Objective To explore the culturing strategies,curiculum provision,courses conferring methods,teaching effects as well as the associated managerial evaluations on the basis of Sino-French cooperation on medical education with the hope of summarizing helpful suggestions to Sino-Foreign cooperation on medical education. Methods The achievements of our Sino-French cooperation on medical education were analyzed and compared in the teaching models,culturing strategies along with courses conferring processes among seven-year medical students from both English-teaching and French-teaching classes. Results Our Sino-French cooperation on medical education was featured in its distinct culturing purposes and effective teaching model.Its scientifically formulated culturing strategy found its full expression in French-teaching atmosphere.The Sino-French cooperation on medical education was consistently welcomed and favorably recommended by both faculties and students. Conclusion The Sino-French cooperation on medical education has not only gained precious experience in culturing the cutting-edge medical talents with the international visions but also conduced to fulfill the goal to establish a modernized and internationalized medical school.

Objective To investigate the possible function of integrin-linked kinase (ILK)/protein kinase B (PKB/Akt) signaling in repair of neonatal rat hypoxia-ischemia brain damage (HIBD). Methods Postnatal day 10 SD rats were randomly divided into hypoxia ischemia (HI) group and sham control group. Rat brains were collected at 0 h, 4 h, 6 h, 12 h, 24 h, 48 h and 72 h after hypoxia ischemia damage. Immunolfuorescence staining was used to observe the distribution and expression of ILK. Western blot was used to detect the expression of ILK, Akt, phosphorylated Akt (p-Akt) and vascular endothelial growth factor (VEGF). Lentiviral vectors expressing ILK shRNA were constructed to inhibit the expression of ILK in neonatal rats. After intracerebroventricular injections of LV-ILK shRNA lentivirus and LV-control respectively, HIBD model was established. Rat brains were collected at 4 h and 24 h after HIBD. Western blot was used to detect the expression of ILK, p-Akt, and VEGF. TdT-mediated dUTP-biotin nick end labeling (TUNEL) staining was used to detect cell apoptosis. Results Immunolfuorescence staining showed that ILK was widely distributed in cortex and hippocampus both in HI group and sham control group. ILK located at cell membrane and cytoplasm. Western blot results demonstrated that ILK protein increased after HI, with a peak at 24 h, and maintained higher level than those in sham control group. The p-Akt protein signiifcantly increased at 4 h after HI, and signiifcantly decreased in the following 24 h, and then increased again, with a peak at 48 h, but the level of p-Akt protein was higher than that of sham control group. The VEGF protein increased at 4 h after HI, with a peak at 12 h, higher than that of sham control group. The expression of Akt protein showed no signiifcant difference between HI group and sham control group. Lentiviral vectors containing RNAi targeting ILK was applied successfully in vivo. At 4 h and 24 h after HIBD model, the expression of ILK, p-Akt, and VEGF proteins in right side brain received LV-ILK shRNA signiifcantly decreased compared with those of right side brain received LV-control at the same time point. And cell apoptosis signiifcantly increased in LV-ILK shRNA group. Conclusions The expression of ILK, p-Akt, VEGF proteins increased after HI. By inhibiting the expression of ILK, the expression of p-Akt and VEGF proteins can be reduced, and cell apoptosis could increase in newborn rats after HIBD. The results suggest that ILK may induce the expression of VEGF through activating the PI3K/Akt signaling pathway, and promote cell survival and angiogenesis after HIBD.

