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Biomedical subjects

B X Zhang

Publications and source records attributed to B X Zhang.

At least 19 recordsLinked to original sources

Autoantibody production from a thymoma and a follicular dendritic cell sarcoma associated with paraneoplastic pemphigus.

BACKGROUND: Paraneoplastic pemphigus (PNP) is an autoimmune mucocutaneous disease. We previously reported that B cells in a Castleman tumour associated with PNP produced autoantibodies. However, it is uncertain whether the production of autoantibodies from the associated tumour is a common mechanism in PNP. OBJECTIVES: To investigate autoantibody production in a thymoma and a follicular dendritic cell sarcoma that were excised from two patients with PNP. METHODS: Tumour cells were cultured, and their surface markers were identified. Indirect immunofluorescence, immunoblotting and enzyme-linked immunosorbent assay (ELISA) using culture media from the tumours were used to detect PNP autoantibodies. RESULTS: B cells with markers (CD22+, surface membrane IgG+ and surface membrane IgM+) of mature B lymphocytes constituted a proportion of cultured tumour cells in both tumours. Western blot showed that the medium from both the thymoma and the follicular dendritic cell sarcoma cells recognized 190-kDa periplakin and 210-kDa envoplakin bands of human epithelial proteins as well as recombinant linker regions of periplakin, envoplakin, desmoplakin and bullous pemphigoid antigen 1. ELISA was positive for antidesmoglein 3 antibody. CONCLUSIONS: The presence and localization in tumours of B-lymphocyte clones against proteins of the plakin family and desmoglein 3 in skin may not be confined to PNP with Castleman disease, but is possibly a common mechanism in PNP associated with various tumours.

Adult↗

Involvement of hypoxia-inducible factor-1-alpha in multidrug resistance induced by hypoxia in HepG2 cells.

Aim of the study was to explore the influence of hypoxia on multidrug resistance related genes and the potential role of hypoxia-inducible factor-1-alpha (HIF-1alpha) in formation of multidrug resistance in HepG2 human hepatocellular carcinoma cell line. HepG2 cells were subjected to hypoxia in a cohort of exposed time. A cell model stably expressing HIF-1alpha was established by liposome-mediated transfection of plasmid pcDNA3/HIF-1alpha into HepG2 cells. Apoptosis of HepG2 cells exposed to hypoxia or transfected by plasmid pcDNA3/HIF-1alpha was detected by Flow Cytometry after administration of chemotherapeutic drug (5-Fu). Real-time fluorescent quantitative PCR and Western-blot technique were used to analyze the expressions of multidrug resistance related genes mdr1, MRP1 and LRP at mRNA and protein level, respectively. Apoptosis Index of HepG2 cells exposed to hypoxia stepped down as exposed time extended after administration of 5-Fu. The expression of mdr1, MRP1 and LRP gene and protein revealed a hypoxic time-dependent induction and was synchronous with the alterations of HIF-1alpha in HepG2 cells exposed to hypoxia. The expressions of these multidrug resistance related genes were remarkably increased in HIF-1alpha transfected HepG2 cells as compared to empty vector transfected cells. Apoptosis index of HIF-1alpha transfected cells was obviously less than that of control cells when they were simultaneously exposed to 5-Fu for 24hrs. In conclusion, ambient hypoxia might be one of the causes for the formation of multidrug resistance in HepG2 human hepatocellular carcinoma cell line. Hypoxia-elicited multidrug resistance related protein expression might be a pathway for resistance of HepG2 cells to chemotherapeutics and HIF-1alpha might be involved in this process.

Apoptosis↗

QTL analysis of fertility restoration in cytoplasmic male sterile pepper.

