Isolation of tetranucleotide microsatellites from the Mexican jay Aphelocoma ultramarina.
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Animals↗
Biomedical subjects
S H Li
Publications and source records attributed to S H Li.
[Suppressive effects of a plant-origin polyol, dulcitol on collagen-induced arthritis in mice].
Dulcitol was isolated chemically from Celastrus obiculatus Thumb and determined by HPLC. Effects of dulcitol were examined on collagen-induced arthritis (CIA) in DBA/1J mice. From 6 weeks after the first immunization with bovine type II collagen, dulcitol (100 mg/kg body weight/day) was administered orally to immunized mice for 9 weeks. Clinical score of CIA was improved significantly by dulcitol intervention compared with the non-treated CIA mice. Radiographic score of phalangeal destruction was also improved by dulcitol treatment. These findings suggest that dulcitol may play a role in regulation of some inflammatory responses in the present arthritis model. Significant reduction of percentage of CD4+ and CD8+ T cell subsets in the spleen leucocytes of CIA mice was observed by flow cytometry. Almost normal level of CD4+ and CD8+ T cells was observed in dulcitol-treated groups, suggesting T cell-modifying effect of dulcitol in CIA. Weight of spleen was larger in CIA mice and it was not affected by dulcitol. Anti-collagen antibody titer was increased in CIA mice, and it was not affected by dulcitol, either. Improvement of the changes of CD4+ and CD8+ T cells in the spleen by dulcitol may suggest its modulatory effect on cellular immunity.
Animals↗
[Progress in the study on left ventricular diastolic dysfunction in traditional Chinese medicine].
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Animals↗
Is quantitative urinalysis more sensitive?
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Cocaine↗
Lymphocyte apoptosis: mediation by increased type 3 inositol 1,4,5-trisphosphate receptor.
B and T lymphocytes undergoing apoptosis in response to anti-immunoglobulin M antibodies and dexamethasone, respectively, were found to have increased amounts of messenger RNA for the inositol 1,4,5-trisphosphate receptor (IP3R) and increased amounts of IP3R protein. Immunohistochemical analysis revealed that the augmented receptor population was localized to the plasma membrane. Type 3 IP3R (IP3R3) was selectively increased during apoptosis, with no enhancement of type 1 IP3R (IP3R1). Expression of IP3R3 antisense constructs in S49 T cells blocked dexamethasone-induced apoptosis, whereas IP3R3 sense, IP3R1 sense, or IP3R1 antisense control constructs did not block cell death. Thus, the increases in IP3R3 may be causally related to apoptosis.
Amino Acid Sequence↗
Huntingtin-associated protein (HAP1): discrete neuronal localizations in the brain resemble those of neuronal nitric oxide synthase.
Huntington disease stems from a mutation of the protein huntingtin and is characterized by selective loss of discrete neuronal populations in the brain. Despite a massive loss of neurons in the corpus striatum, NO-generating neurons are intact. We recently identified a brain-specific protein that associates with huntingtin and is designated huntingtin-associated protein (HAP1). We now describe selective neuronal localizations of HAP1. In situ hybridization studies reveal a resemblance of HAP1 and neuronal nitric oxide synthase (nNOS) mRNA localizations with dramatic enrichment of both in the pedunculopontine nuclei, the accessory olfactory bulb, and the supraoptic nucleus of the hypothalamus. Both nNOS and HAP1 are enriched in subcellular fractions containing synaptic vesicles. Immunocytochemical studies indicate colocalizations of HAP1 and nNOS in some neurons. The possible relationship of HAP1 and nNOS in the brain is reminiscent of the relationship of dystrophin and nNOS in skeletal muscle and suggests a role of NO in Huntington disease, analogous to its postulated role in Duchenne muscular dystrophy.
Animals↗
Analysis of thirteen trinucleotide repeat loci as candidate genes for schizophrenia and bipolar affective disorder.
