[Oxidative stress and lens opacity: a study on the mechanism of treating and preventing cataract by scavengers of free radicals].
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Biomedical subjects
Publications and source records attributed to X Han.
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Flow cytometric DNA analysis was performed on formalin fixed paraffin-embedded samples taken from 43 cases of peripheral nerve tumors. Fourteen samples were taken from benign tumors, 11 from actively proliferative tumors and 12 from malignant tumors. Ploidy pattern and proliferative index of tumors were estimated. All samples of benign tumors showed a diploid model of DNA content whereas DNA aneuploidy was encountered in 75% (12/16) of the malignant tumors and 25% (4/16) of the actively proliferative tumors. The proliferative index (PI) of benign tumors (medium: 24.8%) was lower than that of proliferative tumors (medium: 42.7%). The proliferative index of malignant tumors was the highest in the experimental group (medium: 51.2%). These results were conformable to the malignant degree of histologic grading and prognosis.
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Recombinant interleukin 4 (rIL4) inhibited the proliferation and induction of lymphokine activated killer (LAK) cells in human peripheral blood mononuclear cells (PBMC) cultured in recombinant interleukin 2 (rIL2). Other recombinant cytokines, such as rIFN gamma, rTNF alpha, rIL1, and rIL3, did not inhibit LAK cell induction. rIL4-mediated suppression was dose dependent. As little as 1 U/ml of rIL4 significantly decreased both LAK activity and proliferation of cells induced by incubation of PBMC with 200 U/ml rIL2. Suppression was specific for the induction phase of LAK activity, because rIL4 did not suppress the cytotoxic capability of previously activated LAK cells. rIL4 directly suppressed rIL2-induced activation of precursors into LAK cells, since it inhibited both rIL2-induced proliferation and LAK cell activity in LGL-enriched cell fractions or in purified CD16+ NK cells. Suppressive effects of rIL4 were overcome by adding rIFN gamma to the culture. These results suggest that rIL4 is a potent inhibitor of rIL2-induced activation of PBL, and that the net LAK response in the host may be a function of the production of IL-2, IL-4 and rIFN gamma.
This article reports a new grafting technique--microskin grafting. These experiments were carried out in rabbits, and used a small amount of autograft minced into tiny pieces and then spread on a piece of homograft. The combined autograft plus homograft was then transplanted onto the wound of a rabbit. In 12 rabbits, the microskin grafts took well and covered the wound completely in 8 rabbits. The expansion ratios of the micrografts were from 7:1 to 15:1. The healing time of the wound was from 19 to 35 days. The operation failed in 4 rabbits because of the homograft moving. Histological sections revealed that microskin grafts orientated upwards can grow well and those orientated in a lateral or downward direction can grow too. This technique is an effective procedure for repairing extensive wounds with smaller donor sites.
A technique for microskin grafting for treating extensively burned patients is presented. Eight extensively burned patients were treated in this way with encouraging results. The recipient area covered by microskin grafts ranged from 2.5 per cent to 44 per cent of the total body surface area (TBSA). The expansion ratio of the micrografts was 15:1 maximum. The micrografts took well in seven patients with the healing time ranging from 22 to 45 days post-operatively. One case failed because of sloughing of the homograft. The advantages of the microskin grafting are: (1) economical use of autografts, (2) the procedure is simple, (3) there is less scar on the recipient site. This new technique is effective, simple and feasible in extensive burns.
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The metabolism of 7-(4-chlorbenzyl)-7,8,13,13a-tetrahydroberberine chloride (CTHB), a compound with promising pharmacological effects against arrhythmia, was investigated in rat bile. A metabolite and unchanged CTHB were found in the bile. Characterization and structural elucidation of the metabolite was achieved by LC/MS and LC/NMR. The following metabolic pathway is proposed: CTHB is metabolized by demethylation at position 10 to produce a new entity.
