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Objective:To investigate the clinical effect of oxcarbazepine combined with ziprasidone in the treatment of acute excitatory agitation in patients with schizophrenia.Methods:From January 2016 to January 2019, a total of 110 patients with acute excitatory schizophrenia who admitted in the Third Hospital of Quzhou were enrolled, and they were divided into observation group and control group according to the random digital table method, with 55 cases in each group.The control group was given ziprasidone capsule, and the observation group was given oxcarbazepine combined with ziprasidone capsule treatment for 4 weeks.The PANSS excitatory agitation factor(PANSS-EC), explicit aggressive behavior scale(MOAS), clinical efficacy rating scale(CGI-SI) score, serum neurocytokines[brain-derived nutritional factors(BDNF), nerve growth factor(NGF), glial-derived neurotrophic factor(GDNF)], homocysteine (Hcy), inflammatory factors[interleukin 1β(IL-1β), interleukin 6(IL-6), interleukin 12(IL-12), tumor necrosis factor α(TNF-α)] before and after treatment and the incidence of adverse reactions were compared between the two groups.Results:After treatment, the PANSS-EC, MOAS, CGI-SI scores, Hcy, IL-1β and TNF-α levels were decreased in the two groups( t=7.829, 14.952, 3.417, 15.511, 18.948, 7.193, 18.453, 24.161, 1.995, 3.378, 3.968, 6.820, all P<0.05), which of the observation group were lower than those of the control group[(15.34±3.56)points vs.(11.08±3.17)points, (5.36±1.68)points vs.(4.15±1.46)points, (5.56±1.21)points vs.(4.18±1.35)points, (14.29±2.42)μmol/L vs.(10.63±2.24)μmol/L, (48.15±15.63)ng/L vs.(42.18±10.51)ng/L, (29.57±8.76)ng/L vs.(23.48±6.76)ng/L]( t=6.628, 4.032, 5.645, 8.231, 2.351, 4.082, all P<0.05), while the BDNF, NGF, GDNF levels were increased( t=6.253, 6.346, 3.513, 13.906, 15.874, 7.507, all P<0.05), which of the observation group were higher than those of the control group[(9.34±1.23)μg/L vs.(11.35±1.34)μg/L, (21.37±2.85)μg/L vs.(26.87±3.21)μg/L, (439.51±56.42)ng/L vs.(489.63±58.15)ng/L], the differences were statistically significant( t=2.351, 3.523, 3.204, all P<0.05). There was no statistically significant difference in the incidence of adverse reactions between the two groups[25.45%(14/55) vs.12.73%(7/55), χ 2=2.884, P=0.089]. Conclusion:Oxcarbazepine combined with ziprasidone in the treatment of acute excitatory patients with schizophrenia can control the clinical symptoms, improve the serum levels of cytokines, Hcy and inflammatory factors, and has high safety.
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Objective:To explore the relationship between smoking and the effect of antipsychotics in schizophrenics.Methods:From July 2017 to July 2019, 142 schizophrenics in the mental health center were treated with olanzapine, and the serum drug concentration and concentration/dose ratio (C/D) were calculated.The age, sex, liver function, smoking, combined medication and other clinical data of the two groups were collected, and the influencing factors of serum olanzapine concentration in schizophrenic patients were analyzed by multivariate logistic regression.Results:Forty-four patients were in the non-compliance group(serum olanzapine concentration <20ng/mL), and 98 patients were in the compliance group(serum olanzapine concentration 20-80ng/mL). In the non-compliance group, males accounted for 72.2%, the average age was (61.6±10.5)years old, smoking history accounted for 90.1%, and serum C/D was (2.5±1.1)ng·mL -1·mg -1·d -1, and in the compliance group, males accounted for 51.0%, the average age was (57.9±9.6)years old, smoking history accounted for 41.8%, and serum C/D was (3.2±1.8)ng·mL -1·mg -1·d -1, and there were statistically significant differences in sex, age, smoking history and serum C/D between the two groups ( t=5.86, χ 2=2.06, χ 2=5.43, t=2.38, all P<0.05). Multivariate logistic regression analysis showed that smoking and CYP1A2 genes were independently related to whether the plasma concentration of olanzapine was up to standard in schizophrenic patients.Compared with non-smokers, previous smoking increased the probability of blood concentration non-compliance by 11% and current smoking by 15% respectively( OR=1.15, P=0.001). And compared with CYP1A2 gene AA, CYP1A2 gene AC reduced the probability of blood concentration non-compliance by 15% and CYP1A2 gene CC by 13%( OR=0.87, P=0.002). Conclusion:There is an independent correlation between smoking and serum C/D value of olanzapine in schizophrenics.Quitting smoking can reduce the probability of substandard blood concentration.
