When acral malignant melanoma facades as diabetic foot!

An 85-year-old Indian man presented with non-healing foot ulcer over the left heel. There was initial response to wound size with standard treatment including offloading, debridement and antibiotic therapy. However, subsequently, there was no progress noted.

Adaptor protein-2 sigma subunit mutations causing familial hypocalciuric hypercalcaemia type 3 (FHH3) demonstrate genotype-phenotype correlations, codon bias and dominant-negative effects.

The adaptor protein-2 sigma subunit (AP2σ2) is pivotal for clathrin-mediated endocytosis of plasma membrane constituents such as the calcium-sensing receptor (CaSR). Mutations of the AP2σ2 Arg15 residue result in familial hypocalciuric hypercalcaemia type 3 (FHH3), a disorder of extracellular calcium (Ca(2+) o) homeostasis. To elucidate the role of AP2σ2 in Ca(2+) o regulation, we investigated 65 FHH probands, without other FHH-associated mutations, for AP2σ2 mutations, characterized their functional consequences and investigated the genetic mechanisms leading to FHH3.

Effect of a serotonin reuptake inhibitor on irritability, apathy, and psychotic symptoms in patients with Alzheimer's disease.

Objective: To ascertain the impact of treatment with citalopram on irritability, apathy, delusions, and hallucinations in nondepressed behaviorally disturbed Alzheimer's disease (AD) patients.

Method: This was a retrospective analysis of data from the 36-week Clinical Antipsychotic Trials of Intervention Effectiveness in Alzheimer's Disease in which patients with probable AD (diagnosed according to criteria of the National Institute of Neurological and Communicative Disorders and Stroke and Alzheimer's Disease and Related Disorders Association [NINCDS/ADRDA]) were treated in a naturalistic manner. Scores were compared on the irritability, apathy, delusions, and hallucinations subscales of the Neuropsychiatric Inventory.

Present and prospective clinical therapeutic regimens for Alzheimer's disease.

Alzheimer's disease (AD) is an incurable neurodegenerative disorder that produces cognitive impairments that increase in severity as the disease progresses. The clinical symptoms are related to the presence of neuritic plaques and neurofibrillary tangles in the cerebral cortex which represent the pathophysiological hallmarks of AD. The debilitating nature of the disease can result in clinical burden for the patient, emotional strain for those that care for patients with Alzheimer's, and significant financial burden to society.