This study was aimed to investigate the effects of Chai-Hu Shu-Gan Tang (CHSGT) on levels of TNF-α and 5-HT in lithium chloride–pilocarpine caused epilepsy–depression comorbidity rat model, in order to discuss the intervention effect of CHSGT on TNF-α and 5-HT in epilepsy–depression comorbidity. The lithium chloride–pilocarpine caused epilepsy–depression comorbidity rat model was established. After 6 weeks of animal establishment, rats were randomly divided into 5 groups, which were citalopram group (A), physiological saline group (B), CHSGT high dose group (C), medium dose group (D), and low dose group (E). Intragastric administration was given for 4 weeks, twice a day. Before and after the treatment, RT-PCR was performed to detect hippocampal TNF-αlevels. Liquid chromatography-mass spectrometry was performed to detect hippocampal 5-HT levels. Both forced swimming test (FST) and saccharin preference test were carried out to monitor the depressive behaviors of rats. In the meantime, 24 hours a day video camera surveillance were performed to record the number of seizures of rats. The results showed that after treatment, the number of seizures of rats were significantly reduced, the accumulative immobility time in FST was shortened, and the consumption of sucrose increased significantly (P < 0.01) in group A, C and D. Compared with group B, after the treatment, the expressions of hippocampal TNF-α mRNA of rats in group A, C, D were distinctly downregulated, with the level of 5-HT significantly increased (P < 0.05,P < 0.01). Compared with group A, group C and D showed no significant changes. It was concluded that TNF-α played a role in the pathogenesis of epilepsy–depression comorbidity through mediating the level of 5-HT. High and medium doses of CHSGT can downregulate the expression of TNF-α mRNA in depression comorbidity of chronic temporal lobe epilepsy, increase 5-HT level, reduce the number of seizures of rats, and improve depressive behaviors.

Objective · To investigate the expression of the regulator of calcineurin 1 (RCAN1) and calcineurin A (CnA) in tissues of in-stent restenosis after intervention of arteriosclerosis obliterans (ASO), and to explore the relationship between their expression levels and the occurance of in-stent restenosis. Methods · Superficial femoral arterial tissues were collected from 15 ASO patients undergoing lower extremity amputation for in-stent restenosis in Department of Vascular Surgery, The First Affiliated Hospital of Chongqing Medical University from September 2013 to June 2016. H-E staining and Masson staining were performed on the stenosis tissues, as well as on the proximal and distal tissues, and the morphological changes of these tissues were observed under optical microscope. Western blotting was used to detect the protein levels of RCAN1, CnA and proliferating cell nuclear antigen (PCNA). The distribution of RCAN1 and CnA proteins was observed by immunohistochemistry and immunofluorescence methods. In addition, co-immunoprecipitation was used to validate the protein-protein interaction between RCAN1 and CnA in vascular tissues. Results · The expression of RCAN1 in the distal tissues was significantly elevated compared with the proximal tissues and the stenosis tissues (P<0.05). The expression of RCAN1 in the proximal tissues was higher than that in the stenosis tissues (P <0.05). The expression of CnA and PCNA in the stenosis tissues was significantly elevated compared with the proximal tissues and the distal tissues (P<0.05). Immunohistochemistry and immunofluorescence analyses showed that RCAN1 and CN proteins were mainly expressed in the cytoplasm of vascular smooth muscle cells. Co-immunoprecipitation analysis showed there is protein-protein interaction between RCAN1 and CnA in arterial tissues. Conclusion · The low expression of RCAN1 and the high expression of CnA are probably related to the occurrence of in-stent restenosis.

OBJECTIVE: To analyze the clinical manifestations, diagnosis, therapy and prognosis of Langerhans cell histiocytosis (LCH) of the temporal bone in children. METHOD: Seven children with LCH of the temporal bone n our hospital were retrospectively summed up from April 2009 to April 2014. The patients were followed up 1-5 years, their clinical manifestations, imaging findings, diagnosis, therapy and prognosis were studied. Correlation between clinical classifications and prognosis was also analyzed. RESULT: Among the 7 patients, 4 were boys and 3 were girls. 5 cases belonged to the single system group and 2 cases belonged to the multisystem group. The most common clinical characters were temporal tumor, otorrhea, otalgia, hearing loss and granulation of external auditory canal. CT of the temporal bones showed extensive osteolytic destructions with diffuse soft tissure density, without border sclerotization. The cases were. received different therapies. Followed up for 1-5 years, 4 cases were regressive, 1 case kept stable, while 2 cases showed progressive. The two boys then received standard treatment combined steroids with vinblastine. The prognosis in the multisystem group was significantly different from the single system group (P < 0.05). CONCLUSION The clinical manifestations of LCH vary a lot. The diagnosis is based on histological and immunophenotypic examination of lesion tissue. The main therapy includs surgery, chemotherapy and radiotherapy. The prognosis of the single system group is much better than the multisystem group.
Child ; Combined Modality Therapy ; Deafness ; etiology ; Ear Canal ; pathology ; Ear Diseases ; etiology ; Female ; Histiocytosis, Langerhans-Cell ; diagnosis ; pathology ; therapy ; Humans ; Male ; Prognosis ; Retrospective Studies ; Steroids ; therapeutic use ; Temporal Bone ; pathology

