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Biomedical subjects

X J Li

Publications and source records attributed to X J Li.

At least 37 records · Page 2Linked to original sources
PubMed2001

Experimental research on TECA-I bioartificial liver support system to treat canines with acute liver failure.

AIM: To evaluate the efficacy and safety of the TECA-I bioartificial liver support system (BALSS) in treating canines with acute liver failure (ALF). METHODS: Ten canines with ALF induced by 80% liver resection received BALSS treatment (BALSS group). Blood was perfused through a hollow fiber tube containing 1X10(10) porcine hepatocytes. Four canines with ALF were treated with BALSS without porcine hepatocytes (control group), and five canines with ALF received drug treatment (drug group). Each treatment lasted 6 hours. RESULTS: BALSS treatment yielded beneficial effects for partial liver resection induced ALF canines with survival and decreased plasma ammonia, ALT, AST and BIL. There was an obvious decrease in PT level and increase in PA level, and there were no changes in the count of lymphocytes, immunoglobulins (IgA, IgG and IgM) and complement (C3 and C4) levels after BALSS treatment. In contrast, for the canines with ALF in non-hepatocyte BALSS group (control group) and drug group, there were no significant changes in ammonia, ALT, AST, BIL, PT and PA levels. ALF canines in BALSS group, control group and drug group lived respectively an average time of 108.0h +/- 12.0h, 24.0h +/- 6.0h and 20.4h +/- 6.4h,and three canines with ALF survived in BALSS group. CONCLUSION: TECA-I BALSS is efficacious and safe for ALF canines induced by partial liver resection.

Animals↗
PubMed2001

TECA hybrid artificial liver support system in treatment of acute liver failure.

AIM: To assess the efficacy and safety of TECA type hybrid artificial liver support system (TECA-HALSS) in providing liver function of detoxification, metabolism and physiology by treating the patients with acute liver failure (ALF). METHODS: The porcine liver cells (1-2) x 10(10) were separated from the Chinese small swine and cultured in the bioreactor of TECA-BALSS at 37.0 degrees C and circulated through the outer space of the hollow fiber tubes in BALSS. The six liver failure patients with various degree of hepatic coma were treated by TECA-HALSS and with conventional medicines. The venous plasma of the patients was separated by a plasma separator and treated by charcoal adsorbent or plasma exchange. The plasma circulated through the inner space of the hollow fiber tubes of BALSS and mixed with the patients' blood cells and flew back to their blood circulation. Some small molecular weight substances were exchanged between the plasma and porcine liver cells. Each treatment lasted 6.0-7.0 h. Physiological and biochemical parameters were measured before,during and after the treatment. RESULTS: The average of porcine liver cells was (1.0-3.0) x 10(10) obtained from each swine liver using our modified enzymatic digestion method. The survival rate of the cells was 85%-93% by trypan blue stain and AO/PI fluorescent stain. After cultured in TECA-BALSS bioreactor for 6 h, the survival rate of cells still remained 70%-85%. At the end of TECA-HALSS treatment, the levels of plasma NH(3), ALT, TB and DB were significantly decreased. The patients who were in the state of drowsiness or coma before the treatment improved their appetite significantly and regained consciousness, some patients resumed light physical work on a short period after the treatment. One to two days after the treatment, the ratio of PTA increased warkedly. During the treatment, the heart rates, blood pressure, respiration condition and serum electrolytes (K(+), Na(+) and Cl(-)) were stable without thrombosis and bleeding in all the six patients. CONCLUSION: TECA-HALSS treatment could be a rapid, safe and efficacious method to provide temporary liver support for patients with ALF.

Acute Disease↗
PubMed2001

Enhanced photo--catalytic activity of gold ion and gold modified.

The gold ion modified TiO2 was prepared by means of sol-gel whereas gold deposited TiO2 was prepared by means of photo-reduction. The physical properties were influenced significantly by the presence of gold ion or gold. The enhanced photo-activity of gold modified TiO2 was quantified in terms of methylene blue degradation. The presence of gold ion in TiO2 lattices or gold on TiO2 surface enhanced their photo-activity. The optimum molar content of gold ion doping and gold deposition all was 0.5%. The first-order rates constants of gold modified TiO2 was more than that of pure TiO2, and decreased by increasing the content of gold ion and gold when their contents were more than 0.5%. Gold ion doped in TiO2 lattices was more effective to enhance the photo-activity than gold on TiO2 surface. Moreover, the relationship between physical properties, chemical properties and photo-activity has been discussed.

