Objective To establish a neonatal transport network in order to improve the diagnosis and treatment levels of the basic medical unit and to decrease medical disputes and fatality rate of the new born Methods The first neonatal transport network in the Southwest of China, covering Chongqing and the adjacent areas, was established During the process of transport, warm keeping, unobstructed respiratory tracts, oxygen treatment, establishment of venous passage and placement of gastric canal were included Meanwhile, the vital signs, colors of the skin and mucosa and consciousness should be closely observed Corresponding measures could be taken at any time when needed Results Satisfactory results were achieved by means of the neonatal transport network Conclusion The neonatal transport network can play a very important role in strengthening the treatment of the newborn, decreasing the fatality rate and sequela and improving the diagnosis and treatment levels of the basic medical unit

Objective To observe the effect of GPR30 agonist G1 on high glucose-induced endoplasmic reticulum stress ( ERS) in endothelial EA .hy926 cells.Methods EA.hy926 endothelial cells were divided into three groups:nor-mal control group (Con, 17.51 mmol /L glucose), high glucose (HG, 33.3 mmol /L), high glucose +G1 group (HG+G1, HG +1 μmol/L G1).The apoptosis rate of endothelial cells was measured by flow cytometry , the protein expres-sion changes of ERS related molecules Bip , IRE1, PERK and apoptotic molecules Bax , Bcl-2 were measured by Western blot, the mRNA expressions of Bip and CHOP were measured by RT-PCR assay.Results Compared with Con group , the apoptosis in HG group was significantly increased (P <0.01), Bip, IRE1, PERK and apoptotic molecule Bax were upreg-ulateded (P <0.05, P<0.01 or P <0.001), Bcl-2 downregulatted (P <0.01) and Bip mRNA, CHOP mRNA expres-sion were upregulated (P <0.001 and P<0.01).Compared with the HG group, apoptosis rate in HG +G1 group was significantly lower (P <0.05), BIP, IRE1, PERK and apoptotic molecules Ba.0 downregulated ( P <0.05 or P <0.01), Bcl-2 expressions was increased (P <0.05), Bip mRNA and CHOP mRNA expression were decreased (P<0.001 or P<0.01).Conclusion GPR30 agonist G-1 inhibits EA.hy926 ERS in endothelial cells.

Objective To study the effect of forpart operation on reducing death rate of patients with severe acute pancreatitis.Methods A retrospective study was conducted to analyze 56 patients with severe acute pancreatitis.Results Among 56 patients,11 cases died,5 patients died from MODS after operation in 24 hours;6 patient died of abdominal infection etc;and other patients were cured.Conclusion To patients with severe acute pancreatitis,making use of different method according as clinic sign in appropriate time can reduce death rate and obtain satisfactory treatment outcome.

Objective. To study the role of endogenous carbon monoxide (CO) in endotoxin shock. Methods. The changes of CO levels and the effects of zinc protoporphyrin IX (ZnPP),an inhibitor of heme-oxygenase (HO), in endotoxin shock and the efficacy of hemin,an inducer of HO were investigated.Results. The plasma CO levels were found to be significantly increased during the course of endotoxin shock. Injection of ZnPP was shown to abrogate the endotoxin-induced hypotension and metabolic derangements markedly. Administration of hemin to healthy rabbits revealed the hypotension and metabolic derangements similar to the animals given endotoxin.Conclusion.CO is a newly found endogenously produced mediator which may play an important role in the pathogenesis of endotoxin shock.

Both delayed posttraumatic intracerebral hemorrhage and epidural hematoma have been well described in the neurosurgical literatures. However, delayed posttraumatic acute subdural hematoma which happens more than a week with a rapid progress after mild traumatic brain injury and causes death of patient is rarely reported. We show two such cases and briefly review the literature and discuss the probable pathogenesis of their rapid progress.
Aged ; Brain Injuries ; complications ; Fatal Outcome ; Female ; Hematoma, Subdural, Acute ; etiology ; Humans ; Male ; Middle Aged

