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Biomedical subjects

Y Meng

Publications and source records attributed to Y Meng.

At least 73 records · Page 4Linked to original sources
PubMed1998

The effect of sequential injuries on splanchnic perfusion and eicosanoid release.

BACKGROUND: This study examines the hypothesis that sequential burn injury followed by intraabdominal sepsis induces significantly greater splanchnic hypoperfusion and reduced intestinal PGI2 release than either injury independently. MATERIALS AND METHODS: Anesthetized Sprague-Dawley rats were randomized to one of four groups: BURN (45% body surface area scald burn) + cecal ligation and puncture (CLP); BURN alone; CLP alone; or uninjured controls (SHAM). Twenty-four hours following injury, superior mesenteric artery (SMA) blood flow was measured with a doppler flow probe. Splanchnic eicosanoid release (6-keto-PGF1alpha, metabolite of PGE2; TxB2, metabolite of TxA2; and PGE2) was measured in mesenteric venous effluent utilizing an isolated, perfused bowel preparation. RESULTS: SMA blood flow was no different than that of controls 72 h following BURN injury alone; whereas CLP alone resulted in a 80% reduction in splanchnic blood flow when compared with controls (P < 0.001). SMA blood flow in animals sustaining BURN + CLP was only modestly reduced from controls (P = 0.04) and 3.6 times greater than that of animals sustaining CLP alone (P < 0.001). PGI2 was the dominant eicosanoid released by the intestine with levels 10 times greater than TxB2 and nearly 50 times greater than PGE2. CLP either alone or when combined with BURN was associated with a 60% decrease in splanchnic PGI2 release when compared to controls (P < 0.05). CONCLUSIONS: These data suggest that moderate BURN injury in rats attenuates the severe reduction in splanchnic perfusion associated with intraabdominal sepsis and that this occurs despite profound reductions in the release of the endogenous splanchnic vasodilator PGI2.

Animals↗
PubMed1998

Alveolar macrophage response to remote organ injury.

Intestinal reperfusion (IR)-induced pulmonary edema has been related to endogenous pulmonary thromboxane A2 (TxA2) release. This study examines the hypothesis that alveolar macrophages (aMphis) activated during IR are an important cellular source of TxA2 in this model. Anesthetized Sprague Dawley rats underwent 120 min of intestinal ischemia and 60 min of reperfusion (IR) or sham operation (Sham). aMphis were isolated by bronchoalveolar lavage and incubated in Krebs buffer for 30 min, after which the supernatant was analyzed for TxB2 (metabolite of TxA2) and prostaglandin E2. Other parameters of aMphi activation measured included lysosomal enzyme release (beta-glucuronidase), superoxide (O2-) release, and procoagulant activity. aMphis from animals sustaining IR generated more than twice as much TxA2 and prostaglandin E2 as did those isolated from controls (p < .05). Other evidence of aMphi activation included a nearly 100-fold increase in procoagulant activity, a 7-fold increase in beta-glucuronidase release, and a 2.5-fold increase in O2- release over that of controls (p < .05). These data suggest that TxA2 is a major eicosanoid product of aMphis during IR and that aMphis may be an important cellular participant in IR-induced pulmonary microvascular injury, either directly by releasing O2-, lysosomal enzymes, and pro-coagulant factors, or indirectly by generating TxA2.

Animals↗
PubMed1998

[Successful media exchange and network communication of CT digital image].

The digital image standard in medical is discussed. Based on the DICOM standard by using the media exchange and establishing the network communication between PC and CT system, we successfully acquired the CT original digital image and convert it to DICOM standard image. The CT image can easitly be read and adjusted on the PC platform.

Computer Communication Networks↗
PubMed1998

[Detection of HFRSV in Eulaelaps shanghaiensis and Ornithonyssus bacoti by using in situ hybridization].

