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There has been increasing interest in the psycho-socio-relational and sexual disorders of infertility, as the risk of psychological burden among infertile men with sexual dysfunctions is significant. The purpose of this study was to develop and to validate a predictive model to estimate individual psychological burden among infertile men with sexual dysfunction and study the association between them. Comprehensive data were collected for infertile men (n = 480) who sought treatment for infertility in a reproductive medicine center between June 2012 and December 2013. Using independent predictors of psychological burden from the least absolute shrinkage and selection operator, univariable and multivariable analyses were developed into two models. Predictive accuracy was compared between the models. We explored the association between sexual dysfunction and psychological burden. A total of 480 patients were analyzed using 10-fold cross-validation. Independent predictors of psychological burden were incorporated into a model to measure anxiety (corrected-area under curve (AUC): 77.3%) and a model to measure depression (corrected-AUC: 70.2%). Anxiety and depression were both associated with erectile dysfunction (P < 0.05), with anxiety demonstrating the strongest association. Only anxiety was associated with premature ejaculation (P < 0.05). Premature ejaculation was not found to be associated with depression (P > 0.05). Predictive models for psychological burden among infertile men with sexual dysfunction are presented, and we found that there is an association between psychological burden and sexual dysfunction. According to the models, proper counseling and treatment of sexual dysfunction in infertile men may reduce the psychological burden, help attain natural pregnancy, and improve the quality of life., Competing Interests: None

Background: Pancreatic beta-cell apoptosis induced by lipotoxicity, to a large extent, contributes to the progression of type 2 diabetes. To investigate the mechanism of free fatty acid induced apoptosis, we aimed to study the effects of palmitic acid (PA) on the apoptosis and peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) expression in βTC3 cells as well as the possible role of nuclear factor-κB (NF-κB) in this process., Methods: Hoechst 33258 was used to detect βTC3 cell apoptosis, which was induced by PA stimulation for 12 hours. PGC-1α expression was analyzed by reverse transcription polymerase chain reaction, IκB kinase β (IKKβ), IκBα, NF-κB-inducing kinase (NIK) and Rel-B expressions were analyzed by Western blotting. MG132 was employed to block the endogenous IκBα degradation before PA administration, and then its effect on PA-inducing cell apoptosis and PGC-1α mRNA expression was analyzed., Results: Significant increased cell apoptosis was found at the concentration of 0.5 mmol/L and 1.0 mmol/L PA administration. PA (0.5 mmol/L) could extensively reduced the expression of PGC-1α mRNA. After exposing βTC3 cells to 0.5 mmol/L PA for different time periods (0, 4, 6, 8, 10 and 12 hours), IKKβ protein expression increased while IκBα, NIK and Rel-B protein expression declined in a time-dependent manner. Pretreatment with MG132 to inhibit the degradation of IκBα, partially prevented the down-regulation of PGC-1α mRNA expression after 12-hour PA treatment in accordance with the decrease of PA induced apoptosis., Conclusions: NF-κB canonical pathway was activated in PA-mediated βTC3 cell apoptosis, whereas non-canonical pathway was inhibited. Reduced PGC-1α expression by PA in βTC3 cells could involve the activation of canonical NF-κB pathway, so as to deteriorate the PA induced apoptosis.

Objective: To investigate the effects of FFA(free fatty acid)on the expression of PANDER (pancreatic derived factor) in β-cells and to explore the possible relationship between PANDER and Akt signaling pathway at the anti-apoptotic effects of GLP-1 (glucagon-like peptide-1)., Methods: β-TC3 cells were cultured in vitro with palmitic acid (PA) of different concentrations and different time courses. The expression of PANDER mRNA was analyzed by realtime quantitative PCR (polymerase chain reaction). β-TC3 cells were cultured with vehicle, 0.5 mmol/L PA, 0.5mmol/L PA + 10nmol/L GLP-1 and 10nmol/L GLP-1 respectively with or without Akti-1/2, a selective inhibitor of Akt, for 12 hours. The protein levels of PANDER, p-Akt and pro-caspase3 were detected by Western blot. And cell apoptosis was analyzed by Hoechst33258 staining., Results: (1) PA could dose and time dependently increased the expression of PANDER mRNA in β cells (vs. control, P < 0.05); (2) PA increased the PANDER protein expression [(148 ± 18)% vs control 100%, P < 0.05)]. However, these effects were attenuated by GLP-1 [(70 ± 17)% vs PA group, P < 0.01]; (3) Akt inhibitor-1/2 alleviated the effects of GLP-1 on PA inducing the expression of PANDER. The expression of PANDER increased significantly in PA + GLP-1 + Akti-1/2 group [(249 ± 49)% vs PA + GLP-1 group (110 ± 54)%, P < 0.01], and cell apoptosis increased significantly as well [(37.8 ± 1.5)% vs PA + GLP-1 group (20.1 ± 3.5)%, P < 0.01]., Conclusion: PA induces the expression of PANDER and the apoptosis of β cell while GLP-1 counteracts the above effects through an activation of Akt signaling pathway.

