Biomedical subjects

F Zhang

Publications and source records attributed to F Zhang.

At least 379 records · Page 21Linked to original sources

PubMed1998

[A endothelial coverage in the autogenous vein graft for arterial reconstruction in the early stage].

OBJECTIVE: To sequentially study the endothelial cell(EC) in the autogenous vein graft(AVG) for arterial construction in the early stage. METHODS: Forty dogs were divided in to two groups. After the artery reconstructed and intravenous injection or nonintravenous injection of PGE1, the dogs were divided in to groups. The deendothelialization and reendothelialization of AVG were determined by the portrayal apparatus. RESULTS: Excellent results in renovation of EC to the AVG were observed after establishment of running off of was reconstructed artery without intravenous injection of PGE1. The valve of AVG is very important in renovation of EC. CONCLUSION: It must be protected when artery is reconstructed by AVG.

Animals↗

PubMed1998

[Recovery of submandibular gland function following transoral sialolithectomy].

OBJECTIVE: Investigate the recovery of the submandibular gland function following transoral sialolithectomy. METHODS: The glandular function of 26 patients who received the transoral sialolithectomy were investigated by sequential scintigraphy with 99m Tc pertechetate. RESULTS: Most glandular function recovers normal in short time after operation. Glandular infection, calculus diameter and patients's age could influence the recovery of function. CONCLUSION: In the treatment of sialolithiasis, breaking up the pathogenic process of calculus formation and effectively controlling the glandular infection are very important in preventing from the function reduction. After transoral sialolithectomy preserving the anatomical normal orifice of the duct, and using silivators may be very favorable for the function recovery.

Adolescent↗

PubMed1998

[Surgical treatment of epispadias].

OBJECTIVE: To analyse the surgical treatment of 124 cases of epispadias (incomplete 27 cases, complete 21 and complex 76). METHOD: Leadbetter's operation was used for anti-incontinence. Urethral tightening was used in 4 cases of complete female epispadias. Penile straightening was adopted for incomplete epispadias and penile lengthening for complete and complex male epispadias. RESULT: In 97 cases of urinary incontinence, complete continence was achieved in 73. CONCLUSION: The orthopedic effects of external genitals were satisfactory.

Adolescent↗

PubMed1998

[Hepatitis B virus replication status and its response to surgery for tumor in hepatocellular carcinoma patients with positive markers of HBV].

OBJECTIVE: To investigate the status of hepatitis B virus (HBV) activity in patients with hepatocellular carcinoma (HCC) and its response to surgical interventions for tumor in HBV positive HCC patients. METHOD: We analyzed HBV marker results and detected HBV DNA in sera of 97 HCC patients (pre-operation 66 cases, post-operation 31 cases) with polymerase chain reaction (PCR) assay. We also investigated the HBV DNA titer in sera before and one week after operation in 20 HCC patients with positive HBV markers by quantitative polymerase chain reaction (Q-PCR). RESULT: HBV DNA positive rate in sera was 40.9% and 64.52% in the two subgroup respectively (P < 0.05). HBV DNA titer in sera increased after operation (P < 0.01). CONCLUSION: The infection rate of HBV in Chinese HCC patients is very high. The replication of hepatitis B virus is strong in partial HBV marker positive HCC patients and surgical interventions may promote the virus replication.

Carcinoma, Hepatocellular↗

PubMed1998

[Application of diode laser in the operation of retinal diseases].

OBJECTIVES: To evaluate the effects of diode laser photocoagulation applied on 43 cases of various kinds of fundus diseases with media opacity and on 40 cases during vitreo-retinal surgery. METHODS: Indirect ophthalmoscope laser photocoagulator was used for fundus diseases, and endolaser used during surgery. RESULTS: Vision was improved in 24.7% of the eyes, and was unchanged in 62.9% of the eyes. The neovascularization in proliferative diabetic retinopathy regressed in 78.3% of the eyes. All the retinal holes were closed. CONCLUSIONS: Diode laser can be used for treatment of some retinal diseases and in the operation. Good results can be obtained in the eyes with some extent of media opacity. No obvious side-effect was observed.

Adolescent↗

PubMed1998

[Effects of IL-1 and TNF-alpha on the proliferation and cytosolic Ca2+ of lens epithelial cell in vitro].

