Results: Between February 2008 and December 2009, 325 adult patients admitted for elective heart surgery were included. Analyses showed that low selleckchem fat-free mass index, present in 8.3% of patients, was independently associated with occurrence

of infections after cardiac surgery (18.5% vs 4.7%; adjusted odds ratio, 6.9; 95% confidence interval, 1.8-27.7; P = .01). Low fat-free mass index also tended to be associated with higher risk of longer postoperative intensive care unit stay (adjusted hazard ratio, 0.7; 95% confidence interval, 0.4-1.1; P = .09). When classifying patients as undernourished by traditional methods (body mass index <= 21.0 kg/m(2) or >= 10% weight loss in preceding 6 months), half of patients with low fat-free mass index were misclassified as well nourished.

Conclusions: Low fat-free mass index is associated with increased occurrence of adverse outcomes after cardiac surgery. We advocate fat-free mass index as the leading parameter in classifying and treating undernourished cardiac surgical patients, which might improve recovery PRI-724 rates after cardiac surgery. (J Thorac Cardiovasc Surg 2011;142:1263-9)”
“Organophosphate (OP)-induced brain damage is defined as progressive damage to the brain,

resulting from the cholinergic neuronal excitotoxicity and dysfunction induced by OP-induced irreversible AChE inhibition. This delayed secondary neuronal damage that occurs mainly in the cholinergic regions of the brain that contain dense accumulations of cholinergic neurons and the majority over of cholinergic projection, might be largely responsible for persistent profound neuropsychiatric and neurological impairments (memory, cognitive, mental, emotional, motor and sensory deficits) in the victims of OP poisoning. Neuroprotective strategies for attenuating OP-induced brain damage should target

different development stages of OP-induced brain damage, and may include but not limited to: (1) Antidote therapies with atropine and related efficient anticholinergic drugs; (2) Anti-excitotoxic therapies targeting attenuation of cerebral edema and inflammatory reaction, blockage of calcium influx, inhibition of apoptosis program, and the control of seizures; (3) Neuroprotective strategies using cytokines, antioxidants and NMDAR antagonists (a single drug or a combination of drugs) to slow down the process of secondary neuronal damage; and (4) Therapies targeting individual symptoms or clusters of chronic neuropsychiatric and neurological symptoms. These neuroprotective strategies may help limit or prevent secondary neuronal damage at the early stage of OP poisoning and attenuate the subsequent neuropsychiatric and neurological impairments, thus reducing the long-term disability caused by exposure to OPs. (c) 2012 Elsevier Inc. All rights reserved.”
“Current therapeutic strategies are proving inadequate to deal with growing obesity rates because of the inherent resistance of the human body to weight loss.