Binding Sites↗
PubMed2001

[High-level expression of human calmodulin in E. coli and its effects on cell proliferation].

The gene coding for human CaM was amplified by PCR in which pUC/hCaM3 cDNA was usd as template. After inserting the hCaM III cDNA into the expression plasmid pBV220, we constructed the hCaM3 cDNA-recombinant expression vector(hCaM3/pBV220). The recombinant plasmid was then transformed into E. coli DH5 alpha. After heat induction, a high level expression of CaM protein was obtained. SDS-PAGE analysis showed that the recombinant E. coli could express a 17 kD protein which accounted for about 20% of the total cellular protein. Western blot analysis showed that anti-CaM monoclonal antibody(McAb) specifically bound to the 17 kD band of expression product. rhCaM was purified by Phenyl-sepharose CL-4B affinity chromatography from recombinant bacterial lysate. 3-4 mg of the purified protein were obtained from 1 liter of bacterial culture. The rhCaM was able to activate NAD kinase to the same extent as the standard human brain CaM (Sigma). K562 cells and SP2/0 cells were seeded in 24-well or 96-well plate and cultured for 48 h with rhCaM and CaM-antagonist trifluoperazine(TFP). Cell proliferation rates was determined by MTT assay. There was a significant positive correlation between the concentrations of rhCaM and the cell proliferation rates. CaM-antagonist TFP had an inhibitory effect on cell proliferation rate. The inhibition could be corrected by the addition of extracellular rhCaM.

Animals↗
PubMed2001

[Basic assessment of trust level in medical apparatus and instruments sales systems by medical organization].

Purchase of medical apparatus and instruments is a strict work of taking the patient as a consuming objection. To analyze the trust level in medical apparatus and instruments sales systems and to set up the method of trust level assessment before the purchase, is an important link of ensuring the reality of medical products and consumerism. According to the principle mentioned about, the present article analyses the basic content of assessing factors and their inter-relationship, summarizes their expressions, studies and sets up the mathematical modal and it method. All these are of some value to medical organization in choosing factory owners and their products while the purchasing.

Commerce↗
PubMed2000

Transplanted fetal striatum in Huntington's disease: phenotypic development and lack of pathology.

Neural and stem cell transplantation is emerging as a potential treatment for neurodegenerative diseases. Transplantation of specific committed neuroblasts (fetal neurons) to the adult brain provides such scientific exploration of these new potential therapies. Huntington's disease (HD) is a fatal, incurable autosomal dominant (CAG repeat expansion of huntingtin protein) neurodegenerative disorder with primary neuronal pathology within the caudate-putamen (striatum). In a clinical trial of human fetal striatal tissue transplantation, one patient died 18 months after transplantation from cardiovascular disease, and postmortem histological analysis demonstrated surviving transplanted cells with typical morphology of the developing striatum. Selective markers of both striatal projection and interneurons such as dopamine and c-AMP-related phosphoprotein, calretinin, acetylcholinesterase, choline acetyltransferase, tyrosine hydroxylase, calbindin, enkephalin, and substance P showed positive transplant regions clearly innervated by host tyrosine hydroxylase fibers. There was no histological evidence of immune rejection including microglia and macrophages. Notably, neuronal protein aggregates of mutated huntingtin, which is typical HD neuropathology, were not found within the transplanted fetal tissue. Thus, although there is a genetically predetermined process causing neuronal death within the HD striatum, implanted fetal neural cells lacking the mutant HD gene may be able to replace damaged host neurons and reconstitute damaged neuronal connections. This study demonstrates that grafts derived from human fetal striatal tissue can survive, develop, and are unaffected by the disease process, at least for 18 months, after transplantation into a patient with HD.

Corpus Striatum↗
PubMed2000

Intranuclear huntingtin increases the expression of caspase-1 and induces apoptosis.

