ANALYSIS OF AGOMELATINE TREATMENT WITH DEPRESSIVE SYMPTOMS

Objective: Agomelatine is a new mechanism of antidepressants, which is approved by Taiwan Food and Drug Administration and available in Taiwan.Agomelatine behaves both as a potent agonist at melatonin MT1 and MT2 receptors and as a neutral antagonist at 5-HT2C receptors. The structuresof agomelatine are similar to melatonin with not only the effects to maintain depression symptoms but also can help patients who have insomnia.Methods: This is a retrospective study. In a mental hospital in Taoyuan, we analyzed the prescriptions of the outpatients who were prescribedagomelatine to realize the effects of agomelatine and whether the prescriptions were prescribed appropriately.Results: Catastrophic illnesses were found to be associated with significantly used multiple hypnotics (χ2 =22.02, p<0.001). When patients’ ageincreased by 1 year, multiple hypnotics used increased by 1.013 times (Exp(B)=1.013, p<0.01). Catastrophic illnesses were found to be associatedwith significantly used augmentation with other antidepressants (χ2=54.07, p<0.001).Conclusions: Doctors should be evaluating the benefits and risks when they prescribe a medicine to patients, and they should be written in medicalrecord. This study is the hope to provide relevant units as a reference for formulating health policies

Loss of vesicular dopamine release precedes tauopathy in degenerative dopaminergic neurons in a Drosophila model expressing human tau.

While a number of genome-wide association studies have identified microtubule-associated protein tau as a strong risk factor for Parkinson's disease (PD), little is known about the mechanism through which human tau can predispose an individual to this disease. Here, we demonstrate that expression of human wild-type tau is sufficient to disrupt the survival of dopaminergic neurons in a Drosophila model. Tau triggers a synaptic pathology visualized by vesicular monoamine transporter-pHGFP that precedes both the age-dependent formation of tau-containing neurofibrillary tangle-like pathology and the progressive loss of DA neurons, thereby recapitulating the pathological hallmarks of PD. Flies overexpressing tau also exhibit progressive impairments of both motor and learning behaviors. Surprisingly, contrary to common belief that hyperphosphorylated tau could aggravate toxicity, DA neuron degeneration is alleviated by expressing the modified, hyperphosphorylated tau(E14). Together, these results show that impairment of VMAT-containing synaptic vesicle, released to synapses before overt tauopathy may be the underlying mechanism of tau-associated PD and suggest that correction or prevention of this deficit may be appropriate targets for early therapeutic intervention

Radiographic Disclosure of Fournier’s Gangrene

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