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Biomedical subjects

Z H Liu

Publications and source records attributed to Z H Liu.

At least 37 records · Page 2Linked to original sources
PubMed2000

Endogenous BDNF is required for myelination and regeneration of injured sciatic nerve in rodents.

Following a peripheral nerve injury, brain-derived neurotrophic factor (BDNF) and the p75 neurotrophin receptor are upregulated in Schwann cells of the Wallerian degenerating nerves. However, it is not known whether the endogenous BDNF is critical for the functions of Schwann cells and regeneration of injured nerve. Treatment with BDNF antibody was shown to retard the length of the regenerated nerve from injury site by 24%. Histological and ultrastructural examination showed that the number and density of myelinated axons in the distal side of the lesion in the antibody-treated mice was reduced by 83%. In the BDNF antibody-treated animals, there were only distorted and disorganized myelinated fibres in the injured nerve where abnormal Schwann cells and phagocytes were present. As a result of nerve degeneration in BDNF antibody-treated animals, subcellular organelles, such as mitochondria, disappeared or were disorganized and the laminal layers of the myelin sheath were loosened, separated or collapsed. Our in situ hybridization revealed that BDNF mRNA was expressed in Schwann cells in the distal segment of lesioned nerve and in the denervated muscle fibres. These results indicate that Schwann cells and muscle fibres may contribute to the sources of BDNF during regeneration and that the deprivation of endogenous BDNF results in an impairment in regeneration and myelination of regenerating axons. It is concluded that endogenous BDNF is required for peripheral nerve regeneration and remyelination after injury.

Animals↗
PubMed2000

Triptolide: a potent inhibitor of NF-kappa B in T-lymphocytes.

AIM: To study the effect of triptolide on the activity of nuclear factor-kappa B (NF-kappa B) and gene expression of I kappa B alpha, a major inhibitor of NF-kappa B, in human Jurkat T cell line. METHODS: Jurkat cells treated with or without PMA/PHA were incubated with varied doses of triptolide for different time periods. The activity of NF-kappa B in Jurkat cells was measured with electrophoretic mobility shift assays (EMSA), and the mRNA expression of I kappa B alpha in Jurkat cells was detected by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: PMA/PHA treatment was found to induce NF-kappa B activation rapidly. Triptolide treatment decreased the activity of NF-kappa B in both PMA/PHA treated and untreated Jurkat cells. This effect of triptolide was in a dose-dependent manner and was more obvious in cells treated with PMA/PHA. The mRNA expression of I kappa B alpha were upregulated by triptolide, while this effect was more potent in cells without PMA/PHA treatment. CONCLUSION: Triptolide is a potent inhibitor of NF-kappa B activation in T lymphocyte and this effect is partly due to the upregulation of I kappa B alpha mRNA expression.

DNA-Binding Proteins↗
PubMed2000

Long-term outcome of acute renal injury induced by Aristolochia manshuriensis Kom in rats.

AIM: To investigate the long-term functional and morphological changes of the kidney induced by acute intoxication of Aristolochia manshuriensis Kom in rats. METHODS: Experimental model of acute renal injury was established in the Sprague-Dawley rats with oral administration of decoctions of Chinese herb, Aristolochia manshuriensis Kom, at dosages of 50 g.kg-1.d-1 and 30 g.kg-1.d-1 for 7 consecutive days, and 20 g.kg-1.d-1 for 15 consecutive days. Renal function was assayed at months 0 (right after treatment), 1, 3, and 6 of the experiment. Renal histological examination was also performed. RESULTS: 1) At month 0, the renal functional changes of acute renal injury included azotemia, low molecular weight proteinuria, glycosuria, hypoosmotic urine, and NAG enzymuria. Histopathological changes showed acute tubular necrosis, predominantly at the corticomedullary junction. 2) At months 1 and 3, the renal function of rats of the experiment was gradually restored and histopathologic examination suggested that the tubular lesions gradually recovered. In HE sections, basophilic deposits were observed in the tubular cytoplasm. And interstitial infiltration of inflammatory cells was not prominent. 3) At months 6, renal preneoplastic lesions, renal tumors, and extrarenal tumors occurred in rats. The occurrence of renal preneoplastic lesions at dosages of 50 g.kg-1.d-1, 30 g.kg-1.d-1, and 20 g.kg-1.d-1 were 100.0% at all three doses, renal tumors 42.8%, 25.0%, and 0%, respectively, extrarenal tumors 14.4%, 12.5%, and 12.5%, respectively, and systemic tumors 57.2%, 37.5%, and 12.5%, respectively. The occurrence of basophilic deposits, renal preneoplastic lesions, renal tumors, and extrarenal tumors in normal control group was nil. CONCLUSIONS: 1) Administration of large dosage of Aristolochia manshuriensis Kom induces acute renal failure in rats. 2) The long-term renal function and histopathologic changes of acute renal injury induced by Aristolochia manshuriensis Komrecover spontaneously. 3) Aristolochia manshuriensis Kom has been proved to be oncogenic for the first time.

