Highly collimated broadside emission from room-temperature GaAs distributed Bragg reflector lasers

Highly collimated laser beams have been observed to be coupled out by second-order Bragg scattering from GaAs distributed Bragg reflector lasers. The beams are perpendicular to the waveguide plane and have an angular width of less than 1°. The diodes have a separate confinement structure and operate at room temperature with thresholds as low as 1.4 kA/cm^2

Quantification of neurodegeneration by measurement of brain-specific proteins

Quantification of neurodegeneration in animal models is typically assessed by time-consuming and observer-dependent immunocytochemistry. This study aimed to investigate if newly developed ELISA techniques could provide an observer-independent, cost-effective and time-saving tool for this purpose. Neurofilament heavy chain (NfH(SM135)), astrocytic glial fibrillary acidic protein (GFAP), S100B and ferritin, markers of axonal loss, gliosis, astrocyte activation and microglial activation, respectively, were quantified in the spinal cord homogenates of mice with chronic relapsing experimental allergic encephalomyelitis (CREAE, n=8) and controls (n=7). Levels of GFAP were found to be threefold elevated in CREAE (13 ng/mg protein) when compared to control animals (4.5 ng/mg protein, p<0.001). The inverse was observed for NfH(SM135) (21 ng/mg protein vs. 63 ng/mg protein, p<0.001), ferritin (542 ng/mg protein vs. 858 ng/mg protein, p<0.001) and S100B (786 ng/mg protein vs. 2080 ng/mg protein, N.S.). These findings were confirmed by immunocytochemistry, which demonstrated intense staining for GFAP and decreased staining for NfH(SM135) in CREAE compared to control animals. These findings indicate that axonal loss and gliosis can be estimated biochemically using the newly developed ELISA assays for NfH(SM135) and GFAP. These assays may facilitate the quantification of pathological features involved in neurodegeneration

Zależność między stężeniem wolnego testosteronu w surowicy a występowaniem stanu przedrzucawkowego

Introduction: Hyperandrogenism may be implicated in the pathogenesis of pre-eclampsia. We hypothesised that there may be a difference between the levels of testosterone in pregnant women complicated with pre-eclampsia and those of matched women without this complication. Material and methods: A case-control study conducted in Tehran, Iran between January and June 2006 included 20 women with moderate to severe pre-eclampsia and 20 normotensive pregnant women without complications who were matched for age, body mass index and gravity. Maternal levels of free testosterone was measured in the two groups and compared. Results: Free testosterone levels were significantly higher in the pre-eclamptic group (mean = 1.97, SD = 0.58, median = 1.90 ng/dL) than in the control group (mean = 0.58, SD = 0.29, median=0.50 ng/dL) (P < 0.001). Conclusions: An increase in serum free testosterone concentration may be considered an important risk factor for pre-eclampsia and might be implicated in the pathogenesis of pre-eclampsia. (Pol J Endocrinol 2008; 59 (5): 390-392)Wstęp: Hiperandrogenizm może mieć wpływ na patogenezę stanu przedrzucawkowego. Autorzy założyli, że istnieją różnice w zakresie stężeń testosteronu u kobiet w ciąży powikłanej stanem przedrzucawkowym i dobranych odpowiednio ciężarnych kobiet z grupy kontrolnej bez tego powikłania. Materiał i metody: W badaniu kliniczno-kontrolnym przeprowadzonym w Teheranie w okresie od stycznia do czerwca 2006 roku uczestniczyło 20 kobiet z umiarkowanym lub ciężkim stanem przedrzucawkowym i 20 ciężarnych kobiet z prawidłowym ciśnieniem tętniczym bez powikłań, dobranych pod względem wieku, wskaźnika masy ciała i parametrów ciążowych. Stężenie wolnego testosteronu w surowicy ciężarnych kobiet zmierzono i porównano między grupami. Wyniki: Stężenie wolnego testosteronu w surowicy było istotnie wyższe u kobiet, u których ciąża była powikłana stanem przedrzucawkowym (średnia = 1,97, SD = 0,58, mediana = 1,90 ng/dl) niż w grupie kontrolnej (średnia = 0,58, SD = 0,29, mediana = 0,50 ng/dl) (P < 0,001). Wnioski: Zwiększenie stężenia wolnego testosteronu w surowicy kobiet ciężarnych może być ważnym czynnikiem ryzyka stanu przedrzucawkowego i odgrywać znaczącą rolę w patogenezie tego powikłania ciąży. (Endokrynol Pol 2008; 59 (5): 390-392

Activity of 3β-hydroxysteroid dehydrogenase associated with progesterone production in bovine granulosa cells cultured under different concentrations of serum, insulin-like growth factor I, and gonadotropin

