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Biomedical subjects

A Li

Publications and source records attributed to A Li.

At least 343 records · Page 19Linked to original sources
PubMed1989

Abnormalities of serum proteins following thermal injury.

Suppressive factors were found to be present in serum and considered to be one of the causes of the suppression of body defences following thermal injury. The purpose of this study was to find out any abnormality of the postburn serum proteins by the comparison of burned and normal sera using immunoprecipitation in gel. The results of SDS-polyacrylamide gel electrophoresis, crossed immunoelectrophoresis, tandem crossed immunoelectrophoresis, and fused rocket immunoelectrophoresis showed that differing precipitation bands or peaks existed between burned and normal sera, and abnormal constituents with relatively low molecular weight were present in the burned serum.

Blood Protein Electrophoresis↗
PubMed1989

Pathogenetic role of anti-vascular endothelial cell antibodies in systemic lupus erythematosus.

In order to study the relationship between vascular endothelial cell (VEC) antigen system and systemic lupus erythematosus (SLE), including lupus nephritis, Terasaki's microcytotoxicity test and indirect immunofluorescence were used to detect anti-VEC antibody. VEC was identified by electron microscopy. Sera of 21 SLE patients and of 100 healthy donors were examined. Among the 21 SLE patients evaluated, 17 had kidney injury and 13 were in active stage SLE. Results showed that anti-VEC antibody was found in 76.2% of 21 SLE patients, while only 1% of the controls were positive (P less than 0.05). This antibody was detected in 84.6% of patients in active stage SLE and in 62.5% of patients in inactive stage (P greater than 0.05). In patients with and without kidney injury, it was detected in 82.4% and 50%, respectively (P greater than 0.05). These data show that anti-VEC antibody does exist in the sera of SLE patients, the presence of which is closely related to SLE onset and is independent of whether the patient is in active stage of SLE or has kidney injury. In summary, our data suggest that anti-VEC antibody may be one of the triggering factors in the vasculitis of SLE. It is proposed that renal VEC may act as a target cell which can be attacked by anti-VEC antibody to constitute an in-situ immune complex formation in the kidney, leading to lupus nephritis.

Adolescent↗
PubMed1988

Antidepressant-like effects of (+)-oxaprotiline on a behavioral screen.

(+)-Oxaprotiline (1.25-10 mg/kg), a highly selective and stereospecifically acting norepinephrine (NE) uptake inhibiting drug, increased the reinforcement rate, decreased the response rate, and enhanced temporal discrimination in rats performing under a differential-reinforcement-of-low-rate 72-s schedule of reinforcement similar to other antidepressant drugs. (-)-Oxaprotiline did not affect the reinforcement rate, response rate or temporal discrimination. Since the most prominent known difference between the oxaprotiline enantiomers is the greater potency for inhibition of norepinephrine (NE) uptake by the (+) enantiomer, the effects of (+)-oxaprotiline in the present studies is probably due to inhibition of NE or epinephrine uptake. The present work also predicts that the therapeutic effects of oxaprotiline in the treatment of affective disorders is due to the (+) enantiomer.

Animals↗
PubMed1988

Bone marrow granulopoietic response to scalds and wound infection in mice.

Phagocytic cell function is often suppressed after thermal injury. It has been suggested that one of the mechanisms of suppression is a direct effect of thermal injury upon these cells. In the present study we examined whether bone marrow haemopoietic stem cells were suppressed by thermal injury similar to the effect seen on mature haemopoietic cells. Results of both in vitro bone marrow cell cultures and in vivo spleen colony assays showed that granulopoiesis was not suppressed but activated early on day 3 following scald injury or scald plus wound infection in mice. In the latter group, stimulation of granulopoiesis persisted throughout the entire observation period of 9 days. These studies indicate that bone marrow pluripotent stem cells are capable of modulating their direction of differentiation according to body demand and deviate toward the granulocyte series following thermal injury.

Agranulocytosis↗
PubMed1988

Effect of smoke inhalation injury on thromboxane levels and platelet counts.

