Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The tools available for monitoring necrotic enteritis caused by Clostridium perfringens in broiler chickens have been limited, particularly for identifying subclinical disease. In this study, a modified enzyme-linked immunosorbent assay was used to quantify levels of specific immunoglobulin G to C. perfringens alpha-toxin in serum from broilers. We found significantly higher antibody levels in broilers with a history of subclinical necrotic enteritis compared with a zinc-bacitracin-treated group with a low level of gut lesions. Furthermore, in 4.5-week-old commercial broiler flocks, there was an association between the occurrence of C. perfringens-associated hepatitis at slaughter and the immune response to alpha-toxin. Practical solutions for defining cut-off levels for positive serum samples at individual and flock levels are proposed, and were found to be useful on a set of samples available from flocks with different histories regarding the occurrence of C. perfringens-associated disease. This serological approach seems promising as a diagnostic tool in research and disease monitoring regarding C. perfringens-associated disease.
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PMID:Diagnosing Clostridium perfringens-associated necrotic enteritis in broiler flocks by an immunoglobulin G anti-alpha-toxin enzyme-linked immunosorbent assay. 1452 9

Hepatic metabolism of biological toxins, industrial poisons, and medicinal agents involves disturbed hepatic cell biochemistry with augmented generation of reactive oxygen species and free radicals and redox imbalance with secondary damage to proteins, nucleic acids, lipids, and carbohydrates. The xenobiotic hepatotoxicity ranging from a subclinical anicteric state to severe necroinflammatory hepatitis (acute, recurrent or chronic) and cirrhosis depends on the nature, dosage, and duration of exposure to the xenobiotic, the antioxidant defence, and concomitant exposure to other diseases or xenobiotics. Experimental and clinical studies suggest that xenobiotic hepatotoxicity with variable depletion of antioxidants can be avoided or ameliorated by administration of an unusually high dosage of zinc or by a combination of antioxidants above normal daily requirements. Therefore reassessment of optimal prophylactic and therapeutic nutritional requirements of antioxidants (particularly zinc) to defend humans against xenobiotic induced oxidative stress is advocated.
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PMID:Oxidative stress, toxic hepatitis, and antioxidants with particular emphasis on zinc. 1461 18

Dominant types of viral hepatitis are presently A, B, and C with prophylactic immunization available only for A and B. Hepatitis B and C and human immunodeficiency virus (HIV) infection constitute a worldwide scourge and treatment is far from satisfactory. Each produces severe oxidative stress (OS) and secondary cellular damage of varying severity and, as in toxic hepatitis, progression and regression are dependent on redox balance between oxidation and antioxidation. Experimental and clinical studies suggest that xenobiotics and co-infections exert cumulative, detrimental effects on their pathogeneses and further deplete antioxidants. It is proposed therefore that in the clinical management of these infections and especially in their early stages, considerable benefit should accrue from antioxidant repletion at dosages substantially above recommended daily allowances (RDAs) in conjunction with a nutritious high protein diet. Because plasma zinc and selenium concentrations are very low, their replenishment by high dosages is urgent and mandatory particularly in advanced HIV infections bordering on acrodermatitis enteropathica. Also recommended is their long-term continuance at high normal levels.
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PMID:Oxidative stress in viral hepatitis and AIDS. 1535 Dec 35

Hepatic encephalopathy is a complex neuropsychiatric syndrome, which derives from liver failure associated with severe liver damage such as fulminant hepatitis and liver cirrhosis, and vascular abnormalities associated with liver cirrhosis. Although the cause is explained by a multifactorial theory, the accumulation of ammonia has traditionally been considered to have an important role in the pathogenesis of hepatic encephalopathy. In addition, a number of other possible mechanisms have recently proposed, including production of false neurotransmitter, activation of central gamma-aminobutyric acid-benzodiazepine receptors by ligands of endogenous origin, altered cerebral metabolism. These pathogenetic mechanisms are not necessarily exclusive. The principle of treatment is to remove or correct aggravating factors and inhibit the transfer of toxic substances such as ammonia into the bloodstream by minimizing the interaction of intestinal bacteria and nitrogen substances. Most treatments of proved value are based on the ammonia hypothesis. Ammonia metabolism is regulated by numerous factors, among which zinc has long been indicated to be involved, and its clinical application has drawn attention recently.
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PMID:Ammonia metabolism and hepatic encephalopathy. 1560 43

