Objective:To explore the feasibility of ADSCs in the clinical treatment of traumatic femoral neck fracture.Methods: After the intervention by ADSCs,femoral neck fracture repair was observed by hematoxylin-eosin staining.The vascular endothelial growth factor expression levels at the fracture segment were quantitatively measured by immunohistochemical staining,RT-qPCR was utilized to detect the mRNA formation in callus tissue.Results: In the study group,we observed less fracture repair than in the sham surgery group but more than in the blank group.Conclusion: ADSCs administration can promote osseous tissue and osteoblast repair,thereby contributing to the healing of traumatic femoral neck fracture in rats.

Objective: To observe the automatic ventricular capture management (VCM) conifrmed by paced depolarization integral (PDI) evoked response detection via the follow-up study in patients with Zephyr5826 pacemaker implantation. Methods: A total of 102 relevant patients were enrolled. In order to conduct PDI calculation, pacemakers were set by bipolar sensing and bipolar pacing at immediately after implantation. VCM functions were observed at 1 day, 7 days and 1 month, 3, 6, 12 months after implantation, the ventricular threshold by VCM test and manual test were compared. The symptoms of pectoralis major stimulus, diaphragm stimulus and palpitation were observed in all follow-up patients. Results: There was 1 patient died by MI at 1 month after Zephyr5826 pacemaker implantation, the rest 101 patients were followed-up for 12 months. VCM function was successfully turned-on at immediately after implantation in all patients, no pectoralis major stimulus and diaphragm stimulus occurred. VCM function was turned-off in 6/101 (5.9%) patients at 7 days after implantation due to intolerable palpitation caused by daily automatic VCM, instead they received manual test at follow-up visit. The coincidence rate of ventricular thresholds between VCM test and manual test were 100%. Ventricular pacing output voltage by VCM was (0.99 ± 0.48) V,n=608. Compared with regular pacing output voltage (2.5V, 0.4ms), VCM function may save 84% of energy consumption; compared to high pacing output voltage (3.5V, 0.4ms), VCM may save 92%. Loss of ventricular capture and poor sensation were not found by ECG and 24 h dynamic monitoring. Conclusion: Zephyr5826 pacemaker may conduct bipolar pacing and scanning with VCM function, it can be effectively and safely operated by low energy output. A few patients may not use VCM function due to intolerable palpitation.

Objective To evaluate effects of interleukin-36α (IL-36α) on psoriasiform skin lesions and C-C motif chemokine ligand 20 (CCL20) expression in mice.Methods Totally,30 BALB/c female mice were randomly and equally divided into 3 groups:control group treated with topical vaseline cream on the shaved back and intracutaneous injection with phosphate buffer saline (PBS),model group treated with topical imiquimod cream on the shaved back and intracutaneous injection with PBS,experimental group treated with topical imiquimod cream on the shaved back and intracutaneous injection with IL-36α solution.Psoriasis area severity index (PASI) was used to evaluate changes of psoriasiform skin lesions in mice,and light microscopy to observe morphological changes of skin lesions and to measure the thickness of the epidermis.Real-time fluorescence-based quantitative PCR (qRT-PCR) and Western blot analysis were performed to determine the expression of IL-36α in skin lesions in the control group and model group,and qRT-PCR,Western blot analysis and immunohistochemical study to evaluate changes of CCL20 levels in skin lesions.Results The model group showed significantly increased mRNA (△ Ct value:0.0195 ± 0.0059) and protein expression (3.922 ± 0.248) of IL-36α compared with the control group (mRNA:0.0012 ± 0.0004,P ＜ 0.05;protein:0.690 ± 0.025,P ＜ 0.05).The mRNA and protein expression of CCL20 were significantly higher in the experimental group than those in the model group (mRNA:2.152 ± 0.793 vs.0.999 ± 0.178;protein:0.397 ± 0.033 vs.0.145 ± 0.030;both P ＜ 0.05),and higher in the model group than those in the control group (mRNA:0.378 ± 0.075;protein:0.025 ± 0.009;both P ＜ 0.05).Immunohistochemical study showed that the expression intensity of CCL20 in skin lesions significantly increased in the experimental group compared with that in the model group (Z =2.294,P ＜ 0.05).Conclusion IL-36α may aggravate psoriasiform skin inflammation in mice by promoting CCL20 expression.

