[Prevalence and treatment of anemia in chronic kidney disease patients based on regional medical big data].

Objective: To assess the prevalence, risk factors and treatment of anemia in patients with chronic kidney disease (CKD). Methods: A descriptive method was used to analyze the prevalence and treatment of anemia in CKD patients based on regional health data in Yinzhou District of Ningbo during 2012-2018. The multivariate logistic regression analysis was used to identify independent influence factors of anemia in the CKD patients. Results: In 52 619 CKD patients, 15 639 suffered from by anemia (29.72%), in whom 5 461 were men (26.41%) and 10 178 were women (31.87%), and anemia prevalence was higher in women than in men, the difference was significant (P<0.001). The prevalence of anemia increased with stage of CKD (24.77% in stage 1 vs. 69.42% in stage 5, trend χ2 test P<0.001). Multivariate logistic regression analysis revealed that being women (aOR=1.57, 95%CI: 1.50-1.63), CKD stage (stage 2: aOR=1.10, 95%CI: 1.04-1.16;stage 3: aOR=2.28,95%CI: 2.12-2.44;stage 4: aOR=4.49,95%CI :3.79-5.32;stage 5: aOR=6.31,95%CI: 4.74-8.39), age (18-30 years old: aOR=2.40,95%CI: 2.24-2.57, 61-75 years old: aOR=1.35,95%CI:1.28-1.42, ≥76 years old: aOR=2.37,95%CI:2.20-2.55), BMI (<18.5 kg/m2:aOR=1.29,95%CI: 1.18-1.41;23.0-24.9 kg/m2:aOR=0.79,95%CI: 0.75-0.83;≥25.0 kg/m2:aOR=0.70,95%CI: 0.66-0.74), abdominal obesity (aOR=0.91, 95%CI: 0.86-0.96), chronic obstructive pulmonary disease (aOR=1.15, 95%CI: 1.09-1.22), cancer (aOR=3.03, 95%CI: 2.84-3.23), heart failure (aOR=1.44, 95%CI: 1.35-1.54) and myocardial infarction (aOR=1.54, 95%CI:1.16-2.04) were independent risk factors of anemia in CKD patients. Among stage 3-5 CKD patients with anemia, 12.03% received iron therapy, and 4.78% received treatment with erythropoiesis-stimulating agent (ESA) within 12 months after anemia was diagnosed. Conclusions: The prevalence of anemia in CKD patients was high in Yinzhou. However, the treatment rate of iron therapy and ESA were low. More attention should be paid to the anemia management and treatment in CKD patients.

Human umbilical cord mesenchymal stem cell-derived exosomes carrying hsa-miRNA-128-3p suppress pancreatic ductal cell carcinoma by inhibiting Galectin-3.

BACKGROUND: Pancreatic ductal adenocarcinoma (PDAC) is one of the most fatal malignant tumors of the digestive system. Many patients are diagnosed at an advanced stage and lose eligibility for surgery. Moreover, there are few effective methods for treating pancreatic ductal cell carcinoma. Increasing attention has been given to microRNAs (miRNAs) and their regulatory roles in tumor progression. In this study, we investigated the effects of exosomes extracted from human umbilical cord mesenchymal stem cells (HUCMSCs) carrying hsa-miRNA-128-3p on pancreatic cancer cells. METHODS: Based on existing experimental and database information, we selected Galectin-3, which is associated with pancreatic cancer, and the corresponding upstream hsa-miRNA-128-3p. We extracted HUCMSCs from a fresh umbilical cord, hsa-miRNA-128-3p was transfected into HUCMSCs, and exosomes containing hsa-miRNA-128-3p were extracted and collected. The effect of exosomes rich in hsa-miRNA-128-3p on pancreatic cancer cells was analyzed. RESULTS: The expression of Galectin-3 in normal pancreatic duct epithelial cells was significantly lower than that in PDAC cell lines. We successfully extracted HUCMSCs from the umbilical cord and transfected hsa-miRNA-128-3p into HUCMSCs. Then we demonstrated that HUCMSC-derived exosomes with hsa-miRNA-128-3p could suppress the proliferation, invasion, and migration of PANC-1 cells in vitro by targeting Galectin-3. CONCLUSION: Hsa-miRNA-128-3p could be considered as a potential therapy for pancreatic cancer. We provided a new idea for targeted therapy of PDAC.

