Sugar-sweetened beverage intake and serum testosterone levels in adult males 20-39 years old in the United States.

BACKGROUND: This population-based study was designed to investigate whether consumption of sugar-sweetened beverages (SSB) is associated with lower serum total testosterone concentration in men 20-39 years old. METHODS: All data for this study were retrieved from the National Health and Nutrition Examination Survey (NHANES) 2011-2012. The primary outcome was serum testosterone concentration, and main independent variable was SSB intake. Other variables included age, race/ethnicity, poverty/income ratio, body mass index (BMI), serum cotinine, heavy drinking, and physical activity. RESULTS: Among all subjects (N = 545), 486 (90.4%) had normal testosterone levels (defined as ≥231 ng/dL) and 59 (9.6%) had low testosterone levels (defined as < 231 ng/dL). Multivariate logistic regression revealed the odds of low testosterone was significantly greater with increasing SSB consumption (Q4 [≥442 kcal/day] vs. Q1 [≤137 kcal/day]), adjusted odds ratio [aOR] = 2.29, p = 0.041]. After adjusting for possible confounding variables, BMI was an independent risk factor for low testosterone level; subjects with BMI ≥ 25 kg/m2 had a higher risk of having a low testosterone level than those with BMI < 25 kg/m2 (aOR = 3.68, p = 0.044). CONCLUSION: SSB consumption is significantly associated with low serum testosterone in men 20-39 years old in the United States.

Continuous positive airway pressure and diabetes risk in sleep apnea patients: A systemic review and meta-analysis.

BACKGROUND: The study assessed the effect of continuous positive airway pressure (CPAP) therapy on the risk of developing type 2 diabetes by evaluating change in the homeostasis model assessment of insulin resistance (HOMA-IR) fasting blood glucose (FBG) and fasting insulin following CPAP treatment in non-diabetic patients and pre-diabetic with obstructive sleep apnea (OSA). METHODS: Medline, PubMed, Cochrane, and EMBASE databases were searched until August 24, 2015. The analysis included randomized controlled trials (RCTs), two arm prospective studies, cohort studies, and retrospective studies. The primary outcome measure was change of HOMA-IR in pre-diabetic patients receiving CPAP treatment. RESULTS: Twenty-three studies were included with 965 patients who had OSA. Nineteen studies were prospective studies and four were RCTs. CPAP therapy resulted in a significant reduction in the pooled standard difference in means of HOMA-IR (-0.442, P=0.001) from baseline levels compared with the control group. Change in FBG and fasting insulin from baseline levels was similar for the CPAP and control groups. For RCT studies (n=4), there was no difference in change in HOMA-IR or FBG levels from baseline between CPAP and control groups. The combined effect of RCTs showed that CPAP was associated with a significant reduction in change from baseline in fasting insulin than the control group (standardized diff. in means between groups=-0.479, P value=0.003). CONCLUSION: These findings support the use of CPAP in non-diabetic and pre-diabetic patients with OSA to reduce change of HOMA-IR and possibly reduce the risk of developing type 2 diabetes in this patient population.

Predictors of cardiorespiratory fitness in female and male adults with different body mass index: National Health and Nutrition Examination Survey 1999-2004 dataset.

BACKGROUND: The aim of this study was to explore factors affecting cardiorespiratory fitness in males and females with different body mass index (BMI). METHODS: The National Health and Nutrition Examination Survey 1999-2004 data were used for this retrospective study. Estimated maximal oxygen uptake (VO2max) is surrogate for cardiorespiratory fitness (CRF). Univariate and multivariate linear regression analyses were performed to explore whether study variables were associated with estimated VO2max stratified by gender and BMI categories. RESULTS: A total of 3292 subjects 20-49 years of age were included in the analysis. CRF significantly decreased as BMI increased in both females and males. Ethnic difference was found in normal BMI in both genders and obese females; homocysteine was significantly negatively associated with estimated VO2max, as was total cholesterol. Obese male subjects with diabetes had a lower estimated VO2max than those without diabetes, and C-reactive protein (CRP) level and vitamin B12 level were significantly negatively associated with CRF. Female subjects with diabetes had higher estimated VO2max than those without diabetes. Folate was significantly positively correlated with estimated VO2max, whereas CRP was negatively correlated in obese female. CONCLUSIONS: There are different predictors of CRF in males and females, and in individuals with different BMI. Key messages Different BMI classes are associated with different predictors of cardiorespiratory fitness. Indicators of cardiorespiratory fitness differ between sexes.

