OBJECTIVE To investigate antibiotic resistance in nosocomial infections with Acinetobacter baumannii from lower respiratory tract in the intensive care unit(ICU) and guide clinically rational use of drug.METHODS Antibiotics susceptibility tests in 109 clinical isolates of A.baumannii from lower respiratiory tract were performed by K-B disk diffusion method.The results were judged according to CLSI 2007.As controls,standard strain was used simultaneously.RESULTS The sensitivity rate to cefoperazone/sulbactam was the highest,arriving at 77.1% and followed by imipenem(57.8%) and meropenem(54.9%).The other antibiotics were below 50.0%,generally.The serious cross-resistance phenomenon was in present.Pan-resistant strains had been detected.CONCLUSIONS The drug-resistant status in nosocomial infections with A.baumannii from lower respiratory tract in ICU is very serious.We should continue to strengthen the monitoring of the antibiotic resistance and prevent the outbreak epidemics of drug resistant strains in ICU.

Restless legs syndrome (RLS) is a common sensorimotor disorder. Although it does not pose a threat to life, it seriously affects the quality of life of patients. RLS pathogenesis is still unclear, and its incidence is associated with a variety of risk factors, including genetic factors and non-genetic factors. Genetic factors involve more than 20 risk genes, such as meis homeobox 1 ( MEIS1), BTB domain containing 9 ( BTBD9), mitogen-activated protein kinase kinase 5 ( MAP2K5), and protein tyrosine phosphatase receptor type Db ( PTPRD). Non-genetic factors include regional age, gender, obesity, medical related diseases, neuropsychiatric diseases and drugs. This paper reviews the recent advance in risk factors and related pathogenesis of RLS to provide references for early prevention and treatment of the disease.

Objective:To evaluate the effects of heparin on focal adhesion kinase (FAK)/Ras homolog gene family member A (RhoA)/Rho-associated coiled-coil-containing protein kinase (ROCK) signaling pathways during acute lung injury (ALI) in septic mice.Methods:Thirty SPF healthy adult male C57BL/6J mice, aged 6-8 weeks, weighing 20-23 g, were assigned into 3 groups ( n=10 each) using a random number table method: control group (group C), ALI group, and heparin group (group H). Septic ALI model was prepared by intraperitoneal injection of lipopolysaccharide 15 mg/kg, while group C received the equal volume of normal saline. In group H, heparin sodium solution 10 U was injected via the tail vein at 30 min before developing the model. The equal volume of normal saline was injected in C and ALI groups. Venous blood samples were collected from the eyeballs under deep anesthesia at 24 h after lipopolysaccharide injection. The mice were subsequently sacrificed and lung tissues were obtained for determination of the serum concentrations of interleukin-1beta (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) (using enzyme-linked immunosorbent assay), wet/dry lung weight (W/D) ratio, expression of vascular endothelial adhesion factor 1 (VCAM-1) (by immunohistochemical staining) and expression of FAK, phosphorylated FAK (p-FAK), RhoA, GTP-bound RhoA (RhoA-GTP) and ROCK (by Western blot) and for examination of the pathological changes. The lung injury was assessed and scored. Results:Comparison with group C, the serum concentrations of IL-1β, IL-6 and TNF-α, W/D ratio and lung injury scores were significantly increased, and the expression of VCAM-1, p-FAK, RhoA-GTP and ROCK was up-regulated in ALI group ( P<0.05). Compared with ALI group, the serum concentrations of IL-1β, IL-6 and TNF-α, W/D ratio and lung injury scores were significantly decreased, and the expression of VCAM-1, p-FAK, RhoA-GTP and ROCK was down-regulated in H group ( P<0.05). Conclusions:The mechanism through which heparin mitigates ALI is associated with the inhibition of the FAK/RhoA/ROCK signaling pathway in septic mice.