Adaptive synapse-based neuron model with heterogeneous multistability and riddled basins.

Biological neurons can exhibit complex coexisting multiple firing patterns dependent on initial conditions. To this end, this paper presents a novel adaptive synapse-based neuron (ASN) model with sine activation function. The ASN model has time-varying equilibria with the variation of externally applied current and its equilibrium stability involves transitions between stable and unstable points through fold and Hopf bifurcations, resulting in complex distributions of attractive regions with heterogeneous multi-stability. Globally coexisting heterogeneous behaviors are studied by bifurcation diagram, phase portrait, dynamical distribution, and basin of attraction. The results show that the number of coexisting heterogeneous attractors can be up to 12, but for a simple neuron model, such a large number of coexisting heterogeneous attractors has not been reported in the relevant literature. Most interestingly, the ASN model also has riddled-like complex basins of attraction and four illustrative examples are depicted by the phase portraits with small changes of the initial conditions. Besides, the ASN model is implemented using a simple microcontroller platform, and various heterogeneous coexisting attractors are acquired experimentally to validate the numerical results.

[Correlation of serum ADAMTS13 and TSP1 levels with myocardial injury and prognosis in patients with acute coronary syndrome].

OBJECTIVE: To investigate serum levels of von Willebrand factor lytic protease (ADAMTS13) and thrombospondin-1 (TSP1) in patients with different types of acute coronary syndrome (ACS) and their correlation with the patients' clinical prognosis. OBJECTIVE: According to their disease history, results of angiography and clinical biochemical tests, a total of 405 patients undergoing coronary angiography, were divided into unstable angina (UAP) group (n=215), acute myocardial infarction (AMI) group (n=96), and angiographically normal group (n=94). Serum ADAMTS13 and TSP1 levels were detected in all the patients, who were followed up for 15 months to evaluate the occurrence of long-term major cardiac adverse events (MACE). OBJECTIVE: Serum ADAMTS13 level was significantly lower and TSP1 level was significantly higher in AMI group and UAP group than in the normal group (P < 0.001). Serum ADAMTS13 and TSP1 levels were negative correlated in ACS patients (R=-0.577, P < 0.001). The patients experiencing MACE had significantly different serum TSP1 level from those without MACE (P < 0.05). Cox proportion regression model analysis showed that TSP1 was a risk factor affecting the occurrence of MACE in ACS patients; Kaplan-Meier survival analysis showed that the patients with high levels of TSP1 had a higher incidence of longterm MACE than those with low TSP1 levels. OBJECTIVE: A lowered serum ADAMTS13 level and an elevated TSP1 level can support the diagnosis of ACS. An elevated TSP1 level may serve as an indicator for predicting the risk of MACE in patients with ACS.

[Xinfeng capsule inhibits immune inflammation in osteoarthritis by inhibiting the miR- 23a-3p/PETN/PI3K/AKT/mTOR pathway].