Three-β-hydroxysteroid dehydrogenase (3β-HSD) is the enzyme responsible for progesterone production. This study aimed to determine whether 3β-HSD activity can be shown to reflect progesterone production by granulosa cells cultured under different serum conditions and follicle stimulating hormone (FSH), luteinising hormone (LH), and insulin-like growth factor I (IGF-I) concentrations. Large bovine follicles were dissected from abattoir ovaries to recover granulosa cells. Cells were washed, stained for viability, and plated for 48 h in basic medium with or without 5% foetal calf serum (FCS). Subsequently, cells were exposed to FSH (1 ng/mL), LH (10 or 100 ng/mL), or FSH (1 ng/mL) + IGF-I (1 or 10 ng/mL) in a serum-free medium for another 96 h to predict degree of luteinisation. Before and after incubation, granulosa cells were stained for 3β-HSD activity. The high dose of IGF-I (10 ng/mL) increased (P &#60; 0.05) progesterone secretion over 2.5-fold compared with FSH alone or the low dose of IGF-I (1 ng/mL) in cells preincubated with FCS. This was clearly reflected by darker 3β-HSD staining than in cells exposed to FSH and low dose IGF-I

Can μ\mu--ee Conversion in Nuclei be a Good Probe for Lepton-Number Violating Higgs Couplings ?

Motivated by the improving sensitivity, $R$, of experiments on $\mu~Ti \rightarrow e~Ti$ and the enhanced Higgs nucleon interaction, we study this lepton number violating process induced by Higgs exchange. Taking the possible sensitivity, $R \simeq 10^{-16}$, we obtain the constraint on the Higgs-muon-electron vertex, $\kappa_{\mu e}$, to be less than $2.4\times10^{-7}$ if the masses of the Higgs scalar and $W$ gauge boson are the same. $\kappa_{\mu e}$ is also calculated for some models.Comment: 11 pages(revtex 3), TRI-PP-93-7

Białko CTRP3 zwiększa wrażliwość na insulinę adipocytów 3T3-L1 przez hamowanie procesu zapalnego i poprawę przekazywania sygnału insulinowego