The treatment of Wilson's disease has changed considerably in recent times, from the use of penicillamine (Cuprimine, Merck) for all stages and types of disease, to the use of three other anticopper drugs at appropriate times for appropriate patients. Each type and stage of the disease can be considered as a therapeutic target, for which specialised therapy is appropriate. This paper systematically reviews the various types and stages of Wilson's disease presentation, and provides opinion on the appropriate therapy for each. For patients presenting with neurological disease, the use of tetrathiomolybdate is optimum; for patients presenting with mild-to-moderate hepatic failure, a combination of trientine (Syprine, Merck) and zinc is recommended, whereas liver transplantation is necessary for those with severe failure; zinc therapy alone or trientine alone as second choice is recommended for patients presenting with hepatitis or cirrhosis without liver failure, for maintenance therapy, for treatment of presymptomatic patients and for treatment of paediatric and pregnant patients.
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PMID:Novel therapeutic approaches to the treatment of Wilson's disease. 1644 26

Herpes simplex is a common viral infection of the skin or mucous membranes. The lesions caused by this infection are often painful, burning, or pruritic, and tend to recur in most patients. Short-term treatment with acyclovir can accelerate the healing of an acute outbreak, and continuous acyclovir therapy is often prescribed for people with frequent recurrences. While this drug can reduce the recurrence rate by 60-90 percent, it can also cause a wide array of side effects, including renal failure, hepatitis, and anaphylaxis. Safe and effective alternatives are therefore needed. There is evidence that certain dietary modifications and natural substances may be useful for treating active Herpes simplex lesions or preventing recurrences. Treatments discussed include lysine, vitamin C, zinc, vitamin E, adenosine monophosphate, and lemon balm (Melissa officinalis).
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PMID:Natural remedies for Herpes simplex. 1681 59

Wilson disease is an autosomal recessive disorder of copper overload. A principal characteristic of this disease is its wide phenotypic and genotypic variability. Its results from mutations of the ATP 7B gene located on chromosome 13, that encodes a hepatic copper transport protein. More than 300 mutations of this gene have been identified. This protein ensures the transport of copper in the hepatocyte, its incorporation with the apoceruloplasmin and its biliary excretion. The clinical manifestations are heterogeneous as well in their presentation, dominated by the neuropsychiatric and hepatic symptoms, as in the age of the first symptoms. Early recognition and initiation of therapy with chelators or zinc are essential for prognosis. Liver transplantation is indicated in cases with fulminant hepatitis, end-stage liver cirrhosis and should be considered in the therapy resistant neurological forms. A regular follow-up with monitoring of adverse effects of treatment and compliance is essential. Any discontinuation of treatments will involve, within a very variable time, but in constant manner, a reappearance or a reaggravation of the signs. Such relapses are often brutal and can be extremely serious, especially since response to subsequent treatment is often poor.
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PMID:[Wilson disease]. 1684 Sep 91

The severe acute respiratory syndrome coronavirus (SARS-CoV) possesses a large 29.7-kb positive-stranded RNA genome. The first open reading frame encodes replicase polyproteins 1a and 1ab, which are cleaved to generate 16 "nonstructural" proteins, nsp1 to nsp16, involved in viral replication and/or RNA processing. Among these, nsp10 plays a critical role in minus-strand RNA synthesis in a related coronavirus, murine hepatitis virus. Here, we report the crystal structure of SARS-CoV nsp10 at a resolution of 1.8 A as determined by single-wavelength anomalous dispersion using phases derived from hexatantalum dodecabromide. nsp10 is a single domain protein consisting of a pair of antiparallel N-terminal helices stacked against an irregular beta-sheet, a coil-rich C terminus, and two Zn fingers. nsp10 represents a novel fold and is the first structural representative of this family of Zn finger proteins found so far exclusively in coronaviruses. The first Zn finger coordinates a Zn2+ ion in a unique conformation. The second Zn finger, with four cysteines, is a distant member of the "gag-knuckle fold group" of Zn2+-binding domains and appears to maintain the structural integrity of the C-terminal tail. A distinct clustering of basic residues on the protein surface suggests a nucleic acid-binding function. Gel shift assays indicate that in isolation, nsp10 binds single- and double-stranded RNA and DNA with high-micromolar affinity and without obvious sequence specificity. It is possible that nsp10 functions within a larger RNA-binding protein complex. However, its exact role within the replicase complex is still not clear.
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PMID:Crystal structure of nonstructural protein 10 from the severe acute respiratory syndrome coronavirus reveals a novel fold with two zinc-binding motifs. 1687 46

