Biomedical subjects

H Meng

Publications and source records attributed to H Meng.

At least 91 records · Page 5Linked to original sources

PubMed1996

[Association of polymorphism in 5'-regulatory region of angiotensinogen gene with essential hypertension].

The association of the variant in the 5'-regulatory region of angiotensinogen gene with primary hypertension in the Han Nationality in China was studied by applying PCR-SSCP analysis and DNA cycle sequencing. The frequencies of three identified SSCP-patterns (pattern-A, B, C) in 73 hypertensive subjects were compared with those in 74 normal controls. It was found that the number of pattern-C was higher in the study group (5/73) than in the controls (1/74). The results of DNA sequencing showed that the difference of three SSCP-patterns was caused by a nucleotide substitution G-->A at -216 locus in the 5'-upstream region of angiotensinogen gene, and the subjects with pattern-C were homozygous for mutant A-allele (genotype A/A). These results suggest that the identified gene variant may be associated with primary hypertension.

Aged↗

PubMed1996

[On diagnostics of malignant meningioma and invasive meningioma].

We have made a clinicopathological study of 90 cases of malignant meningiomas and 18 cases of invasive meningiomas. The results show that the diagnostic features of malignant meningioma include increased cellularity, nuclear pleomorphism, tumorous giant cells, numerous mitotic figures, focal necrosis, cystic change and hemorrhage. The diagnosis of malignant meningioma can be more positively made when invasive growth, recurrence and metastasis are present. In making the diagnosis of invasive meningioma, both changes of benign meningioma and invasive growth should be present.

Adolescent↗

PubMed1996

[Report of clinical use of fixed-removable prosthesis].

Thirty-two patients provided with the fixed-removable prosthes is were followed up 3 month to 2.5 years. A total of 52 abutments were included, 17 of which were telescopic retainer, 14 were bar attachment retainer, 4 were rod attachment, 12 were stud attachment and 5 were slide attachment. Few technical failures were recorded. All found the prosthesis satisfactory and well functioning.

Adult↗

PubMed1996

[Evaluation of ligature-induced periodontitis in minipig].

We evaluated the progressing period of ligature induced periodontitis in chinese minipig. Plaque index (PLI), bleeding index (BI), probing pocket depth (PD) and clinical attachment level (CAL) were measured in 3 minipigs. On weeks 4 and 8, there was a significant increase of the mean values of PD and CAL. After this active phase, there was no further destruction up to 20 weeks. Following ligature removed probing depths decreased in 3 weeks, but they did not restore to the baseline. It suggests that using ligature induced periodontitis model to evaluate the treatment therapy and medicine effect have to consider the self-healing of lesions, when a treatment trail is carried out in a model.

Animals↗

PubMed1995

Mast cells are potent regulators of endothelial cell adhesion molecule ICAM-1 and VCAM-1 expression.

To investigate the possible role of mast cells (MC) in regulating leukocyte adhesion to vascular endothelial cells (EC), microvascular and macrovascular EC were exposed to activated MC or MC conditioned medium (MCCM). Expression of intercellular and vascular adhesion molecules (ICAM-1 and VCAM-1) on EC was monitored. Incubation of human dermal microvascular endothelial cells (HDMEC) and human umbilical vein endothelial cells (HUVEC) with activated MC or MCCM markedly increased ICAM-1 and VCAM-1 surface expression, noted as early as 4 hr. Maximal levels were observed at 16 hr followed by a general decline over 48 hr. A dose-dependent response was noted using incremental dilutions of MCCM or by varying the number of MC in coculture with EC. At a ratio as low as 1:1,000 of MC:EC, increased ICAM-1 was observed. The ICAM-1 upregulation by MCCM was > 90% neutralized by antibody to tumor necrosis factor alpha (TNF-alpha), suggesting that MC release of this cytokine contributes significantly to inducing EC adhesiveness. VCAM-1 expression enhanced by MCCM was partly neutralized (70%) by antibody to TNF-alpha; thus other substances released by MC may contribute to VCAM-1 expression. Northern blot analysis demonstrated MCCM upregulated ICAM-1 and VCAM-1 mRNA in both HDMEC and HUVEC. To evaluate the function of MCCM-enhanced EC adhesion molecules, T cells isolated from normal human donors were used in a cell adhesion assay. T-cell binding to EC was increased significantly after exposure of EC to MCCM, and inhibited by antibodies to ICAM-1 or VCAM-1. Intradermal injection of allergen in human atopic volunteers known to develop late-phase allergic reactions led to marked expression of both ICAM-1 and VCAM-1 at 6 hr, as demonstrated by immunohistochemistry. These studies indicate that MC play a critical role in regulating the expression of EC adhesion molecules, ICAM-1 and VCAM-1, and thus augment inflammatory responses by upregulating leukocyte binding.

