Snakes may lack arms and legs, but their supple bodies squeeze through naarrow openings and slither —a motion that depends on the combination of a flexible spinal column,strong muscles, and specialized scales on their undersides called scutes.


Adult humans have 26 vertebrae in their spines; a snake may have more than 400.each pair of ribs is attached to a vertebrae.overlapping scutes on the snake`s belly attach by muscles to animals ribs.

when the snake is moving ,the back edges of the scutes catch and hold the ground as the muscles pull the snake forward.snakes Move according to the terrain they travel through.Sidewinding snakes in sandyy habitats have ways to keep from slipping. The snake swings its head and upper body forward and sideways.Its lower  body and tail follow,with the belly raised above the hot sand,leaving a j-shaped pattern in sand.

Some snakes climb do that ,a snake coils up like an accordion,anchors with its tail,then strtches its head forward,gathering momentum,so the rest of the body catches up.


Do animals ever use drugs in nature?

Oh yes! Animals aren’t any less than us, many animals get high, like dolphins nibbling on puffer fish, Dogs licking toads (SEE IT: Druggie dogs risk death getting high on poison toads) , and bees resemble humans when they get drunk on fermented plants, and alcholic drinks left out in the open for them to get into. Once they make their way back to the hive, they “beegin” (Pun intended) to start fights with other bees and are more aggressive when they do. Some may forget to make it back to the hive and the ones that do are jumped on and killed due to their behavior almost like the death penalty in the bee world for being drunk.(9 Animals That Get Drunk Or High).

Agile scrum model

In Agile model Scrum is the most popular way  due to its simplicity and flexibility. Because of this popularity, many organizations using this model.Scrum word is actually related to Rubby game .Scrum stands for formation of two teams as one team.Developers and testers together work as a team and this team is called as scrum team.from scrum methodology we can develop a software piece by piece ,called as  sprints.

Sprint:  It is apiece of software,which is potentially shippable to customer site and which have previous sprint features versions.

Sprint software testing:

Sprint software testing was done by conducting below  functional and non functional tests.


How to select all options in a drop down using selenium.

To get all  the options in a dropdown,we have a method called getoptions() in selenium. By using this method we can retrive all the options in dropdown.

Select s= new select(driver.findElement(“………….”));

//get list of options

list<webElement> x= s.getOptions();



//print size of the list


//print each and everyone element in dropdown list

for(int i=0;i<=y;i++)





Get methods in Selenium Webdriver.

Webdriver class Get methods


The method  is used to get or launch the specific site or website.

Syntax: get(url)
Example: driver.get();


The method  is used to get  text of a located element in the current page..

Syntax: getText()

string x=driver.findElement(“………….”)).getText();


The method  is used to get attribute value for a located element in the current page.

Syntax: getAttribute()

string y=driver.findElement(“………….”)).getAttribute();


The method  is used to get style attribute value for a located element in the current page.

Syntax: getcssValue();


string s=driver.findElement(“………….”)).getcssValue();

5.getTitle():The method  is used to get title of currently active page.

Syntax: getTitle()

string a =driver.getTitle();


The method  is used to know weather the current site is securable or not.

Syntax: getCurrenturl();

string u =driver.getCurrenturl();


The method  is used to get the HTML source of current page.

Syntax: getPagesource();

string p =driver.getPagesource();


The method  is used to get the all handle numbers of browser window into an array.

Syntax: getwindowHandles();

Arraylist<string> q =new Arraylist<string>(driver.getwindowHandles(1));

9.getfirstSelectedOption();The method  is used to get the first selected option in a drop down.


Select s= new select(driver.findElement(“………….”))

webElement x= s.getfirstSelectedOption();




The method  is used to get the first selected option in a drop down.


Select s= new select(driver.findElement(“………….”))

list<webElement> x= s.getAllSelectedOptions();



for(int i=0;i<=y;i++)






The method  is used to get the all options in a drop down.


