DBMS Practical File

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DBMS Practical File

  3. 3. INTRODUCTION TO ORACLECLIENT SERVER COMPUTING ARCHITECTURE It consists of two or more computers designated as client machine runningan application program which communicates with remote computer designated as server machine whichserves request from client machine. In basic model of client server computing, RDBMS resides onserver machine. The application program which resides on client machine interfaces with client softwarecalled middleware that are responsible for communicating request & results between their applicationprograms and RDBMS. CLIENTS CLIENTS LAN / WAN CLIENTS RDBMS SERVER DATA PRINTERS STORAGECLIENT The Client is the front END application of a database which interactswith the server. The Client has more responsibility for accessing the data, it concentrates on the requests.The processing and presentation is managed by the server.SERVER The Server executes the Oracle software and these with the function required for simultaneousand shared data excess. The server receives and processes the SQl and PL/SQL declaration and thatoriginates in the client application. ***** 3 *****
  4. 4. There are two types of Client Server Model are  Two tier Client Server Model  Three tier client Server Model  Two tier Client Server Model: It improves the scalability by allowing upto 100’s of user and is very flexible for data sharing. Client requests services whereas the server it provides its services. There is one limitation of this tier i.e. the design of this architecture scales up. There are three components of client of this tier:  User System interface  Processing Management  Database Management Three Tier Client Server Model: When the less software is on the client, there is less worry about security. Since the importance software is on a server and in a more controlled environment. The support and installation cost of maintaining the software on a single server is much less than trying to maintain the same software on 100’s of PC’s.ADVANTAGES OF CLIENT SERVER MODEL  It allows the user to work in extensible form.  It can work on any type of operating system eg. UNIX, LINUX, Win 98.  It provides the facility to establish the link between remote databases.  It provides the facility of fast accessing of information and processing of data.  Better application performance and network usage i.e. it reduces the network time.  It is multiplatform and centralized.  Distributed computing as the servers act as a focal point for data management.  Provides flexibility and full utilization of all resources.  The same database is shared by different clients.DISADVANTAGES OF CLIENT SERVER MODEL  Bottleneck: If a significant portion of application layer is moved to a server, the server may become a bottle neck in the processing and distribution of data to the client  Server limited resources will be in over higher demanding by the increasing no. of resource consumers.  Security features: It has to take care of the security of the database from unauthorized access. ***** 4 *****
  5. 5. ORACLE Oracle is one of the powerful RDBMS product that provide efficient solutions for databaseapplications. Oracle is the product of Oracle Corporation which was founded by LAWRENCEELLISION in 1977. The first commercial product of oracle was delivered in 1970. The first version oforacle 2.0 was written in assembly language. Nowadays commonly used versions of oracle areORACLE 8, 8i & 9i Oracle 8 and onwards provide tremendous increase in performance, features andfunctionality.FEATURES OF ORACLE  Client/Server Architecture  Large database and Space Management  Concurrent Processing  High transaction processing performance  High Availability  Many concurrent database users  Controlled availability  Openness industry standards  Manageable security  Database enforced integrity  Distributed systems  Portability  CompatibilityORACLE SERVER TOOL Oracle is a company that produces most widely used server based multi-user RDBMS. Oracleserver is a program installed on server hard-disk drive. This program must be loaded in RAM to that itcan process the user requests. Oracle server takes care of following functions. Oracle server tools arealso called as back end. Functions of server tool:  Updates the data  Retrieves the data sharing  Manages the data sharing  Accepts the query statements PL/SQL and SQL ***** 5 *****
  6. 6.  Enforce the transaction consistencyORACLE CLIENT TOOL Once Oracle engine is loaded into sever memory userwould have to log in to engine in order to work done. Client tools are more useful in commercialapplication development. It provides facilities to work on database objects. These are more commonlyused in commercial applications. Oracle client tools are also called front end.DDL – DATA DEFINATION LANGUAGE The SQL sentences that are used to create these objects are calledDDL’s or Data Definition Language. The sql provides various commands for defining relation schemas,deleting relations, creating indexes and modify relation schemas. DDL is part of sql which helps a userin defining the data structures into the database. Following are the various DDL commands are Alter table & Create table & drop table Create index & drop index Create view & drop viewDML – DATA MANIPULATION LANGUAGE The SQL sentences used to manipulate data within these objects are called DML’s orData Manipulation Language. It is language that enables users toaccess or manipulate data as organized by appropriate data model. By data manipulation we have  Retrieval of information stored in database.  Insertion of new information into database.  Deletion of information from database.  Modification of data stored in database.Two types of DML are  Procedural DML  Non-procedural DMLFollowing are DML commands are  Select  Update  Delete  Insert ***** 6 *****
  7. 7. DCL – DATA CONTROL LANGUAGE The SQL sentences, which are used to control the behavior ofthese objects, are called DCL’s or Data Control Language. It is language used to control data and accessto the database. Following are some DCL commands are  Commit  Rollback  Save point  Set transaction DATA TYPES OF SQL  CHAR : This data type is used to store character strings values of fixed length. The size in brackets determines the number of characters the cell can hold. The maximum number of characters (i.e. the size) this data type can hold is 255 characters. Syntax is CHAR(SIZE) ***** 7 *****
  8. 8. Example is CHAR (20)  VARCHAR : This data type is used to store variable length alphanumeric data. The maximum this data type can hold is 4000 characters. One difference between this data type and the CHAR data type is ORACLE compares VARCHAR values using non-padded comparison semantics i.e. the inserted values will not be padded with spaces. Syntax is VARCHAR(SIZE) Example is VARCHAR (20) OR VARCHAR2 (20)  NUMBER : The NUMBER data type is used to store numbers (fixed or floating point). Numbers of virtually any magnitude maybe stored up to 38 digits of precision. Numbers as large as 9.99 * 10 to the power of 124, i.e. followed by 125 zeros can be stored. The precision, (P), determines the maximum length of the data, whereas the scale, (S), determines the number of places to the right of the decimal. If scale is omitted then the default is zero. If precision is omitted values are stored with their original precision up to the maximum of 38 digits. Syntax is NUMBER (P, S) Example is NUMBER (10, 2)  LONG : This data type is used to store variable length character strings containing up to 2GB. LONG data can be used to store arrays of binary data in ASCII format. LONG values cannot be indexed, and the normal character functions such as SUBSTR cannot be applied to LONG values. Syntax is LONG (SIZE) Example is LONG (20)  DATE : This data type is used to represent data and time. The standard format id DD-MM-YY as in 13-JUL-85. To enter dates other than the standard format, use the appropriate functions. Date Time stores date in the 24-hour format. By default, the time in a date field is 12:00:00 am, if no time portion is specified. The default date for a date field is the first day of the current month. Syntax is DATE  LONG RAW : LONG RAW data types are used to store binary data, such as Digitized picture or image. Data loaded into columns of these data types arestored without any further conversion. LONG RAW data type can contain up to 2GB. Values stored incolumns having LONG RAW data type cannot be indexed. Syntax is LONGRAW (SIZE) ***** 8 *****
  9. 9.  RAW : It is used to hold strings of byte oriented data. Data type can have a maximum length of 255 bytes. Syntax is RAW(SIZE)TRANSACTION STATEMENTS COMMIT: A COMMIT ends the current transaction and makes permanent any changes made during the transaction. All transactional locks acquired on tables are released. Syntax is COMMIT [work] [comment text]; Where Work is optional and comment text is used to specify comment ROLLBACK : A ROLLBACK does exactly the opposite of COMMIT. It ends the transaction but undoes any changes made during the transaction. All transactional locks acquired on tables are released. Syntax is ROLLBACK [WORK] [TO [SAVEPOINT] save point] Where WORK is optional and is provided for ANSI compatibility. SAVEPOINT is optional and is used to rollback a partial transaction, as far as the specified save point. SAVEPOINT is a save point created during the current transaction. SAVEPOINT : SAVEPOINT marks and saves the current point in the processing of a transaction. When a SAVEPOINT is used with a ROLLBACK statement, parts of a transaction can be undone. An active save point is one that is specified since the last COMMIT or ROLLBACK. Syntax is SAVEPOINT savepointname; Where Save point is an identifier and it is not to declared in declare section. ***** 9 *****
  10. 10. SQL COMMANDS CREATE TABLE: A table is basic unit of storage. It is composed of rows and columns. To create a table we will name the table and the columns of the table. We follow the rules to name tables and columns:-  It must begin with a letter and can be up to 30 characters long.  It must not be duplicate and not any reserved word. Syntax to create a table is CREATE TABLE tablename (column_name1 datatype (size), column_name2 datatype (size) …); Example is CREATE TABLE student (rollno number (4), name varchar2 (15)); ***** 10 *****
  11. 11.  SELECT : The select command of sql lets you make queries on the database. A query is a command that is given certain specified information from the database tables. It can be used to retrieve a subset of rows or columns from one or more tables. Syntax to create a table is SELECT <column_name1>,<column_name2> FROM <tablename>; Example is SELECT empno, ename, sal from emp; CREATE TABLE FROM ANOTHER TABLE : We can create a table by applying as subquery clause from another clause. It will create the table as well as insert the rows returned from subquery. Syntax to create table from another table is CREATE TABLE tablename(<column1>,<column2>,……) AS SELECT <column1>,<column2> FROM <tablename>; Example is CREATE TABLE stud(empno,ename,salary) AS SELECT empno,ename,sal FROM emp; ALTER TABLE : After creating a table one may have need to change the table either by add new columns or by modify existing columns. One can do so by using alter table command. Syntax to add a column is ALTER TABLE tablename ADD(col1 datatype,col2 datatype); Syntax to modify a column is ALTER TABLE tablename MODIFY(col1 datatype,col2 datatype); DROP TABLE : To remove the definition of oracle table, the drop table statement is used. Syntax to drop table is DROP TABLE tablename RENAME : One can change the name of a table by rename command Syntax to rename table is RENAME oldname TO newname DELETE : One can delete data fron table by using delete from statement. The delete statement removes rows from table but it doesn’t release storage space. Syntax of delete rows from table is ***** 11 *****
