Biomedical subjects

Wei Zou

Publications and source records attributed to Wei Zou.

49 records · Page 3Linked to original sources

PubMed2003

Measurements of the longitudinal wave speed in thin materials using a wideband PVDF transducer.

A flat transducer was constructed, using a 9-microm-thick PVDF (polyvinylidene fluoride) film for generation and detection of high-frequency ultrasonic waves, and used for measurements of the phase velocity of longitudinal waves traveling along the thickness direction in a very thin material. The transducer has a useful wideband frequency characteristic extending from 10 MHz to over 150 MHz. Measurements of the phase velocity of the longitudinal waves are carried out using a 0.212-mm-thick glass slide and a 0.102-mm-thick stainless-steel shim, using water as a coupling medium. The thickness limit for this measurement appears to be approximately 20 microm. The phase velocity of the longitudinal mode is obtained as a function of frequency in the frequency domain by using a modified sampled continuous wave (cw) technique. It can also be measured in the time domain by using a broadband pulse of short duration.

Journal Article↗

PubMed2003

[Drug resistance of HIV-infected patients after the failure of highly active antiretroviral treatment].

OBJECTIVE: To find out the mechanism of drug resistance by detecting the mutations of HIV RNA in patients who failed in the anti-HIV therapy, to direct the clinical use of anti-HIV drugs and to complement the existing drug resistant database. METHODS: HIV RNA and DNA were extracted from the plasma of 10 HIV-infected patients who developed drug resistance in the Clinic of AIDS, Ruhr University, Bochum, Germany. Then HIV-RNA was amplified in the reverse transcriptase (RT) and protease regions by polymerase chain reaction (PCR). After purified, the PCR products was sequenced. The acquired sequences were compared with the international standard strain HXB2CG and the resistant database of Stanford University. RESULTS: Some mutations were found to cause the corresponding resistance to certain drugs and were consistent with the clinical results. Some mutations existed in some patients, such as V179I in RT and K20T, K20I in protease, which hadn't been reported in the resistant database of Stanford University yet. CONCLUSION: Patients who fail in HAART have different mutations in RT and protease regions. Mutations such as V179I in RT and K20T, K20I etc in protease may be related to drug resistance.

Adult↗

PubMed2003

The potential role of IGF-I receptor mRNA in rats with diabetic retinopathy.

OBJECTIVE: To evaluate the potential role of insulin-like growth factor-1 receptor mRNA (IGF-IR mRNA) in the onset and development of retinopathy in diabetic rats. METHODS: A diabetic model was duplicated in Wistar rats. The early changes in the retina were examined using light and transmission electron microscopy. Expression of IGF-IR mRNA was analyzed using in situ hybridization. RESULTS: Weak expression of IGF-IR mRNA (5%) was found in retinas of normal rats, but was significantly increased (15% and 18%) in the retinas of diabetic rats after 3 and 6 months of diabetes (P < 0.01). In situ hybridization and morphological study demonstrated that there was a positive correlation between IGF-IR mRNA expression and retinal changes at various stages. CONCLUSION: Increased IGF-IR mRNA might play an important role in the onset and development of diabetic retinopathy.

Animals↗

PubMed2003

Preliminary research on the co-infection of human immunodeficiency virus and hepatitis virus in intravenous drug users.

OBJECTIVE: To confirm the close relationship of high co-infection rate between HIV and hepatitis virus in intravenous drug users (i.v.DUs). METHODS: Anti-HIV, HBV and HCV were detected by ELISA in the serum from 35 scattered and 15 massed i.v.DUs. PCR and RT-PCR were performed to confirm the infection of HIV, HBV, HCV, HGV and TTV among the 15 massed intravenous drug abusers. RESULTS: Among the 50 i.v.DUs, the positive rates of anti-HCV1 HBsAg, anti-HBe and anti-HBc were 92% (46/50), 12% (6/50), 10% (5/50) and 66% (33/50), respectively. In the samples of HBsAg positive, their HBeAg was also positive. Although the positive rate of serum markers was different in the massed i.v.DUs compared to the scattered i.v.DUs, no significant difference was shown. In the cases of massed i.v.DUs, the positive rates of HIV DNA, HBV-DNA, HCV-RNA, HGV-RNA, and TTV-DNA were 100% (15/15), 26.6% (4/15), 53.3% (8/15), 33.3% (5/15) and 26.6% (4/15), respectively. Among the 15 massed intravenous drug users, one was infected with HIV, HBV, HCV, HGV and TTV; two were infected with HIV, HBV, HCV and HGV; three were infected only with HIV; and the remaining had other forms of co-infection. CONCLUSION: The co-infection rate of HIV, HBV, HCV, HGV and TTV in intravenous drug users is very high.

