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Biomedical subjects

Z Tang

Publications and source records attributed to Z Tang.

At least 217 records · Page 12Linked to original sources

[An observation of protective effect of acupuncture on the cardiac function and anti-hemorrhagic shock].

This paper reports the study of the effect of the cardiac function and arterial pressure on rabbits with hemorrhagic shock by electroacupuncture Neiguan point. The result showed that PEP was shortened, ET was lengthened, SV, CO and Map were raised by needling Neiguan and the each index was significant difference (P < 0.001). Above results indicated that needling may strengthen myocardial contractile force, protect the cardial pump function, raise the blood pressure, play a positive role during anti-hemorrhagic shock.

Animals↗

[Evaluation of chemosensitivities of human breast cancers by primary culture assay in vitro].

Chemosensitivities of 32 human breast cancer to 6 antitumor drugs were assayed in vitro using MTT colorimetric method. The results showed that the chemosensitivity of primary breast cancer cultures varied remarkably from one patient, and from one drug, to another with hundred-to thousand-fold differences. The distribution of 50% inhibition concentration (IC50) was significantly deviated from normal distribution (P < 0.0001), and the drug sensitivity could be divided into four different catagories by means of percentile method. Preliminary results showed that the in vitro chemosensitivities of different antitumor drugs were consistent with the clinical therapeutic responses It seems that the herein reported assay might be useful on an individual basis to optimize chemotherapy of human breast cancer.

Antineoplastic Agents↗

[Preliminary studies on the effects of tumor necrosis factor gene transfer on the growth of human hepatocellular carcinoma cells in nude mice].

An eukaryotic expression vector containing tumor necrosis factor alpha (TNF alpha) gene (psVK3-tnf) was transduced into hepatocellular carcinoma (HCC) cell line, SMMC7721, by calcium phosphate coprecipation method. The TNF-gene-transduced SMMC7721 cell began to secrete TNF after 24h (50 0/ml), reached peak level at 48-72h (90U/ml), and declined after 96h (40U/ml). Three weeks after the pSVK3-tnf DNA entrapped with calcium phosphate was introduced directly into subcutaneous nodules of human HCC in nude mice (treated mice), the growth of HCC was significantly delayed as compared to the pSVK3 group (control mice) (2.5 +/- 1.6 cm vs. 3.2 +/- 1.8 cm, n = 6, P < 0.05). There was a transient increase in TNF alpha level in peripheral blood in the treated but not in the control mice. The survival time of the treated mice was markedly prolonged as compared to the control (44.0 +/- 3.3d vs. 28.2 +/- 2.0d, n = 6, P < 0.01). The above results suggest that TNF alpha gene transfer might be a hopeful therapy for HCC.

Animals↗

[Clinicopathologic characteristics of primary liver cancer in patients younger than 35 years].

To investigate clinicopathologic characteristics of primary liver cancer (PLC) in young adults, 77 patients younger than 35 years were compared with 603 patients older than 35 years during the same period. In the young patients, PLC showed a low incidence of PLC detected at mass survey (young 15.6% versus older 28.7%, P < 0.05); a low incidence of hepatitis history (young 36.8% versus older 66.3%, P < 0.01); a high incidence of positive hepatitis B virus surface antigen (HBsAg) (young 79.2% versus older 67.6%, P < 0.05); a low incidence of associated cirrhosis (young 64.9% versus older 90.7%, P < 0.01); larger tumor size (PLC > 5cm; young 87.0% versus older 73.0%, P < 0.01); a more advanced stage of the disease in TNM classification (stage III; young 29.9% versus older 18.2%, P < 0.05). It is suggested that hepatitis B virus (HBV) may play an important role in the development of PLC without associated liver cirrhosis in the young patients. A close periodic surveillance of young adults with a positive HBsAg is important to detect PLC at an early stage.

Adolescent↗

[Clinical significance of fungi-bearing status of hospitalized patients].