  12. 12. DELETE FROM tablename WHERE <condition>; DESCRIBE : To find information about columns like column name, their data types and other attributes of a table we can use DESCRIBE command. Syntax to describe table is DESCRIBE tablename; INSERT : To add new rows in an existing oracle table the insert command is used. Syntax to add new fields is INSERT INTO tablename(col1,col2,col3,..) VALUES(value1,value2,value3); Example is INSERT INTO employee(emp_id,ename,desg,basic_pay) VALUES(100001,’MOHIT’,’MANAGER’,55000); UPDATE : The update command enables user to change the values of existing rows. Syntax to update value of table is UPDATE tablename SET col1=value1,col2=value2; Example is UPDATE emp_info SET salary =salary +100; DISTINCT CLAUSE : The distinct keyword duplicates all rows from results of a select statement. Syntax to remove distinct rows is SELECT DISTINCT <col1>,<cols2> FROM tablename; Example is SELECT DISTINCT job FROM emp; WHERE CLAUSE : The where clause specifies the criteria for selection of rows to be returned. Syntax is SELECT <col1>,<col2> FROM tablename WHERE <cond>; Example is SELECT ename,sal FROM emp WHERE sal > 2000; ORDER BY CLAUSE : You can sort the results of query ina specific order using order by clause. It allows sorting of query results by one or more columns. It can be done either in ascending or descending. Syntax to sort result of query is ***** 12 *****
  13. 13. SELECT * FROM tablename ORDER BY col1,col2,col3; Example is SELECT * FROM emp ORDER BY ename desc; GROUP BY CLAUSE : The group clause is sued in select statement to divide the table into groups. Grouping can be done by column name or wih aggregate functions in which case the aggregate producing a value for each group. Syntax is SELECT col1,col2 FROM tablename GROUP BY <col>; Example is SELECT deptt,avg(salary) FROM emp_infoGROUP BY deptt; HAVING CLAUSE : The having clause filters the group values created by group by clause. This clause can precede the group by clause but it is more logical if we place group by first. Syntax is SELECT col1,col2 FROM tablename GROUP BY <col> HAVING <condition>; Example is SELECT deptt,max(salary) FROM emp_info GROUP BY deptt HAVING max(salary) > 12000; IN: In operator is used to check a value as search from a domain of multiple values to perform a query. Not In acts as reverse of In. Syntax is SELECT <col1>,<col2> FROM tablename WHERE <col> IN (value1,value2,value3); Example is SELECT ename,address,city,state FROM employee WHERE deptt IN (‘comp’,’electronics’,’english’); ALL : It retains duplicate output rows. All is essentially a clarifier rather than a functional argument. Syntax is SELECT ALL <column1>,<column2> FROM <tablename>; ***** 13 *****
  14. 14. Example is SELECT ALL city FROM suppliers;SET OPERATORS Set keywords are used to combine information of similar typefrom one or more than one table. Set operations and the operators are based on set theory. It consumestwo or more queries into one result. The types of set operators are:-  UNION : The union clause merges the outputs of multiple queries into a single set of rows and columns. It combines rows returned by two select statements by eliminating duplicate rows. Syntax is SELECT <statement> UNION SELECT <statements>; Example is SELECT designation FROM emp_info WHERE deptt=’comp’ UNION SELECT designation FROM emp_info WHERE deptt=’eco’;  INTERSECT : The intersect operator combines two select statements and return only those rows that are returned by both queries. Syntax is SELECT <statement> INTERSECT SELECT <statements>; Example is SELECT designation FROM emp_info WHERE deptt=’comp’ INTERSECT SELECT designation FROM emp_info WHERE deptt=’eco’;  MINUS : It combines the result of two queries and returns only those values that are selected by first query but not in second query. Syntax is SELECT <statement> MINUS SELECT <statements>; Example is SELECT desgination FROM emp_info WHERE deptt=’comp’ MINUS SELECT desgination FROM emp_info WHERE deptt=’eco’; ***** 14 *****
  15. 15. ENHANCING PERFORMANCEViews : A view is very commonly used database object that is derived at runtime. A view contains dataof its own. Its contents are derived from another table. The command for creating view is CREATEVIEW command. Editing in the tables are automatically reflected in the views. It is virtual table & doesnot have any data of its own. Syntax to create a view is CREATE [OR REPLACE] VIEW view name AS sub query [WITH CHECK OPTION] [WITH READ ONLY];Example is CREATE VIEW mohit AS SELECT empno, ename, sal, comm FROM emp;Types of views are as follows:  Join View:- It is defined as view that has more than one table specified in from clause and does not contain following clauses i.e. distinct, aggregation, group by. This type of view allows update, insert and delete command to change data in table. Syntax is CREATE OR REPLACE VIEW mohit AS SELECT ename, empno, sal FROM emp, dept WHERE emp.deptno = dept.deptno; ***** 15 *****
  16. 16. The views to be updateable must not include the following are  Set operators , aggregate functions  Distinct operator , rownum pseudo columns  Group by clause , having clause  Inline View: - Oracle also offers an inline view that is very handy and inline view is part of SQL statements. It allows you in body of SQL statement to define SQL for view that SQL statement will use to resolve its query.  Materialized View: - Snapshot also called materialized view. It is defined as copy of part of table or entire table. It reflects the current status of table that is being copied. The original status table is also called master table. Two types are Read only and update. Read-only does not allow changes to be made in view. It simply publishes and subscribes the replications. It allows changes in local copy which periodically updates master table.Sequences : Oracle provides an object called a Sequence that can generatenumeric values. The value generated can have a maximum of 38 digits. A sequence can be defined to  generate numbers in ascending or descending order.  provide intervals between numbers.  Caching of sequence numbers in memory.A sequence is a database object used to generate unique integers for use as primary keys. Syntax is CREATE SEQUENCE sequence name [INCREMENT BY integervalue START WITH integervalue MAXVALUE integervalue / NOMAXVALUE MINVALUE integervalue / NOMINVALUE CYCLE / NOCYCLE CACHE integervalue / NOCACHE ORDER / NOORDER]Example is CREATE SEQUENCE mohit INCREMENT BY 1 START WITH 1 MINVALUE 1 ***** 16 *****
  17. 17. MAXVALUE 9999 CYCLE;Indexes : Index is a way to store and search records in the table. These are used to improve the speed withwhich records can be located and retrieved from the table. Oracle retrieves rows in table in one of twoways are:  By ROWID  By full table scanThe creation and dropping of index doesn’t affect the storage of data in the underlying tables.Indexes are primarily used for 2 reasons are:  To ensure the uniqueness of the indexed column’s values.  To enhance performance.Syntax to create an index is CREATE INDEX <index name> ON <tablename>(column name);Syntax to drop an index is DROP INDEX <index name>;The types of indexes are:-  UNIQUE : It doesn’t allow duplicate values for indexed columns. Example is CREATE UNIQUE INDEX mohit ON EMP (ename);  DUPLICATE : It allows duplicate values for indexed columns. Example is CREATE DUPLICATE INDEX mohit ON EMP (ename);  COMPOSITE : multi column indexes. Example is CREATE UNIQUE INDEX mohit ON EMP (ename, sal);  FUNCTIONAL : perform some functions on fields and then indexes it. Example is CREATE INDEX mohit ON EMP (sal+100); ***** 17 *****
  18. 18. GRANTING AND REVOKING PERMISSIONS GRANT : The Grant statement provides various types of access to database objects such as tables, views and sequences. A privilege is consent to execute an action or to access another user object. These consents can be given by grant statement. Syntax is GRANT {object privileges} ON object name TO username [WITH GRANT OPTION]; The WITH GRANT OPTION allows the grantee to in turn grant object privileges to other users.Object privileges Each object privileges that is granted authorizes the grantee toPerform some operation on the object. The user can grant all the privileges or grant only specific objectprivileges.ALTER allows the grantee to change the table definition with the. ALTER TABLE command.DELETE allows the grantee to remove the records from the table with the DELETE command.INDEX allows the grantee to create an index on the table with the ***** 18 *****
  19. 19. CREATE INDEX command. INSERT allows the grantee to add records to the table with the INSERT Command. SELECT allows the grantee to query the table with the SELECT Command. UPDATE allows the grantee to modify the records in the tables with the UPDATE command. Example to grant select & insert privileges on table item to user named as mohit. GRANT SELECT, INSERT ON item TO mohit; Example to grant all privileges on table EMP to user named as chiku. GRANT ALL ON EMP TO mohit; REVOKE : Privileges once given can be denied to a user using the REVOKE command. The object owner can revoke privileges granted to another user. A user of an object who is not the owner, but has been granted the GRANT privilege, has the power to REVOKE the privileges from a grantee. The REVOKE statement is used to deny the grant given on an object. Syntax is REVOKE {object privileges} ON object name FROM username; Example to revoke select & insert privileges on table item to user named as mohit. REVOKE SELECT, INSERT ON item TO mohit; Example to revoke all privileges on table EMP to user named as chiku. REVOKE ALL ON EMP TO mohit; PATTERN MATCHING SQL includes string matching operator LIKE for comparison on character string using patterns. The LIKE predicate allows for a comparison of one string with another string value, which is not identical. This is achieved by using wildcard characters. The patterns are case ***** 19 *****
  20. 20. sensitive and that is uppercase letters do not match lower case characters. The keyword NOT LIKE isused to select those rows that do not match the specified pattern of characters.Two wildcard characters that are available are:For character data types: The percent sign (%) matches any string The Underscore (_) matches any single characterExample is SELECT * FROM EMP WHERE ename LIKE ‘_B%’; SELECT * FROM EMP WHERE ename LIKE ‘MOH__’;RANGE SEARCHING BETWEEN operator acts as range searching operator. To get a range ofvalues from a query, you may use between operators. You must specify the lower and upper limit forrange search. Syntax is SELECT <col1>,<col2> FROM table name WHERE <col> BETWEEN lower limit and upper limit;Example is SELECT empname, deptt, basic pay FROM employee WHERE basic pay BETWEEN 5000 and 10000; ***** 20 *****
