Search PubMed⌕ Search

Biomedical subjects

P Zhou

Publications and source records attributed to P Zhou.

At least 127 records · Page 7Linked to original sources
PubMed1997

Genetic and environmental factors affecting the de novo appearance of the [PSI+] prion in Saccharomyces cerevisiae.

It has previously been shown that yeast prion [PSI+] is cured by GuHCl, although reports on reversibility of curing were contradictory. Here we show that GuHCl treatment of both [PSI+] and [psi-] yeast strains results in two classes of [psi-] derivatives: Pin+, in which [PSI+] can be reinduced by Sup35p overproduction, and Pin-, in which overexpression of the complete SUP35 gene does not lead to the [PSI+] appearance. However, in both Pin+ and Pin- derivatives [PSI+] is reinduced by overproduction of a short Sup35p N-terminal fragment, thus, in principle, [PSI+] curing remains reversible in both cases. Neither suppression nor growth inhibition caused by SUP35 overexpression in Pin+ [psi-] derivatives are observed in Pin- [psi-] derivatives. Genetic analyses show that the Pin+ phenotype is determined by a non-Mendelian factor, which, unlike the [PSI+] prion, is independent of the Sup35p N-terminal domain. A Pin- [psi-] derivative was also generated by transient inactivation of the heat shock protein, Hsp104, while [PSI+] curing by Hsp104 overproduction resulted exclusively in Pin+ [psi-] derivatives. We hypothesize that in addition to the [PSI+] prion-determining domain in the Sup35p N-terminus, there is another self-propagating conformational determinant in the C-proximal part of Sup35p and that this second prion is responsible for the Pin+ phenotype.

Fungal Proteins↗
PubMed1997

Interleukin-12 modulates the protective immune response in SCID mice infected with Histoplasma capsulatum.

Infection with Histoplasma capsulatum results in a subclinical infection in immunocompetent hosts due to an effective cellular immune response. By contrast, immunodeficient individuals can have a severe disseminated and potentially fatal disease. In a previous study, it was demonstrated that normal mice infected intravenously with H. capsulatum and treated with interleukin-12 (IL-12) at the time of infection were protected from a fatal outcome. In this study, we examined the immunomodulatory effects of IL-12 on disseminated histoplasmosis in immunodeficient SCID mice. SCID mice infected with H. capsulatum and treated with IL-12 showed an increase in survival and a reduction in the colony counts of H. capsulatum in internal organs at 14 days after infection. The protective effect of IL-12 was abrogated if animals were also treated with a neutralizing antibody to gamma interferon (IFN-gamma). IL-12 treatment also resulted in an increase in mRNA expression and protein production for IFN-gamma, tumor necrosis factor alpha (TNF-alpha), and nitric oxide from spleen cells. When IL-12 was combined with amphotericin B (AmB) treatment, there was a significant increase in survival compared with either modality alone. Moreover, combined treatment resulted in an increase in both IFN-gamma and TNF-alpha production, as well as in a substantial reduction in H. capsulatum burden at 35 and 90 days postinfection. This study demonstrates that IL-12 modulates the protective immune response to histoplasmosis in SCID mice and also suggests that IL-12 in combination with AmB may be useful as a treatment for H. capsulatum in immunodeficient hosts.

Amphotericin B↗
PubMed1997

Gene transcription and chromosome replication in Escherichia coli.

Transcript levels of several Escherichia coli genes involved in chromosome replication and cell division were measured in dnaC2(Ts) mutants synchronized for chromosome replication by temperature shifts. Levels of transcripts from four of the genes, dam, nrdA, mukB, and seqA, were reduced at a certain stage during chromosome replication. The magnitudes of the decreases were similar to those reported previously ftsQ and ftsZ (P. Zhou and C. E. Helmstetter, J. Bacteriol. 176:6100-6106, 1994) but considerably less than those seen with dnaA, gidA, and mioC (P. W. Theisen, J. E. Grimwade, A. C. Leonard, J. A. Bogan, and C. E. Helmstetter, Mol. Microbiol. 10:575-584, 1993). The decreases in transcripts appeared to correlate with the estimated time at which the genes replicated. This same conclusion was reached in studies with synchronous cultures obtained with the baby machine in those instances in which periodicities in transcript levels were clearly evident. The transcriptional levels for two genes, minE and tus, did not fluctuate significantly, whereas the transcripts for one gene, iciA, appeared to increase transiently. The results support the idea that cell cycle timing in E. coli is not governed by timed bursts of gene expression, since the overall findings summarized in this report are generally consistent with cell cycle-dependent transient inhibitions of transcription rather than stimulations.