Objective:To study the effects of endothelial progenitor cells(EPCs)on the osteogenesis of bone marrow mesenchymal stem cell (BMSCs)sheet-implant complex.Methods:EPCs were added to the BMSC sheets,and the expression of osteogenesis-relat-ed genes was examined by real time PCR.Cell sheets were wrapped around implants to construct cell sheet-implant complexes and the complexes were subcutaneously transplanted into SCID mice.The complexes were harvested 8 weeks after operation and observed by micro-CT and histological examination.Results:The BMSC sheet with EPCs showed higher expression of Runx2,ALP,BMP2 and VEGF in the in vitro test;higher bone volume ratio,greater amount of new bone tissue and higher expression of Runx2 and BMP2 in the in vivo test.Conclusion:EPCs can improve the osteogenesis of BMSC sheet-implant complex.

BACKGROUND:According to the core functional zone of amino acid sequence of the osteoinduction in bone morphogenetic proteins, our research group synthesized bone morphogenetic protein (BMP) active polypeptides Ⅰ and Ⅱ by artificial solid-state synthesis method. OBJECTIVE: To evaluate the osteoinductive ability of BMP active polypeptides Ⅰ and Ⅱ in animals. METHODS:Forty-two Sprague-Dawley rats were randomly divided into seven groups, and respectively implanted with hydroxyapatite/polylactic acid carrying 0.2, 0.4, 0.8 g/L BMP active polypeptides I, hydroxyapatite/polylactic acid carrying 0.2, 0.4, 0.8 g/L BMP active polypeptides Ⅱ, and hydroxyapatite/polylactic acid alone. At 3 and 5 weeks postoperatively, X-ray, CT and histological detection were conducted to evaluate osteoinductive conditions in the seven groups. RESULTS AND CONCLUSION:At 3 and 5 weeks postoperatively, there were better local osteoinductive effects in the groups hydroxyapatite/polylactic acid carrying BMP active polypeptides Ⅰ and Ⅱ than the group of hydroxyapatite/polylactic acid, indicating both two kinds of BMP active polypeptides possessed a certain osteoinductive ability. Moreover, this osteoinductive ability became stronger with time. At 5 weeks postoperatively, the osteoinductive effect in the 0.4 and 0.8 g/L BMP active polypeptides I groups was better than that in the 0.2 g/L BMP active polypeptides I group and the 0.2, 0.4 and 0.8 BMP active polypeptides Ⅱ groups (P < 0.05). In addition, there was no difference in the osteoinductive effect of 0.4 and 0.8 g/L BMP active polypeptides I groups. These results indicate that BMP active polypeptides I has a stronger osteoinductive ability than BMP active polypeptides Ⅱ.

Objective To investigate the effect of hosphocreatine therapy on the plasma cardiotrophin-1(CT-1) and N terminal probrain natriuretic (NT-proBNP) in elderly hypertensive patients with heart failure. Methods A total of 76 hy-pertensive patients with heart failure, aged 65 or over, were randomly divided into treatment group and control group (n=38 for each group). The control group received routine anti-heart failure treatment. The treatment group received conventional therapy plus creatine phosphate sodium for 2 weeks. The plasma levels of CT-1 and NT-proBNP were determined in two groups. The plasma CT-1 level was measured by a double antibody sandwich enzyme-linked immunosorbent assay (ELISA). The plasma level of NT-proBNP was tested by Rui Pu fluorescent dry quantitative analyzer. Results The plasma levels of CT-1 and NT-proBNP were significantly lower after treatment in two groups (P＜0.01). The plasma levels of CT-1 and NT-proBNP were significantly decreased in treatment group than those in control group (P＜0.05). The total effective rate was 89.47%in treatment group, which was significantly higher than that of control group (71.05%, P＜0.05). Symptoms of heart failure improved in one week (21 cases in treatment group/9 cases in control group) and in two weeks (13 cases in treatment group/18 cases in control group). Conclusion The conventional therapy plus creatine phosphate sodium can decrease the plasma CT-1 and NT-proBNP levels in elderly hypertensive patients with heart failure, which improves symptoms of heart failure in a shorter period of time.

lusionsThe CEUS findings are different between benign and malignant gallbladder adenomas. The enhancement pattern and speed are useful for differentiating benign from malignant adenomas.