Fertility restoration of Peterson's cytoplasmic male-sterility in pepper (Capsicum annuum L.) is quantitative and environment-dependent. QTL analysis of fertility restoration was performed based on the test-cross progeny of 77013A (a strict cytoplasmic-genetic male sterile line) and a doubled haploid population of 114 lines obtained from an F1 hybrid between Yolo wonder (a sterility maintainer line) and Perennial (a fertility-restorer line). The fertility of the test-crossed lines was assessed under greenhouse and open field conditions using three criteria related to pollen or seed production. One major QTL for fertility restoration was mapped to chromosome P6. It was significant in all the environments and for all the traits, accounting for 20-69% of the phenotypic variation, depending on the trait. Four additional minor QTLs were also detected on chromosomes P5, P2, and linkage groups PY3 and PY1, accounting for 7-17% of the phenotypic variation. Most of the alleles increasing fertility originated from the restorer parent, except for two alleles at minor QTLs. Phenotypic analysis and genetic dissection indicated that breeding pepper for complete sterility of female lines and high hybrid fertility requires complex combinations of alleles from both parents and a strict control of the environment.

Breeding↗

Chinese experience with hepatectomy for huge hepatocellular carcinoma.

BACKGROUND: The risks and outcome of hepatic resection for huge hepatocellular carcinoma (HCC) are controversial. METHODS: The clinical records of 525 patients who underwent resection of HCC greater than 10 cm in diameter were studied retrospectively. Prognostic factors for long-term survival were evaluated by univariate and multivariate analyses. RESULTS: Postoperative complications were common (26.8 per cent) and five patients (0.9 per cent) required relaparotomy. The 30-day mortality rate was 2.7 per cent. The main causes of postoperative death were liver failure (nine patients) and bleeding (four). The 3-, 5- and 10-year crude survival rates after liver resection were 34.3, 16.8 and 2.9 per cent respectively. CONCLUSION: Prognostic factors for long-term survival mainly reflected the biological behaviour of the tumour. They can be used only as a guide in balancing the risks of operation against the potential benefits of resection in a patient in poor general condition or with poor liver function. They cannot be used alone to exclude patients from liver resection with curative intent. Liver resection for huge HCC was safe and efficacious. It should be used to treat patients with acceptable surgical risks and resectable tumours.

Aged↗

[A new method of bone defect repairing after bone cyst curettage].

OBJECTIVE: To introduce a new method of bone defect repairing after bone cyst curettage. METHODS: Eight cases with bone cyst were treated with this new method. The pieces of autogenous periosteum were implanted into the hematoma within the enveloped bone defect created after the bone cyst curettage. Among these patients, there were 5 males and 3 females, aged from 14 to 36 years old. All the lesions located in the upper of femur except one being located in humerus. The results were evaluated through the postoperative radiological findings with the preoperative ones and analysis of clinical functions. RESULTS: All the patients were followed up for 2 to 11 years. X-ray films showed that osteogenesis developed well and that the enveloped bone defects had been repaired. No recurrence was found and the function of the affected limbs were maintained. CONCLUSION: Autogenous periosteum grafting is effective in the treatment of solitary bone cyst.

Adolescent↗

Differential regulation of the phosphatidylinositol 3-kinase/Akt and p70 S6 kinase pathways by the alpha(1A)-adrenergic receptor in rat-1 fibroblasts.

Phosphatidylinositol (PI) 3-kinase and its downstream effector Akt are thought to be signaling intermediates that link cell surface receptors to p70 S6 kinase. We examined the effect of a G(q)-coupled receptor on PI 3-kinase/Akt signaling and p70 S6 kinase activation using Rat-1 fibroblasts stably expressing the human alpha(1A)-adrenergic receptor. Treatment of the cells with phenylephrine, a specific alpha(1)-adrenergic receptor agonist, activated p70 S6 kinase but did not activate PI 3-kinase or any of the three known isoforms of Akt. Furthermore, phenylephrine blocked the insulin-like growth factor-I (IGF-I)-induced activation of PI 3-kinase and the phosphorylation and activation of Akt-1. The effect of phenylephrine was not confined to signaling pathways that include insulin receptor substrate-1, as the alpha(1)-adrenergic receptor agonist also inhibited the platelet-derived growth factor-induced activation of PI 3-kinase and Akt-1. Although increasing the intracellular Ca(2+) concentration with the ionophore A23187 inhibited the activation of Akt-1 by IGF-I, Ca(2+) does not appear to play a role in the phenylephrine-mediated inhibition of the PI 3-kinase/Akt pathway. The differential ability of phenylephrine and IGF-I to activate Akt-1 resulted in a differential ability to protect cells from UV-induced apoptosis. These results demonstrate that activation of p70 S6 kinase by the alpha(1A)-adrenergic receptor in Rat-1 fibroblasts occurs in the absence of PI 3-kinase/Akt signaling. Furthermore, this receptor negatively regulates the PI 3-kinase/Akt pathway, resulting in enhanced cell death following apoptotic insult.