The samples for fungi culture were collected from 11 body parts of 1109 patients who had been admitted to hospitals in Wuhan for more than 3 days. The body parts included the cavities and foramina (inner canthus, nasal vestibule, external auditory canal), skin (finger raphe, cubital fossa, axillary fossa, nipple), and mucosa (pharynx, vagina, coronary sulcus and anal canal). 201 healthy subjects were also examined and served as controls. It was found that the total fungus-bearing rate in hospitalized patients was 88.73% (984/1109), while the rate in healthy subject was 76.62% (154/201) (X2 = 21.61). Among the hospitalized patients, the fungus-bearing rate in patients with leukemia, tumors, connective tissue diseases or severe infectious diseases was significantly higher than other patients (X2 = 4.30-9.87). In the hospitalized patients, the body parts with highest fungus-bearing rates were cavities and foramina, 80.70% (895/1109) for patients and 71.64% (144/201) for healthy subjects respectively. The skin had lowest fungus-bearing rate. 20.02% (222/1109) and 13.43% (26/201), and the mucosa had a rate of 50.77% (563/1109) for patients and 32.34% (65/201) respectively. The fungi in the hospitalized patients included 1884 strains (mean = 1.92 strains per case) in which the Candida accounted for 29.78% (561/1884) and Aspergilla 24.31% (458/1884) and those identified in healthy subjects covered 234 strains (mean = 1.52 strains per person) in which Penicillia accounted for 45.30% (106/234) and Saccharomycetes 26.07% (61/234). The patients who had been hospitalized for 3-10 days and over 20 days had higher fungus-bearing rate as compared with those who had been hospitalized for 10 to 20 days (X2 = 5.633-97.09). The patients before the administration of antibiotics and adrenocortical steroid and those who had been given these medicines for over 20 days had a higher fungus-bearing rate than those who had been on these medicines for 1-20 days.

Adolescent↗

Treatment of 23 patients with advanced gastric cancer by intravenously transfer of autologous tumor-infiltrating lymphocytes combined with rIL-2.

Tumor-infiltrating lymphocytes (TIL) isolated from metastatic lymph nodes in patients with nonoperable advanced gastric cancer were induced to become LAK-like cytotoxic activity of TIL after in vitro culture with rIL-2. Twenty-three patients with advanced gastric cancer were treated by intravenously transfer of autologous TIL combined with rIL-2. The tumor focus disappeared (complete remission, CR) in 3 patients (13.0%) and significantly decreased (partial remission, PR) in 5 patients (21.7%). Fifteen patients did not respond to the treatment. The amount of soluable IL-2 receptor in serum was significantly decreased after treatment, the cytotoxicity of NK cells and OT test were significantly increased. No significant difference in CD4/CD8 was found between before and after treatment. No serious side effect was observed in the treatment.

Adenocarcinoma↗

[Growth pattern and metastatic behaviour of orthotopically metastatic model of human hepatocellular carcinoma in nude mice].

Growth pattern, metastatic behaviour and serial alph-a-fetoprotein (AFP) level of highly metastatic model of human hepatocellular carcinoma in nude mice (LCI-D20), which constructed by using orthotopic implantation of histologically intact patient specimens, were studied by implanting into the liver, subcutis and peritoneum of nude mice. Pathologic (by light and electronmicroscopic examination) and biologic (chromosome karyotype and DNA contents by flow cytometry) characteristics of LCI-D20 were also observed. The results showed that transplantability of LCI-D20 was 100% in 12 generations (passage time: 20 days) and all of these mice implanted tumors died within 40 days after transplantation due to serious metastasis. After LCI-D20 implanted into the liver of nude mice, growing implant-tumors in progress were negatively related to their double time during animal survival. LCI-D20 maintained 100% (70/70) metastatic rate in nude mice that showed early intrahepatic metastasis and late lymphatic and pulmonary metastasis. The high metastatic potentials of LCI-D20 tumor cells were kept in subcutis and peritoneum (70%, 100% respectively). The increase of the serial AFP secreting from the tumor cells was correlated with the implantation tumor growth rate (797.5 micrograms/L/5th week). The data from histological and electronmicroscopic findings, chromosome karyotype and DNA content analysis of the tumor cells revealed characteristics of human hepatocellular carcinoma. The results indicated that LCI-D20 exhibited the variety of clinical behaviours seen in hepatoma patients and it could be a useful model for investigating the metastasis mechanism of human hepatoma and anti-metastasis therapy.

Adult↗

[The relation between p53 mutations and tumor invasiveness of human hepatocellular carcinoma].

We have combined the polymerase chain reaction (PCR) with the HaeIII enzyme restriction analysis to study the mutations at codon 249 of p53 gene in L02 human liver cell line, Bel-7402, SMMC-7721 human hepatocellular carcinoma cell lines and 19 surgical specimens of hepatocellular carcinoma (HCC) and their surrounding non-cancer liver tissues. None of the three cell lines and the non-cancer liver tissues was found to have p53 mutation; but 10 of 19 HCC samples (52.6%) had p53 point mutations, and the p53 gene mutated more frequently in HCC with incomplete capsule, intrahepatic metastasis, or multiple nodules than in those with well encapsulated (70% vs 33.3%, P < 0.05), no intrahepatic metastasis (71.4% vs 41.6%, P < 0.05) and single nodule (83.3% vs 38.5%, P < 0.05). These suggested that the codon 249 was a mutational hotspot of the p53 gene in human HCC seen in China, and p53 mutations may be related to invasiveness of human HCC.

