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We conclude that the highly renoprotective capacity of mesenchymal stem cells opens the possibility for a cell-based paradigm shift in the treatment of I/R ARF.

While symptoms did not improve and dietary compliance was problematic, there was substantial histologic improvement after 4 weeks on the elemental diet. EoE in adults is substantially triggered by foods.

Biomarkers of disease activity have come into wide use in the study of mechanisms of human disease and in clinical medicine to both diagnose and predict disease course; as well as to monitor response to therapeutic intervention. Here we review biomarkers of the involvement of mast cells, basophils, and eosinophils in human allergic inflammation. Included are surface markers of cell activation as well as specific products of these inflammatory cells that implicate specific cell types in the inflammatory process and are of possible value in clinical research as well as within decisions made in the practice of allergy-immunology.

Conditional deletion of β1 integrins in the intestinal epithelium, unlike in epidermal and mammary epithelia, of mice does not result in decreased cell adhesion and proliferation, but instead causes a profound increase in epithelial proliferation with dysplasia and polypoid structures. The increased epithelial proliferation inhibited epithelial differentiation that caused severe malnutrition and early postnatal lethality. The striking similarities between β1 integrin–deleted mice and neonatal mice with defective Hedgehog signaling led to the discovery that Hedgehog expression was markedly reduced in the former mice. β1 integrins were found to drive the expression of Hedgehogs in intestinal epithelial cells in an HNF-3β (Foxa2)–dependent fashion. The expression of Tcf-4, a transcription factor known to be required for intestinal epithelial stem cell proliferation, was increased and mislocalized in the intestinal epithelia of the β1 integrin–deleted mice and in newborn mice treated with the Hedgehog signaling inhibitor cyclopamine. This study shows that β1 integrins are key regulators of proliferation and homeostasis in the intestine and achieve this not through anchorage-dependent effects but by generating Hh expression and signaling.

SUMMARYThe goal of this study was to examine the changes in lymphocyte populations in rectal mucosa during HIV infection and to study their relationship to mucosal immunity and to systemic depletion of CD4 lymphocytes. Rectal biopsies from 58 HIV-infected subjects and eight controls were studied. Frozen rectal tissue sections were stained with antibodies to CD4, CD3, CD8, and markers for macrophages. HIV-infected subjects were divided into early stage (no opportunistic infections) and AIDS groups. There was profound depletion of rectal lamina propria CD4 lymphocytes (16% and 6% of normal content in early and AIDS groups, respectively). However, lymphoid aggregate CD4 lymphocytes were far less severely depleted (69% and 40% of normal content, respectively). The extent of lymphoid aggregate CD4 lymphocyte depletion generally parallelled the CD4 lymphocyte depletion in the blood. CD8 lymphocyte content in both the lamina propria and lymphoid aggregates usually were increased, particularly in early-stage patients. Macrophage contents were usually normal in the HIV-infected groups. We conclude that rectal lamina propria and lymphoid aggregates are distinct compartments differing markedly in their CD4 lymphocyte content during HIV infection. In light of this and an increased number of apoptotic cells which were noted in rectal lamina propria in HIV-infected subjects, we hypothesize that intestinal lamina propria could be a site of rapid CD4 lymphocyte destruction during HIV infection.

Pathologic features of 378 breast carcinomas without axillary lymph node metastases were correlated with long‐term prognosis. Mitotic count, the feature best predicting prognosis, was most useful at lower mitotic count levels than usually studied. Cases with less than 4.5 mitotic figures per ten high‐power fields had a 20‐year tumor‐related survival of 73% versus 48% for those with higher mitotic counts. Low and high mitotic count groups had significantly different prognoses for T1c, T2, and T3 tumors. Multivariate analysis showed that the best combination of features predicting tumor‐related death were high mitotic count (relative risk, ×2.8), large tumor size (relative risk, ×1.7), lymphatic invasion (relative risk, ×1.7), and skin or subjacent muscle or chest wall invasion (relative risk, ×2.5). Nuclear grade, Bloom‐Richardson grade, modified Scarff‐Bloom‐Richardson grade, Fisher's grade, and necrosis correlated well with survival but had no significant additional predictive value when adjusted for the mitotic count.

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