Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Since the mid-1970s, evidence has accumulated that cholecystokinin (CCK) has a role as a neuromodulator or neurotransmitter in the central nervous system as well as in the periphery. CCK has been shown to have a variety of effects on gastrointestinal functions and is one of the main candidates for a role as a peripheral negative feedback signal to stop feeding behavior. CCK produces satiety not only in animals but also in man: it reduces appetite and activation arising from the preparation of a meal and inhibits intake of liquid and solid food in both lean and obese subjects. The closely related peptide caerulein has similar effects. The site of action of peripherally administered CCK seems to be on an abdominal organ innervated by gastric vagal branches and relayed to the brain by afferent vagal fibres, since selective gastric vagotomy blocks the satiety effect, but pharmacological antagonism of vagal motor effects or lesions of the ventromedial hypothalamus do not. CCK also may have a role in the regulation of pain perception. In mice, CCK and caerulein were shown to produce a decrement in response to noxious stimulation after peripheral and central administration. In man, caerulein was demonstrated to relieve pain originating from biliary and renal colic as well as from cancer and ischemia. A series of studies in healthy man revealed that caerulein also alleviates experimentally induced cutaneous pain. Data from animal studies suggest that CCK-like peptides not only are able to produce analgesic effects on their own, but also are involved in the modulation of opioid systems mediating analgesia. Further study of these effects of CCK should elucidate the regulatory connections between the life-sustaining functions of feeding and pain sensation.
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PMID:Effects of cholecystokinin and caerulein on human eating behavior and pain sensation: a review. 308 29

Free radicals have been implicated in many pathological processes, including ischemia, inflammation, and malignancy. Since a reduction in extrathyroidal outer ring monodeiodination of T4 and rT3 occurs in virtually all systemic illnesses, we have studied the effect of free radicals on iodothyronine (T4 and rT3) 5'-monodeiodinating activity (MA) of liver tissue in vitro. Rat liver microsomes or homogenate were preincubated in Tris buffer for 30 min with a free radical-generating system (FRGS) and then incubated with T4 (2.5 microM) or [125I]rT3 (0.4 nM) and dithiothreitol (DTT; 5-20 mM with T4 and 20-150 mM with [125I]rT3) in the same buffer for 10 or 30 min. T3 generated during incubation was quantified by RIA of ethanol extracts of the incubation mixture. 125I generated from [125I]rT3 was quantified after precipitation of the incubation mixture with trichloroacetic acid or by paper chromatography. Free radicals caused 55% or more reduction in hepatic T4 MA and 44% or more reduction in rT3 MA in various experiments. The inhibition of hepatic rT3 MA after incubation with FRGS persisted despite removal of FRGS and washing of microsomes preincubated with FRGS before studying the MA. However, inclusion of DTT (1-60 mM) during preincubation of tissue with FRGS prevented the FRGS-induced inhibition of rT3 MA. Depletion of the iodothyronine substrate did not occur when FRGS inhibited T4 and rT3 5'-monodeiodination. Free radical scavengers, i.e. superoxide dismutase (600 IU/ml), catalase (300 U/ml), tocopherol (10 mg/ml), thiourea (0.15 M), and tert-butanol (0.15 M), all significantly reduced the inhibition of hepatic rT3 MA caused by FRGS. The FRGS-induced inhibition of hepatic T4 MA was reduced by the same doses of tocopherol, thiourea, and tert-butanol, but not by superoxide dismutase or catalase. Since free radicals may effect tissue damage by lipid peroxidation and since the latter results in generation of malondialdehyde (MDA) as a by-product of the reaction, we studied MDA by its reaction with 2-thiobarbituric acid. Incubation with FRGS caused an approximately 100-fold increase in MDA formation in liver microsomes. Serum MDA was significantly higher in 16 NTI patients than in 8 normal subjects and also higher in turpentine oil-injected rats [an experimental model of nonthyroidal illness (NTI)] than in saline-injected control rats. The data suggest that generation of free radicals may contribute to the reduced extrathyroidal 5'-monodeiodination of T4 and rT3 in NTI.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The effect of free radicals on hepatic 5'-monodeiodination of thyroxine and 3,3',5'-triiodothyronine. 310 83

