Robotic surgery does not affect upstaging of T1 renal masses

Partial nephrectomy is the mainstay of treatment for localized kidney cancer. A proportion of patients are upstaged post-operatively to locally advanced di     

Beyond C4d: Other Complement-Related Diagnostic Approaches to Antibody-Mediated Rejection

Complement is a multifunctional system of receptors and regulators as well as effector molecules. Both the pathogenic and diagnostic power of complement is based on the capacity of the complement system to amplify innate and adaptive immunity. This amplification is accomplished through two strategies: (1) enzymatic reactions in the complement cascade, and (2) stimulation of leukocytes, platelets and parenchymal cells through specific receptors or receptor-independent pore formation. The mechanisms by which complement mediates and modifies nonspecific inflammation, antibody-mediated injury and T-cell responses are of particular significance to the pathogenesis of transplant rejection. Understanding the mechanisms by which complement integrates the interactions of leukocytes, platelets and parenchymal cells offers opportunities to further refine the diagnosis of rejection.     

Intracellular trafficking of fluorescently tagged proteins associated with pathogenesis in Candida albicans.

Proteins that enter the secretory pathway play important roles in virulence and pathogenesis in Candida albicans, but our understanding of the trafficking of these proteins is in its early stages. In Saccharomyces cerevisiae, dominant negative alleles of YPT1 and SEC4 interrupt secretory traffic at pre- and post-Golgi steps, respectively. We therefore used a dominant negative genetic approach to examine the intracellular trafficking of several proteins associated with virulence or azole resistance. When the dominant negative ypt1(N121I) allele of C. albicans was overexpressed, yellow-fluorescent protein (YFP) tagged forms of two plasma membrane transporters (Cdrlp and Ftrlp) and the vacuolar membrane ABC transporter Mltlp accumulated in intracellular structures that appeared related to the ER, but localization of Cdc10p and Int1p was unaffected. When the dominant negative sec4(S28N) allele of C. albicans was overexpressed, Cdrlp and Ftrlp accumulated intracellularly, and localization of Mltlp, Cdc10p and Int1p was unaffected. These results imply that (i) Cdrlp and Ftrlp are transported to the plasma membrane by the general secretory pathway, (ii) Mlt1p enters the secretory pathway but is diverted to the vacuole at an early post-Golgi step, and (iii) like Cdc10p, Int1p does not enter the general secretory pathway.     

全科医生札记--布朗医生日记

汽车机械学 Bobby是我的汽车修理师，他有一种我喜欢效仿的工作风格。首先他是一位伟大的诊断专家；如果你告诉他汽车出现了什么问题，他会帮你做出鉴别诊断。“运货车是否发动不着了？发动机是否转动？你是否听到了滴滴答答的声音？”问了几个问题后，他便会做出判断。比如我的发动机供不上汽油了，排除了几种可能性后他认为是由燃油泵造成的。     

Combined prostacyclin and thromboxane synthetase inhibitor UK 38485 in flap survival

Thromboxane, a prostanoid derivative, is a central mediator of the progressive dermal ischemia seen in the distal dying flap. Prostacyclin; a vasoactive prostanoid derivative, has been found to enhance ischemic flap survival. This study examines the effects of prostacyclin and UK 38485 (specific thromboxane synthetase inhibitor), separately and combined, in axial flap survival in the pig. Each increased flap survival over control flaps; their combined use demonstrated an even greater flap survival (p less than 0.005).