Cell Adhesion↗

PubMed1995

Cervical dilation from laminaria tents and synthetic osmotic dilators used for 6 hours before abortion.

OBJECTIVE: To compare thick laminaria tents with two synthetic osmotic devices for softening and dilating the cervix before abortions. METHODS: This was a randomized clinical trial comparing cervical dilation by thick laminaria tents with two commercially made devices, 3-mm Hypan and 3-mm anhydrous magnesium sulfate-impregnated plastic tents, used for 6 hours. Subjects were 7-14 weeks pregnant, and all 93 were assigned to devices in permuted randomized groups of three. Physicians and patients were not blinded to the type of device used. Need for a tenaculum for insertions, ease of introduction, cramps, removal ease, hourglassing, achieved dilation, and ease of forced dilation were compared. The effects of parity and gestational length on achieved dilation were also analyzed. RESULTS: Parity did not affect dilation. Significant positive, linear slopes of regression were found for achieved dilation versus weeks of gestation for thick laminaria tents and magnesium sulfate devices but not for Hypan tents. Forcible dilation was easiest with thick laminaria tents and most difficult with magnesium sulfate devices. CONCLUSION: All devices provided safe cervical dilation and softening, but thick tents were most effective.

Abortion, Induced↗

PubMed1995

Sister-chromatid exchanges in lymphocytes of workers at a phosphate fertilizer factory.

The frequencies of sister-chromatid exchange (SCE) in peripheral blood lymphocytes of 40 workers at a phosphate fertilizer factory in North China were studied. HF and SiF4 are main air pollutants in the factory, there is also some dust containing fluoride, phosphate fog, NH3 and SO2. It was shown that the chemicals caused an increase in SCE, and also induced cell mitotic delays. The mean SCEs/cell of the workers and the non-exposed controls were 7.47 +/- 0.31 and 4.94 +/- 0.14 (p < 0.01) respectively. SCEs/cell in 75% of 40 workers were higher than 6 while 40 controls all had values lower than 6. SCE frequencies of the workers increased with length of the chemical exposure period up to 10 years. Smoking enhanced the SCE frequencies induced by the chemicals.

Air Pollutants, Occupational↗

PubMed1995

Mast cells induce T-cell adhesion to human fibroblasts by regulating intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 expression.

The capacity of mast cell products to mediate T-cell adhesion to fibroblasts was explored using heterotypic coculture systems or by exposing fibroblasts to mast-cell-conditioned media (MCCM), prepared by degranulating mast cells with calcium ionophore. Experimental results indicated that fibroblasts exposed to MCCM for 24 h bound fivefold more T cells than control fibroblasts. Binding was inhibited with intercellular adhesion molecule-1 (ICAM-1) or vascular cell adhesion molecule-1 (VCAM-1) neutralizing antibodies. Enzyme-linked immunosorbent assay and fluorescence-activated cell sorter analysis revealed that fibroblasts exposed to MCCM markedly increased ICAM-1 and VCAM-1 surface expression by 4 h, with levels maximal at 16 h and returning toward baseline by 48 h. A dose-dependent response of ICAM-1 and VCAM-1 expression was noted using serial dilutions of MCCM or by altering the ratio of degranulated mast cells cocultured with fibroblasts. Similar results were obtained using human fibroblasts derived from the dermis, synovium, and lung, although lung fibroblasts were generally less responsive. Northern analysis confirmed that MCCM regulated ICAM-1 and VCAM-1 expression at the mRNA level. In summary, mast cell products stimulated fibroblast surface expression, steady-state mRNA levels, and functional expression of ICAM-1 and VCAM-1. Experimental data suggest that mast-cell-derived tumor necrosis factor-alpha may be in large part responsible for these observations, although further studies using human mast cells will be required. Using a skin-equivalent organotypic coculture model with fibroblasts admixed with mast cells, we observed increased ICAM-1 expression in both keratinocytes and fibroblasts after activation of the mast cells.

