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Biomedical subjects

F Zheng

Publications and source records attributed to F Zheng.

At least 55 records · Page 3Linked to original sources

[Genetic polymorphism analysis of apoE intron 1 enhancer in patients with coronary heart disease and the association with serum lipid level].

OBJECTIVE: To investigate the association between the polymorphism of apolipoprotein E (apoE) intron 1 enhancer (IE1) and the level of serum lipid in patients with coronary heart disease (CHD). METHODS: ApoE IE1 genotypes of 81 patients with CHD and 108 healthy subjects were detected by polymerase chain reaction and restriction fragment length polymorphism. RESULTS: The frequency of G/G genotype in patients with CHD was significantly higher than that in control group (P < 0.05). The frequency of G allele was significantly higher in patients than in control group (P < 0.05). The gene polymorphism of apoE IE1 obviously influenced the serum lipid levels. The concentrations of TC, and LDL-C among different genotype groups were significantly different, and the level in G/G group was higher than that in C/C group (P < 0.05). CONCLUSION: ApoE IE1 gene polymorphism is closely related to serum lipid, and G/G genotype of apoE IE1 may be a risk factor of coronary heart disease in Han Chinese.

Aged↗

Epidemiology of human ancylostomiasis among rural villagers in Nanlin County (Zhongzhou Village), Anhui Province, China: II. Seroepidemiological studies of the age relationships of serum antibody levels and infection status.

Anti-hookworm antibody serologic responses were measured in residents of an Anhui provincial Chinese village where Ancylostoma duodenale is the predominant hookworm. Antibody responses were measured against either soluble infective third-stage larval (L3) or adult antigens. Immunoglobulins of the IgG class, especially IgG4 correlated with both the prevalence and intensity of A. duodenale hookworm infections. In contrast, there was an inverse correlation with IgM, but no correlation with IgA or IgE. Circulating IgG4 antibody responses might serve as a surrogate marker for active A. duodenale hookworm infection.

Ancylostomiasis↗

Gene polymorphism in apolipoprotein E and presenilin-1 in patients with late-onset Alzheimer's disease.

OBJECTIVE: To evaluate the association of apolipoprotein E (apoE) and presenilin-1 (PS-1) gene polymorphism with late-onset Alzheimer's disease (AD). METHODS: A case-control study was undertaken to detect the polymorphism of apoE and PS-1 by polymerase chain reaction and digestion with the endonucleases of BspL I, Hha I and BamH I. RESULTS: The frequencies of apoE epsilon 3/4 genotype and epsilon 4 allele in late-onset AD (n = 42) were significantly higher than those of age-matched controls (P < 0.05). The frequencies of the apoE intron 1 enhancer (IE1) G/G genotype and G allele in late-onset AD were also significantly higher than those in controls (P < 0.05). The frequencies of the PS-1 1/1 genotype but not the 1 allele in AD were significantly higher than those in controls (P < 0.05). The apoE epsilon 4 allele was associated with a tripling of risk for late-onset AD compared with that with no epsilon 4 allele (odds ratio: 2.932). Homozygosity of the G allele in IE1 and 1/1 genotype in PS-1 was associated with a doubling of risk for late-onset AD, and odds ratios were 2.223 and 2.066, respectively. When the apoE epsilon 4 was controlled, the association between the IE1 G/G genotype AD was no longer statistically significant (P > 0.05). We sequenced the exon 4 of apoE in patients with late-onset AD, and found no other genetic polymorphism or mutation except for apoE epsilon 4 and IE1 G alleles associated with AD. CONCLUSION: apoE epsilon 4 gene appears to be the strongest gene risk factor for late-onset AD and its apparent association between the IE1 G/G genotype and late-onset AD is a consequence of the association between the epsilon 4 and IE1 G/G genotype. The PS-1/1 genotype is weakly associated with late-onset AD.

Aged↗

Aristolochic acid I-induced apoptosis in LLC-PK1 cells and amelioration of the apoptotic damage by calcium antagonist.

