外科手术中产生的烟气:仅仅是大量的热空气吗?

外科医生和手术室人员经常接触手术设备产生的烟气,病人也会暴露于烟气中,特别是腹腔镜手术中产生的烟气滞留于腹腔内这一密闭空间并被吸收.这些烟气是一种与香烟烟气相似的毒性物质,然而对这种毒性物质的影响还未引起足够重视.应该采取必要措施尽可能减少手术中烟气的不良影响.     

The Sigma-trial protocol: a prospective double-blind multi-centre comparison of laparoscopic versus open elective sigmoid resection in patients with symptomatic diverticulitis

Backround  

Diverticulosis is a common disease in the western society with an incidence of 33–66%. 10–25% of these patients will develop diverticulitis. In order to prevent a high-risk acute operation it is advised to perform elective sigmoid resection after two episodes of diverticulitis in the elderly patient or after one episode in the younger (< 50 years) patient. Open sigmoid resection is still the gold standard, but laparoscopic colon resections seem to have certain advantages over open procedures. On the other hand, a double blind investigation has never been performed. The Sigma-trial is designed to evaluate the presumed advantages of laparoscopic over open sigmoid resections in patients with symptomatic diverticulitis.     

Selection of U937 histiocytic lymphoma cells highly responsive to phorbol ester-induced differentiation using monoclonal antibody to the eosinophil cytotoxicity-enhancing factor

Monoclonal antibodies (MoAbs) to the eosinophil cytotoxicity-enhancing factor (ECEF) were used to detect ECEF in U937 cells before and after phorbol ester (PMA)-induced differentiation into ECEF-secreting macrophages. Membrane-associated ECEF (mECEF), apparently an integral membrane component, is found in U937 cells and in 70% of monocytes and, at lower levels, on blood T lymphocytes. Expression of mECEF in U937 cells is heterogeneous, as is responsiveness to PMA. In PMA-treated cultures, the strongest mECEF expression is on adherent, differentiated macrophages, rather than on activated, nonadherent cells. To study the relationship of mECEF to PMA responsiveness, we positively selected by "panning" a cell line (U937 P+) with significantly higher mECEF expression than that of U937. U937 P+ cells respond to PMA as a differentiation stimulus more effectively than do U937 cells, with a fourfold increase in the number of differentiated macrophages (P less than .001) and a faster rate of differentiation (a fourfold increase at t = 12 hours, P less than .001). U937 P+ cells also show a 7.4-fold increase in response to suboptimal doses of PMA (P less than .001). These findings suggest that mECEF expression correlates with responsiveness to a differentiation stimulus in a histiocytic lymphoma cell line that is widely used as a model of monocyte maturation.     

Age-dependent neurological phenotypes in a mouse model of PRRT2-related diseases

Paroxysmal kinesigenic dyskinesia is an episodic movement disorder caused by dominant mutations in the proline-rich transmembrane protein PRRT2, with onset in childhood and typically with improvement or resolution by middle age. Mutations in the same gene may also cause benign infantile seizures, which begin in the first year of life and typically remit by the age of 2 years. Many details of PRRT2 function at the synapse, and the effects of mutations on neuronal excitability in the pathophysiology of epilepsy and dyskinesia, have emerged through the work of several groups over the last decade. However, the age dependence of the phenotypes has not been explored in detail in transgenic models. Here, we report our findings in heterozygous and homozygous Prrt2 knockout mice that recapitulate the age dependence of dyskinesia seen in the human disease. We show that Prrt2 deletion reduces the levels of synaptic proteins in a dose-dependent manner that is most pronounced at postnatal day 5 (P5), attenuates at P60, and disappears by P180. In a test for foot slippage while crossing a balance beam, transient loss of coordination was most pronounced at P60 and less prominent at age extremes. Slower traverse time was noted in homozygous knockout mice only, consistent with the ataxia seen in rare individuals with biallelic loss of function mutations in Prrt2. We thus identify three age-dependent phenotypic windows in the mouse model, which recapitulate the pattern seen in humans with PRRT2-related diseases.