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

To elucidate the heart involvement associated with influenza virus infection, the authors studied the hearts of influenza A/PR/8/34 virus-inoculated ICR mice by light and electron microscopy, cardiac catheterization, virus assay, and indirect immunofluorescence. Light microscopy showed small necrotic foci with inflammatory cell infiltration spreading in the myocardium on days 3 to 7 and evidence of healing by day 9 after inoculation. Electron microscopy demonstrated that necrotic cell debris was phagocytosed by macrophages, and that degenerating cardiocytes, macrophages, and lymphocytes were often in close contact, suggesting immunologic interactions, and that platelet thrombi were present in some capillaries on days 3 to 5. Both systolic and diastolic functions of the left ventricle (LV) were impaired on days 3 to 9 and recovered almost to normal by day 14. The virus could be isolated from the heart on days 3 to 7. Immunofluorescent preparations showed virus antigens in the vascular walls and cardiocytes until day 7. These results suggest that the acute cardiac injury was related to cytotoxic immunologic interactions, virus-induced cytolysis and, at least in part, to ischemia due to intracapillary thrombosis. Compared with coxsackie B3 myocarditis in mice, the influenza myocarditis was mild in degree and short in duration, but the influenza infection is a most common and repetitive disease in humans. The clinical implications of this animal model with myocarditis are discussed.
 ...
PMID:Experimental influenza A virus myocarditis in mice. Light and electron microscopic, virologic, and hemodynamic study. 215 29

Infection following breast implants is an uncommon event. This is somewhat surprising, since the human breast is not a sterile anatomical structure. The flora found in the breast are derived from the nipple ducts and closely resemble those of normal skin. These organisms, predominantly S. epidermidis, may in some cases be responsible for firmness secondary to capsular contracture. Treatment of the periprosthetic infection usually involves implant removal, but salvage by systemic antibiotics is sometimes possible. Atypical mycobacteria are very rarely the cause of infection, but can be extremely difficult to eradicate when involved. Toxic shock syndrome has been reported to occur following breast implants and is a life-threatening problem requiring immediate removal of the implant. It may be significant that in some cases with effusion and infection occurring many months or years after implant placement, there has been a preceding event such as a laryngitis or flu-like illness. This suggests the possibility of a bacteremia being involved in the causation of the infection. If this were the case, then these patients should be handled in a fashion similar to those with prosthetic heart valves. Accordingly, in our own practice, we advise that penicillin "V" be given beforehand when a patient with breast implants is to have any dental procedure. It must be stressed that there is no statistical or scientific proof at the present time that this is of any value. In conclusion, when dealing with these large foreign bodies, absolute sterility is essential, and excellent surgical technique to obviate hematoma and the occurrence of tissue ischemia is mandatory. Evidence of severe infection necessitates implant removal, but in less severe cases a trial of intravenous antibiotics is permissible. Having removed an implant, further insertion should be deferred, preferably for 6 months. If the new implant can be placed in a different plane, that is, submuscular, this is desirable. Exposed implants can be salvaged but this requires considerable judgment and one should be prepared for re-exposure or frank infection.
 ...
PMID:Infections in breast implants. 266 82

Recombinant gamma interferon (r-GIFN) demonstrates in vitro and in vivo characteristics that contrast with those of alpha and beta interferons. It has relatively weak antiviral properties, yet relatively potent immunomodulatory effects. A phase I trial was performed with r-GIFN (specific activity 2.6 X 10(6) IU/mg protein), administered as a continuous intravenous (IV) infusion over 24 hours for five days (Cl X 5) and repeated every 28 days. This schedule was chosen based on the short half-life of r-GIFN in animal systems and the in vitro augmentation of biologic effects with continuous exposure to interferons. Twenty-one patients with refractory solid tumors received 46 evaluable courses of therapy. The dose-limiting toxicities included fever, flu-like symptoms, cardiovascular toxicity, and neurotoxicity. The cardiovascular toxicity included hypotension and one episode of cardiac ischemia with chest pain. Neurotoxicity consisted of lethargy and confusion. These toxicities were reversible, and although dose-limiting, occurred sporadically throughout all dosage levels. Mild to moderately severe non-dose-limiting toxicities included nausea and vomiting, leukopenia, and liver function abnormalities. Other infrequent toxicities included hypocalcemia, diarrhea, constipation, and alopecia. The maximally tolerated dose of r-GIFN on this schedule is 0.5 X 10(6) IU/m2/d. Partial responses were seen in one patient with metastatic melanoma and in one patient with renal cell carcinoma. Toxicity and antitumor activity were seen at doses where interferon serum levels could not be detected by radioimmunoassay. In addition, the toxicity and antitumor activity seen were at much lower doses than previously described for shorter infusion schedules of other recombinant gamma interferon preparations. Differences in biologic activity of interferon preparations and/or differences in scheduling may account for this variability. Although this study defines a recommended phase II dose of r-GIFN based on the maximally tolerated dose, the optimal therapeutic index may exist at a lower dosage level.
 ...
PMID:A phase I clinical trial of recombinant DNA gamma interferon. 310 84

