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)

Interest in ornithine decarboxylase (ODC) and the therapeutic effects of its inhibition with the consequent depletion of polyamine biosynthesis has been widespread since the late 1970s and 1980s. This review covers new information about the properties of ODC, recent findings with ODC inhibitors and a discussion of the mechanism of inactivation of ODC by eflornithine. Recent in vivo therapeutic approaches of ODC inhibition are also discussed including: cancer and cancer chemoprevention; autoimmune diseases; polyamines and the blood-brain barrier, ischemia and hyperplasia; the NMDA receptor and modulation by polyamines; hearing loss; African trypanosomiasis; Pneumocystis carinii pneumonia and Cryptosporidium in AIDS; and other infectious diseases/organisms.
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PMID:Ornithine decarboxylase as an enzyme target for therapy. 143 32

We examined 11 brains of human immunodeficiency virus (HIV) seropositive cases who died from unnatural causes (10 intravenous drug abusers who died from heroin overdose and 1 homosexual dead from a gunshot injury); 10 brains of HIV seronegative heroin addicts who died from overdose and 1 seronegative drug abuser who died from gunshot injury served as controls. Complete postmortem examination did not show evidence of acquired immune deficiency syndrome (AIDS) or AIDS related complex. Terminal changes including nerve cell ischemia, edema and diffuse vascular congestion were observed in all cases. Perivascular pigment deposition with macrophages was a constant finding in drug addicts and was probably related to chronic intravenous injection. In contrast, cerebral vasculitis was significantly more frequent and marked in HIV seropositive cases and was often associated with lymphocytic meningitis. Granular ependymitis, myelin pallor with reactive astrocytosis and microglial proliferation were also more frequent and more severe in HIV seropositive cases. Immunocytochemistry was negative for HIV antigens. Our study further supports the view that early central nervous system changes occur in HIV infection.
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PMID:Early brain changes in HIV infection: neuropathological study of 11 HIV seropositive, non-AIDS cases. 153 41

Three male patients with the acquired immunodeficiency syndrome revealed perforations of the intestine (jejunum-ileum; colon ascendens; coecum). The cause was necrosis due to cytomegalovirus infection. The characteristic findings were cytomegalic inclusion bodies in endothelial cells of the capillaries. These lesions caused alterations of the microcirculation. Therefore it seems reasonable to conclude that in these cases necrosis and perforation were due to ischemia. Cytomegalovirus infection must be taken into consideration in any patient with the acquired immunodeficiency syndrome and gastrointestinal ulcerations.
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PMID:[Cytomegalovirus infection as a cause of intestinal perforation]. 283 28

Electroretinographic (ERG) investigations were performed in three AIDS patients. The first had cotton wool-like spots in both eyes (AIDS "retinopathy"). The second presented with the same changes in his right eye and an acute cytomegalovirus (CMV) in his left eye. In the third patient signs of healed peripheral retinochoroiditis were found. In CMV retinitis the retinal damage demonstrated by ERG correlated well with the ophthalmoscopic findings. As the ERG improved concurrently with Ganciclovir therapy, retinal function can be monitored by means of ERG controls. In the cases of AIDS "retinopathy" with only a few cotton wool-like spots and with healed peripheral retinochoroiditis, pronounced changes in the ERG were seen regularly; these were most probably caused by ischemia of the inner retinal layers.
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PMID:[Electroretinography in AIDS retinopathy and AIDS cytomegalovirus retinitis with ganciclovir therapy]. 283 55

A gross, light, and electron microscopic study of the eyes from 35 consecutive autopsy cases of the acquired immune deficiency syndrome revealed cotton-wool spots (71% of cases), retinal hemorrhage in areas without cytomegalovirus infection (40%), cytomegalovirus retinitis (34%) with associated retinal detachment, Roth's spots (23%), retinal microaneurysms (20%), papilledema (14%), conjunctival Kaposi's sarcoma (9%), cryptococcal chorioretinitis (6%), Mycobacterium avium-intracellulare in retina and in choroidal granulomas (6%), ischemic maculopathy (6%), bilateral keratitis (3%), and herpes simplex retinitis (3%). Ocular infection with candida or toxoplasmosis were not found in this autopsy series. Immunocytologic studies demonstrated deposition of immunoglobulins in arteriolar walls, consistent with immune complex mediated disease. Ultrastructural studies showed a vasculopathy in the areas near cotton-wool spots. A mechanism is proposed linking the deposition of immune complexes with subsequent small vessel lesions, ischemia, cotton-wool spots and later spread of cytomegalovirus to retina via damaged vascular endothelium.
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PMID:Acquired immune deficiency syndrome. Pathogenic mechanisms of ocular disease. 298 69