[Efficacy of ultrasound-guided lauromacrogol sclerotherapy for benign thyroid cysts and factors affecting the therapeutic effect].

OBJECTIVE: To evaluate the clinical efficacy of ultrasound-guided lauromacrogol sclerotherapy for benign thyroid cysts and analyze the factors affecting the efficacy. METHODS: Ultrasound-guided lauromacrogol sclerotherapy was performed in 97 patients with a total of 99 benign thyroid cysts. The changes in cystic volume and other thyroid parameters were evaluated at 1, 3, 6, and 12 months after sclerotherapy. According to changes in the cystic volume, the efficacy of sclerotherapy was defined as therapeutic failure (with a volume reduction <50%), treatment success (volume reduction ≥50%) and cure (volume reduction ≥90%). The factors of affecting the efficacy of sclerotherapy was analyzed using COX regression. RESULTS: The mean cystic volume at 1, 3, 6 and 12 months after sclerotherapy were reduced from the baseline volume of 12.08∓11.56 cm3 to 5.63∓8.51 cm3, 5.96∓8.42 cm3, 3.80∓5.50 cm3 and 2.85∓3.98 cm3, respectively, with an average cystic volume reduction rate of (70.02∓33.72)%. Therapeutic success was achieved 82 of the 99 cysts (82.83%) and cure was achieved 63cysts (63.64%) at 12 months after the procedure. A second sclerotherapy was performed for 13 cysts which did not show a volume reduction at 1-3 months after the initial procedure. A disease course of over 12 months was an independent risk factor for a second sclerotherapy (23.7% [9/38] vs 6.6% [4/61], OR=4.473 [1.238-16.169], P=0.022). The efficacy of sclerotherapy was related to cystic cavity separation, cystic fluid viscosity, cystic/solid ratio and cystic wall thickness. COX regression analysis revealed that cystic cavity separation (HR=2.25, 95%CI: 1.19-4.25) and cystic fluid viscosity (HR=2.02, 95%CI: 1.19-3.43) were the major factors affecting the treatment efficacy. CONCLUSION: Ultrasound-guided lauromacrogol sclerotherapy is effective and safe for treatment of benign thyroid cysts, and the maximal treatment effect can be achieved at 6 months after sclerotherapy and in cases of uncomplicated cysts with non-viscous cystic fluid, no solid cystic cavity separation and a disease course of less than 12 months.

[A preliminary study of long-term mitochondrial dysfunction in rat brain caused by lipopolysaccharide-induced sepsis].

OBJECTIVE: To preliminarily investigate the long-term structural and functional injuries of mitochondria in rat brain caused by sepsis. METHODS: Wistar rats were randomly assigned into sepsis and control groups. A rat model of sepsis was prepared by an intraperitoneal injection of 10 mg/kg lipopolysaccharide (LPS) of gram-negative bacteria, and the survival assay was performed. Eight rats in the sepsis group were sacrificed at 12, 24, 48, or 72 hours after LPS injection, while rats in the control group were sacrificed after an intraperitoneal injection of an equal volume of normal saline. Mitochondria were extracted from rat brain tissue. Mitochondrial membrane potential (MMP) and mitochondrial swelling level were determined by flow cytometry, and the activities of electron transport chain complexes (I-V) were measured using enzyme assay kits. Hematoxylin-eosin (HE) staining and electron microscopy were used to observe morphological changes in brain tissue and mitochondria. RESULTS: The sepsis group had a significantly lower survival rate than the control group (P<0.01). The MMP and activities of electron transport chain complexes (I-V) in the sepsis group, which were significantly lower than those in the control group (P<0.05), were reduced to the lowest levels at 48 hours and partially recovered at 72 hours. The mitochondrial swelling level in the sepsis group, which was significantly higher than that in the control group (P<0.05), increased to the peak level at 48 hours and partially recovered at 72 hours. Hematoxylin and Eosin staining revealed substantial damages in the structure of brain tissue, and electron microscopy showed mitochondrial swelling, and vacuolization in a few mitochondria. CONCLUSIONS: In the rat model of LPS-induced sepsis, both structural and functional injuries are found in cerebral mitochondria, and achieve the peak levels probably at around 48 hours.

