FIRST    BACK   document 3 of 6      FORWARD    LAST    The subepithelial gland in ants: a novel exocrine gland closely associated with the cuticle surface   Acta Zoologica,  October 2003, vol. 84, no. 4,   pp. 285-291(7)   Gobin B.[1]; Ito F.[2]; Billen J.[1]   [1] Laboratory of Entomology, K.U. Leuven, Naamsestraat 59, B-3000 Leuven, Belgium; [2] Faculty of Agriculture, Kagawa University, Ikenobe, Miki 761-0795, Japan   Abstract: Gobin, B., Ito, F. & Billen, J. 2003. The subepithelial gland in ants: a novel exocrine gland closely associated with the cuticle surface. Acta Zoologica (Stockhom) 84: 285291 Two glandular systems were discovered that secrete their products onto the cuticular surface in ants. The first, the subepithelial gland, was previously undescribed in ants, and is found throughout the body just beneath the epithelium. This gland consists of independent secretory units, each made up of a single gland cell and an associated duct cell that penetrates the cuticle. Its ultrastructural appearance is consistent with possible hydrocarbon production. Examining 84 ant species, the subepithelial gland was found in eight subfamilies (out of 13), although not necessarily in all species. In a single ant species, Harpegnathos saltator, it was the epithelium itself that was enlarged and functioned as a gland. The enlarged epithelial cells secrete their products directly onto the cuticle through distinct cuticular crevasses.   Keywords: chemical communication; desiccation; fertility signal; Formicidae; hydrocarbons; kin recognition   Document Type: Research article ISSN: 0001-7272

Uneducated few give snakes bad rap; they only bite as last line of defense   What are you afraid of? Death, the unknown, pain, bad grades, that roommate from your freshman year who liked to play the banjo in the nude? Whatever it is, we're all afraid of something. But some people let their fears control them and some people are afraid of silly things. VIEWPOINT Jason Rucker is a senior in animal science. You can contact him by e-mail at <anubis@ksu.edu>. You can also read him previous columns. One of the biggest fears I saw firsthand during my days as a zoo volunteer was the rampant and ridiculous fear of snakes-the general attitude of which can be summed up by a quote from one of my professors who said, "All snakes kill in one of two ways. Some kill by poison, and the rest kill by heart attack." The people who think this way are the ones who walk quite nervously through the herpetarium (reptile house) at the zoo. The worst of them refuse to come within 10 feet of the exhibit windows. That kind of behavior is obviously foolish - let's examine why. Does a snake have any hands or other appendages with which to strike the glass? No. Which leaves only its head. How many of you, without first downing a case of Southern Comfort, willingly would put your face through plate glass? The snake has no desire to do so, either. In the Kansas wilderness, the big fear is the dreaded rattlesnake. Here is an animal that does everything in its power to let you know right where it is so you can avoid it. The rattling does not mean, "You want some of this? Let's go, cowboy!" By rattling, the snake is saying, "Hey! I'm down here, please don't hurt me! I was just leaving! You wouldn't hit a guy with glasses, would ya?" When the rattlesnake hunts, it holds its rattle perfectly still so it can move silently. The snake's fangs and venom are not meant for defensive purposes. In fact, 25 percent of defensive bites are dry bites, meaning the snake doesn't inject venom. Venom is for securing prey, and because you are a bit bigger than the average field mouse, the snake would be wasting his venom to use it on you. I'm not saying snakes won't bite. They will give you every chance to leave them alone long enough for them to escape. But if you push them, they have no other choice (remember that lack of appendages thing we discussed earlier). They also may bite if you surprise them and are suddenly too close for them to have any time to warn you of their presence. I think you would react similarly if an animal 10 times your size suddenly stepped or sat on you. People continue to demonize snakes, though. Of course, it wasn't the person's fault the rattlesnake bit them; after all, they were only trying to kick it out of the way. Worse than fearing them, people pass this unjustified fear on to their children. Children learn about the world from their parents. So when their moms or dads pick up the picnic basket in the park, find a garter snake curled up under it and run away, arms flailing, screaming, "Mommy! Help, get it away!," the children are going to be traumatized into thinking snakes are deadlier than nuclear weapons. The fear becomes entrenched and is almost impossible to get over later in life. Psychologists tested this theory. They used baby monkeys, some raised with parents and others raised by people. Those raised by people reacted with curiosity when presented with a rubber snake or garter snake. Those raised with their parents, seeing their parents flee in terror of the rubber snake, were horrified by snakes. The psychologists then showed the human-raised monkeys a video of adult monkeys reacting fearfully to snakes. After this, the monkeys raised by humans developed a fear of snakes. Many of us share this primal fear, though we should know better. It's a crying shame so many people are ignorant about snakes. I hardly can count the number of times I've heard morons spout off about how they would go out of their way to kill a snake. From a pseudo-Freudian perspective, I would have to say the reason for this is snakes remind these guys of their inadequate ... well, manhood, and thus they feel the need to express their self-loathing through violence. For women who enjoy killing snakes, I have two words of warning for the men who date or marry them: Lorena Bobbit. Australia is the only place in the world where there are more venomous snakes than non-venomous snakes. We are not in Australia; in fact, Kansas is home to only a few species of venomous snakes. So chances are if you see a snake, it's harmless. Some snakes can be dangerous, and thus it is a good idea to respect snakes. If you have children, don't pass on your fears; teach them to respect snakes in the same way they respect any other wild animal. This item was published on April 14, 1998 Copyright 1998, Student Publications Inc. All rights reserved. This document may be distributed electronically, provided it is distributed in its entirety and includes this notice. However, it cannot be reprinted without the express written permission of Student Publications Inc., Kansas State University.

