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)

Less than a decade ago, the use of continuous mammalian cell lines for the production of cloned proteins was considered strictly a research tool. At that time, few thought it possible to allay the many safety concerns associated with transformed cells. It soon became clear that mammalian expression systems had numerous advantages over bacteria for production of therapeutic proteins, initiating a multidisciplinary effort to address these concerns in a thorough and reliable manner. The success of these efforts is exemplified by the emergence of product molecules into the market. Today, there are seven recombinant human therapeutics that have received FDA approval. Almost half of them (OKT3, t-PA, and EPO) are produced in mammalian cells, with the remainder produced in bacteria (insulin, growth hormone, and alpha-interferon) or yeast (hepatitis vaccine). At least a dozen more recombinant cell culture products are in advanced human clinical trials. With the accumulation of data and experience, continuous mammalian cell lines will no doubt be the preferred hosts for many future products of biotechnology.
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PMID:Downstream processing of proteins from mammalian cells. 136 66

"Wasting" or "fading" syndromes are common causes of puppy and kitten mortality. Numerous infectious and toxic, metabolic, or nutritional factors could potentially be responsible for wasting and death in young animals. Evidence has been presented that infectious canine hepatitis virus infection, beta-hemolytic streptococcus infection, and feline infectious peritonitis virus infection are responsible for a significant number of deaths due to wasting syndrome. However, many cases of wasting syndrome cannot be attributed to infectious agents or other specific etiologies. The thymus gland warrants special attention when one is evaluating an animal with a wasting syndrome because it is known that, in some species, neonatal thymectomy results in wasting and death. Unfortunately, most reports describing fading syndromes in puppies and kittens do not mention the gross or histologic appearance of the thymus gland at postmortem examination. When examining the thymus gland, one must keep in mind that the thymus may be hypoplastic owing to a congenital or genetic defect in its structure and function or it may be atrophic secondary to whatever is causing the fading syndrome. If a thorough history, clinical examination, and/or postmortem examination do not reveal a cause for the fading syndrome, then defective thymus function should be considered as a possible causative or contributing factor to the fading syndrome. In these cases, therapy designed to replace or improve the defective thymus function should be considered. At least one form of wasting syndrome in puppies (immunodeficient dwarfism) has been found to respond to short-term therapy with a thymus hormone (thymosin fraction 5) or with bovine growth hormone (which is thymotropic) in limited clinical trials. It is possible that other forms of wasting or fading syndromes would also respond to therapy with thymus hormone or growth hormone. Certain thymus hormones (thymopoietin pentapeptide, thymosin alpha 1, facteur thymique serique, and rabbit thymus acetone powder) and bovine growth hormone are commercially available. Before initiating therapy, one should consider that if the cause of the wasting syndrome is genetic, then successful treatment may perpetuate a genetic defect. More research (both basic and clinical) is needed to determine the role of thymus gland dysfunction in fading syndromes of puppies and kittens and if therapy with one or several of the thymus hormones or with growth hormone could reverse the symptoms of wasting.
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PMID:Possible association of thymus dysfunction with fading syndromes in puppies and kittens. 349 4

Two strains of transplantable rat pituitary tumors, MtT SA5 and MtT SA6, have been established in female nude mice from a single original pituitary tumor which had spontaneously occurred in a female Wistar rat at 759 days of age. MtT SA5 tumor produces prolactin (PRL), growth hormone, and adrenocorticotropic hormone, and MtT SA6 tumor secretes PRL and growth hormone. Additionally, both tumors induce severe nephropathy and promote pathogenicity of murine hepatitis virus, resulting in hepatic necrosis. Electron micrographs of MtT SA5 and MtT SA6 tumors revealed three and two types of cells, respectively, in reference to secretory granules. The tumors seem to consist of mixed population, each cell secreting each hormone. Since marked adrenal enlargement and relatively low serum corticosterone levels were found in MtT SA5-bearing rats, it is suggested that MtT SA5 tumor secretes adrenocorticotropic hormone and/or its related peptides which induce adrenal hyperplasia with little or no stimulation of corticoid production. In nude mice bearing MtT SA5 tumor, concentrations of growth hormone in serum and tumor tissue were exceedingly higher than those of PRL, while they were in the same magnitude in MtT SA6-bearing nude mice. We also found that PRL levels in serum and tumor tissue of MtT SA5-bearing nude mice were much higher in males than females, although those of MtT SA5-bearing rats were not significantly different in both sexes.
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PMID:Functional and morphological characteristics of transplantable rat pituitary tumors established in nude mice. 654 Jun 21