HIV Infections↗

PubMed2002

Overexpression of PEMT2 downregulates the PI3K/Akt signaling pathway in rat hepatoma cells.

Phosphatidylethanolamine N-methyltransferase 2 (PEMT2) is an isoform of PEMT that converts phosphatidylethanolamine to phosphatidylcholine in mammalian liver. Overexpression of PEMT2 led to inhibition of proliferation of hepatoma cells [J. Biol. Chem. 269 (1994) 24531]. The present study aims to unravel the molecular mechanism of the reduced proliferation, especially the signaling transducer proteins involved in this process. Thus, we chose PI3K/Akt pathway that is initiated by growth factors and leads to cell survival and proliferation. Rat hepatoma CBRH-7919 cells transfected with pemt2-cDNA showed that: (1) signaling proteins including c-Met, PDGF receptor, PI3K, Akt and Bcl-2 all had reduced expression as shown by Western blotting studies; (2) flow cytometric and DNA ladder assays showed that 22.9% of the pemt2-transfected cells were undergoing apoptosis; (3) the activity of Akt was decreased as shown by Western blotting using antibody directed against p-Akt (Thr308); (4) wortmannin and PD98059, inhibitors of PI3K and MEK, respectively, both inhibited Akt activity, indicating that PI3K and MAPK pathways were merging at Akt in CBRH-7919 cells. The above results suggest that overexpression of PEMT2 strongly downregulated the PI3K/Akt signaling pathway at multiple sites and induced apoptosis. This, at least partly, explains the molecular mechanism of impaired proliferation induced by pemt2 transfection.

Androstadienes↗

PubMed2002

Novel zinc (II)-mediated epimerization of 2'-carbonylalkyl-alpha-C-glycopyranosides to their beta-anomers.

2'-Aldehydes and 2'-ketones of alpha-C-glycosides, including the gluco-, galacto-, and manno- series, were epimerized exclusively to their beta-anomers in good-to-excellent yields under basic conditions and in the presence of zinc acetate. The beta-stereoselectivity is independent of the neighboring group at 2-O-substitution of sugar substrates. Therefore, this provides a particularly useful method for the preparation of manno-beta-C-glycosides. The epimerization is likely initiated by the formation of Zn-enolate that is stabilized by intramolecular chelation to the pyranose ring-oxygen to form a syn chair-boat structure. Due to the activation generated by the Zn-O coordination, fission of the C1-O bond occurs, leading to opening of the pyranose ring, which is spontaneously followed by a change in conformation. The more stable anti chair-boat transition state is favored, and the subsequent hetero-intramolecular Michael addition results in the formation of beta-C-glycoside in a ring-closure step.

Carbohydrate Conformation↗

PubMed2002

Defected expression of E-cadherin in non-small cell lung cancer.

Reduced expression of E-cadherin, a cell-cell adhesion molecule, was frequently observed in several types of human carcinomas, and the protein plays a role as an invasion suppressor in vitro. In an attempt to evaluate the significance of E-cadherin gene in non-small cell lung cancer (NSCLC), we undertook the immunohistochemical and molecule structural analyses of E-cadherin gene in 40 resection specimens of NSCLC and the corresponding paracarcinoma controls. E-cadherin expression was explored by immunohistochemistry with a monoclonal antibody, and the E-cadherin gene was studied by polymerase chain reaction single-strand conformation polymorphism analysis (PCR-SSCP). The analysis represented in this study demonstrated clear reduction in the expression of E-cadherin proteins in the cancer tissues. However, only in one amplicon were aberrant bands detected, which was a single polymorphic site (codon 692; exon 13), and no somatic mutation was found. These results indicated that defected E-cadherin expression might play a role in the development of malignant phenotype in NSCLC, even though the genetic mutation of E-cadherin gene is not involved in the pathogenesis of NSCLC and does not appear to be direct cause for the reduced expression of E-cadherin gene.

