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X Meng

Publications and source records attributed to X Meng.

At least 37 records · Page 2Linked to original sources

Vascular cell adhesion molecule--1 expression is obligatory for endotoxin-induced myocardial neutrophil accumulation and contractile dysfunction.

BACKGROUND: Sepsis-induced cardiac dysfunction occurs commonly in critically ill patients and is associated with high mortality rates. Neutrophils play a central role in sepsis-induced lung and liver injury; however, the mechanism of sepsis-induced cardiac dysfunction remains unclear. Vascular cell adhesion molecule-1 (VCAM-1) has been implicated in neutrophil-mediated liver injury during endotoxemia and is also expressed in myocardium. The purposes of this study were to examine the temporal relationship of myocardial VCAM-1 expression with neutrophil accumulation during endotoxemia and to determine whether VCAM-1 mediates neutrophil accumulation and cardiac dysfunction during endotoxemia. METHODS: Mice were subjected to lipopolysaccharide (LPS; 0.5 mg/kg, intraperitoneally). Myocardial VCAM-1 expression and neutrophil accumulation were determined by immunofluorescence staining. Cardiac performance with or without VCAM-1 blocking antibody (5 mg/kg, intravenously) was determined by the Langendorff technique. RESULTS: LPS caused a time-dependent increase in both myocardial VCAM-1 expression and neutrophil accumulation. At 6 hours after LPS, the immunofluorescent intensity for VCAM-1 increased from 2.5 +/- 0.6 x 10(6) in saline solution controls to 19.9 +/- 3.5 x 10(6) (P <.05, analysis of variance), and neutrophil count increased from 2.4 +/- 1.7/mm(2) in saline solution controls to 13.0 +/- 2.5/mm(2) (P <.05). Left ventricular developed pressure was decreased maximally at 6 hours after LPS compared with saline solution controls (29.1 +/- 1.1 mm Hg vs 53.1 +/- 3.9 mm Hg; P <.05). Treatment with VCAM-1 monoclonal antibody abrogated both myocardial neutrophil accumulation and cardiac dysfunction during endotoxemia. CONCLUSIONS: LPS-induced myocardial dysfunction is associated with increased expression of VCAM-1 and with neutrophil accumulation. Blockade of VCAM-1 abrogates myocardial neutrophil accumulation and preserves cardiac function during endotoxemia, which supports a role for VCAM-1 as a therapeutic target for myocardial protection during sepsis.

Animals↗

Divergence of volatile anesthetic effects in inhibitory neurotransmitter receptors.

BACKGROUND: The mechanism of volatile anesthetic (VA) action is unknown. Inhibitory receptors for the neurotransmitters gamma-aminobutyric acid (GABA) or glycine are typically positively modulated by VAs and may be important targets for their action. The existence of a GABA receptor subtype (p), which is uniquely inhibited by VAs, suggested a chimeric receptor approach to identify portions of these proteins that may be necessary for anesthetic effects. METHODS: A silent mutation resulting in the addition of a unique restriction enzyme recognition site was introduced in GABA receptor type A alpha2, glycine alpha1, and p subunit cDNAs. Chimeras were constructed by rejoining restriction digest fragments and were expressed in Xenopus oocytes. Modulation of submaximal agonist-evoked peak currents by the VAs chloroform, enflurane, halothane, or isoflurane was measured using two-electrode voltage clamp. RESULTS: Four chimeras were constructed and designated glyrho, rhogly, alpha2rho, and rhoalpha2. Glyrho formed glycine-gated receptors with currents that were enhanced by chloroform or halothane but were inhibited by enflurane or isoflurane. Chimeras rhogly and rhoalpha2 each formed GABA-gated receptors with currents that were inhibited by chloroform or halothane but enhanced by enflurane or isoflurane. CONCLUSIONS: These data show, for the first time, functional divergence of VA action on a single protein target. The VAs in this study fall into two distinct groups with respect to their effects on these receptors. This grouping parallels the chemistry of these compounds. Our results support the involvement of multiple protein domains in the mechanism of VA modulation of GABA and glycine receptors.

Amino Acid Sequence↗

Post-hemorrhagic shock mesenteric lymph lipids prime neutrophils for enhanced cytotoxicity via phospholipase A2.

