Post-traumatic stress disorder among the injured of theintifada

The current study aimed to assess the prevalence of PTSD among Palestinians who sustained serious bodily injuries during theintifada, as well as to delineate factors having an effect on the development and attenuation of PTSD symptomatology. Results indicated evidence of high prevalence of PTSD among the injured. No significant differences in PTSD prevalence for demographic, situational, and trauma-related variables were found except for the age factor. Prevalence of PTSD among adolescents was significantly higher than among adults. It seemed that the injury itself was so intensely overwhelming that the other variables were overshadowed. Implications for further research and stress management techniques were discussed.     

Superior mesenteric artery is more important than inferior mesenteric artery in maintaining colonic mucosal perfusion and integrity in rats

Mucosal hemodynamics (by reflectance spectrophotometry) and mucosal damage (by histologic examination) following acute colonic ischemia were evaluated in different anatomic locations in the colon of anesthetized rats. The reflectance spectrophotometer provides an index of mucosal hemoglobin concentration (IHB) and an index of oxygen saturation of hemoglobin (ISO₂). The patterns of ischemia without congestion (IHB, ISO₂) during superior mesenteric artery occlusion, and ischemia with congestion (IHB, ISO₂) during portal vein occlusion, previously demonstrated in the stomach and duodenum, are also applicable to the colon. The significant linear correlations between changes (as percent of baseline) in IHB, ISO₂, and hydrogen gas clearance suggest that changes in these indices are adequate indicators of changes in colonic mucosal perfusion. Superior mesenteric artery ligation produced significant reductions in both indices, and an increase in damage in the mucosa of the cecum, transverse colon, splenic flexure, and left colon, but not the rectum. Inferior mesenteric artery ligation produced only slight reduction in these indices and minimal damage only in the mucosa of the splenic flexure. These results support the hypothesis that the superior mesenteric artery is more important than the inferior mesenteric artery in maintaining colonic perfusion and colonic mucosal integrity in the rat.Supported by the American Society for Gastrointestinal Endoscopy Career Development Award (H850208, H870212), Veterans Administration Medical Research Funds; and in part by research grants (0162-01, 0162-02; 0291-01) from the Smokeless Tobacco Research Council, Inc.; and by funds provided by the Cigarette and Tobacco Surtax Fund of the State of California through the Tobacco Related Disease Research Program of the University of California.     

Über funktionelle Unterschiede zwischen Dünn-und Dickdarm—dargestellt an den verschiedenen Reaktionen der Darmschleimhaut bei Angebot von Lösungen nicht penetrabler Solute und steigender Osmolarität

Zusammenfassung Bei Instillation von Mannitlösungen steigender Osmolarität in durchblutete, in situ belassene Jejunum- und Colonschlingen von Ratten reagieren beide Darmabschnitte unterschiedlich.Während die durch Enterosorption binnen 30 min in das Jejunum gelangte Flüssigkeitsmenge 250% des Instillats ausmacht, beträgt der analoge Wert beim Colon nur 100%. Die enterosorbierten Mengen an Na⁺, Cl^– und Urea sind im Jejunum wesentlich größer als im Colon, da nicht nur die enterosorbierte Flüssigkeitsmenge größer ist, sondern weil auch die intraintestinalen Konzentrationen höher liegen.Zwischen den Ca⁺⁺-Konzentrationen im Jejunum und Colon bestehen keine Unterschiede, die K⁺-Konzentration ist im Colon höher. Bei Berücksichtigung der Wasserbewegungen ist die enterosorbierte Ca⁺⁺-Menge im Jejunum, die K⁺-Menge dagegen im Colon größer.Während der Versuchszeit — 30 min — erfolgt im Jejunum ein osmolarer Konzentrationsausgleich aller Lösungen mit dem Plasma, deren Konzentration kleiner als die 1,66 fache Blutisotonie ist. Im Colon stellt sich dieser Ausgleich auch für eine Lösung von 1,33 facher Blutisotonie nicht mehr ein.Die Colonschleimhaut verhält sich demnach so, als ob hier die Exsorption von Wasser, Na⁺, Cl^–, Ca⁺⁺ und Urea wesentlich stärker behindert wäre als die durch die Schleimhaut des Jejunums.Instillation großer Volumina stark hypertoner (ca. 2000 mOsmol/l) Lösungen, deren Solute nur schwer absorbiert werden können, führen zu einem so großen Einstrom von Blut- und Körperflüssigkeit in den Intestinaltrakt, daß Ratten in schwerer Exsiccose sterben. Dabei steigt der Anteil von Zellen am Blutvolumen von 48% auf 68% der Wassergehalt der geprüften Gewebe — quergestreifte und Herzmuskulatur, Gehirn — sinkt ab.     