iASPP can prompt the cell proliferation and inhibit the apoptosis of many cells. There are putative binding sites of transcription factor GATA-2 upstream of iASPP transcription start site. GATA-2 plays an important role in the proliferation and differentiation of hematopoietic stem cells (HSC) and progenitors. This study was aimed to explore the role of GATA-2 protein in iASPP gene transcription. Firstly, the expression of iASPP and GATA-2 protein in some leukemia cell lines was detected by Western blot. Second, The expressive vector of pCMV5-GATA2 and the luciferase reporter vectors containing possible binding sites of GATA-2 were constructed and co-transfected into HEK293 and CV-1 cells. Then the luciferase activity was assayed by luminometer. Also, ChIP assays were performed to further confirm the specific binding of GATA-2 to iASPP promoter. The results showed that GATA-2 was overexpressed in most cell lines with high level of iASPP. GATA-2 exhibited a significant effect on luciferase activity of reporter gene iASPP and in a dose-dependant manner. The relative luciferase activity was up-regulated to about two-fold of the empty vector control when the transfection dose of pCMV5-GATA2 plasmid was increased to 100 ng. While the effect was more significant in CV-1 cells and showed a 6.7-fold increase. The ChIP assay demonstrated the in vivo specific binding of GATA-2 to iASPP. The binding sites of GATA2 were located between nt -361 ∼ -334 in upstream of iASPP gene transcription start site. It is concluded that transcription factor GATA-2 can bind with the cis-regulatory region of the iASPP promoter and up-regulate iASPP expression.
Animals ; Cell Line ; Cercopithecus aethiops ; GATA2 Transcription Factor ; genetics ; Gene Expression Regulation, Leukemic ; Humans ; Intracellular Signaling Peptides and Proteins ; genetics ; K562 Cells ; Repressor Proteins ; genetics ; Transcription, Genetic ; Transcriptional Activation ; Transfection

OBJECTIVESome neonates especially premature infants, low birth weight infants and extremely low birth weight infants have limited endogenous energy stores. It is necessary to establish continuous administration of postnatal nutrition. The use of parenteral nutrition (PN) in neonates with immaturity of digestive system and intentionally delayed feedings has gained widespread acceptance. PN has been shown to provide sufficient nutrients to maintain growth in newborn infants. The major complication of PN in neonates is PN-associated cholestasis (PNAC). It remains a significant and frequent clinical problem for neonatal practitioners. In some cases, progressive liver damage, liver failure and death may become inevitable. In order to analyze the risk factors of the PNAC in neonates and to provide the evidence of safety and efficiency in clinical nutrition support, the clinical data of 612 neonates who had received PN for more than 5 days during the past 20 years were reviewed.

METHODSRetrospective analysis on data collected from April 1985 to March 2005 was performed. The records of 612 neonates were divided into two groups according to the established Nutrition Support Team (NST) in our hospital. Each group included two sub-groups. Seventy neonates of the first group were divided into PNAC group (n = 6) and non-PNAC group (n = 64); these patients were seen between 1st April 1985 and 31st March 1995. The remaining 542 neonates of the second group who were also divided into 2 groups, i.e. PNAC group (n = 12) and non-PNAC group (n = 530) who were seen from 1st April 1995 through 31st March 2005. The incidence of PNAC between the first group and the second group was compared and the associated factors were analyzed. The PNAC was defined when serum level of direct-bilirubin exceeded 1.5 mg/dl or direct-bilirubin greater than 50% of the bilirubin and excluding cholestasis resulted from other diseases.

RESULTSThe total incidence of PNAC in neonates who had received TPN for more than 5 days was 2.94%. The incidence of PNAC of the first and the second decade was 8.57% and 2.21%, respectively (OR = 0.242, 95% CI = 0.088 approximately 0.666). The average gestational age (GA) and birth weight (BW) of PNAC group were less than those of the non-PNAC group (GA: (33 +/- 5) w vs. (36 +/- 4) w, P = 0.009; OR = 0.827, 95% CI = 0.698 approximately 0.980. BW: (2003 +/- 743) g vs. (2393 +/- 764) g, P = 0.045; OR = 1.001, 95% CI = 0.999 approximately 1.002). The PN duration and calorie intake of PNAC group was longer than that of the non-PNAC group (PN duration: 32 +/- 30 d vs. (13 +/- 10) d, P = 0.000; OR = 1.072, 95% CI = 1.032 approximately 1.112. Calorie intake: [(272 +/- 46) kJ/(kg.d)] [(65.0 +/- 10.9) kcal/(kg.d)] (1 kcal = 4.184 kJ) vs. [(232 +/- 55) kJ/(kg.d) (55.5 +/- 13.1) kcal/(kg.d)], (P = 0.002; OR = 1.066, 95% CI = 1.012 approximately 1.122), but the weight gain in the non-PNAC group had a tendency to increase as compared to that of the PNAC group [(20 +/- 27) g/d vs. (9 +/- 19) g/d, P = 0.175].

