Search PubMed⌕ Search

PubMed · 15309250

Sinus node dysfunction secondary to hyperparathyroidism.

Abstract

We present two patients who were diagnosed with symptomatic sinus node dysfunction in the setting of hypercalcemia secondary to hyperparathyroidism. An extensive review of the literature has not revealed previous reports of this pathologic process.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Atman P Shah, Angela Lopez, Robin Y Wachsner, Sheba K Meymandi, Adel K El-Bialy, Anne M Ichiuji. 2004. Sinus node dysfunction secondary to hyperparathyroidism.. https://doi.org/10.1177/107424840400900209

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Prolactin stimulates prostate cell proliferation by increasing endoplasmic reticulum content due to SERCA 2b over-expression.

Prolactin (PRL) has been shown to be involved in the differentiation and proliferation of numerous tissues, including the prostate gland. Moreover, variations in [Ca2+]ER (calcium concentration within the endoplasmic reticulum) may play a role in cell growth. However, few studies have focused on the regulation of calcium homoeostasis by prolactin. The present study evaluates the regulation of calcium pools as well as the possible role of [Ca2+]ER variations as a signal for growth modulation by PRL. We show that PRL stimulates the proliferation of normal SV40 immortalized epithelial prostate (PNT1A) cells with a maximum effect at a dose of 100 ng/ml. We also show that 100 ng/ml PRL increases the [Ca2+]ER when measured either by indirect quantification with Fura-2AM after application of 1 mM thapsigargin or by direct quantification with Mag-Fura-2AM within the endoplas-mic reticulum. Western blot analysis shows that the SERCA 2b (sarcoendoplasmic calcium ATPase 2b) is over-expressed in PNT1A cells treated with 100 ng/ml PRL for 24 h. A small inter-fering RNA SERCA 2a/b, used to down-regulate endogenous SERCA 2b expression, reduced both PNT1A cell proliferation and [Ca2+]ER. We thus identify [Ca2+]ER and SERCA 2b as protagonists in PRL-induced proliferation.

Calcium↗

Binding of calcium ions and SNAP-25 to the hexa EF-hand protein secretagogin.

Secretagogin is a hexa EF-hand protein, which has been identified as a novel potential tumour marker. In the present study, we show that secretagogin binds four Ca2+ ions (log K1=7.1+/-0.4, log K2=4.7+/-0.6, log K3=3.6+/-0.7 and log K4=4.6+/-0.6 in physiological salt buffers) with a [Ca2+](0.5) of approx. 25 microM. The tertiary structure of secretagogin changes significantly upon Ca2+ binding, but not upon Mg2+ binding, and the amount of exposed hydrophobic surface in secretagogin increases upon Ca2+ binding, but not upon Mg2+ binding. These properties suggest that secretagogin belongs to the 'sensor' family of Ca2+-binding proteins. However, in contrast with the prototypical Ca2+ sensor calmodulin, which interacts with a very large number of proteins, secretagogin is significantly less promiscuous. Only one secretagogin-interacting protein was reproducibly identified from insulinoma cell lysates and from bovine and mouse brain homogenates. This protein was identified as SNAP-25 (25 kDa synaptosome-associated protein), a protein involved in Ca2+-induced exocytosis in neurons and in neuroendocrine cells. K(d) was determined to be 1.2x10(-7) M in the presence of Ca2+ and 1.5x10(-6) M in the absence of Ca2+. The comparatively low Ca2+ affinity for secretagogin and the fact that it undergoes Ca2+-induced conformational changes and interacts with SNAP-25 raise the possibility that secretagogin may link Ca2+ signalling to exocytotic processes.

Calcium↗

Cell signaling and neuronal death.

The past few decades have revealed that cell death can be precisely programmed with two principal forms, apoptosis and necrosis. Besides pathophysiological alterations, physiologic processes, such as the pruning of neurons during normal development and the involution of the thymus, involve apoptosis. This review focuses on the role of inter- and intracellular signaling systems in cell death, especially in the nervous system. Among neurotransmitters, glutamate and nitric oxide have been most extensively characterized and contribute to cell death in excitotoxic damage, especially in stroke and possibly in neurodegenerative diseases. Within cells, calcium, the most prominent of all intracellular messengers, mediates diverse forms of cell death with actions modulated by many proteins, including IP3 receptors, calcineurin, calpain, and cytochrome c.

Calcium↗