谷氨酸诱导体外培养的鸡胚脊髓神经细胞释放NO

用鸡胚脊髓神经细胞的原代培养,测定细胞中亚硝酸盐的含量,研究了谷氨酸(Glu)对原代培养神经细胞中NO的影响。结果表明,谷氨酸作用于原代培养的鸡胚脊髓神经细胞,在诱导神经细胞释放乳酸脱氢酶(LDH)的同时,还可诱导细胞释放一氧化氮(NO)。如先用NO合成酶抑制剂L-NOARG作用细胞,再加入Glu,则发现L-NOARG能降低Glu导致的培养液中LDH活性升高。提示NO可能参与介导Glu的神经毒性作用。     

Editorial

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How thick is the glycocalyx of human erythrocytes?]

The aim of the experiment was to determine the thickness of the glycocalyx of human erythrocytes of the blood group A. For that purpose, the distance between the electron dense contrasted lipid layer of the plasmalemma and gold sol particles loaded with Helix pomatia lectin was determined. The mean thickness of the glycocalyx under this conditions was 5.9 nm.     

The mixed lipoxygenase/cyclooxygenase inhibitor SK&F 105809 reduces cerebral edema after closed head injury in rat.

Closed head injury in rats induces edema formation, which is indicated by a decrease in cerebral specific gravity and an increase in water content. We previously described the activation of the eicosanoid metabolic cascade, namely, activation of PLA2 and accumulation of products of both 5-lipoxygenase (5-LO) and cyclo-oxygenase (CO) in the same model of head injury. The present study was designed to determine the effect of a novel drug, SK&F 105809, a dual inhibitor of 5-LO and CO on cerebral edema formation after head injury in rats. Rats, under ether anesthesia, were subjected to sham operation or trauma induced by weight-drop device impacting over the left calvarium. One group of traumatized rats received 0.9% saline and served as control and two other groups were treated with SK&F 105809, 20 or 30 mg/kg, i.p. immediately after the impact. In one group treatment was repeated additionally 2.5 h post-trauma. Four hours after trauma, rats were sacrificed and brain edema was evaluated. SK&F 105809 treated rats which received 30 mg/kg had significantly less brain edema, as measured by both gravimetry and water content, at 4 h after trauma. The lower dose, 20 mg/kg, had no effect. Our results suggest that treatment with a mixed 5-LO/CO inhibitor shortly after head injury will result in less brain edema and ultimately improved functional outcome.     

Industrial back belts and low back pain: Mechanisms and outcomes

The recent increased utilization of industrial back belts as personal protective equipment in the workplace has generated considerable controversy among occupational health and safety professionals in the United States. The purpose of this article is to review the literature regarding proposed mechanisms of action of these devices and studies related to outcome of belt utilization in the prevention of low back pain and disability in the workplace. At the present time, neither the suspected mechanisms of action nor the efficacy of these devices in the primary, secondary, and tertiary prevention of work-related low back pain has been adequately demonstrated in clinical trials. As a result, generally accepted guidelines regarding the safe use of belts in the occupational setting have not been established. Based on this review it is recommended that further well-controlled, prospective, randomized clinical trials are necessary to evaluate the effectiveness of these devices as personal protective equipment. During the interim, the decision to prescribe belts to employees in the workplace should be at the discretion of an adequately trained occupational health care provider. These devices should not be provided as an alternative to appropriate administrative and/or engineering controls.     

Quantitative comparison of magnetic resonance imaging (MRI) and histologic analyses of focal ischemic damage in the rat

Hemispheric swelling and area of infarction, two parameters of cerebral focal ischemic damage, were identified and quantified from T2-weighted magnetic resonance imaging (MRI) two days after occlusion of the middle cerebral artery (MCAO) in spontaneously hypertensive rat (SHR) brains. Results were compared with these measures quantified from 2,3,5-triphenyltetrazolium hydrochloride (TTC)- and hematoxylin and eosin (H&E)-stained histologic sections in the same brains. The degree of hemispheric swelling and infarct size determined by MRI were highly correlated to the measurements as determined in the TTC- and H&E-stained tissues. These results demonstrate that the focal ischemic damaged area and associated tissue swelling identified by MRI is quantitatively similar to, and thus, is representative of actual tissue damage/changes that can be identified by gross or histologic examination.     