CONCLUSIONSThe incidence of PNAC was associated with the longer duration of PN, the smaller age at initiation of PN, the higher calorie intake, prematurity and lower birth weight. Establishment of the nutrition support team can normalize the practice of the PN administration and decrease the incidence of the complication with nutrition support. It is a favorable mode and it can provide a safer, more effective and reasonable means in clinical nutrition support. To avoid PNAC, it is suggested that the administration of enteric feeding should start as soon as possible, which may enhance effective contraction of gallbladder and secretion of gastrointestinal hormones, and it is best to avoid high calorie of PN and control the calorie intake under 251.04 approximately 334.72 kJ/(kg.d) [60 approximately 80 kcal/(kg.d)].

Cholestasis ; complications ; epidemiology ; etiology ; Female ; Gestational Age ; Humans ; Incidence ; Infant ; Infant, Low Birth Weight ; physiology ; Infant, Newborn ; Infant, Premature ; growth & development ; Male ; Parenteral Nutrition ; adverse effects

Objective: To retrospectively analyze the prognostic value of platelet count recovery in the early stage post burn for patients with extremely severe burn, so as to evaluate their severity. Methods: A study involving 244 adult patients with extremely severe burn admitted to our hospital from January 2006 to December 2015, conforming to the inclusion criteria, was conducted. Data of their demography, injury, transmission, disease change in hospital, and platelet count from post injury day (PID) 1 to 10 were collected. (1) Patients were divided into survival group (n=212) and non-survival group (n=32) according to whether death or not. The dynamic change characteristic of platelet count in patients of two groups from PID 1 to 10 was analyzed and compared. (2) Patients were divided into return to normal group (RN, n=163) and non-return to normal group (NRN, n=81) according to whether platelet count returned to normal within one week post burn. The proportion of patients who received mechanical ventilation and mortality in groups RN and NRN, and length of stay in ICU between patients with platelet count that returned to normal and that did not return to normal in the early stage post burn in survival group were compared. Data were processed with independent samples t test , analysis of variance of repeated measurement, chi-square test, and binomial distribution test. Correlation was analyzed between data of sex, age, weight, total burn area, full-thickness burn area, inhalation injury, length of hospital stay, receiving mechanical ventilation, platelet count recovery condition within one week post burn and death of patients using the univariate and multivariate Cox regression analysis. Receiver operating characteristic (ROC) curve of platelet count on PID 8 was drawn to evaluate predicting value for death of 244 patients. Results: (1) The platelet count kept declining from PID 1 to 4, declined to below the normal low limit on PID 2, and reached its lowest level on PID 4 both in survival group and non-survival group. The platelet count both in survival group and non-survival group rose gradually from PID 4 to 10, and returned to normal on PID 8 and 10, respectively. There was no significant difference in platelet count of patients in two groups on PID 1 (t=1.01, P>0.05), while platelet count of patients in non-survival group was obviously lower than that in survival group from PID 2 to 10 (with t values from 2.64 to 7.17, P values below 0.01). The daily increment of platelet count in survival group from PID 4 to 10 was (26±13)×10⁹/L, obviously higher than that in non-survival group [(19±11)×10⁹/L, t=2.76, P<0.01]. (2) The proportion of patients who received mechanical ventilation was obviously lower than that of patients who did not receive mechanical ventilation in group RN (P<0.01), while the proportion of patients who received mechanical ventilation was obviously higher than that of patients who did not receive mechanical ventilation in group NRN (P<0.05). The proportion of patients who received mechanical ventilation in group NRN was obviously higher than that in group RN (χ²=32.93, P<0.01). The mortality of patients in group NRN was obviously higher than that in group RN (χ²=20.99, P<0.01). The length of stay in ICU of patients whose platelet count did not return to normal in the early stage was significantly longer than that of patients whose platelet count returned to normal in the early stage in survival group (t=4.20, P<0.01). (3) Total burn area, receiving mechanical ventilation, and platelet count did not return to normal within one week post burn were independent risk factors for death of patients with extremely severe burn (with hazard ratio respectively 1.073, 16.552, and 2.249, 95% confidence interval respectively 1.033-1.115, 2.147-127.580, and 0.993-5.096, P<0.05 or P<0.01). (4) The area under the ROC curve of platelet count on PID 8 to predict death of 244 patients with extremely severe burn was 0.745 (with 95% confidence interval 0.645-0.845, P<0.01), and 150×10⁹/L was chosen as the optimal threshold value, with sensitivity of 71.4% and specificity of 71.0%. Conclusions Platelet count recovery in the early stage post burn of patients with extremely severe burn was significantly associated with their prognosis and could be used as an important indicator to evaluate the severity of illness.