In accordance with the clonal selection theory the authors intended to prevent the development of autoimmune hepatitis in rabbits with the aid of radiolabelled liver specific membrane (LSP) antigen administered prior to the antigen immunization. The autoimmune hepatitis was produced in rabbits by allogen LSP antigen. The inflammatory reaction was characterized by the serum glutamic oxaloacetic transaminase activity in the sera, by the parameters of immune reaction as well as by lysosomal membrane alterations in the liver and by morphological findings. The process was inhibited by pre-treatment with hot labelled LSP antigen. Neither the radioactively labelled growth hormone pre-treatment, nor the application of hot labelled antigen at the last week of the experiment were able to prevent the humoral and lysosomal, as well as the morphological data characteristic for autoimmune hepatitis. The results obtained may be understood considering the mechanism of clonal selection.
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PMID:Inhibition of autoimmune hepatitis with hot labelled liver specific antigen. 669 67

During the course of woodchuck hepatitis virus (WHV) replication three virus-specific mRNA transcripts that encode four essential proteins are produced. The transcripts are 3.6, 2.3, and 0.7 kb in size. The 3.6-kb transcript serves as the replicative intermediate as well as the template for translation of the nucleocapsid and polymerase proteins. The 2.3-kb mRNA serves as the template for translation of the virus envelope proteins. Both the 3.6- and 2.3-kb transcripts are polyadenylated and are readily found in the cytoplasm of infected hepatocytes. However, the 0.7-kb transcript, specific for the X gene, accumulates in the nucleus of infected cells and is polyadenylated poorly in hepatocytes. Thus, while it is likely that the 0.7-kb transcript is the template for translation of the X protein, it is possible that it also has a function at the RNA level to regulate virus replication or gene expression. In order to characterize the WHV X promoter we cloned the region of the WHV8 genome encompassing the viral enhancer through the amino terminus of the X gene into the vector pSV0CAT. We transfected Huh-7 and WLC-3 cells with the WHV X promoter construct, along with a plasmid encoding human growth hormone to control for transfection efficiency, and assayed for the presence of chloramphenicol acetyl transferase activity. We found that the WHV X promoter was about one-half as active as the well-studied simian virus 40 early or Rous sarcoma virus promoters. Next, we made a series of 5' and 3' deletion mutants and mapped the WHV X promoter to a 21-nucleotide domain (1482-GGGGAAGCTGACGTCCTTTCC-1502) which is approximately 100 bp downstream of the corresponding promoter in hepatitis B virus. Further analysis, using oligonucleotide-directed mutagenesis, demonstrated that the essential nucleotides comprising the WHV X promoter are located in a 10-nucleotide domain near the initiation codon of the X gene. Mutation of either nucleotide T at position 1490 or G at position 1491 within this domain was sufficient to reduce the level of promoter activity by 100-fold. Thus, we have defined the important nucleotides within the promoter of the WHV X transcript which is a first step in understanding the role of this transcript in WHV replication and gene expression.
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PMID:Analysis of the X gene promoter of woodchuck hepatitis virus. 797 27

We routinely measured plasma neurotransmitters and hormone levels in order to investigate the role of stress on many types of diseases. In this study, we present results obtained from patients with severe chronic diseases. The study sample consisted of 88 patients (asthmatics, ulcerative colitis, Crohn's disease, chronic active hepatitis, chronic relapsing hepatitis, multiple sclerosis, trigeminal neuralgia, systemic lupus erithematous, and rheumatoid arthritis), and their respective controls. Noradrenaline (NA), adrenaline (Ad), dopamine (DA), platelet-serotonin (pS), free-serotonin (fS), growth hormone (GH) and cortisol (CRT) were determined during both exacerbation and improvement periods. A profile compatible with uncoping stress disorder (raised NA-Ad-DA + fS + CRT as well as low pS and NA/Ad ratio) was found during exacerbation periods when compared with improvement, as seen in controls. However, during improvement periods the neurochemical profile remained significantly different from that of normal controls. The neurochemical plus hormonal plasma profiles registered in chronic illness, both during exacerbation and improvement periods, strongly suggest that an uncoping stress mechanism underlies diseases of these patients.
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PMID:Plasma neurotransmitters and cortisol in chronic illness: role of stress. 799 62

