[Studies on the chemical constituents of Chaenomeles speciosa].

OBJECTIVE: To study the chemical constituents of Chaenomeles speciosa. METHODS: Isolation and purification were carried out by varied chromatographies, and structure identifications of compounds were carried out by physical methods, chemical methods and spectral data. RESULTS: Seven compounds were obtained from the ethyl acetate fraction of C. speciosa, and were identified as cinnamic acid (I), 2'-methoxyaucuparin (II), 2-hydroxyl-butanedioic acid-4-methylester (III), esculetin (IV), p-hydroxybenzoic acid (V), chlorogenic acid (VI), caffeic acid (VII). CONCLUSION: Compounds I - IV are obtained from Chaenomeles genus for the first time.

[Study on safe use of 10% difenoconazole in GAP of Gentiana scabra].

OBJECTIVE: To investigate the safe use of 10% difenoconazole in planting Gentiana scabra. METHOD: The degradation dynamics of 10% ifenoconazole in the stems and leaves of G. scabra collecting in different time were determined by GC with ECD detection, and the half life of difenoconazole in the plant was calculated, and then the safe use method of 10% difenoconazole was formulated. RESULT: Under the local climatic conditions, the half life of 10% difenoconazole was 6.84-6.90 days. CONCLUSION: In the good agricultural practice (GAP) of G. scabra, the maximal concentration of 10% difenoconazole is 400 g x ha(-1), the safety interval of using 10% difenoconazole is 40 days.

Reduced plasma total antioxidant status in first-episode drug-naive patients with schizophrenia.

Excessive free radical production leading to oxidative stress may be involved in the pathophysiology of schizophrenia. Determination of total antioxidant status (TAS) provides an index of the sum of activities of all antioxidants. However, there have been few systematic studies to examine the relationship between TAS levels and psychopathology in first-episode and drug-naive patients with schizophrenia. TAS levels were determined in the plasma of 60 never-medicated first-episode patients with schizophrenia and 68 healthy control subjects. The schizophrenia symptomatology and the depressive symptoms were assessed by the positive and negative syndrome scale (PANSS) and the Hamilton rating scale for depression (HAMD). The results showed that TAS levels were significantly lower in first-episode patients with schizophrenia than in healthy control subjects (159.8 ± 45.8 U/ml vs 211.4 ± 46.8 U/ml, F=39.5, df=1, 126, p < 0.001). A trend toward significant inverse correlation between TAS levels and PANSS negative subscore was observed (r = 0.25, df=60, p = 0.06). Our results suggest that oxidative stress occurs in an early course of schizophrenia and may have an important role in pathogenesis and perhaps, negative symptomatology of schizophrenia.

Smoking initiation and schizophrenia: a replication study in a Chinese Han population.

Schizophrenia is associated with a greater probability of ever smoking daily and with higher rates of initiation of daily smoking after age 20 in Caucasian populations. The aims of the current study were to replicate that schizophrenia is associated with smoking and higher risk of initiating daily smoking before schizophrenia starts among a large sample of male Chinese patients. A survival analysis of onset age for daily smoking compared 776 DSM-IV male inpatients with schizophrenia to 560 male controls. The results showed that the cumulative hazard curves for age of smoking initiation in schizophrenia and controls were significantly different (p<0.001), even after controlling for education (p<0.001). After excluding the patients who started smoking within 5 years before schizophrenia started, the cumulative hazard curve for schizophrenia was significantly different from ever-smoked controls (p<0.001), even after adjusting for education (p<0.001). These findings suggest that schizophrenic patients have a higher risk of starting daily smoking suggesting that vulnerability to schizophrenia may be associated with a higher risk of becoming a daily smoker.

The study of BDNF Val66Met polymorphism in Chinese schizophrenic patients.

Accumulating evidence showed that brain-derived neurotrophic factor (BDNF) may be involved in the pathophysiology of schizophrenia. Recent studies have reported that the Val66Met polymorphism of the BDNF gene may be associated with susceptibility for schizophrenia and age of onset of this disease, with mix results. In the present study, the BDNF Val66Met gene polymorphism was examined in 387 inpatients (259 men and 128 women) meeting the DSM-IV criteria for schizophrenia and unrelated 365 healthy controls (255 men and 110 women). The schizophrenia symptomatology was assessed by the Positive and Negative Syndrome Scale (PANSS). Age of onset was defined as the age at which the psychotic symptoms first appeared. Our results showed that genotype frequency distributions and allelic frequencies did not differ between patients and controls. No interaction was found between sex and genotypes. Analysis of covariance (ANCOVA) showed a significance of the BDNF Val66Met genotypes on the age of onset (F=3.76, p<0.02), after adjusting sex, age and duration of illness. Furthermore, ANCOVA showed that the significance of the BDNFVal66Met genotypes on age of onset was increased comparing the Val66Met heterozygotes with the combination of Val66Val and Met66Met homozygotes (F=5.85, p<0.01). Our results suggest that the BDNF Val66Met polymorphism may not contribute directly to the susceptibility to schizophrenia, but to the onset of the disease. Furthermore, our results show the heterozygous effect of the BDNF Val66Met gene on the clinical variability of schizophrenia phenotype.

