In recent years, the number of ICU survivor is ever-growing with the increase of cure rate. The survivors′ outcome has aroused more and more attentions from medical personnel. ICU survivors tend to experience lasting physical, psychological and cognitive injuries, the post-traumatic stress disorder is one kind of significant psychological injury associated with patients′ critical experience. This review aims to summarize relevant literatures, introduces the prevalence, risk factors, complications, and interventions of ICU survivors′ post-traumatic stress disorder symptom, in order to prevent ICU survivors from post-ICU psychological injury and improve their long-term outcome.

Objective To observe the effects of propofol on the hippocampal astrocytes and microglia in the nenotal mice . Methods 15 healthy mice from the same litters on postnatal 7 d were randomized into 3 groups:high dose propofol group ,low dose propofol group and 10% intralipid control group .All mice were treated with drugs on postnatal 7 d by intraperitoneal injection and were sacrificed at 24 h after drugs treatment .The high dose group was injected with propofol 60mg · kg -1 ;the low dose group was injected with propofol 30mg · kg -1 ;the control group was injected with the equal volume of 10% intralipid .The immunohistochem‐istry assay was used to detect the expression of glial fibrillary acidic protein (GFAP) and ionized calcium binding adapter molecular 1 (Iba1) for observing the effect of propofol on the astrocytes (AST ) and microglia in the hippocampus .Results Compared with the control group ,the number of GFAP‐labeled AST in the dentate gyms (DG) molecular layer of hippocampus in P7 mice of the high dose propofol group was significantly reduced (P<0 .01) ,while no obvious effect of the low‐dose propofol on the number of AST was observed ;high dose and low dose propofol all significantly decreased the number of Iba1‐labeled microglia .Conclusion Propofol can inhibit the growth of the hippocampal AST and microglia in a dose‐dependent manner .

Rhizome atractylodes macrocephalae is the dry roots of Atractylodes macrocephala Koidz. It is one of commonly used Chinese medicine. In the ″Shennong's Herbal″, it was listed as the top grade. It mainly contains volatile oil, atractylenolides, atractylodes polysaccharides, glycosides and amino acids.And it has the medical functions of good for spleen and intestine, diuretic and dehumidifi?cation, hidroschesis, miscarriage prevention and soon.In order to provide references for further devel?opment and utilization, this paper systematic arranged the Chinese medicine atractylodes chemical composition, pharmacological effects, processing technology and effect of processing technology on chemical composition and pharmacological action.

Objeclive To explore relationship between TCM constitution and primary dysmenorrhea of female students in adolescent age,and to observe clinical effect of treating dysmenorrhea of students whose constitution tends toward Qi-deficiency and Yang-deficiency with wanning meddian therapy.Methods Relationship between TCM constitution and dysmenorrhea was performed in 789 students by questionnaire.Results Students with dysmenorrhea accounted for 50.3%,in which students with mild constitution accounted for 70.2%,and students with constitution tending toward Qi-deficiency and Yang-deficiency accounted for 80%.Conclusion Dysmenorrhea is associated with constitution.Warming meridian therapy can adjust constitution tending toward Qi-deficiency and Yang-deficiency.