Chronic liver diseases are disastrous to health. Many factors are associated with their prevalence, hence endemicity. These are mainly infectious, parasitic and toxic. A survey was conducted in a village south to Cairo. Large industries concerned with iron and steel industry, metals smelting, cement manufacturing and electric station were located north to the village. A systematic random sample of houses was selected. All individuals inside the houses were invited to share in the study. Sample size was 84 individuals. Hepatitis markers were done (HBsAg and anti-HCV antibodies). The levels of some heavy metals were assessed; which were lead, mercury, arsenic, aluminum, manganese, nickel, chromium and cadmium. Levels of some trace elements were assessed. These were copper, iron, selenium and zinc. Aflatoxin B1 was assessed in serum. Assessment of schistosomal circulating antigen and antibodies was carried out. Abdominal ultrasonograghy was done to assess liver condition. Univariate logistic regression analysis was done to assess the association between studied variables and HBsAg or anti-HCV sero-positive subjects. The association between studied variables and bilharzial or fatty liver, diagnosed by ultrasonography, were also assessed. The univariate logistic regression analysis revealed odds ratios at the following results. For HBsAg seropositive subjects, aflatoxin B1, lead, chromium and schistosomal antigen and antibodies were higher than negative ones where odds ratios were; 6.2, 1.6, 1.6, 1.6 and 1.7, respectively. None of the variables showed statistically significant difference. For anti-HCV antibodies sero-positive subjects, aflatoxin B1 and chromium had the highest odds ratios among the studied variables, (odds ratios were 2.5 and 2.4, respectively). Bilharzial liver showed higher significant positivity of anti-HCV antibodies and insignificant decreased level of zinc than negative ones (odds ratios were 7.2 and 4.5, respectively). Fatty liver cases showed higher statistically significant positivity of anti-HCV antibodies and chromium than negative ones. Odds ratios were 8.0 and 7.1, respectively. Statistically significant lower level of aflatoxin B1 was shown in fatty liver than normal liver subjects. Multivariate logistic regression analysis for fatty liver showed that only anti-HCV antibodies sero-positivity had statistically significant odds ratio in comparison to chromium level and aflatoxin B1. It is concluded that some heavy metals, and Aflatoxin B1 had a definite association with liver diseases in the area under study. Having anti-HCV antibodies had a relation with fatty liver and with bilharzial liver more than having HBsAg. It is recommended that environmental management to factories nearby the village is urgently needed to decrease exposure to heavy metals. Prevention of hepatitis infection and aflatoxin exposure through different means is also recommended, other wise health care authorities would be confronted with unusual cases of HCC in the nearby future.
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PMID:A cross sectional study of hepatitis B, C, some trace elements, heavy metals, aflatoxin B1 and schistosomiasis in a rural population, Egypt. 1690 Jun 14

Myelin transcription factor 1 (Myt1) is a zinc-finger DNA binding protein that influences developing oligodendrocyte progenitor (OP) cell proliferation, differentiation, and myelin gene transcription in vitro. The potential of Myt1 to play a role in OP responses leading to remyelination was examined using murine hepatitis virus strain A59 (MHV) to induce spinal cord demyelination and potential relevance to human pathology was evaluated in multiple sclerosis (MS) lesions. In MHV-infected mice, the density of Myt1 expressing cells markedly increased in lesioned areas of spinal cord white matter. Myt1 expressing cells proliferated most extensively during active demyelination and subsequently accumulated to maximal levels during early remyelination. Cells with nuclear Myt1 immunoreactivity were mainly OP cells, identified by co-localization with platelet-derived growth factor alpha receptor, with additional phenotypes being either oligodendrocytes or neural stem cells, identified by CC1 antigen and Musashi1, respectively. The density of OP cells expressing Myt1 was significantly increased in white matter of MHV-infected mice during demyelination and early remyelination then as remyelination advanced the values returned to levels comparable to PBS-injected control mice. In MHV lesions, Myt1 was not expressed in astrocytes, lymphocytes, or macrophage/microglial cells. MS lesions demonstrated increased Myt1 expression in both the periplaque white matter adjacent to lesions and within early remyelinating lesions. These results suggesta potential role for Myt1 in the regeneration of oligodendrocyte lineage cells in response to demyelination.
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PMID:Myelin transcription factor 1 (Myt1) expression in demyelinated lesions of rodent and human CNS. 1733 Aug 75


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