Child ; Child Health Services ; trends ; Delivery of Health Care ; organization & administration ; Education, Medical ; Hospitals, Pediatric ; economics ; organization & administration ; Humans ; Pediatrics ; trends ; Specialization ; Urban Population

Adenoma, Pleomorphic ; pathology ; Adult ; Ear Neoplasms ; pathology ; Humans ; Male

Objective To explore the causes of subclinical hypothyrodism in children and the effects of the interventional therapy with thyroixine on the course of it.Methods Two hundreds children with subclinical hypothyroidism were measured for thyroglobulin antibody(TGAb),thyroid microsomal antibody(TMAb) in the blood serum,examined by colord Dopplor ultrasonic,examined by fine needle aspiraton cytology of the throid and measured the rate of 131I absorbed by thyroid in order to find out the causes of the disease.Two hundreds cases were randomly divided into two groups on the base of the cause of diseases,treatment group 100 cases and control group 100 cases.The treatment group were treated by throxine 25-75 ?g/d and the therapeutic dosage were chosen with the normal value of free triiodothyronine(FT3),free thyroxine(FT4)and high sensitive thyrotropin(sTSH) in the blood serum .After one year thyroxine therapy were stopped.Thyroid function was examined 6 months later after stopping the thyroxine.Results Among all of the causes of subclinical hypothyroidism in children,Hasgumoto′s thyroiditis accounts for 56%,simple goiter accounts for 26%,antithyroid drug accounts for 6%,the lack of thyroxine substitution therapy on the hypothyroidism accounts for 5% and undefined causes accounts for 7% .The thyroid function could keep normal for 1 year with an alternative therapy with thyroxine on subclinical hypothyroidism in children.Half a year later after stopping thyroxine,the thyroid function turned normal in most of the children.There were obvious differences in the ratio of cure and the ratio of effectiveness between treatment group and control group (t=20.2,3.2 Pa

Objective To evaluate the role of AMP-activated protein kinase (AMPK)-dependent autophagic signaling pathway in ketamine-induced reduction of diabetic neuropathic pain (DNP) in rats.Methods Sixty male Wistar rats,aged 3 months,weighing 200-250 g,were equally randomized into 5 groups using a random number table:control group (C group),normal saline group (NS group),ketamine group (K group),ketamine + Compound C group (KC group),and ketamine + 3-methyladenine (3-MA) group (KM group).DNP model was established by intraperitoneal injection of streptozocin (STZ)65 mg/kg in anesthetized rats.Four weeks later,the equal volume of normal saline,ketamine 10 mg/kg,ketamine 10 mg/kg + Compound C1 mg/kg,and ketamine + 3-MA 2 μl were injected intraperitoneally once a day for 7 consecutive days in NS,K,KC and KM groups,respectively.The mechanical paw withdrawal threshold (MWT) was measured on 8th day.The rats were then sacrificed,and the lunbar segment (L1-5) of the spinal cord was removed for determination of the expression of AMPKαt,Beclin-1,microtubule-associated protein 1 light chain (LC) 3B (by Western blot) and dendritic spine density in the dorsal root ganglia.Results Compared with group C,the MWT,expression of AMPKα,Beclin-1,and LC3B,and dendritic spine density were significantly decreased in group NS (P＜0.05).Compared with group NS,the MWT,expression of AMPKαt,Beclin-1,and LC3B,and dendritic spine density were significantly increased in group K (P＜0.05).Compared with group K,the MWT,expression of AMPKα,Beclin-1,and LC3B,and dendritic spine density were significantly decreased in KC and KM groups (P＜0.05).Conclusion Activation of AMPK-dependent autophagic pathway is involved in ketamine-induced reduction of DNP in rats.

Objective To assess the influencing factors of the progression of carotid atherosclerotic stenosis using color Doppler flow imaging (CDFI). Methods From January 2009 to December 2014, a total of data 279 consecutive patients first assessed by CDFI as moderate stenosis of carotid atherosclerosis (stenosis rate 50 -69%)and regularly reexamined with CDFI at 12,24 and 36 months after initial examination were enrolled retrospectively. The residual diameter of vascular lesions and the changes of hemodynamic parameters were documented,and they were divided into either a progression group (n = 40)or a non-progression group (n = 239,and the non-progression group was divided into steady group[n = 210]and improved group [n = 29])according to whether the degree of stenosis progressed into severe stenosis (stenosis rate 70 -99%)or occlusion. The effects of the risk factors for common cerebrovascular disease and taking lipid lowering drugs (atorvastatin 20 mg/ d)on stenosis progression were compared in patients between the 2 groups. There were significant differences in hypertension,smoking and the regular use of atorvastatin . The effects of those factors on the progression of carotid stenosis were compared further through Logistic regression analysis. Results The residual vascular diameters of stenosis at 24,and 36 months were reduced obviously in the progression group compared with those of the non-progression group. There was significant difference (all P < 0. 05),and both the stenotic sites and distal peak systolic flow velocity ratio were significantly higher than those of the steady group and improved group (all P < 0. 05). Among the risk factors for cerebrovascular disease,hypertension (OR,2. 686,95% CI 1. 120 -6. 442,P = 0. 027)and smoking (OR,2. 265,95% CI 1. 081 -4. 746,P = 0. 030)were the major risk factors for affecting the progression of carotid stenosis. Regularly taking atorvastatin was a protective factor of delaying the progression of carotid stenosis (OR,0. 383,95% CI 0. 178 -0. 827,P = 0. 015). Conclusions CDFI may objectively evaluate the progression of carotid stenosis. Smoking and hypertension are the independent risk factors for affecting the progression of carotid stenosis,and regularly taking atorvastatin contributes to delay the progression of carotid stenosis.