Objective Though paraquat (PQ) is highly toxic, there is still no effective treatment for PQ poisoning .The aim of the article was to study the protective effect and mechanism of the p 38 mitogen-activated protein kinase ( MAPK) inhibitor SB203580 on PQ-induced acute lung injury in rats . Methods 72 SD rats were randomly divided into three groups ( n=24 ): normal saline (NS) group, PQ poisoning group and p38 inhibitor SB203580 intervention (PQ+SB) group.The arterial blood gas analysis, lung wet and dry ratio (W/D),the expression of tumor necrosis factor-α(TNF-α), the superoxide dismutase (SOD) level and the pathological changes of lung tissues were recorded at different time points after drug intervention . Results On the 1st , 3rd, 5th days after drug intervention in PQ group, the alveolo-arterial oxygen partial pressure difference (PA-aO2) [(45.67 ±4.17), (68.78 ±6.63), (80.23 ±7.12 ) mmHg ], the lung tissue TNF-αexpression (14.63 ±3.10], [18.24 ±2.98], [16.22 ±2.79] pg/mg) and W/D ([4.931 ±0.034], [5.020 ±0.064], [5.079 ±0.016]) in-creased gradually to a peak on the 3rd day, while the SOD level de-creased respectively on the 1st , 3rd, 5th days after drug intervention ([175.26 ±7.98], [167.57 ±8.05], [160.24 ±6.78] U/ug) (P<0.05).Compared with PQ group, PQ+SB group got a decrease in the PA-aO2([80.23 ±7.12] vs [44.17 ±4.16]), the lung tissue TNF-αexpression ([16.22 ±2.79] vs [9.48 ±2.72]) and W/D ([4.805 ±0.070] vs [5.079 ±0.016]) (P<0.05), while the pulmonary SOD level increased in comparison with PQ group ([125.89 ±6.65] vs [160.24 ±6.78]) (P<0.05). Conclusion The p38MAPK inhibitor SB203580 plays a certain protective role in PQ-induced acute lung injury by reducing inflammation and improving antioxidant capacity .

BACKGROUNDResolvin D1 (RvD1) is a newly found anti-inflammatory bioactive compound derived from polyunsaturated fatty acids. The current study aimed to explore the protective effect of RvD1 on lipopolysaccharide (LPS)-induced acute kidney injury (AKI) and its possible mechanism.