Objective To investigate the inhibitory effects of rosiglitazone on the synthesis of reactive oxygen species (ROS) and the expression of monocyte chemoattractant protein 1 (MCP-1) induced by high glucose in rat mesangial cells. Methods The mesangial cells were divided into six groups: control group ( C, 5.6 mmol/L glucose), mannitol group (M, 24.2 mmol/L mannitol+group C), high glucose group( H, 30 mmol/L glucose), R1 group(R1, group H+10 μmol/ L rosiglitazone), R2 group (R2, group H+20 μmol/L rosiglitazone), N-acetylcysteine (NAC) group (N, group H+5 mmol/L NAC, NAC was added 1 h before the stimulation of high glucose). The level of ROS was measured by confocal laser scanning microscopy. The mRNA and the protein expression of MCP-1 were semi-quantitatively determined with reverse transcription-polymerase chain reaction and ELISA respectively. Results No significant differences of ROS and MCP-1 were found between control group and mannitol group. The intracellular ROS induced by high DOI:10.3760/cma.j.issn. 1001-7097.2009.01.011glucose increased by 4.1-fold compared to control group (P<0.01), which was prevented by rosiglitazone (20 μmol/L) and NAC respectively. The MCP-1 mRNA expression in group R2 and group N was significantly lower than that in group H (P<0.01). The MCP-1 protein level in group H [(940.9±20.3) ng/L] was higher than that in group C [(403.0±8.1) ng/L] (P<0.01), and the expression of MCP-1 protein in group R2 [(562.5±15.3) ng/L] and group N [(539.8±8.3) ng/L] was lower than that in group H (P<0.01). Conclusion Rosiglitazone may suppress high glucose-induced MCP-1 expression by reducing the level of ROS, which may be one of the mechanisms that rosiglitazone plays a direct role in the protection of kidney.

Local focal adhesion kinase (FAK) is a non-receptor intracellular tyrosine kinase that plays an important role in tumor initiation, development, metastasis and invasion, and is considered to be an important target for the development of antineoplastic drugs. It has both kinase-dependent and non-kinase-dependent scaffolding functions. However, traditional small molecular inhibitors can only inhibit its kinase-dependent activity, so it is difficult to target the kinase-independent scaffolding function. Therefore, there is an urgent need for novel strategies to enhance FAK targeting to lay the foundation for determining the druggability and discovery of FAK inhibitors. Proteolysis targeting chimera (PROTAC) is a new drug development strategy that can recruit E3 ligase to specifically ubiquitinylate target proteins for degradation through the proteasome system. The unique mechanism of action of the PROTAC system could be used to target and degrade the FAK protein, thus eliminating the scaffolding function of FAK. In this review, FAK protein, the signaling pathway, and small molecule inhibitors are briefly described, and the latest research progress in targeting the degradation of FAK using PROTAC technology is summarized.

Objective: To learn the characteristics of adolescent pregnancy in Wenzhou from 2015 to 2019, so as to provide basis for protecting adolescent physical and mental health. Methods: Data of demographic characteristics, pregnancy and delivery outcomes of the women aged under 19 years ( adolescent pregnant ) and 20 to 34 years ( right-age pregnant ) who delivered in Wenzhou from 2015 to 2019 were collected from Wenzhou Maternal and Child Health Information Management System. The incidence of pregnancy complication, comorbidity and adverse delivery outcomes of adolescent pregnant women was compared with that of right-age pregnant women. Results: Among 536 753 parturients reported in Wenzhou from 2015 to 2019, there were 22 419 ( 4.18% ) of adolescent pregnancy and 430 163 ( 80.14% ) of right-age pregnancy. The average age of adolescent pregnant women was (18.11±0.82) years ( range, 10-19 years ). The majority of adolescent pregnant women were migrant population (19 437 cases, 86.70%), had an education level of junior high school and below ( 18 594 cases, 82.94% ), and had no occupation (19 192 cases, 85.61%). The incidence rates of anemia, gestational diabetes, postpartum hemorrhage, perineal laceration and premature delivery in adolescent pregnant women increased from 2015 to 2019 ( all P<0.05 ). The incidence rates of gestational diabetes, anemia, gestational hypertension, placental abruption, postpartum hemorrhage, perineal laceration, premature delivery, low birth weight, fetal death and stillbirth were 1.65%, 11.76%, 0.19%, 0.26%, 3.19%, 24.52%, 6.03%, 5.53%, 0.50% and 0.04% in adolescent pregnant women, which were significant different from 5.49%, 8.94%, 0.13%, 0.01%, 0.17%, 23.46%, 4.66%, 3.08%, 0.26% and 0.01% in the right-age pregnant women, respectively ( all P<0.05 ). Conclusions The adolescent pregnant population in Wenzhou are mainly migrant population with lower education level and no occupation. The incidence rates of pregnancy complication, comorbidity and adverse birth outcomes in adolescent pregnant population are higher than those in right-age pregnant population, and are increasing year by year.