Adenocarcinoma↗

PubMed2002

Protective effect of magnesium on the endothelial function mediated by endothelium-derived hyperpolarizing factor in coronary arteries during cardioplegic arrest in a porcine model.

OBJECTIVES: Hyperkalemia in cardioplegia impairs the function mediated by endothelium-derived hyperpolarizing factor. This study examined the effect and mechanism of magnesium ion on the relaxation mediated by endothelium-derived hyperpolarizing factor. METHODS: In the isometric force study, porcine coronary microarteries in a myograph (diameter 200-450 microm) were incubated in Krebs solution (subgroups Ia, IIa, and IIIa), potassium ion (20 mmol/L, subgroups Ib, IIb, and IIIb), magnesium ion (16 mmol/L, subgroups Ic, IIc, and IIIc), or potassium ion plus magnesium ion (subgroups Id, IId, and IIId) for 1 hour at 37 degrees C in group I or II, followed by washout for 45 minutes in group III (n = 8). Relaxation to bradykinin (groups I and III) or sodium nitroprusside (group II) in U(46619)-stimulated contraction was established. In the electrophysiologic study, the membrane potentials of single smooth muscle cells of arteries were measured by microelectrode after superfusion with the previously described solutions (subgroups IVa-IVc). RESULTS: In group I, 20-mmol/L potassium ion greatly reduced the bradykinin-induced relaxation (35.0% +/- 4.9% vs 86.0% +/- 5.3%, P <.001), which was significantly restored by magnesium ion (51.9% +/- 4.0%, P =.017). In groups II and III, the bradykinin- or nitroprusside-induced relaxation had no significant differences. In group IV, potassium ion depolarized the smooth muscle and decreased the bradykinin-induced hyperpolarization (-72.0 +/- 1.5 vs -61.7 +/- 0.7 mV, n = 7, P <.001), which was significantly restored by magnesium ion (-68.0 +/- 2.5 mV vs -72.5 +/- 1.5 mV, n = 6, P =.029). CONCLUSIONS: Magnesium ion, either alone or added to hyperkalemic solutions, preserves or helps to restore the endothelial function mediated by endothelium-derived hyperpolarizing factor. The mechanism is related to preservation of the membrane hyperpolarization and reversal of the potassium-induced membrane depolarization of the smooth muscle cell.

Analysis of Variance↗

PubMed2002

CpG oligonucleotides: novel regulators of osteoclast differentiation.

The macrophage capability to recognize bacterial DNA is mimicked by oligodeoxynucleotides containing unmethylated CG dinucleotides ('CpG' motifs) in specific sequence contexts (CpG ODN). CpG ODN stimulates NF-kappaB activation in murine macrophages. In light of the pivotal role played by NF-kappaB in osteoclast differentiation, we examined the ability of CpG ODN to modulate osteoclastogenesis. CpG ODN alone induced TRAP-positive cells in bone marrow macrophage (BMM) cultures, but not multinucleation or calcitonin receptor expression. CpG ODN inhibited RANKL-induced osteoclastogenesis when present from the beginning of BMM culture, but strongly increased RANKL-induced osteoclastogenesis in RANKL-pretreated BMMs. CpG ODN enhanced the expression of interleukin 1beta (IL-1beta) and tumor necrosis factor alpha (TNF-alpha). Antibodies to TNF-alpha and the TNF type 1 receptor, but not the addition of IL-1 receptor antagonist, blocked CpG ODN-induced osteoclastogenesis in RANKL-pretreated cultures. On the other hand, CpG ODN reduced expression of the M-CSF receptor, which is critical during the initiation of osteoclast differentiation. These results suggest that CpG ODN, via the induction of TNF-alpha, support osteoclastogenesis in cells that are committed to the osteoclast differentiation pathway but, due to down-modulation of M-CSF receptor, inhibit early steps of osteoclast differentiation. Thus, CpG ODN represents a potential therapeutic tool for treating bone diseases.

Acid Phosphatase↗

PubMed2002

Male fertility is compatible with an Arg(840)Cys substitution in the AR in a large Chinese family affected with divergent phenotypes of AR insensitivity syndrome.