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OBJECTIVE:To compare the efficacy and safety of only paroxetine vs. paroxetine combined with alprazolam in the treatment of diabetes complicated with anxiety and depression. METHODS:Totally 86 patients with diabetes complicated with anxi-ety and depression were randomly divided into observation group and control group. The patients in observation group were given paroxetine 20 mg,qd,and alprazolam 0.4 mg,tid;patients in control group were given paroxetine alone. The treatment course lasted for 8 weeks in 2 groups. The clinical data was compared,including fasting plasma glucose(FPG),2 h postprandial glucose (2 h PG),glycated hemoglobin (HbA1c),cortisol,adrenocorticotropic hormone (ACTH) levels and scores of Hamilton anxiety scale (HAMA) and Hamilton depression scale (HAMD). The adverse reactions were observed. RESULTS:After treatment,FP-BG,2 h PG,HbA1c,cortisol,ACTH levels and scores of HAMA and HAMD in observation group were significantly lower than control group,with significant difference(P0.05). CONCLUSIONS:Compared with paroxetine alone,paroxetine combined with alprazolam can improve more in blood glucose,endocrine levels and adverse mood symptoms in the treatment of diabetes complicated with anxiety and de-pression,with similar safety.
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BACKGROUND: Reports regarding adipose-derived stern cells (ADSCs) differentiation into dopaminergic (DN) neurons are few in addition, there is not experimental evidence of the effect of ADSCs on maintaining the survival of DN neurons.OBJECTIVE: To investigate the effect of glial cell-derived neurokophic factor (GDNF)-modified adipose-derived stem cells on survival of DN neurons under co-cultured condition.DESIGN, TIME AND SETrlNG: The in vitro cytology experiment was conducted at the Institute of Otolaryngology-Head and Neck Surgery and Key Laboratory of Zoonoses of Ministry of Education between March and December 2007.MATERIALS: Wistar rats with 3-weeks-old, or 14 days of pregnancy were provided by Norman Bethune College of Medicine, Jilin University.METHODS: The GDNF recombinant adenovirus was constructed by using pAdTrackCMV and pAdEasy-1 system. DN neurons were obtained from the rostral mesencaphalic tegmentum of Wistar rat embryos by using trypsin and collagenase method. ADSCs isolated from rat inguinal fat pads were digested with collagenase Ⅱ, cultured and passaged in vitro. When the cells reached 60% cenfluency at the 3rd passage, cells were transfectad with 1×109vp/mL of Ad-GDNF for 1 hour and then transferred into growth medium for another 24 hours, and GDNF level in cell supematant was detected by ELISA assay. Meanwhile, the co-cultured of ADSCs and DN neurons were carried out for following 7 days. With GFP-modified ADSCs was served as a control group.MAIN OUTCOME MEASURES: The effect of co-cultured condition on the survival of DN neurons, as well as the differentiation of GDNF-modified ADSCs was detected by immunofluorescence staining.RESULTS: GDNF appeared in ADSCs supematant at 24 hours after Ad-GDNF transfection and reached a peak at 72 hours.There was approximately 80% GFP-positive labeled in ADSCs. The tyrosinase hydroxylase staining results demonstrated that the rate of survival DN neurons were significantly increased than in DA neurons cultured alone, co-cultured group of GFP-modified ADSCs and GDNF-modified ADSCs groups (55%, 15%, 25%, P < 0.01). However, there were no co-expressing TH and GFP positive cells appeared at 7 days of co-culture, which indicated that the co-cultured condition was not available to ADSCs differentiation.CONCLUSION: The co-cultured of GDNF modified ADSCs and DN neurons can promote the survival and growth of cultured DN neurons, however, it can not induce ADSCs differentiate into DN neurons.