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Objective To identify a clinical isolate of Mycobacterium abscessus.Methods A pus sample was collected from a patient with suspected nontuberculous mycobacterial infection who visited the Affiliated Hospital of Weifang Medical University on December 18,2017,and was subjected to bacterial culture,Gram staining and acid-fast staining.Drug sensitivity test was conducted by the proportion method.The genome DNA of the strain was extracted and amplified by PCR with the universal primer of 16S rRNA.The PCR products were sequenced after collection and purification,and were compared with the known sequence of Mycobacterium abscessus in GenBank database.The isolate was identified by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS).Results The clinical isolate was identified as Mycobacterium abscessus both by MALDI-TOF MS and 16S rRNA gene sequencing.The drug sensitivity test showed that the strain was sensitive to amikacin,moxifloxacin,levofloxacin,but was resistant to streptomycin,isoniazid,rifampicin,ethambutol,ofloxacin,kanamycin,capreomycin,aminosalicylic acid,protionamide and rifabutin.The patient was diagnosed with subcutaneous soft tissue infection in the left knee joint.According to the results of drug sensitivity test,the patient was treated with amikacin and levofloxacin,and her condition was improved after treatment.Conclusion The 16S rRNA gene detection and MALDI-TOF MS both can be applied in the identification of Mycobacterium abscessus.
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BACKGROUND:Matrix metaloproteinases are now generaly considered to be able to degrade al extracelular matrices. Hypersecretion of matrix metaloproteinases or reduction in tissue inhibitors of matrix metaloproteinases leads to destruction of the dynamic balance of extracelular matrix. OBJECTIVE: To elucidate the role of matrix metaloproteinase-1 and tissue inhibitor of matrix metaloproteinase-1 in the pathogenesis and progression of intervertebral disc degeneration. METHODS:A total of 60 patients with intervertebral disc degeneration were included. Mild, moderate, and severe degeneration signals appeared on MRI imaging of the patients. Meanwhile, 20 patients with vertebral fracture, mainly cervical spine fracture, were selected as the control group. Venous blood samples were colected before the surgery; the intervertebral disc specimens were sequentialy colected. RESULTS AND CONCLUSION: Serum and tissue levels of matrix metaloproteinase-1 in patients with intervertebral disc degeneration were significantly increased compared with the control group (P 0.05). These results indicate that hypersecretion of matrix metaloproteinase-1 occurs in patients with intervertebral disc degeneration; however, the expression of tissue inhibitor of matrix metaloproteinase-1 is not correlated with intervertebral disc degeneration.
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OBJECTIVE:To systematically review the effect of organic cation transporter 2 [(OCT2)808G>T] gene polymor-phism on the metformin hydrochloride pharmacokinetics in vivo,and to provide evidence-based reference for clinical medication. METHODS:Retrieved from PubMed,EMBase,Foreign Medical Journey Service,CJFD,VIP database and Wanfang database,re-lated studies about the effect of (OCT2)808G>T gene polymorphism on the metformin hydrochloride pharmacokinetics in vivo were collected,and Meta-analysis was performed by using Rev Man 5.1 statistics software. RESULTS:A total of 5 retrospective studies were included,involving 172 patients. The result of gene type was type GT,type TT and type GG. Results of Meta-analysis showed,compared with type GT volunteers,type TT could prolong the half-time period of metformin hydrochloride;compared with type TT,type GG could increase the peak concentration. However,(OCT2)808G>T gene polymorphism had no effects on the renal clearance rate,creatinine clearance rate and area under the drug-time curve. CONCLUSIONS:(OCT2)808G>T gene poly-morphism has certain effect on the half-time period and peak concentration of metformin hydrochloride in vivo of health volunteer, and has no effect on the renal clearance rate,creatinine clearance rate and area under the drug-time curve. Due to the limit of re-search methodological quality,large-scale and high quality studies are required for further validation of the conclusions.
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Objective To study the changes of reactive astrocytosis after heat shock protein 70 (HSPT0) was blocked by anti-HSP70 antibody. Methods We established cell model of scratch inju-ries by in situ culture and prurification of rat astrocytcs. Anti-HSP70 antibody was added into the nutrient medium at once after injury for intervention (intervention group). Then, immunocytochemical staining of glial fibrillary acidic protein (GFAP) was done at different time points in control group and intervention group to observe astrocytosis and morphologic changes, mRNA expression of GFAP was observed by means of reverse transcriptase-polymerase chain reaction (RT-PCR). Results Compared with the con-trol group, average cell area, average dentritic length and number of dentrities of astrocytes were signifi-cantly reduced in the intervention group(P < 0.05 or P < 0.01), with down-regulated mRNA expression of GFAP (P < 0.05). Conclusion HSP70 plays a facilitative role in reactive astrocytosis after injury of astrocytes. Reactive astrocytosis can be controlled to some extent by blocking HSP70 with anti-HSP70 antibody.