  21. 21. JOINS A JOIN can be recognized in sql select statement if its has more than one table after fromkeyword. This join condition is based on primary keys and foreign keys. There must be n-1 joinconditions for n joins to tables. If join condition is omitted then the result is Cartesian product.Syntax is SELECT “list of columns” FROM table1, table2 WHERE “condition”;Types of joins are  Equi join : It returns all rows from tables where there is a match. Tables are joined on columns that have the same datatype & size in table. It is also known as equality join or simple join or inner join. Syntax is SELECTfield1,field2 FROM table1,table2 WHERE table1.field=table2.field; Example is SELECTename, dname FROM emp, dept WHERE emp.deptno=dept.deptno;  Cartesion join : When the join condition is omitted the result is Cartesian join of two or more tables in which all the combinations of rows will be displayed. All the rows are joined to all rows of the second table. Syntax is SELECT field1, field2 FROM table1, table2; Example is SELECTename, dname FROM emp, dept; ***** 21 *****
  22. 22.  Outer join : While using equi join we see that if there exists certain rows in one table which don’t have corresponding values in the second table thn those rows will not be selected. We can forcefully select those rows by outer join. The rows for those columns will have NULL values. Syntax is SELECT table1.col, table2.col FROM table1, table2 WHERE table1.col (+) = table2.col; Example is SELECT empno, ename, emp.deptno, dname FROM emp, dept WHERE emp.deptno (+) = dept.deptno;  Self Join : The self join can be seen as join of two copies of the same table. The table is not actually copied but sql performs the command as though it were. Example is SELECT e.ename, m.ename FROM emp e, emp m WHERE e.mgr=e.empno;SUBQUERIES A sub query is a form of an SQL statement that appears inside another SQLstatement. It is also termed as nested query. The statement containing a sub query is called a parentstatement. The parent statement uses the rows returned by the sub query. It can be used by the followingcommands:  To insert records in a target table.  To create tables and insert records in the table created.  To update records in a target table.  To create views.  To provide values for conditions in WHERE, HAVING, IN etc. used with SELECT, UPDATE, and DELETE statements.Types of sub queries are  Single row : It returns one row from inner nested query. Example is SELECT deptno FROM emp WHERE ename =’MILLER’;  Multiple row : Subqueries that return more than one row called multiple row queries. Operators like IN,ALL,ANY are used. Example is ***** 22 *****
  23. 23. SELECT ename,sal,deptno FROM emp WHERE sal IN (SELECT min(sal) FROM emp GROUP BY deptno);  Multiple column : It returns more than one column .Example is SELECT ordid , prodid , qty FROM item WHERE (qty,prodid) IN (SELECT prodid,qty FROM item WHERE ordid = 605 AND ordid <> 605); CONSTRAINTS Constraints are the rules that restrict the data values inserted in columnsof a table. It helps in maintaining integrity of table at database level instead of application level. All applicatcan take advantage of these global constraints, rather than building similar logic in individual applicatiConstraints can constrain single column or group of columns in a table. Constraints can be specified as two typ  Column level constraint  Table level constraintColumn level constraint : Column constraints are specified as part of columndefinition to constrain single column.Table level constraint : Table constraints is specified at end of create tablestatement to constraint more than one column.Following are the constraints used in tables are NULL/NOT NULL : Specifies if the column must contain value or might not contain any. By default all columns in a table allows nulls, ie. Absence of a value in a column. NOT NULL specifies that all rows in the table to have value for specified column. All NOT NULL columns are mandatory fields. Syntax is COLUMN_NAME DATA_TYPE(SIZE) NOT NULL Example is CREATE TABLE employee(empname varchar2(25) NOT NULL) ; ***** 23 *****
  24. 24.  UNIQUE : Specifies that all values in a column must be unique. Values in field cannot be duplicated. More than one Null value can be inserted in the column. Unique constraint can be placed on multiple columns. Syntax is COLUMN_NAME DATA_TYPE(SIZE) UNIQUE -- at column level UNIQUE COLUMN_NAME DATA_TYPE(SIZE) -- at table level Example is CREATE TABLE dept(deptt varchar2(25) UNIQUE); CREATE TABLE dept(deptt varchar2(25),UNIQUE(dept)); PRIMARY KEY : Primary key refers to one or more column values in a table that can uniquely identify each row in a table. A primary key column cannot contain nulls and is unique by default. Syntax is COLUMN DATA_TYPE(SIZE) PRIMARY KEY -- at column level PRIMARY KEY COLUMN DATA_TYPE(SIZE) -- at table level Example is CREATE TABLE dept(deptt varchar2(25) PRIMARY KEY); CREATE TABLE dept(deptt varchar2(25),PRIMARY KEY(dept)); FOREIGN KEY : A foreign key is a one or more column with values based on the primary key values from another table. A foreign key constraint specifies that the values stored in foreign column correspond to values of the primary key in the other table. Foreign key is also known as referential integrity constraint. The table containing foreign key is known as Dependent table and the table that is referenced by foreign key is called Referenced table. Syntax is COLUMN DATA_TYPE(SIZE) REFERENCES TABLE -- at column level FOREIGN KEY COLUMN DATA_TYPE(SIZE) REFERENCES TABLE Example is CREATE TABLE dept(deptt varchar2(25) REFERENCES emp_info); CREATE TABLE dept(deptt varchar2(25),PRIMARY KEY(dept) FOREIGN KEY(dept) REFERENCES emp_info); ***** 24 *****
  25. 25. FUNCTIONS Functions make the result of the query easier and are used to manipulate the data values.Following are the functions are  String or character functions  Number functions  Aggregate functions or group functions  Date functions  Conversion functionsCharacter Manipulation functions  Ascii : It returns the ASCII decimal equivalent of a character passed as an argument. Example is select ascii(‘b’)from dual;  Chr : This function gives the result as a character corresponding to the value in the database set. Example is select char (97) from dual;  concat(x1,x2) : This function concates the string x1 with x2. This function is equivalent to the | | operator. Examples select concat(‘mohit’,’garg’)from dual;  instr :This function returns the first position of the character x in the string. Example is select instr(‘mohit’,’o’) from dual;  length : It returns the length of the string x. Example is select length (‘mohit’) from dual; ***** 25 *****
  26. 26.  lpad : It pads the leading spaces to the left side of the column char1 with the char2, so that the total width becomes equal to the value n. If char2 is absent, it pads the char1 on the left side with blank spaces to the total width of n. Example is select lpad(dname,12,’*’) from dept; Ltrim : It removes all the blank spaces from the left side of the stringif no char is specified. If we give a char, then it removes the leading occurrences of that charcter from the string. Example is select ltrim(dname.’S’) from dept; Rpad : This function pads the leading spaces to the right side of the column char1 with the char2, so that the total width becomes equl to the value n. Example is select rpad(dname,12,’*’)from dept; Rtrim : This function removes all the blank spaces from the right side if no char is specified. Example is select rtrim(dname,’S’) from dept; Replace : Where c1,c2,c3 and c3 are all character string .this function returns c1 with all occurenes of c2 replaced with c3, the default value of c3 is NULL. Example is select replace (uptown,’up’,down’)from dual; Substr : It returns the substring from z, of length equal to y starting at position x . Example is select substr(‘mohitgarg’2,5) from dual; Initcap : This function returns the string with letter in caps. Example is select initcap (dname) from dept; Lower : This function converts the string into lower case. Example is select lower (dname)from dept; Upper : It converts the string into upper case. Example is select upper(dname)from dept; ***** 26 *****
  27. 27.  Translate : This function is used to find a char and replace it with new character. Example is select dname, translate (dname,’E’,2) from dept;Group functions  Count : This function returns the number of rows or non-null values for column x. Syntax is count([distinct|all]column name) Example is select count(empno)from emp;  Sum : This function ireturns the sum of values for the column x. This function is applied on columns having numeric datatype and it returns the numeric value. Syntax is sum([distinct|all]column name) Example is select sum(sal) from emp;  Avg : Ths function returns the average of values for the column x. It ignores the null values in the column x. Syntax is avg([distinct|all]column name) Example is select avg(sal),count(sal) from emp;  Min : This function returns the minimum of values for the column x for all the rows. Syntax is min([distinct|all]column name) Example is select min(sal) from emp;  Max : This function returns the maximum of values for the column x for all the rows. Syntax is max([distinct|all]column name) Example is select min(sal),max(sal) from emp;Number functions  Abs : It obtains the absolute value for the number x. Example is Select abs(-10) from dual;  Ceil : Where is a number. This function returns the smallest integer that is greater than or equal to n. Example is select ceil (9.8), ceil (-32.85) from dual; ***** 27 *****
  28. 28.  Cos : It returns trigonometric cosine of the number n. Example is select cos(45) from dual; Exp : It returns the e raised to the x power. Example is select exp (4) from dual; Floor : This function returns the largest integer that is less than or equal to n. Example is select floor (9.8), floor (-32.85) from dual; Mod : It returns the remainder when x is divided by the number y. Example is select mod (10.3),mod (10.5)from dual; Power : This function returns the value of x raised to the power of y. The argument y should be an integer. Example is select power (2, 3) from dual; Round : It rounds off x to the decimal precision of y. If y is negative, rounds to the precision of y places to the left of the decimal point. Example is select round (55.849,1 ), round(55.849) from dual; Sign : This function returns the sign of the value x. If x is a negative number it returns -1 otherwise it returns 1. Example is select sign (-2) from dual; Sqrt : This function returns the square root of the given number x. Example is select sqrt(36) from dual; ***** 28 *****
  29. 29. Date functions  Add_months : It adds the months in specified date with the function. Syntax is ADD_MONTHS(date,m) where date refers to date & m is number value. Example is select add_months(sysdate,2) from dual;  Last_day : It returns the last day of given month which is specified with function. Syntax is LAST_DAY(d) where d is date Example is select last_day(sysdate) from dual;  Months_between : It computes & returns the number of months b/w two dates. Syntax is MONTHS_BETWEEN(date1,date2) Example is select months_between(’13-mar-05’,’01-dec-05’) from dual;  Next_day : It returns the date of first day of the week specified in a string after the beginning date. Syntax is NEXT_DAY(date,ch) where ch refers to character value. Example is select next_day(’13- mar-05’,’sunday’) from dual; ***** 29 *****