[Effect of UCP2-siRNA on inflammatory response of cardiomyocytes induced by septic serum].

OBJECTIVE: To study the effect of uncoupling protein 2 (UCP2)-siRNA on the inflammatory response of rat cardiomyocytes (H9C2) induced by septic serum and to investigate the possible role of UCP2 in the development of septic cardiomyopathy. METHODS: Serum samples were separately collected from normal rats and septic rats. Cultured rat cardiac cells (H9C2) were randomly divided into blank control, normal serum, 10% septic serum, UCP2-siRNA+10% septic serum and negative siRNA+10% septic serum groups. Stimulation with 10% septic serum was performed for 12 hours in relevant groups. The mRNA expression of tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1ß) was measured by RT-PCR. The expression of phosphorylated p38 mitogen-activated protein kinase (p-p38 MAPK) and nuclear factor-kappa B (NF-κB) was measured by Western blot. RESULTS: The expression levels of p-p38 and NF-κB in the UCP2-siRNA+10% septic serum group were significantly higher than in the 10% septic serum group (P<0.05). The UCP2-siRNA+10% septic serum group had a significantly higher TNF-α mRNA expression than the 10% septic serum group (P<0.01), but IL-1ß mRNA expression showed no significant difference between the two groups. CONCLUSIONS: UCP2 plays a regulatory role in the activation of p38 MAPK and NF-κB and the expression of downstream inflammatory mediators in H9C2 cells stimulated with septic serum.

[Non-nascent hydrogen mechanism of plumbane generation].

The mechanism of plumbane generation in dichromate system was studied via investigation of the relationship between the plumbane yield and the molar number of the reactants. A flow injection hydride generator was used in the study. Reactant moler number was calculated by the injected volume and the reactant concentration, and the plumbane yield was measured via an AAS spectrometer equipped with an electrothermal quartz tube atomizer. Experimental results show that the acid was first used for the neutralization of NaOH and successively participated in the redox reaction of borohydride with dichromate with a constant molar ratio of 9.95 +/- 0.42 (expressed in terms of mean +/- standard deviation). At the same time, plumbane generation was displayed as synchronously taking place with the redox reaction, and the yield increased with the increase of acid. The mechanism of plumbane generation was thus deduced as an induced reaction or a catalytic reaction by the redox reaction. Up to this end, the non-nascent hydrogen mechanism of hydride generation has been verified for all the IVA elements.

Multiple regions of the NG2 proteoglycan inhibit neurite growth and induce growth cone collapse.

The NG2 chondroitin sulfate proteoglycan, an integral membrane proteoglycan, inhibits axon growth from cerebellar granule neurons and dorsal root ganglia (DRG) neurons in vitro. The extracellular domain of the NG2 core protein contains three subdomains: an N-terminal globular domain (domain 1), a central extended domain that has the sites for glycosaminoglycan (GAG) attachment (domain 2), and a juxtamembrane domain (domain 3). Here, we used domain-specific fusion proteins and antibodies to map the inhibitory activity within the NG2 core protein. Fusion proteins encoding domain 1 (D1-Fc) or domain 3 (D3-Fc) of NG2 inhibited axon growth from cerebellar granule neurons when the proteins were substrate-bound. These proteins also induced growth cone collapse from newborn DRG neurons when added to the culture medium. Domain 2 only inhibited axon growth when the GAG chains were present. Neutralizing antibodies directed against domain 1 or 3 blocked completely the inhibition from substrates coated with D1-Fc or D3-Fc. When the entire extracellular domain of NG2 was used as a substrate, however, both neutralizing antibodies were needed to reverse completely the inhibition. When NG2 was expressed on the surface of HEK293 cells, the neutralizing anti-D1 antibody was sufficient to block the inhibition, whereas the anti-D3 antibody had no effect. These results suggest that domains 1 and 3 of NG2 can inhibit neurite growth independently. These inhibitory domains may be differentially exposed depending on whether NG2 is presented as an integral membrane protein or as a secreted protein associated with the extracellular matrix.

Simulation of the effects of space charge and Schottky barriers on ferroelectric thin film capacitor using Landau Khalatnikov theory.