One factor at a time design and first order exponential model were applied to investigate the effects of the four major factors(temperature,ionic strength,pH and osmo-regulator) in the preservation process of nitrite oxidization bacteria(NOB),and a first order decay kinetics was introduced.The result showed that the anoxic decay rate of nitrifying bacteria reduced from 0.25 to 0.015,the half life was extend to 53d at 4℃,pH7.60,ionic strength 0.035mol/kg.The protecting effect of glycerin showed obviously better than that of other cryoprotectants at 4℃.

Objective To measure vitamin D levels in newborn cord blood inorder to ascertain appropriate supplementation regimes.Methods A total of 6420 newborn umbilical cordblood 25-hydroxyvitamin D [ 25-( OH ) D ] concentrations were measured by enzyme linked immunosorbent assay, and the correlation between 25-( OH ) D and gestational or birth weight or season was retrospectively analyzed.Results There were 5358(83.5℅)of the 6420,had umbilical cord blood concentrations of 25-(OH)D <50. 0 nmol/L. The 25-(OH)D levels M(Q1,Q3)increased from very preterm births, moderately preterm, later preterm, full-term infants to post-term infants [ 29. 0 ( 22. 5, 38.9),33.4(26.3,41.6),35.1(26.9,43.3),35.7(28.1,45.0),43.3(33.5,52.8)nmol/L, P <0. 001]. The 25-(OH) D levels M(Q1,Q3) increased from very low birth weight infants, low birth weight, normal birth weight infants to macrosomia [29. 0(22. 4,38. 8),34. 6(27. 5,44. 2),35. 1(28. 1, 44. 7),35. 7(28. 0,47. 5), P<0. 001]. The 25- (OH)D levels were positively correlated respectively in gestational ages and body weights ( r =0. 619 , 0. 180 , P <0. 05 ) . Newborn umbilical cord blood concentration of 25- ( OH ) D levels varied with season ( P all <0. 001 ) , the lowest in spring [ 30. 4 (24.1,38.3)]and highest in autumn[39.3(31.6,50.9)].Conclusions Premature and low birth weight infants are especially at high risk of vitamin D deficiency and should receive appropriate vitamin D supplementation. In addition, there should be an ongoing promotion of vitamin D supplements to pregnant women and the awareness of sun exposure to achieve vitamin D sufficiency.

Aim To explore the protective roles of lic-ochalcone A ( LA) on mice with cigarette smoke-medi-ated acute lung injury and the related mechanisms. Methods In vivo: Mice were exposed to cigarette smoke ( CS) to establish acute lung injury model. The bronchoalveolar lavage fluid ( BALF ) was conducted for cell counting. The mRNA and protein expression of keratinocyte-derived chemokine ( KC ) , tumor necrosis factor alpha ( TNF-α) , interleukin 1β ( IL-1β) and matrix metalloproteinases ( MMP)-9 in lungs were de-termined. The myeloperoxidase ( MPO ) , superoxide dismutase ( SOD ) activities and glutathione ( GSH ) levels in lungs were quantified. The paraffin sections of lungs were prepared and stained with HE. In vitro:Human lung epithelial cells (BEAS-2B) were exposed to cigarette smoke extract ( CSE ) , which induced cell injury. The releases of interleukin 8 (IL-8) and MMP-9 were assessed. The phosphorylation of mitogen-acti-vated protein kinases ( MAPKs, including ERK1/2, p38 and JNK ) and nuclear factor-κB ( NF-κB ) p65 protein were analyzed by Western blot. Results In vi-vo: The accumulation of inflammatory cells was lower in LA groups than that in model group. In comparison with normal control group, the mRNA and protein lev-els of KC, TNF-α, IL-1βand MMP-9 were significant-ly increased in model group. Following treatment with LA, the above indicators were significantly decreased as compared to model group. In the CS-exposed mice, the MPO activity in lungs was significantly increased, meanwhile the SOD activity and GSH level were signif-icantly decreased compared with the air-exposed ani-mals. CS-induced activity of MPO was significantly in-hibited, which were accompanied by increases in SOD and GSH levels by LA. In vitro: CSE-induced mRNA levels of IL-8 and MMP-9 were significantly inhibited by LA at 2 . 5 and 5 μmol · L-1 . The CSE-induced phosphorylation of ERK1/2 and nucleus NF-κB p65 protein expression were prevented by pretreatment with LA. Conclusions LA has protective effects on CS-ex-posed acute lung injury in mice by preventing CS-in-duced pulmonary inflammation, oxidative stress and protease rise. The exploration of the mechanisms sug-gests that LA exerts protective effects via suppressing ERK1/2/NF-κB pathways.