Art Print

Captain Lazarus

by Jessica Beebe - Photography

The Captain has been on the high seas for so long, he can't even walk on land anymore. Some say he has an enchanted pipe that does his bidding, others say, he has an octopus in place of an eye. Regardless, he was a fun project that let me play with some new techniques.

people photography humor


Scientific Publications

Sequencing the nuclear genome of the extinct woolly mammoth.

Publication TypeJournal Article
AuthorsMiller, W., Drautz DI, Ratan A., Pusey B., Qi J., Lesk AM, Tomsho LP, Packard MD, Zhao F., Sher A., Tikhonov A., Raney B., Patterson N., Lindblad-Toh K., Lander E. S., Knight JR, Irzyk GP, Fredrikson KM, Harkins TT, Sheridan S., Pringle T., and Schuster SC
AbstractIn 1994, two independent groups extracted DNA from several Pleistocene epoch mammoths and noted differences among individual specimens. Subsequently, DNA sequences have been published for a number of extinct species. However, such ancient DNA is often fragmented and damaged, and studies to date have typically focused on short mitochondrial sequences, never yielding more than a fraction of a per cent of any nuclear genome. Here we describe 4.17 billion bases (Gb) of sequence from several mammoth specimens, 3.3 billion (80%) of which are from the woolly mammoth (Mammuthus primigenius) genome and thus comprise an extensive set of genome-wide sequence from an extinct species. Our data support earlier reports that elephantid genomes exceed 4 Gb. The estimated divergence rate between mammoth and African elephant is half of that between human and chimpanzee. The observed number of nucleotide differences between two particular mammoths was approximately one-eighth of that between one of them and the African elephant, corresponding to a separation between the mammoths of 1.5-2.0 Myr. The estimated probability that orthologous elephant and mammoth amino acids differ is 0.002, corresponding to about one residue per protein. Differences were discovered between mammoth and African elephant in amino-acid positions that are otherwise invariant over several billion years of combined mammalian evolution. This study shows that nuclear genome sequencing of extinct species can reveal population differences not evident from the fossil record, and perhaps even discover genetic factors that affect extinction.
Year of Publication2008
Date Published (YYYY/MM/DD)2008/11/20
ISSN Number0028-0836


Shenmue HD is Finished, Claims Report

Source claims it's coming to XBLA and PSN.

A new report is claiming that Sega has been sitting on finished HD remakes of Shenmue and Shenmue II for over a year, waiting for an apt release window.

GamerZines cites a person with "ties to Sega" as the source of this information. "Shenmue HD is real [and has been] finished for well over a year, as is Shenmue II HD," says the source.

The reason for the delay, evidently, has been uncertainty over the series' future and whether Shenmue III would ever happen (short answer: no). The HD remakes are reportedly headed to PSN and XBLA.

With Jet Set Radio heading to Xbox Live, and re-releases (not remakes) of Sonic Adventure, Space Channel 5 and Crazy Taxi already widely available, it's not absolutely out of the question that Shenmue I and II might make their way to modern consoles after all. Shenmue II was remade for the original Xbox in 2002 following a Dreamcast release the previous year.

In their day, the Shenmue games were amongst the most ambitious video games ever made, featuring huge, living cities - Sega's Yakuza series is often considered their spiritual successor. If an HD remake does indeed exist, would Shenmue stand the test of time?


The bones’ cut marks do not fit hoof, claw, or tooth damage, but look like parallel grooves made by multiple slices with a stone knife. Researchers verified the marks–along with “percussion marks” evidently left by someone trying to break the bone open for its marrow–by electron microscopy.

The oldest tools had previously been dated at 2.6 million years. But these bones, likely the rib of a hoofed mammal and the thigh bone of a smaller animal, were dated “as long ago as 3.4 million years.”1

This presents a huge problem, since evolutionary history held for decades that man did not evolve until 2.5 million years ago. Prior to that time, only ape-like creatures like “Lucy,” which hypothetically later “give rise” to humans, were supposed to have existed.

Rather than do the work of reorganizing–yet again–the evolutionary story about which ape supposedly evolved into man and when, anthropologists have interpreted this new evidence with a predictably evolution-friendly spin. Instead of being the work of actual people, known to possess foresight and purpose, the butchering of these animals was supposedly accomplished by “early hominins” resembling Lucy.3

In contrast, the creation model does not restrict man’s presence to a truncated time in earth’s history. Because mankind has been living alongside all animals since the creation week was completed, the discovery of fully human artifacts–like footprints and tool marks–from these post-Flood deposits fits perfectly well with creation thinking.

  3. “This, he says, means that early hominins–presumably Australopithecus afarensis–were not only using tools, but also venturing out of the safety of the forests and onto the plains in search of meat.” Shannon McPherron, cited in Lovett, Butchering dinner 3.4 million years ago.

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The human sympathetic nervous system: its relevance in hypertension and heart failure

Gianfranco Parati, Murray Esler
DOI: http://dx.doi.org/10.1093/eurheartj/ehs041 1058-1066 First published online: 16 April 2012

Evidence assembled in this review indicates that sympathetic nervous system dysfunction is crucial in the development of heart failure and essential hypertension. This takes the form of persistent and adverse activation of sympathetic outflows to the heart and kidneys in both conditions. An important goal for clinical scientists is translation of the knowledge of pathophysiology, such as this, into better treatment for patients. The achievement of this ‘mechanisms to management’ transition is at different stages of development with regard to the two disorders. Clinical translation is mature in cardiac failure, knowledge of cardiac neural pathophysiology having led to the introduction of beta-adrenergic blockers, an effective therapy. With essential hypertension perhaps we are on the cusp of effective translation, with recent successful testing of selective catheter-based renal sympathetic nerve ablation in patients with resistant hypertension, an intervention firmly based on the demonstration of activation of the renal sympathetic outflow. Additional evidence in this regard is provided by the results of pilot studies exploring the possibility to reduce blood pressure in resistant hypertensives through electrical stimulation of the area of carotid baroreceptors. Despite the general importance of the sympathetic nervous system in blood pressure regulation, and the specific demonstration that the blood pressure elevation in essential hypertension is commonly initiated and sustained by sympathetic nervous activation, drugs antagonizing this system are currently underutilized in the care of patients with hypertension. Use of beta-adrenergic blocking drugs is waning, given the propensity of this drug class to have adverse metabolic effects, including predisposition to diabetes development. The blood pressure lowering achieved with carotid baroreceptor stimulation and with the renal denervation device affirms the importance of the sympathetic nervous system in hypertension pathogenesis, and perhaps suggests a wider role for anti-adrenergic antihypertensives, such as the imidazoline drug class (moxonidine, rilmenidine) which act within the CNS to inhibit central sympathetic outflow, although the lack of large-scale outcome trials with this drug class remains a very material deficiency.

  • Chronic heart failure
  • Arterial hypertension
  • Sympathetic activity
  • Arterial baroreflex
  • Microneurography
  • Catecholamines
  • Baroreceptor stimulation
  • Renal denervation
  • Beta-blockers

Willis, in 1664, provided the first anatomically correct depiction of the sympathetic nervous system.1 Histological examination two centuries later demonstrated dense innervation of walls of blood vessels, leading Stelling in 18402 to correctly conclude that the vasomotor fibres were in sympathetic nerves carried from the central nervous system. In the mid-nineteenth century, building on these observations, Brown-Sequard, Waller, and Bernard2 laid the foundation for modern concepts of neural circulatory control, through demonstration of vasoconstriction with electrical stimulation of the cut nerves, and vasodilatation on the nerve section, which indicated that sympathetic fibres exerted a tonic, vasoconstrictor influence.

The sympathetic nervous system was brought to public awareness in the early decades of the twentieth century by Cannon, through his research on, and popularization of the concept of the ‘fight and flight’ response to stress.3 In the past three decades, the sympathetic nervous system has moved towards centre stage in cardiovascular medicine, with demonstration of the importance of aberrations of the sympathetic nervous system in heart failure, essential hypertension, disorders of postural circulatory control causing syncope, and ‘psychogenic heart disease’, heart disease attributable to mental stress and psychiatric illness.4

This review makes the claim that sympathetic nervous system activation is important in heart failure and hypertension, but in contrasting ways. In heart failure, sympathetic activation occurs subsequently to the development of the heart failure, and then impacts adversely on the clinical outcome. In essential hypertension the causal chain is different, with sympathetic nervous system activation being important in the initiation, and then maintenance of the hypertension, on the background of a complex interaction between multiple other mechanisms. Despite these differences, the sympathetic nervous system becomes a ‘culprit’, and therapeutic target in both conditions. Clinical translation of these concepts is mature in cardiac failure, knowledge of cardiac neural pathophysiology having led to introduction of beta-adrenergic blockers, an effective therapy. With essential hypertension, the positive results obtained with more recently developed beta-adrenergic receptor blockers, and recent successful testing of a device for electrical carotid baroreceptor stimulation as well as of selective catheter-based renal sympathetic nerve ablation in patients with resistant hypertension, hint at pathophysiology to therapy translation that might occur.

The sympathetic nervous system: methods of measurement

Von Euler5 definitively demonstrated the sympathetic transmitter to be norepinephrine, using bioassay systems allowing comparison of the biological actions of the sympathetic transmitter extracted from tissues with those of epinephrine and norepinephrine. This discovery quickly led to the application of neurochemical methods, initially measurement of norepinephrine excretion in urine, now largely obsolete, in efforts to quantify sympathetic nervous system activity in humans. The development of a sympathetic nerve recording technique applicable to humans (clinical microneurography) in 1968 by Hagbarth and Vallbo6 and the publication of the first sensitive and specific plasma-catecholamine assay, also in 1968, by Engelman et al.7 were subsequent milestones in the field. The application of these neurophysiological and neurochemical methods, and later refinements of them, came to dominate the investigation of sympathetic neural mechanisms in clinical research.

