Objective To investigate the correlation between serum osteocalcin and type 2 diabetes mellitus (T2DM) in elderly patients.Methods A total of 55 T2DM patients (diabetic group) and 50 non-diabetic subjects (control group) aged ≥60 years were enrolled in this study.The levels of fasting blood glucose (FBG),glycated hemoglobin (HbAlc),insulin resistance index (HOMA IR),osteocalcin (OC),body mass index (BMI) and bone mineral density (BMD) in groups were compared.The correlations between serum osteocalcin and the above indicators were analyzed.Results The levels of OC and BMD were higher in control group than in diabetic group [(11.2±3.2)μg/Lvs.(4.1±3.0)μg/L,(-1.3±0.3) vs.(-2.6±0.5),respectively,both P＜0.05].The levels of FBG,HbAlc,FINS,HOMA-IR were lower in control group than in diabetic group [(4.7±2.0) mmol/L vs.(9.4±2.1) mmol/L],[(4.8±1.5) ％ vs.(7.6±1.6)％,(7.4±3.2) U/L vs.(23.7±3.0) U/L,(1.5±0.7) vs.(9.9±1.2),respectively,all P＜0.05].Serum osteocalcin concentration was negatively correlated with the levels of FBG,HbAlc,FINS and HOMA-IR in elderly patients with T2DM (r=-0.739,-0.713,-0.613,-0.092,all P＜0.01).Conclusions Serum osteocalcin concentration is correlated with the levels of blood sugar and insulin resistance index in elderly patients with T2DM.A further study on the correlation between osteocalcin and T2DM may provide a new target for the treatment of type 2 diabetes mellitus.

Rheumatoid Arthritis (RA) is a chronic systemic autoimmune disease. Moxibustion treatment for RA has significant efficacy, with high security and without dependency. It can alleviate the symptoms and make the body gradually return to normal level of immunity at the same time. This article reviewed the study on mechanism of moxibustion for the treatment of RA in recent years from the aspects of innate immunity, humeral immunity, cellular immunity, cytokines and immune organs, discussed the existing problems in relevant study, and provided a basis for clinic and future research.

Objective To observe the effect of oxidized low-density lipoproteins (Ox-LDL),15-Deoxy-△ 12,14-prostaglandin J2 ( 15d-PGJ2 ),leukotrienes B4 ( LTB4 ) on mRNA expressions of peroxisome proliferator activated receptor γ2 ( PPARγ2 ),receptor activator of NF-κB ligand (RANKL),alkaline phosphatase ( ALP),and osteoprotegerin(OPG) in osteoblastic cells of rats; and to investigate the influence of these PPARγ2 endogenous ligands on bone metabolism.Methods Rat osteoblastic cells were cultured in vitro for 24 h in medium with different PPARγ2 endogenous ligands at various concentrations ( the final concentrations of Ox-LDL were 0,12.5,25,50μg/ml; the final concentrations of 15 d-PGJ2 were 0,10,20,30 μmol/L; the final concentrations of LTB4 were 0,0.1,1.0,10 μ mol/L).RT-PCR was performed to determine the mRNA expressions of PPARγ2,RANKL,ALP,and OPG in osteoblastic cells.Results RT-PCR analysis showed that Ox-LDL,15d-PGJ2,and LTB4 all down-regulated the mRNA expressions of RANKL,ALP,and OPG,while up-regulated the mRNA expressions of PPARγ2 in osteoblastic cells in a dose-dependent manner.Significant differences were found in interclass comparisons( P＜0.05 or P＜ 0.01 ).Conclusions These findings suggest that Ox-LDL,15d-PGJ2,and LTB4 suppress the expressions of osteogenic genes through activating the transcription activity of PPARγ2,and this may be a plausible mechanism of senile osteoporosis.

