Key pointsr Acutely isolated rat magnocellular neurosecretory cells (MNCs) display reversible hypertrophy when exposed to hypertonic saline (325 mosmol kg −1 ) for tens of minutes.r Osmotically evoked hypertrophy is prevented by agents that block Na + channels, TRPV1 channels (which mediate an osmotically evoked depolarization in these cells), L-type Ca 2+ channels, and exocytotic fusion and is associated with an increase in whole-cell capacitance.r Exposure to hypertonic saline activates phospholipase C leading to a decrease in plasma membrane phosphatidylinositol 4,5-bisphosphate.r Inhibition of phospholipase C or protein kinase C prevents osmotically evoked hypertrophy and activation of protein kinase C evokes hypertrophy in the absence of an increase in osmolality.r These results suggest that osmotically evoked hypertrophy is triggered by an increase in MNC action potential firing, leading to Ca 2+ influx, the activation of phospholipase C, an increase in diacylglycerol, and the activation of protein kinase C. AbstractThe magnocellular neurosecretory cells of the hypothalamus (MNCs) synthesize and secrete vasopressin or oxytocin. A stretch-inactivated cation current mediated by TRPV1 channels rapidly transduces increases in external osmolality into a depolarization of the MNCs leading to an increase in action potential firing and thus hormone release. Prolonged increases in external osmolality, however, trigger a reversible structural and functional adaptation that may enable the MNCs to sustain high levels of hormone release. One poorly understood aspect of this adaptation is somatic hypertrophy. We demonstrate that hypertrophy can be evoked in acutely isolated rat MNCs by exposure to hypertonic solutions lasting tens of minutes. Osmotically evoked hypertrophy requires activation of the stretch-inactivated cation channel, action potential firing, and the influx of Ca 2+ . Hypertrophy is prevented by pretreatment with a cell-permeant inhibitor of exocytotic fusion and is associated with an increase in total membrane capacitance. Recovery is disrupted by an inhibitor of dynamin function, suggesting that it requires endocytosis. We also demonstrate that hypertonic solutions cause a decrease in phosphatidylinositol 4,5-bisphosphate in the plasma membranes of MNCs that is prevented by an inhibitor of phospholipase C (PLC). Inhibitors of PLC or protein kinase C (PKC) prevent osmotically evoked hypertrophy, and treatment with a PKC-activating phorbol ester can elicit hypertrophy in the absence of changes in osmolality. These studies suggest that increases in osmolality cause fusion of internal membranes with the plasma membrane of the MNCs and that this process is mediated by activity-dependent activation of PLC and PKC.L. Shah and V. Bansal have contributed equally to this work.
Legionnaires disease is primarily a pneumonic illness with possible multisystem involvement. Major risk factors include immunodeficiency, smoking, alcoholism and chronic obstructive pulmonary disease among others. We report a peculiar case of Legionnaires disease presenting with diarrhea as the chief complaint and no respiratory symptoms throughout the course of disease. The patient had no risk factors for the disease and had no recent travel history or sick contacts. Acute diarrhea is not an uncommon manifestation of Legionnaires disease, although isolated diarrhea symptoms with the absence of concurrent respiratory symptoms and no risk factors for Legionella makes this case a diagnostic challenge, leading to possible delay in appropriate management. We are presenting this case to inform physicians of the possibility of Legionnaires disease presenting as an isolated gastrointestinal involvement with no clinical symptoms of pneumonia at presentation.
We present the case of a 50-year-old man presenting with new heart failure symptoms. He had no evidence of any ischaemic cardiomyopathy, however, further cardiac imaging showed a left ventricular non-compaction cardiomyopathy. He was noted to have muscular weakness and an exhaustive search for associated comorbidities yielded a diagnosis of Becker muscular dystrophy. In this report, we review the pathophysiology, comorbidities and diagnostic workup in patients presenting with left ventricular non-compaction in the context of dystrophinopathy. Ultimately, we suggest the consideration of rare cardiomyopathies in all patients presenting with neuromuscular syndromes and vice versa.
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