Adult↗

PubMed1995

[Analysis of HLA-DRB1 alleles in patients with IDDM].

HLA-DR association with IDDM in local population in Beijing was studied by PCR/SSP typing. The frequency of HLA-DR9 was significantly higher in diabetic patients (30.3% [45/148] vs 17.92% [38/212], chi 2 = 6.97, P < 8.3 x 10(-3)). DR3 was higher in diabetic patients in this study (7.0% [10/148] vs 2.36% [5/212], chi 2 = 3.19, P > 0.05) and DR2 was lower in patients with IDDM (7.4% [11/148] vs 19.8% [42/212], chi 2 = 9.67, P < 1.9 x 10(-3)). These results suggest that DR9 and DR3 both were positively associated with IDDM, but DR2 was negatively associated with IDDM.

Adolescent↗

PubMed1994

Antisense oligonucleotide to AT1 receptor mRNA inhibits central angiotensin induced thirst and vasopressin.

Antisense oligodeoxynucleotides (AS-ODN) to AT1 receptor mRNA inhibit high blood pressure in Spontaneously Hypertensive Rats (SHR) when injected into the brain. The effect is presumably through inhibition of the actions of brain angiotensin II (Ang II). Central injection of Ang II elicits several physiological responses including release of vasopressin and motivation to drink. The angiotensin II type-I (AT1) receptor is located in brain regions which have been implicated in mediating these effects. Therefore we hypothesized that AS-ODN to AT1 mRNA would inhibit the drinking and AVP response to central administration of Ang II in adult male SHR. AS-ODN were constructed to bases +63 to +77 (15-mer) of the AT1 receptor RNA. 24 h after AS-ODN treatment (50 micrograms/4 microliters) (intracerebroventricularly, i.c.v.), the drinking response to Ang II (50 ng, i.c.v.) was significantly reduced in the SHR (P < 0.05). The drinking response to Ang II (i.c.v.) was also reduced in the Sprague-Dawley rats (P < 0.05). There was no reduction of water intake in the control animals treated with scrambled ODN (SC-ODN). Repeated injection of AS-ODN did not produce a greater reduction in drinking response. Arginine vasopressin (AVP) release to central Ang II was significantly decreased after AS-ODN treatment when compared to vehicle (P < 0.05) and to SC-ODN injections (P < 0.05). Radioligand binding assays of the hypothalamic block after AS-ODN treatment showed a significant decrease of AT1 receptor binding (P < 0.05). The results show that the antisense inhibition of brain AT1 receptor gene expression decreases the Ang II induced drinking and AVP release responses.

Animals↗

PubMed1993

Temperature dependence of oxygen diffusion and consumption in mammalian striated muscle.

This study investigated the effect of temperature on the oxygen diffusion coefficient (DO2) of hamster retractor muscle from 11 to 37 degrees C. DO2 was measured using a non-steady-state technique, whereas muscle O2 consumption (VO2) was estimated after steady state was reached. DO2 was 0.84 +/- 0.04 x 10(-5) cm2/s at 11 degrees C and rose exponentially to 2.41 +/- 0.19 x 10(-5) cm2/s at 37 degrees C, producing a temperature coefficient for DO2 of 4.60%/degrees C for this temperature range. To measure DO2 directly at 37 degrees C, it was necessary to inhibit tissue VO2 with Amytal. The DO2 measurements made at 37 degrees C were significantly higher than previously reported values, which had been based on extrapolations from lower temperatures (6). Further analysis suggests a possible transition in the diffusion pathway between 23 and 30 degrees C, resulting in a DO2 higher than that previously expected. This larger DO2, together with a recently published value of oxygen solubility (alpha) (21), results in an in vitro Krogh's diffusion coefficient (KO2) that is 2.4 times larger than that previously reported (24) and therefore significantly reduces an order of magnitude discrepancy between in vitro and estimated in vivo KO2 values (24). Muscle VO2 was 0.35 ml O2.min-1.100 g-1 at 11 degrees C and increased with temperature, resulting in an activation energy of the rate-limiting reaction from the Arrhenius equation of -10.5 kcal/mol between 11 and 30 degrees C.