The roles of space charge induced in the ferroelectric thin film and the presence of Schottky barriers at the two electrode/film interfaces are studied by numerical simulation using Landau-Khalatnikov theory. In this work, the whole film is considered as the stacking of dipolar layers, each of which contains multilayers of perovskite cells. In the presence of a local electric field, the double-well thermodynamic potential of each layer is modified into an asymmetric manner. The local electric field distribution is determined both by the space charge and the boundary conditions imposed by the Schottky barrier heights. The asymmetric and skewed hysteresis loops are generated.

Inhibition of axon growth by oligodendrocyte precursor cells.

The glial scar that forms at the site of injury is thought to be a biochemical and physical barrier to successful regeneration, although the molecules responsible for this barrier function are not well understood. Glia scars contain large numbers of oligodendrocyte precursor cells (OPCs) and these cells can produce several different growth-inhibitory chondroitin sulfate proteoglycans (CSPGs), including NG2, neurocan, and phosphacan. Here, we used membrane-based assays to show that the surface of OPCs is both nonpermissive and inhibitory for neurite outgrowth. Inhibition of growth by OPC is reversed by treatment with antibodies against the NG2 CSPG and the expression of NG2 is sufficient to change a growth-permissive cell surface to a nonpermissive surface. These result suggest that the OPCs that accumulate rapidly at sites of CNS injury can contribute to the creation of an environment that inhibits nerve regeneration and that NG2 is a necessary feature of that environment.

[The expression of neuronal nitric oxide synthase in caudal medulla of two-kidney one clip Goldblatt hypertension rat].

Experiments were performed in male Sprague-Dawley rats (150-200 g). A silver clip (0.2 mm internal diameter) was placed on the left renal artery of rats. After operation the rats were divided into 4 groups sham group, 2K1C (two-kidney one clip) group, 2K1C+Arg (2K1C and L-Arg 150 mg/kg x d(-1) by drinking) group, and 2K1C+NAME (2K1C and L-NAME 10 mg/kg x d(-1) i.p.) group. The animals were studied at two time points (4 and 7 weeks after operation) corresponding to phases I and II of Goldblatt hypertension. The animals were deeply anesthetized with pentobarbital and perfused by the cardiac route with saline (100 ml) and freshly prepared 4% paraformaldehyde in phosphate buffer (300 ml). The caudal medulla was removed, then placed in 25% sucrose in PB for 12 h in a 4 degrees C fridge. The 40 microm coronal slices of brainstems were cut with cryostat, collected in PBS for nNOS study by immunohistochemistry. The results showed that (1) only a few neuronal nitric oxide synthase (nNOS) positive neurones were found in caudal medulla, including the depressor area of the ventral surface of medulla oblongata (VSMd) and the caudal pressor area (CPA) of the sham operated animals. The number of nNOS positive neurons in caudal medulla was significantly increased in 2K1C Goldblatt hypertension rats at 4 and 7 weeks. (2) The number of nNOS positive neurons in VSMd and CPA were 2K1C+Arg > 2K1C >2K1C +NAME > sham. (3) L-Arg enhanced the expression of nNOS whereas L-NAME inhibited the expression of nNOS in caudal medulla. (4) The character of nNOS expression was similar in Goldblatt hypertension rats at 4 weeks with that of the rats at 7 weeks.

Oligodendrocyte precursor cells: reactive cells that inhibit axon growth and regeneration.

Oligodendrocyte precursor cells (OPCs) are a newly recognized glial component of the adult central nervous system of unknown function. Antibodies against the NG2 chondroitin sulfate proteoglycan have been useful tools to identify these cells in intact tissue. Here we review studies that show that OPCs react to several types of experimentally induced brain injury. Injury stimulates OPCs to re-enter the cell cycle, divide, and accumulate at the site of damage. OPCs, together with microglia and astrocytes, form the glial scar. Glial scars are thought to inhibit or prevent axonal regeneration and reactive OPCs contribute to this inhibition by producing growth-inhibiting chondroitin sulfate proteoglycans, particularly NG2. In developing animals, NG2 is found in areas, such as the perinotochordal mesenchyme, that are avoided by growing motor and sensory axons. Within the developing CNS, NG2-expressing cells surround the developing optic chiasm and tract and separate it from the overlying diencephalon. Thus, NG2-expressing cells are well positioned to inhibit axonal growth from developing as well as regenerating neurons.