Hemorrhagic shock induced mesenteric hypoperfusion has long been implicated as a key event in the pathogenesis of the adult respiratory distress syndrome (ARDS) and multiple organ failure (MOF). Previous work links post-hemorrhagic shock mesenteric lymph (PHSML) lipids and neutrophil (PMN) priming in the pathogenesis of ARDS. We hypothesize that gut phospholipase A2 (PLA2) liberates proinflammatory lipids following hemorrhagic shock, which are responsible for enhanced PMN cytotoxicity. Mesenteric lymph was collected from rats (n > or = 5) before hemorrhagic shock, during hemorrhagic shock (MAP 40 mm Hg x 30 min), and after resuscitation (shed blood + 2x lactated Ringers). PMNs were incubated with physiologic concentrations (1-5%, v:v) of (a) buffer control, (b) sham (c) pre-shock lymph, (c) PHSML, (d) PHSML lipid extracts, (e) heat-denatured PSHML, and (f) PHSML harvested after i.v. pretreatment with a known PLA2 inhibitor (quinacrine, 10 mg/kg). PMNs were activated with fMLP (1 micromol), and the maximal rate of superoxide production measured by reduction of cytochrome c. Gut morphology was assessed histologically using hematoxalin and eosin (HE) staining. PHSML and PHSML lipid extracts (5%, v:v) primed for enhanced superoxide production compared to buffer controls (2.5-fold and 3.6-fold), sham (2.5-fold) and pre-shock lymph (2.0-fold). Lymph collected after systemic PLA2 inhibition, in contrast, abrogated the PMN priming response. Gut mucosal morphology, at end-resuscitation, was intact on HE staining both with and without PLA2 inhibition. Heat denaturing the PHSML (eliminating cytokines and complement), on the other hand, did not reduce PMN priming. Physiologic concentrations of PHSML lipids prime the PMN respiratory burst. Lymph priming is diminished with systemic PLA2 inhibition, implicating gut PLA2 as a source of proinflammatory lipids that may be central in the pathogenesis of hemorrhagic shock induced ARDS/MOF.

Animals↗

Differential cardiopulmonary recruitment of neutrophils during hemorrhagic shock: a role for ICAM-1?

Hemorrhagic shock and subsequent resuscitation can result in acute lung injury and cardiac dysfunction. Previous studies have demonstrated that tissue neutrophil accumulation contributes to cardiopulmonary injury associated with trauma. Thus, suppression of tissue neutrophil recruitment in an early therapeutic window after hemorrhagic shock may protect the cardiopulmonary system. It is unclear whether hemorrhagic shock induces cardiopulmonary recruitment of neutrophils before resuscitation. Intercellular adhesion molecule-1 (ICAM-1) is one of the important factors that mediate tissue neutrophil recruitment. The physiologic significance of ICAM-1 expression after hemorrhage before resuscitation is not well delineated. The present study examined the role of ICAM-1 in neutrophil accumulation in the heart and lung after severe hemorrhage without resuscitation. Mice were subjected to hemorrhagic shock by removal of 30% of total blood volume. Lung neutrophil number as determined by immunofluorescent staining increased by 1 h after hemorrhage and was maximal at 4 h whereas myocardial neutrophil number was not changed. Lung neutrophil accumulation was not associated with an up-regulation of ICAM-1 expression or an alteration in ICAM-1 subcellular distribution. Surprisingly, deletion of the ICAM-1 gene enhanced hemorrhagic shock-induced lung neutrophil accumulation. These results suggest that hemorrhagic shock induces preferential neutrophil accumulation to the lung that appears to occur independent of ICAM-1-expression.

Animals↗

TNF receptor I is required for induction of macrophage heat shock protein 70.