 Introduction: C1q/TNF-related Protein-3 (CTRP3) is a novel adipokine with multiple effects such as lowering glucose levels, inhibiting glyconeogenesis in the liver, and increasing angiogenesis and anti-inflammation. But little is known about the effects of CTRP3 on insulin resistance in adipose tissue. This study aims to investigate the effects and mechanisms of CTRP3 on the insulin sensitivity of 3T3-L1 adipocytes.Material and methods: Insulin resistant 3T3-L1 adipocytes were induced by palmic acid cultivation. Such adipocytes were treated with recombinant CTRP3 protein at different concentrations (0, 10, 50, 1,250 ng/mL）for 12 hours, and at a concentration of 250 ng/mL for differing times (2, 6, 12, and 24h). Another group was pre-treated with wortmannin, the special inhibitor of phosphatidylinositol-4,5- bisphosphate 3-kinase (PI3K), for 20 minutes before the treatment with 250 ng/mL CTRP3. The glucose consumption, the glucose uptake, the expression and release of tumour necrosis factor α (TNF-α) and interleukin-6(IL-6) in supernatant, and the protein relative expression of PI3K and protein kinase B (PKB)(ser437) were detected.Results: Compared to the control group, glucose consumption in the CTRP3 intervention group at concentrations of 10, 50, 250, and 1,250 ng/mL was increased by 22.1%, 42.9%, 76.6% and 80.5% respectively (all P &lt; 0.01); the glucose uptake was increased by 39.0%, 68.0%, 108.0% and 111.0% respectively (all P &lt; 0.01); the content of TNF-α in the culture media of CTRP3 (10, 50, 250 ng/mL) intervention group was decreased by 7.6% (P &gt; 0.05), 13.0% (P &lt; 0.05) and 17.4% (P &lt; 0.01) respectively; the content of IL-6 was decreased by 7.1%, 12.4% and 17.1% respectively (all P &lt; 0.01); the protein relative expression of PI3K was increased by 0.63-, 1.00- and 1.36-fold respectively (all P &lt; 0.01), and PKB(ser437) increased by 0.65-, 1.61- and 1.93-fold respectively (all P &lt; 0.01); the mRNA relative expression of GLUT-4 was increased by 23.0%, 47.0% and 62.0% respectively (all P &lt; 0.01). After the treatment with wortmannin, glucose consumption, glucose uptake, PI3K and PKB(ser437) protein relative expression, as well as GLUT-4 mRNA relative expression, was decreased by 53.2%, 44.7%, 43.4%, 56.1 and 30.9% respectively (all P &lt; 0.01).Conclusions: CTRP3 could improve insulin sensitivity of insulin resistant 3T3-L1 adipocytes by decreasing inflammation and ameliorating insulin signalling transduction, indicating that CTRP3 may be a new target for the prevention and cure of insulin resistance and type 2 diabetes. (Endokrynol Pol 2014; 65 (4): 252–258) Wstęp: Białko związane z C1q/TNF typu 3 (CTRP3, C1q/TNF-related Protein-3) jest nowo odkrytą adipokiną o wielorakim działaniu obejmującym obniżenie stężenia glukozy we krwi, hamowanie glukoneogenezy w wątrobie, pobudzanie angiogenezy i działanie przeciwzapalne, Niewiele jednak wiadomo na temat wpływu CTRP3 na insulinooporność komórek tłuszczowych. Badanie to przeprowadzono w celu oceny mechanizmów działania tej adipokiny i jej wpływu na wrażliwość na insulinę adipocytów 3T3-L1.Materiał i metody: Insulinooporne adipocyty 3T3-L1 uzyskano poprzez dodanie do hodowli tych komórek kwasu palmitynowego. Następnie adipocyty te poddano działaniu rekombinowanego białka CTRP3 w różnych stężeniach (0, 10, 50, 1250 ng/ml przez 12 godzin oraz w stężeniu 250 ng/ml przez różny czas (2, 6, 12, 24 godz.). Inną grupę hodowli komórkowych przed dodaniem CTRP3 w stężeniu 250 ng/ml inkubowano wstępnie z wortmaniną, inhibitorem kinazy fosfatydyloinozytolu-4,5 (PI3K, phosphatidylinositol-4,5- bisphosphate 3-kinase) przez 20 minut. Określono zużycie glukozy, wychwyt glukozy, ekspresję i uwalnianie czynnika martwicy nowotworów typu alfa (TNF-α, tumor necrosis factor α) i interleukiny 6 (IL-6, interleukin-6,) w supernatancie oraz ekspresję PI3K i kinazy białkowej B (PKB, protein kinase B) (ser437).Wyniki: Zużycie glukozy w hodowlach poddanych działaniu CTRP3 w stężeniach 10, 50, 250, 1250 ng/ml było większe niż w hodowli kontrolnej odpowiednio o 22,1%, 42,9%, 76,6% i 80,5% (dla wszystkich porównań p &lt; 0,01). Wychwyt glukozy był większy o 39,0%, 68,0%, 108,0% i 111,0% (dla wszystkich porównań p &lt; 0,01) Zawartości TNF-α w medium hodowli komórkowej z dodatkiem CTRP3 (10, 50, 250 ng/ml) były mniejsze odpowiednio o 7,6% (p &gt; 0,05), 13,0% (p &lt; 0,05) i 17,4% (p &lt; 0,01), a zawartości IL-6 były mniejsze o odpowiednio 7,1%, 12,4% i 17,1% (dla wszystkich porównań p &lt; 0,01). Związana z białkami ekspresja PI3K stanowiła odpowiednio 0,63-, 1,00- i 1,36-krotność wartości uzyskanej w hodowli kontrolnej (dla wszystkich porównań p &lt; 0,01), a ekspresja PKB(ser437) stanowiła odpowiednio 0,65-, 1,61- i 1,93-krotność (dla wszystkich porównań p &lt; 0,01); Względna ekspresja mRNA GLUT-4 była większa odpowiednio o 23,0%, 47,0% i 62,0% (dla wszystkich porównań p &lt; 0,01). W hodowlach poddanych wstępnie działaniu wortmaniny zużycie glukozy, signifiwychwyt glukozy, ekspresja PI3K i PKB(ser437) oraz ekspresja mRNA GLUT-4 były mniejsze odpowiednio o 53,2%, 44,7%, 43,4%, 56,1% i 30,9% (dla wszystkich porównań p &lt; 0,01).Wnioski: Białko CTRP3 może powodować zwiększenie wrażliwości na insulinę insulinoopornych adipocytów 3T3-L1 przez hamowanie procesu zapalnego i poprawę przewodzenia sygnałów insulinowych, co wskazuje, że białko to może być nowym celem w zapobieganiu i leczeniu insulinooporności i cukrzycy typu 2. (Endokrynol Pol 2014; 65 (4): 253–258)

Effects of Dietary Fatty Acids on Insulin Resistance, Tissue Lipid Profile and Adipose Tissue Cellularity in Sprague-Dawley Rat

