Highly malignant endometrial stromal sarcoma in a cat.

An 11-year-old female Persian cat underwent ovariohysterectomy due to dilation of the uterine cavity with irregular thickening of the wall. Macroscopically, the middle and distal regions of the left uterine horn were swollen and the uterine wall was irregularly thickened due to the development of multiple coalescent, variably sized nodules. Microscopically, the nodules had originated in the endometrium and were composed of round to polygonal neoplastic cells arranged in dense sheets or ill-defined fascicles. The neoplastic cells had locally invaded the myometrium and reached the subserosa, with lymphovascular invasion. Immunohistochemically, the neoplastic cell population was partially positive for CD10, an established marker of endometrial stromal sarcoma (ESS) in humans, with focal and diffuse nuclear immunopositivity for oestrogen and progesterone receptors and immunonegativity for desmin and α-smooth muscle actin. Based on these findings, the uterine tumour was diagnosed as ESS and was considered to correspond morphologically to high-grade ESS in humans.

Characterization of muscarinic receptor-mediated cationic currents in longitudinal smooth muscle cells of mouse small intestine.

In mouse intestinal smooth muscle cells held at -50 mV, carbachol evoked an atropine-sensitive inward current in the intracellular presence of Cs(+). The current response consisted of an initial peak followed by a smaller plateau component on which oscillatory currents frequently arose. Results from various experimental procedures indicated that the inward current is a muscarinic receptor-operated cationic current (mI(cat)) sensitive to cytosolic Ca(2+) concentration ([Ca(2+)](i)) and that the initial peak and oscillatory components are contaminated by Ca(2+)-activated Cl(-) currents. Under conditions of [Ca(2+)](i) buffered to 100 nM, the mI(cat) response to cumulative carbachol applications was inhibited competitively by an M(2)-selective antagonist but non-competitively by an M(3)-selective one. Also it was severely reduced by pertussis toxin (PTX) treatment or a phospholipase C (PLC) inhibitor. Comparative analysis of mI(cat) in mouse and guinea-pig intestinal myocytes indicated that the underlying channels resemble between those myocytes in agonist sensitivity, current-voltage relationship, and unitary conductance. The results suggest that in mouse intestinal myocytes, mI(cat) arises mainly via an M(2)/M(3) synergistic mechanism involving PTX-sensitive G-proteins and PLC activity in the absence of current modulation by [Ca(2+)](i) changes, as described for guinea-pig ileal mI(cat). The channels underlying mI(cat) are also indistinguishable in gating properties between both types of myocytes.