Expression of heat shock proteins (HSP) is an adaptive response to cellular stress. Stress induces tumor necrosis factor (TNF)-alpha production. In turn, TNF-alpha induces HSP70 expression. However, osmotic stress or ultraviolet radiation activates TNF-alpha receptor I (TNFR-I) in the absence of TNF-alpha. We postulated that TNF-alpha receptors are involved in the induction of HSP70 by cellular stress. Peritoneal Mphi were isolated from wild-type (WT), TNF-alpha knockout (KO), and TNFR (I or II) KO mice. Cells were cultured overnight and then heat stressed at 43 +/- 0.5 degrees C for 30 min followed by a 4-h recovery at 37 degrees C. Cellular HSP70 expression was induced by heat stress or exposure to endotoxin [lipopolysaccharide (LPS)] as determined by immunoblotting. HSP70 expression induced by either heat or LPS was markedly decreased in TNFR-I KO Mphi, whereas TNFR-II KO Mphi exhibited HSP70 expression comparable to that in WT mice. Expression of HSP70 after heat stress in TNF-alpha KO Mphi was also similar to that in WT mice, suggesting that induction of HSP70 by TNFR-I occurs independently of TNF-alpha. In addition, levels of steady-state HSP70 mRNA were similar by RT-PCR in WT and TNFR-I KO Mphi despite differences in protein expression. Furthermore, the effect of TNFR-I appears to be cell specific, since HSP70 expression in splenocytes isolated from TNFR-I KO was similar to that in WT splenocytes. These studies demonstrate that TNFR-I is required for the synthesis of HSP70 in stressed Mphi by a TNF-independent mechanism and support an intracellular role for TNFR-I.

Animals↗

L-arginine attenuates lipopolysaccharide-induced lung chemokine production.

Chemokines stimulate the influx of leukocytes into tissues. Their production is regulated by nuclear factor-kappaB (NF-kappaB), an inducible transcription factor under the control of inhibitory factor kappaB-alpha (IkappaB-alpha). We have previously demonstrated that L-arginine (L-Arg) attenuates neutrophil accumulation and pulmonary vascular injury after administration of lipopolysaccharide (LPS). We hypothesized that L-Arg would attenuate the production of lung chemokines by stabilizing IkappaB-alpha and preventing NF-kappaB DNA binding. We examined the effect of L-Arg on chemokine production, IkappaB-alpha degradation, and NF-kappaB DNA binding in the lung after systemic LPS. To block nitric oxide (NO) production, a NO synthase inhibitor was given before L-Arg. LPS induced the production of chemokine protein and mRNA. L-Arg attenuated the production of chemokine protein and mRNA, prevented the decrease in IkappaB-alpha levels, and inhibited NF-kappaB DNA binding. NO synthase inhibition abolished the effects of L-Arg on all measured parameters. Our results suggest that L-Arg abrogates chemokine protein and mRNA production in rat lung after LPS. This effect is dependent on NO and is mediated by stabilization of IkappaB-alpha levels and inhibition of NF-kappaB DNA binding.

Animals↗

A low level of TNF-alpha mediates hemorrhage-induced acute lung injury via p55 TNF receptor.

Acute lung injury after hemorrhagic shock (HS) is associated with the expression of tumor necrosis factor (TNF)-alpha in the lung. However, the role of TNF-alpha and its receptors in this pulmonary disorder remains obscure. This study examined the temporal relationship of pulmonary TNF-alpha production to neutrophil accumulation during HS and determined the role of TNF-alpha in neutrophil accumulation and lung leak. HS was induced in mice by removal of 30% of total blood volume. Lung TNF-alpha was measured by ELISA. Neutrophil accumulation was detected by immunofluorescent staining, and microvascular permeability was assessed using Evans blue dye. Although HS induced a slight and transient increase in lung TNF-alpha, neutrophil accumulation preceded the increase in TNF-alpha. However, lung neutrophil accumulation and lung leak were abrogated in TNF-alpha knockout mice, and both were restored by administration of recombinant TNF-alpha to TNF-alpha knockout mice before HS. Neutrophil accumulation and lung leak were abrogated in mice lacking the p55 TNF-alpha receptor, but neither was influenced by p75 TNF-alpha receptor knockout. This study demonstrates that a low level of pulmonary TNF-alpha is sufficient to mediate HS-induced acute lung injury during HS and that the p55 TNF-alpha receptor plays a dominant role in regulating the pulmonary inflammatory response to HS.

Acute Disease↗

[Expression of rasp21, C-myc, C-erbB-2, and AFP in 2-FAA induced experimental hepatocarcinogenesis].

