Epithelial-stromal interactions in the mouse vagina exposed neonatally to diethylstilbestrol.

BACKGROUND: In neonate mice exposed to diethylstilbestrol (neoDES), vaginal epithelium shows persistent proliferation and stratification even after ovariectomy. Tissue recombination studies suggest that neonatally-estrogenized vaginal stroma can induce vaginal epithelial hyperplasia depending on the stromal age. This study examined the proliferative effect of the vaginal stroma from 8-day-old mice treated with DES on the vaginal epithelia of 8-day-old and adult mice. MATERIALS AND METHODS: Vaginal epithelium and stroma from 8-day-old and adult mice was recombined, and grafted to ovariectomized host mice. RESULTS: The 5-bromo-2'-deoxyuridine (BrdU)-labeled cells in the epithelium and the number of epithelial cell layers were not significantly different between epithelia from 8-day-old and adult mice when combined with stroma from 8-day-old control mice. BrdU-labeled cells in the vaginal epithelia from both age groups combined with the stroma from 8-day-old neoDES mice exhibited higher values. The epithelium from neoDES adult mice had a lower percentage of BrdU-labeled cells. CONCLUSION: The stroma from 8-day-old neoDES mice induces epithelial cell proliferation, but lower stromal cell proliferation.

Selective optical control of synaptic transmission in the subcortical visual pathway by activation of viral vector-expressed halorhodopsin.

The superficial layer of the superior colliculus (sSC) receives visual inputs via two different pathways: from the retina and the primary visual cortex. However, the functional significance of each input for the operation of the sSC circuit remains to be identified. As a first step toward understanding the functional role of each of these inputs, we developed an optogenetic method to specifically suppress the synaptic transmission in the retino-tectal pathway. We introduced enhanced halorhodopsin (eNpHR), a yellow light-sensitive, membrane-targeting chloride pump, into mouse retinal ganglion cells (RGCs) by intravitreously injecting an adeno-associated virus serotype-2 vector carrying the CMV-eNpHR-EYFP construct. Several weeks after the injection, whole-cell recordings made from sSC neurons in slice preparations revealed that yellow laser illumination of the eNpHR-expressing retino-tectal axons, putatively synapsing onto the recorded cells, effectively inhibited EPSCs evoked by electrical stimulation of the optic nerve layer. We also showed that sSC spike activities elicited by visual stimulation were significantly reduced by laser illumination of the sSC in anesthetized mice. These results indicate that photo-activation of eNpHR expressed in RGC axons enables selective blockade of retino-tectal synaptic transmission. The method established here can most likely be applied to a variety of brain regions for studying the function of individual inputs to these regions.

Trichosporon asahii-induced asthma in a family with Japanese summer-type hypersensitivity pneumonitis.

BACKGROUND: Trichosporon species frequently induce summer-type hypersensitivity pneumonitis (SHP), which is the most prevalent type of hypersensitivity pneumonitis (HP) in Japan, but have not been reported to induce asthma. OBJECTIVE: Evaluation of a case of asthma induced by Trichosporon asahii. METHODS AND RESULTS: This report describes a 46-year-old Japanese man who developed asthma induced by T. asahii, following symptoms of HP attributable to the same pathogen, in a case of familial occurrence of SHP. This patient lacked typical findings of HP in his radiograph but had an elevated level of eosinophils in his bronchoalveolar lavage fluid. Open lung biopsy, however, revealed typical pathologic findings of HP when he was free of asthmatic symptoms. His serum was also positive for anti-T asahii antibody, as are the sera of SHP patients. Nevertheless, provocation tests, including returning home and inhalations of T. asahii antigen, reproduced asthmatic features such as airway hyperresponsiveness and reversible bronchoobstruction, but not the features of HP. A skin test with the same antigen also evoked an immediate allergic reaction. An IgE mechanism was suspected but could not be proven by radioallergosorbent test. The patient's son and daughter displayed typical features of SHP, associated with compatible results in their radiographs, bronchoalveolar lavage fluid analysis, serologic and pathologic examinations, and provocation and skin tests. CONCLUSIONS: To our knowledge, this is the first case of extrinsic asthma, and of coexistent asthma and HP, induced by T. asahii. The patient initially displayed symptoms typical of SHP, which were subsequently replaced by more typical asthmatic symptoms.