Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034067 (emphysema)
 11,506 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Experience gained in performing 3615 laparoscopic sterilizations in India over a 10-year period is reported. A simplified technique was developed for performing sterilization under local anesthesia without neuroleptanalgesia, avoiding uterine manipulators, performing direct trocar insertion without prior pneumoperitoneum, and using air for pneumoperitoneum. Beginning in 1973 laparoscopic sterilizations were performed using monopolar electrocoagulation and Hulka clips. The first 100 cases were done under local anesthesia with neuroleptanalgesia (75 mg meperidine, .6 mg atropine intravenously), using uterine manipulators and creating pneumoperitoneum with a Cerres needle and CO2. In 1974, neuroleptanalgesia was no longer used and air was used instead of CO2 for penumoperitoneum (3515 cases). The patients did not fast but were allowed to have liquids and given a glucose drink just prior to survery. The air was insufflated with a sigmoidoscopy bulb or a fish tank minicompressor. Since 1977 the trocar cannula has been inserted directly, without creating a pneumoperitoneum (1035 cases). Since 1980 the semilithotomy position and uterine manipulators are no longer used. A simple supine position with knees bent at right angles and a 30 degree Trendelenburg position was used in the last 435 cases. Of the 3515 cases performed under local anesthesia without neuroleptanalgesia, only 12 (.34%) needed medication during surgery. 20 patients developed vasovagal attacks and required atropine. None needed general anesthesia. Of the 3515 cases in which air was used for pneumoperitoneum, none developed air embolism. When preperitoneal (8 cases), omental (3 cases), and mediastinal (1 case) emphysema developed, it took 3-4 days to subside because the air was absorbed slowly. Postoperative shoulder pain persisted in 1038 cases (29.5%), but it was more of an annoyance than a complication. Of the 1035 cases of direct trocar insertion, there was no injury to the bowel or a blood vessel. In 14 cases (1.3%) the trocar was found to be extraperitoneal and reinserted for correct placement. Pneumoperitoneum with a Verres or spinal needle was created in 21 technically difficult cases (2%), which included obesity, previous scars, and a bulky postpartum uterus. A uterine manipulator wwas used in 9 technically difficult cases (2.07%).
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PMID:Development of a simplified laparoscopic sterilization technique. 623 98

Anaphylactic shock was produced in guinea-pigs by sensitizing them with oval albumin and challenging them with an intracardial dose (rapid shock) or intraperitoneal dose (slow shock) of the same protein 4 weeks later. The animals died within 5 min or 30 min, respectively. Blood for biochemical assays was taken by cardiac puncture and tissue samples were excised for histamine assay and histological studies. High concentrations of histamine (4-5 times the control values) were measured in the animals which died rapidly, but not in the others, whereas the histamine content of the stomach wall and lungs was decreased both in rapid and slow shock. Plasma cortisol was low in the rapid shock group. Plasma free fatty acids were high in both groups, but glucose only in the slow shock group. The lungs were distended, indicating bronchial obstruction. Occasional platelet agglutinations were seen in the lung veins. The most promising signs regarding the diagnosis of death from anaphylaxis were the high plasma histamine values and acute emphysema.
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PMID:Histamine, cortisol and organ changes in fatal anaphylactic shock in guinea-pigs. 670 65

This paper reports that substitution of Glucosidorum Tripterygii Totorum (GTT) for cortical hormone used to treat corticosteroid-dependent type of aspirin asthma, 60 mg, 3 times a day. The result showed that total effective rate was 100% including 31 cases of marked effective (86.11%) and 5 cases of effective (13.89%). Corticosteroid in the blood was significantly elevated to normal level after treatment (P < 0.001), Cushing's syndrome was cleared up gradually. The blood glucose in 9 cases complicated with diabetes mellitus was recovered and glucosuria test was negative. The value of peak expiratory flow (PEF) was increased to some extent (P of male < 0.01, of female < 0.05), especially on those not complicated with emphysema. There was no side-effect during the treatment and could avoid the side-effect of cortical hormone. This therapy was valuable.
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PMID:[Treatment of 36 corticosteroid-dependent type of aspirin asthma patients with Glucosidorum Tripterygii totorum]. 771 7