OBJECTIVE: To study the effects of interleukin 1 (IL-1) and tumor necrosis factor alpha (TNF-alpha) on the proliferation and cytosolic Ca(2+) of bovine lens epithelial cells (BLEC) in vitro. The effects of IL-1 and TNF-alpha on posterior capsular opacification (PCO) and the mechanism of effect on the proliferation were investigated. METHODS: The effects of IL-1 and TNF-alpha on the proliferation of BLEC were detected with MTT staining colorimetry, and cytosolic Ca(2+) was measured by fluorescence determination with Fura-2. RESULTS: IL-1 10(2) - 10(5) ng/ml, TNF-alpha 10(2) - 10(4) U/ml obviously could promote BLEC proliferation (P < 0.05 - 0.01), and increase cytosolic Ca(2+) (P < 0.05 - 0.01) at the same doses. CONCLUSIONS: IL-1, TNF-alpha contribute to the PCO. One of the mechanisms of IL-1 and TNF-alpha on proliferation is by cytosolic Ca(2+).

Animals↗

PubMed1998

[Clinical features of 31 cases with bilateral Duane's retraction syndrome].

OBJECTIVES: To summarize the clinical features of 31 cases with bilateral Duane's retraction syndrome (DRS) and discuss its differential diagnosis. METHODS: We retrospectively summarized 31 cases with bilateral DRS from 1979 to 1996. Its clinical features including chief complaints, age and sex distribution, types of presentation, defects in abduction and adduction, retraction of the globe, upshots and downshots in abduction, etc. were analyzed. RESULTS: There were 14 males and 17 females with a female-to-male ratio 1 : 0.8. The chief complaints comprised 14 cases (45%) with ocular motility disorders and 10 cases (32%) with ocular deviations. The most common form of the syndrome was type 1 (29 cases, 94%), the remaining 2 cases (6%) with type III. Its clinical features consisted of retraction of the globe with narrowing of the palpebral fissure in attempted adduction, limitation in abduction with variable extent also in adduction, and upshot and/or downshot of the affected eye during adduction. CONCLUSIONS: In atypical cases, the retraction of the globe in adduction was not obvious and the diagnosis of DRS must be differentiated from the following ocular motility disorders, namely, abducens nerve palsy, Möebius syndrome, congenital oculomotor apraxia and congenital or infantile esotropia.

Adolescent↗

PubMed1998

[Seeds collecting of Ephedra sinica and treatment before sown].

Seeds collecting of Ephedra sinica and treatment before sown were studied. These results indicated that time collecting seeds and treating such as threshing, washing, drying, storing at low temperature and immersing seeds with chemical were available measures. Which could supply a reference for the culture of E. sinica.

Desiccation↗

PubMed1998

[Analysis of rhodopsin and peripherin/RDS genes in Chinese patients with retinitis pigmentosa].

PURPOSE: To disclose the mutation of rhodopsin and peripherin/RDS genes among Chinese patients with retinitis pigmentosa as there was no identified mutation through sequencing reported in Chinese. METHODS: Genomic DNA was prepared from the peripheral lymphocytes. Gene fragments of the rhodopsin and peripherin/RDS genes were amplified by the polymerase chain reaction. The PCR products were analyzed by Heteroduplex-SSCP technique. PCR samples with aberrant migrational bands were identified through direct sequencing or cloning sequencing. RESULTS: Three different mutations in the rhodopsin gene were found in 3 of the 83 patients with retinitis pigmentosa(Va1104Phe, Lys311Glu, Pro347Leu). Two of the three mutations have not been reported before. One of the two (heterozygous, Va1104Phe) was found in an isolated patient and the other (homozygous, Lys311Glu) in a family with autosomal recessive retinitis pigmentosa. Mutation of peripherin/RDS gene was not found in the 83 patients. CONCLUSION: Mutation in the rhodopsin gene is the common cause in Chinese patients with retinitis pigmentosa, either autosomal dominant, recessive or sporadic.

Base Sequence↗

PubMed1998

Butyrate attenuates BCLX(L) expression in human fibroblasts and acts in synergy with ionizing radiation to induce apoptosis.