OBJECTIVE: To investigate the distribution of oncogenes and their relationships in 2-FAA induced experimental hepatocarcinogenesis. METHODS: Rasp21, C-myc, C-erbB-2, and AFP were detected and analyzed by the SP method of immunohistochemistry. RESULTS: Some cells expressed rasp21, C-myc, and AFP in peripheral liver lobules and alternated hepatocyte foci in the early stage of the experiment. And with the formation and progression of hyperplastic hepatocytic nodules, expressed cells increased and often accompanied each other. Expression of C-erbB-2 appeared in the middle stage of the hepatocarcinogenesis. CONCLUSIONS: Expression of rasp21, C-myc, and AFP in the experimental hepatocarcinogenesis is an early molecule change, which may relate to the initiation of hepatocarcinogenesis and be considered to be one of the molecular bases for the morphogenesis of hepatocarcinogenesis. During the development of lesion, C-erbB-2 may have promoting effects. It is also clear that malignant transformation of hepatocyte needs the cooperation of multiple oncogenes.

2-Acetylaminofluorene↗

Formation and identification of 4'-O-methyl-(-)-epigallocatechin in humans.

The possible beneficial effects of tea consumption have attracted a great deal of attention. Many of the biological effects have been attributed to tea catechins, but the metabolic fate of these compounds is not clear. In the present study, a major metabolite observed in human blood and urine samples after green tea administration was identified as a O-methylated derivative of (-)-epigallocatechin (EGC) by comparison with products from chemical and enzymatic O-methylation of EGC. The structure of this metabolite was elucidated as 4'-O-methyl-(-)-epigallocatechin (4'-O-MeEGC) by (1)H and (13)C NMR and heteronuclear multiple bond connectivity experiment. The human plasma level of 4'-O-MeEGC reached its peak value within the first 2 h following tea ingestion. Its maximum concentration was 4 to 6 times higher than that of EGC. The half-lives of EGC and 4'-O-MeEGC in the blood were 1.02 +/- 0.07 and 4.39 +/- 1.14 h, respectively. The amount of 4'-O-MeEGC excreted in urine was about 3 times higher than that of EGC, and 88% of 4'-O-MeEGC was excreted in urine within 8 h. The present structural information and concentration-time profile of this metabolite provide the basis for understanding the biotransformation of EGC and for future elucidation of its biological activities.

Catechin↗

[Significance on expressions of Annexin-I and its correlative gene proteins in endometrial hyperplasia, atypical hyperplasia and endometrial carcinoma].

OBJECTIVE: To investigate expression of Annexin-I in various endometrial lesions and its significance in differential diagnosis of endometrial borderline lesions. METHODS: We collected 37 specimens with different endometrial lesions, and reclassified them according to China and FIGO's standard, which included 12 cases of endometrial hyperplasia (EH), 10 cases of atypical hyperplasia (ATH) and 15 cases of endometrial carcinoma (EC). Immunohistochemical staining for AX-I, c-erbB-2, p53 protein, ER, PR, EGF and IGF were performed by LSAB. RESULTS: The results showed that for AX-I, 1 cases of EH was weakly positive and others were negative; 9 cases of ATH showed strong positivity in the cytoplasm and the cell membrane, and 1 weakly positive; 7 cases of EC were positive and 8 negative. c-erbB-2 was expressed in 9 cases of ATH and 1 was negative. Expressions of EGFR, ER and PR were strong in all cases, but IGFR was negative in almost all cases. P53 expression was higher in EC than in ATH. CONCLUSIONS: AX-I expression suggests that (1) AX-I protein may play an important role in the pathogenesis of cancer, the expression decreased and disappeared after malignant change. (2) High expression for AX-I can be used to differentiate ATH and EC. In addition, c-erbB-2 expression appeared to parallel the expression of AX-I in both ATH and EC, but in ATH it was higher than that in EC.

Annexin A1↗

[The effect of human follicular fluid on mouse embryo culture].

OBJECTIVE: To evaluate the effect of human follicular fluid (HFF) on mouse embryo culture. METHODS: Compare the effects of HFF and serum as a protein supplement on the in vitro development of mouse embryos. Measure the concentration of the epidermal growth factor (EGF) in HFF and human serum. RESULTS: HFF significantly enhanced the developmental potential of mouse embryos in vitro, even in the presence of meiotic inhibitors. HFF significantly increased frequency of development from the 2-cell stage to the 8-cell stage (72.9%), blastocyst stage (50.9%) and hatching (26.3%), compared with human serum(48.0%, 24.5%, 6.9%, P < 0.05). There was higher concentration of EGF with an average of 0.50 microgram/L in HFF group compared with human serum (0.26 microgram/L, P < 0.05). CONCLUSION: Human follicular fluid is effective in increasing the developmental potential of mouse embryos in vitro.