Background Eicosapentaenoic acid(EPA)function as the critical lipid mediators involved in several biological events in human body and play important role in suppressing the genesis of vascular endothelial growth factor (VEGF),migration and proliferation of vascular endothelial cells.Many ocular diseases were proved to be associated with neovascularization.Objecfive The purpose of this study was to investigate the inhibitory effect of EPA on the proliferation of human umbilical vein endothelial cells (HUVEC) indueed by VEGF. Methods HUVEC strain was cultured and passaged,and difierent concentrations of EPA were added to the medium with and without VEGF.The cultured cells were identified by antiofactor Ⅷ polyclonal antibody.The suppressing role of different concentrations of EPA on the proliferation of VEGF-induced or-uninduced HUVEC was assessed by MTT method.The influence of difierent concentrations of EPA on the cellular cycle of VEGF-induced HUVEC was assayed using flow eytometry.The expression of Flk-1,a receptor of VEGF,in the HUVEC Was detected by immunohistochemistry. Results Cultured HUVEC showed the ftlsiform in shape and presented with the cobblestone-like arrangement with the positive response for Ⅷ factor-related antigen.Various concentrations of EPA showed obviously inhibitory effect on VEGF-induced or-unindueed HUVEC at a dose-dependent manner (F=23.072.P=0.000).The inhibitory ability of EPA on VEGF-induced HUVEC was stronger than VEGF-uninduced HUVEC(F=41.417,P=0.000).In 24,48 and 72 hours,the action of EPA on the proliferation of HUVEC was gradually enhanced with the prolong of time(F=1.495,P=0.236).Cell cycle analysis indicated that EPA arrested VEGF-induced HUVEC in G0/G1 phase.The ratio of HUVEC in G0/G1 phase in EPA group was(75.83±1.56)%,and that in control groups was(68.62±1.44)%,showing a significant difference between them(t=-5.88,P=0.00),and no apoptosis of HUVEC was found in both groups.Flk-1 was strongly expressed in the cellular nucleus and cytoplasm in control group.However,the positive expressing intensity of Flk-1 in the HUVEC weakened,and the positive cell number was evidently less in EPA group. Conclusion EPA can inhibit the proliferation of VEGF induced HUVEC through arresting the synthesis of DNA of HUVEC and downregulate the expression of Flk-1 in HUVEC.These results suggest that EPA might exert an antiangiogenic effect.

Objective To study the effect of bromocriptine(BRC) on the activation of T lymphocyte stimulated by phytohemagglutinin(PHA).Methods After CD4+ T cell line Jurkat E6-1 cells were stimulated by PHA,prolactin(PRL) and BRC,respectively,the expression of linker for activation of T cells(LAT) and zeta-chain T cell receptor associated protein kinase 70 000(ZAP-70) mRNA of T lymphocytes were checked by RT-PCR.The expression of PRL mRNA of T lymphocytes was detected by Real time PCR.The expression of CD25(cluster of differentiation) as a marker of early activation on the surface of T lymphocytes was detected by flow cytometry,and the activation of nuclear factor-?B(NF-?B) was detected by luciferase reporter system.Results 1.BRC inhibited the expression of ZAP-70 as the common signal molecules both in the T lymphocyte activation pathway and PRL-prolactin-prolactin receptor(PRLR) signal transduction pathway,and decreased the expression of PRL mRNA produced by activation T lymphocytes.2.BRC enhanced the expression of LAT mRNA as another important signal molecular on the T lymphocytes and CD25 on the surface of the T lymphocytes.3.The activation of NF-?B of T lymphocytes was decreased.Conclusions BRC might inhibit the activation of T lymphocytes by inhibiting the expression of ZAP-70,the common signal molecules between T lymphocytes activation and PRL-PRL pathway,and PRL mRNA,the like-T lymphocyte growth factor.

Cardiac Catheterization ; Child ; Echocardiography, Three-Dimensional ; Heart Septal Defects ; diagnostic imaging ; Humans ; Prosthesis Implantation ; Time Factors