Expansion of a polyglutamine repeat in huntingtin causes Huntington's disease (HD). Although full-length huntingtin is predominantly distributed in the cytoplasm, N-terminal fragments of huntingtin with expanded polyglutamine tracts are able to accumulate in the nucleus and kill neurons through apoptotic pathways. Transgenic mice expressing N-terminal mutant huntingtin show intranuclear huntingtin accumulation and develop progressive neurological symptoms. Inhibiting caspase-1 can prolong the survival of these HD mice. How intranuclear huntingtin is associated with caspase activation and apoptosis is unclear. Here we report that intranuclear huntingtin induces the activation of caspase-3 and the release of cytochrome c from mitochondria in cultured cells. As a result, cells expressing intranuclear huntingtin undergo apoptosis. We show that intranuclear huntingtin increases the expression of caspase-1, which may in turn activate caspase-3 and trigger apoptosis. We propose that the increased level of caspase-1 induced by intranuclear huntingtin contributes to HD-associated cell death.

Animals↗
PubMed2000

Long glutamine tracts cause nuclear localization of a novel form of huntingtin in medium spiny striatal neurons in HdhQ92 and HdhQ111 knock-in mice.

Huntington's disease (HD) is caused by an expanded N-terminal glutamine tract that endows huntingtin with a striatal-selective structural property ultimately toxic to medium spiny neurons. In precise genetic models of juvenile HD, HdhQ92 and HdhQ111 knock-in mice, long polyglutamine segments change huntingtin's physical properties, producing HD-like in vivo correlates in the striatum, including nuclear localization of a version of the full-length protein predominant in medium spiny neurons, and subsequent formation of N-terminal inclusions and insoluble aggregate. These changes show glutamine length dependence and dominant inheritance with recruitment of wild-type protein, critical features of the altered HD property that strongly implicate them in the HD disease process and that suggest alternative pathogenic scenarios: the effect of the glutamine tract may act by altering interaction with a critical cellular constituent or by depleting a form of huntingtin essential to medium spiny striatal neurons.

Animals↗
PubMed2000

Expression of huntingtin-associated protein-1 in neuronal cells implicates a role in neuritic growth.

Huntingtin-associated protein-1 (HAP1) binds more tightly to mutant huntingtin, but its function and distribution in neurites are not clear. Using PC12 cells and cultured hippocampal neurons, we found that two HAP1 isoforms, HAP1-A and HAP1-B, have different subcellular localizations. While most HAP1-B is diffusely distributed within the cytoplasm, HAP1-A is enriched in the growth cones and neuritic puncta of developing neurons. In mature neurons and adult brain neurons, however, HAP1-A is concentrated in axon terminals and associated with synaptic vesicles. Transfection of HAP1-A in PC12 cells significantly promotes neurite extension, with HAP1-A distributed in the distal regions of the growing neurites. Cotransfection of mutant huntingtin with HAP1-A in PC12 cells results in the accumulation of HAP1-A on huntingtin aggregates and the inhibition of neurite promotion by HAP1-A. This study suggests that HAP1-A has a function in neuritic development and synaptic function and that mutant huntingtin may alter this function.

Amino Acid Sequence↗
PubMed2000

Amino-terminal fragments of mutant huntingtin show selective accumulation in striatal neurons and synaptic toxicity.

Huntington disease (HD) is caused by expansion of a glutamine repeat in the amino-terminal region of huntingtin. Despite its widespread expression, mutant huntingtin induces selective neuronal loss in striatal neurons. Here we report that, in mutant mice expressing HD repeats, the production and aggregation of N-terminal huntingtin fragments preferentially occur in HD-affected neurons and their processes and axonal terminals. N-terminal fragments of mutant huntingtin form aggregates and induce neuritic degeneration in cultured striatal neurons. N-terminal mutant huntingtin also binds to synaptic vesicles and inhibits their glutamate uptake in vitro. The specific processing and accumulation of toxic fragments of N-terminal huntingtin in HD-affected striatal neurons, especially in their neuronal processes and axonal terminals, may contribute to the selective neuropathology of HD.

Animals↗
PubMed2000

Mxi1 is a potential cellular target of carcinogens and frequently mutated in experimental rat tumors and tumor cell lines.