An assumption underlying the use of the early neurochemical tests of the sympathetic nervous system was that the sympathetic nervous system acts in a global, undifferentiated fashion. This was in accord with the teaching of Cannon,3 exemplified in his ‘fight and flight’ concept of sympathetic mass action, but is untrue. Sympathetic nervous system responses are often regionalized, activation in one sympathetic outflow commonly being accompanied by no change, or a reduction, in others.8,9 Quantification of individual regional sympathetic nervous outflows can be achieved with the sympathetic nerve recording technique, and by radiotracer-derived measurements of regional norepinephrine spillover to plasma, from individual organs (Figure 1). These methods are complementary; neither is ‘best’. The microneurography method is online, providing instantaneous data on electrical transmission in sympathetic nerves, with multi-unit or single-fibre recordings, but may be open to an investigator bias in case of studies based on manual and not blinded analysis of recordings obtained in small groups of subjects. The regional spillover method provides objective information on neurotransmitter release in individual organs consequent to this firing, including in internal organs for which the nerve recording technique is not applicable. Another commonly used method to explore autonomic cardiovascular modulation is based on computer analysis of heart rate and blood pressure variability. However, while heart rate variability largely reflects selective autonomic control of the heart, blood pressure fluctuations are the result of complex interactions between multiple mechanisms, including cardiac and vascular neural regulation, mechanical influences of ventilation, humoral and endothelial factors, large arteries stiffening, and genetic factors. Nevertheless, when properly applied, methods based on time or frequency domain analysis of either blood pressure or heart rate variability can provide a valuable insight into integrated cardiovascular regulation. The advantages of this approach, in spite of a possible limited specificity in some circumstances, consist in its easy applicability also in daily practice and in the avoidance of any external intervention on subjects under evaluation.10

Figure 1

Sympathetic nervous system responses are often regionalized, activation in one sympathetic outflow commonly being accompanied by no change, or a reduction, in others. Precise quantification of individual regional sympathetic nervous outflows can be achieved with clinical microneurography, a nerve recording technique measuring firing in sympathetic nerves directed to the skeletal muscle vasculature, and by radiotracer-derived measurements of regional norepinephrine spillover to plasma from individual organs not accessible to nerve recording, including the heart and kidneys.

Hagbarth and Vallbo6 in 1968 reported a method for measuring efferent multi-fibre traffic in sympathetic nerves. This technique of clinical microneurography provides a method for studying nerve firing in subcutaneous sympathetic nerves distributed to skin and the skeletal muscle vasculature. Multi-fibre recordings of ‘bursts’ of nerve activity, synchronous with the heart beat, are generated in skeletal muscle vascular efferents. More recently, single fibre sympathetic recording has also been successfully performed in humans.11,12

Noradrenaline spillover

A special impetus to the development of techniques for studying the rates of overflow of noradrenaline to the circulation was provided by the lack of clinical methods for studying sympathetic nervous outflow in humans to otherwise inaccessible organs, such as the heart and kidneys. Measurement of organ-specific norepinephrine release to plasma8,9,13 became the gold standard for doing this. During constant rate infusion of tritiated norepinephrine, outward flux of endogenous norepinephrine from an organ (regional norepinephrine ‘spillover’) can be measured by isotope dilution:Embedded Image where CV and CA are the plasma concentrations of norepinephrine in regional venous and arterial plasma, E is the fractional extraction of tritiated noradrenaline in transit of blood through the organ, and PF is the organ plasma flow.

Heart rate variability, blood pressure variability, and arterial baroreflex sensitivity

Variability in cardiovascular parameters such as blood pressure and heart rate has been shown to reflect the activity of cardiovascular control mechanisms, including sympathetic cardiovascular modulation, both in health and disease.1416 Several methodological approaches are available to this aim, respectively focusing on estimates of blood pressure or heart rate variance, their spectral powers,1416 heart rate turbulence,17 entropy, self-similarity and symbolic logic,18 or on blood pressure–heart rate interactions to quantify the sensitivity of baroreflex control of heart rate (BRS).19,20 Evidence that cardiovascular variability does represent an index of autonomic control of circulation comes from either animal or human studies, the latter performed both in normal subjects and in patients affected by diseases where the autonomic nervous system was primarily or indirectly affected.10

Heart rate variability

Vagal and sympathetic cardiac influences operate on the heart rate in different frequency bands. While vagal regulation has a relatively high cut-off frequency, modulating heart rate both at low and high frequencies, up to 1.0 Hz, sympathetic cardiac control operates only <0.15 Hz.14,21,22 It has to be acknowledged, however, that although heart rate variability is certainly affected by sympathetic cardiac modulation, no individual heart rate spectral component is a specific marker of sympathetic cardiac modulation, because of the interference by other participating factors, including humoral mechanisms, gender, age, respiration and resonance in the baroreflex loop ∼0.1 Hz.23 Normalization of LF powers by total variance, or computation of the LF/HF power ratio, may help increase the reliability of spectral parameters in reflecting sympathetic cardiac modulation.14,15 Recent evidence suggests that also non-linear models for cardiovascular variability analysis, such as heart-rate self-similarity, may reflect autonomic cardiovascular regulation.24 The clinical relevance of the information on autonomic cardiac control provided by heart rate variability parameters is supported by the evidence that reduced heart rate variability and BRS is associated with increased mortality after myocardial infarction as well as in heart failure patients, and with increased risk of sudden arrhythmic death.25

Blood pressure variability

Blood pressure variability increases in conditions characterized by sympathetic activation. Indeed, increased daytime blood pressure variability in humans is associated with an increase in sympathetic efferent traffic in the peroneal nerve.26 When considering blood pressure spectral powers, while HF fluctuations largely depend on the mechanical effects of respiration, LF and VLF powers are predominantly caused by fluctuations in the vasomotor tone and systemic vascular resistance and are influenced by complex interactions between neural, humoral, genetic and endothelial factors, by myogenic tone and by thermoregulation.14 Thus, while blood pressure and heart rate LF powers have been repeatedly suggested as markers of sympathetic cardiovascular control,16 their specificity in this regard is limited.14

Arterial baroreflex sensitivity

The ability of cardiovascular variability to reflect autonomic cardiovascular control is improved by use of multivariate models for its assessment. The simplest ones consider the relationship between spontaneous fluctuations in blood pressure and heart rate, either in the time (sequence technique)19,20 or frequency domain (alpha-coefficient, transfer function analysis) to assess BRS and its modulation in daily life19,27,28 (Figure 2).

Figure 2

Number and slope of +PI/+SBP and −PI/−SBP sequences during each hour of a 24-h intra-arterial ambulatory blood pressure recording (means ± SE) for 10 normotensive (open circle) and 10 hypertensive (closed circle) subjects. (From Ref.20, modified with permission). PI, pulse interval; SBP, systolic blood pressure.

Cardiovascular variability and autonomic cardiovascular regulation

In conclusion, while spontaneous variations in blood pressure and heart rate clearly depend on autonomic mechanisms, caution is needed in taking their assessment as a quantitative index of sympathetic nervous efferent activity to the vessels and the heart. In fact, in a variety of clinical situations, including heart failure, LF heart rate spectral power has little or no relation to rates of noradrenaline spillover from the heart and sympathetic nerve firing quantified by microneurography. Indeed, in heart failure, LF heart rate spectral power is reduced, but cardiac noradrenaline spillover is remarkably increased.29

Heart failure

Sympathetic nervous system activation in heart failure

The contemporary picture of the neural pathophysiology of heart failure emerged slowly over three decades, with the first evidence for activation of the sympathetic nervous system being the finding of increased excretion of noradrenaline in urine.30

Urine and plasma noradrenaline

Noradrenaline in urine derives primarily from two sources, filtration at the glomerulus of noradrenaline in plasma originating systemically from sympathetic nerves, and preferentially, from noradrenaline released within the kidneys by the renal sympathetic nerves. The activation of the renal sympathetic outflow, subsequently demonstrated in cardiac failure,12,31 meant that measurement of the transmitter in urine was well placed to identify the sympathetic activation present. There was an early report of high concentrations in plasma of the sympathetic transmitter,32 but the plasma noradrenaline assays in use at the time were non-specific and unreliable, giving values 5–10-fold higher than those documented later with valid assays.

The modern era commenced when Marks and colleagues,33 applying a newly developed, valid plasma noradrenaline assay, demonstrated elevated plasma concentrations of the transmitter in heart failure patients. But that was not the end of the story; there is a drawback with plasma noradrenaline concentration measurements. The application of isotope dilution methodology with tritiated noradrenaline to heart failure research subsequently demonstrated that the rate of removal of noradrenaline from plasma in heart failure patients is, in fact, slowed due to reduced cardiac output and regional blood flows; the elevation in the plasma concentration of noradrenaline is partly attributable to this reduction in noradrenaline plasma clearance.13 Plasma noradrenaline measurements in fact overestimate the degree of sympathetic nervous activation present in heart failure.

Myocardial β-adrenoceptors

The next milestone was the demonstration by Bristow et al.34 of a reduction in the concentration of adrenoceptors in failing human myocardium, this being selective for β1 adrenoceptors, and excluding β2 adrenoceptors. The results were interpreted by the authors to signify that, most likely, the β1 adrenoceptors, which are in close proximity to sympathetic nerve varicosities, had been selectively down-regulated by increased rates of sympathetic nerve firing and transmitter release in the failing heart. β2 adrenoceptors are extrajunctional and are excluded from this neural influence.34 But a paradox existed, as an earlier, pioneering study by Chidsey et al.35 had demonstrated that the concentration of noradrenaline in failing human myocardium was markedly lowered, which they took to be indicative of the presence of cardiac sympathetic denervation.

Cardiac noradrenaline spillover

This theoretical impasse was overcome with application of regional noradrenaline kinetics methodology, which demonstrated very high rates of noradrenaline spillover from the heart in cardiac failure.13 The low tissue noradrenaline content was misleading; cardiac sympathetic tone is actually remarkably elevated in heart failure patients. Parallel studies demonstrated activation of the sympathetic outflows to the kidneys, evident in high rates of renal noradrenaline spillover,13,31 and to the skeletal muscle vasculature, documented with microneurography.36

Adverse effects of chronic sympathetic activation

Inappropriate and excessive activation of the sympathetic nervous system has been invoked as a cause of heart disease. This pathophysiological linkage can take two forms. The most direct and explicit is when acute sympathetic nervous activation triggers adverse cardiac events (myocardial infarction, atrial fibrillation, ventricular arrhythmias, and Takotsubo cardiomyopathy have all been documented) during acute severe mental stress.37 The case is no less strong that chronic sympathetic activation similarly is adverse. Research in patients with heart failure was central to establishing this principle.