Acute Kidney Injury↗
PubMed1999

Glucose transporter (GLUT1) allele (XbaI-) associated with nephropathy in non-insulin-dependent diabetes mellitus.

BACKGROUND: Although multiple factors contribute to the initiation and progression of diabetic nephropathy (DN), hyperglycemia and genetic predisposition are two major components implicated in the development of DN. Several pieces of experimental evidence suggest that glucose transporter (GLUT1) activity is an important modulator for the cell hypertrophy and extracellular matrix formation of glomerular mesangial cells. METHODS: To evaluate the role of the GLUT1 gene mutation in the development of DN in Chinese patients with non-insulin-dependent diabetes mellitus (NIDDM), the polymorphic XbaI site of GLUT1 gene was analyzed by polymerase chain reaction in 124 normal subjects and 131 patients with NIDDM, among whom 64 were complicated with DN. DN was defined as persistent albuminuria with or without impaired renal function with no known cause of renal disease other than diabetes. RESULTS: The frequencies of XbaI (+/-) genotype (75 vs. 44%, P < 0.01) and XbaI (-) allele (44 vs. 29%, P < 0.05) were significantly higher in NIDDM patients with DN than those without nephropathy. There were no significant differences for GLUT1 genotype and allele frequency between NIDDM patients without nephropathy and normal subjects. The presence of the XbaI (-) allele appeared to have a strong association with the development of DN. The odds ratio was 1.915, and the 95% confidence interval was 1.044 to 3.514. In addition, no strong association was found between GLUT1 gene polymorphism and retinopathy in NIDDM patients. CONCLUSION: Our results indicate that the XbaI (-) allele of the GLUT1 gene might be a genetic marker of NIDDM with DN, and this genetic susceptibility is independent of its retinopathy in Chinese subjects.

Adult↗
PubMed1999

Dihydroetorphine-induced place preference was mediated by dopamine D1 receptors in rats.

AIM: To study the influence of dopamine (DA) receptor antagonists upon the rewarding property of dihydroetorphine (DHE). METHODS: Conditioned place preference (CPP) paradigm was used to characterize the rewarding effect of DHE. DA receptor antagonists were injected administered subcutaneously or peritoneally and microinjected into nucleus accumbens (NAcc). RESULTS: DHE (0.05, 0.5, and 5.0 micrograms.kg-1, s.c.) produced place preference (P < 0.01). Both the DA receptor antagonist haloperidol and the selective D1 receptor antagonist Sch-23390 attenuated the place preference produced by DHE (0.5 microgram.kg-1, s.c.). l-Sulpiride and spiperone, selective D2 receptor antagonists, had no such effects. CONCLUSION: The D1 (but not D2) receptors in NAcc are crucial in the mediation of the rewarding effect of DHE.

Animals↗
PubMed1999

[Chromosomal mapping of ld gene which causes congenital limb deformity syndrome in KM-ld mouse].

Fourteen biochemical marker loci and 61 SSLP loci in congenic strain C57BL/6.KM-ld were screened to determine the loci linkage to ld gene, an autosomal recessive mutant gene in KM mouse which causes congenital limb deformity in mouse by means of electrophoresis and PCR amplification. The result showed that ld gene linked to D2Mit30, D2Mit62 and D2Mit63. To locate ld gene more accurately on chromosome 2, 86 backcross offsprings (C57BL/6 x KM-ld) F1 x KM-ld were produced for linkage analysis. From the backcross progeny genomic DNAs were amplified for D2Mit13, D2Mit30, D2Mit62 and D2Mit63 loci in vitro. According to phenotypes, the linkage between the four SSLP loci and ld gene was analysed by calculating genetic distance, ld gene was located exactly on Chr. 2, 76cM, with distances of 25.58cM to D2Mit30, D2Mit62 and D2Mit63, of 31.39cM to D2Mit13.

Animals↗
PubMed1999

Effect of tetrandrine on morphine dependence in isolated guinea pig ileum.