Objective To study the effects of Panax Notoginseng Saponins (PNS) on the damaged expression of ZO-1 of brain microvascular endothelial cells caused by Aβ42.MethodsBrain microvascular endothelial cells were divided into normal control group, model group, PNS low-, medium- and high concentration groups. They were incubated for 24h in 5% CO2 incubator at 37℃ . Then cell vitality was detected by MTT colorimetric method and ZO-1 protein expression was tested by Western blot.Results Stimulation of Aβ42 reduced the activity of microvascular endothelial cells (P<0.01) and suppressed the expression of ZO-1 protein (P<0.01). Compared with the model group, the activity of microvascular endothelial cells of PNS groups, especially the high and medium dose groups (P<0.05), and increased the ZO-1 protein expression. Conclusion PNS can partly recover the barrier function of blood brain barrier through inhibiting the decrease of the activity of microvascular endothelial cells caused by Aβ42.

Objective To investigate the changes and significances of peripheral blood CD34,KDR/CD34,CD133/CD34,and CD117/CD34 positive cell levels in patients with hemorrhagic stroke at the acute phase. Methods Thirty patients with acute hemorrhagic stroke admitted to the Department of Neurosurgery, Jiangsu Haimen People’s Hospital from September 2013 to April 2014 were enrolled retrospectively. At the same time,20 healthy subjects were selected as a control group. CD34 +,KDR+ /CD34 +,CD133 + /CD34 +, and CD117 + /CD34 +cell levels in peripheral blood were detected in patients with hemorrhagic stroke at day 1 to day 7 after cerebral hemorrhage and the day of physical examination of the control group using FACSCalibur flow cytometry. The data were obtained and analyzed using CELLQuest software. Results Peripheral blood CD34 + cells and KDR+ /CD34 +, CD133 + /CD34 +, CD117 + /CD34 + cells at day 1 to day 7 after ischemic stroke were all lower than control group (all P<0. 05). CD34 + and CD117 + /CD34 + cells decreased firstly at day 1 and 2, then increased gradually;KDR+ /CD34 + and CD133 + /CD34 + cells increased gradually at day 1 to day 5,they were all reached the peak at day 5,which were (14. 8±3. 5) í105 and (16. 7±3. 3) í105 respectively. Compared with that at day 1,CD34 + cells at day 5 and 6 were (27. 4 ±6. 3) í105 and (25. 4 ±5. 7) í105 respectively;KDR+ /CD34 + and CD133 + /CD34 + cells at day 4,5,and 6 were (10. 2±3. 1) í105,(14. 8±3. 5) í105,(12. 1±3. 4) í105 and (14. 3±3. 6) í105,(16. 7±3. 3) í105,and (13. 1±4. 0) í105,respectively;CD117 + /CD34 + cells at day 5 was (21. 3 ±4. 2) í105,which were all higher than the first day after cerebral hemorrhage (P<0.05). In the CD34 + cells,the proportion of KDR+ /CD34 + cells at day 1 to day 7 all decreased compared with the control group (all P<0. 05);the proportion of CD133 + /CD34 + cells at day 4 was (65±4)%,it was higher than the control group (P<0. 05);the proportion of KDR+ /CD34 + cells at day 5 was (55±6)% compared with day 1;the proportion of CD133 + /CD34 + at day 4 was (65 ±4)%;the proportions of CD117 + /CD34 + cells at day 4 and day 5 were (69 ±6)% and (72 ±6)% respectively,and they all increased (all P <0. 05). Conclusion Peripheral blood CD34 + cells and their cell subsets are change in patients with hemorrhagic stroke in acute phase. Speculating the different cell subsets may have different functions and potential. KDR+ /CD34 + and CD133 + /CD34 + may be the early sensitive indicators of acute hemorrhagic stroke,and CD117 + /CD34 + is largely mobilized in early stage.

