BACKGROUND: Homocysteine is associated with the attack of cerebral infarction, and cystathionine-beta-synthase (CBS) is a key enzyme of the metabolism of homocysteine, but it is still not clear whether its gene mutation is the potential candidate genic factor of cerebral infarction.OBJECTIVE: To observe the correlation of CBS base mutation at T833C and G919 sites with the attack of ischemic stroke in youths from the angle of genic mutation.DESIGN: A patient-control analysis.SETTING: Department of Neurology, China-Japan Friendship Hospital of Jilin University.PARTICIPANTS: Patient group (n=100): Young inpatients with cerebral infarction ≤ 45 years old in the China-Japan Friendship Hospital of Jilin University between April 2003 and December 2004, admitted within 2 days after attack. Control group (n=100): Normal young physical examinees in this hospital at the same period.METHODS: The levels of fasting and loaded homocysteine in plasma were detected with high performance liquid chromatography (HPLC), CBS genes at T833C and G919A sites with polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and amplification refractory mutation system in all the subjects.RESULTS: All of the 200 subjects entered the analysis of results. ① Detection of CBS genes at T833C and G919A sites: The distribution of genotype, frequency of homozygote and that of allele had no significant differences between the patient group and control group (P ＞ 0.05). ② Concentration of homocysteine in plasma: There were significant differences among the genotypes at G919A and T833C sites (P ＜ 0.001). The results of LSD-t test of the mutation at the two sites showed that there were significant differences between homozygote and heterozygote, homozygote and wild type,as well as C heterozygote and wild type (P ＜ 0.05).CONCLUSION: ① The CBS gene mutations at both T833C and G919A sites can lead to the obvious increase of the concentration of homocysteine in plasma. ② The CBS gene mutations at T833C and G919A sites had no direct association with the attack of cerebrovascular disease in youths.

BACKGROUND: The increase of concentration of plasma homocysteine is the independent risk factor of atherosclerotic and thrombotic cerebral infarction. Genic mutation of methylene tetrahydrofolate reductase (MTHFR), which is the metabolic enzyme of homocysteine in thansulfuration and remethylation,can induce the elevation of the concentration of plasma homocysteine.OBJECTIVE: To explore the relationship of hyperhomocysteinemia and genic mutation of MTHFR of homocysteine with ischemic cerebrovascular disease in youths.DESIGN: Case-control observation,SETTING: Department of Neurology, China-Japan Friendship Hospital,Jilin UniversityPARTICIPANTS: 100 young patients with cerebral infarction, who were hospitalized within 2 days after episode at the Department of Neurology,China-Japan Union Hospital, Jilin University between April 2003 and December 2004, were enrolled as case group, 73 males and 27 females, aged 27-45 years old with an average of (42±5) years. 100 cases in control group were healthy people receiving health examination in the same period, 70 males and 30 females, aged 18-45 years old with an average of (39±4) years.METHODS: The homocysteine in fasting plasma of testees was detected with high performance liquid chromatograpy (HPLC). C677T site and A1298C site of MTHFR gene were analyzed with polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and detected with armplification refractory mutation system (ARMS).MAIN OUTCOME MEASURES: Detection of MTHFR C677T and A1298C gene; Relationship between concentration of plasma homocysteine and MTHFR genotype.RESULTS: A total of 100 inclusive patients and 100 normal control people were involved in the result analysis. ①Detection of MTHFR C677Tand A1298C gene: Distribution of genotype, frequency of homozygote and frequency of allele of MTHFR C677T in the case group and control group had significant difference (P ＜ 0.01 ) while the distribution of genotype,frequency of homozygote and frequency of allele of MTHFR A1298C gene in the case group and control group had insignificant difference (P ＞ 0.05 ). ②Relationship between the concentration of plasma homocysteine and MTHFR genotype: The concentration of plasma homocysteine between MTHFR C677T and A1298C genotype had significant difference (P＜ 0.001 ). The mutant result LSD-t check of the 2 sites showed that mean difference of homozygote and heterozygote, homozygote and concentration of wild type homocysteine had statistical significance (P ＜ 0.05). The mean difference of MTHFR C677T and A1298C heterozygote and concentration of wild type homocysteine in plasma had no statistical significance (P＞ 0.05 ).CONCLUSION: The mutation of MTHFR C677T and A1298C leads to the marked increase in the concentration of plasma homocysteine. The MTHFR C677T polymorphism site is the independent risk factor of is chemic cerebrovascular disease in youths. The genic mutation of MTHFR A 1298C has no correlation with the attack of ischemic cerebrovascular disease of youths.

Objective To study the effects of lactate peritoneal dialysis solution(L-PDS) with different concentrations on apoptosis of human peritoneal mesothelial cells(HPMC),the expressions of bcl-2,bax and activity of caspase-3.Methods HPMC were separated using enzyme digestion and cultivated stably in vitro.After HPMC were co-cultivated with different concentrations(1.50%,2.50%,4.25%) L-PDS,flow cytometry was used to test the apoptosis of HPMC,RT-PCR was used to observe the expressions of bcl-2 and bax,fluorometric method was used to detect the activity of caspase-3.Results Compared with control group, L-PDS could induce the apoptosis of HPMC,especially in high concentration.With the increasing of L-PDS concentration,the expression of bcl-2 mRNA decreased,the expression of bax mRNA increased,the activity of caspase3 raised.There were significant differences of the indexes mentioned above between 4.25%,2.50% L-PDS groups and control group(P0.05).Conclusion L-PDS could induce HPMC apoptosis,which may be executed by alternating of the expressions of bcl-2,bax and activating of caspase3.