Select s= new select(driver.findElement(“………….”))

list<webElement> x= s.getOptions();



for(int i=0;i<=y;i++)





Above getOptions(),getfirstSelectedOption(),getAllSelectedOptions() are used  to handle the dropdowns.

selenium program based on testng priority

package kolli;

import org.junit.Assert;
import org.openqa.selenium.By;
import org.openqa.selenium.WebDriver;
import org.openqa.selenium.firefox.FirefoxDriver;
import org.testng.annotations.Test;

public class Seltng2 {
WebDriver obj= new FirefoxDriver();
public void seltng()

String pageTitle = obj.getTitle();

@Test(priority =2)
public void seltng1()

public void seltng2() throws InterruptedException
public void seltng3()

Data retriving and Data writing using Jxl jar file in selenium

 Jxl is available as jar file. It  is the most widely used API for executing Selenium data-driven tests, which allows users to read, write, create, and modify sheets in an Excel(.xls) workbook at runtime. It is useful to access .xls file only.


  • Reads data from Excel 95, 97, 2000, XP, and 2003 workbooks
  • Reads and writes formulas (Excel 97 and later only)
  • Generates spreadsheets in Excel 2000 format
  • Supports font, number and date formatting
  • Supports shading, bordering, and coloring of cells
  • Modifies existing worksheets
  • Is internationalized, enabling processing in almost any locale, country, language, or character encoding (formulas are currently only supported in English, French, Spanish, and German, but more can be added if translated)
  • Supports copying of charts
  • Supports insertion and copying of images into spreadsheets
  • Supports logging with Jakarta Commons Logging, log4j, JDK 1.4 Logger, etc


How to download and configure  Jxl jar file with eclipse IDE

Download jxl Zip file from click here (57KB)).

Extract files from zip file and save in a folder.

Now launch Eclipse IDE and go to the project.

Right click on project—>go to properties—>java buildpath—>libraries—>add external  libraries–>browse jxl jar file.


.xls sheet

0th row Input 1 Input 2  Output
1st row XX  XX
2nd row XX  XX
3rd row XX  XX
4th row XX  XX
5th row XX  XX
6th row XX  XX

Output= Input 1+Input 2

From above table we have to read data (Input 1,2) and write the output in the same sheet with the help of jxl in selenium.


public class Jxl {

public static void main (String[] args) throws JXLException, IOException

File f =new File(“E:\\Yamini\\xl\\xx.xls”);

Workbook rwb = Workbook.getWorkbook(f);
Sheet rsh = rwb.getSheet(0);
int nor = rsh.getRows();
WritableWorkbook wwb = Workbook.createWorkbook(f, rwb);
WritableSheet wsh = wwb.getSheet(0);
for (int i=1;i<nor;i++)
int x = Integer.parseInt(rsh.getCell(0 ,i).getContents());
int y= Integer.parseInt(rsh.getCell(1, i).getContents());
int z=x+y;
Number n =new Number (2,i,z);




The liver is an essential body organ that forms an important barrier between the gastrointestinal blood, which contains large amounts of toxins and antigens, and the body. Around 60% of the liver is formed by liver cells, hepatocytes, which are radially grouped into thick unicellular layers around the terminal hepatic veins, forming the smaller anatomic units of the liver, the classic lobes.

It is responsible for the production of bile which is stored in the gallbladder and released when required for the digestion of fats. The liver stores glucose in the form of glycogen which is converted back to glucose again when needed for energy. It also plays an important role in the metabolism of protein and fats.It stores the vitamins A, D, K, B12 and folate and synthesizes blood clotting factors.Another important role is as a detoxifier, breaking down or transforming substances like ammonia, metabolic waste, drugs, alcohol and chemicals, so that they can be excreted. These may also be referred to as xenobiotic chemicals.


Acute liver failure is a complex and devastating consequence of acute liver injury. It is characterized by hepatic encephalopathy, jaundice, coagulopathy and high mortality rates.Emergency liver transplantation is currently the only effective treatment for those patients who are unlikely to spontaneously recover. Donor shortages however remain a serious problem as the number of patients requiring orthotropic liver transplantation has far outpaced the number of donor livers and many patients die before a suitable organ is identified. This has generated interest in designing devices that would support or replace normal liver function until a donor liver became available for liver transplantation, or the patients own liver recovered.