A group of diseases are due to abnormal expansions of trinucleotide repeats. These diseases all affect the nervous system. In addition, they manifest the phenomenon of anticipation, in which the disease tends to present at an earlier age or with greater severity in successive generations. Many additional genes with trinucleotide repeats are believed to be expressed in the human brain. As anticipation has been reported in schizophrenia and bipolar affective disorder, we have examined allele distributions of 13 trinucleotide repeat-containing genes, many novel and all expressed in the brain, in genomic DNA from schizophrenic (n = 20-97) and bipolar affective disorder patients (23-30) and controls (n = 43-146). No evidence was obtained to implicate expanded alleles in these 13 genes as causal factors in these diseases.
Base Sequence↗
cDNA cloning and characterization of an atrophin-1 (DRPLA disease gene)-related protein.
Dentatorubral and pallidoluylsian atrophy (DRPLA) is a progressive neurological disorder characterized by neuronal degeneration, especially in the cerebellar dentate nucleus. DRPLA is caused by an unstable expansion of a CAG trinucleotide repeat coding for glutamine in a gene of unknown function, termed atrophin-1, located on chromosome 12. To gain additional understanding of atrophin-1, we have isolated a second member of the atrophin-1 gene family by screening rat cDNA libraries. The 1006-amino-acid product of this gene, which we have termed rat atrophin related protein(rARP), does not contain a glutamine repeat, but it does contain two regions of alternating acidic and basic amino residues similar to those found in atrophin-1. rARP is widely expressed as both a 7.4- and a 9.4-kb message, with enrichment in cerebellum and testis. Like atrophin-1, the rARP in vitro translation product migrates more slowly on SDS-polyacrylamide gel electrophoresis than predicted by molecular weight. We conclude that, at least in the rat, polyglutamine is not an essential feature of the atrophin family of genes.
Amino Acid Sequence↗
Psychosis and genes with trinucleotide repeat polymorphism.
Abnormal expansion of genes with trinucleotide repeat (TNR) polymorphism has been found in a number of neuropsychiatric disorders. These disorders and the major psychoses, schizophrenia and bipolar affective disorder, appear to share an interesting phenomenon: genetic anticipation. Because TNR expansion correlates with anticipation, these unstable DNA sites are considered important candidate loci for the major psychoses. We investigated genes with TNR polymorphisms, including B1, B33, B37, and the N-cadherin gene, in unrelated Caucasian North American and Italian schizophrenics (n = 53 to 74), and matched controls. Also, unrelated Caucasian North American patients with bipolar I affective disorder were screened for the B33 and N-cadherin genes (n = 49 and 63, respectively). No unusually long alleles that would suggest abnormal expansion of the TNR were observed for any of these genes. Also, no statistically significant results were found in tests for genetic association between any of these genes and schizophrenia. For B37, a trend toward a difference in allele counts between schizophrenics and controls was observed. However, no clear evidence for a role of these TNR-containing genes in schizophrenia or bipolar affective disorders was found.
Bipolar Disorder↗
DRPLA gene (atrophin-1) sequence and mRNA expression in human brain.
Dentatorubral pallidoluysian atrophy (DRPLA, Smith's disease) is one of five disorders currently known to result from expansion of a CAG trinucleotide repeat encoding glutamine. The reported full length cDNA sequence encodes a serine repeat and a region of alternating acidic and basic amino acids, as well as the glutamine repeat. We now report the nucleic acid and deduced amino acid sequences of the open reading frame of this gene, obtained from a series of independently isolated and sequenced cDNA clones. Eight nucleotide differences from the originally published sequence result in a change of 34 amino acids, most prominently in the region of alternating acidic and basic residues. Northern analysis and in situ hybridization indicate that atrophin-1 mRNA is expressed in multiple brain regions. The level of mRNA expression as determined by in situ hybridization in a DRPLA-diseased brain is indistinguishable from the level observed in a matched control brain. These results indicate that the correlation between atrophin-1 expression and regions of pathology in DRPLA is at best partial, and that the expanded allele does not cause a major loss of mRNA expression. The pathology of the disorder may therefore arise from the altered structure and function of the abnormal protein.
Amino Acid Sequence↗
Prostaglandin E2 control of T cell cytokine production is functionally related to the reduced lymphocyte proliferation in atopic dermatitis.