Cirrhosis By Howard J. Worman, M. D. What is Cirrhosis? Cirrhosis is characterized anatomically by widespread nodules in the liver combined with fibrosis. The fibrosis and nodule formation causes distortion of the normal liver architecture which interferes with blood flow through the liver. Cirrhosis can also lead to an inability of the liver to perform its biochemical functions. To understand the pathophysiology of cirrhosis, the normal anatomy and physiology of the liver must first be briefly reviewed. Liver Blood Flow Oxygenated blood that has returned from the lungs to the left ventricle of the heart is pumped to all of the tissues of the body. This is called the systemic circulation. After reaching the tissues, blood is returned to the right side of the heart, from where it is pumped to the lungs and then returned to the left side of the heart after taking up oxygen and giving off carbon dioxide. This is called the pulmonary circulation. Blood from the gut and spleen flow to and through the liver before returning to the right side of the heart. This is called the portal circulation and the large vein through which blood is brought to the liver is called the portal vein. After passing through the liver, blood flows into the hepatic vein, which leads into the inferior vena cava to the right side of the heart. The liver also receives some blood directly from the heart via the hepatic artery. In the esophagus, stomach, small intestine and rectum, the portal circulation and veins of the systemic circulation are connected. Under normal conditions, there is little to no back flow from the portal circulation into the systemic circulation. Bilirubin Secretion The liver is the site of bile formation. Bile contains bile salts, fatty acids, cholesterol, bilirubin and other compounds. The components of bile are synthesized and modified in hepatocytes (the predominant cell type in the liver) and secreted into small bile ducts within the liver itself. These small bile ducts form a branching network of progressively larger ducts that ultimately become the common bile duct that takes bile to the small intestine. Bilirubin is a yellow pigment that derives primarily from old red blood cells. Bilirubin is taken up by hepatocytes from the blood, modified in the hepatocytes to a water soluble form and secreted into the bile. Biochemical Functions The liver performs many biochemical functions. Blood clotting factors are synthesized in the liver. Albumin, the major protein in the blood, is also synthesized in and secreted from the liver. The modification and/or synthesis of bile components also takes place in the liver. Many of the body's metabolic functions occur primarily in the liver including the metabolism of cholesterol and the conversion of proteins and fats into glucose. The liver is also where most drugs and toxins, including alcohol, are metabolized. What Goes Wrong in Cirrhosis? Cirrhosis results from damage to liver cells from toxins, inflammation, metabolic derangements and other causes. Damaged and dead liver cells are replaced by fibrous tissue which leads to fibrosis (scarring). Liver cells regenerate in an abnormal pattern primarily forming nodules that are surrounded by fibrous tissue. Grossly abnormal liver architecture eventually ensues that can lead to decreased blood flow to and through the liver. Decreased blood flow to the liver and blood back up in the portal vein and portal circulation leads to some of the serious complications of cirrhosis. Blood can back up in the spleen causing it to enlarge and sequester blood cells. Most often, the platelet count falls because of splenic sequestration leading to abnormal bleeding. If the pressure in the portal circulation increases because of cirrhosis and blood back up (note: this can also sometimes occur in severe cases of acute hepatitis and liver damage), blood can flow backwards from the portal circulation to the systemic circulation where they are connected. This can lead to varicose veins in the stomach and esophagus (gastric and esophageal varices) and rectum (hemorrhoids). Gastric and esophageal varices can rupture, bleed massively and even cause death. Hypertension in the portal circulation, along with other hormonal, metabolic and kidney abnormalities in cirrhosis, can also lead to fluid accumulation the abdomen (ascites) and the peripheral tissue (peripheral edema). Decreased bilirubin secretion from hepatocytes in cirrhosis leads to the back up of bilirubin in the blood. This leads to jaundice, the yellow discoloration of the skin and eyes. As the water-soluble form of bilirubin also backs up in the blood, bilirubin can also spill into the urine giving it a bright yellow to dark brown color. Abnormal biochemical function of the liver in cirrhosis can lead to several