Base Sequence↗

CGRP in the serum of endotoxin-treated rats suppresses lymphoproliferation.

Mouse mesenteric lymph node cells were incubated with concanavalin A (Con A) with or without the rat form of calcitonin gene-related peptide (rCGRP) (0.1 fM-1 microM) +/- human (h)CGRP8-37 (1 microM) for 48 h. DNA synthesis was assessed by [3H]thymidine incorporation. Con A-stimulated DNA synthesis was suppressed by 13, 20, and 30% at 10 fM, 1 pM, and 100 pM of rCGRP, respectively. hCGRP8-37 (1 microM), a selective blocker of CGRP1 receptor, completely inhibited the suppression of DNA synthesis by rCGRP (10 fM-100 pM). rCGRP caused concentration-dependent elevations of cAMP levels, which were potentiated by pretreatment with 3-isobutyl-1-methylxanthine (0.3 mM, 10 min), an inhibitor of cAMP-phosphodiesterase. hCGRP8-37 (1 microM) significantly inhibited cAMP elevations induced by rCGRP at the lower concentrations, but not at the highest concentrations of rCGRP. These data suggest that rCGRP, at circulating levels (1-10 pM), appears to directly interact with receptors on mouse mesenteric lymph node cells that are coupled to cAMP generation, ultimately inhibiting lymphocyte proliferation. To test the involvement of CGRP in suppression of lymphocyte proliferation by serum from endotoxin-treated rats, mouse mesenteric lymph node cells were stimulated with Con A with or without dilutions of endotoxin treated rat serum. At a 1:20 dilution, DNA synthesis was suppressed 30%, at a 1:40 dilution, DNA synthesis was suppressed by 34%, and at a 1:80 dilution, DNA synthesis was suppressed 25%. At all serum dilutions, coincubation with hCGRP8-37 (1 microM) significantly inhibited the suppressive effect of the endotoxin treated rat serum. These data suggest that the immunosuppression observed during endotoxin shock may be due, at least in part, to CGRP in serum.

Animals↗

Absence of insulin receptor gene mutations in three insulin-resistant women with the polycystic ovary syndrome.

Women with polycystic ovary syndrome (PCOS) are markedly insulin-resistant, but the molecular mechanisms of these changes and their relationship to the hyperandrogenic state remain to be clarified. Mutations have recently been identified in the insulin receptor gene of patients with extreme forms of insulin resistance associated with hyperandrogenism (eg, type A insulin resistance), and these mutations account for the insulin resistance in such patients. We performed this study to determine whether mutations in the coding portion of the insulin receptor gene were responsible for insulin resistance in PCOS. Insulin binding studies using cultured skin fibroblasts of three obese (body mass index > 27 kg/m2) women with PCOS (ie, mild hyperandrogenemia and chronic anovulation of unknown etiology) and documented insulin resistance showed no apparent abnormalities in either the number or affinity of insulin binding sites. Direct sequencing of all 22 exons of the insulin receptor gene from two of the women with PCOS did not reveal any mutations. Furthermore, both alleles of the gene were expressed at equal levels. In a third insulin-resistant PCOS woman, there was no evidence for a mutation in the coding portion of the insulin receptor gene as determined by denaturing gradient gel electrophoresis (DGGE). We conclude that the insulin resistance in these PCOS women was caused by a defect extrinsic to the insulin receptor.

Adult↗

Cell aging of human diploid fibroblasts is associated with changes in responsiveness to epidermal growth factor and changes in HER-2 expression.

The limited replicative life span of diploid human cells in vitro (cellular senescence) serves as a cellular model of aging. We examined the proliferative response of 2BS cells of different population doubling levels to epidermal growth factor (EGF). DNA synthesis was measured by thymidine incorporation. As the cells aged, there was a significant decrease both in the baseline level of DNA synthesis and in the stimulation of DNA synthesis by EGF addition. The effective concentration of EGF and the latent period prior to DNA synthesis did not change. EGF receptor mRNA expression also remained unchanged as the cells aged, in the absence or presence of EGF, suggesting that the defect in old cells lies downstream in the EGF signaling pathway. As the cells reached 100% of their life span, however, there was a 70% decrease in EGF receptor mRNA. Expression of the EGF receptor homologue HER-2 was also examined. The HER-2 mRNA level was significantly reduced in old cells. Moreover, HER-2 expression was stimulated by EGF addition in young cells but not in old cells. The results suggest that cell aging is associated with a progressive loss in the ability of cells to respond to growth factors.