Bacterial Proteins↗
PubMed1997

Replication and segregation of a miniF plasmid during the division cycle of Escherichia coli.

Replication of the miniF plasmid pML31 was examined during the division cycle of Escherichia coli growing with doubling times between 40 and 90 min at 37 degrees C and compared to the replication of plasmid pBR322 and the minichromosome pAL70. The replication pattern of pML31 was indistinguishable from that of pBR322 at all growth rates and very different from the cell-cycle-specific replication of the minichromosome. It is concluded that both pML31 and pBR322 plasmids can replicate at all stages of the division cycle, with a probability of replication that increases gradually, but perhaps not exponentially, during the cycle. In contrast, the modes of segregation of pML31 and pBR322 plasmids into daughter cells at division appeared to differ, raising the possibility that pML31 may segregate in a nonrandom fashion similar to that of chromosomes and minichromosomes.

Cell Division↗
PubMed1997

Genetically divergent strains of simian immunodeficiency virus use CCR5 as a coreceptor for entry.

Entry of human immunodeficiency virus type 1 (HIV-1) requires CD4 and one of a family of related seven-transmembrane-domain coreceptors. Macrophage-tropic HIV-1 isolates are generally specific for CCR5, a receptor for the CC chemokines RANTES, MIP-1alpha, and MIP-1beta, while T-cell line-tropic viruses tend to use CXCR4 (also known as fusin, LESTR, or HUMSTR). Like HIV-1, simian immunodeficiency virus (SIV) requires CD4 on the target cell surface; however, whether it also requires a coreceptor is not known. We report here that several genetically divergent SIV isolates, including SIVmac, SIVsmSL92a, SIVsmLib-1, and SIVcpzGAB, can use human and rhesus CCR5 for entry. CXCR4 did not facilitate entry of any of the simian viruses tested, nor did any of the other known chemokine receptors. Moreover, SIVmac251 that had been extensively passaged in a human transformed T-cell line retained its use of CCR5. Rhesus and human CCR5 differed at only eight amino acid residues, four of which were in regions of the receptor that could be exposed, two in the amino-terminal extracellular region and two in the second extracellular loop. The human coreceptor was as active as the simian for SIV entry. In addition, HIV-1 was able to use the rhesus homologs of the human coreceptors, CCR5 and CXCR4. The SIV strains tested were specific for CCR5 regardless of whether they were able to replicate in transformed T-cell lines or macrophages and whether they were phenotypically syncytium inducing or noninducing in MT-2 cells. However, SIV replication was not restricted to cells expressing CCR5. SIV strains replicated efficiently in the human transformed lymphoid cell line CEMx174, which does not express detectable amounts of transcripts of CCR5. SIV also replicated in human peripheral blood mononuclear cells that were genetically deficient in CCR5. These findings indicated that, in addition to CCR5, SIV can use one or more unknown coreceptors that are expressed on human PBMCs and CEMx174 cells.

Amino Acid Sequence↗
PubMed1997

Effective laser ablation of enamel and dentine without thermal side effects.

We present a feasibility study into laser treating dental materials by using femtosecond pulses generated by a titanium:sapphire laser system which consisted of an oscillator and a regenerative amplifier. The pulse duration was varied between 200 fs and 2 ps. The observed energy thresholds for the ablation process of dentine and enamel were clearly smaller than those observed when longer pulse durations were used. The consequence of this observation is a lower thermal load within the vicinity of the radiated area. Thus no thermal damage or mechanical damage, such as cracks, were produced during the laser treatment. Commercially available femtosecond laser systems can produce ablation rates in healthy and in-vitro demineralized dental material 2 mm3 per min and 6-16 mm3 per min, respectively. These values are an order of magnitude larger than those produced by picosecond laser systems at the same time pulse energy and pulse repetition rate. The brightness of the plasma spark generated by the laser treatment depended on the dimineralization of the teeth. This may allow online control of the laser treatment.

