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Biomedical subjects

Nian-Sheng Tzeng

Publications and source records attributed to Nian-Sheng Tzeng.

2 recordsLinked to original sources

[Cognitive behavioral therapy for eating disorders].

Eating disorders include anorexia nervosa and bulimia nervosa. The former is characterized by failure to maintain a minimum normal body weight, while the latter is typified by recurrent binge eating followed by inappropriate compensating behavior, which may include self-inducing vomiting; abuse of laxatives, diuretics or other medications; fasting; and over-exercise. Because eating disorders are difficult to detect in the early stages and patients frequently try to hide their condition and avoid seeking medical help, medical treatment is sometimes sought only once a patient's condition poses an immediate threat to his/her health, or even life. Some patients suffer from chronic and treatment-refractory disorders. Cognitive behavioral therapy, administered through partially-structured guidance and education, has been shown to treat eating disorders effectively by correcting associated maladaptive and distorted cognitions and behaviors. A review of articles published in the domestic and international literature over the past five years show that cognitive behavioral therapy is more effective in treating eating disorders than other traditional approaches. Therefore, we chose to focus this study on the cognitive behavioral therapy model. Nurses can employ cognitive behavioral therapy to help eating disordered patients address and overcome the core beliefs that underpin their disorder (e.g., compulsive concern about body weight or figure) and recover health.

Anorexia Nervosa↗

Valproate pretreatment protects dopaminergic neurons from LPS-induced neurotoxicity in rat primary midbrain cultures: role of microglia.

Parkinson's disease is a neurodegenerative disorder characterized by progressive degeneration of dopaminergic (DA) neurons in the substantia nigra. Accumulating evidence supports the notion that neuroinflammation is involved in the pathogenesis of this disease. Valproate (VPA) has long been used for the treatment of seizures and bipolar mood disorder. In vivo and in vitro studies have demonstrated that VPA has neuroprotective and neurotrophic actions. In this study, using primary neuron-glia cultures from rat midbrain, we demonstrated that VPA is a potent neuroprotective agent against lipopolysaccharide (LPS)-induced neurotoxicity. Results showed that pretreatment with 0.6 mM VPA for 48 h robustly attenuated LPS-induced degeneration of dopaminergic neurons as determined by [(3)H] dopamine uptake and counting of the number of TH-ir neurons. The neuroprotective effect of VPA was concentration-dependent and was mediated, at least in part, through a decrease in levels of pro-inflammatory factors released from activated microglia. Specifically, LPS-induced increase in the release of TNFa, NO, and intracellular reactive oxygen species was markedly reduced in cultures pretreated with VPA. These anti-inflammatory effects of VPA were time and concentration-dependent correlated with a decrease in the number of microglia. Thus, our results demonstrate that protracted VPA pretreatment protects dopaminergic neurons from LPS-induced neurotoxicity through a reduction in levels of released pro-inflammatory factors, and further suggest that these anti-inflammatory effects may be contributed by VPA-induced reduction of microglia cell number. Taken together, our study reinforces the view that VPA may have utility in treating Parkinson's disease.

Analysis of Variance↗