No abstract available.
Mortality*

No abstract available.
Aged* ; Drug Therapy* ; Humans

No abstract available.
Aged* ; Drug Therapy* ; Humans

No abstract available.
Education, Distance*

No abstract available.
Hernia, Inguinal*

The chronic fatigue immune dysfunction syndrome (abbreviated CFIDS or CFS) is a disorder characterized by debilitating fatigue(over 6 months), along with cognitive, musculoskeletal, and sleep abnormalities. The etiology of this illness is unlikely to be a single agent. Findings to date suggest that physiological and psychological factors work together to predispose and perpetuate the illness. Diagnosis is made difficult by the nonspecific clinical findings and no available diagnostic testing. With no known cause or cure for the chronic fatigue and immune dysfunction syndrome, treatment is based on relieving symptoms and improving the quality of life of affected patients. There is emerging evidence that chronic fatigue syndrome may be familial. In the future, studies will examine the extent to which genetic and environmental factors play a role in the development of chronic fatigue syndrome. Most patients with CFS have psychiatric problems such as a generalized anxiety disorder, or major or minor depression, therefore, these mental health disorders may be correlated with the pathophysiology of the CFS. The treatment for CFS must be individualized, due to the heterogeneity of the CFS population. Also the treatment of CFS is built on a foundation of patient-physician relationship, respect and advocacy.
Anxiety Disorders ; Depression ; Diagnosis ; Diagnostic Tests, Routine ; Fatigue ; Fatigue Syndrome, Chronic* ; Humans ; Mental Health ; Population Characteristics ; Psychology ; Quality of Life

PURPOSE: Angiogenesis is a critical determinant of tumor growth and the development of metastasis. Angiostatin and endostatin have been used in a variety of in vitro and in vivo animal models as effective inhibitors of angiogenesis. However, human angiostatin and endostatin have not been tested against an intact human tissue target in vitro to determine its ability to achieve an antiangiogenic response. We performed our study to determine if human angiostatin and endostatin would inhibit the development of an angiogenic response (initiation) and to determine the subsequent growth (angiogenic index) of human vessels in a dose-dependent manner with a human placental vein angiogenesis model (HPVAM). METHODS: We used full thickness human placental vein discs cultured in three-dimensional fibrin-thrombin clots with an overlay of liquid media. Human angiostatin and endostatin were evaluated in concentrations ranging from 10-9 M to 10-4 M. A positive control containing 20% fetal bovine serum and a negative control using heparin and hydrocortisone 21-phosphate were also tested. RESULTS: Human angiostatin did not inhibit the initiation of an angiogenic response and the subsequent development of the angiogenic response (angiogenic index) at any concentration. Human endostatin significantly inhibited the initiation rate of an angiogenic response at a concentration of 10-4 M (p<0.001) and the subsequent development of an angiogenic response (angiogenic index) from a concentrations of 10-5 M to 10-4 M (p<0.001, p<0.001, respectively). CONCLUSION: We conclude that a very high concentration of human endostatin can inhibit the angiogenic response in human vascular tissue and that human angiostatin will not inhibit angiogenesis of normal human blood vessels in vitroThese results suggest that human endostatin has a more powerful antiangiogenic effect than human angiostatin, but we need further investigations of human angiostatin against an intact human tissue target.
Angiostatins* ; Blood Vessels ; Endostatins* ; Heparin ; Humans* ; Hydrocortisone ; Models, Animal ; Neoplasm Metastasis ; Veins

