Stroke is one of the most common diseases among middle and senior - aged people,and depressive disorder,which hinders severely recovery and prognosis,is one of the complications of stroke.This paper analyzes the efficiency of social intervention mode on patients with post - stroke depressive disorder,and comes up with the conclusion that social intervention mode can not only help to ameliorate the occurrence of post - stroke depressive disorder,but also promote the recovery of patients' nervous function.Therefore,the social intervention mode can be regarded as an effective means for medical treatment.

Adolescent ; Adult ; Aged ; Female ; Humans ; Male ; Middle Aged ; Organophosphate Poisoning ; Pancreatitis, Acute Necrotizing ; etiology ; Pesticides ; poisoning ; Retrospective Studies ; Young Adult

Objective To investigate mechanisms of resistance to adriamycin(ADR)by human breast cancer cell line MCF-7 and to find the alteration of features and celluar behavior of MCF-7 after exposure to ADR.MethodsProliferation speed,population doubling time of MCF(wild type),MCF-7/ADR(exposure to adriamycin)and withdrawl group were respectively tested.Cell phenotype alteration was detected using SP immunohiatochemistry methods.Results No significant difference of proliferation speed was found between MCF-7/ADR and MCF cells.As exposure time prolonged,withdrawl group cells grew faster,thus population doubling time shortened.Differentiation of MCF-7/ADR and wthdrawl group was lower than wild group.The expression of drug resistance associated marker of MCF-7/ADR such as Pgp,LRP,GST-pi,TOPOⅡwas higher than that of MCF-7,ER turned to express negatively,and expression of PR gradually decreased as exposure continued.Conclusion MCF-7 cells exposed to ADR got drug resistant,their proliferation was not suppressed by withdrawl of ADR and even grew faster.Drug resistant cells gained dedifferentiation ability.Their heredity and biochemistry features changed,expression of target enzyme also altered and was reversible by drug withdrawl.

Air Pollutants, Occupational ; analysis ; Chromatography, Gas ; methods ; Methyl Ethers ; analysis ; Workplace

Objective To investigate the brain glucose metabolism in different stage of mixed-type multiple system atrophy (MSA).Methods Forty-six MSA patients with cerebellar or Parkinsonian symptoms and 18 healthy controls with similar age as patients were included.According to the disease duration,the patients were divided into three groups: group 1 (≤ 12 months,n=14),group 2 (13-24 months,n=13),group 3 (≥ 25 months,n =19).All patients and controls underwent 18F-FDG PET/CT brain imaging.To compare metabolic distributions between different groups,SPM 8 software and two-sample t test were used for image data analysis.When P＜0.005,the result was considered statistically significant.Results At the level of P＜0.005,the hypometabolism in group 1 (all t＞3.49) was identified in the frontal lobe,lateral temporal lobe,insula lobe,anterior cingulate cortex,caudate nucleus and anterior cerebellar hemisphere.The regions of hypometabolism extended to posterolateral putamen and part of posterior cerebellar hemisphere in group 2 (all t＞3.21).In group 3,the whole parts of putamen and cerebellar hemisphere were involved as hypometabolism (all t＞4.08).In addition to the hypometabolism regions,there were also stabled hypermetabolism regions mainly in the parietal lobe,medial temporal lobe and the thalamus in all patient groups (all t＞3.27 in group 1,all t＞3.02 in group 2,all t＞3.30 in group 3).Conclusions Disease duration is closely related to the FDG metabolism in the MSA patients.Frontal lobe,lateral temporal lobe,anterior cingulate cortex and caudate nucleus can be involved at early stage of the disease.Putaminal hypometabolism begins in its posterolateral part.Cerebellar hypometabolism occurs early at its anterior part.Besides,thalamus shows hypermetabolism in the whole duration.18F-FDG metabolic changes of brain can reflect the development of mixed-type MSA.

Esophageal Atresia ; complications ; Humans ; Infant, Newborn ; Male ; Respiratory System Abnormalities ; complications ; Trachea ; abnormalities ; Tracheoesophageal Fistula ; complications

Objective To study the effect of red cell and plasma protein parameters on progression, prognosis and recurrence of cerebral infarction. Methods Clinical data from 105 patients with cerebral infarction were analyzed. The pa?tients were divided into four paired groups:progressive stroke group and complete stroke group, short-term favorable progno?sis group and short-term unfavorable prognosis group, long-term favorable prognosis group and long-term unfavorable prog?nosis group, relapsed cerebral infarction group and not relapsed group by different criterion. The red cell and plasma protein parameters were compared between groups. Results There were significantly higher mean corpuscular volume(fL:85.92± 4.50 vs 83.79±4.64,t=2.164,P<0.05), red cell distribution width(fL:13.50±2.45 vs 11.90±2.90,t=2.694,P<0.01), globu?lin(g/L:27.46±4.33 vs 24.79±4.03,t=3.029,P<0.01)and lower albumin(g/L:39.00±3.86 vs 42.89±4.45,t=4.242,P<0.01)in progressive stroke group than those of complete stroke group. The elevated red cell distribution width, reduced albu?min were the risk factors of progressive stroke. In the short-term unfavorable prognosis group, red cell distribution width was significantly higher than that in short-term favorable prognosis group(fL:13.90 ± 2.45 vs 12.00 ± 2.12,t=2.905,P<0.01). The red cell distribution width was positively correlated with mRS scores assessed 3 months and 18 months after cerebral in?farction(P<0.01). Conclusion Progressive stroke rate increases in cerebral infarction patients with elevated red cell distri?bution and reduced albumin;Red cell distribution width has a certain reference value for forecasting the prognosis of cere?bral infarction .