Objective:To evaluate the clinical characteristics and identify potential factors of the early-stage hip involvement in patients with ankylosing spondylitis (AS) based on the magnetic resonance imaging (MRI).Methods:A retrospective group control study was carried out in 570 AS patients who were consecutively admitted to our hospital from 2014 to 2018. Patients with hip pain or hip function limitation but lacking definitive evidence of hip involvement on radiography were underwent hip MRI. Patients were divided into three groups: no hip involvement, early-stage hip involvement (hip involvement detected by MRI but with negative radiographs) and advanced-stage hip involvement (Bath Ankylosing Spondylitis Radiology Index-hip score ≥2). The study factors included demographic, laboratory, clinical and radiographic data. Simple and multiple ordinal logistic regression analysis were used to identify factors associated with the early-stage hip involvement and advanced-stage hip involvement.Results:A total of 236 patients (41.4%) presented with hip involvement, in which 146 cases (25.6%) were diagnosed with early-stage hip involvement, while 90 cases (15.8%) were diagnosed with advanced-stage hip involvement. Multivariate logistic regression analysis demonstrated that older age at onset [ OR=0.80, 95% CI (0.72, 0.90), P<0.01], more active inflammation in the sacroiliac joints [ OR=1.13, 95% CI(1.07, 1.18), P<0.01] and worse BASMI score [ OR=3.06, 95% CI(2.14, 4.13), P<0.01] were associated with the occurrence of early-stage hip involvement. Conclusion:MRI is superior to radiography in detecting early-stage hip involvement. MRI is more suitable for hip involvement assessment in AS patients with suspected symptoms or risk factors of hip involvement.

Objective To investigate the incidence and risk factors of neonatal asphyxia in Hubei Enshi Tujia and Miao Autonomous Prefecture. Methods Live born infants, including those diagnosed with neonatal asphyxia, were recruited from 16 different hospitals in Hubei Enshi Tujia and Miao Autonomous Prefecture from January to December of 2016. The 16 hospitals included four grade A tertiary hospitals (three general hospitals and one traditional Chinese medicine hospital) and 12 grade A secondary hospitals (eight general hospitals, one maternal and child health hospital and three traditional Chinese medicine hospitals). A retrospective investigation was conducted using questionnaire to analyze the basic information, perinatal risk factors and prognosis of those infants. Chi-square test was used for statistical analysis. Results Among 22 294 recruited live born infants, 733 (3.29%) were diagnosed with neonatal asphyxia on discharge, including 627 (85.54%) mild cases and 106 (14.46%) severe cases. And neonatal asphyxia resulted in deaths of 27 cases (3.68%). The risk factors for neonatal asphyxia included multiple pregnancy, pregnancy conceived with assisted reproductive technology, premature infant, low birth weight infant, fetal malposition, congenital malformation, male infant, born during transfer, mother of Tujia nationality, low educational level (primary school or lower), living in rural area, the number of antenatal visits ≤3, history of early threatened abortion, anemia in pregnancy, hypertensive disorders of pregnancy, chorioamnionitis, abnormal pregnancy history and abnormality of umbilical cord, amniotic fluid or placenta. Conclusions The incidence of neonatal asphyxia in Enshi area is obviously higher than the national average. The main risk factors for neonatal asphyxia in this area are related to maternal background and the living condition of the mother during pregnancy, delivery as well as the newborn at birth.

Objective To evaluate the role of M3 receptor in penehyclidine hydrochloride(PHC)-induced reduction of increased permeability of human pulmonary microvascular endothelial cells (PMVECs) caused by endotoxin and the relationship with mitogen-activated protein kinase (MAPK) signaling pathway.Methods Human PMVECs were seeded in 6-well plates (2 ml/hole) or in culture flasks (4 ml/flask) at the density of 1 × 105 cells/ml and randomly divided into 6 groups (n=5 each):control group (group C),M3 receptor shRNA transfection group (group shRNA),lipopolysaccharide (LPS) group,penehyclidine plus LPS group (group P+LPS),LPS plus M3 receptor shRNA transfection group (group LPS+shRNA) and PHC plus LPS plus M3 shRNA transfection group (group P+LPS+shRNA).The cells were transfected with shRNA plasmid containing 2.5 nmol/L M3 receptors in shRNA,LPS+shRNA and P+LPS+shRNA groups.LPS at the final concentration of 0.1 μg/ml was added at 24 h of incubation and then cells were incubated for 1 h in LPS and LPS+shRNA groups.PHC at the final concentration of 2 μg/ml was added at 24 h of incubation,cells were incubated for 1 h,then LPS at the final concentration of 0.1 μg/ml was added,and cells were incubated for another l h in P+LPS and P+LPS+shRNA groups.The permeability of PMVECs was measured using Transwell assay.The expression of phosphorylated p38 MAPK (p-p38 MAPK)and phosphorylated extracellular signal-regulated protein kinase 1/2 (p-ERK1/2) was detected by Western blot,the expression of heat shock protein 27 (HSP27) using immunofluorescent staining,and the expression of M3receptor mRNA by real-time polymerase chain reaction.Results Compared with group C,M3 receptor mRNA expression was significantly down-regulated in group shRNA,and the permeability of cells was significantly increased,and the expression of p-p38 MAPK,p-ERK1/2,HSP27 and M3 receptor mRNA was up-regulated in group LPS (P＜0.05).The permeability of cells was significantly decreased,and the expression of p-p38 MAPK,p-ERK1/2,HSP27 and M3 receptor mRNA was down-regulated in P+ LPS,LPS+shRNA and P+LPS+shRNA groups as compared with group LPS,and in group P+LPS+shRNA as compared with group LPS+shRNA (P＜0.05).Conclusion The mechanism by which PHC reduces endotoxin-caused increased permeability of human PMVECs is related to inhibiting activation of MAPK signaling pathway after down-regulating M3 receptor.