METHODSBoth in vivo and in vitro studies were conducted. Male BALB/c mice were randomly divided into control group (saline), LPS group (LPS 5 mg/kg), RvD1 group (RvD1 5 μg/kg + LPS 5 mg/kg), and blockage group (Boc-MLP 5 μg/kg + RvD1 5 μg/kg + LPS 5 mg/kg). Boc-MLP is a RvD1 receptor blocker. The mice were intraperitoneally injected with these drugs and recorded for general condition for 48 h, while the blood and kidneys were harvested at 2, 6, 12, 24, and 48 h time points, respectively (n = 6 in each group at each time point). Human proximal tubule epithelial cells (HK-2) were randomly divided into control group (medium only), LPS group (LPS 5 μg/ml), RvD1 group (RvD1 10 ng/ml + LPS 5 μg/ml), and blockage group (Boc-MLP 10 ng/ml + RvD1 10 ng/ml + LPS 5 μg/ml). The cells were harvested for RNA at 2, 4, 6, 12, and 24 h time points, respectively (n = 6 in each group at each time point). Blood creatinine was tested by using an Abbott i-STAT portable blood gas analyzer. Tumor necrosis factor-α (TNF-α) level was detected by ELISA. Kidney pathology was observed under hematoxylin and eosin (HE) staining and transmission electron microscope (TEM). We hired immune-histological staining, Western blotting, and fluorescence quantitative polymerase chain reaction to detect the expression of RvD1 receptor ALX, nuclear factor-kappa B (NF-κB) signaling pathway as well as caspase-3. Kidney apoptosis was evaluated by TUNEL staining.

RESULTSRvD1 receptor ALX was detected on renal tubular epithelials. Kaplan-Meier analysis indicated that RvD1 improved 48 h animal survival (80%) compared with LPS group (40%) and RvD1 blockage group (60%), while RvD1 also ameliorated kidney pathological injury in HE staining and TEM scan. After LPS stimulation, the mRNA expression of toll-like receptor 4, myeloid differentiation factor 88, and TNF-α in both mice kidneys and HK-2 cells were all up-regulated, while RvD1 substantially inhibited the up-regulation of these genes. Western blotting showed that the phosphorylated-IκB/IκB ratio in LPS group was significantly higher than that in the control group, which was inhibited in the RvD1 group. RvD1 could inhibit the up-regulation of cleaved-caspase-3 protein stimulated by LPS, which was prohibited in RvD1 blockage group. RvD1 group also had a lower proportion of apoptotic nuclei in mice kidney by TUNEL staining compared with LPS group.

CONCLUSIONIn LPS-induced AKI, RvD1 could decrease TNF-α level, ameliorate kidney pathological injury, protect kidney function, and improve animal survival by down-regulating NF-κB inflammatory signal as well as inhibiting renal cell apoptosis.

Acute Kidney Injury ; chemically induced ; prevention & control ; Adaptor Proteins, Signal Transducing ; analysis ; Animals ; Apoptosis ; drug effects ; Docosahexaenoic Acids ; pharmacology ; Down-Regulation ; Kidney ; drug effects ; pathology ; Lipopolysaccharides ; pharmacology ; Male ; Mice ; Mice, Inbred BALB C ; NF-kappa B ; antagonists & inhibitors ; Tumor Necrosis Factor-alpha ; analysis

To assess the neurotoxic effects and redox responses of Aroclor 1254 (A1254) on perinatally exposed rat offspring, A1254 was administered by gavage from gestational day (GD) 6 to postnatal day (PND) 21. Neurobehavioral development, antioxidant enzyme activities, lipid peroxidation (LPO), nitric oxide (NO), and NO synthase (NOS) levels were analyzed in the offspring. Neurobehavioral development analysis revealed delayed appearance of the righting reflex, negative geotaxis, and cliff drop test responses in A1254 exposed group. Developmental A1254 exposure also caused oxidative stress in the brain of PND 22 offspring via reductions in the activity of SOD and GSH-Px, and by promoting a rise in the levels of NO and NOS.
Aging ; metabolism ; Animals ; Cerebral Cortex ; drug effects ; enzymology ; metabolism ; Chlorodiphenyl (54% Chlorine) ; toxicity ; Female ; Glutathione Peroxidase ; metabolism ; Kidney ; drug effects ; enzymology ; metabolism ; Lipid Peroxidation ; drug effects ; Liver ; drug effects ; enzymology ; metabolism ; Mice ; Nervous System ; drug effects ; growth & development ; metabolism ; physiopathology ; Nervous System Diseases ; chemically induced ; Nitric Oxide ; metabolism ; Nitric Oxide Synthase ; metabolism ; Oxidative Stress ; drug effects ; Pregnancy ; Prenatal Exposure Delayed Effects ; chemically induced ; Random Allocation ; Rats ; Superoxide Dismutase ; metabolism