Animals↗

[Retrospective analysis of endometrial neoplasms treated by different therapeutic modalities].

OBJECTIVE: To compare the therapeutic effects of different remedies in patients with endometrial carcinoma. METHODS: Total of 386 patients with metracarcinoma underwent 3 different treatments: (1) operation only 145 cases; (2) operation and complemental radiotherapy 161 cases; (3) radiotherapy only 80 cases. Then they were followed up for 5 years and more. RESULTS: The 5-year survival rates of operation group were 78.9% (56/71), 61.0% (25/41) and 18.2% (6/33) in stage I, stage II, and stage III-IV respectively, for operation and complemental radiotherapy, they were 75.0% (33/44), 59.5% (44/74) and 48.8% (21/43), for radiotherapy, 34.8% (8/23), 18.8% (3/16) and 0.0% (0/41). There was no difference between operation group and operation plus radiotherapy in patients with stage I and stage II (P > 0.05). However the 5-year survival rates were significantly higher in operation plus complemental radiotherapy group and those only received operation in stage III stage IV patients (P < 0.001). And no matter in what stages, the therapeutic effect was worse in radiotherapy group than other two groups (P < 0.001). CONCLUSION: The remedies with operation as main measure are the best choice for metacarcinoma, radiotherapy merely is fit with those who can not be operated on.

Adult↗

[Experimental study and application of extracellular matrix of conjunctiva].

OBJECTIVE: To investigate the characteristics and application of extra-cellular matrix (ECM) of conjunctiva. METHODS: Pieces of conjunctival ECM were made, and then the conjunctival defect was repaired with that in an experimental group. Control group 1 received the heterogeneous conjunctiva, and in control group 2, the refrigerated ECM was used for transplantation. All of them were photographed and examined by light microscope, electron microscope (EM), immunohistochemical examination and lymphocyte toxicity test. RESULTS: There were blood vessels growing into the grafts on the 3rd day in the experimental group. The grafts became mildly congestive and similar to normal conjunctival ones in the 4(th) week. But in control group 1, the grafts became white and necrotic in the second week; the conjunctiva was congestive, cicatricial and hyperplastic in the 4(th) week. Under the light microscope, the epithelium covered the most part of the region with the graft in the 2nd week, covered completely in the 4(th) week, and its appearance was as an approximately normal conjunctival epithelium in the experimental group. But the epithelium became ulcerative and a lot of lymphocytes infiltrated in the 2nd week in control group 1. Under the EM, the line of demarcation between the covering region of the regenerative conjunctival epithelium and the naked ECM was quite clear in the 1st week in the experimental group. And the ultrastructure of regenerative conjunctival epithelium was basically the same as an normal one in the 8(th) week. Both before and after transplantation, the immunohistochemical examinations verified that ECM was type I and IV collagen. The lymphocyte toxicity test showed that no obvious humoral immunoreaction existed. CONCLUSION: Conjunctival ECM has the characteristics of tissue activity and low antigenicity. It is an ideal conjunctival succedaneum in the plastic surgery of conjunctiva.

Animals↗

[A discussion on diagnosis and typing of viral hepatitis].

OBJECTIVE: To bring forward a suggestion about clinical diagnostic standard and clinical typing for chronic and severe hepatitis. METHODS: To make a comprehensive study on clinical features and pathology of 895 cases of severe and chronic hepatitis, liver cirrhosis after hepatitis based on the viral prevention and control plan laid down in 1995. RESULTS: The chronic hepatitis can still be divided into mild, moderate and severe types clinically, but the PTA should be changed for normol-71, 70-61, 60-51, the A/G value for normal, 1.5-1.3, 1.2-1.0 respectively. ALT, BIL, alpha-globulin are kept unchanged. The albumin value can be cut out from the reference indexes of clinical typing for chronic hepatitis. Acute severe hepatitis can be divided into early stage (taking edema as the main type) and late stage (taking necrosis as the main type); subacute severe hepatitis can be divided into ascite type, coma type and mixed type; if those lacking of coma and ascite with PTA about 60%. 50% can be treated as earlier stage. Subacute and chronic severe hepatitis still can be divided into early, middle and late stages. The disease course of subacute severe hepatitis may prolong to six months. Chronic severe hepatitis can be divided into type B (typical chronic hepatitis type) type C (liver cirrhosis type) and type c (acute liver failure type developed from chronic hepatitis and viral carriers). CONCLUSIONS: The original procedure of 1995 are feasible on the whole.

