Objective:To investigate the influence of lumbar disc degeneration on the efficacy of lumbar fixed-point rotation manipulation in sitting position in treating lumbar intervertebral disc herniation (LIDH). Methods:We simulated lumbar fixed-point rotation manipulation of sitting position using three finite element models including a normal model, a mild degeneration model and a moderate degeneration model of L3-5, in which the herniated disc was assumed at the left rear of L4 disc and the rotation manipulation was carried out on the right side. The displacement and stress at the left rear of L4 disc of the three models were analyzed. Results:When lumbar fixed-point rotation manipulation in sitting position was carried out, a displacement and stress were generated at the left rear of L4 intervertebral disc of the three models directing forward. The displacement and stress in degeneration models were less than those in the normal model, and the smallest values were found in the moderate degeneration model. From normal model to mild and then to the moderate degeneration model, the displacement decreased by 36% and 59%, and the stress decreased by 22.3% and 45.2%, respectively. Conclusion:The lumbar disc degeneration affects adversely the effectiveness of lumbar fixed-point rotation manipulation in sitting position in the treatment of LIDH. The severer the lumbar degeneration, the greater the influence.

Objective To establish a human HepG2 cell growth model under the low oxygen environment induced by cobalt chloride in order to observe the impacts of human HepG2 cell proliferation,cellular cycles and apoptosis,namely cellular growth conditions,under the low oxygen environment induced by cobalt chloride with different concentrations and to study the HepG2 cell growth mechanism under the low oxygen environment induced by cobalt chloride.Methods The human HepG2 cells in the logarithmic phase were randomized grouping as control group and CoCl2 experimental group with different concentrations (50 μm/L,100 μm/L,150 μm/L and 200 μm/L).① HepG2 cell proliferation was tested by MTT assay to calculate cell's suppression rate and draw HepG2 cell growth inhibition curves.② The move ability of HepG2 cells was observed by scratch test.③ The cellular apoptosis and periodic changes were detected using the flow cytometer Annexin-V FITC/PI double-staining and PI single staining methods.④HepG2 cell's Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and Bcl-2 protein expression were detected by Western Blot.Results ① The test results obtained via MTT assay showed that CoCl2 suppressed the human HepG2 cell proliferation within a certain amount of time and concentration and presented a time-dose dependent relation.② Scratch damage trial suggested that the cobalt chloride suppressed the HepG2 cell migration and wound repair capacity and presented a concentration dependent relation.③ Flow cytometer' s test results revealed that the apoptosis rates (％) in control group and experimental group with different concentrations (50 μm/L,100 μm/L,150 μm/L and 200 μm/L) were 3.42,7.74,13.07,20.56,28.53 and 44.45 (P ＜0.05),respectively.The apoptosis rate of the experimental group was significantly increased compared with the control group,as well as showing a concentration dependency.The results of cellular cycles revealed that the cobalt chloride significantly suppressed the HepG2 cell's periodic changes along with increases of concentration,as well as blocked the cell cycle staying in phase G1,thereby suppressing cell proliferation.④Western Blot test:Compared with the control group,the Bcl-2 protein expression was significantly decreased in the experimental group after treatment of cobalt chloride with different concentrations.Conclusion Within a certain range,CoC12-indiuced low oxygen environment can suppress the human HepG2 cell proliferation and healing migration capacity,induce apoptosis and present a time-dose dependent relation.The mechanism is likely associated with decreases of Bcl-2 protein expression.

OBJECTIVETo explore the significance of multi-detector CT (MDCT) in differential diagnosis of papillary renal cell carcinoma and chromophobe renal cell carcinoma.

METHODSClinical data of forty-one cases of renal cancers confirmed pathologically were collected, including 21 cases of papillary renal cell carcinoma (PRCC) (14 type I, 7 type II) and 20 cases of chromophobe renal cell carcinoma (ChRCC). Their morphological and MDCT characteristics were retrospectively analyzed. Receiver operator characteristic curve (ROC) was used to analyze the value of MDCT in differential diagnosis of PRCC and ChRCC. Two senior radiologists analyzed the morphological and the dynamic enhancement characteristics of the images. The attenuation of the lesions and the adjacent renal parenchyma were measured. The morphological indexes were compared with chi-square test and the quantitative indexes were compared with independent sample T-test. Receiver operator characteristic curve (ROC) was used to analyze the sensitivity, specificity and accuracy of diagnosis of PRCC and ChRCC.