complications. The serum albumin concentration falls which can lead to aggravation of ascites and edema. The metabolism of drugs can change requiring dose adjustments. In men, breast enlargement (gynecomastia) sometimes occurs because metabolism of estrogen in the liver is decreased. Decreased production of blood clotting factors can lead to bleeding complications. Derangements in the metabolism of triglycerides, cholesterol and sugar can occur. In earlier stages, cirrhosis frequently can cause insulin resistance and diabetes mellitus. In later stages or in severe liver failure, blood glucose may be low because it cannot be synthesized from fats or proteins. Cirrhosis, especially in advanced cases, can cause profound abnormalities in the brain. In cirrhosis, some blood leaving the gut bypasses the liver as blood flow through the liver is decreased. Metabolism of components absorbed in the gut can also be decreased as liver cell function deteriorates. Both of these derangements can lead to hepatic encephalopathy as toxic metabolites, normally removed from the blood by the liver, can reach the brain. In its early stages, subtle mental changes such as poor concentration or the inability to construct simple objects occurs. In severe cases, hepatic encephalopathy can lead to stupor, coma, brain swelling and death. Cirrhosis of the liver can also cause abnormalities in other organ systems. Cirrhosis can lead to immune system dysfunction causing an increased risk of infection. Ascites fluid in the abdomen often becomes infected with bacteria normally present in the gut (spontaneous bacterial peritonitis). Cirrhosis can also lead to kidney dysfunction and failure. In end-stage cirrhosis, a type of kidney dysfunction called hepatorenal syndrome can occur. Hepatorenal syndrome is almost always fatal unless liver transplantation is performed. Clinical Symptoms and Diagnosis of Cirrhosis Cirrhosis is usually an easy diagnosis to make when any or all of the above abnormalities and complications are present. This is especially true when the underlying liver disease can be identified. The underlying liver disease (see below) is identified in most patients, however, sometimes it will not be discovered. Such cases are called "cryptogenic" cirrhosis. Sometimes, other conditions such as metastatic cancer, hepatic or portal vein thrombosis, severe acute hepatitis or acute bile duct obstruction can cause some of the abnormalities seen in cirrhosis. A careful history combined with special diagnostic tests will usually identify these conditions. Some patients with cirrhosis, especially early in the course of the disease, will have no overt clinical signs or symptoms. Some may have only subtle physical changes such as red palms, red spots that blanch on their upper body (spider angiomata), hypertrophy of the parotid glands, gynecomastia or fibrosis of tendons in the palms. Some patients may only have subtle abnormalities on blood tests, and in some cases, all blood tests may be normal. Radiological and nuclear medicine tests may give clues as to the presence of cirrhosis, but the diagnosis of cirrhosis must often be made by liver biopsy. Causes of Cirrhosis Although most often associated with alcohol abuse, cirrhosis of the liver can result from many causes. Almost any chronic liver disease can lead to cirrhosis. This list gives some of the many causes: Alcoholic liver disease - most common cause in the U. S. A. Chronic viral hepatitis B, C and D Chronic autoimmune hepatitis Inherited metabolic diseases (e. g. hemochromatosis, Wilson disease) Chronic bile duct diseases (e. g. primary biliary cirrhosis) Chronic congestive heart failure Parasitic infections (e. g. schistosomiasis) Nonalcoholic steatohepatitis (liver inflammation that can be caused by fatty liver) Long term exposure to toxins or drugs Treatment Cirrhosis of the liver is irreversible but treatment of the underlying liver disease may slow or stop the progression. Such treatment depends upon the underlying etiology. Termination of alcohol intake will stop the progression in alcoholic cirrhosis and for this reason, it is important to make the diagnosis early in a chronic alcohol abuser. Similarly, discontinuation of a hepatotoxic drug or removal of an environmental toxin will stop progression. Treatment of metabolic diseases, such as treatment of iron overload in hemochromatosis or copper overload in Wilson disease, are also effective therapies. Chronic viral hepatitis B and C may respond to treatment with interferon and autoimmune hepatitis may improve with prednisone and azathioprine (Imuran). Drugs such as ursodiol (Actigall) may slow the progression of primary biliary cirrhosis and possibly sclerosing cholangitis. In patients with cirrhosis of the liver, treatment must also be