The varepsilon4 allele of apolipoprotein E (apoE) is a genetic risk factor for Alzheimer's disease (AD). In order to gain a better understanding of the molecular mechanisms by which apoE and possibly other apolipoproteins produced in the central nervous system (CNS) influence AD pathogenesis, we have purified and characterized the two most abundant apolipoproteins produced in the CNS, apoE and apoJ. We purified apoE and apoJ from primary cultures of mouse astrocytes, which were derived from transgenic mice expressing human apoE isoforms in the absence of mouse apoE. Utilizing antibody affinity columns, we were able to purify both human apoE3 and apoE4, as well as mouse apoJ-containing lipoproteins. Astrocyte-secreted human apoE was present in high density-like lipoproteins of three predominant sizes ranging from 8 to 15 nm in diameter. Mouse apoJ was in particles between 10 and 17 nm in diameter with a peak size range of approximately 11 nm. ApoE and apoJ were in distinct lipoproteins. Utilization of quick-freeze, deep-etch electron microscopy revealed the apoE particles were discs while the apoJ particles were smaller and more irregular in appearance. The lipid composition of apoE particles was very different from those containing apoJ. ApoE-particles contained a similar mass of apoE and lipid, with cholesterol and phospholipid being about equal in mass per particle. ApoJ-particles were relatively lipid poor (three parts protein, one part lipid), with phospholipids being much more abundant than cholesterol. Detailed characterization of phospholipid composition by electrospray ionization mass spectrometry analysis revealed ethanolamine glycerophospholipids to be the most abundant phospholipid present in both apoE and apoJ particles. Analysis of cerebrospinal fluid from apoE3 and apoE4 transgenic mice revealed that human and mouse apoE were in particles the same size as those secreted by astrocytes. Further use of physiological preparations of CNS-derived lipoproteins may allow for a detailed understanding of the role of these molecules in the normal brain and in diseases such as AD.
It is just in recent years that mitochondrial DNA (mtDNA) mutations have been found in solid tumors. Although a direct link between the presence of mtDNA mutations and the development of tumors has not been made, mtDNA mutations might prove significant in the detection of tumor recurrence and possibly in the detection of genotoxic damage. To investigate the relationship between mtDNA variation and endometrial cancer, we collected blood samples from subjects with Han native background in Yunnan province in China, 49 of them with pathologically conformed endometrial cancer and 31 as controls with no cancer disease and sequenced two hypervariable segments of control region, part of 16sRNA gene, tRNA(leu) (tRNA is transfer RNA) gene and ND1 gene of mtDNA and identified some diagnostic polymorphisms by restriction fragment length polymorphism of coding region of mtDNA. We could not identify the suspected mutations that are related to diabetes and obesity from our endometrial cancer patients. However, our data showed that patients with endometrial cancers clustered in haplogroup D in a significantly higher frequency when compared with controls, implicating a possible association of haplogroup D to endometrial cancer. We concluded that mitochondrial polymorphisms in haplogroup D might play a genetic role in predisposing to endometrial cancer.
Taurine transport undergoes an adaptive response to changes in taurine availability. Unlike most amino acids, taurine is not metabolized or incorporated into protein but remains free in the intracellular water. Most amino acids are reabsorbed at rates of 98-99%, but reabsorption of taurine may range from 40% to 99.5%. Factors that influence taurine accumulation include ionic environment, electrochemical charge, and post-translational and transcriptional factors. Among these are protein kinase C (PKC) activation and transactivation or repression by proto-oncogenes such as WT1, c-Jun, c-Myb and p53. Renal adaptive regulation of the taurine transporter (TauT) was studied in vivo and in vitro. Site-directed mutagenesis and the oocyte expression system were used to study post-translational regulation of the TauT by PKC. Reporter genes and Northern and Western blots were used to study transcriptional regulation of the taurine transporter gene (TauT). We demonstrated that (i) the body pool of taurine is controlled through renal adaptive regulation of TauT in response to taurine availability; (ii) ionic environment, electrochemical charge, pH, and developmental ontogeny influence renal taurine accumulation; (iii) the fourth segment of TauT is involved in the gating of taurine across the cell membrane, which is controlled by PKC phosphorylation of serine 322 at the post-translational level; (iv) expression of TauT is repressed by the p53 tumour suppressor gene and is transactivated by proto-oncogenes such as WT1, c-Jun, and c-Myb; and (v) over-expression of TauT protects renal cells from cisplatin-induced nephrotoxicity.