Background: We found microRNA (miR)-1246 to be significantly differentially expressed between severe active alopecia areata (AA) patients and healthy individuals. Objective: To explore the role and mechanism of miR-1246 in severe AA. Methods: Expression of miR-1246, dual-specific tyrosine phosphorylation-regulated kinase 1A (DYRK1A), and nuclear factor of activated T cells 1c (NFATc1) in peripheral CD4+ T cells and in scalp tissues of patients were detected using RT-qPCR, Western blot, and immunohistochemistry assays. Peripheral CD4+ T cells from the AA patients were transfected with lentiviral vectors overexpressing miR-1246. RT-qPCR and Western blot analysis were used to measure mRNA or protein expression of retinoic-acid-receptor-related orphan nuclear receptor gamma (ROR-γt), interleukin (IL)-17, DYRK1A, NFATc1, and phosphorylated NFATc1. Flow cytometry was used to assay the CD4+ IL-17+ cells proportion. ELISA was used to measure cytokine levels. Results: miR-1246 levels decreased and DYRK1A and NFATc1 mRNA levels significantly increased in the peripheral CD4+ T cells and scalp tissues of severe active AA samples.NFATc1 protein expression was also significantly increased in the peripheral CD4+ T cells but not in the scalp tissues. NFATc1 positive cells were mainly distributed among infiltrating inflammatory cells around hair follicles. In peripheral CD4+ T cells of severe active AA, overexpression of miR-1246 resulted in significant downregulation of DYRK1A, NFATc1, ROR-γt, and IL-17 mRNA and phosphorylated NFATc1 protein, as well as a decrease in the CD4+ IL-17+ cells proportion and the IL-17F level. Conclusion miR-1246 can inhibit NFAT signaling and Th17 cell activation, which may be beneficial in the severe AA treatment.

Chemical constituents of Leonurus japonicus were isolated and purified by a combination of various chromatographic techniques including column chromatography over silica gel, Sephadex LH-20, MCI, and Rp C18. Structures of the isolates were determined by spectroscopic analysis as 10 coumarins: bergapten (1), xanthotoxin (2), isopimpinellin (3), isogosferal (4), imperatorin (5), meransin hydrate(6), isomeranzin(7), murrayone(8) , auraptenol(9), and osthol(10). In addition to compound 9, the others were isolated from the genus Leonurus for the first time. In the in vitro assay, compounds 4 and 8 significantly inhibited the abnormal increase of platelet aggregation induced by ADP.
Blood Platelets ; drug effects ; Coumarins ; chemistry ; pharmacology ; Leonurus ; chemistry ; Platelet Aggregation ; drug effects ; Platelet Aggregation Inhibitors ; chemistry ; pharmacology

OBJECTIVETo evaluate the predictive value of admission plasma B-type natriuretic peptide (BNP) and pulmonary capillary wedge pressure (PCWP) for long term cardiovascular events in patients with chronic heart failure (CHF).

METHODSA total of 134 patients [70 males and 64 females, mean age (71.28 +/- 8.22) years] with CHF were included in this study. PCWP was measured with a Swan-Ganz catheterization and plasma BNP level was determined by a rapid immunofluorescence assay (Triage, Biosite, USA) in all patients on admission day. Left ventricular end diastolic diameter (LVEDD) and cardiothoracic ratio (CRT) were measured within 24 hours before or after catheterization. All CHF patients received conventional therapy and the rates of cardiac death and rehospitalization were used as end points during 3-year follow up.

RESULTS(1) LVEDD, CRT, PCWP and BNP were increased in patients with cardiac events compared with patients without cardiac events (P < 0.01). (2) Multivariant logistic analysis showed that PCWP (OR = 1.423, 95% CI 1.163 - 1.741) and BNP (OR = 1.005, 95% CI 1.002 - 1.007) were the independent factors for cardiac events. (3) The area under the receiver operating curve (ROC) of BNP and PCWP to predict cardiac death was 0.846 (95% CI 0.771 - 0.922) and 0.762 (95% CI 0.666 - 0.875), respectively. The sensitivity was 76.5% and the specificity was 75.2% with BNP cutoff point of 720.5 ng/L, and the sensitivity was 68.1% and the specificity was 76.2% with PCWP cutoff point of 19.5 mm Hg (1 mm Hg = 0.133 kPa) for predicting cardiac deaths. (4) The survival rate of patients with BNP < or = 702.5 ng/L and PCWP < or = 19.5 mm Hg were significantly higher than that in patients with BNP > 702.5 ng/L (OR = 4.383, 95% CI 1.407 - 13.650) and PCWP > 19.5 mm Hg (OR = 2.843, 95% CI 1.013 - 8.854).

