Abstract: Objective　To investigate the distribution and drug resistance characteristics of pathogenic bacteria in patients with neutropenic acute leukemia (AL) and bloodstream infections (BSI). Methods　The clinical data of 258 neutropenic acute leukemia patients with bloodstream infections, who admitted to Shengjing Hospital of China Medical University from January 2016 to December 2021, were collected and analyzed for pathogenic bacteria and drug resistance. Results A total of 268 strains of pathogenic bacteria were isolated from 258 patients, including 180 strains of gram-negative bacteria (67.16%), 61 strains of gram-positive bacteria (22.76%), and 27 strains of fungi (10.07%). Gram-negative bacteria were mainly Klebsiella pneumoniae (53/268, 19.78%), Escherichia coli (49/268, 18.28%) and Pseudomonas aeruginosa (41/268, 15.30%). Gram-positive bacteria were mainly coagulase negative Staphylococcus (31/268, 11.57%) and Staphylococcus aureus(17/268, 6.34%). The main fungi were Candida tropicalis (25/268, 9.33%). Escherichia coli (33/268, 12.31%) was the most common pathogen isolated from acute myeloid leukemia (AML), followed by Pseudomonas aeruginosa (25/268, 9.33%), coagulase-negative Staphylococcus (18/268, 6.72%) and Candida tropicalis (18/268, 6.72%). Klebsiella pneumoniae (35/268, 13.06%) was the most common pathogen isolated from acute lymphoblastic leukemia (ALL),followed by Pseudomonas aeruginosa (15/268, 5.60%) and Escherichia coli (14/268, 5.22%). The resistance of Gram-negative bacteria to piperacillin/tazobactam, cefoperazone/sulbactam, imipenem, meropenem, ertapenem, amikacin, cefoxitin, amoxicillin/clavulanic acid was low. Gram-positive bacteria were sensitive to linezolid and vancomycin. Candida was sensitive to flucytosine, amphotericin B and itraconazole. Conclusions　In patients with granulosa after AL chemotherapy combined with BSI, the pathogenic bacteria isolated from AML are diverse, and the pathogenic bacteria isolated from ALL are mainly gram-negative bacteria. Pathogenic bacteria have different degrees of drug resistance to commonly used antibacterial drugs, so it is important to strengthen the monitoring of the distribution of pathogenic bacteria and the change of drug resistance and rational use of antibacterial drugs to minimize the death of patients.

Abstract: Objective　To understand the situation of drug-resistant tuberculosis screening and epidemiological characteristics of multi-drug resistant tuberculosis (MDR-TB) and pre-extensively drug resistant tuberculosis (pre-XDR-TB) in Changsha, in order to provide a scientific basis for improving the quality of drug-resistant tuberculosis prevention and control in the city. Methods　Demographic information and drug susceptibility date of etiologically positive pulmonary tuberculosis patients in Changsha from 2018 to 2021 were collected, the successful rate of resistance screening, incidence and tendency in MDR-TB and pre-XDR-TB in patients included in this study were statistically analyzed accordingly. 　　Results From 2018 to 2021, the successful screening rates were 86.2%, 87.7%, 81.9% and 71.5% for MDR-TB and 82.2%, 84.8%, 76.9% and 68.2% for pre-XDR-TB, respectively. In each year, MDR-TB patients identified accounted for 7.6% (101/1 222), 6.5%(124/1 774), 6.6%(110/1 555) and 6.3%(99/1 478), and pre-XDR-TB patients identified accounted for 3.6%(46/1 219), 3.8%(69/1 766), 4.4%(69/1 495) and 4.6%(69/1 436), correspondingly. The incidence of MDR-TB showed a slowly downward trend, while the incidence of pre-MDR-TB showed a slowly upward trend, with neither decreasing nor increasing trends being statistically significant (（χ2=1.947，0.806，P>0.050). The incidence of MDR-TB in the retreatment failure population was 66.6% (2/3), and the others, failure initial treatment and recrudescence populations were 23.5% (19/81), 16.7% (2/12) and 15.2% (70/461), respectively. Similar to the incidence above, the incidence of pre-XDR-TB was 16.7% (2/12) among patients who failed in initial treatment, and 12.2% (9/74), 9.8% (43/439), and 4.5% (2/44) among the others, recrudescence and returned patients, respectively. The incidence rates of MDR-TB and pre-XDR-TB in different populations were significantly different (χ2=117.600，59.030，P<0.05). Conclusions There are still areas for improvement in tuberculosis drug resistance surveillance system in Changsha. On the premise of paying attention to patients in retreatment failure, other, initial treatment failure and relapse patients, high sensitivity molecular drug susceptibility testing, and scientifically efficient screening strategies must be explored.