Insulin resistance describes a dysfunctional state of glucose metabolism which often occurs in advance of any metabolic diseases in human population. Dietary fatty acids are closely linked to insulin resistance as they are known to modulate fatty acid and glucose metabolism in mammals. In this study, fatty acids from butter, soybean and menhaden oil were separately incorporated into rat chow diet to assess the differential effect of dietary fatty acids on the various indicators and risk factors of insulin resistance. These include glucose clearance functions, plasma insulin, body composition, tissue and plasma fatty acid profiles, blood lipids, adipose cellularity and leptin level. A total of 40 male Sprague-Dawley rats of 9 weeks age, randomly allocated to four treatment groups of ten animals each, were employed in this study. The treatment groups consisted of rats fed with chow diet (CD), rats fed chow diet fortified with 10% w/w butter (BCD), rats fed chow diet added with 6.67 % w/w menhaden oil and 3.33% w/w soybean oil (MCD), and rats fed chow diet added with 3.33 % w/w menhaden oil and 6.67 % w/w soybean oil (SCD). The rats were subjected to their respective treatment diets for 22 weeks and body weight was measured weekly. Intraperitoneal glucose tolerance test (IPGTT) and intraperitoneal insulin tolerance test (IPITT) were carried out on day 0, and then later in the 12th and 20th weeks of dietary intervention to assess changes as a result of insulin resistance. Serial plasma insulin levels were also quantified on day 0 and in the 20th week. Upon termination of the trial at the end of the 22nd week, post mortem body composition and inguinal fat cellularity were performed on the rats. Plasma leptin and blood lipids in all treatment groups were measured. Determination of fatty acid profile of selected tissues (plasma, red blood cell membrane, liver and skeletal muscle) were also carried out. Generally, tissue and plasma fatty acid profiles were reflective of the dietary fatty acid composition. Results showed that glucose clearance in all treatment groups was not compromised as a result of dietary intervention. However, the BCD group consistently showed higher blood glucose spike 15 minutes after initial glucose loading, and higher blood glucose readings even after insulin challenge during IPITT compared to the other groups. The glucose clearance capacities of MCD and SCD fed animals remained similar to that of their initial baseline values even after 20 weeks of treatment. Unlike glucose concentration, plasma insulin level was significantly (P<0.05) higher in a majority of time points in the BCD rats compared to the MCD and SCD rats in the 20th week. The corresponding total amount of plasma insulin by time as indicated by the area under the plasma insulin curve, (AUC) for the BCD rats was 456.7±27.7 ng/L min. This was significantly higher (P<0.05) than those of the CD (335.5±38.5 ng/L min), MCD (273.7±37.6 ng/L min) and SCD (265.9±21.7 ng/L min) rats. Area under the curve (AUC) values also showed that all treatment groups, (CD, MCD and SCD) had much higher (P<0.05) plasma insulin values after 20 weeks of treatment, compared to their baseline concentration of 200.3±21.6 ng/L min. Apart from being hyperinsulinaemic, the insulin sensitivity index of BCD rats was found to be significantly (P<0.05) compromised unlike those of the MCD and SCD rats. Risk factors associated with insulin resistance such as excessive body fat accumulation and adipocyte cellularity were altered by dietary fatty acids. Inguinal fat cellularity results showed large and hypertrophied adipocytes in the BCD rats, while adipocytes in the MCD and SCD rats became hyperplastic but significantly smaller (P<0.05) than those of BCD rats. Plasma leptin was elevated significantly (P<0.05) in the BCD rat (3.22±0.32 ng/mL) compared to MCD (2.37±3.2 ng/mL), SCD (2.29±0.35 ng/mL) and CD (2.16±0.11 ng/mL) groups. Blood lipid picture was found to be healthier in the MCD and SCD supplemented groups. These two groups had significantly (P<0.05) lower total cholesterol and triacylglycerol (TAG) contents than the BCDfed rats. This was accompanied by significantly reduced high density lipoprotein cholesterol (HDL-C) in the MCD (0.15±0.05 mmol/L) and SCD (0.19±0.05 mmol/L) rats, compared to a value of 0.34±0.07 mmol/L observed for the BCD rats. Therefore, it was concluded that 10% dietary fat supplementation from menhaden and soybean oil could delay the onset of hyperinsulinaemia, and possibly insulin resistance in the rat model. Furthermore, PUFA was also shown to have an effect on the risk factors and other indicators for insulin resistance such as adipocyte cellularity, blood lipids and leptin

Room-temperature operation of GaAs Bragg-mirror lasers

Room-temperature operation of GaAs distributed Bragg reflector lasers is reported. The diodes are fabricated from conventional double heterostructures involving only a single step of liquid-phase epitaxy. For gratings with a period of 3700 Å, the diodes lased at 8770 Å, which corresponds to the high-absorption side of the spontaneous emission spectrum. Thresholds as low as 6 kA/cm^2 have been realized