Mxi1, a member of the Myc family of transcription factors, negatively regulates Myc oncoprotein activity and thus may be a tumor suppressor gene. It is mutated in a few human prostate cancers. Rat Mxi1 was isolated as a selective overexpressive message in rat esophageal cancer induced by N-nitrososarcosine ethyl ester using differential display and polymerase chain reaction cloning. Reverse transcription, single-strand conformation polymorphism analysis and subsequent DNA sequencing were used to screen mutations for the rat Mxi1 coding region including the functional domains, Sin3-interacting, helix-loop-helix and leucine zipper in samples from 24 rat tumor tissues and various cell lines. Seven mutations were revealed to exist in six rat tumors (including two esophageal tumors and a breast cancer), and three rat tumor cell lines: Leydig cell tumor, osteogenic sarcoma, and pituitary tumor. No coding changes were detected in 34 samples of human sporadic gastric adenocarcinoma. A silent base substitution (GAG to GAA) at codon 131 was also identified in six rat tumors as well as in one human gastric cancer. Our results indicate that Mxi1 is often mutated in experimental rat tumors but mutations are rare in human sporadic cancers. The Mxi1 tumor suppressor gene may be a cellular target of strong carcinogens. Considering the frequency of mutations in chemical carcinogen-induced tumors, searches for Mxi1 mutation in human tumors should be directed toward patients with a specific epidemiological background.

Adenocarcinoma↗
PubMed2000

Combined free toe and free deep inferior epigastric perforator flap for reconstruction of the thumb and thumb web space.

To repair a complexly injured hand with composite loss of the thumb and the thumb web space in one stage, the combined transfer of a free second toe and a free deep inferior epigastric perforator flap was designed. It was used to simultaneously reconstruct the thumb and thumb web space of the injured hand in five cases. All flaps survived and there were no complications at any donor site after the reconstructions. In follow-up averaging 35.6 months, the final functional and cosmetic outcomes of the reconstructed thumbs and thumb web spaces were satisfactory. Results demonstrated that the combined transfer of a free second toe and a free deep inferior epigastric perforator flap is a valid method for simultaneous reconstruction of the thumb and the thumb web space of the injured hand.

Abdominal Muscles↗
PubMed2000

MDM2 overexpression with alteration of the p53 protein and gene status in oral carcinogenesis.

In this study, to better understand the mechanism of oral squamous cell carcinoma (SCC) carcinogenesis, alterations of the p53 gene and overexpression of MDM2 and p53 were analyzed in 38 oral SCC samples. Twelve of the 38 specimens revealed mutant-type p53. Moreover, coexpression of MDM2 and p53 was found most frequently in dysplastic lesions (P < 0.05). Expression of MDM2 and p53 was significantly increased in accordance with the histological progression of multistep carcinogenesis (P < 0.05). No significant correlation was found between the expression of MDM2 and the alteration of p53 protein or p53 gene status. MDM2 overexpression with mutant p53 was significantly associated with poorly differentiated SCCs (P < 0.05) and tumor stages III and IV of oral SCCs (P < 0.05). These results suggest that MDM2 overexpression is an early event in oral carcinogenesis through the functional inactivation of the wild-type p53, and corresponding alterations of MDM2 and p53 contribute to the oral carcinogenesis. We propose that it would be clinically more instructive to evaluate MDM2 overexpression combined with p53 gene status, compared to the evaluation of either MDM2 or p53 alteration alone.

Carcinoma, Squamous Cell↗
PubMed2000

Xenotransplantation of microencapsulated bovine chromaffin cells into hemiparkinsonian monkeys.

This study examines the effects of xenografts of microencapsulated bovine chromaffin cells (BCCs) on the rotational behavior of hemiparkinsonian monkey recipients. In addition, it determines the content of monoamine neurotransmitters and their major metabolites in the neostriatum in hemiparkinsonian monkeys. The hemiparkinsonian model in monkeys was induced by a unilateral intracarotid injection of methyl-phenyl-tetrahydropyridine (MPTP). Unencapsulated BCCs, BCCs microencapsulated in alginate-polylysine-alginate (ALA) membranes as well as empty microencapsules were grafted into the neostriatum of the hemiparkinsonian monkeys. Following the transplantation the hemiparkinsonian symptoms subsided and the number of rotations induced by apomorphine decreased for up to nine months in the group of recipients grafted with microencapsulated BCCs, while only a temporary improvement (one month) was detected in the recipients of the unencapsulated BCCs. No change was observed in the recipients of empty microencapsules. Dopamine and its metabolites were found considerably depleted in the MPTP-lesioned side versus the unlesioned side of the neostriatum in the hemiparkinsonian monkeys(P<0.05).