The most common approaches used to induce experimental ALF include surgical strategies, hepatotoxic drugs such as paracetamol, carbon tetra chloride and D-Galactose, and viral models. Among surgical approaches, many strategies have been developed: total hepatectomy , partial hepatectomy , complete hepatic devascularization (a portacaval anastomosis followed by ligation of the hepatic artery, and combined surgical/hepatotoxic models . The development of an ideal model of ALF has been remarkably difficult to achieve. The reproducibility of surgical models relies extensively on the availability of appropriate surgical expertise; hepatotoxins have been used extensively in the development of animal models of ALF.

As most hepatoxins are taken orally the liver is the portal to the tissues for such compounds following absorption from the gastrointestinal tract. The liver is, therefore a vulnerable organ, being exposed to both the parent drug carried from the G.I. tract via the portal vein and to any metabolites produced which then enter the systemic circulation via the hepatic vein. However, despite this vulnerability, the liver is not the major target for adverse drug reactions, only about 9.5% of these involve the liver ). Although drug-induced hepatic damage may not be particularly common in general patient populations the case fatality rate is often high, and the severity of drug-induced hepatic injury is such that drugs are a major cause of hepatic failure . Several hepatotoxins have been used over the last 30 years in particular; D-Galactosamine (D-Gal), acetaminophen (paracetamol/APAP), carbon tetrachloride (CCl 4 ) and thioacetamide (TAA), and more recently, Concanavalin A (Con A) and lipopolysaccharide (LPS) have been investigated.As compared with other pharmacological agents D- Galactosamine works more effectively to induce liver damage.

D-Galactosamine is a hepatotoxin that induces liver damage in vivo, similar to human viral hepatitis, via depletion of uridine nucleotides and subsequently diminishes the synthesis of RNA and plasma membrane proteins . Oxidative tissue damage triggered by D-galactosamine is believed to be due to the formation of highly reactive hydroxyl radical which are the initiators of lipid peroxidation chain reaction which subsequently provokes inflammatory reaction and hence destruction and damage to cell membrane  .

Renal failure is often associated with end stage of liver damage and also reported that kidney injury induced by D-Gal along with liver damage.

Pharmacological agents induced hepatotoxicity


Acetaminophen (paracetamol) is among the most commonly used analgesics. It effectively reduces fever and mild to moderate pain, and is regarded, in general, as a very safe drug. Hepatic injury with acetaminophen is not only associated with overdose or use of high doses; rather, it can be encountered with chronic use at lower doses (<4g/ day), particularly in the presence of other predisposing factors, such as chronic alcohol consumption (Rao RR. et  al.,1977  ). Damage to the liver following acetaminophen ingestion is not due to the drug itself, but due to a toxic metabolite that is generated through the cytochrome P450 group of enzymes in the liver. This metabolite is usually rendered harmless through an interaction with the endogenous antioxidant, glutathione. However, when there is overproduction of the acetaminophen metabolite, glutathione stores in the liver become depleted, and the metabolite begins to accumulate and cause tissue injury. Hepatic injury can be limited through administration of N-acetylcysteine, which replenishes liver levels of glutathione. In the United Kingdom acetaminophen or paracetamol poisoning is the most common cause of AHF.

Acetaminophen-induced animal models of AHF are widely used to improve our insight into the metabolic and physiological derangements of AHF and to facilitate the development of new therapeutic modalities.

Carbon tetrachloride

The hepatotoxic effects of CCl4 have been known for a long time . It was used extensively in animal models of AHF in the seventies and early eighties but it was found to be poorly reproducible and also species variation was significant . It has been used in the development of cirrhosis animal models following its gastric and intraperitoneal administration.

Clinically the syndrome of AHF is poorly reproduced by CCl4intoxication with little encephalopathy and late stage hepatic coma. This model is infrequently used to represent AHF.


The anti-hyperlipidemic drug with the highest potential for hepatic injury is the sustained-release formulation of niacin. HMG CoA reductase inhibitors, otherwise known as statins, very rarely cause clinically significant liver injury, although asymptomatic elevation in aminotransferases is common.

Anaesthetic Agents:

Halothane, the most widely used anaesthetic is now accepted as causing hepatic injury. Multiple exposures are a major factor which may predispose the patient to liver injury, particularly if re-exposure occurs within 3 months. Obese patients and females seem more susceptible but children and young adults less so.


