1.First Case of Mycobacterium longobardum Infection.
Sung Kuk HONG ; Ji Yeon SUNG ; Hyuk Jin LEE ; Myung Don OH ; Sung Sup PARK ; Eui Chong KIM
Annals of Laboratory Medicine 2013;33(5):356-359
Mycobacterium longobardum is a slow-growing, nontuberculous mycobacterium that was first characterized from the M. terrae complex in 2012. We report a case of M. longobardum induced chronic osteomyelitis. A 71-yr-old man presented with inflammation in the left elbow and he underwent a surgery under the suspicion of tuberculous osteomyelitis. The pathologic tissue culture grew M. longobardum which was identified by analysis of the 65-kDa heat shock protein and full-length 16S rRNA genes. The patient was cured with the medication of clarithromycin and ethambutol without further complications. To the best of our knowledge, this is the first report of a M. longobardum infection worldwide.
Aged
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Anti-Bacterial Agents/therapeutic use
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Bacterial Proteins/genetics
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Chaperonin 60/genetics
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Clarithromycin/therapeutic use
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Elbow/pathology
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Ethambutol/therapeutic use
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Humans
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Male
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Mycobacterium Infections, Nontuberculous/*microbiology
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Nontuberculous Mycobacteria/classification/genetics/*isolation & purification
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Osteomyelitis/diagnosis/drug therapy/*microbiology/pathology
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RNA, Ribosomal, 16S/genetics
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Treatment Outcome
2.Diosgenin alleviates NAFLD induced by a high-fat diet in rats via mTOR/SREBP-1c/HSP60/MCAD/SCAD signaling pathway.
Su-Wen CHEN ; Guo-Liang YIN ; Chao-Yuan SONG ; De-Cheng MENG ; Wen-Fei YU ; Xin ZHANG ; Ya-Nan FENG ; Peng-Peng LIANG ; Feng-Xia ZHANG
China Journal of Chinese Materia Medica 2023;48(19):5304-5314
This study aims to observe the effects of diosgenin on the expression of mammalian target of rapamycin(mTOR), sterol regulatory element-binding protein-1c(SREBP-1c), heat shock protein 60(HSP60), medium-chain acyl-CoA dehydrogenase(MCAD), and short-chain acyl-CoA dehydrogenase(SCAD) in the liver tissue of the rat model of non-alcoholic fatty liver disease(NAFLD) and explore the mechanism of diosgenin in alleviating NAFLD. Forty male SD rats were randomized into five groups: a control group, a model group, low-(150 mg·kg~(-1)·d~(-1)) and high-dose(300 mg·kg~(-1)·d~(-1)) diosgenin groups, and a simvastatin(4 mg·kg~(-1)·d~(-1)) group. The rats in the control group were fed with a normal diet, while those in the other four groups were fed with a high-fat diet. After feeding for 8 weeks, the body weight of rats in the high-fat diet groups increased significantly. After that, the rats were administrated with the corresponding dose of diosgenin or simvastatin by gavage every day for 8 weeks. The levels of triglyceride(TG), total cholesterol(TC), alanine transaminase(ALT), and aspartate transaminase(AST) in the serum were determined by the biochemical method. The levels of TG and TC in the liver were measured by the enzyme method. Oil-red O staining was employed to detect the lipid accumulation, and hematoxylin-eosin(HE) staining to detect the pathological changes in the liver tissue. The mRNA and protein levels of mTOR, SREBP-1c, HSP60, MCAD, and SCAD in the liver tissue of rats were determined by real-time fluorescence quantitative polymerase chain reaction(RT-qPCR) and Western blot, respectively. Compared with the control group, the model group showed increased body weight, food uptake, liver index, TG, TC, ALT, and AST levels in the serum, TG and TC levels in the liver, lipid deposition in the liver, obvious hepatic steatosis, up-regulated mRNA and protein expression levels of mTOR and SREBP-1c, and down-regulated mRNA and protein expression levels of HSP60, MCAD, and SCAD. Compared with the model group, the rats in each treatment group showed obviously decreased body weight, food uptake, liver index, TG, TC, ALT, and AST levels in the serum, TG and TC levels in the liver, lessened lipid deposition in the liver, ameliorated hepatic steatosis, down-regulated mRNA and protein le-vels of mTOR and SREBP-1c, and up-regulated mRNA and protein levels of HSP60, MCAD, and SCAD. The high-dose diosgenin outperformed the low-dose diosgenin and simvastatin. Diosgenin may prevent and treat NAFLD by inhibiting the expression of mTOR and SREBP-1c and promoting the expression of HSP60, MCAD, and SCAD to reduce lipid synthesis, improving mitochondrial function, and promoting fatty acid β oxidation in the liver.
Rats
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Male
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Animals
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Non-alcoholic Fatty Liver Disease/genetics*
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Sterol Regulatory Element Binding Protein 1/metabolism*
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Diet, High-Fat/adverse effects*
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Diosgenin/metabolism*
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Chaperonin 60/therapeutic use*
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Rats, Sprague-Dawley
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Liver
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Signal Transduction
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TOR Serine-Threonine Kinases/metabolism*
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Triglycerides
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RNA, Messenger/metabolism*
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Simvastatin/therapeutic use*
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Body Weight
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Lipid Metabolism
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Mammals/metabolism*