CONCLUSIONBoth plasma BNP and PCWP on admission day are independent predictors for long term cardiac events in patients with CHF.

Aged ; Chronic Disease ; Female ; Follow-Up Studies ; Heart Failure ; diagnosis ; mortality ; physiopathology ; Humans ; Male ; Middle Aged ; Natriuretic Peptide, Brain ; blood ; Predictive Value of Tests ; Prognosis ; Pulmonary Wedge Pressure ; ROC Curve ; Survival Rate

OBJECTIVETo investigate the effect of chemokine stromal cell-derived factor-1 (SDF-1) and its receptor CXCR4 on liver metastasis of human colon cancer.

METHODSExpression of CXCR4 in different colon cancer cell lines and SDF-1 in different tissues were detected by using Western-blot technique. Effect of SDF-1 and anti-CXCR4 monoclonal antibody (McAb) on proliferation and migration of HT-29 cells were measured using MTT methods. Model mimicking liver metastasis of human colon cancer was established by injecting HT-29 cells intrasplenically into BALB/C nude mice. Mice were randomly divided into AMD3100 treated group and control group. Liver metastatic rate and tumor foci were measured 7 weeks after.

RESULTSHT-29 cells expressed higher level of CXCR4 protein, and liver tissue expressed higher level of SDF-1 protein. Compared with the control, SDF-1 could significantly induced the proliferation and migration of the HT-29 cells, and anti-CXCR4 McAb could inhibited both functions of SDF-1. The liver metastasis rate in the control group was 100%, and it was 40% in the AMD3100 treating group (P < 0.05). The mean liver metastasis number also significantly decreased by AMD3100 (7.8 +/- 2.6 vs 22.4 +/- 8.6, P < 0.05).

CONCLUSIONSSDF-1/CXCR4 biological axis play an important role in liver metastasis of human colon cancer. Arrest of CXCR4 can inhibit liver metastasis of colon cancer through blocking cell proliferation and migration induced by SDF-1.

Animals ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Chemokine CXCL12 ; metabolism ; physiology ; Colonic Neoplasms ; metabolism ; pathology ; HT29 Cells ; Humans ; Liver Neoplasms, Experimental ; secondary ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Receptors, CXCR4 ; metabolism ; physiology ; Xenograft Model Antitumor Assays

OBJECTIVEThe application and therapeutic effect of hyperbaric oxygen (HBO) in hypoxic-ischemic brain damage (HIBD) remains controversial. Previous studies have focused on the early pathological and biochemical outcomes and there is a lack of long-term functional evaluation. This study was designed to evaluate the long-term pathological and behavioral changes of early HBO therapy on neonatal rats with HIBD.

METHODSPostnatal 7 days (PD7) rat pups were randomly assigned into Control (n=18), HIBD (n=17) and HBO treatment groups (n=17). HIBD was induced by ligating the left common carotid, followed by 2 hrs hypoxia exposure in the HIBD and HBO treatment groups. The Control group was sham-operated and was not subjected to hypoxia exposure. The HBO therapy with 2 atmosphere absolutes began 0.5-1 hr after HIBD in the HIBD treatment group, once daily for 2 days. The spatial learning and memory ability were evaluated by the Morris water maze test at PD37 to PD41. The morphological and histological changes of the brain, including brain weight, survival neurons, AchE positive unit and NOS positive neurons in hippocampal CA1 region, were detected at PD42.