It is an amino sugar and is metabolized in the liver leading to depletion of uridine nucleotides and hepatic transcriptional blockade. Depression of protein synthesis cannot explain d-Gal induced hepatic failure and it was suggested that d-Gal sensitized the liver towards other stimuli in part reflecting the role of uridine-containing compounds in hepatic biotransformation.

D-galactosamine is a hepatotoxic agent, which induces diffuse injury of liver tissue followed by the regeneration process. D-galactosamine (GalN) is known for inducing the features of acute hepatitis in rats. The toxic effect of GalN is connected with an insufficiency of UDP-glucose and UDP-galactose and the loss of intracellular calcium homeostasis. These changes affect cell membranes and organelles and the synthesis of proteins and nucleic acids. After GalN application, the location of proteoglycans is changed in the rat liver . GalN also inhibits the energy metabolism of hepatocytes.

Laboratory Tests to Perform in the Initial Evaluation of Acute Liver Failure

Laboratory tests to assess the ALF include a complete blood count, complete metabolic panel with serum chemistries and liver-associated enzymes, arterial blood gases, and lactate.

Enzymes that detect Liver failure

The liver contains thousands of enzymes, some of which are also present in serum in very low concentrations. These enzymes have no known function in serum and behave like other serum proteins. They are distributed in plasma and intestinal fluid and have characteristic half lives of disappearance, usually measured in days. The elevation of a given enzyme activity in serum is thought to primarily reflect its increased rate of entrance into serum from damaged liver cells. Serum enzyme tests can be grouped into two categories: enzymes whose elevation in serum reflects generalized damage to hepatocytes and enzymes whose elevation in serum primarily reflects cholestasis.

  1. Serum glutamate pyruvate transaminase (SGPT) or ALT
  2. Serum glutamate oxaloacetate transaminase (SGOT) or AST
  3. Serum alkaline phosphatase (ALP)
  4. Serum direct bilirubin
  5. Serum total bilirubin
  6. Total protein
  7. Total albumin
  8. Glucose.



Undoubtedly, gold is one of the most precious materials on earth. Besides its common use in art and jewelry, gold is also an essential component of our modern computers and cell-phones.


Cupriavidus metallidurans (previously Ralstonia metallidurans ) type strain CH34 (hereafter C. metallidurans) is a Gram-negative , motile, non-spore forming, rod-shaped bacterium known for its ability to resist toxic heavy metals; metallidurans literally translates to “metal-enduring”. When cultured on trypticase soy agar (TSA) at 30°C for 24h, C. metallidurans forms round, smooth, flat and convex colonies that are transparent and about 0.5mm in diameter. C. metallidurans is a mesophile; it has not been shown to grow under conditions outside of a range of 20-37°C.

This bacteria consist of high number of heavy metal resistance genes and ability to thrive in toxic environments make it an important model organism in studying the mechanisms by which diverse microbes deal with heavy metal stress . C. metallidurans is also able to precipitate solid gold from aqueous gold (III) tetrachloride, which is a potent heavy metal toxin to most organisms

Ecology and Pathology

Cupriavidus metallidurans  is normally found in industrial sediments or wastes which contain high heavy metal concentrations . C. metallidurans was initially isolated from the wastewater of a zinc factory in Liège, Belgium . Later, this bacterium was found in another unusual place; it was the dominant organism present in biofilms on gold grains found in the Prophet gold mine in Queensland, Australia . This bacterium is able to survive in these environments due to the abundance of metal-resistance genes dispersed throughout its genome which code for heavy metal exporters, regulators,and potential metal-binding proteins used to detoxify the cell . These abilities have earned C. metallidurans some fame. When placed in an environment containing aqueous Gold (III) chloride, this bacterium reduces the complex – by a mechanism yet to be fully understood – leading to the precipitation of solid gold nanoparticles within  the


Cupriavidus metallidurans living in biofilms on gold nuggets. The bacteria detoxify dissolved gold by accumulating it in inert nanoparticles inside their cells.Some biofilms also contained a second species of bacterium Delftia acidovarans.was somehow creating gold particles outside its cell wall, instead of inside as C. metallidurans does.