Necrotizing sialometaplasia is a benign disorder that histologically can mimic carcinoma. It is thought to develop as a result of ischemia or adjacent tissue injury. A patient is described who underwent a Mohs' micrographical fresh-tissue excision of one-third of the upper lip for basal cell carcinoma. By the time she was ready for reconstruction, a marked eczematous reaction developed to a polymyxin neomycin preparation (Neosporin ointment) at the wound edges. Reexcision of the wound margins before a flap reconstruction revealed necrotizing sialometaplasia on histopathological examination. This incidental finding fortunately was not mistaken for residual tumor. To prevent over-diagnosis and over-treatment of presumed malignancies, an awareness of necrotizing sialometaplasia is essential for all surgeons operating on mucosal surfaces in the head and neck.
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PMID:Necrotizing sialometaplasia masquerading as residual cancer of the lip. 317 23

A total of 512 colectomy and endoscopic biopsy specimens were reviewed to define the prevalence and possibly the significance of dystrophic goblet cells (DGCs) in neoplastic and nonneoplastic colonic diseases. As compared with an incidence of 1% in disease-free specimens, DGCs were observed in 38% of cases of inflammatory bowel disease, 23% of colonic malignancies, 30% of nonneoplastic polyps, 22% of adenomas, and 8% of cases showing acute self-limited colitis. In contrast, no dystrophic cells were seen in a group of miscellaneous diseases including diverticulitis, diverticulosis, abscesses, fistulas, ischemia, pseudomembranous colitis, melanosis coli, amyloidosis, shock, and mechanical trauma. Although dystrophic cells occur in association with dysplasia and carcinoma, their presence in nonpremalignant lesions, including acute self-limited colitis, raises doubt as to their diagnostic significance. Histochemical studies of the mucin composition in DGCs were unrevealing, failing to show any differences between DGCs and their morphologically normal counterparts in the same region of the colon.
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PMID:The incidence and carbohydrate histochemistry of dystrophic goblet cells in colon. 323 12

Fiberoptic colonoscopy is 25 years old this year. Improvement in instruments led rapidly to wide acceptance of colonoscopy in diagnosis and therapy of colorectal diseases. The diagnosis of benign and malignant neoplasms was revolutionized by colonoscopy. The differential diagnosis of inflammatory bowel disease, assessment of its extent and severity, response to treatment, and potential for development of cancer are all made easier by colonoscopy. Colonoscopy has improved the diagnosis of diverticular disease, rectal bleeding, identification of ischemia, and other problems. Therapeutic colonoscopy has radically changed the management of colonic polyps, and colonoscopic polypectomy is now the standard form of treatment for most of these lesions. Treatment of bleeding lesions, decompression of obstruction, and removal of foreign bodies are other examples of therapeutic colonoscopic procedures.
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PMID:Conceptual developments through colonoscopy. 324 46

Serotherapy and plasma therapy have proved to be effective in the treatment of diverse neoplasms. The mechanisms of the tumoricidal or growth-inhibitory effects are unknown. We previously reported that activation of the alternative pathway of complement in absorbed sera correlated with the presence of anti-tumor activity. Complement components generated during absorption may serve as the initial mediators of cytotoxicity; for example, C5a may function in its role as a chemo-attractant. To further investigate the anti-tumor mechanisms, we undertook a series of sequential histological studies of in vivo changes in tumors following i.v. serotherapy. We found diffuse inflammatory cellular infiltrates in the interstitial compartments of primary mammary carcinomas of rats within 3-4 hr of administration of protein A-Sepharose absorbed syngeneic serum. The number of inflammatory cells was significantly higher in tumors from treated rats: total infiltrating cells (p = 0.002), eosinophils (p = 0.001), neutrophils (p = 0.001), macrophages (p = 0.001), lymphocytes (p = 0.004) and plasma cells (p = 0.001). Also, the mitotic index of tumor cells was significantly lower 4 hr after serotherapy when compared with that of untreated rat tumor cells. C3 in tumor tissue was decreased at 4 hr following serotherapy. Fibrosis was present in tumor nodules with retarded growth 5 weeks after the start of serotherapy. Localization of the infiltrating cells to tumor interstitial compartments prevents direct contact between inflammatory cells and neoplastic cells, making it unlikely that direct cell-cell killing occurs. Indirect cell killing within the tumor bed apparently occurs through several mechanisms involving interactions between serotherapy-initiated humoral mediators and inflammatory cells. The resulting anti-tumor effects include microvascular injury leading to localized ischemia, tumor infarction, and fibroblastic reactions obstructing tumor invasion and growth.
Int J Cancer 1988 Jul 15
PMID:Serotherapy of cancer: cellular changes in primary rat mammary carcinomas after infusion of syngeneic sera absorbed with protein A-Sepharose. 329 44