RESULTSThe rats in the HIBD group displayed significant morphological and histological deficits, as well as severe spatial learning and memory disability. In the Morris water maze test, the mean escape latency were longer (56.35 +/- 22.37 s vs 23.07 +/- 16.28 s; P < 0.05) and the probe time and probe length were shorter in the HIBD group (29.29 +/- 6.06 s vs 51.21 +/- 4.59 s and 548 +/- 92 cm vs 989 +/- 101 cm; both P < 0.05) compared with the Control group. The left brain weight in the HIBD group was lighter than that in the Control group (0.601 +/- 0.59 g vs 0.984 +/- 0.18 g; P < 0.05). The survival neurons in the hippocampal CA1 region were less (100 +/- 27/mm vs 183 +/- 8/mm; P < 0.05), as well as the AchE-positive unit and NOS-positive neurons (18.50 +/- 2.24% vs 27.50 +/- 2.18% and 19.25 +/- 4.33 vs 33.75 +/- 5.57 respectively; P < 0.05) after HIBD. Early HBO treatment improved the abilities of spatial learning and alleviated the morphological and histological damage. The mean escape latency (39.17 +/- 21.20 s) was shortened, the probe time (36.84 +/- 4.36 s) and the probe length (686 +/- 76 cm) were longer, and the brain weight (0.768 +/- 0.85 g), the survival neurons (133 +/- 25/mm) and the AchE-positive unit (21.94 +/- 2.73%) increased significantly compared with those of the HIBD group (P < 0.05).

CONCLUSIONSEarly HBO treatment resulted in a protective effect against HIBD-induced long-term brain morphological and histological deficits and spatial learning and memory disability.

Acetylcholinesterase ; analysis ; Animals ; Brain ; pathology ; Escape Reaction ; Female ; Hippocampus ; enzymology ; pathology ; Hyperbaric Oxygenation ; Hypoxia-Ischemia, Brain ; enzymology ; pathology ; therapy ; Male ; Maze Learning ; Nitric Oxide Synthase ; analysis ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo observe antiasthmatic and anti-inflammatory actions mechanisms of CDCA.

METHODThe content of NO was determined by method of nitroreductase chromatometry in serum and trachea tissue. The content of cAMP was analysed by method of competitive protein-binding assay. The content of PGE2 was determined by method of ultraviolet spectrophotometry.

RESULTCDCA significantly decreased the content of NO of serum and trachea tissue in mice. CDCA increased greatly the content of cAMP of trachea tissue in rats. CDCA significantly decreased the content of PGE2 of trachea and lung tissue in mice.

CONCLUSIONMechanisms of antiasthmatic and anti-inflammatory actions of CDCA are related to increasing the content of cAMP in trachea tissue and decreasing the constituent of NO and PGE2 in body.

Animals ; Anti-Asthmatic Agents ; pharmacology ; Anti-Inflammatory Agents, Non-Steroidal ; pharmacology ; Chenodeoxycholic Acid ; pharmacology ; Cyclic AMP ; metabolism ; Dinoprostone ; metabolism ; Female ; Lung ; metabolism ; Male ; Materia Medica ; pharmacology ; Mice ; Nitric Oxide ; metabolism ; Rats ; Rats, Wistar ; Trachea ; metabolism

Objective To analyze the clinical characteristics ,causes of death and their changes of hospitalized neonates so as to provide theoretical basis for improving the level of intensive medical care and reduce neonatal mortality .Methods The clinical data of 108 neonates who died between January 2012 and December 2016 were collected .We compared the mortality rate of neonates with different gestational age ,birth weight ,sex ,family background and abnormal high-risk pregnancy .The causes of death and death rate were analyzed .Results Among the 8869 hospitalized neonates ,108 died and the mortality rate of the neonates was 1 .22% .The avoidable mortality rate of the neonates was 0 .86% and the avoidable mortality ratio was 71 .29% .Infectious diseases remained to be the leading cause of neonatal death in hospitals . The top five most common causes of death in our hospitalized neonates were infectious diseases ,respiratory diseases ,asphyxia ,congenital malformations ,and genetic metabolic diseases .The three most common causes of death in full-term infants were infectious diseases ,genetic metabolic diseases ,and asphyxia . The three most common causes of death in preterm infants were infectious diseases , respiratory diseases ,and asphyxia .The neonatal mortality rate in our hospital decreased from 2 .02% in 2012 to 1 .09% in 2016 .Sepsis was the leading cause of death between 2012 and 2015 and dropped to the third place in 2016 . Respiratory diseases were the leading cause of death in 2016 . Asphyxia was the second cause of death in 2016 . Congenital malformations dropped from the third cause of death to the fifth .Conclusion In recent years ,thetreatment of neonates has improved and mortality rate of hospitalized neonates is gradually decreased .Controlling infectious diseases should be the primary measure to reduce the avoidable mortality in hospitalized neonates .