The pivotal observation was made by Cohn et al.,38 who demonstrated that the prevailing plasma concentration of noradrenaline was a predictor of heart failure patient survival, survival being worse at the highest plasma concentrations of the transmitter. Direct demonstration of a strong relation of cardiac sympathetic activity specifically to survival followed in a prospective study, with high sympathetic activity, independent of the severity of the heart failure, causing death both by arrhythmias and by progressive left ventricular failure.39 In a later instructive study, both high cardiac noradrenaline spillover and reduced myocardial noradrenaline stores (measured with radiolabelled noradrenaline) were shown to impact on survival in heart failure, the high cardiac sympathetic activity being linked to risk of death from arrhythmias and reduced myocardial noradrenaline content to death from progressive left ventricular failure.40

Subsequently, when most heart failure patients were under treatment with β-adrenergic blockade, high renal sympathetic activity (gauged from renal noradrenaline spillover measurements) emerged as a predictor of early death.31 Excessive retention of sodium from activation of the renal sympathetic nerves directly innervating the renal tubules41 may be the culprit here. Whether the level of activation in the sympathetic outflow to the skeletal muscle vasculature, which is accentuated when hypertension, obesity, and the metabolic syndrome co-exist with heart failure42,43, also predicts survival in heart failure patients is less clear. In this case, the mechanism by which risk would be conferred is not as obvious as with activation of the cardiac and renal sympathetic outflows. Perhaps the burden of heightened cardiac afterload from skeletal muscle vasoconstriction is important.

Heart rate variability and baroreflex sensitivity

In patients with chronic heart failure heart rate variability and baroreflex sensitivity are markedly reduced, and their reduction has been found to be a predictor of arrhythmic mortality both in univariate and multivariate analysis.44 A few studies on cardiac patients have also suggested a predictive value of heart rate turbulence.45 Finally, when examined in conjunction with depressed LVEF, also BRS contributes to risk stratification.25 In spite of these results, however, the evidence linking impaired short-term HRV to sudden death in heart failure patients is still limited, which implies caution with the clinical use of HRV for arrhythmic risk stratification in these conditions.

Antagonism of sympathetic activation in heart failure

These observations linking sympathetic activation to clinical outcome in heart failure provided the theoretical basis for trials of pharmacological antagonism of the sympathetic nervous system.

Beta-adrenergic blockade

An apparently favourable response to propranolol had been reported in several small series of heart failure patients treated with propranolol in the mid-1970s, but these and subsequent more formal trials remained underpowered to show benefit. Then with the strong theoretical foundation that β1-adrenoceptors were selectively down-regulated in the failing heart, and noradrenaline release from cardiac sympathetic nerves was markedly increased,46 subsequent large, randomized beta-blocker trials followed, demonstrating clear prolongation of survival, with carvediolol,47 metoprolol,48 bisoprolol,49 and nebivolol,50 in turn. Benefit was demonstrated in moderate heart failure, severe heart failure, and heart failure in the elderly. But this is not a ‘class effect’, holding for all beta-blockers. Bucindolol and xamoterol provide no benefit with long-term dosing.51 An explanation lies in the fact that these drugs share the property of possessing intrinsic agonist activity, which causes cardiac adrenergic stimulation.

Central inhibition of sympathetic outflow

A logical extension of these beta-blocker trials was the evaluation of central inhibition of sympathetic outflow in heart failure, which was performed with the imidazoline agent moxonidine.52 Central sympathetic inhibition with moxonidine actually increased mortality in heart failure patients, for uncertain reasons. Whether this was because the central premise that inhibition of central outflow would be beneficial was in fact false, or was due to a faulty trial design, specifically the adoption of a fixed, forced titration to high doses,52 remains an unsettled question.

History: early ideas that essential hypertension might be ‘neurogenic’, the pressure rise being initiated and sustained by the sympathetic nervous system

In the early decades of the twentieth century, faced with the high mortality of severe hypertension, and the absence of effective pharmacological therapy, a number of operations on the sympathetic nervous system were devised in an attempt to lower blood pressure (Figure 3). Notable among these was radical lumbodorsal splanchnicectomy, developed in 1938 by Smithwick,53 which lowered blood pressure and reduced mortality, but at the cost of often incapacitating side effects. By the late 1960s, of the available antihypertensives, which by then had been developed, most antagonized the autonomic nervous system, either generally, with ganglionic blockers, or specifically its sympathetic division, with central sympathetic inhibitors methydopa and clonidine, sympathetic neuronal blockers such as guanethidine, and alpha- and beta-adrenergic blockers. The potency and clinical usefulness of these drugs helped sustain the argument that the sympathetic nervous system was important in the pathogenesis of essential hypertension.

Figure 3

The historical antecedents to the current understanding of the importance of sympathetic nervous system pathophysiology in the pathogenesis of essential hypertension.

For the past three decades, the major focus in high blood pressure research has been the renin–angiotensin system. The proven value of anti-hypertensive drugs that block this system has led to neglect of other blood pressure-raising systems, including the sympathetic nervous system. Despite this, undeniable evidence now exists for the importance of chronic activation of the sympathetic nervous system in essential and renal hypertension.

Sympathetic nervous system activation in essential hypertension

Application of the norepinephrine spillover methodology has demonstrated activation of the sympathetic nervous outflows to the kidneys and heart.8,54 Renal norepinephrine spillover, on average, is elevated two- to three-fold in both normal weight patients with essential hypertension and in obesity-related hypertension.8,54 Multi-unit recordings from sympathetic nerve fibres directed to the skeletal muscle vasculature similarly show a doubling or trebling of the sympathetic outflow.12,5557 Single-fibre sympathetic recording demonstrates increased fibre firing frequencies, and multiple firings within a cardiac cycle (firing salvos), not seen in health.12,56

The syndrome of neurogenic essential hypertension appears to account for ≥50% of all cases of high blood pressure. This estimate is based on both the proportion of untreated patients with essential hypertension who have demonstrable sympathetic excitation, and the number in whom substantial blood pressure lowering is achieved, and the extent of this lowering, with anti-adrenergic drugs. The application of sympathetic nerve recording and norepinephrine spillover methodologies, in multiple studies from different research groups,8,12,5457 has identified activated sympathetic outflow to the skeletal muscle vasculature and kidneys in ∼50% of patients (Figure 4).

Figure 4

Renal noradrenaline spillover to plasma in patients with untreated essential hypertension, in relation to their age, compared with measurements in healthy volunteers. Individual and mean values are shown. Renal sympathetic activation is evident in patients under 60 years of age. *P< 0.05 **P< 0.01.

If we consider, even with the limitations mentioned above, an overall measure of autonomic cardiac modulation such as the sensitivity of arterial baroreflex control of the heart rate, both laboratory and ‘spontaneous’ methods for arterial baroreflex sensitivity analysis provide consistent evidence of reduced cardiac baroreflex sensitivity in hypertension, mainly due to impaired parasympathetic cardiac control.19,20 Given the reciprocal interactions between sympathetic and parasympathetic cardiovascular regulation, reduced cardiac parasympathetic activity implies an increase in the activity of the sympathetic nervous system to the heart. The occurrence of such a systematic imbalance between parasympathetic and sympathetic cardiac modulation in hypertensive patients was demonstrated not only in the laboratory, but also over the 24h in ambulatory conditions20 (Figure 2).

Does this sympathetic activation cause blood pressure elevation?

Once it was thought that the sympathetic nervous system exerts minute by minute circulatory control only, and was not important in the pathogenesis of hypertension. This is not correct. It now seems certain that the renal sympathetic nerves are pivotal in the pathogenesis of experimental and essential hypertension, through influences on renin release, glomerular filtration rate and renal tubular reabsorption of sodium.41,58 Experimental studies establish the important concept that sub-vasoconstrictor levels of renal sympathetic activity can increase renin secretion and renal sodium retention, without changing renal haemodynamics.41 A parallel is seen in essential hypertension. Younger patients with mild essential hypertension very commonly have ‘high renin essential hypertension’, where renal sympathetic activity is sufficiently elevated to increase renal secretion of renin, but not to reduce renal blood flow.54 In patients with resistant hypertension, responding inadequately to concurrent treatment with multiple anti-hypertensive drug classes, including ACE inhibitors, angiotensin receptor blockers, dihydropyridine calcium channel blockers, and diuretics, radiofrequency ablation of the renal sympathetic nerves lowers blood pressure remarkably,59,60 as described below.

Consequences of sympathetic nervous system activation in hypertension, beyond blood pressure elevation: left ventricular hypertrophy, insulin resistance

A growth promoting effect of high cardiac sympathetic activity on human myocardium was evident in a clinical study that demonstrated proportionality between increases in LV mass (normalized for blood pressure) and cardiac noradrenaline spillover in patients with essential hypertension.57 Glucose utilization by skeletal muscle through the action of insulin, which is the process largely determining measured insulin resistance, is influenced by sympathetic nervous outflow to the limbs and skeletal muscle blood flow and glucose delivery to muscle. Reduced skeletal muscle blood flow in essential hypertension resulting from sympathetically mediated vasoconstriction is the probable primary cause of insulin resistance and attendant hyperinsulinaemia commonly present.61,62

Sympathetic nervous system activation in secondary forms of hypertension

In end-stage renal disease sympathetic nervous activation is at a very high level, higher than in essential hypertension and equal to or exceeding that seen in cardiac failure.63 Renal transplantation restores renal function but does not abolish the hypertension. Nephrectomy on the other hand does reduce blood pressure, through normalization of sympathetic tone63 via removal of the sympathetic excitatory influence of renal afferents from the diseased kidneys.64 In experimental models of renal injury, involving, for example, injection of phenol into the renal parenchyma, projection of activated renal afferent imputs to the hypothalamus has been demonstrated to activate CNS sympathetic outflow, causing hypertension.64 The hypertension of renal failure is explicitly a neurogenic hypertension.63 Less studied are renovascular hypertension and pregnancy hypertension, where the sympathetic nervous system is activated, and primary aldosteronism and Cushing's syndrome, where the sympathetic system is suppressed.

Obstructive sleep apnoea is another cause of resistant hypertension associated with increased sympathetic activity to cardiac and vascular targets,65 acknowledged by Hypertension Management Guidelines.66 The blood pressure increase associated with obstructive sleep apnoea is due to a complex interaction of different mechanisms, among which changes in autonomic cardiovascular regulation play a major role.65 Indeed, obstructive apnoea, besides determining sleep fragmentation and periodic changes in intra-thoracic pressure, activates hypoxic and hypercapnic chemoreflexes involving central autonomic neural mechanisms that generate a profound elevation in sympathetic nerve activity and cyclical changes in parasympathetic nerve activity.6769 The pathogenetic role of sympathetic activation in the obstructive sleep apnoea (OSA)-related blood pressure increase is clearly supported by the finding of enhanced muscle sympathetic nervous activity during wakefulness and sleep in patients with OSA.70,71

The origins of sympathetic nervous system activation in essential hypertension

These do remain enigmatic. For obesity-related hypertension the list of possible causes is long, but for none of these is the supporting evidence totally convincing. Does the sympathetic activation represent an ongoing response to continuing overfeeding, which is suggested by the experimental models, or is it perhaps a consequence of sedentary life style, or chronic mental stress?61 Or is it driven by the pathophysiological and clinical changes that accompany obesity once it has developed, including hyperinsulinaemia, high plasma leptin levels, or obstructive sleep apnoea?61 Research by Noll et al.72 identified accentuated sympathetic nervous system responses to mental stress in normotensive offspring of parents with essential hypertension. Patients with essential hypertension do have demonstrable increases in forebrain noradrenaline turnover,73 suggesting that brainstem noradrenergic projections to the hypothalamus and amygdala, and presumably behavioural mechanisms, are commonly operative in activation of their CNS sympathetic outflow.