Objective To study the effect of pioglitazone on the differentiation and function of rat osteoclast-like cells (OLC), and to probe the relationship between activated PPARγ2 and osteoclasts. Methods On day 1 of OLC formation from nonadherent bone marrow ceils (BMC) obtained from rats induced by M-CSF and receptor activator of NF-кB ligand (RANKL), 1, 5 and 10μmol/L pioglitazone hydrochloride was added. RT- PCR was performed to determine the mRNA expressions of PPARγ2 and receptor activator of NF-кB (RANK) on day 3, 5 and 7 during incubation, the number of tartrate-resistant acid phosphatase (TRAP)-positive cells,the number of bone resorption pits and the ratio of its area on dentin slice were counted, the activity of TRAP and the mean fluorescence intensity of integrin β3 (CD61) of OLC were also measured. Results (1) The effect on the differentiation of OLC: The addition of pioglitazone at the start of the culture period induced a dose-dependent decrease in TRAP-positive OLC and the activity of TRAP (P < 0.01 or P < 0.05) ; the mRNA expression of PPARγ2 was up-regulated by 5 and 10 μmol/L pioglitazone in the early stage of incubation and attenuated with thematuration of OLC on the contrary, however, the expression of RANK was down-regulated by 5 and 10 μmol/L piolitazone in every stage of incubation (P < 0.05 or P < 0.01), combined with decrease in TRAP-positive OLC from day 3 by 10 μmol/L pioglitazone. (2) The effect on the function of OLC: the number of bone resorption pits and the ratio of its area on dentin slice were decreased in groups of 5 and 10 μmol/L pioglitazone (P < 0.01 orP < 0.05), no obvious change was noted in the group with 1 μmol/L pioglitazone compared with the control group; the mean fluorescence intensity of CD61 were down-regulated in groups of 5 and 10 μmol/L pioglitazone (P < 0.05 or P <0.01). Conclusion Activation of PPARγ2 pathway by pioglitazone could partially inhibit differentiation and function of OLC derived from rat BMC.

Objective To explore the correlation between thyroid nodules and uric acid levels and to find their gender differences.Methods A total of 68 056 subjects in a regional medical physical examination center of Shanxi Province from January 2013 to June 2015 were enrolled in this study.All the participants′ general information and parameters were recorded.Thyroid nodules were detected by color Doppler ultrasonography.Results The total prevalence of thyroid nodule was 35.5%, 30.7% in males and 40.0% in females.The prevalence of single nodule was 50.1%, and multiple 49.9%.Compared with no nodule group, thyroid nodule group tended to be older, with higher BMI, and with a worse metabolic status(all P<0.01).The uric acid levels were lower[(352.37±78.14 vs 357.70±77.51) μmol/L, P<0.01] in thyroid nodule group in male and higher[(260.22±61.91 vs 253.91±59.18) μmol/L, P<0.01] in female.Conclusion Thyroid nodules may be associated with metabolism and inflammation.In males, hyperuricemia group had lower, while in females, hyperuricemia ones were with a higher prevalence of thyroid nodules.

Objective To explore the changes of hepatic and pancreatic fat content in patients with type 2 diabetes mellitus(T2DM)using quantitative MRI,and to discuss the relationship with pancreatic β-cell function and bone mineral density(BMD).Methods A total of 118 patients with T2DM(T2DM group)were selected as the research subjects.At the same time,100 healthy control(HC)(HC group)who received physical examination were selected.All patients were examined with MRI.Hepatic fat fraction(HFF)and pancreatic fat fraction(PFF)were detected using the iterative decomposition of water and fat with echo asymmetry and least square estimation quantitation(IDEAL-1Q)technology.The homeostasis model assessment of β-cell function(HOMA-β)and homeostasis model assessment of insulin resistance(HOMA-IR)were performed.BMD of L2-L4,femoral neck and total hip were measured by dual-energy X-ray absorptiometry.The correlations among HFF,PFF and HOMA-β,HOMA-IR and BMD of L2-L4,femoral neck and total hip were analyzed by Pearson method.Results HFF and PFF in the T2DM group[(14.12±2.19)％and(8.23±1.60)％]were higher than those in the HC group[(5.30±0.83)％and(4.36±0.85)％],with statistically significant differences(P＜0.05).HOMA-βand BMD of L2-L4,femoral neck and total hip in the T2DM group[14.50±3.63,(0.92±0.13)mg/cm3,(0.77±0.10)mg/cm3 and(0.83±0.12)mg/cm3]were lower than those in the HC group[25.22±5.43,(1.05±0.23)mg/cm3,(0.85±0.18)mg/cm3 and(0.91±0.20)mg/cm3].HOMA-IR in the T2DM group(3.56±1.22)was higher than that in the HC group(1.90±0.45).The differences were statistically significant(P＜0.05).Pearson correlation analysis found that HFF and PFF were negatively correlated with HOMA-β and BMD of L2-L4,femoral neck and total hip,and were positively correlated with HOMA-IR(P＜0.05).Conclusion MRI can be used to quantitatively evaluate hepatic and pancreatic fat content in patients with T2DM.In addition,hepatic and pancreatic fat content are closely related to pancreatic HOMA-β,HOMA-IR and BMD.