Ionizing radiation is a poor inducer of apoptosis in many cell types. In this study we investigated what effect the differentiation agent butyrate had on the cellular levels of the apoptosis regulators BCL2, BCLX(L) and BAX and on radiation-induced apoptosis. It was found that butyrate significantly lowered the level of the apoptosis antagonist BCLX(L) in a time- and dose-dependent manner in diploid human fibroblasts. The reduction of the level of BCLX(L) protein by butyrate correlated with an increased induction of apoptosis in cells irradiated with ionizing radiation. Butyrate also acted in synergy with ultraviolet (UV) light and cisplatin to induce apoptosis in human fibroblasts. Radiosensitization was obtained when butyrate was added before and/or after irradiation, although the combination of treatment both before and after irradiation was the most effective. Our results suggest that butyrate acts in synergy with ionizing radiation, UV light and cisplatin to induce apoptosis, perhaps by lowering the level of the apoptosis antagonist BCLX(L) in cells.

Apoptosis↗

PubMed1997

Development of an epithelium-specific expression cassette with human DNA regulatory elements for transgene expression in lung airways.

The efficient expression of therapeutic genes in target cells or tissues is an important component of efficient and safe gene therapy. Utilizing regulatory elements from the human cytokeratin 18 (K18) gene, including 5' genomic sequences and one of its introns, we have developed a novel expression cassette that can efficiently express reporter genes, as well as the human cystic fibrosis transmembrane conductance regulator (CFTR) gene, in cultured lung epithelial cells. CFTR transcripts expressed from the native K18 enhancer/promoter include two alternative splicing products, due to the activation of two cryptic splice sites in the CFTR coding region. Modification of the K18 intron and CFTR cDNA sequences eliminated the cryptic splice sites without changing the CFTR amino acid sequence, and led to enhanced CFTR mRNA and protein expression as well as biological function. Transgenic expression analysis in mice showed that the modified expression cassette can direct efficient and epithelium-specific expression of the Escherichia coli LacZ gene in the airways of fetal lungs, with no detectable expression in lung fibroblasts or endothelial cells. This is the first expression cassette which selectively directs lung transgene expression for CFTR gene therapy to airway epithelia.

Animals↗

PubMed1997

Constitutive internalization of cystic fibrosis transmembrane conductance regulator occurs via clathrin-dependent endocytosis and is regulated by protein phosphorylation.

Although the cystic fibrosis transmembrane conductance regulator (CFTR) is primarily implicated in the regulation of plasma-membrane chloride permeability, immunolocalization and functional studies indicate the presence of CFTR in the endosomal compartment. The mechanism of CFTR delivery from the cell surface to endosomes is not understood. To delineate the internalization pathway, both the rate and extent of CFTR accumulation in endosomes were monitored in stably transfected Chinese hamster ovary (CHO) cells. The role of clathrin-dependent endocytosis was assessed in cells exposed to hypertonic medium, potassium depletion or intracellular acid-load. These treatments inhibited clathrin-dependent endocytosis by >90%, as verified by measurements of 125I-transferrin uptake. Functional association of CFTR with newly formed endosomes was determined by an endosomal pH dissipation protocol [Lukacs, Chang, Kartner, Rotstein, Riordan and Grinstein (1992) J. Biol. Chem. 267, 14568-14572]. As a second approach, endocytosis of CFTR was determined after cell-surface biotinylation with the cleavable sulphosuccinimidyl-2-(biotinamido)ethyl-1,3-dithio- propionate. Both the biochemical and the functional assays indicated that arresting the formation of clathrin-coated vesicles inhibited the retrieval of the CFTR from the plasma membrane to endosomes. An overall arrest of membrane traffic cannot account for the inhibition of CFTR internalization, since the fluid-phase endocytosis was not effected by the treatments used. Thus the efficient, constitutive internalization of surface CFTR (5% per min) occurs, predominantly by clathrin-dependent endocytosis. Stimulation of protein phosphorylation by cAMP-dependent protein kinase A and by protein kinase C decreased the rate of internalization of cell-surface biotinylated CFTR, and contributed to a substantial diminution of the internal CFTR pool compared with that of unstimulated cells. These results suggest that the rate of CFTR internalization may participate in the determination of the CFTR channel density, and consequently, of the cAMP-stimulated chloride conductance of the plasma membrane.

Animals↗

PubMed1997

Delayed reduction of ischemic brain injury and neurological deficits in mice lacking the inducible nitric oxide synthase gene.