Objective: A previously reported female diagnosed with type A insulin resistance syndrome bearing a heterozygous missense mutation of R1174W in the insulin receptor gene was followed for 7 years since the age of 16 years., Methods: Five-hour oral glucose tolerance tests (OGTT) were done on baseline, the 3(rd), 6(th) and 7(th) year respectively, with serum insulin and C-peptide measured at the same time points. Areas under of curve (AUC) of glucose, insulin and C-peptide were compared between the years. Acute insulin response (AIR) was determined at baseline and the 7(th) year. The dose response were insulin secretion rates at each time point during OGTT being plotted over the corresponding glucose levels, and the slopes of which quantified the insulin secretion responding to glucose., Results: The follow up data showed that the glucose metabolism of the subject did not deteriorate over time with yearly glycosylated hemoglobin A1c (HbA1c) being normal (4.6% - 5.5%), and hyperinsulinemic hypoglycemia was a persistent phenomenon observed at 4 - 5 hours post-load. The fasting and AUCs of serum insulin and C-peptide tended to decline without simultaneously increase of those of plasma glucose. The AIR decreased by 56% as compared to baseline. The dose response curves shifted downward as years went by., Conclusions: It supports that with the alleviation of physiological insulin resistance after puberty, the gross hyperinsulinemia tends to ameliorate, and β-cell secretion does not deteriorate over time as glucose homeostasis maintains.

Objective: To study the effect of smoking on resting energy expenditure (REE) and the relationships among REE, smoking, inflammation and oxidative stress in patients with diabetic kidney disease., Methods: A case control study of 31 smokers and 40 non-smokers with early stage of diabetic kidney disease (stage III) were performed to evaluate the chronic effect of smoking on REE. REE/fat free mass (FFM), biomarkers of oxidative stress malondialdehyde (MDA), superoxide dismutase (SOD) and inflammation high-sensitivity C-reactive protein (hs-CRP), adiponectin, TNFα were also measured in these subjects. Data were analyzed by Pearson correlation analysis., Results: Compared with non-smokers, REE/FFM in smokers group was significantly increased by 15.96% (P = 0.001). Pearson analysis showed that smoking was significantly correlated with REE/FFM (t = 0.395, P = 0.001). There were significantly different between smokers and non-smokers in MDA, SOD and hs-CRP (P < 0.05). But no difference between two groups in adiponectin and TNFα (P > 0.05). No significant relationships between REE/FFM and MDA, SOD, hs-CRP, adiponectin, TNFα was found (P > 0.05)., Conclusion: Chronic smoking can lead to increased REE, arouse oxidative stress and inflammatory in patients with early stage of diabetic kidney disease. However, there is no relationship between increased REE due to smoking and oxidative stress and inflammatory.

Objective: To analyzed the role of genetic factors in pathogenesis of acute intermittent porphyria (AIP)., Methods: Peripheral blood sample was collected from a Chinese female AIP patients, aged 36, to undergo direct sequencing to analyze all the exons and flanking introns of the porphobilinogen deaminase (PBGD) and protoporphyrinogen oxidase (PPOX) genes. The sequencing results were compared with the established human PBGD and PPOX sequences (GenBank Accession No. M95623; NC&#95;000001.9)., Results: Direct sequencing showed three kinds of single nucleotide polymorphism (SNP) in the PBGD gene. No mutation was found in the coding regions of either PBGD or PPOX gene., Conclusion: The three SNPs may underlie the genetic defects of AIP in Chinese. SNP may serve as genetic markers for linkage analysis to track presymptomatic carriers in AIP families.