Objective To explore response element that maintains basic transcriptional activity of intestinal trefoil factor (ITF) promoter.Methods Truncated and mutant 5' flanking sequences of ITF gene were cloned from ITF promoter sequences by PCR,and then they were inserted into the pGL3-basic vector to construct truncated and mutant luciferase vectors to conduct the following experiments.(1) Human embryonic kidney 293 (HEK293) cells were divided into pGL3-basic group,pGL3-300 group,pGL3-280 group,pGL3-260 group,pGL3-240 group,pGL3-220 group,and pGL3-200 group according to the random number table (the same grouping method below),with 3 wells in each group,and they were respectively transfected with 500 ng corresponding plasmids and 15 ng renilla luciferase reporter plasmids pRL-TK.After being cultured for 48 hours,the relative luciferase activity of cells was measured by single tube detection system.(2) Another batch of HEK293 cells were divided into pGL3-basic group,pGL3-300 group,mutant 1,2,3,and 4 groups,with 3 wells in each group,and they were respectively transfected with 500 ng pGL3-basic,pGL3-300,mutant 1,2,3,and 4 plasmids and 15 ng pRL-TK plasmids.After being cultured for 48 hours,the relative luciferase activity of cells was measured as in (1).(3) Another batch of HEK293 cells were divided into blank control group and 10,50 μmol/L mithramycin groups,with 3 wells in each group.After being transfected with 500 ng pGL3-300 plasmids and 15 ng pRL-TK plasmids,cells in blank control group were not transfected with mithramycin,while cells in the latter two groups were respectively transfected with 10 and 50 μmol/L mithramycin.After being cultured for 24 hours,the relative luciferase activity of cells was measured as in (1).(4) Another batch of HEK293 cells were divided into blank control group and 0.1,0.2,and 0.3 μg pcDNA3,1-Sp1 groups,with 3 wells in each group.After being transfected with 500 ng pGL3-300 plasmids and 15 ng pRL-TK plasmids,cells in blank control group were not transfected with pcDNA3.1-Spl plasmids,while cells in the latter three groups were respectively transfected with 0.1,0.2,and 0.3 μg pcDNA3.1-Sp1 plasmids.After being cultured for 48 hours,the relative luciferase activity of cells was measured as in (1).Data were processed with one-way analysis of variance and LSD test.Results (1) The relative luciferase activity of cells in pGL3-basic group,pGL3-300 group,pGL3-280 group,pGL3-260 group,pGL3-240 group,pGL3-220 group,and pGL3-200 group was 1.00,7.99 ±0.51,2.03 ±0.55,2.50 ±0.40,2.50 ±0.15,1.72 ±0.19 and 2.10 ± 0.21,respectively.The relative luciferase activity of cells in pGL3-280 group,pGL3-260 group,pGL3-240 group,pGL3-220 group,and pGL3-200 group was significantly lower than that in pGL3-300 group (with P values below 0.01).(2) The relative luciferase activity of cells in pGL3-basic group,pGL3-300 group,mutant 1,2,3,and 4 groups was 1.00,7.99 ±0.51,2.10 ±0.56,7.03 ± 1.05,5.09 ± 1.40 and 8.15 ± 1.48,respectively.The relative luciferase activity of cells in mutant 1 group was significantly lower than that in pGL3-300 group (P ＜ 0.01).The relative luciferase activity of cells in pGL3-300 group,mutant 2,3,and 4 groups was similar (with P values above 0.05).(3) The relative luciferase activity of cells in 10 and 50 μmol/L mithramycin groups was respectively 3.07 ± 0.60 and 2.93 ± 0.55,which was significantly lower than that in blank control group (8.05 ± 0.83,with P values below 0.01).(4) The relative luciferase activity of cells in 0.1,0.2,and 0.3 μg pcDNA3.1-Sp1 groups was respectively 12.74 ± 1.12,14.52 ± 1.25,and 15.66 ± 1.82,which was significantly higher than that in blank control group (8.13 ± 0.71,with P values below 0.05).Conclusions One Sp1 binding site,locating in the region from-301 to-293 bp of ITF promoter,is the core element for regulating the basic transcriptional activity of ITF.

Activation of the heart normally begins in the sinoatrial node (SAN). Electrical impulses spontaneously released by SAN pacemaker cells (SANPCs) trigger the contraction of the heart. However, the cellular nature of SANPCs remains controversial. Here, we report that SANPCs exhibit glutamatergic neuron-like properties. By comparing the single-cell transcriptome of SANPCs with that of cells from primary visual cortex in mouse, we found that SANPCs co-clustered with cortical neurons. Tissue and cellular imaging confirmed that SANPCs contained key elements of glutamatergic neurotransmitter system, expressing genes encoding glutamate synthesis pathway (Gls), ionotropic and metabotropic glutamate receptors (Grina, Gria3, Grm1 and Grm5), and glutamate transporters (Slc17a7). SANPCs highly expressed cell markers of glutamatergic neurons (Snap25 and Slc17a7), whereas Gad1, a marker of GABAergic neurons, was negative. Functional studies revealed that inhibition of glutamate receptors or transporters reduced spontaneous pacing frequency of isolated SAN tissues and spontaneous Ca