OBJECTIVE: To examine the effect of different concentrations of aristolochic acid I (AAI) in inducing apoptosis of cultured porcine renal cell line LLC-PK1 and to investigate the relationship between intracellular free calcium concentration ([Ca++]i) and LLC-PK1 apoptosis induced by AAI and the influence of a calcium antagonist, lacidipine on apoptosis and [Ca++]i. METHODS: LLC-PK1 cells were treated in different groups: a. the normal group without treatment; b. the group with AAl alone (0.01 g.L-1, 0.02 g.L-1, 0.04 g.L-1, 0.08 g.L-1); c. the group with lacidipine alone (10 ng.L-1, 10(2) ng.L-1, 10(3) ng.L-1); d. the group with AAI (0.04 g.L-1) plus lacidipine (10 ng.L-1, 10(2) ng.L-1, 10(3) ng.L-1). Light microscopy, agarose gel electrophoresis, Annexin-V-Flous apoptosis detection kit and flow cytometry using propidium iodide staining to identify or quantify the apoptosis of LLC-PK1 cells. Mean [Ca++]i was measured by laser confocus microscopy using Fluo-3/AM staining. RESULTS: A series of morphologic changes that were characteristic of apoptosis, Annexin-V-Flous staining positive apoptotic cells and "DNA ladder" were identified in AAI (0.02 g.L-1-0.08 g.L-1) treated LLC-PK1 cells. Quantitative analysis of apoptotic cells showed that the percentage of apoptotic cells in AAI (0.02 g.L-1, 0.04 g.L-1 or 0.08 g.L-1) group was significantly higher than that in normal group (5.3%, 48.5%, 78.7% vs 2.6%, P < 0.001). Mean [Ca++]i was significantly higher in cells treated with AAI (0.04 g.L-1) than that in normal cells (58.01 +/- 18.89 vs 22.66 +/- 4.78, P < 0.001). In group treated with AAI plus lacidipine (102 ng.L-1, 103 ng.L-1), mean [Ca++]i was significantly lower than that treated with AAI alone (35.47 +/- 12.85, 28.55 +/- 10.16 vs 58.01 +/- 18.89, P < 0.001). And the percentage of apoptotic cells in group treated with AAI plus lacidipine (10(2) ng.L-1, 10(3) ng.L-1) was also significantly lower than that treated with AAI alone (19.0%, 27.8% vs 34.7%, P < 0.001). CONCLUSIONS: High concentrations of AAI may induce apoptosis of LLC-PK1 cells. The mean [Ca++]i in AAI-treated LLC-PK1 cells was increased significantly, suggesting that the increase of [Ca++]i may be related to apoptosis in LLC-PK1 cells. Lacidipine may decrease the raised mean [Ca++]i levels caused by AAI and the percentage of apoptotic cells, and lacidipine may ameliorate AAI-induced apoptotic damage by inhibiting the increase of [Ca++]i in LLC-PK1 cells.

Animals↗

[Study on the antitumor effect of angiostatin on LA795 adenocarcinoma cells].

OBJECTIVE: To study the antitumor effect of angiostatin on LA795 adenocarcinoma cells inoculated on T739 mice. METHODS: Affinity chromatography purified plasminogen was digested by pancreatic elastase and angiostatin was obtained by purifying the digestion with affinity chromatography and dialysis. T739 mice were inoculated with LA795 cells. Angiostatin was given to part of inoculated and uninoculated mice by intraperitoneal injection fourteen days after the inoculation. The treatment lasted 20 days and the size of tumor, survival period, behavior of the mice and pathology of lungs, livers and kidneys were observed. RESULTS: The size of tumor decreased from (2.35 +/- 0.26) cm to (0.97 +/- 0.34) cm after angiostatin treatment. The number of metastases in lung was significantly fewer in angiostatin treated mice than in untreated ones, which lived much shorter. No obvious side effects were observed. CONCLUSION: Angiostatin markedly inhibits the growth and metastasis of LA795 cells on T739 mice and no obvious side effects of angiostatin were found during the treatment.

Adenocarcinoma↗

[The clinical and biochemical manifestations of Fanconi syndrome: a report of 42 cases].

OBJECTIVE: To recognize the etiologies, clinical, and biochemical manifestations of Fanconi syndnome (FS). METHODS: 42 patients with FS were analyzed retrospectively. RESULTS: 21 cases were idiopathic in 42 (50%) cases, and the other 21 (50%) cases were acquired (sjogren's 5, and interstitial nephritie 8). The patients were characterized by proximal renal tubular acidosis (n = 41) and multiple renal tubular transport dysfunctions, including hypokalemia (n = 21), hypophorphatemia (n = 29), hypourecemia (n = 19), renal glucosuria (n = 38), aminoaciduria (n = 36), low-molecular-weight proteinuria (n = 21). The clinical manifestations commonly presented with muscle weakness, polydipsia, polyuria and renal bone diseases. 18 patients presented with impaired renal function. Renal pathohistological studied in 14 patients showed renal tubulointerstitial changes of different degrees in all cases, and glomerular changes in 4. CONCLUSIONS: The etiology of FS is various and secondary FS is not uncommon. FS usually present proxmal RTA and renal tubulointerstitial lesions in pathology.

Acidosis, Renal Tubular↗

[Synergistic effect of monocyte chemotactic protein-1 and aristolochic acid I on transdifferentiation of human tubular epithelial cells in vitro].