AIM: To evaluate the effects of tetrandrine (Tet) and nimodipine (Nim) on the morphine (Mor) withdrawal response in the isolated guinea pig ileum. METHODS: The withdrawal contracture was elicited by addition of naloxone (Nal) (1 mumol.L-1) to the isolated naive ileum incubated with Mor (3 mumol.L-1) at 37.5 degrees C for 4 h or to the ileum obtained from Mor-dependent guinea pig. RESULTS: When Nim (0.01, 0.05, and 0.1 mumol.L-1) or Tet (1, 10, and 50 mumol.L-1) was added 1 min before Nal in the naive ilea bathed in Krebs solution containing Mor, or when the ilea from Mor-dependent guinea pigs were incubated with Nim (0.01, 0.05, and 0.1 mumol.L-1) or Tet (1, 10, and 50 mumol.L-1) for 15 min, or when Nim (5 and 10 mg.kg-1, i.p.) or Tet (15 and 30 mg.kg-1, i.p.) was administered in vivo to Mor-dependent guinea pigs, the Nal-precipitated withdrawal contracture was significantly decreased in a dose-dependent manner. CONCLUSION: Tet and Nim, Ca2+ channel blockers, could inhibit the Nal-precipitated Mor withdrawal response in the isolated guinea pig ileum.

Alkaloids↗
PubMed1999

[Biological effects of space flight on purple nonsulfur photosynthetic bacteria].

OBJECTIVE: To study biological effects of space flight on purple nonsulfur photosynthetic bacteria. METHODS: Two purple nonsulfur photosynthetic bacteria, Rhodopseudomonas palustris H3 and Rhodobacter sphaeroides ZGY, were carried on satellite for 15 days and some of their biological effects were studied after recovery. RESULTS: In space condition, survival rate of bacteria was promoted. The purification of organic wastewater, removal of nitrite, degradation of phenol and decolorization of acid red B were enhanced, and the resistance of both strains to medicine was stable. CONCLUSION: The major morphological and physiological characteristics of loaded strains H3-S and ZGY-S were not changed after space flight.

Biodegradation, Environmental↗
PubMed1999

[Studies on microinjection of mouse spermatozoa into rabbit oocytes].

The methods of intracytoplasmic sperm injection (ICSI) and subzonal injection (SUZI) were used to study heterologous fertilization and embryonic development between the mouse and the rabbit. Results were as follows: 1. The mouse sperm nuclei decondensed and formed pronuclei following microinjection into cytoplasm and perivitelline space (PVS) of rabbit oocytes; 2. The hybrid embryos developed to the stage of 8-cell when cultured in vitro; 3. The karyotype analysis showed a normal complement of rabbit oocyte and mouse sperm chromosomes in the 4-cell hybrid embryos; 4. The ultrastructure of 4-cell hybrid embryos was similar to that of normal 4-cell rabbit embryos; 5. The fertilization rate (32.4%) and cleavage rate (22.2%) when 5-10 mouse spermatozoa were injected were higher than those of injection of a single spermatozoon into PVS of the rabbit oocyte, but the difference was not significant (P > 0.05). The fertilization rate (42.3%) and cleavage rate (30.8%) in rabbit oocytes in vitro matured for 11-12 h were higher than those in the oocytes which were in vitro matured for 24-25 h following microinjection of 1-2 mouse spermatozoa into PVS, but the difference was not significant (P > 0.05).

Animals↗
PubMed1999

[Study on the separation of optical chromatography].

The relationship between the particle radius with the intensity of the applied laser radiation force is theoretically studied using a ray-optics model by analyzing the forced-status of the separated particles in the mobile phase. The laser radiation force is proportional to the square of the particle radius when the particle radius is much smaller than the laser beam radius under the condition of using a single-transverse-mode laser beam with a Gaussian intensity distribution and the particle refractive index being larger than that of the mobile phase. The retention distance is calculated and the dynamic range is discussed. Theoretically, the dynamic range of the optical chromatography can be extended by increasing laser power, decreasing the flow rate of mobile phase and focusing the laser beam.

Chromatography↗
PubMed1998

Saccharopolyspora spinosporotrichia sp. nov., a novel actinomycete from soil.

The generic position of an aerobic, Gram-positive, non-acid-alcohol-fast actinomycete was determined following isolation of the PCR-amplified 16S rRNA genes and alignment of the resultant sequence with corresponding sequences from representatives of the family Pseudonocardiaceae. The assignment of the organism to the genus Saccharopolyspora was strongly supported by chemotaxonomic and morphological data. The strain was distinguished from representatives of validly described Saccharopolyspora species by a number of phenotypic properties. It is proposed that the organism, strain AS4.198T, be classified in the genus Saccharopolyspora as Saccharopolyspora spinosporotrichia sp. nov.