OBJECTIVE: To observe the inhibitory effect of Xinfeng capsule (XFC) on immune inflammatory response in the coculture system of chondrocytes and CD4+ T cells from patients with osteoarthritis (OA). OBJECTIVE: Thirty OA patients and 30 healthy subjects were examined for the expression of miR-23a-3p/PTEN/PI3K/AKT/mTOR. The changes in the miR-23a-3p/ PTEN/PI3K/AKT/mTOR pathway and the clinical indicators of the OA patients after XFC treatment were observed. OA-CD4+ T cells and OA-Chondrocytes cells were cultured in Transwel chambers, and the expressions of miR-23a-3p, PTEN, PI3K, AKT and mTOR mRNA were detected by RT-PCR; the levels of IL-1ß, IL-6, IL-10 and TNF-α were detected by ELISA. The protein expressions of PTEN, PI3K, AKT, p-AKT, mTOR and p-mTOR were detected by Western blotting. OBJECTIVE: Compared with healthy individuals, OA patients showed significantly increased expressions of miR-23a-3p, PTEN, PI3K, AKT, IL-1ß, IL-6 and TNF-α and lowered expressions of PTEN and IL-10 (P < 0.01). Positive correlations were found between miR-23a-3p and IL-6 and between PI3K and IL-10; mTOR was positively correlated with IL-6, IL-10, complement C3 and C4 (P < 0.01 or 0.05). Intervention with XFC obviously down-regulated the expressions of IL-1ß, IL-6, and TNF-α and up-regulated the expression of IL-10 (P < 0.01). In the cell co-culture systems, the expressions of miR-23a-3p, PI3K, Akt, mTOR, IL-1ß, IL-6 and TNF-α were up-regulated while the expressions of PTEN and IL-10 were down-regulated in the model group (P < 0.01). Overexpression of miR-23a-3p significantly up-regulated the expressions of IL-1ß, IL-6, TNF-α, miR-23a-3p, PI3K, AKT and mTOR and lowered the expressions of PTEN and IL-10 (P < 0.01 or 0.05). The expressions of IL-1ß, IL-6, TNF-α, miR-23a-3p, PI3K, AKT and mTOR were down-regulated and the expressions of IL-10 and PTEN were up-regulated in XFC-treated cells (P < 0.01 or 0.05). OBJECTIVE: XFC can reduce the inflammatory response in patients with OA by down-regulating the expression of miR-23a-3p, inhibiting the activation of the PTEN/PI3K/AKT/ mTOR pathway, and regulating the expression of IL-1ß, IL-6, IL-10 and TNF-α.

Initial-switched boosting bifurcations in 2D hyperchaotic map.

Recently, the coexistence of initial-boosting attractors in continuous-time systems has been attracting more attention. How do you implement the coexistence of initial-boosting attractors in a discrete-time map? To address this issue, this paper proposes a novel two-dimensional (2D) hyperchaotic map with a simple algebraic structure. The 2D hyperchaotic map has two special cases of line and no fixed points. The parameter-dependent and initial-boosting bifurcations for these two cases of line and no fixed points are investigated by employing several numerical methods. The simulated results indicate that complex dynamical behaviors including hyperchaos, chaos, and period are closely related to the control parameter and initial conditions. Particularly, the boosting bifurcations of the 2D hyperchaotic map are switched by one of its initial conditions. The distinct property allows the dynamic amplitudes of hyperchaotic/chaotic sequences to be controlled by switching the initial condition, which is especially suitable for chaos-based engineering applications. Besides, a microcontroller-based hardware platform is developed to confirm the generation of initial-switched boosting hyperchaos/chaos.

[Red blood cell lifespan detected by endogenous carbon monoxide breath test in patients with polycythemia vera].

Objective: To detect the red blood cell lifespan in patients with polycythemia vera (PV), and explore the influencing factors. Methods: From February 2017 to December 2018, 27 patients with PV at Blood Diseases Hospital, Chinese Academy of Medical Science and 18 normal controls were recruited. Red blood cell lifespan was detected by endogenous carbon monoxide (CO) breath test. The related factors were analyzed. Results: The average red blood cell lifespan of 27 PV patients was 80 (range, 35-120) days (d), which was significantly shorter than that of the normal controls [110.5(69-166) d, P<0.05], namely 35.3 d shorter. The red blood cell lifespan of ten newly diagnosed patients and 17 patients who were treated with hydroxyurea and/or interferon were 98 (35-117) d and 69 (45-120) d, respectively, which were both shorter than that of the normal control (P=0.010, 0.000). Correlation analysis showed that red blood cell lifespan of patients with newly diagnosed PV was associated with JAK2 mutation allele burden (r=0.900, P=0.037), peripheral blood lymphocyte count (r=-0.742, P=0.014) and the level of serum vitamin B(12) (r=-0.821, P=0.023). Conclusion: The lifespan of red blood cells in patients with PV is about one-third shorter than normal, and is related to JAK2 mutation allele burden, absolute lymphocyte count, and serum vitamin B(12) level.

Long noncoding RNA TPTE2P1 promotes the migration and invasion of hepatocellular carcinoma.