OBJECTIVE: To test the possible role of monocyte chemotactic protein-1 (MCP-1) and its synergistic effect with aristolochic acid I (AAI) on tubular epithelial-myofibroblast transdifferentiation (TEMT) of human renal tubular epithelial cells (HKC) in vitro. METHODS: The cultured HKC cells were divided into four groups: (1) negative control (serum-free); (2) MCP-1 group; (3) AAI group; (4) AAI + MCP-1 group. The expression of alpha-smooth muscle actin (alpha-SMA), vimentin and cytocreatin was assessed by indirect enzyme immunohistochemistry and the percentages of alpha-SMA((+)) HKC cells were assessed by flow cytometry. RESULTS: The expression of cytocreatin of HKC cells decreased, while the expression of alpha-SMA, vimentin increased when treated with MCP-1 or with AAI and MCP-I concomitantly. Alpha-SMA((+)) HKC cells cultured in serum-free medium was 3.1% by flow cytometry. The percentages of alpha-SMA((+)) HKC cells were 8.6%, 9.6%, 13.4% (P < 0.05 vs control) when treated with 20, 40, 80 microg/L of AAI. The percentages of alpha-SMA((+)) HKC cells were 0.5% and 1.4% (P > 0.05 vs control) when treated with 5, 10 microg/L. The percentages of alpha-SMA((+)) HKC cells were 20%, 26.2%, 20.3%, 23.2% (P < 0.05 vs control) when treated with 0.001, 0.01, 0.05, 0.1 microg/L of MCP-1. When the HKC cells were treated with MCP-1 (0.1 microg/L) and AAI (5, 10, 20, 40 microg/L), the percentage of alpha-SMA((+)) cells increased markedly to 23.2%, 98.7%, 81.5%, 65.1% (P < 0. 01 vs group 1, 2, 3, respectively). CONCLUSIONS: These findings suggest that: (1) MCP-1 may induce the transdifferentiation of HKC cells into myofibroblasts in vitro; (2) AAI at some doses may partially induce HKC cells transdifferentiation. (3) MCP-1 and AAI may have a synergistic effect on transdifferentiation of HKC cells in vitro.

Actins↗

[The clinical significance of the change of blood testosterone in burned patients].

OBJECTIVE: To investigate the patterns and significance of the change in blood testosterone in burned patients. METHODS: The changes of blood testosterone and luteinizing hormone (LH) were dynamically monitored in 21 male patients with moderate burn injury. RESULTS: The blood testosterone levels in this group decreased persistently after burn, and the decrement degree was related to the burn severity. But LH exhibited no regular change and its change exerted no effects on the blood testosterone levels. CONCLUSION: Decrease in blood testosterone in burned patients was related to gonadal injury, which caused the shortage and insufficiency of anabolic hormone and also of protein synthesis. The correction of the shortage of testosterone might be beneficial to protein synthesis and to the restoration of positive nitrogen equilibrium in burned patients.

Adolescent↗

[Coordination chemistry and Raman spectra of acetylide dianion].

This paper shows the syntheses of double salts of silver acetylide with various soluble silver salts, investigations on the coordination modes of acetylide dianion and their Raman spectra, discussion of the relationship between the coordination chemistry of acetylide dianion and the bind mode of N2 molecule in the FeMoco factor of nitrogenase. The results present that the bind mode of N2 molecule inside the FeMoco factor of nitrogenase is more reasonable.

English Abstract↗

Epidemiology of human hookworm infections among adult villagers in Hejiang and Santai Counties, Sichuan Province, China.

Hookworm infection as well as other intestinal nematodiases are endemic to Sichuan Province in China. In order to research the prevalence and intensity of these infections we visited two villages in Hejiang County (southern Sichuan Province) and Santai County (northwestern Sichuan Province) between July and October of 1997. Fecal examinations were performed on adult villagers over the age of 15 years (currently children under this age are dewormed annually with anthelmintic drugs). Among 310 residents of Lugao Village (Hejiang County), 87, 63 and 60% were infected with hookworm, Ascaris or Trichuris, respectively. The prevalence of hookworm determined to rise linearly with age (r = 0.97). High intensity infections with hookworm still occur in this region as 22% of the residents have over 3000 eggs per gram (PEG) of feces as determined by quantitative egg counts. The majority of these individuals harbored mixed infection with Necator americanus and Ancylostoma duodenale, although the former predominated when adult hookworms were collected from 30 village residents treated with pyrantel pamoate. In contrast, among the 334 Xinjian villagers examined (Santai County) the majority harbored predominantly light hookworm infections--66.1% of the residents has less than 400 EPG by quantitative fecal examination and only 3.7% exhibited greater than 3000 EPG. Again, N. americanus was the predominant hookworm seen after worm expulsion. We have round that despite economic development which is occurring in some parts of China, significant hookworm infections and clinical hookworm anemia still exist in areas of Sichuan Province. In Hejiang County we found that the intensity of hookworm infection has actually risen within the last 10 years. Hookworm is a medical problem among the elderly in Sichuan.