3,4-Dihydroxyphenylacetic Acid↗
PubMed2000

Alteration of tumor phenotypes of B16 melanoma after genetic remodeling of the ganglioside profile.

Gangliosides have been thought to be tumor markers of various neuroectoderm-derived cancers. However, their roles in malignant phenotypes of cancer cells are not well understood. We have performed the remodeling of ganglioside profiles of mouse melanoma B16 (B78 subline) by introducing GM2/GD2 synthase cDNA, and analyzed the phenotypic changes such as cell morphology, growth, adhesion and c-fos gene expression. Although newly expressed GM2 was clearly detected, GM2-positive transfectant cells showed rather reduced growth rates in vivo and in vitro, lower expression levels of c-fos gene and increased levels of cell adhesion to extracellular matrices compared to control cells. These results suggested that GM2 is involved in the regulation of cell-cell or cell-extracellular matrix interaction, and negatively control cell proliferation.

Animals↗
PubMed2000

Cytochrome P450 2E1 polymorphism in gastric cancer in Brazil: case-control studies of Japanese Brazilians and non-Japanese Brazilians.

Cytochrome P450 2E1 (Cyp2E1) is involved in the metabolic oxidation of carcinogenic nitroso compounds, including N-nitrosoamines. There is an RsaI polymorphism in the transcriptional regulatory region of this gene, and in vitro evidence suggests that the variant type of this polymorphic site has higher transcriptional activity but less chlorzoxazone-metabolizing activity. Interindividual differences in the metabolic capacity of Cyp2E1 are assumed to be associated with cancer susceptibility, but the results of the previous studies on the relation between Cyp2E1 RsaI polymorphism and cancer susceptibility have been inconsistent. Two case-control studies of gastric cancer in Japanese Brazilians (96 cases, 192 controls) and Brazilians not of Japanese ancestry (non-Japanese Brazilians; 236 cases, 236 controls) in São Paulo were designed to clarify the role of the Cyp2E1 RsaI genotype in susceptibility to gastric cancer after considering multifactorial environmental influences. The subjects with variant RsaI genotypes amounted to 47% (28 of 59) and 48% (64 of 133), respectively, of the Japanese cases and controls, and 6% (11 of 187) and 10% (19 of 192), respectively, of the non-Japanese cases and controls. As expected, a difference in the distributions of the two groups was observed. The odds ratio of the RsaI variant genotype of Cyp2E1 was 0.46 (95% confidence interval, 0.21-1.04) in the non-Japanese Brazilian population and 0.98 (95% confidence interval, 0.50-1.90) in the Japanese Brazilian population after adjusting for sex, age, tobacco use, and meat consumption. Additional adjustment for potential confounding factors did not change the odds ratio substantially. No significant interactions were observed between the polymorphism and environmental factors. In regard to the histological type of gastric cancer, the variant genotype was significantly more prevalent than the common genotype in Japanese subjects with diffuse type gastric cancer. Our study suggests that the Cyp2E1 RsaI polymorphism is associated with a reduced risk of gastric cancer, although how the assumed increase in Cyp2E1 expression produced by this polymorphism is related to a reduced risk of cancer remains unclear. The observations in this study are consistent with the recent observations of esophageal cancer in endemic areas of China.

Aged↗
PubMed2000

Current trends and new approaches in the management of diabetes mellitus.

Current trends in the management of type 2 diabetes mellitus, based on the 20-year United Kingdom Prospective Diabetic Study, include intensive treatment to control the blood glucose level and blood pressure in order to prevent or delay microvascular and cardiovascular complications. In the new millennium, type 2 diabetes will become epidemic in developing countries. If diabetes were to develop in 10% of the 1.2 billion population of China, the expense of intensive treatment would be immense. Laboratory tests are useful for detecting risk factors before the onset of the disease and convincing the general public to take preventive measures. Glucose tolerance testing is one of these tests. When glucose tolerance is impaired, 25% of beta-cell function is lost. Determining the plasma proinsulin level is another useful evaluation; impaired glucose tolerance accompanied by increased plasma proinsulin level is indicative of an enhanced risk that type 2 diabetes will develop within 5 years. Educating the public about eating a healthy diet and exercising may prevent the development of diabetes and thereby reduce the global prevalence of type 2 diabetes.

Diabetes Mellitus, Type 2↗