For determination the ionic mechanisms of the hypoxic acclimatization at the level of channels, male Spradue-Dawley rats were divided into two groups: control normoxic group and chronic intermittent hypoxic group [O2 concentration: (10 +/-0.5)%, hypoxia 8 h a day]. Using whole cell patch-clamp technique, voltage-gated potassium channel currents (IK(V)) were recorded in freshly isolated pulmonary arterial smooth muscle cells (PASMCs) of rat with acute isolated method. The effect of acute hypoxia on IK(V) of PASMCs from chronic intermittent hypoxia group was investigated to offer some basic data for clarifying the ionic mechanisms of the hypoxic acclimatization. The results showed: (1) In control normoxic group, after acute hypoxia free-Ca(2+) solution, the resting membrane potential (Em) of PASMCs was depolarized significantly from -47.2+/-2.6 mV to -26.7+/-1.2 mV, and the IK(V) of PASMCs was decreased significantly from 153.4+/-9.5 pA/pF to 70.1+/-0.6 pA/pF, the peak current percent inhibition was up to (57.6+/-3.3)% at +60 mV, and current-voltage relationship curve shifted to the right. (2) In chronic intermittent hypoxic group, the IK(V) of PASMCs was decreased significantly by exposure to intermittent hypoxia in a time-dependent manner, appeared to start on day 10 and continued to day 30 (the longest time tested) of hypoxia, and current-voltage relationship curve shifted to the right in a time-dependent manner. (3) Compared with the control normoxic group, the percent IK(V) inhibition by acute hypoxia was significantly attenuated in the chronic intermittent hypoxia group and this inhibition effect declined with time exposure to hypoxia. The results suggest that K(V) inhibition was significantly attenuated by chronic intermittent hypoxia, and this effect may be a critical mechanism of the body hypoxic acclimatization.
Animals ; Cell Separation ; Hypoxia ; complications ; physiopathology ; Male ; Muscle, Smooth, Vascular ; cytology ; metabolism ; physiology ; Potassium Channels, Voltage-Gated ; antagonists & inhibitors ; Pulmonary Artery ; metabolism ; pathology ; Rats ; Rats, Sprague-Dawley

Objective: To investigate the effects of two-step retraction and en-masse retraction on tooth movement pattern of anterior teeth and posterior anchorage with clear aligners using three-dimensional finite element analysis. Methods: A finite element model of maxillary first premolar extraction case undergoing clear aligner treatment was established based on maxillofacial cone-beam CT data of a 24-year-old adult male with individual normal occlusion, who visited Department of Oral Surgery, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine for impacted mandibular third molar in June, 2022. The initial tooth displacement of five anterior retraction protocols (two-step with canine retraction, two-step with incisor bodily retraction, two-step with incisor retraction-overtreatment, en-masse bodily retraction, and en-masse retraction-overtreatment) were evaluated. Results: Two step with canine retraction caused distal tipping of the canine and labial tipping of the incisors (0.18° for central incisor and 0.13° for lateral incisor). Two step with incisor retraction caused mesial tipping of the canine. In two step with bodily retraction protocol, uncontrolled lingual tipping was found in central incisor (0.29°) and lateral incisor (0.32°). In two-step with incisor retraction-overtreatment protocol, the movement pattern of the incisors didn't change, but the inclinations reduced to 0.21° and 0.18°. En-masse retraction caused distal tipping of the canine. In en-masse bodily retraction protocol, uncontrolled lingual tipping was also found in central incisor (0.19°) and lateral incisor (0.27°). In en-masse retraction-overtreatment protocol, the central incisor showed controlled lingual tipping (0.02°) and the lateral incisor showed palatal root movement (0.03° labial inclination). Posterior teeth exhibited mesial tipping in all five protocols. Conclusion: En-masse retraction with incisor overtreatment was beneficial to incisor torque control in clear aligner treatment.