1. Endosulfan insecticide is a polychlorinated compound used for controlling a variety of insects; it is practically water-insoluble, but readily adheres to clay particles and persists in soil and water for several years. Its mode of action involves repetitive nerve-discharges positively correlated to increase in temperature. This compound is extremely toxic to most fish and can cause massive mortalities. In fish, it causes marked changes in Na and K concentrations, decrease in blood Ca(2+) and Mg levels and inhibits Na, K and Mg-dependent ATPase (in brain). 2. Bioaccumulation of endosulfan is reported for marine animals; however, freshwater animals (e.g., crayfish) accumulate it to some extent, but they lose the compound rapidly during depuration. Endosulfan is generally less toxic to aquatic invertebrates than fish. However, it causes decreases in adenylate energy charge, oxygen consumption, hemolymph amino acids, succinate dehydrogenase, heart-beat (mussel) and altered osmoregulation. 3. Generally, mammals are less susceptible to endosulfan's toxicity than aquatic animals. The majority of studies conducted on laboratory mammals can be summarized. (a) Neurotoxicity: male rats are more sensitive than females to endosulfan, which decreases brain and plasma acetylcholinesterase activity. Endosulfan I (a metabolite) causes a significant change in norepinephrine, 5-HT and GABA. (b) Renal toxicity: inhibition of MFOs activity was noticed in rats; other effects included changes in proximal convoluted tubules and necrosis of the tubular epithelium. (c) Hepatotoxicity: chemically-induced aminopyrine N-demethylase and aniline hydrolase were found in rat liver, and reduction in the glycogen level occurred. (d) Hematologic toxicity: endosulfan exposure resulted in a significant decrease in the level occurred. (d) Hematologic toxicity: endosulfan exposure resulted in a significant decrease in the erythrocyte glutathione reductase, hemoglobin amount, RBC number and mean corpuscular volume. 4. Respiratory toxicity: involved dyspnea, acute emphysema, cyanosis and hemorrhages in teh interalveolar portions of rat's lungs. 5. Biochemical: in rats, endosulfan caused increased glucose-6-phosphate dehydrogenase activity, blood glucose level, phospholipid contents of the microsomal and surfactant system, and profoundly induced the activity of alcohol dehydrogenase and cytosolic glutathione S-transferases. It also decreased significantly Na+, K+ and Mg(2+) ATPases, plasma calcium level and alkaline phosphatase in the intestinal epithelium. 6. Immunologic toxicity: rat serum antibody titer to tetanus toxin, IgG, IgM and gammaglobulins were significantly reduced. 7. Reproductive toxicity: degenerative changes in the seminiferous epithelium, induction of the rate-limiting enzyme in testosterone production (3beta-hydroxysteroid transferase and 17 beta-hydroxysteroid transferase), histological changes in reproductive organs, testicular atrophy and the occurrence of ovarian cysts were noticed in rat. Reduction in the weight of secondary sex organ was also observed.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Bioaccumulative potential and toxicity of endosulfan insecticide to non-target animals. 790 Sep 59

A 75-g oral glucose tolerance test (OGTT) was performed on 18 patients with chronic respiratory failure and without fasting hyperglycemia, positive urine glucose, or hepatic/pancreatic disorders. Underlying diseases in these patients were pulmonary emphysema (11 cases, 61%), pulmonary tuberculosis (5 cases, 28%), and chronic bronchial asthma (2 cases, 11%). The body mass index (mean +/- SD, 17.6 +/- 2.2 kg/m2, P < 0.001) in these patients was significantly lower than that (23.8 +/- 3.1 kg/m2) in normal subjects. The OGTT results showed an impaired glucose tolerance pattern in 9 cases (50%) and a diabetes mellitus pattern in 6 cases (34%). The mean two-hour plasma glucose value in the patients was 9.8 mmol/L. However, insulin secretion responded well to glucose loading. These results suggest that a high proportion of chronic respiratory failure patients may have an intolerance for glucose loading but a normal insulin secretion pattern.
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PMID:Glucose intolerance in chronic respiratory failure. 797 7

Previously by selection and inbreeding of Wistar rats susceptible or resistant to the cataractogenic effect of galactose the S and R rat strains differing in the intensity of hexose transport into the animal cells were developed. High level of OH-radical generation and enhanced lipid peroxidation are revealed in the liver and myocardium of the S rats in contrast to the R rats. Data are obtained supporting the view that enhanced generation of OH-radicals within the S rat tissues is due to oxidation and autooxidation of the abundant amounts of monosacharides intensely accumulating in the rat cells. In spite of continuous inbreeding for more than 40 generations and a high rate of homozygosity, numerous DNA rearrangements are revealed in the S rat genomes. Fragility of the S rat cell membranes is detected. Cataracts and other lens lesions, emphysema, tumors, cardiomyopathy-like changes in the myocardium, scoliosis, brain disfunctions are characteristic of the S rats, as well as low fertility and short life-span indicative of premature aging.
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PMID:Inherited enhancement of hydroxyl radical generation and lipid peroxidation in the S strain rats results in DNA rearrangements, degenerative diseases, and premature aging. 813 16