RESULTSAngioid enhancement and filled enhancement were more common in ChRCC than in PRCC, while delayed enhancement was more often seen in PRCC than in ChRCC. Calcification was more common in type I than type II PRCC. The enhancement value (ΔCT value) in corticomedullary phase was (29.08 ± 20.12) Hu for PRCC, significantly lower than the (48.29 ± 26.70) Hu for ChRCC (t = -2.611, P = 0.013). The ΔCT value of type I PRCC in corticomedullary phase was (26.36 ± 18.16) Hu, showing a significant difference from that of ChRCC (t = -2.666, P = 0.012). The lesion to kidney ratio (LKR) in corticomedullary phase was 0.44 ± 0.19 for PRCC and 0.58 ± 0.15 for ChRCC, with a significant difference between them (t = -2.587, P = 0.014). The LKR of type I PRCC in corticomedullary phase was 0.39 ± 0.15, showing a significant difference from that of ChRCC (t = -3.628, P = 0.001). The difference value (D-value) of the attenuation of lesion between corticomedullary and nephrographic phases was (-3.69 ± 8.90) Hu for PRCC and (8.39 ± 21.98) Hu for ChRCC, with a significant difference between them (t = -2.285, P = 0.031). The D-value of type I PRCC was (-4.55 ± 9.82) Hu, showing a significant difference from that of ChRCC (t = -2.323, P = 0.028). There was no significant difference between the ΔCT, LKR and D-value of the type II PRCC and ChRCC (P > 0.05 for all). The area under the curve (AUC) for ΔCT value, LKR value in corticomedullary phase, and D-value were 0.718, 0.751 and 0.668, respectively, and there were no significant differences among them (z values were 0.896, 0.683 and 0.559, respectively, and P values were 0.370, 0.495 and 0.576, respectively). Using 49.350 Hu as the cutoff value for ΔCT value in corticomedullary phase, resulted in a sensitivity, specificity and accuracy of 50.0%, 90.5% and 70.7%, respectively. Corresponding values were 65.0%, 81.0% and 73.2%, when using a cutoff value of 0.532 for LKR in corticomedullary phase, and were 60.0%, 76.2% and 68.3%, when using a D-value of 0.400 Hu.

CONCLUSIONSThe ΔCT value, LKR value in corticomedullary phase, and the D-value are all useful indexes for the differentiation of PRCC and ChRCC.

Area Under Curve ; Calcinosis ; Carcinoma, Renal Cell ; diagnosis ; Diagnosis, Differential ; Humans ; Kidney ; Kidney Neoplasms ; diagnosis ; ROC Curve ; Retrospective Studies ; Sensitivity and Specificity

This paper summarized Professor ZHANG Junping's clinical experience in treating coronary heart disease （CHD） combined with hypothyroidism. It is believed that yang deficiency was the root cause of CHD complicated with hypothyroidism， and also the key pathogenesis throughout its development. Accordingly， combined with the different focuses on the lesions in the blood， pulse， heart and spirit， Professor ZHANG took warming yang as the basic rule and summarized the four methods of warming yang for syndrome differentiation and treatment. When spleen-kidney yang deficiency， disturbance of qi transformation， dysfunction of blood transportation as the pathological basis of CHD combined with hypothyroidism， the self-prescribed Butian Formula （补天方） could be used for warming yang and benefiting the kidney， thereby regulating Qi and blood； when the cold and dampness blocked the blood vessels， and turbidity-toxin generated gradually， resulting in heart vessel obstruction， the self-prescribed Huazhuo Changmai Decoction （化浊畅脉汤） could be used to warm yang and dissolve the turbidity so that to unblock the heart vessels； when the structure and function of the heart fail， edema due to yang deficiency with pericardial fluid retention， the self-prescribed Yuxin Baomai Formula （育心保脉方） could be used to warm yang and excret water， and protect the heart； when yang deficiency led to emotional and mental stagnation， and the heart impairment aggravated emotional and mental disorders， which resulted in emotional and mental abnormalities， the self-prescribed Jieyu Anshen Decoction （解郁安神汤） could be used to relieve emotional and mental stagnation， and calm mind.

With the increasing incidence of diabetes mellitus in recent years， cardiomyopathy caused by diabetes mellitus has aroused wide concern and this disease is characterized by high insidiousness and high mortality. The early pathological changes of diabetic cardiomyopathy （DCM） are mitochondrial structural disorders and loss of myocardial metabolic flexibility. The turbulence of mitochondrial quality control （MQC） is a key mechanism leading to the accumulation of damaged mitochondria and loss of myocardial metabolic flexibility， which， together with elevated levels of oxidative stress and inflammation， trigger changes in myocardial structure and function. Qi deficiency and stagnation is caused by the loss of healthy Qi， and the dysfunction of Qi transformation results in the accumulation of pathogenic Qi， which further triggers injuries. According to the theory of traditional Chinese medicine （TCM）， DCM is rooted in Qi deficiency of the heart， spleen， and kidney. The dysfunction of Qi transformation leads to the generation and lingering of turbidity， stasis， and toxin in the nutrient-blood and vessels， ultimately damaging the heart. Therefore， Qi deficiency and stagnation is the basic pathologic mechanism of DCM. Mitochondria， similar to Qi in substance and function， are one of the microscopic manifestations of Qi. The role of MQC is consistent with the defense function of Qi. In the case of MQC turbulence， mitochondrial structure and function are impaired. As a result， Qi deficiency gradually emerges and triggers pathological changes， which make it difficult to remove the stagnant pathogenic factor and aggravates the MQC turbulence. Ultimately， DCM occurs. Targeting MQC to treat DCM has become the focus of current research， and TCM has the advantages of acting on multiple targets and pathways. According to the pathogenesis of Qi deficiency and stagnation in DCM and the modern medical understanding of MQC， the treatment should follow the principles of invigorating healthy Qi， tonifying deficiency， and regulating Qi movement. This paper aims to provide ideas for formulating prescriptions and clinical references for the TCM treatment of DCM by targeting MQC.