Inducible nitric oxide synthase (iNOS), an enzyme that produces toxic amounts of nitric oxide, is expressed in a number of brain pathologies, including cerebral ischemia. We used mice with a null mutation of the iNOS gene to study the role of iNOS in ischemic brain damage. Focal cerebral ischemia was produced by occlusion of the middle cerebral artery (MCA). In wild-type mice, iNOS mRNA expression in the post-ischemic brain begun between 24 and 48 hr peaked at 96 hr and subsided 7 d after MCA occlusion. iNOS mRNA induction was associated with expression of iNOS protein and enzymatic activity. In contrast, mice lacking the iNOS gene did not express iNOS message or protein after MCA occlusion. The infarct and the motor deficits produced by MCA occlusion were smaller in iNOS knockouts than in wild-type mice (p < 0.05). Such reduction in ischemic damage and neurological deficits was observed 96 hr after ischemia but not at 24 hr, when iNOS is not yet expressed in wild-type mice. The decreased susceptibility to cerebral ischemia in iNOS knockouts could not be attributed to differences in the degree of ischemia or vascular reactivity between wild-type and knockout mice. These findings indicate that iNOS expression is one of the factors contributing to the expansion of the brain damage that occurs in the post-ischemic period. iNOS inhibition may provide a novel therapeutic strategy targeted specifically at the secondary progression of ischemic brain injury.

Animals↗

PubMed1997

Increased susceptibility to ischemic brain damage in transgenic mice overexpressing the amyloid precursor protein.

We studied the role of the amyloid precursor protein (APP) in ischemic brain damage using transgenic mice overexpressing APP. The middle cerebral artery (MCA) was occluded in FVB/N mice expressing APP695.SWE (Swedish mutation) and in nontransgenic littermates. Infarct volume (cubic millimeters) was assessed 24 hr later in thionin-stained brain sections. The infarct produced by MCA occlusion was enlarged in the transgenics (+32 +/- 6%; n = 12; p < 0. 05; t test). Measurement of APP by ELISA revealed that, although relatively high levels of Abeta were present in the brain of the transgenics (Abeta1-40 = 80 +/- 19 pmol/g; n = 6), there were no differences between ischemic and nonischemic hemispheres (p > 0.05). The reduction in cerebral blood flow produced by MCA occlusion at the periphery of the ischemic territory was more pronounced in APP transgenics (-42 +/- 8%; n = 9) than in controls (-20 +/- 8%; n = 9). Furthermore, the vasodilatation produced by neocortical application of the endothelium-dependent vasodilator acetylcholine (10 microM) was reduced by 82 +/- 5% (n = 8; p < 0.05) in APP transgenics. The data demonstrate that APP overexpression increases the susceptibility of the brain to ischemic injury. The effect is likely to involve the Abeta-induced disturbance in endothelium-dependent vascular reactivity that leads to more severe ischemia in regions at risk for infarction. The cerebral vascular actions of peptides deriving from APP metabolism may play a role in the pathogenic effects of APP.

Amyloid beta-Peptides↗

PubMed1997

Differential screening of a human chromosome 3 library identifies hepatocyte growth factor-like/macrophage-stimulating protein and its receptor in injured lung. Possible implications for neuroendocrine cell survival.

Transient pulmonary neuroendocrine cell hyperplasia and non-neuroendocrine lung tumors develop in nitrosaminetreated hamsters, which we hypothesized might modulate epithelial cell phenotype by expressing gene(s) homologous to human chromosome 3p gene(s) deleted in small cell carcinoma of the lung (SCLC). We differentially screened a chromosome 3 library using nitrosamine-treated versus normal hamster lung cDNAs and identified hepatocyte growth factor-like/macrophage-stimulating protein (HGFL/MSP) in injured lung. HGFL/MSP mRNA is low to undetectable in human SCLC and carcinoid tumors, but the HGFL/MSP tyrosine kinase receptor, RON, is present and functional on many of these neuroendocrine tumors. In H835, a pulmonary carcinoid cell line, and H187, a SCLC cell line, HGFL/ MSP induced adhesion/flattening and apoptosis. Using viable cell counts to assess proliferation after 14 d of treatment with HGFL/MSP, there is growth inhibition of H835 but not H187. Nitrosamine-treated hamsters also demonstrate pulmonary neuroendocrine cell apoptosis in situ during the same time period as expression of the endogenous HGFL/ MSP gene, immediately preceding the spontaneous regression of neuroendocrine cell hyperplasia. These observations suggest that HGFL/MSP might regulate neuroendocrine cell survival during preneoplastic lung injury, which could influence the ultimate tumor cell phenotype.