Adolescent↗

Yeast transcriptional regulator Leu3p. Self-masking, specificity of masking, and evidence for regulation by the intracellular level of Leu3p.

Recent work suggests that the masking of the activation domain (AD) of yeast transactivator Leu3p, observed in the absence of the metabolic signal alpha-isopropylmalate, is an intramolecular event. Much of the evidence came from the construction and analysis of a mutant form of Leu3p (Leu3-dd) whose AD is permanently masked (Wang, D., Hu, Y., Zheng, F., Zhou, K., and Kohlhaw, G. B. (1997) J. Biol. Chem. 272, 19383-19392). In a modified two-hybrid experiment, the ADs of both wild type Leu3p and Leu3-dd were shown to interact with the remainder of the Leu3 protein, in an alpha-isopropylmalate-dependent manner. The finding that masking and unmasking proceed apparently normally when full-length Leu3p is expressed in mammalian cells is also consistent with the notion of intramolecular masking. Here we report on the identification of nine missense mutations (all of them suppressors of the Leu3-dd phenotype) that cause permanent unmasking of Leu3p. The nine mutations map to three short segments located within a 140-residue-long region of the C-terminal part of the middle region of Leu3p. These segments may be part of a spatial trap for the AD. We also performed "domain swaps" between Leu3p and Cha4p, a serine/threonine-responsive activator that, like Leu3p, belongs to the family of Zn(II)2Cys6 proteins. We show that AD masking and response to the appropriate metabolic signal only occur when a given AD remains attached to its own middle region; middle region swapping results in constitutively active proteins. Finally, we show that the extent to which Leu3p regulates reporter gene expression depends on the intracellular concentration of Leu3p. The possible physiological significance of this observation is discussed in light of the known regulation of Leu3p by Gcn4p.

Amino Acid Substitution↗

Uteroglobin: a novel cytokine?

Blastokinin or uteroglobin (UG) is a steroid-inducible, evolutionarily conserved, multifunctional protein secreted by the mucosal epithelial of virtually all mammals. It is present in the blood and in other body fluids including urine. An antigen immunoreactive to UG antibody is also detectable in the mucosal epithelia of all vertebrates. UG-binding proteins (putative receptor), expressed on several normal and cancer cell types, have been characterized. The human UG gene is mapped to chromosome 11q12.2 13.1, a region that is frequently rearranged or deleted in many cancers. The generation of UG knockout mice revealed that disruption of this gene causes: (i) severe renal disease due to an abnormal deposition of fibronectin and collagen in the glomeruli; (ii) predisposition to a high incidence of malignancies; and (iii) a lack of polychlorinated biphenyl binding and increased oxygen toxicity in the lungs. The mechanism(s) of UG action is likely to be even more complex as it also functions via a putative receptor-mediated pathway that has not yet been clearly defined. Molecular characterization of the UG receptor and signal transduction via this receptor pathway may show that this protein belongs to a novel cytokine/chemokine family.

Amino Acid Sequence↗

Morphine reversed formalin-induced CA1 pyramidal cell suppression via an effect on septohippocampal neural processing.

We have investigated the effect of morphine on (i) dorsal hippocampus field CA1 nociceptive response to a formalin injection, and (ii) septohippocampal neural processing. Extracellular recordings were made in urethane (1.0 g/kg)-anaesthetized rats. Previously, we reported that formalin (5%, 0.05 ml, s.c.) injection into a hindpaw evoked, in the CA1 field, a "signal-to-noise processing", i.e. a selective excitation of a few pyramidal cells with high spontaneous extracellular activity against a background of widespread pyramidal cell suppression accompanied by an increase in period of rhythmic slow activity. In the present study, morphine administered i.p. concurrent to a formalin injection reversed the pyramidal cell suppression in conjunction with a decrease in the period of evoked rhythmic slow activity. The effect was dose dependent and was prominent at the dose of 5 mg/kg. This dose, administered as a pretreatment, also truncated CA1 pyramidal cell suppression or excitation to a formalin injection. Furthermore, the drug decreased the power and frequency of the posterior hypothalamus-supramammillary region stimulation-evoked hippocampal field CA1 rhythmic slow activity. Such an effect was observed in a time-frame parallel to the decline in the period of formalin injection-induced field CA1 rhythmic slow activity. However, morphine sulphate administration per se did not alter pyramidal cell excitability or extracellular activity. Together, the above findings are consistent with the notion that morphine influences dorsal hippocampus field CA1 pyramidal cell suppression partly via an effect on the septohippocampal neural processing. However, the effect of the drug does not involve a change in the pyramidal cell basal extracellular responses. The effect of morphine on septohippocampal neural processing might be functionally relevant to the influence of the drug on the affective-motivational component of pain.

Action Potentials↗