Cell Division↗

Caveolae, caveolin and caveolin-rich membrane domains: a signalling hypothesis.

Caveolae, 50-100 nm invaginations that represent a subcompartment of the plasma membrane, have been known for many years, but their exact roles remain uncertain. The findings that the caveolae coat protein caveolin is a v-Src substrate and that G-protein-coupled receptors are present in caveolae have suggested a relationship between caveolae, caveolin and transmembrane signalling. The recent isolation of caveolin-rich membrane domains in which caveolin exists as a hetero-oligomeric complex with integral membrane proteins and known cytoplasmic signalling molecules provides support for this hypothesis. Compartmentalization of certain signalling molecules within caveolae could allow efficient and rapid coupling of activated receptors to more than one effector system.

Journal Article↗

Characterization of caveolin-rich membrane domains isolated from an endothelial-rich source: implications for human disease.

Caveolae are 50-100-nm membrane microdomains that represent a subcompartment of the plasma membrane. Previous morphological studies have implicated caveolae in (a) the transcytosis of macromolecules (including LDL and modified LDLs) across capillary endothelial cells, (b) the uptake of small molecules via a process termed potocytosis involving GPI-linked receptor molecules and an unknown anion transport protein, (c) interactions with the actin-based cytoskeleton, and (d) the compartmentalization of certain signaling molecules, including G-protein coupled receptors. Caveolin, a 22-kD integral membrane protein, is an important structural component of caveolae that was first identified as a major v-Src substrate in Rous sarcoma virus transformed cells. This finding initially suggested a relationship between caveolin, transmembrane signaling, and cellular transformation. We have recently developed a procedure for isolating caveolin-rich membrane domains from cultured cells. To facilitate biochemical manipulations, we have applied this procedure to lung tissue--an endothelial and caveolin-rich source-allowing large scale preparation of these complexes. These membrane domains retain approximately 85% of caveolin and approximately 55% of a GPI-linked marker protein, while they exclude > or = 98% of integral plasma membrane protein markers and > or = 99.6% of other organelle-specific membrane markers tested. Characterization of these complexes by micro-sequencing and immuno-blotting reveals known receptors for modified forms of LDL (scavenger receptors: CD 36 and RAGE), multiple GPI-linked proteins, an anion transporter (plasma membrane porin), cytoskeletal elements, and cytoplasmic signaling molecules--including Src-like kinases, hetero-trimeric G-proteins, and three members of the Rap family of small GTPases (Rap 1--the Ras tumor suppressor protein, Rap 2, and TC21). At least a fraction of the actin in these complexes appeared monomeric (G-actin), suggesting that these domains could represent membrane bound sites for microfilament nucleation/assembly during signaling. Given that the majority of these proteins are known molecules, our current studies provide a systematic basis for evaluating these interactions in vivo.

Amino Acid Sequence↗

Sequential analysis of K-ras mutations in aberrant crypt foci and colonic tumors induced by azoxymethane in Fischer-344 rats on high-risk diet.

Forty Fischer-344 male rats were given a high-risk diet (HRD) that was high in fat, low in fiber and low in calcium. After 4 weeks, the rats were given two weekly s.c. injections of azoxymethane (AOM, 15 mg/kg body wt), and remained on the same diet till death. Eight rats were killed at 12 weeks and again at 20 weeks in order to microdissect aberrant crypt foci (ACF) containing four or more crypts/focus from their colons. The remaining 24 rats were killed at 30 weeks to harvest colonic tumors. The polymerase chain reaction (PCR) was used to amplify specific DNA segments in the K-ras gene from ACF and colonic tumors. The PCR-amplified DNAs were sequenced to identify the point mutations in codons 12 and 13. All the mutations detected in the ACF and colonic tumors were G to A transitions in the second position of codon 12. These mutations were present in the ACF of 2/8 (25%) and 3/8 (37%) rats at 12 and 20 weeks respectively. The mutations were present in colonic tumors of 7/24 (29%) rats. These results provide important evidence for the significance of K-ras mutations in ACF (> 4 crypts/focus) as early markers of malignant potential in the colons of F344 rats exposed to AOM while receiving a high-risk western style diet.

Adenocarcinoma↗