(C) 2009 Wiley Periodicals Inc, Environ Toxicol 25: 48-54, 2010

(C) 2009 Wiley Periodicals. Inc, Environ Toxicol 25: 48-54, 2010.”
“Postoperative hypocalcaemia has been reported to be more common after total thyroidectomy (TT) for Graves’ disease than after TT for benign atoxic multinodular goitre (MNG). The reasons

for this potential association are not clear. In the present study, the frequency and risk factors of hypocalcaemia after TT for Graves’ vs MNG were compared.

Between January 1999 and October 2009, patients with first-time GSK3235025 surgery for Graves’ disease or MNG treated with a TT were included in the study. Postoperative hypocalcaemia was defined by symptoms, calcium levels and treatment with calcium and/or vitamin D analogues during postoperative hospital stay, at discharge, and at the 6-week and 6-month follow-ups. Outcomes were compared with Mann-Whitney, chi(2) and Fishers’ exact test where appropriate and by multivariable logistic regression analysis.

There were 128 patients with Graves’ disease and 81 patients with MNG. Patients with Graves’ disease were younger Angiogenesis inhibitor than patients with MNG (median age, 35 vs 51 years, p < 0.001). Symptoms

of hypocalcaemia were more common in patients with Graves’ disease (p < 0.001; OR, 95 % CI 3.26, 1.48-7.14), but the frequency of biochemical hypocalcaemia, postoperative levels of parathyroid hormone (PTH) and treatment with calcium and vitamin D did not differ between groups of patients.

Apart from more frequent

symptoms of hypocalcaemia in patients with Graves’ disease, there was no difference in the overall frequency of biochemical hypocalcaemia, low levels of PTH and/or treatment with calcium and vitamin D.”
“Recent researches indicated that mitochondrial pathway might play an important role in lead-induced apoptosis. Our previous study also found that lead could induce apoptosis in PC 12 cells, and mitochondrial pathway events were involved in this process. As lead can disturb Ca(2+) homeostasis, the present study was undertaken to determine whether lead can activate key cellular events in the learn more endoplasmic reticulum (ER) pathway, including the expressions of C/EBP homology protein (CHOP) and glucose-regulated protein 78 (GRP78), and the activation of caspase-12 and calpain. The results showed that lead could increase the expression of GRP78, while the expressions of CHOP and procaspase-12 remained unchanged. Moreover, the caspase-12 and calpain were not activated, and the ultrastructure of endoplasmic reticulum was not altered. Therefore, it suggests that lead may induce apoptosis in PC 12 cells through mitochondrial pathway, but not through the endoplasmic reticulum pathway. (C) 2009 Wiley Periodicals. Inc. Environ Toxicol 25: 55-60, 2010.”
“In the present study, an attempt has been made to analyze the changes in the biochemical and mineral contents of lead-intoxicated bones of Catla catla at subchronic (15.

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