Dendritic cells modulate burn wound healing by enhancing early proliferation.

Adequate wound healing is vital for burn patients to reduce the risk of infections and prolonged hospitalization. Dendritic cells (DCs) are antigen presenting cells that release cytokines and are central for the activation of innate and acquired immune responses. Studies have showed their presence in human burn wounds; however, their role in burn wound healing remains to be determined.

Olanzapine treatment of adolescent rats causes enduring specific memory impairments and alters cortical development and function.

Antipsychotic drugs are increasingly used in children and adolescents to treat a variety of psychiatric disorders. However, little is known about the long-term effects of early life antipsychotic drug treatment. Most antipsychotic drugs are potent antagonists or partial agonists of dopamine D2 receptors; atypical antipsychotic drugs also antagonize type 2A serotonin receptors.

Olanzapine treatment of adolescent rats alters adult reward behaviour and nucleus accumbens function.

Antipsychotic drugs are increasingly used in children and adolescents to treat a variety of psychiatric disorders. However, little is known about the long-term effects of early life antipsychotic drug (APD) treatment. Most APDs are potent antagonists or partial agonists of dopamine (DA) D₂ receptors; atypical APDs also have multiple serotonergic activities.

Role for mTOR signaling and neuronal activity in morphine-induced adaptations in ventral tegmental area dopamine neurons.

While the abuse of opiate drugs continues to rise, the neuroadaptations that occur with long-term drug exposure remain poorly understood. We describe here a series of chronic morphine-induced adaptations in ventral tegmental area (VTA) dopamine neurons, which are mediated via downregulation of AKT-mTORC2 (mammalian target of rapamycin complex-2). Chronic opiates decrease the size of VTA dopamine neurons in rodents, an effect seen in humans as well, and concomitantly increase the excitability of the cells but decrease dopamine output to target regions.

Altered oxidative stress levels in Indian Parkinson's disease patients with PARK2 mutations.

The aim of this pilot study was to determine the baseline state of oxidative stress indices in patients with Parkinson's disease (PD). Peripheral blood samples of 15 PD subjects were analyzed and compared with ten age matched healthy controls. Patients with PARK2 mutations were also compared with PD patients without mutations.

Occurrence of PARK2 mutations in a never-smoker population with Parkinson's disease in North India.

Background: Parkinson's disease (PD) is a complex neurological disorder without any well-documented genotype-demography associations among sporadic variants. We recently reported PARK2 mutations to be constituting 40% of PD in this region and thus analysed how demographic variables associate with PARK2 mutations in 70 of these patients.

Methods: PD samples were screened by PCR single-strand conformation polymorphism (SSCP) and sequencing and their demographic data collected.

Genetic screening reveals high frequency of PARK2 mutations and reduced Parkin expression conferring risk for Parkinsonism in North West India.

Background: Among several aetiological factors, PARK2 mutations are the most common cause of Parkinson disease (PD) that result in degeneration of dopaminergic neurons in the substantia nigra.

Methods: In order to examine the contribution of PARK2 mutations and corresponding Parkin expression in blood of North West Indian PD patients, the authors screened 120,000 patients from 2001 to 2006 for features of PD using UK Parkinson disease society brain bank clinical diagnostic criteria (UKPDBBC), and tested PARK2 mutations in 69 of those that fulfilled this criteria. 43 controls lacking extrapyramidal signs were also analysed.

A case of manifesting carrier with DMD phenotype.

A case of a 35-year old female with a history of proximal weakness in lower limbs and bulkiness of both calves manifesting before ten years of age was reported. Clinical findings were suggestive of muscular dystrophy. Genetic analysis using polymerase chain reaction (PCR), single strand conformation polymorphism (SSCP) and direct sequencing revealed several point mutations, which account for dystrophin dysfunction and DMD type pathogenesis.