Aged ; Coal Mining ; Electrocardiography ; Heart Rate ; Humans ; Male ; Middle Aged ; Pneumoconiosis ; complications ; physiopathology ; Tachycardia ; etiology

OBJECTIVETo study clinical value of shear wave elastography (SWE) in the evaluation of neck-shoulder myofascial pain syndrome.

METHODSFrom December 2013 to July 2014,30 patients diagnosed as neck-shoulder myofascial pain syndrome were in the treatment group,including 17 males and 13 females, with an average age of (44 ± 3) years old. Thirty healthy people were in the control group, including 22 males and 8 females, with a mean age of (37 ± 5) years old. The patients in the treatment group were treated with manipulation, once every other day, total 7 times. The SWE was used to detect tension part of trapezius muscle of patients in the treatment group before and after treatment, as well as to detect muscle belly at the descending part of trapezius muscle in the control group. The tissue elasticity and Yang's modulus value were recorded and compared.

RESULTSThe tissue elasticity chart of patients in the treatment group before treatment was mainly greenish blue with the score of 3.70 ± 1.53, and the Yang's modulus was (43.4 ± 15.6) kPa. The tissue elasticity figure after treatment was mainly blue with the score of 2.40 ± 0.87, and the Yang's modulus was (29.0 ± 5.9) kPa. Whereas in the control group, the tissue elasticity figure was mainly blue with the score of 1.60 ± 0.72, and the Yang's modulus was (24.0 ± 7.6) kPa. These were statistical differences between the two groups (P = 0.000).

CONCLUSIONSWE can be used as an evaluation method of manipulation treatment for neck-shoulder myofascial pain syndrome, which is an objective and sensitive detection method.

Adult ; Elasticity Imaging Techniques ; methods ; Female ; Humans ; Male ; Middle Aged ; Musculoskeletal Manipulations ; Myofascial Pain Syndromes ; diagnosis ; therapy ; Neck ; Shoulder

Biomarkers, Tumor ; genetics ; Carcinoma, Hepatocellular ; genetics ; Cell Line ; Hepatocytes ; cytology ; Humans ; Liver Neoplasms ; genetics ; Transfection

Adolescent ; Adult ; Aged ; Aged, 80 and over ; Analgesics, Non-Narcotic ; adverse effects ; Anti-Bacterial Agents ; adverse effects ; Chemical and Drug Induced Liver Injury ; etiology ; Drugs, Chinese Herbal ; adverse effects ; Female ; Humans ; Male ; Middle Aged ; Retrospective Studies

Objective To observe the effect of Compoud Qingqin Liquids on renal function of rat model of uric acid nephropathy, and to discuss its protection of renal function. Methods The rat model was induced by gavaging adenine and feeding yeast. SD rats were randomly divided into control group, model group, positive group, and high-, medium-, low-dose groups of Chinese medicine. Blank control group and model group were daily gavaged with distilled water, positive control group was daily gavaged with allopurinol by 9.33 mg/kg, and high-, medium-, low-dose group of Chinese medicine was daily gavaged with Compound Qinggin Liguids by 3.77, 1.89, 0.09 g/(kg·d) respectively for 6 weeks. General condition of rats were observed, renal pathological changes were observed with light and electron microscope. Urine protein concentration, blood uric acid, blood urea nitrogen, creatinine and kidney weight index were respectively tested before and after treatment. Results There were no significant differences in eating, drinking and body weight between before and after modeling. Compoud Qingqin Liquids can obviously decrease the concentration of urine protein, blood uric acid, serum creatinine, blood urea nitrogen, and kidney weight index (P<0.05) of rats with uric acid nephropathy. Renal tubular epithelial cells atrophy and renal interstitial fibrosis of high-dose group of Chinese medicine were not evident. Conclusion Compoud Qingqin Liquids can protect the rats renal function against uric acid renal injury.

BACKGROUNDObstructive sleep apnea is a frequent medical condition consisting of repetitive sleep-related episodes of upper air ways obstruction and can lead to hypertension. Ang II type 1 receptor (AT1R) played important roles in hypertension since it binds with Ang II, controlling salt-water and blood pressure homeostasis. This study explores rat aorta AT1R expression during intermittent hypoxia (IH) and the signaling pathways involved.