Classification↗
PubMed1998

Genetic analysis of N-acetyltransferase polymorphism in a Chinese population.

AIM: To study the genetic basis of N-acetylatransferase polymorphism in Chinese. METHODS: Genotypes in 120 healthy Han volunteers from 19 provinces of China were assayed. The 3 common mutant alleles (M1, M2, M3) and one normal wild-type (WT) allele of the N-acetyltransferase (NAT2) gene were detected by allele-specific polymerase chain reaction technique. RESULTS: The NAT2 allele frequencies in 120 Chinese (WT = 0.625, M1 = 0.0458, M2 = 0.188, M3 = 0.142) were different (P < 0.01). The NAT2 genotype distribution for all detected combinations of NAT2 alleles in 120 Chinese subjects was consisitent with Hardy-Weinberg equilibrium (chi 2 = 7.27, nu = 8, 0.7 > P > 0.5). Fifty subjects (41.7%) were homozygous wildtypes, 50 subjects (41.7%) were heterozygous mutants, and 20 subjects (16.7%) were homozygous mutants. CONCLUSION: The lower frequency of mutant M1 allele compared with that of Caucasians explains the low frequency of slow acylators in Chinese.

Acetyltransferases↗
PubMed1997

A cysteine protease inhibitor prevents activation-induced T-cell apoptosis and death of peripheral blood cells from human immunodeficiency virus-infected individuals by inhibiting upregulation of Fas ligand.

Activation of T-cell hybridomas, preactivated normal T cells, and peripheral blood lymphocytes (PBL) from human immunodeficiency virus (HIV)-infected individuals results in apoptosis. In the first two cases, apoptosis is caused by the upregulation of Fas ligand (FasL) and its subsequent interaction with Fas; the mechanism for the spontaneous and activation-induced death of lymph node cells and PBL from HIV+ blood is not known. A number of protease inhibitors have been shown to prevent T-cell apoptosis under all of these circumstances, but the mechanism of action has not been determined. Here we show that the cysteine protease inhibitor E64d prevent activation-induced T hybridoma cell death by inhibiting the upregulation of FasL. Quantitative polymerase chain reaction (PCR) demonstrated that mRNA for FasL is expressed at low levels in fresh PBL from HIV-infected blood, but increases in cultured PBL from both uninfected and HIV-infected donors. The ex vivo apoptosis of PBL from HIV+ donors was prevented by adding the soluble extracellular domain of Fas, demonstrating a requisite role for Fas/ FasL interactions in this form of cell death. Furthermore, while having no effect on the death of PBL from HIV-infected blood stimulated directly via Fas, E64d inhibited FasL upregulation. Thus, aberrant apoptosis of cultured PBL from HIV-infected individuals is mediated by FasL and Fas, and E64d blocks this apoptosis by inhibiting the upregulation of FasL. These results are consistent with the hypothesis that the abnormal expression of Fas and the inducible expression of FasL, contributes to the immunodeficiency of patients with acquired immune deficiency syndrome and suggest that modulation of FasL expression could be an effective target for therapeutic intervention.

Apoptosis↗
PubMed1997

Interleukin-1 receptor antagonist allele: is it a genetic link between Henoch-Schönlein nephritis and IgA nephropathy?

Henoch-Schönlein purpura nephritis (HSPN) is a multi-organ systemic vasculitis, which shares many clinical, histological and immunological features with IgA nephropathy (IgAN). To address whether these two diseases have a common genetic background, the polymorphism of the variable number tandem repeat (VNTR) of IL-1 receptor antagonist (IL-1ra) gene has been analyzed using PCR in patients diagnosed with HSPN (N = 43) and IgAN (N = 97), together with normal controls (N = 98) and patients with acute post-infectious glomerulonephritis (APGN), under the concept that IL-1 might play an important role in mediating pathogenesis of vasculitis and glomerulonephritis. It was found that the allele frequency and carriage rate of the interleukin-1 receptor antagonist allele (IL1RN*2) of the IL-1ra gene increased significantly in HSPN patients as compared to IgAN (P < 0.01), APGN (P < 0.05) and normal subjects (P < 0.01). Interestingly, varied carriage rates of IL1RN*2 were found among various groups of IgAN patients presenting with different clinical manifestations. The carriage rate of IL1RN*2 was significantly higher in patients with recurrent gross hematuria than other groups of IgAN patients (P < 0.01). Furthermore, although the carriage rate of IL1RN*2 was higher in HSPN (46.5%) than average IgAN patients (26.8%; P < 0.01), there was no significant difference in the carriage rate of IL1RN*2 between HSPN and those IgAN patients with recurrent gross hematuria (42.8%l P > 0.05). It suggested that the IL1RN*2 allele might be a genetic marker shared by HSPN and a special group of IgAN patients with recurrent gross hematuria. Our preliminary observation provided a genetic evidence to support the hypothesis that HSPN and certain subgroup of IgAN are closely related diseases. Such an association of the gene polymorphism of IL-1ra between HSPN and IgAN with recurrent gross hematuria might serve as a key to explore their pathogenesis and eventually a specific intervention.