Animals↗

PubMed1997

The transcriptional activators BAS1, BAS2, and ABF1 bind positive regulatory sites as the critical elements for adenine regulation of ADE5,7.

Adenine repression of the purine nucleotide biosynthetic genes in Saccharomyces cerevisiae involves down-regulation of the activator protein BAS1 or BAS2 by an unknown mechanism. To determine the minimal cis-acting requirements for adenine regulation, hybrid promoter constructs were made between ADE5,7 promoter fragments and a CYC1-lacZ reporter. A 139-nucleotide fragment containing two BAS1 binding sites was sufficient to confer adenine regulation on the CYC1-lacZ reporter. Analysis of deletion and substitution mutations led to the conclusion that the proximal BAS1 binding site is both necessary and sufficient for regulation, whereas the distal site augments the function of the proximal site. By performing saturation mutagenesis, we found two essential regions that flank the proximal site. An ABF1 consensus sequence is within one of these regions, and mutations that impaired in vitro ABF1 binding impaired promoter activity in vivo. A second region is AT-rich and appears to bind BAS2. No substitution mutations led to high level constitutive promoter activity as would be expected from removal of an upstream repression sequence. Our results indicate that ABF1, BAS1, and BAS2 are required for ADE5,7 promoter function and that adenine repression most likely involves activator modification or a negative regulator that does not itself bind DNA.

Adenine↗

PubMed1997

Crystal structure of the obese protein leptin-E100.

Mutations in the obese gene (OB) or in the gene encoding the OB receptor(OB-R) result in obesity, infertility and diabetes in a variety of mouse phenotypes. The demonstration that OB protein (also known as leptin) can normalize body weight in ob/ob mice has generated enormous interest. Most human obesity does not appear to result from a mutant form of leptin: rather, serum leptin concentrations are increased and there is an apparent inability to transport it to the central nervous system (CNS). Injection of leptin into the CNS of overfed rodents resistant to peripheral administration was found to induce biological activity. Consequently, for the leptin to act as a weight-lowering hormone in human obesity, it appears that appropriate concentrations must be present in the CNS. This places a premium on understanding the structure of the hormone in order to design more potent and selective agonists. Here we report the crystal structure at 2.4A resolution of a human mutant OB protein (leptin-E100) that has comparable biological activity to wild type but which crystallizes more readily. The structure reveals a four-helix bundle similar to that of the long-chain helical cytokine family.

Amino Acid Sequence↗

PubMed1997

Uncoupling of cell cycle arrest from the expression of monocytic differentiation markers in HL60 cell variants.

Differentiation generally leads to cell cycle arrest. Human leukemia HL60 cells respond to the presence of 1,25-dihydroxyvitamin D3 (1,25D3) by expressing a number of markers of the monocyte/macrophage phenotype and become arrested predominantly in the G1 phase of the cell cycle. We have recently reported a series (A) of 1,25D3-resistant variants of HL60 cells which proliferate in the presence of 1,25D3 and do not express differentiation markers (Exp. Cell Res. 224, 312, 1996). We now describe another series (B) of such variants, which differ from A series cells grown in similar concentrations of 1,25D3 in that they express the CD14 antigen and nonspecific esterase, characteristic of the monocyte, while continuing to proliferate and they develop hypotetraploid DNA (4C) content at higher concentrations of ambient 1,25D3 than the A series cells. Cells in the B series with 4C DNA content (100B and 200B) also differed from the A series 4C cells by the absence of DNA binding by the full-length Sp1 transcription factor. However, B series cells resembled the A series cells in exhibiting faster growth rates than the parental HL60 cells and showed high levels of vitamin D receptor and retinoid receptor X proteins. These results show that the initial steps in the 1,25D3 signaling pathway are intact in B series resistant cells and lead to the appearance of early markers of monocytic differentiation. However, the progression to subsequent events which comprise terminal differentiation and cell cycle arrest is halted during the adaptation to the presence of 1,25D3 in these cells. Thus, the availability of these variant cells should provide a system for studying the link between differentiation and cell cycle arrest.

Antigens, Differentiation, Myelomonocytic↗