Surgically debulked malignant pleural mesothelioma: Results and prognostic factors

Background: We analyzed morbidity and mortality, sites of recurrence, and possible prognostic factors in 95 (78 male, 17 female) patients with MPM on phase I–III trials since 1990. A debulking resection to a requisite, residual tumor thickness of ≤ 5 mm was required for inclusion. Methods: Preoperative tumor volumes were determined by three-dimensional reconstruction of chest computerized tomograms. Pleurectomy (n=39) or extrapleural pneumonectomy (EPP; n=39) was performed. Seventeen patients could not be debulked. Preoperative EPP platelet counts (404,000) and mean tumor volume (491 cm³) were greater than that seen for pleurectomy (344,000, 114 cm³). Results: Median survival for all patients was 11.2 months, with that for pleurectomy 14.5 months, that for EPP 9.4 months, and that for unresectable patients 5.0 months. Arrhythmia (n=14; 15%) was the most common complication, and there were two deaths related to surgery (2.0%). Tumor volume of >100 ml, biphasic histology, male sex, and elevated platelet count were associated with decreased survival (p<0.05). Both EPP and pleurectomy had equivalent recurrence rates (27 of 39 [69%] and 31 of 39 [79%], respectively); however, 17 of 27 EPP recurrences as opposed to 28 of 31 pleurectomy recurrences were locoregional (p₂=0.013). Conclusions: Debulking resections for MPM can be performed with low operative mortality. Size and platelet count are important preoperative prognostic parameters for MPM. Patients with poor prognostic indicators should probably enter nonsurgical, innovative trials where toxicity or response to therapy can be evaluated. Presented at the 49th Annual Cancer Symposium of The Society of Surgical Oncology, Atlanta, Georgia, March 21–24, 1996.     

Reperfusion increases neutrophils and leukotriene B4 receptor binding in rat focal ischemia.

BACKGROUND AND PURPOSE: Neutrophils are critically involved with ischemia and reperfusion injury in many tissues but have not been studied under conditions of reperfusion after focal cerebral ischemia. The present studies were conducted to confirm our previous observations quantifying neutrophils in rat permanent focal stroke using a myeloperoxidase activity assay and to extend them to transient ischemia with reperfusion. In addition, leukotriene B4 receptor binding in ischemic tissue was evaluated as a potential marker for inflammatory cell infiltration. METHODS: Histological, enzymatic, and receptor binding techniques were used to evaluate neutrophil infiltration and receptor binding in infarcted cortical tissue 24 hours after permanent middle cerebral artery occlusion (n = 25) or temporary occlusion for 80 (n = 12) or 160 (n = 22) minutes followed by reperfusion for 24 hours in spontaneously hypertensive rats. RESULTS: Sham surgery (n = 26) produced no changes in any parameter measured. After permanent middle cerebral artery occlusion, neutrophil accumulation was observed histologically, but the infiltration was moderate and typically within and adjacent to blood vessels bordering the infarcted cortex. After temporary middle cerebral artery occlusion with reperfusion, marked neutrophil infiltration was observed throughout the infarcted cortex. Myeloperoxidase activity was increased (p less than 0.05) after permanent occlusion and to a greater extent after temporary occlusion with reperfusion. Myeloperoxidase activity (units per gram wet weight) in ischemic cortex was increased over that in nonischemic (control) cortex 32.2-fold, 54.6-fold, and 92.1-fold for permanent occlusion and 80 and 160 minutes of temporary occlusion with reperfusion, respectively (p less than 0.05). Sham surgery produced no changes in myeloperoxidase activity. Leukotriene B4 receptor binding also was increased (p less than 0.05) after focal ischemia and paralleled the increases in myeloperoxidase activity. Ischemic cortex-specific receptor binding (femtomoles per milligram protein) was 3.87 +/- 0.63 in sham-operated rats and 4.57 +/- 0.98, 8.98 +/- 1.11, and 11.12 +/- 1.63 for rats subjected to permanent occlusion and 80 and 160 minutes of temporary occlusion with reperfusion, respectively (all p less than 0.05 different from sham-operated). Cortical myeloperoxidase activity was significantly correlated with the degree of cortical leukotriene B4 receptor binding (r = 0.66 and r = 0.79 in two different studies, p less than 0.01). CONCLUSION: These data indicate that neutrophils are involved in focal ischemia and that there is a dramatic accumulation of neutrophils in infarcted tissue during reperfusion that can be quantified using the myeloperoxidase activity assay. Leukotriene B4 receptor binding increases in infarcted tissue in a parallel manner, which suggests that the increased leukotriene B4 binding is to receptors located on the accumulating neutrophils.