Past studies of peripheral blood mononuclear cells (PBMC) from patients with atopic dermatitis (AD) have demonstrated reduced proliferation. We have studied phytohemagglutinin-induced lymphocyte proliferation in the context of interleukin-4 (IL-4), interferon-gamma (IFN-gamma), and prostaglandin E2 (PGE2) production in cultures of PBMC from patients without and with AD. The proliferation index was found to correlate proportionally to IFN-gamma production and inversely to T-cell IL-4 and monocyte PGE2 production. Assays in parallel cultures showed significantly increased PGE2 production by purified AD monocytes. The proliferation index in PBMC from persons with AD was significantly reduced compared with normal PBMC. This difference was normalized in the presence of extrinsic IFN-gamma but exaggerated when IL-4 was added. Increased AD monocyte production of inflammatory factors (e.g., PGE2) and cytokines appears to increase IL-4 production by Th2 while suppressing IFN-gamma production by Th1. Restoration of the normal proliferation of PBMC by the addition of IFN-gamma may represent one mechanism for the clinical efficacy of IFN-gamma treatment of AD.
Adult↗
Abnormal IL-4 gene expression by atopic dermatitis T lymphocytes is reflected in altered nuclear protein interactions with IL-4 transcriptional regulatory element.
Among the atopic disease, atopic dermatitis is characterized by the highest levels of serum IgE and by increased peripheral blood T-cell interleukin-4 (IL-4) production. IL-4 promotes IgE synthesis by B cells and stimulates the growth of IL-4-producing T cells and may contribute to the pathogenesis of this disease. In this study, in situ hybridization established that atopic dermatitis patients have a higher frequency of IL-4-producing peripheral blood T cell when compared to normal subjects. These in vivo-derived T cells were used to examine the signaling requirements of IL-4 production and the nuclear factors that associate with a critical IL-4 transcriptional regulatory element between -88 and -60 relative to the IL-4 transcription initiation site, the activation responsive element. We demonstrate that, as in T-cell lines, proteins belonging to the NF-AT and AP-1 family of transcription factors are present in stimulated cell extracts and specifically associate with the activation responsive element. Dysregulated IL-4 production is reflected in the nuclear proteins that associated this element. Using gel shift assays, we found that 12 of 12 nuclear extracts from stimulated atopic T cells formed the activation-dependent protein-DNA complex, compared to only 2 of 12 normal T-cell extracts. Activation complex formation correlated with the relative level of IL-4 mRNA and protein produced in stimulated T cells, suggesting that abnormal IL-4 gene expression in atopic disease may be linked to alterations in nuclear protein interactions with these promoter elements.
Base Sequence↗
Suppressive effects of a herbal formula, TBL-1, on type II collagen-induced arthritis in DBA/1J mice.
1. The effects of a formula of traditional Chinese medicine, TBL-1, on collagen-induced arthritis (CIA) were investigated in DBA/1J mice. 2. From 4 weeks after the first immunization with bovine type II collagen (CII), TBL-1 or indomethacin was administered orally for 13 weeks. 3. Clinical scores of CIA were decreased by both TBL-1 and indomethacin intervention compared with the control CII-immunized group. 4. Radiographic scores of phalangeal destruction were markedly improved by TBL-1 intervention (P < 0.001), but indomethacin failed. 5. The suppressive effects of TBL-1, but not indomethacin, were manifested in reduced serum anti-CII antibody titres (P < 0.001). 6. These findings suggest that TBL-1 may play a role in regulating some immune responses in the present arthritis model.
Animals↗
Tissue transglutaminase in apoptosis of photoreceptor cells in rat retina.