Alpha-1-protease inhibitor is susceptible to oxidative impairment by the neutrophil myeloperoxidase (MPO) system. The purpose of this study was to assess the effect of the MPO oxidant system on elastase-induced emphysema in the hamster. Intratracheal instillation of 200 micrograms of human neutrophil elastase (HNE) induced a significant secretory cell metaplasia (SCM) and airspace enlargement [23% increase in mean linear intercept (MLI) as compared with control values]. Instillation of MPO system components [0.6 international units (U) of MPO, 5.5 U of glucose oxidase and glucose (0.02 M)] along with 200 micrograms HNE failed to enhance the severity of the SCM or emphysema induced by HNE alone. A second experiment was carried out using 50 micrograms of porcine pancreatic elastase (PPE) to induce emphysema. PPE produced a significant 45% increase in MLI, but the MPO system combined with PPE failed to enhance the emphysema induced by PPE alone. The MPO system alone had no measurable effect on airspace size or SCM. In vitro studies showed that PPE was partially inactivated by the MPO system; a 56% loss of elastolytic activity occurred during a 6-min incubation of PPE with the MPO system. This may explain why the MPO system did not exacerbate PPE-induced injury, but it does not explain the lack of enhancement for HNE. A 6-minute incubation of HNE with the MPO system resulted in a nonsignificant 10% decrease of elastolytic activity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Oxidants from neutrophil myeloperoxidase do not enhance elastase-induced emphysema in the hamster. 821 Jul 17

A 24-year-old previously healthy man presented with a 3-week history of progressively intensifying symptoms of diabetes mellitus. He had become increasingly unwell during the night preceding his admission to hospital and had developed central pleuritic chest pains with nausea; he had vomited once. On admission, he was clinically dehydrated and acidotic with Kussmaul's respiration. A diagnosis of diabetic ketoacidosis was confirmed by laboratory tests (arterial pH 7.21; bicarbonate 11.6 mmol l-1; blood glucose 40.5 mmol l-1, and heavy ketonuria). Subcutaneous emphysema was palpable in the neck tissues and a chest X-ray revealed mediastinal emphysema. There was no clinical or radiological evidence of acute or chronic pulmonary disease and a barium swallow confirmed the integrity of the oesophagus. He made an uneventful recovery from the ketoacidosis with conventional therapy. The subcutaneous emphysema and pneumomediastinum had completely resolved at review 4 weeks later.
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PMID:Pneumomediastinum complicating diabetic ketoacidosis. 879 65

We have recently identified a novel gene, klotho (kl), which may suppress several aging phenotypes. A defect of kl gene expression in the mouse results in a syndrome resembling human aging, such as arteriosclerosis, skin atrophy, osteoporosis, and pulmonary emphysema. To determine whether mouse homozygotes for the kl mutation (kl/kl) show abnormal glucose metabolism, an oral glucose tolerance test (OGTT) was performed at 6 to 8 weeks of age. Blood glucose levels during the OGTT were significantly lower in kl/kl mice versus wild-type mice. The insulin content of the pancreas was significantly lower in kl/kl mice compared with wild-type mice. Decreased insulin production was also supported by Northern blot analysis showing lower levels of insulin mRNA in kl/kl mice. To examine how lower blood glucose levels may exist in kl/kl mice despite decreased insulin production, insulin tolerance tests (ITTs) were performed. The glucose decline following insulin injection was more severe in kl/kl mice versus wild-type mice, suggesting that insulin sensitivity was higher in kl/kl mice versus wild-type mice. In kl/kl mice, an augmented expression of GLUT4 in skeletal muscle was demonstrated by both Northern blot analysis and Western blot analysis. Thus, we conclude that insulin production is decreased and insulin sensitivity is increased in the klotho mouse, a novel animal model for human aging.
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PMID:Decreased insulin production and increased insulin sensitivity in the klotho mutant mouse, a novel animal model for human aging. 1101 90

Early lactic acidosis has been suggested as negatively influencing the exercise capacity of patients with chronic obstructive pulmonary disease (COPD). We conducted a study to investigate whether the early lactate (La) response to exercise in COPD is related to alterations in exercise-related substrate levels in resting muscle, associated with physical inactivity. Twenty-seven COPD patients and 22 controls (physically inactive [PI] subjects, n = 15; and physically active [PA] subjects, n = 7) performed an incremental cycle test. Venous blood was sampled for La analyses, and the oxygen uptake at which the La level began to rise (La threshold) was calculated. Vastus lateralis biopsy specimens were obtained at rest. In the PA group, muscle glutamate (GLU) and glycogen were higher, but muscle La, pyruvate, and glucose were not different than in the PI group. Moreover, the La threshold was higher in the PA group. The COPD group had lower values for La threshold and muscle GLU, and higher values for muscle La and pyruvate levels than did the PI group. Stratification of patients into those with and without macroscopic emphysema (EMPH+, EMPH-, respectively), with comparable physical activity levels on the basis of previous observations, revealed lower values for La threshold and GLU in EMPH+ patients. Diffusing capacity for carbon monoxide (DL(CO)) and arterial oxygen tension (Pa(O(2))) in the four study groups were positively related to GLU and La threshold. Moreover, La threshold was positively related to GLU. This study illustrates that the early lactic acidosis during exercise in patients with COPD is associated with the physical inactivity-related reduction in these patient's muscle GLU. However, factors other than physical inactivity, such as Pa(O(2)) or DL(CO), play a role in the different La responses during exercise in subjects with different subtypes of COPD.
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PMID:Exercise-induced lactate increase in relation to muscle substrates in patients with chronic obstructive pulmonary disease. 1106 99


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