Objective To compare the effects on neurobiological factors of attributional retraining group therapy (ARGT) or selective serotonin reuptake inhibitors (SSRI) for major depressive disorder (MDD),anxiety disorder (AD) and obsessive-compulsive disorder (OCD).Methods Outpatients with MDD,AD and OCD were divided into ARGT group (n =63) and SSRI group (n =66) according to the sequence of entering the study.MDD,AD and OCD patients were respectively measured with Hamilton Depression Scale (HAMD),Hamilton Anxiety Scale (HAMA),and Yale-Brown Obsessive Compulsive Scale (Y-BOCS) before and after 8 weeks treatment.All subjects were detected of plasma serotonin,norepinephrine,cortisol and adrenocorticotropic hormone by radioimmunoassay before and after treatment.Results After treatment,HAMD scores of MDD patients were reduced significantly in both ARGT group (t =18.411,P =0.000) and SSRI group (t =20.092,P =0.000) ; HAMA scores of GAD patients were reduced significantly in both ARGT group (t =13.989,P=0.000) and SSRI group (t=15.815,P=0.000) ;Y-BOCS scores of OCD patients were reduced significantly in both ARGT group (t =5.465,P =0.000)and SSRI group (t =4.792,P =0.000).In ARGT group,MDD (t =3.145,P =0.006),AD (t =2.785,P =0.012) and OCD patients (t =2.877,P =0.011) decreased plasma cortisol concentrations significantly.In SSRI group,MDD (t =-2.923,P =0.010) and OCD patients (t =-2.301,P =0.035) improved plasma serotonin significantly and MDD patients (t =-2.333,P =0.033) improved plasma norepinephrine significantly.Conclusion ARGT can modulate plasma cortisol level.SSRI can up-modulate plasma serotonin level.The two therapies take effect by different biological ways.

Animals ; Ethanol ; pharmacology ; Female ; Fetal Heart ; drug effects ; growth & development ; Male ; Zebrafish ; embryology

Objective To investigate the inhibitory effect of paclitaxel on rat graft arteriosclero- sis and the mechanism.Methods The rat abdominal aortic allograft model was used.All rats were divided into three groups:isograft control group (Wistar to Wistar),allograft group (Wistar to SD) and allograft paclitaxel-treated group (Wistar to SD).Rats in allograft paclitaxel-treated group re- ceived paclitaxel (2 mg?kg~(-1)?d~(-1)) from the operation day to post-operative day 14 and others received same dosage of vehicle (0.9% normal saline).Animals were sacrificed and the grafts were harvested at 30th day after operation.Intimal proliferation was studied by light microscopy.The apoptosis of vascular smooth muscle cells (VSMCs) was detected by transmission electronic microscopy and termi- nal deoxynucleotidyl transferase biotin nick end-labeling (TUNEL) method.Results Morphological analysis showed that grafts had no change after operation in isograft control group,but in allograft group intimal proliferation,inflammatory cells infiltration in neointima and adventitia and stenosis of allografts were obvious.After treatment with paclitaxel,there was a significant decrease in intimal proliferation,inflammatory cells infiltration and stenosis.Apoptosis index of VSMCs was higher in the allograft paclitaxel-treated group than other groups.Conclusion Paclitaxel can inhibit intimal pro- liferation in aortic allografts and prevent the graft from arteriosclerosis possibly by inducing the apoptosis of VSMCs.

Objective To explore the change and clinical significance of plasma levels of thrombomodulin(TM) in children with Kawasaki disease(KD)(n=44) before and after treatmen with intravenous immunoglobulin(IVIG).Methods Enzyme-linked immunosorbent assay(ELISA) was used to detect the plasma levels of TM in children with KD(n=44) before and after treatment with IVIG and in normal control group(n=15),respectively.Children with KD were enrolled from September 2004 to June 2006,one group(n=20) with coronary artery lesions(CALs) and another group(n=24) without CALs.The control were enrolled from heathy children in clinic service.Results The plasma level of TM in KD group before treatment with IVIG was significantly higher than that in control group(P

Objective To investigate the effect of matrix metalloproteinases(MMPs) in ventilator-induced lung injury inflammatory reaction of newborn rabbits.Methods Seventy-five newborn rabbits aged 1-5 days were randomly arranged to 3 groups:control group(n=3),other 72 rabbits designed by 2?2?3 factorial were divided into high concentration oxygen(100%)and low concentration oxygen(45%) groups,and each group was subdivided into 2 groups:High peak inspiratory pressure(PIP)group and low PIP group.All rabbits were done by mechanical ventilation and killed to obtain lung tissue at 1,3,6 hours after trailing respectively.The concentration of MMP-9 and MMP-2 in lung tissue bomogenate were detected by ELISA,at the same time the ratio of wet to dry was detected and pathological section was analyzed.Results 1.The concentration of MMP-2 in high concentration oxygen group,high PIP group and low PIP group increased compared with that in normal group,and there were significant differences.2.The mean concentration of MMP-9 was lower in high concentration oxygen group than that in normal control group,and there was significant difference between 2 groups.The mean concentration of MMP-9 in low concentration oxygen group was higher than that in normal group,and there was no significant difference between 2 groups.There was no significant difference in effect to mean concentration of MMP-9 by different PIP.3.There were positive correlation between MMP-2 and MMP-9,MMP-2 and the ratio of wet to dry in lung.Conclusions Within 6 hours in newborn rabbits by mechanical ventilation,ventilation with high concentration oxygen up-regulate MMP-2,but down-regulated MMP-9.The lungs stretch by mechanical ventilation increase MMP-9,but decrease MMP-2.Mechanical ventilation can affect the synthesis of MMPs,and MMPs plays an important role in ventilator-induced lung injury of newborn rabbits.