Adolescent↗
PubMed1997

[A follow-up study on correlated factors for intrauterine infection of hepatitis B virus].

One hundred and twenty-two pregnant women with positive serum hepatitis B surface antigen (HBsAg) and their infants were followed-up to study the risk factors related to intrauterine infection of hepatitis B virus (HBV). Infants were immunized with three doses of hepatitis B vaccine within 24 hours after birth, one month and six months of age, respectively, and hepatitis B immunoglobulin (HBIG) was injected simultaneously with the first dose. Markers of HBV infection in pregnant women and infants were detected by enzyme linked immunosorbent assay (ELISA). Results showed that 13 infants were detected positive for HBsAg in their sera, eight of them were positive at their birth and the other five converted positive during follow-up. Simple and multiple logistic regression analyses showed that positivity of hepatitis Be antigen (HBeAg) in mothers and their threatened abortion related to intrauterine infection, with relative risks of 31.27 and 10.87, respectively.

Female↗
PubMed1996

Inhibition of diabetic nephropathy by a GH antagonist: a molecular analysis.

Streptozotocin-treated C57B1/SJL mice developed glomerular hypertrophy and light microscopic lesions mimicking human diabetic glomerulosclerosis. In contrast, there were no glomerular hypertrophy and lesions in diabetic mice transgenic (TG) for a mutated growth hormone (bGH-G119K) that competes with native endogenous GH and results in dwarfism. We examined the molecular events underlying these findings. The non-transgenic (non-TG) diabetic mouse glomeruli had an increase in mRNA coding for alpha 1IV collagen, laminin B1, TGF-beta 1, 72 kDa collagenase, and TIMP-3. In contrast, glomerular type IV collagen and laminin B1 mRNA levels were normal in diabetic TG dwarf mice. However, the 72 kDa gelatinase, TIMP-3, and TGF-beta 1 mRNAs were elevated in the diabetic dwarfs. Type IV collagen and laminin accumulated in the glomeruli of diabetic non-TG, but not of diabetic dwarf mice, by immunofluorescence microscopy, confirming the mRNA data. GH binding protein mRNA levels were comparable in glomeruli from dwarf and non-TG mice, both diabetic and non-diabetic. We did not detect GH receptor mRNA in glomeruli. These data suggest that diabetic glomerulosclerosis is associated with an increase in type IV collagen and laminin synthesis, and that these changes do not occur in mice transgenic for bGH119K, a functional antagonist of GH. The increase of 72 kDa gelatinase, TIMP-3 and TGF-beta 1 mRNAs, independent of GH, suggested that these changes induced by hyperglycemia were not sufficient for the induction of glomerulosclerosis.

Animals↗
PubMed1996

TNF-alpha and IL-1 alpha induce mannose receptors and apoptosis in glomerular mesangial but not endothelial cells.

The macrophage mannose receptor, a carbohydrate-binding membrane protein, mediates endocytosis and phagocytosis. This study was undertaken to determine whether mannose receptors were expressed in resting glomerular mesangial and endothelial cells and whether their level was affected by cytokines. Neither mannose receptor mRNA nor proteins were found in resting mesangial or endothelial cells. Mannose receptor mRNA was induced in a dose- and time-dependent manner in mesangial cells by interleukin-1 alpha (IL-1 alpha) or tumor necrosis factor-alpha (TNF-alpha) but not by platelet-derived growth factor-B or IL-6. Cell surface receptors were found by fluorescence-activated cell sorter analysis. Binding to stimulated mesangial cells was saturable and inhibited by excess mannose-bovine serum albumin (BSA) but not by galactose-BSA. TNF-alpha and IL-1 alpha also induced apoptosis in mesangial cells. Mannose receptor expression was not restricted to apoptotic stimulated mesangial cells. Neither agonist induced mannose receptor expression or apoptosis in endothelial cells. Because immunoglobulin A, M, and G contain mannose residues, immune aggregates may be removed from the mesangium through cytokine-induced mannose receptors.

Animals↗