Association of the manganese superoxide dismutase gene Ala-9Val polymorphism with clinical phenotypes and tardive dyskinesia in schizophrenic patients.

OBJECTIVE: Several recent studies that have investigated the genetic association between the manganese superoxide dismutase (MnSOD) gene Ala-9Val single-nucleotide polymorphism (SNP) and tardive dyskinesia (TD) have produced conflicting results. This study was to investigate whether this SNP was associated with clinical phenotypes and antipsychotic-induced tardive dyskinesia (TD) in schizophrenia in a genetically homogeneous Han Chinese inpatient population. METHODS: Genotyping was performed for the MnSOD gene Ala-9Val SNP in Chinese schizophrenia patients with (n=176) and without TD (n=346). The severity of TD was assessed using the abnormal involuntary movement scale (AIMS), and psychopathology using the Positive and Negative Syndrome Scale (PANSS). RESULTS: The frequencies of genotypes and alleles did not differ significantly between schizophrenic patients with and without TD (both p>0.05). Also, there was no significant difference in the AIMS total score between the Val/Val and Ala allele carrier groups (p>0.05). However, the PANSS negative symptom subscore was significantly higher in patients with Val/Val genotype (21.8+/-7.3) than those with Ala alleles (20.1+/-7.7) (t=2.32, p=0.03). CONCLUSION: While the MnSOD gene Ala-9Val polymorphism did not play a major role in the susceptibility to TD in schizophrenic patients, it might be associated with negative symptoms of schizophrenia.

Decreased serum BDNF levels in chronic institutionalized schizophrenia on long-term treatment with typical and atypical antipsychotics.

Accumulating evidence showed that brain-derived neurotrophic factor (BDNF) may be involved in the pathophysiology of schizophrenia. Decreased BDNF levels have been found in the serum of schizophrenic patients with mixed results. In the present study, we assessed serum BDNF levels in a large group of 364 schizophrenic patients (157 on clozapine, 89 on risperidone and 118 on typical antipsychotics), compared to 323 healthy control subjects matched for age and gender. The schizophrenia symptomatology was assessed by the Positive and Negative Syndrome Scale (PANSS), and serum BDNF levels were measured by sandwich ELISA. The results showed that BDNF levels were significantly lower in chronic patients with schizophrenia than in healthy control subjects (9.9+/-2.0 ng/ml vs.11.9+/-2.3 ng/ml, p<0.0001). Lower BDNF levels were observed in patients treated with risperidone (9.3+/-2.3 ng/ml) compared to those with clozapine (10.2+/-2.0 ng/ml, p<0.001) and typical antipsychotics (10.0+/-2.1 ng/ml, p<0.01). Furthermore, a stepwise multiple regression analysis identified types of antipsychotic drugs (beta=-0.37, t=-3.15, p=0.001) and BDNF levels (beta=-0.26, t=-2.51, p=0.014) as the influencing factor for the positive symptom subscore of PANSS. In addition, there was a sex difference in BDNF levels in patients with schizophrenia (9.7+/-1.9 ng/ml for males vs.10.4+/-2.1 ng/ml for female, p<0.005), but not in normal controls. Our findings indicated decreased BDNF serum levels in chronic patients with schizophrenia, which may be related to clinical phenotypes, including gender, antipsychotic treatment and the severity of psychotic symptoms.

Decreased levels of serum brain-derived neurotrophic factor in drug-naïve first-episode schizophrenia: relationship to clinical phenotypes.

OBJECTIVE: There is accumulating evidence that brain-derived neurotrophic factor (BDNF) may be involved in the pathophysiology of patients with schizophrenia. Clinical studies show reductions in BDNF in schizophrenic patients treated with first generation antipsychotics or second generation antipsychotics. However, there have been few systematic studies to examine the relationship between BDNF levels and psychopathology in first-episode and drug-naïve patients with schizophrenia. MATERIALS AND METHODS: Serum BDNF levels were determined using enzyme-linked-immunosorbent assay (ELISA) in the serum of 88 never-medicated first-episode and 90 healthy controls subjects matched for age and gender. The schizophrenia symptomatology and the depressive symptoms were assessed by the positive and negative syndrome scale (PANSS) and the Hamilton rating (HAMD) scale for depression. RESULTS: The results showed that BDNF levels were significantly lower in first-episode patients with schizophrenia than in healthy control subjects (9.0 +/- 4.2 ng/ml vs 12.1 +/- 2.2 ng/ml; F = 37.6; df = 1, 176; p < 0.0001). A significant positive correlation between BDNF levels and PANSS positive subscore was observed (r = 0.29; df = 88; p = 0.008). Furthermore, higher BDNF levels were observed in patients with paranoid subtype of schizophrenia. However, no significant correlation between BDNF and HAMD total score was found. CONCLUSION: Low BDNF levels at the onset of psychosis suggest that it may contribute to the pathogenesis of schizophrenia and perhaps, could be a candidate biological marker for positive symptoms.