Ischemia causes tissue necrosis in a wide variety of pathologic conditions. Permanent deprivation of blood flow is lethal to any tissue and the prudent therapy for ischemia unquestionably is reperfusion. While reperfusion is necessary to reverse the progression towards ischemic death, reperfusion is also thought to be accompanied by its own component of injury. Oxygen free radicals, formed during ischemia/reperfusion, have been proposed as one of the main causes of reperfusion injury. Free radical attacks on biological membrane, such as mitochondria and endoplasmic reticulum, and can lead to the oxidative destruction of the polyunsaturated fatty acids of the membranes through lipid peroxidation. However, direct association between microsomal lipid peroxidation in vivo after ischemia/reperfusion and changes in secretory function and drug metabolism on the liver have not been established. Therefore, present study was performed to evaluate the hepatic secretory function and the hepatic microsomal drug metabolizing enzyme activity after ischemia/reperfusion preparation in rat liver. Further, the effect of oxygen free radical scavengers was investigated. The animals were divided into sham operation group and ischemia/reperfusion group. The ischemia/reperfusion group was subdivided into non-treated control and treated (with superoxide dismutase, allopurinol, alpha-tocopherol, deferoxamine) groups. Hepatic ischemia was produced by clamping the left branches of portal vein and hepatic artery, resulting in complete ischemia to the median and left lobes while the right lobes remained per Fused to prevent intestinal congestion. Reperfusion was permitted by declamping after 1 hour. After 1 or 5 hours of reperfusion, bile was collected, blood was obtained from abdominal aorta, and liver microsomes were isolated. The results are as follows. Serum aminotransferase was increased 15~20 times by ischemia/reperfusion. However, this increase was attenuated by free radical scavengers, especially 5 hours of reperfusion. The wet weight-to-dry weight ratio of the liver was significantly increased by ischemia/reperfusion. alpha-tocopherol pretreatment minimized the increase of ratio. Malondialdehyde level in the liver microsomal fraction was significantly increased after ischemia/reperfusion, but this increase was attenuated by scavenger pretreatment, especially alpha-tocopherol. Bile flow and cholate output but not the bilirubin output, were decreased after ischemia/reperfusion. The free radical scavenger pretreahnent restored the secretion significantly. Cytochrome P-450 content was significantly decreased after ischemia/reperfusion and ameliorated by free radical scavenger pretreatment. NADPH cytochrome P-450 reductase activity and aminopyrine N-demethylase activity were also decreased and improved by free radical scavengers pretreatment. These results indicate that ischemia/reperfusion deteriorates the hepatic secretory function as well as hepatic microsomal drug metabolizing enzyme activity, and the oxygen free radical scavengers attenuate the functional changes of the liver induced by ischemia/reperfusion.
Allopurinol ; alpha-Tocopherol ; Aminopyrine N-Demethylase ; Animals ; Aorta, Abdominal ; Bile ; Bilirubin ; Cholates ; Constriction ; Cytochrome P-450 Enzyme System ; Endoplasmic Reticulum ; Estrogens, Conjugated (USP) ; Fatty Acids, Unsaturated ; Free Radical Scavengers ; Free Radicals ; Hepatic Artery ; Ischemia ; Lipid Peroxidation ; Liver ; Malondialdehyde ; Membranes ; Metabolism* ; Microsomes, Liver ; Mitochondria ; NADPH-Ferrihemoprotein Reductase ; Necrosis ; Oxygen ; Portal Vein ; Rats* ; Reperfusion ; Reperfusion Injury ; Superoxide Dismutase

To establish whether an association exists between low blood pressure and common symptoms such as fatigue, dizziness, headache, and palpitation, we analysed the data of health center in Yeungnam medical college from January 1993 to June 1993. Total 1,133 subjects were taken and results were analysed by combined stratification and logistic regression. The results were as followed : 1. True confounders were sex, age, and body mass index. 2. No association was found between low blood pressure and all symptoms. 3. Positive associations were found between high blood pressure and self reported palpitation and headache, which persisted after adjusted for confounders. The results suggest that low blood pressure and all neurasthenic symptoms such as fatigue, palpitation, headache and dizziness have no association, but the validity is limited.
Body Mass Index ; Dizziness ; Fatigue ; Headache ; Hypertension ; Hypotension* ; Logistic Models ; Self Report

No abstract available.
Cholesterol* ; Dyslipidemias*