Dental Enamel↗
PubMed1997

Disorders in cell circuitry associated with multistage carcinogenesis: exploitable targets for cancer prevention and therapy.

The development of a malignant tumor involves the progressive acquisition of mutations and epigenetic abnormalities in multiple genes that have highly diverse functions. Some of these genes code for pathways of signal transduction that mediate the action of growth factors. The enzyme protein kinase C plays an important role in these events and in the process of tumor promotion. Therefore, we examined the effects of three inhibitors of protein kinase C, CGP 41251, RO 31-8220, and calphostin C, on human glioblastoma cells. These compounds inhibited growth and induced apoptosis; these activities were associated with a decrease in the level of CDC2 and cyclin B1/CDC2-associated kinase activity. This may explain why the treated cells accumulated in G2-M. In a separate series of studies, we examined abnormalities in cell cycle control genes in human cancer. We have found that cyclin D1 is frequently overexpressed in a variety of human cancers. Mechanistic studies indicate that cyclin D1 can play a critical role in carcinogenesis because: overexpression enhances cell transformation and tumorigenesis; introduction of an antisense cyclin D1 cDNA into either human esophageal or colon cancer cells reverts their malignant phenotype; and overexpression of cyclin D1 can enhance the amplification of other genes. The latter finding suggests that cyclin D1 can enhance genomic instability and, thereby, the process of tumor progression. Therefore, inhibitors of the function of cyclin D1 may be useful in both cancer chemoprevention and therapy. We obtained evidence for the existence of homeostatic feedback loops between cyclins D1 or E and the cell cycle inhibitory protein p27Kip1. On the basis of these and other findings, we hypothesize that, because of their disordered circuitry, cancer cells suffer from "gene addiction" and "gene hypersensitivity," disorders that might be exploited in both cancer prevention and therapy.

Apoptosis↗
PubMed1997

[The research on p53 gene mutation in lung cancer tissue of silicotic patients by PCR-SSCR].

Using polymerase chain reaction single strand conformation polymorphism analysis (PCR-SSCP), the authors mutations in exon 5, 7 and 8 of the p53 gene in lung cancer tissue from 15 of 36 silicotic patients. Mutations existed in exon 5, exon 7 and exon 8, but occured more frequently in exon 8. The authors also found that p53 gene mutation rate in lung adenocarcinomas of silicotic patients was higher than that of those without silicosis. A single base substitution was found by DNA sequencing analysis in sample C8. As a result, No. 144 codon was mutated from CAG to AAG, so Gln was substituted by Lys. The authors' data suggest that p53 mutation may play an important role in the pathogenesis of lung cancer of silicotic patients.

Adenocarcinoma↗
PubMed1997

[Identification of a pure culture of nodular endophyte from Coriaria nepalensis].

A Frankia-like strain, Cs146, was isolated from nodules of Coriaria nepalensis in southwest China. The isolate is an actinomycete with vesicles and sporangia borne on the hyphae, and shown to have an ability to nodulate the host plant. No aerial hyphae is formed, but the substrate hyphae are usually orange and produce soluble yellow pigment. Cs146 could grow quite slow at 28-30 degrees C on both liquid and solid media. However, the isolate is greatly different from other frankiae in physiology (intermediate physiologocal group between A and B trains), cell wall composition of characteristical amino acids (meso-DAP plus glycine) and whole cell sugar patterns (xylose plus little amount of galactose and arabinose). Cs146 thus appears to be a member of a distinct Frankia lineage.

English Abstract↗
PubMed1997

Preparation and characterization of double layered coating composed of hydroxyapatite and perovskite by thermal decomposition.

A new modified thermal decomposition method is described for preparing a double layered coating on titanium plates which includes an initial perovskite (CaTiO3) layer followed by a hydroxyapatite (HA) layer on top. The characterization of the coating was studied by X-ray diffractometry and infrared spectroscopy and indicated that the double layer consisted of carbonate HA and CaTiO3 and the thickness of the layer was 4 microns. The coating was performed on the inner surfaces of 50-200 microns sized pores and was also consistent in the smallest of the pores even those of 50 microns. Bone formation was examined in canines at 2-32 week intervals and was dominant on coated plates and in large-sized pores before 16 weeks. However, after 16 weeks bone ingrowth was similar in non-coated and coated plates and in all pore sizes. The results indicated that HA could only influence early bone ingrowth, though good bone ingrowth into small pores indicated that HA exhibited enhanced osteocompatibility. Our methodology ensured the stability of the HA layer consequently minimizing the problems associated with HA loss.