Objective To observe the influence of exercises on the mRNA expression of peroxisome proliferator-activated receptor (PPAR-α) and its target genes of acyl-CoA oxidase (ACO),Enoyl-CoA-hydratase and 3-hydroxyacyl-CoA-dehydrogenase (EHHADH) in the skeletal muscles in insulin-resistance mice to develop a way to improve the lipid metabolism.Methods Twenty male ApoE knockout mice were randomly divided into two groups,the high-fat diet group (group HFD) and the exercise training group (group Ex).The HFD group were fed with highfat diet,while the Ex group were fed in the same way,with additionally swimming training.And ten healthy male C57BL/6j mice were chosen as the control group(group ND).After 12 weeks of intervention,the serum lipid,blood glucose and insulin levels were determined,and homeostasis model assessment insulin resistance index (Homa-IRI) was calculated.The bilateral gastrocnemiuses were cut to be observed under a transmission electron microscope,and the mRNA expression of PPAR-α,ACO and EHHADH in skeletal muscle were measured using reverse transcription polymerase chain reaction(RT-PCR).Results The transmission electron microscope showed that the sarcolemma edema,mitochondrial swelling,as well as focal myocytolysis and edema within myofibrils were observed in the HFD group.The total cholesterol,low-density lipoprotein cholesterol,free fatty acid,fasting glucose,insulin and HomaIRI of the HFD group were significantly higher than the control group (P ＜ 0.05),while the mRNA expression of PPAR-α,ACO and EHHADH was significantly deceased than the latter(P ＜ 0.05).After swimming,the abovementioned pathological changes disappeared.The serum lipid of the Ex group were significantly lower (P ＜ 0.05),while HDL was significantly higher (P ＜ 0.05).And fasting insulin,glucose and HOMA-IR of the Ex group were significantly lower (P ＜ 0.05),while the mRNA expression of the above in the Ex group were significantly increased (P ＜0.05).Conclusion Swimming training could improve insulin resistance and metabolic disorder of lipid of ApoE knockout mice.The possible mechanisms may be through up-regulating the expression of PPAR-α,which in turn stimulates the expression of ACO and EHHADH mRNA to strengthen fatty acid β-oxidation.

Objective To study the 18F-FDG PET/CT features of tuberculous and malignant diffuse peritoneal lesions and to discuss the diagnostic value of 18F-FDG PET/CT in diagnosing and differentiating the lesions. Methods The 18F-FDG PET/CT features of 72 patients with tuberculous peritonitis,28 primary serous papillary carcinoma of the peritoneum and 135 peritoneal metastases confirmed by clinic and/or histopathology, were retrospectively reviewed. The peritoneal thickening features of tuberculous and malignant peritoneal lesions were observed. The maximal standardized uptake value (SUVmax) of peritoneal lesions and ascites, ascites SUVmax/liver SUVmax (T/NT) were compared between tuberculous peritonitis and cancerous peritonitis. The ROC curve was used to analyze the diagnostic efficiency of T/NT, SUVmax of peritoneal lesions and ascites. Results The typical 18F-FDG PET/CT features of tuberculous peritonitis were uniformity thickening of parietal peritoneum, mesenteric and omental stain like changes, widely and even distribution of the peritoneal 18F-FDG, while the cancerous peritonitis was obvious uneven thickening of parietal peritoneum, mesenteric and omental nodules and pie-shape changes, uneven distribution of the peritoneal 18F-FDG. The degree of 18F-FDG uptake was increased in all peritoneal lesions, and there was no significant difference between the tuberculous group (SUVmax=10.53±5.44) and the cancerous group (SUVmax=11.45±6.78, t=1.017, P>0.05). The 18F-FDG concentration in malignant ascites (SUVmax=1.88±0.65,T/NT=0.73± 0.18) was obvious higher than that of tuberculous ascites (SUVmax=1.67±0.69,T/NT=0.57±0.27, t=2.243 and 5.045,both P<0.05). The area under the ROC curve of T/NT, SUVmax of ascites, SUVmax of peritoneal lesions were 0.707, 0.593, 0.536, respectively. Conclusion The 18F-FDG PET/CT imaging can reflect the morphology and metabolic changes of peritoneal lesions. It is important to combine the SUVmax of ascites in order to improve the efficiency of diagnosing the diffuse peritoneal diseases.

MTM1 gene is essential for SOD2 activity and normal mitochondrial function. MTM1 deletion results in decreased SOD2 activity, impaired mitochondrial function and growth defect on nonfermentable carbon source. A yeast genomic library was transformed into mtm1 deletion mutant to screen for suppressor genes of MTM1. The damage caused by MTM1 deletion is irreversible and even overexpression of MTM1 can not rescue the growth defect of mtm1 deletion mutant. Another screening strategy was adopted: a plasmid overexpressing MTM1 was transformed into wild type before the MTM1 gene on chromosome was deleted. The resulting strain, designated YES2MTM1, was transformed with a yeast genomic library. Transformants lost the plasmid overexpressing MTM1 after 5-FOA treatment. Yeast strains able to grow on nonfermentable carbon source with MTM1 deletion and overexpression of some DNA fragments were picked up and candidate suppressor genes were identified. Overexpression of five genes were identified to be able to rescue the growth defect on nonfermentable carbon source. The study will provide reference for MTM1 gene function and screening for suppressor of genes whose deletion result in irreversible damage.