PURPOSE: The possible involvement of tissue transglutaminase (tTG) in apoptosis during photoreceptor degeneration was examined in retinal photic injury in rats and in retinal dystrophy of Royal College of Surgeons (RCS) rats. METHODS: Retinal photic injury was induced in 48 male Lewis albino rats by exposure to green fluorescent light of 300 to 320 foot-candles. The retinal tTG was examined by enzyme assay, immunohistochemistry, and Western blot analysis after 9, 12, or 24 hours of exposure or at 6 or 24 hours of dark adaptation after 24 hours of light exposure. Retinas from RCS rats at various stages of degeneration also were examined with similar methods. RESULTS: There was a progressive increase in retinal tTG activity after 300 to 320 ft-c of light exposure, reaching a peak after 24 hours of light exposure. In the RCS rats, tTG activity increased with age. Western blot analysis revealed an immunoreactive band at 80 kDa, which increased in accordance with the transglutaminase activity in both models. In normal rat retinas, tTG immunolabeling was present only in the outer segments. There was an increased number of immunolabeled photoreceptor nuclei from 12 hours of light exposure to 24 hours of light exposure. In the RCS rat, increasing numbers of immunopositive photoreceptor nuclei from 20 to 50 days of age were noted. CONCLUSIONS: The data associated increased retinal tTG activity and enzyme levels with photoreceptor cells undergoing apoptosis. The tTG-dependent irreversible cross-linking of intracellular protein may play an important role in causing the structural changes in cells undergoing apoptosis in the retina.
Aging↗
Avoiding serious complications in laparoscopic cholecystectomy--lessons learned from an experience of 2428 cases.
Over a three-and-a-half year period, we performed 2428 cases of laparoscopic cholecystectomy (LC) and encountered 11 cases of serious procedure-related complications, including bile duct injuries in 4 patients, postoperative bleeding requiring laparotomy and haemostasis in 3 patients, bile leakage from the cystic duct stump, jejunal injury related to puncture, intraoperative injury to the duodenum and subdiaphragmatic abscess in 1 patient each respectively. Six patients required re-hospitalisation including 2 patients with pancreatitis, 1 patient with Ascaris cholangitis, 1 patient with residual stone of the common bile duct (CBD) after laparoscopic CBD exploration, 1 patient with a stone in the CBD after LC, and 1 patient with bile leakage from the cystic duct stump and peritonitis. Of the 2428 patients treated, there was only 1 operative mortality. This patient developed frequent episodes of supraventricular tachycardia. She was found to have pnuemonia on the 21st postoperative day and she died. Apart from this, 1 other patient was found to have primary cancer of the liver 1 month after LC. Based on our experience, we think that LC is safe for patients with benign disease of the gallbladder.
Adolescent↗
A huntingtin-associated protein enriched in brain with implications for pathology.
Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder caused by an expanding polyglutamine repeat in the IT15 or huntingtin gene. Although this gene is widely expressed and is required for normal development, the pathology of HD is restricted to the brain, for reasons that remain poorly understood. The huntingtin gene product is expressed at similar levels in patients and controls, and the genetics of the disorder suggest that the expansion of the polyglutamine repeat induces a toxic gain of function, perhaps through interactions with other cellular proteins. Here we report the identification of a protein (huntingtin-associated protein (HAP)-1) that binds to huntingtin. This binding is enhanced by an expanded polyglutamine repeat, the length of which is also known to correlate with the age of disease onset. The HAP-1 protein is enriched in the brain, suggesting a possible basis for the selective brain pathology of HD.
Amino Acid Sequence↗
Resolution of isotoxins in the beta-bungarotoxin family.
Although only five isotoxins of the beta-bungarotoxin family had been claimed, this work indicated the existence of more than sixteen isotoxins. Crude snake (Bungarus multicinctus) venom was divided into four main fractions by gel filtration on a Sephadex G-50 column. beta-Bungarotoxin appeared in a major fraction that contained mainly the M(r) 20,000 protein components. The fraction could be further resolved into eighteen peaks designated P1-P18 by HPLC on a Protein Pak SP 5PW column that was eluted with a linear gradient of 0.1-0.6 M CH3COONa in 20 mM NaH2PO4-Na2HPO4 at pH 7.4 P3-P18 were demonstrated to be isotoxins of the beta-bungarotoxin family. Results of protein sequencing for P8, P9 and P11, the three main isotoxins, confirmed that they shared a common phospholipase A2 subunit, which was very similar to although not completely identical with the A1 chain reported previously.
Amino Acid Sequence↗