Thirteen goats with chronic lung lymph fistula suffering from smoke inhalation injury were studied for a 6-h period. All animals were found to have acute respiratory failure after injury, the arterial TXA2 (thromboxane A2) levels had increased by 5 min after injury, they peaked at 2 h, and then subsequently declined. Peripheral platelet counts decreased progressively within 2 h, then gradually recovered but were still lower than baseline values at 6 h after injury. EVLW (extravascular lung water), Q1 (lung lymph flow rate) and L/P (total lymph protein/plasma protein concentration), all increased and peaked at 2 h after injury. A negative linear correlation was observed between the TXA2 levels and the platelet counts. Furthermore, differences between the venous and arterial platelet counts were markedly increased. All these observations suggested that the increased TXA2 triggered the formation of platelet microaggregates which were then trapped in the microvasculatures of viscera such as the lung. This might be one of the causes of the decreased platelet counts in peripheral blood. Both TXA2 levels and platelet counts were closely correlated with EVLW, suggesting that TXA2 may indirectly cause the increased pulmonary microvascular permeability by promoting platelet aggregation and microaggregate formation in the pulmonary microvasculature. This may be one of the reasons for the developing pulmonary oedema in goats following smoke inhalation injury.

Animals↗
PubMed1987

Blood gas studies in dogs with severe steam inhalation injury.

The dynamic changes in blood gases in 34 dogs suffering severe steam inhalation injury were studied during the first 14 days post-burn to determine the effects of inhalation injury on lung function. Nineteen dogs received only severe steam inhalation injury, while 15 other dogs received both 30 per cent total body surface area (TBSA) deep burns and steam inhalation injury. The results showed marked reductions of PaO2, PaCO2, AB, SBE, T-CO2, SB, BBp, pHNR and SatO2 (P less than 0.05 approximately 0.01), whereas the P(A-a)O2 increased (P less than 0.05 approximately 0.01) within week 1 post-burn in both groups. These data suggest that the injured animals were suffering from hypoxaemia and respiratory alkalosis induced by disturbance of the gas-exchange function of the lungs. There was also metabolic acidosis, which was closely related to high fever, excessive catabolism, and particularly to hypoxaemia in week 1 post-burn. If the animals survived through the critical period (1-7 days post-burn), most of the abnormal gas parameters then gradually returned to the pre-burn levels. It is clear, therefore, that blood gas monitoring in patients with inhalation injury is not only of diagnostic importance but also of prognostic value.

Acidosis, Respiratory↗
PubMed1987

Nonadditive interactive effects of polychlorinated biphenyl congeners in rats: role of the 2,3,7,8-tetrachlorodibenzo-p-dioxin receptor.

Administration of 3,3',4,4',5,5'-hexa-,3,3',4,4',5-penta-, and 2,3,3'4,4'5-hexa-chlorobiphenyl to immature male Wistar rats caused a thymic atrophy at high dose levels (1.25, 1.0, and 100 mumol/kg, respectively) and induced the hepatic cytochrome P-448 dependent monooxygenases (benzo[a]pyrene hydroxylase and ethoxyresorufin O-deethylase) at both high and low (0.25, 0.01, and 5 mumol/kg, respectively) doses. In contrast, 2,2',4,4',5,5'-hexachlorobiphenyl (HCBP) (300 mumol/kg) did not elicit any of these effects but elevated hepatic 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) cytosolic receptor protein levels (threefold) as previously reported. The effects of hepatic receptor modulation by 2,2',4,4',5,5'-HCBP (300 mumol/kg) on the enzyme induction activities of 3,3'4,4',5-penta-, 3,3'4,4',5,5'-hexa-, and 2,3,3',4,4',5-hexa-chlorobiphenyl were dose-dependent; no interactive effects were observed at high (toxic) doses of these compounds, whereas apparent synergistically increased hepatic microsomal monooxygenase induction activities were noted at the lower submaximal induction doses. It was concluded that the increased responsiveness of the rats was due to elevated hepatic 2,3,7,8-TCDD receptor levels.

Animals↗