METHODSA rat model and a cell model used a BioSpherix-OxyCycler A84 system and a ProOx C21 system respectively. The arterial blood pressure was recorded by a Nihon Kohden Polygraph System. Immunohistochemic was used to focus and analyze the expression of AT1R in rat aorta. Real-time PCR and Western blotting were used to explore the signaling pathways that participated in AT1R expression.

RESULTSIn this study, we found that chronic intermittent hypoxia (CIH) induced AT1R transcription which increased the blood pressure in rat aorta compared to normoxia and to sustained hypoxia. The AT1R protein expression in the aorta was similar to the real-time PCR results. We explored the signaling mechanisms involved in the AT1R induction in both rat aorta and the aortic endothelial cells by real-time PCR and Western blotting. Compared to normoxia, CIH increased ERK1 mRNA transcription but not ERK2 or p38MAPK in the aorta; whereas sustained hypoxia (SH) upregulated ERK2 but not ERK1 or p38MAPK mRNA. In cells, IH induced AT1R expression with ERK1/2 phosphorylation but reduced p38MAPKs phosphorylation, whereas SH induced only ERK1/2 phosphorylation. The ERK1/2 inhibitor PD98059 attenuated the IHinduced AT1R increase but the p38MAPK inhibitor SB203580 did not.

CONCLUSIONSOur results indicate that CIH induced the elevation of rat blood pressure and aorta AT1R expression. Moreover, AT1R expression in IH and sustained hypoxia might be regulated by different signal transduction pathways, highlighting a novel regulatory function through ERK1/2 signaling in IH.

Animals ; Aorta ; metabolism ; Blood Pressure ; physiology ; Hypoxia ; genetics ; physiopathology ; MAP Kinase Signaling System ; genetics ; physiology ; Male ; Rats ; Rats, Wistar ; Receptor, Angiotensin, Type 2 ; genetics ; metabolism

BACKGROUNDPosterior pedicle screw device is widely used in treatment of thoracolumbar burst fractures. As the clinical operation is not based upon quantitative data of adjustments, the results are not optimal. At present, no study has assessed the associations between the device adjustments and the restoration of stiffness. We investigated the biomechanical effects that adjustments of a pedicle screw device had on the burst fracture, and explored an optimal adjustment.

METHODSBurst fractures were produced at L1 vertebra in 24 fresh calf spines (T12-L3). The specimens were divided into four groups at random. Pedicle screw devices were attached to T13 and L2. Four device adjustments, consisting of distraction and extension, were applied. Adjustment 1 was pure 6° extension, adjustment 2 was pure 5 mm distraction, adjustment 3 was 6° extension followed by 5 mm distraction, and adjustment 4 was 5 mm distraction followed by 6° extension. The effect of each adjustment on the stiffness restoration, anatomical reduction, and neural decompression for the burst fractures was analyzed and evaluated.

RESULTSPure extension (Group 1) produced the closest segment height and the least restoration of the canal to the intact. Pure distraction (Group 2) restored stiffness most, but with only 60% stiffness of the intact value, and lost the segmental angle most to the intact. The combination of extension-distraction (Group 3 and Group 4) produced the maximum reduction of the anatomy and restoration of the canal in the burst fracture, and the least stiffness restoration. The sequence of extension and distraction did not affect stiffness restoration, anatomical reduction, and neural decompression.

CONCLUSIONSThe device adjustments affected stiffness restoration, anatomical reduction, and neural decompression. The combined extension-distraction adjustment may be the most suitable considering the anatomical reduction and neural decompression, but the stiffness decreased the most; it should be considered to reconstruct L1 vertebra.

Animals ; Biomechanical Phenomena ; Cattle ; Female ; Fracture Fixation, Internal ; instrumentation ; Lumbar Vertebrae ; injuries ; surgery ; Male ; Spinal Fractures ; physiopathology ; surgery ; Thoracic Vertebrae ; injuries ; surgery

OBJECTIVEThe mechanism by which M.tuberculosis persists and survives in host macrophage is not fully understood, however, the M. tuberculosis chromosome-encoded TA loci perform functions possibly of signaling to these processes. To explore the biological functions of M. tuberculosis chromosome-encoded TA loci, the Rv1494 and Rv1495 genes of M.tuberculosis H37Rv strain were cloned and expressed.