Neurogenic essential hypertension: research translation via anti-adrenergic therapies

The sympathetic nervous system is the ‘forgotten pathway’ in the treatment of hypertension in the modern era where anti-hypertensive drugs antagonizing the renin–angiotensin system is the dominant therapeutic mode. Despite the importance of neural pathophysiological mechanisms in pathogenesis, therapy specifically targeting the sympathetic nervous system is currently underutilized.

Non-pharmacological treatment

Two commonly applied non-pharmacological therapies for hypertension, aerobic exercise training and calorie restriction, inhibit the sympathetic nervous system. We have learned post hoc that this effect is congruent with the neural pathophysiology of essential hypertension, and perhaps explains why, of all non-pharmacological therapies, these two seem to be the most effective. This targeting of the pathophysiology is particularly apt for the metabolic syndrome and obesity-related hypertension, where there is a contribution of sympathetic inhibition to reductions in both blood pressure and insulin resistance.61 Another non-pharmacological approach with an anti-adrenergic component is the regular application at night of continuous positive air pressure (CPAP) ventilation in patients with obstructive sleep-apnoea-related resistant hypertension. This therapeutic approach has been shown to prevent nocturnal obstruction of upper airways, reduce sympathetic activity and favour blood pressure reduction.65,7476

Anti-adrenergic drugs

The early anti-hypertensive drugs were commonly anti-adrenergic, and potent, but fell out of favour because of their side effects. Beta-adrenergic blocking drugs are currently following a similar path, due to their adverse effects on plasma lipids and insulin resistance. Alpha-adrenergic blocking drugs similarly are now used less, due to common side effects of postural and exercise hypotension, and their presumptive linkage with heart failure risk in patients with hypertension.

What anti-hypertensive drugs are available to specifically target the sympathetic nervous activation of essential and renal hypertension? Should centrally acting sympathetic suppressants, imidazoline-binding agents, such as moxonidine and rilmenidine, be specifically prescribed in patients with essential hypertension? Both drugs produce the desired sympathetic inhibition in the sympathetic outflows to the heart, kidneys, and skeletal muscle vasculature. They are largely free of the side effects of their progenitor, clonidine, most notably the rebound hypertension seen with clonidine when doses were missed. These drugs are third or fourth tier in most national and professional society guidelines. Sometimes they do not make the list at all. Logic would, perhaps, dictate that this might change, and especially in obesity hypertension, where sympathetic inhibition in skeletal muscle reduces the existing insulin resistance.62 A substantial barrier to wider prescription of this drug class, however, remains, this being the absence of large-scale outcome studies.

Anti-adrenergic devices

The neglect of anti-adrenergic therapies for hypertension appears to be at an end, with the recent testing of anti-hypertensive devices for reducing sympathetic nervous system activity, and as a consequence blood pressure. One of these is the surgically implantable arterial barostimulator, which operates by continuous electrical stimulation of the carotid sinus buffer nerves.77,78 Recent evidence indicates that such a stimulation is accompanied by a reduction in the 24-h mean blood pressure, although this issue still needs further investigation on a larger scale and over a prolonged follow-up time.79

Another revolutionary treatment principle, described in more detail here, which has been recently successfully tested in patients with resistant (uncontrolled) hypertension, involves ablation of the renal sympathetic nerves with a radiofrequency emitting catheter inserted percutaneously into the femoral artery in the groin, and advanced to lie, in turn, in the lumen of both renal arteries59 (Figure 5). Sympathetic nerves enter the human kidneys in the walls of the renal arteries, within reach of ablative energy delivery.

Figure 5

The renal sympathetic nerves pass to the kidney in the wall of the renal artery, within reach of radiofrequency energy delivered by the Symplicity catheter in the artery lumen. The radiofrequency energy is transmitted through the catheter from an external generator, delivered at four to six sites in both arteries, aimed at achieving a full circumference of dosing coverage, to ablate all nerves in passage, but not at a single point on the artery which might, perhaps, predispose to stenosis or aneurysm formation.

In many experimental models of hypertension the sympathetic outflow to the kidneys is activated, and renal sympathectomy typically prevents the development of the hypertension.41 Initiation of the new treatment strategy for hypertension was based on these observations, and the demonstration that the renal sympathetic outflow is activated in essential hypertension8,54 (Figure 4). In participating patients with resistant hypertension, radiofrequency energy in 90° quadrants was delivered in a step-wise fashion to the full circumference of the walls of both renal arteries. To establish whether the catheter ablates renal sympathetic nerves, measurements of renal norepinephrine spillover were made at baseline and at follow-up; sympathetic denervation does, in fact, occur. The level of blood pressure reduction achieved, a mean fall of 24/10 mmHg at 3 months and 29/16 mmHg at 12 months (P< 0.001), was actually greater than anticipated, but it should be emphasized that in this proof of principle trial the experimental design is not blinded. At this point, in those patients with the longest follow-up (2 years), blood pressure reduction is sustained, suggesting that renal sympathetic innervation, if it has occurred, is insufficient to cancel out the blood pressure benefit (Figure 6).

Figure 6

Effect on clinic blood pressures of bilateral denervation of the kidneys using endovascular radiofrequency ablation methodology in patients with essential hypertension resistant to multi-drug therapy. Shown here are the initial 45 patients,63 and 26 additional patients, in whom follow-up results for a minimum of 1 month post-denervation were available. The procedure produced very substantial blood pressure lowering (P< 0.001). Pressures are shown, when available, from 1 to 24 months post-procedure.

Perspective: a cure for essential hypertension?

It has been suggested that renal artery catheter-based renal denervation might, perhaps, provide a cure for essential hypertension in selected patients, those with milder hypertension than treated in the recent study. This speculation remains untested. For the procedure to be applied in milder forms of essential hypertension, a very high level of safety would be mandatory. Further, efferent sympathetic nerve regrowth is possible, although the degree to which this would fully restore sympathetically mediated function in the kidneys, and perhaps cancel out the observed anti-hypertensive effect, is problematic. Also relevant is the fate of renal afferent nerves, which project to the hypothalamus, and stimulate sympathetic outflow.1 This CNS input from renal afferent nerves is critical in producing both the sympathetic activation and hypertension in patients with end-stage renal disease.63,64 It is almost certain that the radiofrequency procedure ablates the renal afferent nerves and that this, by inhibiting systemic sympathetic outflow, contributes to blood pressure lowering.60 Regeneration of renal afferent nerves does not occur. Any blood pressure reduction attributable to renal deafferentation is likely to be permanent.

Conflict of interest: M.E. received research funds, travel expenses and consultancy fees from Ardian Inc. USA, and travel expenses and consultancy fees from Medtronic, USA. M.E. is a member of the International Renal Denervation Advisory Board of Medtronic. M.E. owns no stock or shares in Ardian or Medtronic, and receives no patent royalties.

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96 US 124 Arthur v. Zimmerman

96 U.S. 124

24 L.Ed. 770

October Term, 1877

In 1873 and 1874, Zimmerman imported certain goods from France, which were composed of cotton, and commercially known as 'hat braids.' Arthur, the collector of the port of New York, imposed upon them, and collected, under protest, a duty of ninety per cent of thirty-five per cent ad valorem, under the sixth section of the tariff act of 1864 (13 Stat. 209), which imposes that duty upon 'cotton braids, insertings, lace trimmings, or bobbinets, and all other manufactures of cotton not otherwise provided for.'

It appeared, upon the trial of the suit to recover the excess so paid, that there were goods known as cotton braids, used for other purposes, but that the goods in question were commercially known as 'hat braids,' and used exclusively for making and trimming hats and bonnets.

The court below, being of the opinion that the articles were only liable to duty at thirty per cent, under the eighth section of the act of July 14, 1862 (12 Stat. 551), so instructed the jury, and directed a verdict for the plaintiff. Judgment having been rendered thereon, the collector brought the case here.

Mr. H. E. Davis, Jr., contra.

MR. JUSTICE HUNT delivered the opinion of the court.

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The articles imported by the defendant in error are embraced in the general words of the act of 1864, and, if there were nothing else in the case, would be subject to the duty therein provided.

They are, however, commercially known as 'hat braids,' used exclusively for enamelling hats and bonnets. These articles are specifically enumerated in the acts of 1861 and 1862, and are there made subject to a different and a lower duty.

By these acts, and by the Revised Statutes, Congress establishes and recognizes the distinction between 'cotton braids' and 'other manufactures of cotton not otherwise provided for,' and 'hat braids.' 12 Stat. 178; id. 543, 551; Rev. Stat., sect. 2504.

Under the principles laid down in Arthur v. Morrison, Arthur v. Lahey, and Arthur v. Unkart (supra, pp. 108, 112, 118), the specific designation should prevail; and the judgment in favor of the plaintiff for the excess of duties paid by him was right, and must be affirmed.

Judgment affirmed.


Legit Psychic Readings

Ever wondered Are psychics legitimate or whether the readings offered to you by the psychic are accurate or not? Nowadays, most of the people have started turning to psychic readings to learn about their future and for positive affirmations however you can still find a few people across the globe who do not rely on such readings and even allege that they are false. Well, it all falls back on your individual choices whether you wish to have belief in psychic reading or not however the truth is that there are some genuine psychic readers who can give accurate readings.

There are a lot of psychic readers who claim to offer correct readings but you need to find out whether they are actually saying the facts or not. Some readers simply frame stories to entice people and dupe them. What sets apart people from animals is free will. Animals don’t have free will. Free will is essentially the idea that you are able to believe what you want to believe and not worry about what other people are saying. Your character and lifestyle can be influenced considerably by this free will. When we speak about the psychic science, nothing is eternal. The events and things which people face keep on changing and it is thought that it is even possible to change luck with free will.