Animals↗

G-protein signaling abnormalities mediated by CD95 in salivary epithelial cells.

Salivary epithelial cells from patients with primary Sjögren's syndrome (SS) undergo Fas-mediated apoptosis. Bcl-2 and Bcl-xL are apoptosis suppressing oncogenes. Very little is known about the role of these oncogene molecules in salivary epithelial cells. To investigate the possible prevention of salivary glandular destruction in SS by Bcl-2 and Bcl-xL, stable transfectants expressing these molecules were made from HSY cells, a human salivary epithelial cell line. HSY cells were transfected with an expression vector for human Bcl-2 or Bcl-xL. Stable transfectants were selected and apoptosis was induced by anti-Fas antibody. Apoptosis was quantified by propidium iodide staining followed by flow cytometry. Caspase activity was detected by immunohistochemical analysis and enzyme cleavage of DEVD-AMC, a fluorescent substrate. Response to carbachol, a muscarinic receptor agonist, and EGF was measured by Ca2+ mobilization and influx. Fas-mediated apoptosis was significantly inhibited in Bcl-2 and Bcl-xL transfectants compared to wild-type and control transfectants (empty vector). Surprisingly, caspase activity was not inhibited in Bcl-2 and Bcl-xL transfectants. Activation of the Fas pathway in the Bcl-2 and Bcl-xL transfectants by antibody also inhibited carbachol and EGF responsiveness (i.e., Ca2+ mobilization and/or influx) by 50-60%. This Fas-mediated inhibition of cell activation was partially or completely restored by specific peptide interference of caspase enzyme activity. The prevention of Fas-mediated apoptosis by the overexpression of Bcl-2 and Bcl-xL in salivary gland epithelial cells results in injured cells expressing caspase activity and unable to respond normally to receptor agonists. Such damaged cells may exist in SS patients and could explain the severe dryness out of proportion to the actual number of apoptotic cells seen on salivary gland biopsy.

Apoptosis↗

EGF inhibits muscarinic receptor-mediated calcium signaling in a human salivary cell line.

The effects of epidermal growth factor (EGF) on intracellular calcium ([Ca(2+)](i)) responses to the muscarinic agonist carbachol were studied in a human salivary cell line (HSY). Carbachol (10(-4) M)-stimulated [Ca(2+)](i) mobilization was inhibited by 40% after 48-h treatment with 5 x 10(-10) M EGF. EGF also reduced carbachol-induced [Ca(2+)](i) in Ca(2+)-free medium and Ca(2+) influx following repletion of extracellular Ca(2+). Under Ca(2+)-free conditions, thapsigargin, an inhibitor of Ca(2+) uptake to internal stores, induced similar [Ca(2+)](i) signals in control and EGF-treated cells, indicating that internal Ca(2+) stores were unaffected by EGF; however, in cells exposed to thapsigargin, Ca(2+) influx following Ca(2+) repletion was reduced by EGF. Muscarinic receptor density, assessed by binding of the muscarinic receptor antagonist L-[benzilic-4,4'-(3)HCN]quinuclidinyl benzilate ([(3)H]QNB), was decreased by 20% after EGF treatment. Inhibition of the carbachol response by EGF was not altered by phorbol ester-induced downregulation of protein kinase C (PKC) but was enhanced upon PKC activation by a diacylglycerol analog. Phosphorylation of mitogen-activated protein kinase (MAP kinase) and inhibition of the carbachol response by EGF were both blocked by the MAP kinase pathway inhibitor PD-98059. The results suggest that EGF decreases carbachol-induced Ca(2+) release from internal stores and also exerts a direct inhibitory action on Ca(2+) influx. A decline in muscarinic receptor density may contribute to EGF inhibition of carbachol responsiveness. The inhibitory effect of EGF is mediated by the MAP kinase pathway and is potentiated by a distinct modulatory cascade involving activation of PKC. EGF may play a physiological role in regulating muscarinic receptor-stimulated salivary secretion.