OBJECTIVE: Hepatocellular carcinoma (HCC) is a common malignant tumor that poses a serious threat to human health and life. Metastasis is one of the reasons for high rate of relapse. Due to the lack of effective treatment, the prognosis of HCC patients is far from satisfactory. The aim of this study was to investigate the role of long non-coding RNA (lncRNA)-TPTE2P1 in HCC development. Moreover, we aimed to search for new biomarkers which could predict the metastasis and provide novel therapeutic strategies for HCC. PATIENTS AND METHODS: Quantitative real-time polymerase chain reaction (qRT-PCR) was used to evaluate the expression level of lncRNA-TPTE2P1 in both HCC tissues and cell lines. Wound-healing assay and transwell assay were applied to determine the ability of cell migration. Meanwhile, transwell matrigel assay was applied to detect the invasion of HCC cells. The protein expressions of E-cadherin, Vimentin and N-cadherin in chosen cell lines were detected by Western blotting. RESULTS: Results found that lncRNA-TPTE2P1 was overexpressed in both HCC tissues and cell lines. Further analysis revealed that overexpression of lncRNA-TPTE2P1 was correlated with tumor size, distant metastasis, differentiation degree, as well as tumor node metastasis (TNM) stage of HCC patients. Subsequent wound-healing assay, transwell assay and Matrigel assay confirmed that down-regulated lncRNA-TPTE2P1 could significantly suppress the invasion and migration of cells. However, up-regulation of lncRNA-TPTE2P1 showed the opposite results. Moreover, lowly expressed lncRNA-TPTE2P1 significantly decreased the protein levels of E-cadherin, Vimentin and N-cadherin. These results indicated that lncRNA-TPTE2P1 might stimulate the migration and invasion of HCC cells by promoting epithelial-mesenchymal transition (EMT). CONCLUSIONS: In summary, our results suggested that lncRNA-TPTE2P1 functioned as an oncogene in HCC. Meanwhile, lncRNA-TPTE2P1 stimulated HCC cell migration and invasion by promoting EMT. LncRNA-TPTE2P1 might play a vital role in the development and progression of HCC. Our findings demonstrated that lncRNA-TPTE2P1 could serve as an early biomarker of metastasis and therapeutic target for HCC.

[Clinical effects of simple hallux valgus surgery for transfer metatarsalgia].

Objective: To analyze the clinical effects of simple hallux valgus surgery for transfer metatarsalgia. Methods: From September 2011 to November, a total of 21 patients(30 feets)with transfer metatarsalgia of hallux valgus and underwent the simple hallux valgus surgery without lateral metatarsal shortening osteotomy In Department of Orthopedics, Beijing Tongren Hospital, Capital Medical University, were enrolled in the study.The hallux valgus angle (HVA), intermetatarsal angle (IMA) , AOFAS scale and analogue score (VAS) were measured pre-operation and a half year, one year, two years after operation.The data were measured repeatedly and analyzed with analysis of variance. Results: The mean preoperative HVA changed [(39.6±9.7), (14.2±7.9), (14.8±7.9), (13.2±6.5)°] at 6 months, 1 year and 2 years follow-up; the mean IMA decreased [(13.8±4.0), (4.5±4.3), (5.8±3.9), (5.4±4.9)°] at 6 months, 1 year and 2 years follow-up(all P<0.001).63.5% of metatarsalgia cases improved, and 73.1% of painful callosities disappeared postoperatively.All the patients do not require further surgeries. The mean AOFAS for hallux , AOFAS for lesser toes and VAS were improved from 58.96 to 95.42, from 84.38 to 92.04 and from 7.5 to 1.3, respectively. All the results are statistically significant(P<0.001). Conclusion: These results suggest that a simple osteotomy of the first metatarsal provides excellent outcomes with a low rate of complications when compared with the combining lateral metatarsal shortening osteotomy.

miR-508-5p acts as an anti-oncogene by targeting MESDC1 in hepatocellular carcinoma.

