Objective To investigate the role of subdural puncture(SDP)in the diagnosis and treatment of subdural fluid collection in young children with purulent meningitis.Methods Totally 207

Humans ; Temporomandibular Joint Disorders ; therapy

Cerebral Palsy ; diagnosis ; etiology ; therapy ; Humans ; Magnetic Resonance Imaging ; Prognosis

Adolescent ; Asthma ; blood ; drug therapy ; Case-Control Studies ; Child ; Child, Preschool ; Female ; Humans ; Interleukin-17 ; blood ; Male

Humans ; Quality of Life ; Rhinitis ; Sinusitis

Adult ; Female ; Humans ; Male ; Middle Aged ; Parathyroid Neoplasms ; diagnostic imaging ; surgery ; Retrospective Studies ; Ultrasonography

Objective To investigate the effects of Par-4 gene silence on hydrogen peroxide-induced apoptosis in alveolar epithelial cells. Method The alveolar epithelial cells A549 were cultured and exposed to hydrogen peroxide. The siRNA sequences targeted Par-4 gene was chemically synthesized and transfected to A549 cells with or without the exposure of hydrogen peroxide. The cells were divided into normal control groups, hydrogen peroxide-treated group(The cells were treated with 0. 1 mmol/L hydrogen peroxide), hydrogen peroxide and Par-4-siRNA-treated group(The cells were treated with 0. 1 mmol/L hydrogen peroxide after transfection of Par-4-siRNA), Non-specific DNA sequence transfection control group. The apoptosis of A549 cells was quantified by flow cytometry. The expression of Smac protein was detected by Western blot.Electrophoretic mobility shift assay was applied for evaluating the change of E2F1 DNA binding activity. Relative activity of Caspase-3 was detected by clolorimetric assay. Results The percent of apoptotic cells in hydrogen peroxide and Par-4-siRNA-treated group was (29.7 ± 2.3) %, which was significantly lower than that of hydrogen peroxide-treated group [(54.2 ± 4.1)%, q= 8.91, P ＜ 0.01)]. Par-4 siRNA could significantly suppress the increase of Smac protein, E2F1 DNA binding activity and caspase-3 activity induced by hydrogen peroxide in A549 cells. Conclusions Par-4 gene silence induced by siRNA might inhibit the apoptosis of alveolar epithelial cells, which might be resulted from suppression of the up-regulation of Smac gene expression, E2F1 DNA binding activity and caspase-3 activity.

Objective To build a normal value of serum sex hormone in the healthy children in favour of the diagnosis of children precocious puberty and the evaluation of the growth of the children.Method Serum of 462 healthy children(aged from 1 month to 14 years;205 females,257 males)was collected,and the level of testosterone(T) and 17-estradiol(E2).Results There were no significant deviation in the levels of E2 of deferent genders between 1-12 months,but the level of T in boys and girls were obviously different.The puberty of boys was la-ter than girls.There was no significant deviation in the level of E2 of the boys in different periods,but the levels of T in boys at different ages were obviously different.Conclusions With the improvement the detection methods,the normal values of the serum sex hormone in healthy children have been changing.It is helpful for diagnosis of children precocious puberty by rebuilding normal values of T and E2 .

Objective To study the effect of hypothyroidism on oxidative stress status in developing rat brain and to further explore the mechanism of impaired brain development caused by hypothyroidism. Methods Perinatal hypothyroidism was induced by administering propylthiouracil(PTU) solution to the dams by gavage.The oxidative stress indexes were measured in brain homogenate of normal and hypothyroid pups which were sacrificed on the 21st d after birth. Results As compared to the control,the following indexes were found to be increased in the hypothyroid group: protein carbonyl contents,thiobarbital acid reactive substances,reduced glutathione,total antioxidative capacity,activities of superoxide dismutase and glutathione peroxidase(P0.05). Conclusion Hypothyroidism during rat brain development may cause oxidative stress,which may be related to the brain damage caused by hypothyroidism.