Binding, Competitive↗

[Influence of cleftpalate on middle ear conduction and eustachian function].

OBJECTIVE: To explore the influence and its degree of cleftpalate on middle ear conduction and eustachian function. METHOD: 41 cleftpalate patients (82 ears) were performed with otopharyngeal examinations, form of the ostium pharyngeum tubae auditivae observations and acoustic impedance measurements. The results were compared with healthy persons of normal hearing. RESULT: In the cases with cleftpalate, tympanic membrane pathological change incidence was 89.0% (73/82), ostium pharyngeum tubae auditivae of cracked shape was 59.5% (25/42), abnormal tympanogram was 83.1% (64/77), the negative rate of stapedius muscle reflex was 84.4% (65/77). There are significant different in comparison with healthy persons. In synthetic analyses, the rate of secretory otitis media with varied degree in the cleftpalate cases was 74.0% (57/77). CONCLUSION: There was a high incidence of middle ear pathological change and secretory otitis media in the cleftpalate patients. This high incidence was due to susceptivity of the nasopharynx on the infection, weak strength of the dilator tubae eustachii and the deformed shape of the ostium pharyngeum tubae auditivae.

Acoustic Impedance Tests↗

[Experimental study and clinical application on osteogenesis of percutaneous autogenous bone marrow grafting in bone defects].

OBJECTIVE: To observe the osteogenesis of percutaneous autogenous bone marrow grafting in cicatricial bone defect, to seek a good method for treating fracture nonunion. METHODS: Eighteen rabbits were adopted in this study. 1 cm bone defect model was made in each side of radius, 6 weeks later, 2 ml autogenous bone marrow was injected in the right radial bone defect as experimental group, 2 ml autogenous peripheral blood in the left side as control group. X-ray features, histologic changes, Ca and P content in the site of bone defect were studied in various times. Also 15 patients were treated clinically for the nonunion fracture, the average time from nonunion to bone marrow grafting was 13 months. RESULTS: In experimental group, the increasing new bone tissue were observed in X-ray and histologic examination. While in control group, no osteogenesis was observed. Ca and P content of experimental group was higher than that of control group. For the 15 patients, 13 cases healed in 5-9 months, 2 cases failed. CONCLUSION: Percutaneous autogenous bone marrow grafting is capable of osteogenesis in the cicatricial bone defects. It can be used in nonunion cases which are not fit for operation of bone grafting because of poor condition of the skin.

Adolescent↗

[The comparative study of the ultra-light anaesthesia between N(2)O inhalation and propofol intravenous in tooth extraction]

OBJECTIVE:To study the effect of N(2)O inhalation and propofol intravenous anaesthesia in tooth extraction. METHODS: 40 dental outpatients with the extraction of the mandibular wisdom tooth,ASAI,were randomly allocated to two groups:N(2)O group with the age of 20-36 years old and propofol group with the age of 21-35 years old.All cases undergoing dental extraction were given ultra-light anaesthesia as an adjunct local anaesthesia. RESULTS: The two groups were gained various levels of sedation,there were no significant difference among BP,HR,RR,SPO(2) before,in,and after the operation.Dental treatment could be carried out in cooperating conditin throughout the whole procedure.There was a certain extent of amnesia postoperation,the incidence of postoperative side effects was low,the recovery time was gained within 30 minutes. CONCLUSION: The analgesic effects of N(2)O group were superior to the propofol group.

Journal Article↗

Activation of purinergic receptors triggers oscillatory contractions in adult rat ventricular myocytes.