Objective To evaluate the role of M3 receptors in penehyclidine hydrochloride ( PHC)-induced reduction of lipopolysaccharide ( LPS)-induced injury to human pulmonary microvascular endotheli-al cells ( PMVECs) . Methods Human PMVECs transfected with M3 shRNA were seeded in 6-well plates (2 ml∕hole) or in culture flasks (4 ml∕flask) at the density of 1×105 cells∕ml and divided into 5 groups ( n=5 each) using a random number table method: control group ( group C) , LPS group, PHC plus LPS group ( group P+LPS) , LPS plus M3 shRNA transfection group ( group LPS+shRNA) , and PHC plus LPS plus M3 shRNA transfection group ( group P+LPS+shRNA) . Group C received no mediation, and LPS was added at the final concentration of 0. 1 μg∕ml in the other groups. PHC 2 μg∕ml was added at 1 h before adding LPS in P+LPS and P+LPS+shRNA groups. The cells were transfected with plasmid containing 2. 5 nmol∕L M3 receptor shRNA in LPS+shRNA group and P+LPS+shRNA group. Contents of filamentous actin ( F-actin) in endothelial cells were measured by flow cytometry at 1 h after adding LPS. The expression of myosin light chain kinase ( MLCK) and VE-cadherin protein was examined by immunofluorescence. The ex-pression of nuclear factor kappa B ( NF-κB) p65 and IκB was detected by Western blot. Contents of tumor necrosis factor-alpha ( TNF-α) and interleukin-6 ( IL-6) were determined by enzyme-linked immunosorbent assay. The M3 receptor mRNA transcription was detected by real-time polymerase chain reaction at 10, 30 and 60 min after adding LPS. Results Compared with group C, F-actin content was significantly de-creased, the expression of VE-cadherin and IκB was down-regulated, the contents of TNF-αand IL-6 were increased, and the expression of MLCK and NF-κB p65 was up-regulated in LPS and P+LPS groups ( P<0. 05) . Compared with group C, the expression of M3 receptor mRNA was significantly up-regulated in group LPS ( P<0. 05) , and no significant change was found in group P+LPS ( P>0. 05) . Compared with group LPS, F-actin content was significantly increased, the expression of VE-cadherin and IκB was up-reg-ulated, the contents of TNF-αand IL-6 were decreased, and the expression of MLCK, NF-κB p65 and M3 receptor mRNA was down-regulated in group P+LPS and group LPS+shRNA ( P<0. 05) . Compared with group P+LPS, F-actin content was significantly increased, the expression of VE-cadherin and IκB protein was up-regulated, TNF-α and IL-6 contents were decreased, and the expression of MLCK, NF-κB p65 and M3 receptor mRNA was down-regulated in group P+LPS+shRNA ( P<0. 05) . Conclusion PHC re-duces LPS-induced injury to human PMVECs through interfering with M3 receptors and inhibiting NF-κB-mediated inflammatory responses.

Diabetes has long been considered a risk factor in implant therapy and impaired wound healing in soft and hard oral tissues.Magnesium has been proved to promote bone healing under normal conditions.Here,we elucidate the mechanism by which Mg2+ promotes angiogenesis and osseointegration in diabetic status.We generated a diabetic mice model and demonstrated the alveolar bone healing was compromised,with significantly decreased angiogenesis.We then developed Mg-coating implants with hydrothermal synthesis.These implants successfully improved the vascularization and osseointegration in diabetic status.Mechanically,Mg2+ promoted the degradation of Kelch-like ECH-associated protein 1(Keap1)and the nucleation of nuclear factor erythroid 2-related factor 2(Nrf2)by up-regulating the expression of sestrin 2(SESN2)in endothelial cells,thus reducing the elevated levels of oxidative stress in mitochondria and relieving endothelial cell dysfunction under hyperglycemia.Altogether,our data suggested that Mg2+ promoted angiogenesis and osseointegration in diabetic mice by regulating endothelial mitochondrial metabolism.