AIM: To provide molecular biological evidence of transmission of hemorrhogic fever with renal syndrome virus (HFRSV) by gamasid mites, Eulaelaps shanghaiensis and Ornithonyssus bacoti. METHODS: Frozen sections of the gamasid mites 10 days and more than 100 days after biting suckling mice inoculated with HFRSV were in situ hybridized with dig-labelled HFRSV cDNA probes. RESULTS: RNA was detected in frozen sections of Eulaelaps shanghaiensis, after biting suckling mice inoculated with Hantaan (76-118) and Seoul (UR) virus, respectively. Most of the fine granules of the virus RNA were located in the nuclei, cytoplasm and nuclear membrane of cells of brain cortex, caeca and genitalia of the mites. In situ hybridization results showed that 17 of 31 mites in Hantaan group and 10 of 23 mites in Seoul group were positive. The virus RNA was still detected in tissues of the mites on d132 for Hantaan group and on d102 for Seoul group after infection, respectively. Among 20 Ornithonyssus bacoti detected 12 were positive on d10 after biting suckling mice inoculated with Hantaan virus, and the virus RNA was mainly found in the cells of genitalia (Figs. 1-13). CONCLUSION: Both Eulaelaps shanghaiensis and Ornithonyssus bacoti could be infected with HFRSV by biting HFRSV-positive mice. E. shanghaiensis could be infected with both Hantaan and Seoul virus, and the two types of HFRSV were found to be maintained in the mites for 132 days and 102 days, respectively. These confirmed that E. shanghaiensis and O. bacoti are suitable vectors and reservoirs of both Hantaan and Seoul virus and might play an important role in the cross transmission of the two types of HFRSV.

Animals↗
PubMed1998

[Studies on the experimental transmission of Rattus-borne Hantavirus by Ornithonyssus bacoti].

AIM: To demonstrate the role of rat mite (Ornithonyssus bacoti) in the transmission of Rattus-borne hemorrhagic fever with renal syndrome (HFRS). METHODS: In the transmission experiments, about 100 O. bacoti per pool were isolated and placed in a jar, unfed for 4 d at 23 +/- 1 degrees C. Suckling Wistar rats inoculated with Hantavirus strain Z45 or Seoul virus strain UR were placed in each jar for free attack by the mites for 12 hours. After 14 d the normal suckling Wistar rats were bitten by the mites. Fifteen days later, the lung tissues and sera of the infected rats were collected and detected for Hantaviral antigen by indirect fluorescent antibody technique (IFAT). For demonstration of the infection of O. bacti with Rattus-borne Hantavirus PCR technique was applied to detect Rattus-borne Hantaviral RNA. RESULTS: Sukling Wistar rats inoculted Hantavirus strain Z45 or Seoul virus strain UR were bitten by O. bacoti and then these mites were fed on 4 and 5 of normal suckling rats in each jar, respectively. The antigens of Hantavirus strain Z45 were positive in all the lungs of the normal rats bitten by the mites, the sera titers of the rats were from 1:10 to 1:40. The antigens were positive in 3 of the 4 rats, the sera titers were from 1:20 to 1:40. Both of the viruses could be maintained in O. bacoti for 22 days. The blocking test showed when 1:30 Hantavirus immunosera were exposed to the lung samples and then reacted with the sera from the patients with HFRS, all the specific fluorescence reactions of the samples were blocked, whereas the control group including the normal rat lung tissues and sera were all negative (Fig. 1). CONCLUSION: O. bacoti might play a role as the vector of HFRS and a reservoir host as well.

Animals↗
PubMed1998

[Determination of linear sintering shrinkage rate of slip-casting infiltrated ceramic].

This study tested the linear sintering shrinkage (SS) rate of ceramic infiltrated with different glasses (Vita In-ceram, G I-I La, G I-II La, G I-II Ce), the results showed that the linear SS rate was 0.08%-0.32%, which occurred mainly in the firing stage of alumina (P < 0.05) and glass infiltration had no influences on the dimensional stability of ceramic(P > 0.05). It suggests that the effects of glass infiltration on the dimensional stability of GI glasses were comparable with that of Vita In-ceram.

Aluminum Oxide↗
PubMed1997

Thromboxane A2 mediates increased pulmonary microvascular permeability after intestinal reperfusion.