Animals↗
PubMed1997

Fibroblast growth factor-2 inhibits endothelial cell apoptosis by Bcl-2-dependent and independent mechanisms.

Intact endothelium acts as a sensor and transducer of signals and also provides a nonthrombogenic surface at the blood-vascular wall interface. Hence, mechanisms that maintain the integrity of the endothelium are of interest in physiological and pathological states. In this study we show that apoptosis induced by growth factor and serum deprivation of endothelial cells occurs at all phases of the cell cycle and can be blocked by fibroblast growth factor-2 (FGF-2) independently of its mitogenic activity. As the Bcl-2 family of proteins plays a prominent role in regulating cell survival, we attempted to identify Bcl-2 homologues expressed in endothelial cells. Here we demonstrate that, in addition to the previously identified A1, four other members of the Bcl-2 family, Bcl-2, Mcl-1, Bcl-X(L), and Bax, are expressed in endothelial cells. Of these family members, only Bcl-2 is induced by FGF-2. Overexpression of Bcl-2, using a retroviral vector, protects endothelial cells from serum and growth factor deprivation. There is no difference in FGF-2-induced proliferation between Bcl-2-overexpressing cells and those transduced with the empty retroviral vector. At early time points Bcl-2 is not up-regulated, but FGF-2 still has a protective effect. However, FGF-2 protects only adherent endothelial cells but not those that are cultured in suspension. The early effect of FGF-2 is dependent on tyrosine phosphorylation but not on activation of the MAP kinase pathway. Thus, FGF-2 inhibits endothelial cell apoptosis by Bcl-2-dependent and independent mechanisms.

Apoptosis↗
PubMed1997

[Changes in gamma-amino-butyric acid and N-methyl-D-aspartic acid receptor-gated currents from freshly isolated hippocampal CA1 pyramidal neurons of hepatic encephalopathy rats].

OBJECTIVE: To explore the effects of the changes of the amino acid receptor-gated ion-channel currents on the pathogenesis of hepatic encephalopathy (HE). METHODS: Using rapid drug applicating device, we added 50 mumol/L gamma-amino-butyric acid (GABA) or 1 mmol/L N-methyl-D-aspartic acid (NM-DA) + 10 mumol/L Glycine (Gly) to the surrounding of freshly isolated rat hippocampal CA1 pyramidal neurons to induce receptor-gated ion-channel currents, which was recorded by whole-cell voltage-clamp technique. RESULTS: The intensity of the GABAA-receptor mediated inward Cl- current of hippocampal CA1 pyramidal neurons of HE rats (413.3 +/- 436.8 pA, n = 31) was stronger than that of the controls (233.4 +/- 179.7 pA, n = 28, t = 2.1049, P < 0.05), and the appearance of the Cl- current in HE rats was more frequent than that in the controls. The intensity of the NMDA-receptor gated inward current in HE rats (408.5 +/- 317.2 pA, n = 37) was weeker than that in the controls (882.6 +/- 896.5 pA, n = 26, t = 2.5851, P < 0.05), but the difference of their channel opening frequency was not significant. CONCLUSIONS: The changes of the amino acid receptor-gated ion-channel currents play an important role in the pathogenesis of hepatic encephalopathy.

Action Potentials↗
PubMed1997

[A preliminary study on p53 gene in lung cancer tissues of workers exposed to silica and welding fumes].