Hepatocellular carcinoma (HCC) is the third leading cause of cancer associated mortality. Accumulating evidence has shown that microRNAs (miRNAs) act as critical factors for tumor recurrence and metastasis. MiR-508-5p has been reported as a down-regulated miRNA in the primary gastric cancer tissues. However, the role of miR-508-5p on HCC has not been well elucidated. In this study, we observed that miR-508-5p was downregulated in HCC tissues when compared to the non-tumorous tissues. We then demonstrated that overexpression of miR-508-5p attenuated HepG2 cells proliferation and invasion and induced cell apoptosis in vitro. Furthermore, our further investigations revealed that mesoderm development candidate 1 (MESDC1) is a potential target of miR-508-5p, as well as miR-508-5p overexpression downregulated MESDC1 expression. Overexpression of MESDC1 promoted HepG2 cells migration, invasion and proliferation in vitro. In addition, miR-508-5p markedly suppressed the tumor growth in xenograft model, while MESDC1 promoted the tumor growth in xenograft model. This study provides new insight into molecular mechanisms that miR-508-5p acts as a tumor suppressor by targeting MESDC1 in HCC progression.

Dietary luteolin activates browning and thermogenesis in mice through an AMPK/PGC1α pathway-mediated mechanism.

BACKGROUND: Two brown-like adipocytes, including classical brown adipocytes from brown adipose tissues and beige cells from white adipose tissues, regulate thermogenesis. The developmental and functional induction of brown-like cells provides a defense against obesity and associated metabolic diseases. Our previous study suggests dietary luteolin can improve diet-induced obesity and insulin resistance in mice. Here we further elucidated the action of the natural flavonoid on energy expenditure and adaptive thermogenesis. METHODS: Five-week-old male C57BL/6 mice were fed low-fat diet (LFD), high-fat diet (HFD) and HFD supplemented with 0.01% luteolin. After 12 weeks, their energy expenditure were detected using a combined indirect calorimetry system. Moreover, thermogenic program and associated molecular regulators were assessed in adipose tissues. In another independent study, even-aged mice were fed LFD and luteolin-containing LFD for 12 weeks, and their energy expenditure and thermogenic program were also investigated. Finally, differentiated primary brown and subcutaneous adipocytes were used to identify the critical participation of AMPK/PGC1α signaling in luteolin-regulated browning and thermogenesis. RESULTS: In mice fed either HFD or LFD, dietary luteolin supplement increased oxygen consumption, carbon dioxide production and respiratory exchange ratio. The enhancement in energy expenditure was accompanied by the upregulation of thermogenic genes in brown and subcutaneous adipose tissues. Meanwhile, several important AMPK/PGC1α signaling molecules were activated by dietary luteolin in the tissues. Further, luteolin treatment directly elevated thermogenic gene expressions and activated AMPK/PGC1α signaling in differentiated primary brown and subcutaneous adipocytes, whereas AMPK inhibitor Compound C reversed the efficiencies. CONCLUSIONS: Dietary luteolin activated browning and thermogenesis through an AMPK/PGC1α pathway-mediated mechanism.

Osteítis condensante ilíaca como causa de lumbalgia crónica / Condensing iliac osteitis as a cause of chronic low back pain

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Multistability in Chua's circuit with two stable node-foci.

Only using one-stage op-amp based negative impedance converter realization, a simplified Chua's diode with positive outer segment slope is introduced, based on which an improved Chua's circuit realization with more simpler circuit structure is designed. The improved Chua's circuit has identical mathematical model but completely different nonlinearity to the classical Chua's circuit, from which multiple attractors including coexisting point attractors, limit cycle, double-scroll chaotic attractor, or coexisting chaotic spiral attractors are numerically simulated and experimentally captured. Furthermore, with dimensionless Chua's equations, the dynamical properties of the Chua's system are studied including equilibrium and stability, phase portrait, bifurcation diagram, Lyapunov exponent spectrum, and attraction basin. The results indicate that the system has two symmetric stable nonzero node-foci in global adjusting parameter regions and exhibits the unusual and striking dynamical behavior of multiple attractors with multistability.

Long-range magnetic coupling across a polar insulating layer.

Magnetic interactions in solids are normally mediated by short-range exchange or weak dipole fields. Here we report a magnetic interaction that can propagate over long distances (∼10 nm) across a polar insulating oxide spacer. Evidence includes oscillations of magnetization, coercivity and field-cooled loop shift with the thickness of LaAlO3 in La0.67Sr0.33MnO3/LaAlO3/SrTiO3 heterostructures. Similar modifications of the hysteresis loop appear when two coupled films of La0.67Sr0.33MnO3 are separated by LaAlO3, or another polar insulator, but they are absent when the oxide spacer layer is nonpolar. The loop shift is attributed to strong spin-orbit coupling and Dzyaloshinskii-Moriya interaction at the interfaces. There is evidence from inelastic light scattering that the polar spacer mediates long-range transmission of orbital magnetization. This coupling mechanism is expected to apply for any conducting ferromagnetic oxide with mixed valence; in view of electron hopping frequency involved, it raises the prospect of terahertz tunability of magnetic coupling.