Rhabdomyolysis can be precipitated by trauma, ischemia, metabolic defects, electrolyte abnormalities, drugs, and a wide variety of infectious diseases. At our institution, recent cases of rhabdomyolysis induced by influenza prompted us to review the infectious etiologies of this entity. In addition, a thorough literature search revealed numerous case reports but no general review on this subject. This study describes representative recent cases from our institution and details the wide variety of infections that can cause muscle damage. The pathophysiological mechanisms, muscle histology, and correlation with renal dysfunction are also discussed.
 ...
PMID:Infectious etiologies of rhabdomyolysis: three case reports and review. 911 26

Constrictive bronchiolitis (CB), also termed in lung transplant patients obliterative bronchiolitis, is inflammation and fibrosis occurring predominantly in the walls and contiguous tissues of membranous and respiratory bronchioles with resultant narrowing of their lumens. CB is found in a variety of settings, most often as a complication of lung and heart-lung transplantation (affecting 34% to 39% of patients, usually in the first 2 years after transplantation) and bone marrow transplantation, but also in rheumatoid arthritis, after inhalation of toxic agents such as nitrogen dioxide, after ingestion of certain drugs such as penicillamine and ingestion of the East Asian vegetable Sauropus androgynous, and as a rare complication of adenovirus, influenza type A, measles, and Mycoplasma pneumoniae infections in children. In lung transplants, CB is the single most important factor leading to death thereafter. In one study, the overall mortality rate was 25%. However, at the same time, 87% of patients who were asymptomatic and diagnosed solely by transbronchial biopsy had resolution or stabilization of disease. Decreases in FEV1 from baseline can be used to clinically support CB in transplant patients; the term bronchiolitis obliterans syndrome is used to denote this clinical dysfunction, and a grading system has been established for it that is now widely used in the literature. Significant risk factors for the development of CB in lung transplants include alloantigen-dependent and -independent mechanisms. In the former group are late acute rejection and HLA mismatches at the A loci; in the latter are ischemia/reperfusion injuries to airways that result from the transplantation surgery and cytomegalovirus infection.
 ...
PMID:Constrictive (obliterative) bronchiolitis. 1081 4

We have previously determined that there is a significant benefit of vaccination against influenza in patients hospitalized due to an acute coronary event. The purpose of this study is to determine whether the observed benefits of vaccination were maintained over a 2-year follow-up among those who were re-vaccinated during the subsequent winter season. During the winter season of 2001, a total of 301 acute coronary patients were prospectively enrolled within 72 hours of the onset of symptoms. Follow-up was conducted at 6 and 12 months. Patients who survived participated in a registry 1 year after the 2nd influenza vaccination period (winter 2002), as a cohort of chronic and stable coronary patients. The incidence of the primary endpoint cardiovascular death at 1 year was significantly lower in patients receiving vaccination than in controls (6% vs 17%, respectively) by intention-to-treat analysis. The relative risk with vaccination in comparison with controls was 0.34; 95% confidence interval, 0.17-0.71; P = 0.002. In the winter of 2002, 116 patients were vaccinated according to their physicians' instructions, and 114 subjects remained unvaccinated. The combined endpoints of total death plus myocardial infarction 1 year later were 4 (3.4%) in the vaccinated group vs 11 (9.7%) among those who were not vaccinated (P = 0.05). Influenza vaccination may reduce the risk of death and ischemic events in patients admitted with acute coronary syndromes. There is also a beneficial trend in the quiescent phase of ischemia.
 ...
PMID:Two-year follow-up of the FLU Vaccination Acute Coronary Syndromes (FLUVACS) Registry. 1506 23