This study examines the hypothesis that intestinal reperfusion (IR)-induced pulmonary thromboxane A2 (TxA2) release increases local microvascular permeability and induces pulmonary vasoconstriction. Sprague-Dawley rats underwent 120 min of intestinal ischemia and 60 min of IR. Sham-operated animals (Sham) served as controls. After IR or Sham, the pulmonary vessels were cannulated, and the lungs were perfused in vitro with Krebs buffer. Microvascular permeability was quantitated by determining the filtration coefficient (Kf), and pulmonary arterial (Ppa), venous (Ppv), and capillary (Ppc) pressures were measured to calculate vascular resistance (Rt). After baseline measurements, imidazole (TxA2 synthase inhibitor) or SQ-29,548 (TxA2-receptor antagonist) was added to the perfusate; then Kf, Ppa, Ppv, and Ppc were again measured. The Kf of lungs from IR animals was four times greater than that of Sham (P = 0.001), and Rt was 63% greater in the injured group (P = 0.01). Pc of IR lungs was twice that of controls (5.4 +/- 1.0 vs. 2.83 +/- 0.3 mmHg. IR vs. Sham, respectively; P < 0.05). Imidazole or SQ-29,548 returned Kf to baseline measurements (P < 0.05) and reduced Rt by 23 and 17%, respectively (P < 0.05). IR-induced increases in Pc were only slightly reduced by 500 micrograms/ml imidazole (14%; P = 0.05) but unaffected by lower doses of imidazole (5 or 50 micrograms/ml) or SQ-29,548. These data suggest that IR-induced pulmonary edema is caused by both increased microvascular permeability and increased hydrostatic pressure and that these changes are due, at least in part, to the ongoing release of TxA2.

Animals↗
PubMed1997

[Minor alkaloids from the capsule of Papaver nudicaule L].

Two minor alkaloids were isolated from the capsule of Papaver nudicaule. On the basis of physicochemical methods and spectroscopic analysis, they were identified as chelidonine, 5-hydroxy-2-hydroxymethylpyridine. Chelidonine was isolated from this plant and 5-hydroxy-2-hydroxymethylpyridine was isolated from genus for the first time.

Alkaloids↗
PubMed1996

Pharmacological potency and biodisposition of phencyclidine via inhalation exposure in mice.

The purpose of the present study was to characterize the pharmacological effects and biodisposition of phencyclidine (PCP) following inhalation exposure to mice. Results from these studies indicate that PCP was easily volatilized when heated in a glass pipe. Volatilization was efficient with no significant formation of pyrolytic products. Exposure to the volatilized PCP resulted in a dose-dependent impairment in motor performance in both the rotorod and inverted-screen tests. PCP was equally effective in disrupting performance on the inverted-screen and rotorod with ED50 values corresponding to the volatilization of 10.7 and 13.2 mumol, respectively. The time courses were comparable to those produced following intravenous (i.v.) administration of PCP. In order to determine the dose of drug absorbed by inhalation, mice were exposed to [3H]-PCP. The ED50 values of PCP following i.v. administration were 4.1 and 6.2 mumol/kg in the inverted screen and rotorod, respectively. The biodisposition of PCP following inhalation exposure was similar to that after i.v. injections. At doses that produced approximately 50% of the maximum motor impairment by either administration route, higher ratios of the total drug equivalents were found following i.v. injection than that after inhalation, with the brain/plasma ratios of 1.3 +/- 0.2 versus 0.58 +/- 0.02, and brain/body ratios 0.59 +/- 0.06 versus 0.35 +/- 0.1 for i.v. and inhalation, respectively. However, the brain/plasma ratios of the concentrations of PCP were similar, 1.1 versus 0.9. The body concentration of PCP equivalents that produced 50% of the maximum effect after inhalation was 4.7 +/- 0.6 mumol/kg. These results indicate that inhalation of PCP produces a similar pharmacological profile to that of i.v. administration and suggest that the drug is equipotent by these two administrations routes. Moreover, these findings are consistent with the observation that smoking is becoming the most common route of administration among drug users.

Administration, Inhalation↗
PubMed1996

Estrogen increases male rat aortic endothelial cell (RAEC) PGI2 release.