Objective To investigate the drug resistance genes of extended-spectrum beta- lactamase-producing bacteria in 49 strains.Methods Extended-spectrum ?-lactamase -producing strains were detected by the disc diffusion test.The techniques of polymerase chain reaction,sequence analysis, pulsed-field gel electrophoresis were used to analyze the genotype and homology of extended-spectrum ?- lactamase-producing strains.Results The incidence of ESBL-producing strains from E.coli,K pneumoniae,K oxytoca,was 20% in 2000,and 40% in 2003.Among the 49 ESBLs producers the most common genotype was CTX-M-14( n=33).The others were CTX-M-3,CTX-M-9,CTX-M-12,CTX-M-15, CTX-M-24 and SHVSa.Both two CTX-M subtypes,CTX-M-3 and CTX-M-14,were detected in one strain. However,4 ESBL-producing strains confirmed by phenotype remained untyped.The results showed that the ESBLs producers were not closely related,except for two strains of E.coli and two strains of K.pneumoniae which were homgenic respectively.Concolusions The incidence of ESBL-producing strains increases with years.The most common genotype of ESBLs is CTX-M.There is no evidence for epidemiologic spread of ESBL-producers by pulsed-field gel electrophoresis.

AlM:To discuss the protective effect ofα-mangostin on retinal light damage in mice.METHODS:Totally 30 Balb/c mice, aged 6~8wk, were randomly divided into the control group, light-exposure group and α-mangostin group. Every group contained 10 mice. Mice of α-mangostin group were treated with alpha-mangostin at the dose of 30mg/( kg · d ) body weight by intragastric administration daily for 7d, and then exposed to white light at the 5th d. The light-exposure group and α-mangostin group were exposed to 5 000 ± 200lx white light-emmiting diodes (LEDs) for continuously 1h to establish the mice model of retinal light damage. Flash -electroretinograme was recorded 72h after light exposure. The changes in retinal morphology of mice were observed by light microscopy. Retinas were extracted to detect the malondialdhyde ( MDA ) content change of the retinal homogenate.RESULTS: Flash-electroretinogram ( F-ERG ) showed that retinal dysfunction was less severe in α-mangostin group than in light-exposure group ( P<0. 05 ). Light microscopy test showed that retina structural damage was less severe in α-mangostin group than in light-exposure group (P<0. 05). The level of MDA in retinal tissue of α-mangostin group was significantly lower when compared with light-exposure group (P<0. 05).CONCLUSlON: α-mangostin inhibits lipid peroxidation induced by light damage and protect retina against light damage.

As one of the major sources of infection, viruses could infect all organisms including bacteria, plants, animals, and humans. Infectious diseases caused by viruses pose a great threat and damage to human health and economic activities all over the world. Adaptor-associated protein kinase 1 (AAK1) is a member of the Ark1/Prk1 family of serine/threonine kinases and a specific key kinase regulating the phosphorylation of AP-2 protein μ2 subunit T156. In the past, AAK1 has been regarded as a feasible biological target for the treatment of nerve pain. Recently, scientists have found that inhibiting AAK1 can regulate endocytosis and inhibit virus invasion into cells. Therefore, AAK1 could be the potential target of anti-virus therapy. This paper reviews the research progress of small molecule AAK1 inhibitors in the field of antiviral, analyzes the future research directions and challenges, and provides new ideas for the development of antiviral drugs targeting AAK1.

This study was designed to evaluate the effects of drilling through the growth plate and using adipose-derived stem cells (ADSCs) and bone morphogenetic protein-2 (BMP-2) to treat femoral head epiphyseal ischemic necrosis,which can be done in juvenile rabbits.Passage-four bromodeoxyuridine (BrdU)-labeled ADSCs were cultured,assayed with MTT to determine their viability and stained with alizarin red dye to determine their osteogenic ability.Two-month-old,healthy male rabbits (1.2 to 1.4 kg,n=45) underwent ischemic induction and were randomly divided into five groups (group A:animal model control;group B:drilling;group C:drilling & ADSCs;group D:drilling & BMP-2;and group E:drilling & ADSCs & BMP-2).Magnetic resonance imaging (MRI),X-ray imaging,hematoxylin and eosin staining and BrdU immunofluorescence detection were applied 4,6 and 10 weeks after treatment.Approximately 90％ of the ADSCs were labeled with BrdU and showed good viability and osteogenic ability.Similar results were observed in the rabbits in groups C and E at weeks 6 and 10.The animals of groups C and E demonstrated normal hip structure and improved femoral epiphyseal quotients and trabecular areas compared with those of the groups A and B (P＜0.01).Group D demonstrated improved femoral epiphyseal quotients and trabecular areas compared with those of groups A and B (P＜0.05).In summary,drilling through the growth plate combined with ADSC and BMP-2 treatments induced new bone formation and protected the femoral head epiphysis from collapsing in a juvenile rabbit model of femoral head epiphyseal ischemic necrosis.