Ischemia-induced biliary tract lesions, called ischemic cholangitis, often lead to strictures of biliary ducts and cholestasis. Causes of ischemic changes of the biliary tract can be found in the arterial blood supply or in the peribiliary capillary plexus. Known examples are thrombosis after transplantation, intraoperative ligation, or the application of chemotherapeutic drugs. Rarely, such changes are due to inflammation of the blood vessels, such as occurs in polyarteritis nodosa or giant cell arteritis. We present a report of a 49-year old man with leucocytoclastic vasculitis after viral infection, influenza vaccination, and antibiotic treatment, leading to florid ischemic cholangitis. We conclude that hypersensitivity vasculitis must be included in the differential diagnosis of cholestasis and cholangitis.
 ...
PMID:Florid ischemic cholangitis due to leucocytoclastic vasculitis. 1506 28

The lungs are the richest in oxygen among the various organs of the body and are always subject to harmful reactive oxygen species. Regulation of the reduction/oxidation (redox) state is critical for cell viability, activation, proliferation, and organ functions. Although the protective importance of various antioxidants has been reported, few antioxidants have established their clinical usefulness. Thioredoxin (TRX), a key redox molecule, plays crucial roles as an antioxidant and a catalyst in protein disulfide/dithiol exchange. TRX also modulates intracellular signal transduction and exerts antiinflammatory effects in tissues. In addition to its beneficial effects in other organs, the protective effect of TRX in the lungs has been shown against ischemia/ reperfusion injury, influenza infection, bleomycin-induced injury, or lethal inflammation caused by interleukin- 2 and interleukin-18. Monitoring of TRX in the plasma, airway, or lung tissue may be useful for the diagnosis and follow-up of pulmonary inflammation. Promotion/modulation of the TRX system by the administration of recombinant TRX protein, induction of endogenous TRX, or gene therapies can be a therapeutic modality for oxidative stress-associated lung disorders.
 ...
PMID:Redox regulation of lung inflammation by thioredoxin. 1565 Mar 96

Homeostasis of the reduction-oxidation (redox) state is critical to protection from oxidative stress in the lungs. Therefore, the lungs have high levels of antioxidants, including glutathione, heme oxygenase, and superoxide dismutase. The numbers of inflammatory cells -- particularly eosinophils -- are increased in the airways of asthma patients, and these pulmonary inflammatory cells release large amounts of harmful reactive oxygen species and reactive nitrogen species. Human thioredoxin 1 (TRX1) is a redox-active protein of approximately 12 kDa that contains a (32)Cys-Gly-Pro-(35)Cys sequence necessary for its activity. The strong reducing activity of the sequence results from the cysteine residues acting as proton donors and cleaving disulfide (S-S) bonds in the target protein. Endogenous or exogenous TRX1 or both protect the lungs against ischemia-reperfusion injury, influenza infection, bleomycin-induced injury, or lethal pulmonary inflammation caused by interleukin-2 and interleukin-18. We showed that exogenous TRX1 inhibits airway hyperresponsiveness and pulmonary inflammation accompanied by eosinophilia in mouse models of asthma. Recently, we reported that exogenous TRX1 improves established airway remodeling in a prolonged antigen-exposure mouse asthma model. Exogenous and endogenous TRX1 also prevents the development of airway remodeling. Here, we discuss the role and clinical benefits of TRX1 in asthma.
 ...
PMID:Redox-regulated mechanisms in asthma. 1817 61

Stroke is among the most common causes of death and persisting disability and therefore represents a great social and economic burden worldwide. In order to lower this burden it is essential to identify risk factors and respective preventive strategies. Besides the established stroke risk factors (e.g. hypertension, diabetes, hypercholesterolemia, atrial fibrillation) both acute and chronic infectious diseases have emerged as risk factors for stroke. Mainly acute respiratory tract infection but also urinary tract infections independently increase the risk of ischemic stroke. Such additional risk was shown to be highest for infection within 3 days before ischemia and the risk steadily declines with increasing time intervals between infection and stroke. Associations between stroke incidence and mortality and influenza epidemics have been demonstrated. Observational studies showed an inverse association between influenza vaccination and stroke risk; however, interventional studies in this field have not been performed so far. Chronic infections, presently discussed as stroke risk factors mainly include periodontitis and infections with Helicobacter pylori (Hp) and Chlamydia pneumoniae (Cp). Although most respective studies identified these infectious diseases as independent stroke risk factors interventional trials have not been performed so far and causality is not proven, yet. There is preliminary evidence that the number of pathogens to which a subject had been exposed to rather than single pathogens are associated with the risk of stroke or other cardiovascular diseases. Chronic infectious diseases are treatable conditions and their identification as causal contributors to stroke risk could offer new avenues in stroke prevention.
 ...
PMID:Infection, its treatment and the risk for stroke. 1935 97


1 2 3 Next >>