directed at the complications. Bleeding esophageal varices can be treated with endoscopic sclerotherapy or rubber band ligation. Ascites and edema are often responsive to a low sodium diet and such a diet must be emphasized in patients with these symptoms. More advanced ascites and edema can respond to diuretic therapy. A low protein diet and agents such as lactulose may help hepatic encephalopathy. Infections such as spontaneous bacterial peritonitis must be rapidly treated with appropriate antibiotics. Drugs metabolized in the liver must be given with caution. Coagulation disorders will sometimes respond to vitamin K. Liver transplantation is highly effective for the treatment of end-stage cirrhosis. Transplantation is usually needed when complications such as encephalopathy, ascites or bleeding varices are uncontrollable or when biochemical function is severely depressed. In patients with primary biliary cirrhosis, a rising bilirubin indicates a poor prognosis and such patients should be considered for transplantation as the serum bilirubin concentration begins to rise. Active drug or alcohol abuse are contraindications to liver transplantation. However, alcoholics who have abstained from drinking for an extended period of time (usually more than six months), and have participated in rehabilitation programs and support groups such as Alcoholics Anonymous, can be considered as candidates and will often have a good prognosis. Liver cancer is usually a contraindication to transplantation, except in experimental protocols. Liver transplantation is usually not performed in patients more than 70 years old. Alcoholic Liver Disease By Howard J. Worman, M. D. Alcohol abuse is a leading cause of morbidity and mortality throughout the world. It is estimated that in the United States as many as 10 % of men and 3 % of women may suffer from persistent problems related to the use of alcohol. The Fourth Edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) published by the American Psychiatric Association divides alcohol use disorders into "alcohol dependence" and "alcohol abuse." Alcohol dependence is indicated by evidence of tolerance and/or symptoms of withdrawal such as delirium tremens (DTs) or alcohol withdrawal seizures (rum fits) upon cessation of drinking. Alcohol abuse is characterized by recurrent performance problems at school or on the job that result either from the after effects of drinking alcohol or from intoxication on the job or at school. In addition, patients with alcohol abuse disorders may use alcohol in physically adverse circumstances (e.g. while driving) and may miss work or school or neglect child care or household responsibilities because of alcohol use. Legal difficulties related to alcohol use are also common. Patients with alcohol abuse disorders often continue to consume alcohol despite the knowledge that continued consumption poses significant social or interpersonal problems for them. People with alcohol use disorders often consume alcohol despite knowing that they suffer from alcohol-related medical problems such as liver disease. Alcohol affects many organ systems of the body, but perhaps most notably affected are the central nervous system and the liver. Almost all ingested alcohol is metabolized in the liver and excessive alcohol use can lead to acute and chronic liver disease. Liver cirrhosis resulting from alcohol abuse is one of the ten leading causes of death in the United States. From data obtained in autopsy studies, it appears that between 10 % and 15 % of alcoholics have cirrhosis at the time of death. It is unknown why some alcoholics develop liver disease while others do not. One possibility is that there are genetic factors that predispose some alcoholics to liver disease. Some data also suggest that co-factors such as chronic infection with hepatitis C virus may increase the risk of the development of cirrhosis in an alcoholic. In general, women who drink an equal amount of alcohol are at higher risk than men for the development of liver disease, possibly because of decreased metabolism of alcohol in the stomach prior to absorption. REMEMBER, LIVER DISEASE IS NOT THE ONLY LIFE-THREATENING COMPLICATION OF ALCOHOL USE DISORDERS. ALL ALCOHOLICS MUST ABSTAIN FROM DRINKING AS NUMEROUS OTHER ALCOHOL-RELATED MEDICAL, SOCIAL AND PSYCHOLOGICAL PROBLEMS CAN LEAD TO MORBIDITY AND MORTALITY. Alcohol abuse generally leads to three pathologically distinct liver diseases. In clinical practice, any or all of these three conditions can occur together, at the same time, in the same patient. These three conditions are: Fatty Liver (Steatosis) Alcohol abuse can lead to the accumulation of fat within hepatocytes, the predominant cell type in the liver. A similar condition can also be seen in some obese