Factor XI↗

[A study on bacterial contamination of dental handpieces].

OBJECTIVE: The aim of this study is to evaluate the effects of different factors, including concentration of the bacterial suspension, number of stops set on handpieces, and different disinfectants, on bacterial contamination of handpieces and their clinical significance. METHODS: Bacterial contamination of 20 handpieces were analyzed in different concentration of bacterial suspension, number of stops set on handpieces and after using different out surface disinfectants. RESULTS: Statistical increment (P < 0.05) of handpieces inside contamination was observed relevant to increment of the bacterial suspension concentration. No statistical relevance was seen between handpiece inside contamination and the number of stops set on handpieces(P > 0.05). Disinfection with different disinfectants significantly decreased out surface contamination(P < 0.05), but no statistical change of bacteria (P > 0.05) was observed inside handpieces. CONCLUSION: As the concentration of bacterial suspension is the key factor affecting the inside contamination of handpieces, oral cavity cleanness is essential before dental therapy. The surface disinfection of handpieces is necessary after dental therapy, but cannot prevent cross-contamination between patients.

Cross Infection↗

[The relationship between content of substance P, VIP in pharyngeal tissue and narrow pharyngeal cavity of patients with OSAS].

OBJECTIVE: To investigate the relationship between content of substance P, VIP in the pharyngeal tissue and narrow pharyngeal cavity of patients with OSAS. METHOD: By using semi-quantitative immunohistochemical method, resected pharyngeal tissue from 30 patients with OSAS and 12 normal health adult controls were investigated with rabbit anti-substance P and rabbit anti-VIP. RESULT: SP and VIP were detected in tribution within the epithelium or between epithelium cells, around the pharyngeal glands and gland ducts, around endothelium cells and smooth muscle of blood vessels. SP and VIP levels in pharyngeal tissue of the patients with OSAS were increased than those of the controls. CONCLUSION: Narrow of pharyngeal cavity with OSAS was relative to edema of pharyngeal tissue induced by increased SP and VIP in pharyngeal tissue. A neurogenic inflammation was one of the factors of OSAS.

Adult↗

[Clinical observation on effect of electroacupuncture therapy in treating superficial tumor].

OBJECTIVE: To investigate the clinical effect of electroacupuncture therapy (EAT) in treating superficial tumors. METHODS: The healthy tissue was protected by insulation sleeve, and the platinum electrodes served as needles was inserted into the tumor and connected to an EAT instrument using galvanic current. The electric voltage applied was 6-8 V, the electric current was in a range of 40-80 mA, and 80-100 coulomb electricity for 1 cm diameter of tumor mass was administered. RESULTS: In the 320 cases, 123 were complete remission (CR), 129 partial remission (PR), 36 with their tumor shrinked by 1/4 and 32 with size of tumor unchanged. The total effective rate (CR + PR) was 78.7%. CONCLUSION: EAT shows good effect in treating superficial tumor and provides a new therapeutic means for the patients with tumor of unresectable or relapsed. It is a simple, convenient, safe and effective method with less injury and quick recovery.

Adolescent↗

[An association study of histocompatibility leukocyte antigen-class II with Meniere's disease].

OBJECTIVE: To investigate the relation between histocompatibility leukocyte antigen (HLA)-class II DRB1 and Meniére's disease in Chinese. METHODS: Polymerase chain reaction-sequence specific primers (PCR-SSP) technique was used. HLA-class II allele distribution were measured in 60 patients with Meniére's disease, in comparison with those in 85 normal population. RESULTS: The results showed that the frequency of DRB1*09 allele was significantly lower in Meniére's disease patients than in those of controls (relative risk = 0.17, P < 0.01). CONCLUSION: HLA-DRB1*09 of the patients with Meniére's disease was significant low. It implied that DRB1*09 may be a protective gene for Meniére's disease.

Adolescent↗