Transcription and replication of hepatitis delta virus (HDV) RNA is thought to be performed by host RNA polymerase II. The mechanism which enables polymerase II to use RNA as a template is unclear. However, since extensive intramolecular complementarity allows HDV RNA to form a rod-shaped structure, it is possible that the mostly double-stranded HDV RNA may resemble double-stranded DNA in structure, and can thus be used by RNA polymerase II as a template. To investigate this possibility, we examined whether the cDNA counterpart of HDV RNA contains a promoter and thus can drive the transcription and replication of HDV RNA. Circularized monomers of HDV cDNA, when transfected into various cell lines, were found to generate both monomeric and dimeric forms of HDV RNA and hepatitis delta antigen at levels comparable to those generated with HDV cDNA multimers under the control of a SV40 late promoter, suggesting that HDV cDNA contains endogenous promoters. Using chloramphenicol acetyltransferase and human growth hormone as reporter genes, the specific promoter activity for the synthesis of antigenomic HDV RNA was localized to a 29-nucleotide region (nucleotides 1650-1679), although an additional 224-nucleotide upstream region was also necessary for maximum activity. Similarly, promoter activity for the synthesis of genomic RNA was localized to a 160-nucleotide region around position 1679 that overlapped with the antigenomic promoter region. Since these regions are in a highly conserved double-stranded region of HDV RNA, they may represent RNA promoters recognized by RNA polymerase II. This result also suggests a convenient method, using circularized monomer HDV cDNA, to study HDV RNA replication.
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PMID:Endogenous promoters can direct the transcription of hepatitis delta virus RNA from a recircularized cDNA template. 837 36

This work was designed in an attempt to clarify the effect of growth hormone injection on the serum somatomedin-C (SM-C) levels in Egyptian children with (1) urinary bilharziasis, (2) advanced bilharzial hepatic fibrosis, and (3) children suffering from chronic hepatitis, in comparing with 11 healthy age- and sex-matched children,, served as controls. SM-C levels were studied prior and after injection of human growth hormone (hGH). The basal and hGH-stimulated SM-C levels were significantly reduced in bilharzial patients compared with controls. Patients with hepatitis had significantly lower serum SM-C values prior or post hGH administration. Liver tests carried out for bilharzial patients showed impaired function both on admission and after treatment. It can concluded from this work that shortness in children with bilharzial hepatic fibrosis may be result of hepatic and endocrinal factors and nutritional. Also, our results suggested that the delayed skeletal maturation in chronic hepatitis cases is probably secondary to liver dysfunction, malnutrition and associated endocrinopathies.
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PMID:Effect of growth hormone administration on serum somatomedin-C levels in bilharzial and liver disorders patients. 872 Dec 26

A case of congenital isolated growth hormone deficiency with neonatal giant cell hepatitis is described. Hypoplasia of the pituitary gland was detected by a MR-scan. Values of IGF-I, IGF-II, and IGF-BP-3 were low. Birth length and weight were normal; hypoglycaemia, jaundice, and failure to thrive were the most pronounced symptoms and present from the first day. Substitution therapy with growth hormone induced a remission of all symptoms. Growth was normal at follow-up at the age of two and a half years.
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PMID:[Isolated congenital growth hormone deficiency. Severe hypoglycemia and neonatal giant cell hepatitis]. 899 85

Immunohistochemical study was carried out on D-galactosamine hydrochloride (GaIN)-induced subacute hepatitis in rats of JCL: Wistar-TGN (ARGHGEN) 1Nts strain (Mini rats), in which the expression of growth hormone gene is suppressed by the presence of an antisense transgene. Mini rats were given 1000 mg/kg of GaIN once a week for 4 consecutive weeks and killed at 1, 2, 3 and 4 weeks after the first administration. At 1 week after the first administration, proliferation of small epithelial cells positive for both alpha-fetoprotein and cytokeratin 7, i.e. so-called oval cells, was observed in the whole area of each hepatic lobule, and prominent deposition of fibronectin, laminin and type IV collagen was detected around these oval cells. Together with these extracellular matrix components, many activated Ito cells positive for both desmin and alpha-smooth muscle actin were observed. With time, most of the oval cells formed duct-like structures and lost their positive stainability for alpha-fetoprotein, and many Ito cells became inactive. Deposition of fibronectin decreased rapidly from 2 weeks after the first administration. At 4 weeks after the first administration, deposition of laminin was detected only around the duct-like structures, where that of type IV collagen was also still prominent. These results suggest that a large population of oval cells differentiated into bile duct epithelial cells and that Ito cells and extracellular matrix components might play a role in this process.
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PMID:Immunohistochemical study on galactosamine-induced subacute hepatitis in rats of JCL: Wistar-TGN (ARGHGEN) 1 Nts strain (Mini rats). 925 Apr 81


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