Amobarbital↗

PubMed1993

Enhanced oxygenation in vivo by allosteric inhibitors of hemoglobin saturation.

The in vivo effects on hemoglobin (Hb)-O2 affinity and tissue PO2 were investigated after intraperitoneal administration of 2-[4-(((dichloroanilino)-carbonyl)methyl)phenoxyl]-2-methyl propionic acid (RSR4; 150 mg/kg) or its 3,5-dimethyl derivative (RSR13; 300 mg/kg) in C3Hf/Sed mice. The Hb-O2 dissociation curve was plotted from tail vein blood samples using an O2 dissociation analyzer before and up to 160 min after compound administration. Twenty to 40 min after injection, the PO2 at 50% saturation of hemoglobin (Hb P50) increased by a mean of 25% (range 18-31%) after RSR4 and 53% (range 36-76%) after RSR13. Tissue PO2 was continuously measured using an O2 microelectrode in thigh muscle before and up to 40 min after RSR4 or RSR13 injection. Twenty to 40 min after administration, tissue PO2 increased by a mean of 78% (range 30-127%) after RSR4 and 66% (range 39-97%) after RSR13 administration in anesthetized mice. No change in tissue PO2 was seen in anesthetized controls.

Aniline Compounds↗

PubMed1993

Myoglobin content of hamster skeletal muscles.

Myoglobin (Mb) may facilitate O2 diffusion in muscle tissue, yet models of O2 transport are often simplified by ignoring the role of Mb. A recent analysis of O2 transport in hamster retractor muscle revealed a large discrepancy between the observed O2 diffusion from arterioles and that predicted by a mathematical model that did not include Mb. To establish whether this simplification was justified, we measured Mb content ([Mb]) in three hamster muscles that vary markedly in histochemical fiber type composition. [Mb] was determined spectrophotometrically using freshly excised tissues from hamsters of different ages (5-34 wk). [Mb] increased rapidly up to 15 wk of age and then rose more slowly. [Mb] in hamster muscles paralleled oxidative capacity. Our measurements of rat and dog muscles also show that [Mb] varies greatly among species and among muscles of a given species. The results indicate that in the hamster the variability in [Mb] with age and muscle should be taken into account when the potential role of Mb in studies on O2 transport is interpreted.

Aging↗

PubMed1992

Oxygen diffusion in hamster striated muscle: comparison of in vitro and near in vivo conditions.

To investigate the suggestion of A. S. Popel, R. N. Pittman, and M. L. Ellsworth [Am. J. Physiol. 256 (Heart Circ. Physiol. 25): H921-H924, 1989] that Krogh's diffusion coefficient for O2 in vivo might be an order of magnitude higher than in vitro, O2 diffusion coefficient (DO2) and resting O2 consumption were measured on hamster retractor muscle in vitro and under near in vivo conditions where the muscle remained attached to the animal but the arterial inflow was occluded just before measurement. Experiments were performed on two groups of animals, differing in weight and age. We found that DO2 determined in vitro (extrapolated to 37 degrees C) was 1.81 +/- 0.12 x 10(-5) cm2/s for group I (smaller and younger), which was not significantly different from the value (2.00 +/- 0.08 x 10(-5) cm2/s) determined in group II. In both groups, DO2 under near in vivo conditions tended to be 10-15% larger than the value in vitro, although this trend did not reach statistical significance. It is unlikely that this trend is large enough to reconcile the inconsistency between theoretical and experimental determinations of O2 diffusion from the arteriolar network of this tissue.

Animals↗

PubMed1992

The role of sodium-proton exchange in ischemic/reperfusion injury in the heart. Na(+)-H+ exchange and ischemic heart disease.