Estrogen has been proposed as a negative risk factor for development of peripheral vascular disease yet mechanisms of this protection are not known. This study examines the hypothesis that estrogen stimulates rat aortic endothelial cell (RAEC) release of PGI2. Male Sprague-Dawley rat abdominal aortic 1-mm rings were placed on 35 mm matrigel plates, and incubated for 1 week. The cells were transferred to a Primaria 60-mm dish and maintained from passage 3 in RAEC complete media and experiments performed between passages 4-10. Cells were incubated with Krebs-Henseleit buffer (pH 7.4) containing carrier or increasing concentrations of beta-estradiol or testosterone for 60 min. The effluent was analyzed for eicosanoid release of 6-keto-PGF1 alpha (6-keto, PGI2 metabolite), PGE2 and thromboxane B2 (TXB2) by EIA (hormone stimulated-basal). Cells were analyzed for total protein by the Bradford method and for cyclooxygenase-1 (COX-1) and prostacyclin synthase (PS) content by Western blot analysis and densitometry. Testosterone did not alter RAEC 6-keto-PGF1 alpha release, whereas estrogen increased RAEC 6-keto-PGF1 alpha release in a dose-related manner. Estrogen preincubation (10 ng/ml) decreased COX-1 and PS content by 40% suggesting that the estrogen-induced increase in male RAEC PGI2 release was not due to increased synthesis of COX-1 or PS. These data support the hypothesis that estrogen stimulation can increase endogenous male RAEC release of PGI2.

6-Ketoprostaglandin F1 alpha↗
PubMed1996

Inhalation exposure to volatilized opioids produces antinociception in mice.

The goal of this study was to determine whether opioids of varying potencies are pharmacologically active via the inhalation route of administration in mice. The opioids evaluated included heroin, morphine, codeine, fentanyl and meperidine; each of these drugs has the potential for abuse in humans. Inhalation exposure to each of these compounds produced antinociception in a dose-dependent manner as assessed in the tall-flick test. No pyrolysis products were detected after heating either morphine or codeine at 250 degrees C for 5 min. Although 6-acetylmorphine was found after heating heroin, it accounted for less than 5% of the recovered sample. Heroin was somewhat less potent by inhalation administration than i.v. injection, with ED50 values of 1.6 and 0.69 mumol/kg, respectively. In contrast, the relative potency of morphine was substantially greater when inhaled than when injected, with respective ED50 values of 0.77 and 3.9 mumol/kg. Whereas the body to brain ratios of [3H]morphine were approximately 8 and 20 for inhalation exposure and i.v. injection, respectively, the ratio for heroin was approximately 5 regardless of administration route. This pattern of results suggests that the increase in morphine potency upon inhalation may have resulted from an increased accessibility to the brain compared with i.v. injection. Finally, naloxone reversed the antinociceptive effects of volatilized heroin, but neither the kappa selective antagonist nor-binaltorphimine nor the delta selective antagonist naltrindole blocked this antinociception, which suggests the involvement of mu opioid receptors. These findings taken together suggest the potential for the abuse of a variety of opioids, in addition to heroin, through the inhalation route of administration by humans.

Administration, Inhalation↗
PubMed1996

[A study on p53 gene mutation, protein expression and relationship with clinico-pathological status in large cell carcinoma of the lung].

Immunohistochemistry and in situ hybridization techniques were used to investigate the correlation between p53 gene mutation and the clinico-pathological status as well as prognosis of large cell carcinoma of the lung. p53 expression was found in 40% of the cases by immunohistochemistry and p53 gene mutation was found in 53.3% by in situ hybridization. The concordance ratio was 73.3% between gene mutation and protein expression. No statistically significant correlation was found between p53 gene mutation, its protein expression and sex, age, smoking, histological type, tumor size or lymph node involvement. A significant correlation was found between p53 gene mutation (or its protein expression) and mitotic index. The result of in situ hybridization demonstrated that there was a statistically significant correlation between p53 gene mutation and a poor prognosis. It was found that p53 gene mutation was associated with fast growth of the tumor. Therefore p53 gene mutation is probably an indicator of poor prognosis for large cell carcinoma of the lung.

Adult↗
PubMed1996

[A pathological study on phenotype differentiation and its significance in pulmonary large cell carcinoma].

This study was designed to find the differentiated phenotype and its clinicopathological significance in pulmonary large cell carcinoam (PLCC) by immunohistochemical methods using a panel of antibodies related to the phenotype differentiation: high molecular weight cytokeratin, low molecular weight cytokeratiin, secretory component, chromogranin A and synaptophysin in 60 cases of PLCC. The results demonstrated that all cases of PLCC possessed monophasic, biphasic and triphasic phenotype differentiation features respectively, including squamous (4 cases), adenomatous (20 cases), neuroendocrine (19 cases), adenosquamous (11 cases); and the the coexistence of adenomatous, squamous and neuroendocrine (6 cases). The median survival time was different between patients with various differentiated phenotypes of PLCC. There was a statistically significant difference (P < 0.05) in survival between neuroendocrine and adenomatous phenotypes. The results of this study implies that: (1) PLCC expressed different phenotypes of differentiation, (2) phenotypes of neuroendocrine differentiation has a poor prognosis, (3) it is necessary to classify PLCC according to the phenotype differentiation.