Traditionally, schizophrenia is considered to be a result of dopaminergic hyperactivity while dopaminergic deficiency underlies Parkinson’s disease (PD). This opposing pathophysiology makes comorbid schizophrenia and PD seemingly impossible; however, they do coexist rarely in clinical practice. We present four patients with paranoid schizophrenia diagnosed in their youth who developed parkinsonian symptoms on a stable regimen of quetiapine or clozapine after several years. The diagnosis of comorbid schizophrenia and PD was made mainly according to clinical observation. In addition, dopamine transporter (DAT) imaging with 18F-FP-CIT PET was done in two patients, which showed normal DAT density. It is believed that dopaminergic dysfunction in distinct dopaminergic pathways may explain the coexistence of these two disorders

PURPOSE: Cathepsin K is a potent collagenase implicated in human and animal atherosclerosis-based vascular remodeling. This study examined the hypothesis that serum CatK is associated with the prevalence of coronary artery disease (CAD). MATERIALS AND METHODS: Between January 2011 and December 2012, 256 consecutive subjects were enrolled from among patients who underwent coronary angiography and percutaneous coronary intervention treatment. A total of 129 age-matched subjects served as controls. RESULTS: The subjects' serum cathepsin K and high sensitive C-reactive protein (hs-CRP) and high-density lipoprotein cholesterol were measured. The patients with CAD had significantly higher serum cathepsin K levels compared to the controls (130.8+/-25.5 ng/mL vs. 86.9+/-25.5 ng/mL, p<0.001), and the patients with acute coronary syndrome had significantly higher serum cathepsin K levels compared to those with stable angina pectoris (137.1+/-26.9 ng/mL vs. 102.6+/-12.9 ng/mL, p<0.001). A linear regression analysis showed that overall, the cathepsin K levels were inversely correlated with the high-density lipoprotein levels (r=-0.29, p<0.01) and positively with hs-CRP levels (r=0.32, p<0.01). Multiple logistic regression analyses shows that cathepsin K levels were independent predictors of CAD (odds ratio, 1.76; 95% confidence interval, 1.12 to 1.56; p<0.01). CONCLUSION: These data indicated that elevated levels of cathepsin K are closely associated with the presence of CAD and that circulating cathepsin K serves a useful biomarker for CAD.
Aged ; Biological Markers/blood ; C-Reactive Protein/metabolism ; Cathepsin K/*blood ; Coronary Artery Disease/*blood/metabolism ; Female ; Humans ; Male ; Middle Aged

PURPOSE: Cathepsin K is a potent collagenase implicated in human and animal atherosclerosis-based vascular remodeling. This study examined the hypothesis that serum CatK is associated with the prevalence of coronary artery disease (CAD). MATERIALS AND METHODS: Between January 2011 and December 2012, 256 consecutive subjects were enrolled from among patients who underwent coronary angiography and percutaneous coronary intervention treatment. A total of 129 age-matched subjects served as controls. RESULTS: The subjects' serum cathepsin K and high sensitive C-reactive protein (hs-CRP) and high-density lipoprotein cholesterol were measured. The patients with CAD had significantly higher serum cathepsin K levels compared to the controls (130.8+/-25.5 ng/mL vs. 86.9+/-25.5 ng/mL, p<0.001), and the patients with acute coronary syndrome had significantly higher serum cathepsin K levels compared to those with stable angina pectoris (137.1+/-26.9 ng/mL vs. 102.6+/-12.9 ng/mL, p<0.001). A linear regression analysis showed that overall, the cathepsin K levels were inversely correlated with the high-density lipoprotein levels (r=-0.29, p<0.01) and positively with hs-CRP levels (r=0.32, p<0.01). Multiple logistic regression analyses shows that cathepsin K levels were independent predictors of CAD (odds ratio, 1.76; 95% confidence interval, 1.12 to 1.56; p<0.01). CONCLUSION: These data indicated that elevated levels of cathepsin K are closely associated with the presence of CAD and that circulating cathepsin K serves a useful biomarker for CAD.
Aged ; Biological Markers/blood ; C-Reactive Protein/metabolism ; Cathepsin K/*blood ; Coronary Artery Disease/*blood/metabolism ; Female ; Humans ; Male ; Middle Aged

Objective To investigate the changes of chromosome aberration and micronucleus frequencies in the peripheral blood of patients with cancer before and after treatment, and to provide a basis for clinical prevention and treatment. Methods We collected the physical examination data of 102 patients with cancer before and after treatment from 2016 to 2021 to analyze the changes of chromosome aberration and micronucleus frequencies in peripheral blood. Results Before and after treatment, there were significant differences in chromosome aberration frequency and micronucleus frequency in peripheral blood lymphocytes in patients having radiotherapy or chemoradiotherapy (all P < 0.05), but no significant difference was observed in either index for patients having chemotherapy (both P > 0.05). Before and after radiotherapy, there were significant differences in the numbers of patients with abnormal chromosome aberration frequency and those with abnormal micronucleus frequency in lymphocytes (both P < 0.001). Before and after chemotherapy, there was no significant difference in the number of patients with abnormal chromosome aberration frequency (P = 0.100) or those with abnormal micronucleus frequency (P = 0.110). Conclusion Radiotherapy can cause abnormalities in chromosome aberration and micronucleus frequencies in peripheral blood lymphocytes, which can be useful for monitoring radiotherapy injury to formulate effective emergency plans and evaluate radiation dose in each course of treatment.