Previous work has associated cardiac dysfunction and damage after ischemia/reperfusion with metabolic alterations in the heart or alterations in the myocardial ionic homeostasis. Unfortunately, neither mechanism on its own has been able to conclusively explain the pathology. Instead, recent data suggest that the two mechanisms may be interrelated. The low intracellular pH during ischemia (due to the accumulation of metabolic by-products) may stimulate the Na(+)-H+ exchange pathway during reperfusion to remove H+ from the cell in exchange for will lead to accelerated Ca2+ entry via Na+. The subsequent accumulation of Na+ in the cell Na(+)-Ca2+ exchange, which can ultimately result in intracellular Ca2+ overload, contractile dysfunction and damage. This hypothesis is supported by the known biochemical characteristics of the cardiac Na(+)-H+ exchanger. Pharmacological studies also support this hypothesis as a mechanism involved in ischemic/reperfusion damage. Dimethylamiloride, a blocker of Na(+)-H+ exchange, has provided significant protection against ischemic/reperfusion injury to the heart. A series of studies have indicated that the mechanism through which dimethylamiloride acts is via inhibition of the Na(+)-H+ exchange pathway. The data, therefore, are consistent with an important interaction between metabolism and ionic alterations, which includes a central role for Na(+)-H+ exchange in ischemic/reperfusion damage to the heart.

Animals↗

PubMed1992

The use of an external tibial fixator in the treatment of genu varum.

This paper reports 72 cases of genu varum treated by a U-shaped osteotomy of the tibia and an oblique osteotomy of the fibula in combination with immobilization effected by a specially designed external tibial fixator. Owing to this modified approach, the patients were able to stand up and move about much earlier than usual. Our trial yielded 80.7% excellent, 16.6% good and 2.7% fair results. The treatment course was shortened to two thirds of the time required when using previously described techniques.

Adolescent↗

PubMed1991

Unstable tibio-fibular fractures treated with an external fixator--a clinical report of 1033 cases.

From 1977 to 1987, 1033 cases of unstable tibio-fibular fractures were treated with an external fixator designed by the authors. Among them, 232 involved open fractures. All of the patients were followed up for 4 to 90 months (average 20 months). The duration of bed confinement averaged 8.3 days, and the mean time necessary for clinical bone union was 54 days. Anatomical or nearly anatomical bone apposition was effected in 878 cases (85.0%), functional apposition in 141 cases (13.6%) and malunion in 14 cases (1.4%). The overall functional results were as follows: excellent in 769 cases (74.4%), good in 218 cases (21.1%), fair in 32 cases (3.1%), and poor in 14 cases (1.4%). The design of the device and its indications are also discussed.

Adolescent↗

PubMed1991

Involvement of sodium in the protective effect of 5-(N,N-dimethyl)-amiloride on ischemia-reperfusion injury in isolated rat ventricular wall.

During reperfusion in the isolated right ventricular wall of the rat after 60 min of ischemia, developed tension and resting tension were 35 +/- 4 and 221 +/- 12%, respectively, of preischemic values. Including 35 microM ouabain in the perfusate before and after ischemia resulted in more severe cardiac dysfunction during reperfusion than in drug-untreated hearts. Introduction of the Na(+)-H+ exchange inhibitor, 5-(N,N-dimethyl)-amiloride (DMA), could effectively protect the right ventricular wall against ischemia-reperfusion dysfunction in the presence or absence of ouabain. The ion content in the right ventricular wall was measured with atomic absorbance spectrophotometry. Before ischemia, Na+,Ca++ and K+ content were 53.4 +/- 6.4, 2.70 +/- 0.22 and 262 +/- 7.7 mumol/g of dry weight tissue, respectively. After 60 min of ischemia and 6 min of reperfusion, Na+,Ca++ and K+ content were 73.4 +/- 7.2, 3.79 +/- 0.31 and 180 +/- 15 mumol/g of dry weight tissue, respectively (P less than .05). Introduction of 20 microM DMA normalized ion content in the muscles which was consistent with the contractile function recovery during reperfusion. The data suggest that a rise in intracellular Na+ in the early stage of reperfusion represents a crucial or primary step for the development of cardiac contractile dysfunction. DMA, which protects against severe reperfusion-induced cardiac contractile dysfunction, appears to act via a normalization of tissue sodium levels. This action is consistent with its proposed role as a blocker of transsarcolemmal Na(+)-H+ exchange.

Amiloride↗