Extracellular ATP is an important neurotransmitter that modulates cardiac function by activation of purinergic receptors. In this study, the effect of P2 purinergic receptor activation on contractions and on [Ca2+]i was investigated in adult rat ventricular myocytes. Fura 2 was used to measure [Ca2+]i, and video edge detection was used to measure contraction. Superfusion of 2-methylthio-adenosine-5'-triphosphate (2-M-S-ATP) over quiescent myocytes induced oscillations in contraction and in [Ca2+]i. The frequency of the oscillatory contractions increased with increasing concentrations of 2-M-S-ATP, but the amplitude of contractions varied from cell to cell and was independent of the concentration of 2-M-S-ATP. During electrical stimulation, activation of purinergic receptors in myocytes potentiated the amplitude of contraction and induced arrhythmias. In populations of quiescent myocytes, the plateau phase of the [Ca2+]i signal evoked by 2-M-S-ATP could be shown to represent summed oscillations in [Ca2+]i in individual cells. Pretreatment of quiescent myocytes with thapsigargin or caffeine reduced or abolished the oscillations in contractions and in [Ca2+]i triggered by 2-M-S-ATP, indicating a dependence of the oscillations on uptake and release of Ca2+ by the sarcoplasmic reticulum. These data demonstrate the novel phenomenon that activation of purinergic receptors in quiescent myocytes stimulates oscillations in [Ca2+]i and contraction. In electrically stimulated myocytes, activation of purinergic receptors triggers oscillatory contractions and potentiates the amplitude of electrically triggered contractions.

Adenosine Triphosphate↗

Experimental study of early diagnosis and treatment of fat embolism syndrome.

An experimental animal model has been established using i.v. fat injection to mimic fat embolism syndrome (FES). Fourteen healthy mongrel dogs who were administered 0.7 ml/kg of fluid marrow fat obtained from the long bone marrow cavity of mongrel dogs were divided into control and therapeutic groups. The therapeutic group (n = 7) was given dexamethasone (1.0 mg/kg) and repeated every 6 h i.v. During 48 h of observation, blood gas analysis and frozen sections were performed on blood samples collected from the pulmonary vessels by a floating catheter and from a peripheral vein at different time intervals. The frozen sections were stained with Oil Red O. Positive results were seen 2 h after fat injection in both pulmonary and peripheral blood samples of both control and therapeutic groups. By computer image analysis, the average median number of fat droplets per section and the average median diameter of fat droplets in pulmonary blood of the control group were found to be significantly higher and larger than were those of the therapeutic group. The average median number and diameter of fat droplets in pulmonary blood were significantly higher and larger than were those of peripheral blood in both control and therapeutic groups. These findings correlated well with blood gas changes and the clinical appearance of the experimental animals. The fat droplets from pulmonary or peripheral blood as demonstrated by Oil Red O staining in combination with blood gases changes [PaO2 < 7.99 KPa, difference between the alveolar and arterial oxygen tension (P(A - a)O2) > 6.09 KPa] may be a rapid method for screening of an earlier diagnosis of FES.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Caries prevalence and patterns in 3-6-year-old Beijing children.

A total of 400 Beijing children, 3-6-yr-old, equally distributed by age and sex, were examined for dental cares. Results were analyzed with the traditional dmfs/t index and with the Caries Analysis System. The system differentiated between caries patterns and examined the percentage of affected children (Prevalence), the degree to which these children were affected (Severity), and the proportion of total caries each disease pattern represented (Distribution). Over 67% of the children experienced caries, a level comparable to other reports from China and other developing countries, but 50% greater than those seen in United States preschool children. Nearly all children with caries experienced fissure caries. In 3-yr-olds maxillary anterior caries was the next most prevalent pattern with 43% affected, whilst in the 6-yr-olds, posterior proximal caries was the second most prevalent pattern with 68% affected. Since maxillary anterior caries was so prevalent, and because the presence of this pattern has been shown to be a risk factor for future caries, preventing the maxillary anterior pattern may markedly reduce caries in this population.

Age Distribution↗

Evaluating the social impact and effectiveness of four-year "Love Teeth Day" campaign in China.

A massive campaign on "Love Teeth Day" (LTD) has been celebrated nationwide each year in China since 1989. As announced in an official document, nine government and non-government organizations have jointly issued a circular designating that the 20th of September of each year be kept for the Love Teeth Festival in this country. The main activities were planned and conducted by the National Committee for Oral Health, which was set up in 1988. It aims to motivate the people's awareness of dental self-care, participation, and to promote community involvement in oral health education programs. For feedback, two types of questionnaires were designed and sent to the public and the organizers, respectively, after each campaign, and then returned to the office for data processing. The findings from a four-year study indicated that: (1) The activities started from three municipalities, 29 capitals of provinces, and some large cities (1989), and spread to most cities in the urban area, and about 300 counties in the rural area (1992); (2) 14,000 dental professionals and health workers participated in 1989 as information providers, and increased to 40,000 in 1992; (3) oral health knowledge has increased to 76.2% (1992) from 37% (1989); and (4) the people's will in dental prevention was strengthened.