Androgen insensitivity syndrome (AIS) is a disorder of male sexual development caused by an absent or dysfunctional AR. Fertile cases with mild AIS and slightly impaired AR activity had been reported in literature, and their external genitalia were documented to be usually normal or subnormal. We reported here an Arg(840)Cys substitution in the AR gene in a large Chinese pedigree affected with AIS. The mutant gene may result in infertility for some affected males with or without hypospadias. However, it was also observed that the mutation did not affect the fertility of the other patients. The gonadotropin levels for one of these patients were within the normal range. Thus, whether normal levels of the gonadotropins are necessary for the preserved fertility of patients affected with this genetic disorder remains to be elucidated.

Adolescent↗

PubMed2002

Dual modulation of osteoclast differentiation by lipopolysaccharide.

Lipopolysaccharide (LPS) modulates bone resorption by augmentation of osteoclastogenesis. It increases in osteoblasts the production of RANKL, interleukin (IL)-1, prostaglandin E2 (PGE2), and TNF-alpha, each known to induce osteoclast activity, viability, and differentiation. We examined the role of direct interactions of LPS with osteoclast precursors in promoting their differentiation. To this end, we have used bone marrow mononuclear cell preparations in the absence of osteoblasts or stromal cells. We found that LPS does not induce osteoclast differentiation in these cells. Moreover, the inclusion of LPS blocked the osteoclastogenic activity of RANKL. However, LPS is a potent inducer of osteoclastogenesis in RANKL-pretreated cells, even if present in the absence of exogenous RANKL. Osteoprotegerin (OPG), does not affect the stimulatory phase of LPS modulation of osteoclastogenesis, ruling out involvement of endogenous RANKL. LPS induces the expression of TNF-a and IL-1beta in osteoclast precursors, regardless if they were or were not pretreated with RANKL. These two cytokines induced osteoclast differentiation in RANKL-pretreated cells. To examine if these cytokines mediate LPS effect in an autocrine mechanism, we measured the effect of their neutralization on LPS osteoclastogenic activity. Although neutralization of IL-1beta did not affect LPS activity, a marked inhibition was observed when TNF-alpha was neutralized. However, TNF-a expression was increased also in conditions in which LPS inhibited RANKL osteoclastogenic activity. We found that LPS reduces the expression of RANK and macrophage colony-stimulating factor (M-CSF) receptor. In summary, LPS impacts on osteoclastogenesis also via its interactions with the precursor cells. LPS inhibits RANKL activity by reducing the expression of RANK and M-CSF receptor and stimulates osteoclastogenesis in RANKL-pretreated cells via TNF-alpha.

Animals↗

PubMedDate not supplied

Caveolin-1 haploinsufficiency leads to partial transformation of human breast epithelial cells.

BACKGROUND: Caveolin-1 (Cav-1), a principal component of caveolae membranes, may function as a tumor suppressor in several types of human cancer. MATERIALS AND METHODS: In this report, we employed a retrovirus-mediated poly-A gene trapping approach to inactivate expression of genes that may be involved in transformation of mammary cells and screened for cell growth in soft agar. RESULTS: We found two anchorage-independent clones (ST1 and ST3) that expressed reduced levels (approximately 50%) of Cav-1 mRNA and protein, suggesting the inactivation of one allele of Cav gene. However, haploinsufficiency of Cav-1 expression did not induce significant tumor formation when tested in nude mice. CONCLUSION: Cav-1 haploinsufficiency in human breast epithelial cells can lead to partial transformation.

Animals↗

PubMedDate not supplied

Caveolin-1 down-regulation activates estrogen receptor alpha expression and leads to 17beta-estradiol-stimulated mammary tumorigenesis.

Constitutive activation of estrogen receptor alpha (ER-alpha) expression is an early event in breast cancer tumorigenesis. However, the mechanism whereby ER-alpha is constitutively activated during transformation of normal mammary cells has not been well established. Previously, we reported that haploinsufficiency of caveolin-1, a major structural protein that forms caveolae, resulted in anchorage-independent growth of a normal mammary epithelial cell line, MCF10A. Here, we further demonstrated that ER-alpha but not ER-beta expression was constitutively activated in these caveolin-1 haploinsufficient cells. Transient treatment of MCF10A cells with beta-methyl-cyclodextrin, a chemical that can displace caveolin-1 from the plasma membrane, also stimulated ER-alpha expression. We further found that the 17beta-estradiol (E2) accelerated anchorage-independent growth of these cells in vitro and promoted their tumorigenesis in nude mice. These results suggest that dysregulation of caveolin-1 is one of the mechanisms by which ER-alpha expression is activated during initiation of breast tumorigenesis.

Animals↗