Cerebrovascular lesions were seen in 28 of 83 cases (34%) of acquired immune deficiency syndrome (AIDS). Cerebral hemorrhage was noted in 4 cases, cerebral infarct in 23 cases and both in 1 case. Cerebral hemorrhage was in various locations such as intraparenchymal, subarachnoid space, subdural space and epidural space. Large, clinically evident hemorrhage was noted in 2 of 5 cases and bleeding tendency was noted in 2 cases. Most of the 24 cases with cerebral infarcts were not clinically evident; they were multiple, small and mainly involved the striatum, cerebral cortex and brain stem. Mural thickening of occasional small blood vessels was seen in 12 of the cases (50%) with infarcts. Other changes in blood vessels included vasculitis in one case and perivascular lymphocytic infiltration in another. In addition to thrombo-embolism and systemic ischemia/anoxia, these blood vessel changes may have a role in the development of cerebral infarcts in AIDS.
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PMID:Cerebrovascular lesions in acquired immune deficiency syndrome (AIDS). 318 38

Ophthalmic manifestations were studied in 34 patients suffering from AIDS. Ophthalmic disorders were found in 20 of these (58%), the most frequent being a cotton-wool-type spot (94.7%). Three patients showed an ophthalmic state compatible with choroid ischemia and atrophy of the pigmented epithelium of the retina. Three patients had necrotizing retinitis probably of viral etiology (cytomegalovirus). Other disorders observed were intraretinal hemorrhages, Roth's spots, microaneurysms, periphlebitis and ocular infiltration by Kaposi's sarcoma.
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PMID:Ophthalmic manifestations of acquired immunodeficiency syndrome. A study of thirty-four patients. 323 16

The study of microglial cell biology has become the key to understanding the brain's fundamental tissue reactions as well as the cellular mechanisms underlying CNS disease. This article focuses on glial-neuronal interactions with special reference to human pathology. Three important areas of brain pathology are critically reviewed: multiple sclerosis and CNS inflammation, the brain in AIDS and opportunistic infections, and neurodegenerative disorders. Although microglial cytotoxicity may cause bystander damage, e.g. in ischemia, there is little evidence to support the view that microglial activation per se is pathogenic. Results suggesting that one important normal function of microglia is to protect the integrity of the central nervous system are discussed. The concept is proposed that microglia function as a highly developed guardian to the CNS.
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PMID:Surveillance, intervention and cytotoxicity: is there a protective role of microglia? 770 19

Cytomegalovirus disease is an opportunistic infection that is seen in patients with inmunodeficiencies. The group most commonly affected are AIDS and transplanted patients. Only a few cases of cytomegalovirus disease in non-immunocompromised patients have been reported. In localized disease, the gastrointestinal tract is the most frequently affected. We report two cases of acute abdomen caused by cytomegalovirus enteritis and colitis (histopathological diagnosis) without any underlying immune disorder. The role that the cytomegalovirus infection might play in the development of the clinical manifestations in these two cases is discussed. Without an established immunodeficiency we must be careful to attribute to cytomegalovirus infection the direct responsibility of the lesions. In the reported cases, the existence of intestinal ischemia is more than just a clinical hypothesis and pathological examination is inconclusive. The absence of an immunocompromised state, the presentation as an acute abdomen and the clinical course forwards intestinal occlusion in the first case are not characteristic of cytomegalovirus enteritis and colitis. We conclude that the two reported cases are in fact an ischemic enteritis upon which cytomegalovirus enteritis and colitis was superimposed, an association that has not been reported before.
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PMID:[Cytomegalovirus enteritis and colitis in nonimmunodepressed patients, a primary disease or superinfection?]. 798 12

Increasing evidence supports the hypothesis that escalating levels of excitatory amino acids (EAAs) are responsible for neuronal cell death in a variety of acute neurological conditions including hypoxia/ischemia, trauma, seizures, and hypoglycemia. EAAs may also contribute to several chronic neurodegenerative diseases including Huntington's disease, parkinsonism, and acquired immunodeficiency syndrome dementia. A predominant form of neurotoxicity appears to be mediated by excessive activation of the N-methyl-D-aspartate subtype of glutamate receptor. This laboratory recently reported that memantine, an antiparkinsonian drug, is a potent N-methyl-D-aspartate antagonist capable of preventing the death of central neurons both in vitro and in vivo when given coincident to an EAA insult. In the present study, we found that 12 microM memantine prevented the death of neonatal rat retinal ganglion cells in primary culture when administered up to 4 hours after the initiation of N-methyl-D-aspartate receptor-mediated neurotoxicity.
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PMID:Delayed administration of memantine prevents N-methyl-D-aspartate receptor-mediated neurotoxicity. 809 95


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