people who are not alcohol abusers. Fatty liver is reversible if the patient stops drinking, however, fatty liver can lead to steatohepatitis. Steatohepatitis is fatty liver accompanied by inflammation and this condition can lead to scarring of the liver and cirrhosis. Click to see a microscopic section of a NORMAL LIVER LOBULE and an example of FATTY LIVER in an alcoholic. (Images are part of WebPath and are copyrighted by the Pathology Department of the University of Utah Health Sciences Center. Link with permission of Edward C. Klatt, M. D.) Hepatitis Alcohol can cause acute and chronic hepatitis. The patient who presents with alcoholic hepatitis is usually a chronic drinker with a recent episode of exceptionally heavy consumption. Other presentations are also possible. Alcoholic hepatitis can range from a mild hepatitis, with abnormal laboratory tests being the only indication of disease, to severe liver dysfunction with complications such as jaundice (yellow skin caused by bilirubin retention), hepatic encephalopathy (neurological dysfunction caused by liver failure), ascites (fluid accumulation in the abdomen), bleeding esophageal varices (varicose veins in the esophagus), abnormal blood clotting and coma. Histologically, alcoholic hepatitis has a characteristic appearance with ballooning degeneration of hepatocytes, inflammation with neutrophils and sometimes Mallory bodies (abnormal aggregations of cellular intermediate filament proteins). Click to see a microscopic section of a NORMAL LIVER LOBULE and an example of a liver with ALCOHOLIC HEPATITIS. (Images are part of WebPath and are copyrighted by the Pathology Department of the University of Utah Health Sciences Center. Link with permission of Edward C. Klatt, M. D.) Alcoholic hepatitis is reversible if the patient stops drinking, but it usually takes several months to resolve. Alcoholic hepatitis can lead to liver scarring and cirrhosis, and very frequently occurs in alcoholics who already have cirrhosis of the liver. Cirrhosis Cirrhosis is characterized anatomically by widespread nodules in the liver combined with fibrosis. In the United States, alcohol abuse is the leading cause of liver cirrhosis. Anatomically, alcoholic cirrhosis is almost always micronodular (i.e. the regenerating liver nodules are small). You can click to see a microscopic section of a liver with MICRONODULAR CIRRHOSIS AND FATTY LIVER and a NORMAL SECTION for comparison. (Images are part of WebPath and are copyrighted by the Pathology Department of the University of Utah Health Sciences Center. Link with permission of Edward C. Klatt, M. D.) Cirrhosis can result from many causes other than alcohol such as chronic viral hepatitis, metabolic and biliary diseases. The co-existence of another chronic liver disease in a patient who abuses alcohol likely increases the risk of developing cirrhosis (eg. an alcoholic with chronic viral hepatitis C). Alcoholic cirrhosis can occur in patients who have never had evidence of alcoholic hepatitis. Cirrhosis can lead to end-stage liver disease. Some of the complications of cirrhosis are jaundice, ascites, edema, bleeding esophageal varices, blood coagulation abnormalities, coma and death. You can click to read more about CIRRHOSIS AND ITS COMPLICATIONS. Treatment The most important measure in the treatment of alcoholic liver disease is to ensure the total and immediate abstinence from alcohol. This will sometimes require admission to an in-patient medical ward for prophylactic treatment of withdrawal symptoms such as delirium tremens and seizures. Treatment of other associated neurological conditions may also be required. Chronic alcohol abusers often need treatment with vitamins, especially thiamin, to correct the deficiencies that may have resulted from chronic alcohol abuse. Intensive medical treatment of the complications of acute alcoholic hepatitis or cirrhosis is also sometimes necessary, as is the treatment of concurrent infectious and/or metabolic disorders. Once the patient is medically stable, he/she should receive on-going treatment to ensure abstinence from alcohol. This often includes a period of in-patient alcohol rehabilitation followed by subsequent long-term participation in support groups such as Alcoholics Anonymous and possibly continuous out-patient psychiatric care. Cessation of alcohol use will reverse fatty liver and alcoholic hepatitis. Although cirrhosis is irreversible, alcohol abusers who stop drinking will often have a good prognosis in that progressive liver deterioration can be avoided. There are several sites on the Internet with information about alcohol-related disorders and recovery programs for alcohol abusers. Here is a list of links, some of which will also lead to other sites: Alcoholics Anonymous Al-anon and Alateen