Mutations of suppressor gene p53 was studied in 36 cases of silica related lung cancer and 6 cases of welding fume related lung cancer with immunohistochemical and PCR-SSCP methods. Cancer tissues were embedded in paraffin and stored for 13.4 years in average. Results revealed that there was abnormal mobility shift of electrophoresis in 18 cases with 20 point mutations of 42 specimens tested, accounted for 42.9%, and 50% (10/20) of the mutations were clustered in exon 8. This finding differed from mutational spectrum of gene in non-occupational lung cancer, in which mutation frequency of exon 8 ranged from 17.5% to 23.5%. Gene mutation frequency in varied pathological categories of pneumoconiosis related lung cancer also differed from that in common lung cancer. In the latter, the highest one was in small cell lung cancer (70%) and the lowest in adenocarcinoma (33%), but in the former, the highest in adenocarcinoma (53.9%) and the lowest in small cell lung cancer (30.8%). Immunohistochemical observations also showed a very high prevalence of p53 gene mutation expression (46.9%). Sequencing, which was determined in two cases of this study, revealed that two point mutations all occurred in non-hotspot codon 144 of p53 gene. Difference in gene mutation spectrum suggests that there exist specific carcinogens and carcinogenesis in silica and welding fume related lung cancer.

Adenocarcinoma↗
PubMed1997

[Clinical study of glibenclamide in combination with kelening treatment in non-insulin dependent diabetes mellitus].

OBJECTIVE: To asses the efficacy of combination therapy of glibenclamide and Kelening in treating the non-insulin dependent diabetes mellitus (NIDDM). METHODS: Sixty-five patients with NIDDM were randomly divided into two groups. One group was treated with both glibenclamide and Kelening, the other with glibenclamide alone. RESULTS: After treatment for 12 weeks, the levels of fasting blood glucose (FBG), postprandial blood glucose (PBG) and HBAIC were reduced significantly in glibenclamide-Kelening group. In both groups, the degree dropped of the levels of FBG were almost the same, but the levels of PBG and HBAIC in glibenclamide-Kelening group were reduced more significantly than those in glibenclamide group, and the incidence of hyperinsulinemia had dropped considerably. CONCLUSION: Glibenclamide in combination with Kelening in the treatment of NIDDM is more effective and less toxic, and the combination may reduce the dosage of glibenclamide in NIDDM.

Adult↗
PubMed1997

[New species of Natronobacterium].

An extreme haloalkalophilic bacterium HAM-2 with pleomorphic rods was isolated from Hamatai soda lake in Inner Mongolia Autonomous Region. Growth occurs in 12%-30% NaCl, no growth below 12%, optimum 17.5%. pH range for good growth 7.8-10.4, optimum 9.0-9.5. The strain HAM-2 is non-motile, Gram-negative, pleomorphic, cell of which were 1.0-2.0 by 2.0-5.0 microns in size in liquid medium. The major polar lipids of the organisms are phosphatidylglycerol phosphate and phosphatidyglycerol and contains an unidentified phospholipid as a minor component PL4. G + C contant of DNA is 59.5 mol%. Based on the characteristics, the strain HAM-2 could be included in the genus Natronobacterium, but since HAM-2 differs from reported four species of this genus in cell shape, polar lipids and biochemical features. The name Natronobacterium innemongoliae sp. nov. is proposed. The type strain is designated HAM-2.

Natronobacterium↗
PubMed1996

Human leukocyte antigen-DRB1*1502 (DR2Dw12) transgene reduces incidence and severity of arthritis in mice.

A strong correlation exists between susceptibility to RA in humans and some DRB1 alleles of the MHC region, such as DRB1*0401 and DRB1*0101. Meanwhile, incidences of other DR specificities, such as DR2, DR5, or DR7 have often been found reduced among RA patients. Like RA, susceptibility to mouse CIA is influenced by the MHC class II loci. To analyze the effect of a DRB1 molecule associated with low incidence of RA on mouse CIA, a human DRB1*1502 (DR2Dw12) transgene was introduced into CIA-susceptible B10.RQB3 (H2Aq) mice. Transgene-positive DRB1*1502 mice showed a significant reduction in the incidence and severity of arthritis. Moreover, the clinical reduction of arthritis correlated with the T-cell proliferative response of B10.RQB3-DRB1*1502 mice against a self-derived DRB1 peptide from the third hypervariable region. Our results suggest that the DRB1*1502-mediated protection against CIA can be explained by the DRB1 molecule acting as a source of self-antigenic peptide which interferes with the T-cell response against immunodominant regions(s) of the arthritogenic type II collagen molecule. By analogy, a similar mechanism might play a critical role in influencing the class II-associated predisposition to RA.

Animals↗