Epidemiology and characteristics of the dengue outbreak in Guangdong, Southern China, in 2014.

Dengue is a rapidly spreading mosquito-borne disease caused by the dengue virus (DENV) and has emerged as a severe public health problem around the world. Guangdong, one of the southern Chinese provinces, experienced a serious outbreak of dengue in 2014, which was believed to be the worst dengue epidemic in China over the last 20 years. To better understand the epidemic, we collected the epidemiological data of the outbreak and analyzed 14,594 clinically suspected dengue patients from 25 hospitals in Guangdong. Dengue cases were then laboratory-confirmed by the detection of DENV non-structural protein 1 (NS1) antigen and/or DENV RNA. Afterwards, clinical manifestations of dengue patients were analyzed and 93 laboratory-positive serum specimens were chosen for the DENV serotyping and molecular analysis. Our data showed that the 2014 dengue outbreak in Guangdong had spread to 20 cities and more than 45 thousand people suffered from dengue fever. Of 14,594 participants, 11,387 were definitively diagnosed. Most manifested with a typical non-severe clinical course, and 1.96 % developed to severe dengue. The strains isolated successfully from the serum samples were identified as DENV-1. Genetic analyses revealed that the strains were classified into genotypes I and V of DENV-1, and the dengue epidemic of Guangdong in 2014 was caused by indigenous cases and imported cases from the neighboring Southeast Asian countries of Malaysia and Singapore. Overall, our study is informative and significant to the 2014 dengue outbreak in Guangdong and will provide crucial implications for dengue prevention and control in China and elsewhere.

Newly identified gene muscle segment homeobox C may play a role in intermuscular bone development of Hemibarbus labeo.

Intermuscular bones, ossified from tendons within the myosepta, occur only in teleost fish. Current understanding of the homology and origins of intermuscular bones in fishes is based mainly on morphological data. To date, there is no published data regarding molecular mechanisms of intermuscular bone formation. In this study, we cloned the gene muscle segment homeobox C (MsxC). MsxC potentially plays a role in intermuscular bone development of Hemibarbus labeo, an important species of cyprinid fish in the Chinese aquaculture industry. Sequence analysis of MsxC revealed motifs characteristic of the homeobox domain family. Whole-mount in situ hybridization showed that MsxC was primarily expressed in the myosepta and brain. MsxC was expressed in the myosepta from 26 to 41 days after hatching (DAH); this coincided with the onset of intermuscular bone ossification, which occurred between 35 and 62 DAH. Evidence for localization of MsxC expression by in situ hybridization correlated with its detection by quantitative real-time PCR. In vertebrates, MsxC plays a role in the regulation of mesenchymal cell differentiation during bone formation. We therefore conclude that MsxC may have a role in epithelium-mesenchyme interactions during intermuscular bone formation in H. labeo.

Effect of glycated hemoglobin on heart function of the patients with revascularization of coronary artery.

BACKGROUND: Patients with diabetes after coronary artery bypass graft (CABG) or percutaneous coronary intervention (PCI) treatment for coronary artery disease (CAD) had higher mortality rates than those without diabetes. There were limited data comparing the cardiac and metabolic differences between diabetes and non-diabetes for CABG and PCI and about impact of pre-procedure GHb level on systolic heart function in patients with diabetes. AIMS: To explore the cardio-metabolic differences and to evaluate their potential as significant risk factors. SUBJECTS AND METHOD: 124 patients with diabetes and 170 patients without diabetes were enrolled. Coronary lesions (≥ 70% stenosis in at least one major coronary artery) were documented by angiography. Patients with diabetes were divided into different groups by GHb, Coronary lesions (≥ 70% stenosis in at least one major coronary artery) were documented by angiography. CABG and PCI were performed for all the patients. Cardio-metabolic risk factors before revascularization were compared between them. RESULTS: Diabetics with GHb ≥ 8% had lower cardiac ejection fraction (EF) values than those with GHb<8% (P<0.05) or patients without diabetes (P<0.05). And count of vascular lesions between the groups was not statistically significant. Observed EF as a dependent variable negatively correlated to GHb levels (P<0.05). The levels of glycated hemoglobin A1c (GHbA1c) rose with increased fasted blood glucose (FBG) values (P<0.001). Even with treatment for hyperglycemia and dyslipidemia, overall levels of fasting blood sugar (FBG, P<0.001), GHbA1c (P<0.001), and triglycerides (TG, P<0.05) in patients with diabetes were still higher than those without diabetes respectively. CONCLUSION: Poorer glucose control with GHb ≥ 8% and decreased systolic heart function are significant risk factors that potentially contribute to worse prognosis for CABG or PCI treatment. Elevated levels of FBG, GHbA1c, and TG are evident for patients with diabetes compared to patients without diabetes prior to revascularization.