Three patients developed anterior substernal chest pain in association with ischemic electrocardiographic changes temporally related to continuous infusions of 5-fluorouracil (5-FU). Two patients developed myocardial infarctions and one died. Cardiac toxicity of 5-FU may be more likely when the drug is given by continuous infusion in the presence of preexisting cardiac disease. The pattern of cardiac toxicity suggests cardiac ischemia most likely secondary to coronary artery vasospasm. Patients should not receive 5-FU by infusion if they have significant underlying coronary artery disease or if they develop anterior substernal chest pain while receiving the drug.
Cancer Treat Rep
PMID:Cardiotoxicity of 5-fluorouracil. 330 Sep 68

Tissue damage as a consequence of ischemia is a major medical problem in an industrialized society. Whereas the conventional view has attributed this injury process to ischemia itself, recent studies have found that a variable, but often substantial proportion of the injury is caused by toxic oxygen metabolites that are generated from xanthine oxidase at the time of reperfusion. This mechanism was first identified and characterized in a model of moderately mild partial vascular occlusion in the feline small intestine. Strikingly similar mechanisms have been subsequently confirmed as the basis for ischemia/reperfusion injury in the stomach, pancreas, liver, skin, skeletal muscle, heart, lung, kidney and central nervous system. The potential for clinical application of this concept is related primarily to that proportion of the total post-ischemic injury that is due to this reperfusion mechanism, set against the proportion due to ischemia itself. Ironically, in clinical cases of intestinal ischemia the reperfusion component appears to be proportionately small, and the potential for treatment of ischemic bowel disease is correspondingly limited. On the other hand, there is reason to expect that the ablation of free radical-mediated reperfusion injury, something that can be readily achieved through non-toxic means, may provide substantial benefit for the treatment of ischemic renal disease, myocardial infarction, stroke, cardiac arrest, and of organs preserved for transplantation.
Br J Cancer Suppl 1987 Jun
PMID:Free radical-mediated reperfusion injury: a selective review. 330 76

The current status of superoxide dismutase (SOD) is that it is an enzyme with diverse ramifications. This review attempts an understanding of SOD as a structural, functional, and biological entity. Accordingly, the review is in three parts. The first part discusses SOD in terms of protein structure, proceeding from primary to secondary and three-dimensional structure for the three forms of SOD: copper/zinc SOD, manganese SOD, and iron SOD. This is the order of structural knowledge of the enzyme. Iron SOD is an enzyme of prokaryotes and some higher plants. Manganese SOD is an enzyme of prokaryotes and eukaryotes. Copper/zinc SOD is an enzyme of eukaryotes and certain prokaryotes. The evolutionary relationships of the three forms of SOD, the status of the copper/zinc SOD gene in prokaryotes, and the cloning and sequencing of SOD genes are discussed. The second part of the review deals with the catalytic mechanism of SOD in the three forms of the enzyme. Structural and mechanistic conclusions from various spectroscopic studies are critically considered. A detailed picture is given of the active site of copper/zinc SOD. The third part is a review of SOD in the general context of oxygen toxicity. After consideration of the question of superoxide toxicity and superoxide pathology, several areas in which SOD has been investigated or used as a tool in a biochemical, pharmacological, or clinical context are discussed, including population genetics; trisomy 21; development and senescence; the nutritional copper, zinc, and manganese status; hemolysis and anemia; oxygen toxicity in the lung and nervous system; inflammation, autoimmune disease and chromosome breakage, ischemia and degenerative changes; radiation damage; and malignancy. A comprehensive picture is given of measurements of SOD activity in disease states, and the question of superoxide-related disease is considered at several points.
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PMID:Aspects of the structure, function, and applications of superoxide dismutase. 331 61

Magnetic resonance spectroscopy is able to measure noninvasively a variety of important metabolites involved in cell energetics. These include phosphocreatine, ATP, inorganic phosphate, pH, and lactate. Anoxia, ischemia, and infarction produce rapid loss of high-energy phosphates and accumulation of hydrolysis products. Many animal studies have shown that MRS monitors metabolic changes in various models of human disease. The availability of large, high field magnets and the development of noninvasive localization techniques permits MRS to be performed on selected volumes within the body. It is now clear that MRS in humans will be immediately useful in several areas including studies of malignancy, ischemia, and infarction of various organs and metabolic disorders. It is expected that human MRS will be increasingly used for clinical investigation and eventually for medical diagnosis.
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PMID:NMR spectroscopy for clinical medicine. Animal models and clinical examples. 332 57


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