Some individuals also say that future is already written however it is not completely true because you can make your future by yourself and you only need to possess a free will for that. If you think that you can achieve in life then you would definitely make it happen. So when you get psychic reading it also depends on you, how you take it because it could prove to be accurate at the moment but if you don’t want to believe then the reading might just seem fake to you. As a matter fact, it is completely dependent upon your free will whether you wish the psychic predications to come true or not. The reading may simply tell what could possibly happen at the end of the day or in the near future.

You may have at times questioned yourself on how could the psychics claim to be highly accurate. Quite often, this is just an average figure with the objective to boost their credibility. You need to understand how they profess such high correctness in psychic reading. If an individual totally believes in what a psychic reader predicts, then in that situation the psychic reader would say that his reading is accurate because the person will do nothing to alter the readings. The individual has faith in the readings and it could actually become true. So in actual reality the readings may not be accurate. The psychic readers allege the correctness of their readings based on the feedback which they receive from their clients. With regards to precision it is up to you whether you believe are psychics genuine to give you Positive affirmations and high accuracy in the readings.


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Infants may sleep better when vaccinated in afternoon

Scheduling infantimmunizations in the afternoon may lead to an increase in the infant's sleep over the next 24 hours.

A small rise in body temperature is an expected reaction in infants getting an immunization, and can be a sign of a good immune response.

Sleep also plays an important role in the immune response. Previous research in adults has shown that lack of sleep before or after getting a shot may lead to a weaker immune response to the vaccine.

"Given the importance of sleep for a healthy immune response, our findings suggest that the time of day of vaccine administration and sleep duration after immunization are important to consider," researcher Linda Frank, RN, PhD, of the University of California, San Francisco, writes in Pediatrics.

If the relationship between timing of immunizations and immune response are confirmed by further studies, researchers say afternoon immunizations should be recommended for infants.

Timing of Vaccinations

In the study, researchers compared sleep duration and body temperature in 70 infants about 2 months old in the 24 hours before and after their first immunization.

Half of the parents were also instructed to give their infant a dose of acetaminophen (baby Tylenol) 30 minutes before the immunization and every four hours thereafter for a total of five doses.

Researchers say there are conflicting recommendations about whether parents should give their infants acetaminophen before and after receiving immunizations to ease discomfort or help them sleep.

Overall, the study showed infants slept for an average of 69 minutes longer in the 24 hours following immunization than in the 24-hour period before immunization.

Researchers found acetaminophen was not a significant factor in sleep duration after accounting for other factors, such as fever or discomfort.


Create a positive online learning experience by applying some of these motivational principles in your own home classroom. student motivation, student motivation principles, staying motivated

Get Students Motivated: K-12 Home Classroom Inspiration

By: Beth Werrell
Next Exit Motivation: 12 Principles for the Home Classroom

Learning is the main focus of school, but the school environment has a huge impact on students’ mental, social, and emotional well-being as they grow into young adults. The best way to nurture student well-being and encourage success is to improve a student’s motivation.

As a Learning Coach, you have a huge influence on your virtual school student. Your attitude, your suggestions, and even your body language can influence your student’s confidence and performance. That’s why it’s so important to create a consistently positive learning environment and do everything in your power to improve and maintain your student’s motivation.

While online teachers ensure student motivation in the virtual classroom, Learning Coaches can help create a positive online learning experience by applying some motivational principles in their own home classroom:

  1. Identify the purpose of learning. If your student asks, "Why do I need to learn this?", it’s important to find the right answer. Every lesson should have a purpose, whether it is to help your student understand the world better, prepare your child to apply the concept later on, or challenge your student’s critical-thinking skills. Making sure that your student understands the purpose of a lesson or assignment can help you both set and achieve long-term goals.
  2. Give clear, specific directions. Providing students with clear directions helps avoid confusion and frustration while allowing students to get enthusiastic about the assignment. Consider having your student write down the steps needed to complete a task so as to make the directions even easier to follow. This way, students will also uncover questions upfront and can reach out to their teacher for clarification. Learning Coaches who take some time to organize for virtual school lessons will be able to facilitate the school day more smoothly.
  3. Communicate your expectations. Both teachers and Learning Coaches have to establish expectations not just for assignments but also for student behavior. By showing your student that you think highly of his or her abilities and expect success, your student is much more likely to follow through. Spending time with your student and offering encouragement are great ways to show that you care, helping your student feel good about him- or herself.
  4. Encourage students to think critically. Students are more likely to stay on task if they’re asked to think critically about a question rather than simply recall facts. Open-ended questions also allow students to use their imaginations, building creative and reasoning skills that last for life.
  5. Engage your student’s curiosity. Whenever possible, connect assignments or activities to high-interest topics for your student’s age group. When students are interested in a subject and want to know more, they’re more likely to stay focused and work efficiently. For example, you can take a hot issue from the news or pop culture and use it to demonstrate a concept your student is learning.
  6. Make learning fun. Making learning fun for your student makes learning fun for you, too! Add variety to the school day by getting students active between lessons or by doing some fun, educational crafts or activities. Some examples of fun science activities are building a battery out of a lemon and dusting for fingerprints.
  7. Promote collaboration and competition. Getting students working with others builds teamwork and leadership, whether your student works with siblings or in a study group you arrange. By combining learning with socializing, students have more fun working together or competing against each other to achieve goals.
  8. Be positive, fair, and consistent in your treatment. Learning Coaches can get frustrated just like their students, but it’s important to lead by positive example. When you are fair and consistent as well as positive, your student will know what to expect from day to day, and you can also gain and maintain your student’s trust. Striving to be positive, fair, and consistent ultimately helps your student’s performance remain steady.
  9. Empower students with honest praise. Students who regularly receive positive feedback can become confident learners, and confidence is key to staying motivated. When students are confident and learn to value their successes, they’ll want to continue learning.
  10. Reward both effort and achievement. Part of instilling confidence in a student is offering rewards as well as praise. Remember to reward students for great effort as well as successes in order to emphasize the importance of trying hard. Reward includes intrinsic (internal) rewards and extrinsic (external) rewards. Establishing rewards can help you and your student form the habit of setting goals. Younger students will respond better to extrinsic rewards, with the goal being to eventually teach your student autonomy and a love of learning that are part of intrinsic motivation.
  11. Help students learn from mistakes. When you offer a balance of praise and constructive criticism, you help students learn how to handle their mistakes without getting discouraged. They’ll try new things, taking more risks, because they’re not afraid of failure.
  12. Assess and communicate progress. Students need to know where they stand, and frequent feedback and evaluations help them get a clear sense of their progress. Together with your student and his or her teachers, discuss strengths as well as areas that need improvement, focusing on ways your child can work on both.

Do you use any other methods to get—and keep—your student motivated? Make sure you share your thoughts below!


SN1 vs SN2 reactions

The following is my comment on a forum post on how to decide whether a reaction should be an SN1 or an SN2 reaction.

In my discussion of these reactions, I draw the distinction between what must happen at the extremes. For an SN2 reaction, I suggest it is similar to billiards in which the cue ball must strike a combination of balls before the object ball can move. For an SN1 reaction, it is like trying to find a parking place in a crowded parking lot. You cannot pull in until someone pulls out first.

In practice, the reactions are generally somewhere between these extremes. For some SN2 reactions, the bond breaking may be more advanced than in other examples, or it can be increased by electron withdrawing ability, solvent or heat. The attack can be advanced with electrons better able to hit the nucleus before the leaving group has much movement. In SN1 reactions, you may find some nucleophiles attack occurs before the leaving group has completely diffused away. In that case, the product may have a slight amount of inversion in the product distribution.

I suggest it is easier to rationalize the reactions be starting with those you can best understand as generally SN1 or SN2. For example, SN2 reactions do not occur with tertiary halides and SN1 reactions do not occur on primary halides (unless stabilized by neighboring electrons, allylic and benzylic, for example). In between are the difficult ones, the secondary halides. For some problems, they can be truly difficult to answer, two mechanisms, ambiguous, impossible, not enough data, help…?

My preferred method to learn substitution reactions is to read examples and try to understand why the reactions occur as they do. For example, because carbon is an electron donor (that is why tertiary carbocations are more stable), replacing hydrogens with carbon atoms will make it more difficult for an electron pair to attack the carbon. This retards SN2 reactions and increases the SN1 (carbocation formation) reaction. This will be the same reason for beta substitution to retard SN2 reactions or result in rearrangement in SN1 reactions. The effect of electron donation from the neighboring carbon. (You may find it is called hyperconjugation if CH bond electrons are being donated. However, you may also think it is due to carbon not holding its electrons tightly.)

I also concede there are some examples that become very difficult for me to correctly predict what might happen. This happens with a secondary halide and a protic solvent. Protic solvents are better able to hydrogen bond with the nucleophile or the leaving group. This can provide additional pull to the leaving group and possible carbocation formation. However, I generally assume that if written with a reasonably good negatively charged nucleophile, the reaction is likely to be an SN2 rxn rather than SN1 because increasing the nucleophile concentration can increase the rate. (Dilution can increase SN1 reactions.)

However, that isn’t the greatest dilemma in predicting the products, rather competition from elimination reactions. A rule of thumb I found in the textbook written by Brown and Foote is any nucleophile with a pKa > ~12 will result in elimination.

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Distance Between Birmingham, AL and Mooresville, NC

How many miles? 414 Miles / 666 Km

How many times? 6 hours 9 mins

Distance, Gas Consumption and Emission Notes

Distance from Birmingham, AL to Mooresville, NC is 414Miles or 666 Km. You can get this distance about 6 hours 9 mins. If you want to planning travel with plane for 370 Miles or 596 Km, You can get this distance about 1 hours 17 mins .

A car with an average MPG will needs 19.17 gallons of gas to get the route between these points.

The estimated cost of gas to get between Birmingham, AL and Mooresville, NC is $43.52.

During the route, an average car will release 375.58 pounds of CO2 to the atmosphere. Your carbon footprint is 0.91 pounds of CO2 per mile.

* Average US MPG used for calculations is 21.6 MPG.
* Coordinates of Birmingham, AL is 33.5206608, -86.80249 and coordinates of Mooresville, NC is 35.5848596, -80.8100724