Carcinoma, Non-Small-Cell Lung↗
PubMed1995

Loss of transcriptional attenuation in N-myc is associated with progression towards a more malignant phenotype.

The modulation of RNA polymerase II processivity through the untranslated N-myc first exon represents an important mechanism governing N-myc mRNA levels during normal development. In this study, we employed the rat embryo fibroblast (REF) cooperation assay as a functional means to (i) map N-myc first exon sequences involved in the regulation of N-myc gene expression and specifically their contribution to controlling a block to transcriptional elongation and (ii) determine whether this transcriptional control mechanism plays a role in governing the oncogenic activity of N-myc. Transfection of N-myc expression constructs harboring various deletions within the untranslated first exon revealed that a region encoding a potential stem-loop structure followed by a thymine stretch (stem-loop/T region) was required for efficient transcriptional attenuation. The increase in transcriptional read-through associated with all deletions involving the stem-loop/T region also resulted in a more aggressive malignant phenotype as evidenced by a significant enhancement in the subcloning efficiency of N-myc/ras transformed foci. Most significantly, when cell lines generated from overexpression of the intact N-myc expression construct were selected for anchorage-independent growth, a strong block to transcriptional elongation was completely eliminated in all cases examined. Since the subcloning efficiency of transformed foci and the capacity of permanently established cell lines for anchorage-independent growth are direct correlates of more advanced stages of malignant transformation, our findings suggest that loss of transcriptional attenuation represents an important genetic event in the progression of N-myc-induced cellular transformation.

Animals↗
PubMed1995

IFN-gamma-dependent IL-7 gene regulation in keratinocytes.

IL-7 plays a central role in regulating the growth and differentiation of T cells. We have reported previously that epidermal keratinocytes produce biologically relevant amounts of IL-7, thereby supporting the growth of epidermal gamma delta T cells. In this report, we report that IL-7 gene expression is regulated in keratinocytes by IFN-gamma. Treatment of Pam 212 keratinocytes with IFN-gamma induced a preferential expression of 2.6- and 1.5-kb IL-7 mRNAs, in addition to the 2.9- and 1.7-kb mRNAs that are expressed constitutively. The 2.6- and 1.5-kb mRNAs are produced through the use of alternative transcription initiation sites; these mRNAs are transcribed within 250 bp from the coding sequence, whereas 2.9- and 1.7-kb mRNAs contain > 400 bases in the 5'-untranslated region. IFN-gamma appears to promote this conversion through the IFN-stimulated response element (ISRE), which is located 270 bp upstream from the coding sequence. ISRE is followed by the initiator, a non-TATA-type transcription control element. Functional relevance of the ISRE/initiator complex was suggested by the observations that IFN-gamma-dependent transcription was initiated from immediately downstream of this complex, and that its deletion resulted in an abrogated IFN-gamma responsiveness in transcriptional regulation. These results document a novel mechanism by which IL-7 gene expression is regulated in keratinocytes by a cytokine produced by T cells (IFN-gamma).

Animals↗
PubMed1995

Determination of the protein components of native thin filaments isolated from natural actomyosin: nebulin and alpha-actinin are associated with actin filaments.

A new method was developed for extracting natural actomyosin with full length connectin (titin) and nebulin from rabbit skeletal muscle. To determine the protein components of native thin filaments, thin filaments were isolated from natural actomyosin by sedimentation in a H2O/D2O/sucrose density gradient. Both alpha-actinin and nebulin were cosedimented with actin filaments, while connectin was not. This shows that the native thin filaments contained alpha-actinin and nebulin. This indicates that the native thin filaments were more complicated than synthetic filaments reconstituted from actin, tropomyosin, and troponin. It is known that synthetic filaments are less Ca2+ sensitive than native thin filaments. This difference in Ca2+ sensitivity may be due to the differences in components and/or the different structures of native and synthetic filaments. The newly developed methods described here for extracting natural actomyosin and for isolating native thin filaments are useful for addressing these important problems related to the structure and function of native thin filaments.

Actinin↗