Publications by authors named "J J Halperin"

Infertility in hyperprolactinemic females is attributed to the dysregulation of GnRH release, subsequently affecting gonadotropin levels, and ultimately leading to anovulation. However, in addition to the hypothalamus, prolactin receptor (PRLR) is expressed in ovaries as well, suggesting potential local effects of PRL in cases of hyperprolactinemia. We have developed an experimental model of sulpiride (SPD)-induced hyperprolactinemia using a wild rodent, the plains vizcacha, and studied the implications of pharmacological PRL levels on folliculogenesis and steroid production.

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The plains vizcacha is a rodent that shows reactivation of the hypothalamic-pituitary-ovary (HPO) axis activity at mid-gestation. This process is enabled by the secretion of hypothalamic gonadotropin-releasing hormone (GnRH) at mid-gestation, followed by follicle-stimulating hormone (FSH) and luteinizing hormone (LH) secretion. However, a decrease in the pituitary GnRH receptor (GnRHR) expression is concomitantly determined.

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CD59 is a cell-surface inhibitor of the terminal step in the complement cascade. However, in addition to its complement inhibitory function, a non-canonical role of CD59 in pancreatic beta cells has been identified. Two recently discovered intracellular alternative splice forms of CD59, IRIS-1 and IRIS-2, are involved in insulin exocytosis through interactions with SNARE-complex components.

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Article Synopsis
  • SIRS after mitral transcatheter edge-to-edge repair is linked to worse clinical outcomes in patients with severe mitral regurgitation.
  • Forty-four out of 158 patients (27.9%) developed SIRS post-procedure, which was characterized by elevated white blood cell counts and fever.
  • The presence of SIRS significantly increased the risk of major cardiovascular events, including nonfatal heart attacks and deaths, indicating the need for closer monitoring in these patients.
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  • A patient experienced repeated ischemic strokes after undergoing surgery to repair a mitral valve, despite not having obvious systemic thrombophilia.
  • Even with anticoagulation treatment, the patient's thromboembolism did not improve.
  • After the removal of the prosthetic valve, the patient showed no symptoms and had normal valve function, suggesting an unusual reaction to the prosthetic material may have caused the issues.
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