The RANKL/RANK/OPG signaling pathway is essential for balancing bone resorption and bone formation. Research shows this signaling pathway exists in various tissues, including liver, muscle, adipose tissue, pancreas, and other tissues that might influence glucose metabolism. Blocking the pathway could protect islet β cell function. Furthermore, RANKL also improves insulin resistance by inducing beige adipocytes differentiation and increasing energy expenditure. Currently, the role of RANKL in glucose metabolism remains controversial. This article reviews current research and discusses the potential use of RANKL inhibitors for treating diabetes with osteoporosis.

OBJECTIVETo study pathological and therapeutical problems concerning myocardial cell mitochondria changes during myocardial cell hypertrophy by culturing rat primary myocardial cells.

METHODPrimary myocardial cells were seperated and cultured together with angiotensin II (Ang II) for 72 or 96 hours. The total protein content with the BCA method and the photography and measurement of cell diameter with inverted microscope reflected myocardial cell proliferation. The mitochondrial membrane potential (Delta Psi m) with fluorescence microscope, the mitochondrial single amine oxidase (MAO) activity with spectrophotometer, the mitochondrial cytochrome oxidase (COX) activity and the injury percentage of mitochondrial outer membrane with microplate reader and the contents of ATP, ADP, AMP with high performance liquid chromatography reflected the injury and energy metabolism of myocardial cell mitochondrial structure and function when being cultured together with Ang II. On that basis, cells were treated with Astragali Radix injection and valsartan for observing pharmacological effects on mitochondrial structure and function in restructured myocardial cells.

RESULTIn 72 h and 96 h, compare with the control group, the model group showed significantly increased total protein content and enlarged myocardial cell diameter. During the course of proliferation, the myocardial cell MAO activity and the injury percentage of mitochondrial outer membrane were significantly increased, with significant decrease in mitochondrial COX activity, mitochondrial Delta Psi m and the content of ATP, ADP and rise in the content of AMP. Astragali Radix injection and valsartan reduced myocardial cell total protein content and cell diameter caused by Ang II, decreased myocardial cell MAO activity, significantly increased mitochondrial COX activity and the content of ATP and ADP, and decreased the content of AMP.

CONCLUSIONDuring the process of myocardial hypertrophy, the injury of mitochondrial structure and function and the changes in myocardial cell energy metabolism injury occurred after the injury of mitochondria. Astragali Radix injection and valsartan can reverse myocardial cell mitochondrial structure and function during myocardial cell hypertrophy caused by Ang II. Reversion of myocardial cell hypertrophy and restructuring of myocardial cells helps improve energy metabolism of the myocardial cells.

Animals ; Astragalus Plant ; chemistry ; Cells, Cultured ; Drugs, Chinese Herbal ; administration & dosage ; therapeutic use ; Female ; Hypertrophy ; drug therapy ; Injections ; Male ; Membrane Potential, Mitochondrial ; drug effects ; Mitochondria, Heart ; drug effects ; Myocytes, Cardiac ; drug effects ; pathology ; Rats ; Rats, Sprague-Dawley