We report a case of an 83-year-old man with a high-grade carcinoma of the urinary bladder who underwent cystoprostatectomy. The invasive carcinoma showed mixed, morphologically distinct patterns consisting of conventional high-grade urothelial carcinoma, glandular differentiation resembling enteric type adenocarcinoma, and acinar/tubular type differentiation, morphologically similar to Gleason grade 3 prostatic adenocarcinoma. Immunohistochemical studies revealed the acinar/tubular component of the tumor to be negative for prostate-specific antigen and prostatic acid phosphatase, but positive for cytokeratin 7, cytokeratin 20, high molecular weight cytokeratin (34 beta E12), and thrombomodulin, consistent with origin from the bladder rather than the prostate. Although bladder carcinomas composed of mixed morphologic patterns are not uncommon, to our knowledge, the presence of acinar/tubular type features simulating prostatic adenocarcinoma in such tumors has not been described elsewhere. 相似文献
The ability of a spatial population of cutaneous, Adelta, and C mechano-nociceptors to encode the location and intensity of a noxious, cutaneous indentation was examined using an isolated preparation in a rat model. Skin and its intact innervation were harvested from the medial thigh of the rat hindlimb and placed in a dish, with the corium side down, containing synthetic interstitial fluid. The margins of the skin were coupled to an apparatus that could stretch and apply compression to the skin. The skin was suspended on top of a deformable platform whose bulk, nonlinear, compressive compliance emulated that found in vivo. The isolated preparation facilitated examination of the spatial population response by eliminating the nonlinear geometry and inhomogeneous compressive compliance present in-vivo. Spatial population responses (SPR) were formed from recordings of single neurons that were stimulated by compressing the skin with an indenter (flat cylinder, 3-mm diam) at discrete intervals from the center of their receptive fields. SPR were composed of the neural responses (z axis) at each indentation location (x, y plane), and were analyzed quantitatively using nonlinear regression to fit an equation of a Gaussian surface. Both Adelta and C SPR accurately encoded the location and intensity of noxious indentation. The intensity of the stimulus was encoded in the peak neural response of the SPR, which had a nonlinear relationship to the compressive force. The location of the stimulus was encoded in the x, y position of the peak of the SPR. The position of the peak remained constant with increasing magnitudes of compressive force. The overall form of the SPR also remained constant with changes of compressive load, suggesting a possible role for encoding in the SPR some aspects of shape of a noxious stimulus. 相似文献
The biologically active substance P (SP) N-terminal metabolite SP1–7 has been reported to modulate several neural processes such as learning, locomotor activity and reaction to opioid withdrawal. Although all these processes are believed to be associated with dopaminergic transmission no evidence of an interaction between SP1–7 and dopamine in the case of morphine withdrawal has so far been reported. Therefore, in this work we applied in vivo microdialysis to investigate the effect of SP1–7 injection into the ventral tegmental area on dopamine release in nucleus accumbens of male rats during naloxone precipitated morphine withdrawal. The result showed that the heptapeptide enhances dopamine release and also elevates the level of the dopamine metabolite dihydroxyphenylacetic acid in this brain area. It was suggested that the observed action of the SP fragment on the dopamine system represents the underlying mechanism for a previously observed ability of SP1–7 to counteract the aversion response to morphine withdrawal. 相似文献
Background: Despite years of research, the treatment of acute kidney injury (AKI) remains a significant challenge. Animal studies presented causal links between elevated regulatory T cell (Treg) response and better prognosis in AKI. Previous studies in mice and humans showed that TIM-3+ Treg cells were more potent than TIM-3- Treg cells. In this study, we investigated the role of TIM-3 in Treg in AKI patients.
Methods: Peripheral blood from AKI patients and healthy controls were gathered, and TIM-3+ Treg subset was examined.
Results: Compared to healthy controls, the AKI patients presented a significant upregulation in the frequency of circulating CD4+CD25+ T cells; however, the majority of this increase was from the CD4+CD25+TIM-3- subset, and the frequency of CD4+CD25+TIM-3+ T cells was downregulated in AKI patients. In both healthy controls and AKI patients, the CD4+CD25+TIM-3+ T cells expressed higher levels of Foxp3, and were more potent at expressing LFA-1, LAG-3, CTLA-4, IL-10 and TGF-β. In addition, the CD4+CD25+TIM-3+ T cells from both healthy controls and AKI patients presented higher capacity to suppress CD4+CD25- T cell proliferation than the CD4+CD25+TIM-3- T cells. Interestingly, the total CD4+CD25+ T cells from AKI patients presented significantly lower inhibitory capacity than those from healthy controls, indicating that the low frequency of CD4+CD25+TIM-3+ T cells was restricting the efficacy of the Treg responses in AKI patients.
Conclusions: We demonstrated that TIM-3 downregulation impaired the function of Treg cells in AKI. The therapeutic potential of CD4+CD25+TIM-3+ T cells in AKI should be investigated in future studies. 相似文献