Child↗

Compartmentalization of Ca2+ signaling and Ca2+ pools in pancreatic acini. Implications for the quantal behavior of Ca2+ release.

Streptolysin O-permeabilized pancreatic acini were used to study compartmentalization of Ca2+ signaling and Ca2+ pools. In these cells, the inositol 1,4,5-trisphosphate (IP3)-dependent Ca2+ channels could be activated by a number of agonists (carbachol, cholecystokinin, or bombesin) or by activation of the entire cellular phospholipase C pool with GTP gamma S. Surprisingly, each of the antagonists interacting with acinar cells inactivated the channels after stimulation with GTP gamma S. In addition, when permeabilized cells were stimulated with more than one agonist, any antagonist to the specific agonists employed inactivated the channels. The aberrant behavior of the antagonists in permeable cells was not related to a loss of specificity since (a) when added before GTP gamma S, the antagonists had no effect on Ca2+ release and (b) when cells were stimulated with a single agonist, the antagonists prevented only the effect of their specific agonist. The differential behavior of the antagonists in intact and permeable cells suggests a compartmentalization of Ca2+ signaling into separate, agonist-specific units that is modified by cell permeabilization. Further evidence for compartmentalization of signaling was obtained by showing that the partial agonist (the CCK octapeptide analogue JMV-180) can access and release only 50% of the cholecystokinin- or IP3-mobilizable Ca2+ pool in intact and permeable cells. Kinetic measurements revealed a multiphasic time course of agonist-evoked Ca2+ release in permeable cells. At high agonist concentrations, all phases were fast and merged into an apparent single event of Ca2+ release. The phases were separated by three independent protocols: reduction in agonist concentrations, addition of heparin, or addition of guanosine-5'-O-(thio)diphosphate. Since all protocols that caused phase separation reduce IP3-mediated Ca2+ release, these findings demonstrate heterogeneity in the affinity for IP3 of channels present in compartmentalized Ca2+ pools of the same cells. Compartmentalization of signaling and the heterogeneity in the affinity for IP3 resulted in a quantal agonist-evoked Ca2+ release. The overall findings are discussed in the context of an integrated model of compartmentalization of signaling complexes, Ca2+ pools, and IP3-activated Ca2+ channels.

Animals↗

Antagonists inactivate the inositol 1,4,5-trisphosphate (Ins-1,4,5-P3)-dependent Ca2+ channel independent of Ins-1,4,5-P3 metabolism.

Streptolysin O-permeable pancreatic acini, which retain intact signaling systems, were used to study the regulation of the inositol 1,4,5-trisphosphate (Ins-1,4,5-P3)-activated Ca2+ channel during agonist stimulation and antagonist inhibition. Stimulation of permeable cells with carbachol induced rapid Ca2+ release from internal stores. Addition of heparin prior to or after agonist stimulation inhibited the release, indicating the activation of the Ins-1,4,5-P3-dependent Ca2+ channels by the agonist. Termination of cell stimulation with the specific antagonist atropine rapidly inactivated the release channels. Channel inactivation by the antagonist was independent of Ins-1,4,5-P3 levels since (a) addition of atropine to carbachol-stimulated cells resulted in a slow hydrolysis of Ins-1,4,5-P3, (b) addition of 10-fold excess Ins-1,4,5-P3 together with the agonist did not prevent channel inactivation by the antagonist, and (c) the antagonist inactivated Ca2+ release in the presence of saturating concentration of the nonhydrolyzable Ins-2,4,5-P3. Hence, the antagonist appears to stabilize the Ins-1,4,5-P3-activated Ca2+ channel in a state refractory to Ins-1,4,5-P3. These findings are the first direct evidence that the channel can exist in such a refractory state.

Animals↗