METHODSThe hypothetical proteins Rv1494 and Rv1495 were bioinformatically analyzed by means of Bioedit software, Dnaman software and Pfam database. The complete open-reading frame sequences of Rv1494 and Rv1495 genes were amplified by PCR using M.tuberculosis H37Rv genomic DNA as the template, and the PCR products were cloned into prokaryotic expression vector pET32a(+), respectively. After induction of expressions in E.coli host strain BL21 (DE3), the recombinant proteins were purified and detected by Western blotting.

RESULTSAccording to bioinformatic analysis, the hypothetical proteins of Rv1494 and Rv1495 genes shared some homologies with mazEF family, one of E. coli chromosomal TA loci (homology at 26% and 29.5%). Sequence analysis showed that the inserted target genes and its reading frames were completely correct. The recombinant plasmids were induced with IPTG to effectively express the fusion proteins with relative molecular mass coincident with prediction. The specific positive signals were identified from the immunoblots.

CONCLUSIONFor the first time, the Rv1494 and Rv1495 genes of M.tuberculosis H37Rv strain were cloned and its prokaryotic expression vectors were constructed successfully in this experiment, which may facilitate further functional study of this mazEF-like gene pair.

Bacterial Proteins ; genetics ; metabolism ; Blotting, Western ; Cloning, Molecular ; Electrophoresis, Polyacrylamide Gel ; Escherichia coli ; genetics ; Gene Expression Regulation, Bacterial ; Genes, Bacterial ; Genetic Vectors ; genetics ; Mycobacterium tuberculosis ; genetics ; metabolism ; Polymerase Chain Reaction ; Recombinant Fusion Proteins ; genetics ; metabolism

Endothelial dysfunction induced by intermittent hypoxia (IH) participates in obstructive sleep apnea syndrome (OSAS)-associated cardiovascular disorders. Myeloid differentiation primary response 88 (MyD88) and tumor necrosis factor receptor-associated factor 6 (TRAF6) regulate numerous downstream adaptors like mitogen-activated protein kinases (MAPKs) and the subsequent oxidative stress and inflammatory responses. This study aimed to characterize the role of MyD88/TRAF6 in IH-treated cell function and its associated signaling. Human umbilical vein endothelial cells (HUVECs) were randomly exposed to IH or normoxia for 0, 2, 4 and 6 h. Western blotting was used to detect the expression pattern of target gene proteins [angiotensin 1 receptor (AT1R), p-ERK1/2, p-p38MAPK, MyD88 and TRAF6], and the relationships among these target genes down-regulated by the corresponding inhibitors were studied. Finally, the influence of these target genes on proliferation of HUVECs was also assessed by EdU analysis. Protein levels of AT1R, TRAF6 and p-ERK1/2 were increased after IH exposure, with a slight rise in MyD88 and a dynamic change in p-p38MAPK. The down-regulation of TRAF6 by siRNA reduced ERK1/2 phosphorylation during IH without any effects on AT1R. Blockade of AT1R with valsartan decreased TRAF6 and p-ERK1/2 protein expression after IH exposure. ERK1/2 inhibition with PD98059 suppressed only AT1R expression. IH promoted HUVECs proliferation, which was significantly suppressed by the inhibition of TRAF6, AT1R and ERK1/2. The findings demonstrate that TRAF6 regulates the proliferation of HUVECs exposed to short-term IH by modulating cell signaling involving ERK1/2 downstream of AT1R. Targeting the AT1R-TRAF6-p-ERK1/2 signaling pathway might be helpful in restoring endothelial function.
Cell Hypoxia ; Cell Proliferation ; Cells, Cultured ; Gene Expression Regulation ; Human Umbilical Vein Endothelial Cells ; physiology ; Humans ; MAP Kinase Signaling System ; drug effects ; Phosphorylation ; Receptor, Angiotensin, Type 1 ; genetics ; metabolism ; TNF Receptor-Associated Factor 6 ; genetics ; metabolism ; Valsartan ; pharmacology