Background::In consideration of the difficulty in diagnosing high heterogeneous glioma, valuable prognostic markers are urgent to be investigated. This study aimed to verify that connective tissue growth factor (CTGF) is associated with the clinical prognosis of glioma, also to analyze the effect of CTGF on the biological function.Methods::In this study, glioma and non-tumor tissue samples were obtained in 2012 to 2014 from the Department of Neurosurgery of Nanfang Hospital of Southern Medical University, Guangzhou, China. Based on messenger RNA (mRNA) data from the Cancer Genome Atlas (TCGA) and CCGA dataset, combined with related clinical information, we detected the expression of CTGF mRNA in glioma and assessed its effect on the prognosis of glioma patients. High expression of CTGF mRNA and protein in glioma were verified by reverse transcription-polymerase chain reaction, immunohistochemistry, and Western blotting. The role of CTGF in the proliferation, migration, and invasion of gliomas were respectively identified by methylthiazoletetrazolium assay, Transwell and Boyden assay in vitro. The effect on glioma cell circle was assessed by flow cytometry. For higher expression of CTGF in glioblastoma (GBM), the biological function of CTGF in GBM was investigated by gene ontology (GO) analysis. Results::In depth analysis of TCGA data revealed that CTGF mRNA was highly expressed in glioma (GBM, n= 163; lowly proliferative glioma [LGG], n = 518; non-tumor brain tissue, n = 207; LGG, t = 2.410, GBM, t = 2.364, P < 0.05). CTGF mRNA and protein expression in glioma (86%) was significantly higher than that in non-tumor tissues (18%) verified by collected samples. Glioma patients with higher expression of CTGF showed an obviously poorer overall survival (35.4 and 27.0 months compared to 63.3 and 55.1 months in TCGA and Chinese Glioma Genome Atlas (CGGA) databases separately, CGGA: χ2 = 7.596, P = 0.0059; TCGA: χ2 = 10.46, P = 0.0012). Inhibiting CTGF expression could significantly suppress the proliferation, migration, and invasion of gliomas. CTGF higher expression had been observed in GBM, and GO analysis demonstrated that the function of CTGF in GBM was mainly associated with metabolism and energy pathways ( P < 0.001). Conclusions::CTGF is highly expressed in glioma, especially GBM, as an unfavorable and independent prognostic marker for glioma patients and facilitates the progress of glioma.

The major idea of this article is to discuss standardization and normalization for the product standard of medical devices. Analyze the problem related to the physical performance requirements and test methods during product standard drafting process and make corresponding suggestions.
Device Approval ; Equipment and Supplies ; standards ; Materials Testing ; methods ; Weights and Measures

OBJECTIVETo study the effect of dihydroartemisinin (DHA) combined irradiation on the apoptosis of human lung cancer GLC-82 cells and to study its mechanism.

METHODSThe growth inhibition rate of GLC-82 cells acted by different concentrations DHA was detected using MTT assay at 24, 48, and 72 h, respectively. Clone forming test was used. With multi-target single-hit model, the radiosensitization effect was assessed by calculating sensitizing enhancement ratio (SER).The effect of DHA combined irradiation on the apoptosis of GLC-82 cell cycle distribution and apoptosis were measured by flow cytometry. The protein expression of p53, p21, Bcl-2, and Bax were detected by Western blot.

RESULTSDifferent concentrations DHA (4, 8, 16, 32, 64, and 128 μg/mL) had cytotoxicity on GLC-82 cells. The IC50 for 24, 48, and 72 h was 38.25,20.58, and 10.36 μg/mL, respectively, in obvious dose- and time-dependent manner. The growth inhibition rate was more significantly increased than that of the blank control group (P < 0.01, P<0.05). DHA had sensitization enhancement effect on GLC-82 cells, with SER of 1.4. DHA combined irradiation could obviously change the structure of GLC-82 cells cell cycle and induce apoptosis (with the apoptosis rate of 21.5%), which was significantly different from that of the blank control group (P < 0.05). Western blot showed the expression of p53 and p21 protein could be increased by DHA combined irradiation, and the expression of Bcl-2 protein down-regulated (P <0.01, P <0. 05).

CONCLUSIONSDHA had stronger cytotoxicity and radiosensitization on GLC-82 cells. Its mechanisms might lie in making the arrest of GLC-82 cells' growth at G0/G1 phase, decreasing the ratio of cells at S phase, restoring the function of p53, decreasing the expression of Bcl-2 protein, and inducing apoptosis in GLC-82 cells.

Apoptosis ; drug effects ; Artemisinins ; pharmacology ; Cell Cycle ; drug effects ; Cell Proliferation ; drug effects ; Down-Regulation ; drug effects ; Flow Cytometry ; Humans ; Lung Neoplasms ; metabolism ; Neoplasm Proteins ; metabolism ; Radiation-Sensitizing Agents ; pharmacology ; Tumor Cells, Cultured ; bcl-2-Associated X Protein ; metabolism