Neoglycoprotein binding to colorectal tumour cells: Comparison between primary and secondary lesions

Summary Biotinylated neoglycoproteins are useful to determine the expression of sugar receptors (lectins) histochemically in routinely processed tissue sections. Assessment of the presence of distinct receptor classes with specificity to-galactosides and to- or-N-acetylgalactosamine, selected on the basis of their potential relevance for recognition processes within the metastatic cascade in murine model systems, was performed for a common human tumour type, colorectal cancer. The four different types of neoglycoproteins, derived from covalent attachment of commercially available derivatives of-N-acetylgalactosamine, differed only quantitatively in their capacity to detect specific binding on cultured cells and tissue sections, thus posing no major restriction on the choice of synthetic process for histochemical efficiency of the product. Glycocytological application revealed specific probe binding and a regulation of level of receptor expression for a human colon carcinoma cell line primarily forN-acetylgalactosamine-specific receptors upon retinoic acid-induced differentiation. Monitoring of sections of the 12 cases of primary and secondary colorectal lesions invariably disclosed the presence of the respective receptors, the extent of cell labelling in primary tumours and metastases being similar. Establishment of metastases, even in different target organs, is apparently not followed by a major phenotypic variation in this feature.     

外源性凝血途径和内皮细胞损伤与动脉粥样硬化之间的关系研究

目的探讨外源性凝血途径在动脉粥样硬化(AS)发病中的作用。方法均采用ELISA法测定心肌梗死、脑梗死、脑出血病人及正常对照组血浆TF、FⅦa的含量及不同时期这些物质浓度的变化、同时通过测定内皮细胞损伤的分子标记物vWF、内皮素 -1(ET -1)、总组织因子途径抑制物(TFPI)、组织因子(TF)探讨外源性凝血途径的活化与水平状况及内皮细胞损伤之间的关系。结果心肌梗死、脑梗死、脑出血病人TF、TFPT、ET -1、vWF、FⅦa,血中的浓度较正常对照组高 (P<0.01) ,有非常显著意义。结论外源性凝血途径与内皮细胞损伤和AS有密切相关。     

In Situ Thermal Denaturation of Proteins in Dunning AT-1 Prostate Cancer Cells: Implication for Hyperthermic Cell Injury

The in situ thermal protein denaturation and its correlation with direct hyperthermic cell injury in Dunning AT-1 prostate tumor cells were investigated in this study. The in situ thermal protein denaturation was studied using both Fourier transform infrared spectroscopy (FTIR) and differential scanning calorimetry (DSC). The FTIR spectra at different temperatures show changes in protein secondary structure (from alpha helix to extended beta sheet) during in situ thermal protein denaturation within AT-1 cells. Calorimetric studies using DSC show that endothermic heat release is associated with the in situ thermal protein denaturation. Furthermore, both the secondary structure changes detected by FTIR and the calorimetric changes detected by DSC were quantified and the kinetics of the overall in situ thermal protein denaturation was derived under different heating conditions. The onset temperature where the overall in situ thermal protein denaturation is first detectable was found to be scanning rate dependent (approximately 41 degrees C at 2 degrees C min(-1) and approximately 44 degrees C at 5 degrees C min(-1)). The kinetics of the overall in situ thermal protein denaturation was derived from both DSC and FTIR measurements and was fit using kinetic and statistical models. The kinetic data determined by FTIR and DSC under the same heating conditions match well with each other. The activation energy of the overall in situ thermal protein denaturation is found to be strongly dependent on the temperature range considered (the activation energy ranges from approximately 110 kJ mol(-1) between 44 and 90 degrees C to approximately 750 kJ mol(-1) between 44 and 50 degrees C). However, its dependence on heating rate is negligible. Several denaturation peaks, including a dominant one between approximately 62 and 65 degrees C, are identifiable from both the DSC and the FTIR results. To investigate directly the relationship between thermally induced cell injury and the in situ thermal protein denaturation, both acute (propidium iodide dye exclusion, assessed 3-h postthermal treatment) and chronic (clonogenics, assessed 7-day postthermal treatment) cell injury were quantified using AT-1 cells prepared under the same conditions as for the DSC protein studies. Comparisons of the results from the cell injury studies and the DSC protein denaturation studies show that the overall in situ thermal protein denaturation correlates well with both the acute and the chronic cell injury, which suggests that overall in situ thermal protein denaturation is an important mechanism of direct hyperthermic cell injury in AT-1 cells at the macromolecular level.     

