Studies with an estrogen-dependent murine model of vaginal candidiasis suggest that local cell-mediated immunity (CMI) is more important than systemic CMI for protection against vaginitis. The present study, however, showed that, compared to uninfected mice, little to no change in the percentage or types of vaginal T cells occurred during a primary vaginal infection or during a secondary vaginal infection where partial protection was observed. Furthermore, depletion of polymorphonuclear leukocytes (PMN) had no effect on infection in the presence or absence of pseudoestrus. These results indicate a lack of demonstrable effects by systemic CMI or PMN against vaginitis and suggest that if local T cells are important, they are functioning without showing significant increases in numbers within the vaginal mucosa during infection.

Pheochromocytoma is a well-described cause of paroxysmal hypertension.1 However, pheochromocytoma presenting with cyclical hypertension and hypotension is uncommon. 2,3 Cardiomyopathy in pheochromocytoma is a well-known phenomenon. Only recently has the inverted takotsubo pattern, in which the left ventriculogram shows hypokinetic bases and preserved apical function, been recognized as being associated with such tumors. [4][5][6] This pattern is in contrast with standard takotsubo cardiomyopathy, which is characterized simply by apical ballooning. Here, we describe a case of pheochromocytoma presenting with cyclic blood pressure (BP) fluctuations as well as the inverted takotsubo cardiomyopathy. Three forms of takotsubo cardiomyopathy exist. One involves apical akinesis, another is the midventricular variant, and the other is the newly noted inverted takotsubo variant, as seen in our patient.7 This presence of the inverted variant should arouse suspicion of a pheochromocytoma. We discuss how the excess catecholamines may contribute to this association.A 55-year-old Caucasian man with no known medical problems awoke from sleep with palpitations and chest pain followed by a severe headache. The patient had intermittent palpitations and chest discomfort for several weeks prior to the emergency department visit, with a flu-like illness about 2 months prior. He denied having any sweating or drenching night sweats. He had a remote history of alcohol abuse and smoked 1 pack a day of cigarettes for many years. He did not take any medications and had no family history of coronary artery disease.On initial presentation he was pale and had a pulse rate of 180 beats per minute, with a BP of 80 ⁄ 55 mm Hg. He complained of ongoing severe substernal chest pain and shortness of breath. The physical examination revealed tachycardia without any murmurs, rubs or gallops, or diffuse rales in half the lung fields and no abdominal tenderness or new skin rashes or lesions. There was no clubbing, cyanosis, or edema of the extremities. Telemetry revealed unstable ventricular tachycardia, and the patient was cardioverted to a normal sinus rhythm. Follow-up examination showed significant hypertension (175 ⁄ 90 mm Hg in the left arm and 190 ⁄ 99 mm Hg in the right arm), a heart rate of 80 beats per minute, a respiratory rate of 26 breaths per minute, and hypoxemia at 84% on room air.Electrocardiographic (ECG) results after cardioversion showed a 3-mm ST-segment depression in the inferior leads II, III, and aVF, and leads V3 through V6. ECG findings prior to the arrhythmia had consistently revealed evidence of left ventricular

SUMMARY Mucosal cell-mediated immunity (CMI) by CD4+ T cells is postulated to be important for host defence against several vaginal pathogens. In addition to the recognized phenotypic distinctions of resident vaginal T lymphocytes, we recently provided evidence by¯uorescence-activated cell sorter (FACS) that murine vaginal CD4 + T lymphocytes, are differentially recognized by two epitopedistinct anti-CD4 antibodies, suggesting that the CD4 protein on vaginal CD4+ cells is atypically expressed. In the present study, we con®rm this by FACS and immunohistochemistry under nondenaturing conditions using two additional anti-CD4 antibodies. However, positive immunohistochemical staining of vaginal CD4+ cells under denaturing conditions revealed that the CD4 epitope in question is indeed present within the CD4 protein. Using reverse transcription polymerase chain reaction, ampli®cation of CD3, T-cell receptor-b (TCR-b), and TCR-d mRNA from lymph node and vaginal tissue, and CD4 mRNA from lymph node tissue was demonstrable. In contrast, ampli®cation of CD4 mRNA from vaginal tissue, vaginal enriched lymphoid cells, or a puri®ed (FACS-sorted) population of vaginal-speci®c CD4 + cells using two distinct primer sets was not demonstrable. Altogether, our results provide evidence that the CD4 protein on vaginal CD4 + T cells is conformationally distinct compared with its systemic counterpart, either as a result of a unique CD4 mRNA sequence or from a stable interaction of soluble CD4 with the surface of vaginal T cells.

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