The interaction of serum testosterone levels and androgen receptor CAG repeat polymorphism on the risk of erectile dysfunction in aging Taiwanese men.

Testosterone has been found to play important roles in men's sexual function. However, the effects of testosterone can be modulated by androgen receptor (AR) CAG repeat polymorphism. It could also contribute to the risk of erectile dysfunction (ED). The aim of this study is to evaluate the interaction of serum testosterone levels and AR CAG repeat polymorphism on the risk of ED in aging Taiwanese men. This cross-sectional data of Taiwanese men older than 40 years were collected from a free health screening held between August 2010 and August 2011 in Kaohsiung city, Taiwan. All participants completed a health questionnaires included five-item version of the International Index of Erectile Function (IIEF-5) and the International Prostate Symptoms Score, received a detailed physical examination and provided 20 cm3 whole blood samples for biochemical and genetic evaluation. The IIEF-5 was used to evaluate ED. Serum albumin, total testosterone (TT), and sex hormone-binding globulin levels were measured. Free testosterone level was calculated. AR gene CAG repeat polymorphism was determined by direct sequencing. Finally, 478 men with the mean age of 55.7 ± 4.8 years were included. When TT levels were above 330 ng/dL, the effect of testosterone level on erectile function seemed to reach a plateau and a significantly negative correlation between AR CAG repeat length and the score of IIEF-5 was found (r = -0.119, p = 0.034). After adjusting for other covariates, the longer AR CAG repeat length was still an independent risk factor for ED in subjects with TT above 330 ng/dL (p = 0.006), but not in TT of 330 ng/dL or below. In conclusion, both serum testosterone levels and AR CAG repeat polymorphism can influence erectile function concomitantly. In subjects with normal TT concentration, those with longer AR CAG repeat lengths have a higher risk of developing ED.

Genetic polymorphisms in androgen receptor-binding sites predict survival in prostate cancer patients receiving androgen-deprivation therapy.

BACKGROUND: Activated androgen receptor binds to androgen-responsive elements (AREs) in genome to regulate target gene transcription and, consequently, mediates physiological or tumorigenic processes of the prostate. Our aim was to determine whether genetic variants in AREs are associated with clinical outcomes after androgen-deprivation therapy (ADT) in prostate cancer patients. PATIENTS AND METHODS: We systematically investigated 55 common single-nucleotide polymorphisms (SNPs) in the genome-wide insilico-predicted AREs in a cohort of 601 men with advanced prostate cancer treated with ADT. The prognostic significance of these SNPs on disease progression, prostate cancer-specific mortality (PCSM) and all-cause mortality (ACM) after ADT was assessed by Kaplan-Meier analysis and Cox regression model. RESULTS: In univariate analysis, two, five, and four SNPs were associated with disease progression, PCSM, and ACM, respectively. After adjusting for known prognostic factors, ARRDC3 rs2939244, FLT1 rs9508016, and SKAP1 rs6504145 remained as significant predictors for PCSM and FBXO32 rs7830622 and FLT1 rs9508016 remained as significant predictors for ACM in multivariate analysis. Moreover, strong combined genotype effects on PCSM and ACM were also observed (P(trend) < 0.001). CONCLUSION: Our results suggest that SNPs in AREs influence prostate cancer survival and may further advance our understanding of the disease progression.