Mechanical Characterization of an In Vitro Device Designed to Quantitatively Injure Living Brain Tissue

Due to the nonlinear, viscoelastic material properties of brain, its mechanical response is dependent upon its total strain history. Therefore, a low strain rate, large strain will likely produce a tissue injury unique from that due to a high strain rate, moderate strain. Due to a lack of current understanding of specific in vivo physiological injury mechanisms, a priori assumptions cannot be made that a low strain rate injury induced by currently employed in vitro injury devices is representative of clinical, nonimpact, inertial head injuries. In the present study, an in vitro system capable of mechanically injuring cultured tissue at high strain rates was designed and characterized. The design of the device was based upon existing systems in which a clamped membrane, on which cells have been cultured, is deformed. However, the present system incorporates three substantial improvements: (1) noncontact measurement of the membrane deflection during injury; (2) precise and independent control over several characteristics of the deflection; and (3) generation of mechanical insults over a wide range of strains (up to 0.65) and strain rates (up to 15s^–1). Such a system will be valuable in the elucidation of the mechanisms of mechanical trauma and determination of injury tolerance criteria on a cellular level utilizing appropriate mechanical injury parameters.     

Relative growth of adenomatous polyps of the colon

Summary The volume of the adenomatous mucosa (V), the area of the surface epithelium (Ss), the area of the glandular epithelium (Sg), and theSg:Ss ratio were calculated in a series of 14 adenomatous polyps (APs) of a case of multiple polyposis of the colon. The equation of simple allometry was used to study the relative growth of the four series of values.Ss grew isometrically with size;Sg overgrewSs and accounted for most of the increase inV. TheSg:Ss ratio increased withSg andV.     

FK506 (tacrolimus) improves lung injury through inhibition of Fas-mediated inflammation

Objective To investigate whether FK506 (tacrolimus) can inhibit Fas- or A23187-induced interleukin (IL)-8 expression and cell death in A549 human alveolar epithelial cells, plus Fas-mediated acute lung injury in vivo. Methods Assays for IL-8, cell death, and caspase-3 activity were performed. A549 cells were treated with 25 μmol A23187 or 0.2 μg/ml agonistic anti-Fas antibody plus 5 ng/ml interferon-gamma (IFN-γ). Tacrolimus was treated at 0.1–10 ng/ml. For in vivo experiment, agonistic anti-Fas antibody (Jo2) at 2.5 μg/g was intratracheally instilled into C57BL/6 mice. Neutrophils and protein contents in bronchoalveolar lavage (BAL) fluid were measured within 24 h of instillation. Mice were orally treated with 32 mg/kg of tacrolimus 24 h and 1 h prior to instillation. Results Both Fas and A23187 caused significant IL-8 expression and cell death in A549 cells. Tacrolimus inhibited A23187-induced IL-8 expression alone while it protected all Fas-mediated responses. Mice instilled intratracheally with Jo2 at 2.5 μg/g had significant increases in neutrophils, protein contents in BAL fluid and in expression of chemoattractants for neutrophils. These increases were reversed by tacrolimus. Conclusions Tacrolimus serves as a therapeutic option for improving lung injury through inhibition of Fas-mediated inflammation. Received 7 November 2005; returned for revision 28 December 2005; accepted by G. Wallace 2 February 2006     

肢体缺血/再灌注后氧自由基与Bax蛋白、细胞凋亡的关系

目的　阐明氧自由基与Bax蛋白、细胞凋亡在大鼠肢体缺血 /再灌注不同时相中的变化规律及相互关系。方法　采用大鼠股动脉夹闭模型 ,阻断股动脉血流 5h后再灌注 ,设立缺血组、再灌注组 ,再灌注组设立 1,6 ,12 ,2 4h 4个检测时相 ,应用硫代巴比妥酸法测定肌肉组织中脂质过氧化产物丙二醛 (MDA)水平 ,应用免疫组化方法测定Bax蛋白表达的变化 ,应用原位末端标记法及电镜方法观察细胞凋亡现象。结果　随着再灌注时间的延长 ,MDA水平、Bax蛋白表达强度、细胞凋亡指数 (AI)进行性升高 ,且三者呈显著正相关。结论　氧自由基与细胞凋亡同时参与肢体再灌注损伤 ,氧自由基可能通过调节Bax蛋白表达促进细胞凋亡的发生。