4,417 research outputs found

    Long-term cigarette smoke exposure increases uncoupling protein expression but reduces energy intake

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    The appetite suppressing effect of tobacco is a major driver of smoking behaviour; however few studies have addressed the effects of chronic cigarette smoke exposure (SE) on appetite, body weight and metabolic markers. We compared the effects of SE to equivalent food restriction (pair-fed, PF), against sham-exposure, on body weight, adiposity, cytokines, and levels of uncoupling proteins (UCP) and brain neuropeptide Y (NPY) in male Balb/C mice. SE rapidly induced anorexia, and after 12Ā weeks, SE and PF groups were lighter than control animals (23.9 Ā± 0.2, 25.5 Ā± 0.5, 26.8 Ā± 0.4Ā g respectively, P < 0.05). White fat (WAT) masses were reduced by both SE and PF. Plasma leptin and insulin were reduced in SE mice; insulin was further reduced by PF. Brown fat UCP1 and 3 mRNA were increased in SE animals relative to PF animals, possibly promoting thermogenesis. WAT mRNA expression of the inflammatory cytokine, TNFĪ± was doubled by SE, while IL-6 was reduced by both PF and SE. Hypothalamic NPY content was increased by SE (89.3 Ā± 2.8 vs. 75.9 Ā± 2.4Ā ng control, P < 0.05), and more by PF (100.7 Ā± 3.4Ā ng, P < 0.05 compared to both groups), suggesting disinhibition due to reduced adipose derived leptin. In contrast to equivalent food restriction, cigarette smoke exposure reduced body weight and total hypothalamic NPY, and increased thermogenesis and markers of inflammation. The suppressed hypothalamic NPY and increased UCPs may contribute to the spontaneous hypophagia and extra weight loss in SE animals. These findings contribute to our understanding of weight loss in smoking-related lung disease, suggesting a greater impact than that due to anorexia alone. Crown Copyright Ā© 2008

    Regulation of hypothalamic NPY by diet and smoking

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    Appetite is regulated by a number of hypothalamic neuropeptides including neuropeptide Y (NPY), a powerful feeding stimulator that responds to feeding status, and drugs such as nicotine and cannabis. There is debate regarding the extent of the influence of obesity on hypothalamic NPY. We measured hypothalamic NPY in male Sprague-Dawley rats after short or long term exposure to cafeteria-style high fat diet (32% energy as fat) or laboratory chow (12% fat). Caloric intake and body weight were increased in the high fat diet group, and brown fat and white fat masses were significantly increased after 2 weeks. Hypothalamic NPY concentration was only significantly decreased after long term consumption of the high fat diet. Nicotine decreases food intake and body weight, with conflicting effects on hypothalamic NPY reported. Body weight, plasma hormones and brain NPY were investigated in male Balb/c mice exposed to cigarette smoke for 4 days, 4 and 12 weeks. Food intake was significantly decreased by smoke exposure (2.32 Ā± 0.03 g/24 h versus 2.71 Ā± 0.04 g/24 h in control mice (non-smoke exposed) at 12 weeks). Relative to control mice, smoke exposure led to greater weight loss, while pair-feeding the equivalent amount of chow caused an intermediate weight loss. Chronic smoke exposure, but not pair-feeding, was associated with decreased hypothalamic NPY concentration, suggesting an inhibitory effect of cigarette smoking on brain NPY levels. Thus, consumption of a high fat diet and smoke exposure reprogram hypothalamic NPY. Reduced NPY may contribute to the anorexic effect of smoke exposure. Ā© 2006 Elsevier Inc. All rights reserved

    The lung inflammation and skeletal muscle wasting induced by subchronic cigarette smoke exposure are not altered by a high-fat diet in mice

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    Obesity and cigarette smoking independently constitute major preventable causes of morbidity and mortality and obesity is known to worsen lung inflammation in asthma. Paradoxically, higher body mass index (BMI) is associated with reduced mortality in smoking induced COPD whereas low BMI increases mortality risk. To date, no study has investigated the effect of a dietary-induced obesity and cigarette smoke exposure on the lung inflammation and loss of skeletal muscle mass in mice. Male BALB/c mice were exposed to 4 cigarettes/day, 6 days/week for 7 weeks, or sham handled. Mice consumed either standard laboratory chow (3.5 kcal/g, 12% fat) or a high fat diet (HFD, 4.3 kcal/g, 32% fat). Mice exposed to cigarette smoke for 7 weeks had significantly more inflammatory cells in the BALF (P<0.05) and the mRNA expression of proinflammatory cytokines and chemokines was significantly increased (P<0.05); HFD had no effect on these parameters. Sham- and smoke-exposed mice consuming the HFD were significantly heavier than chow fed animals (12 and 13%, respectively; P<0.05). Conversely, chow and HFD fed mice exposed to cigarette smoke weighed 16 and 15% less, respectively, compared to sham animals (P<0.05). The skeletal muscles (soleus, tibialis anterior and gastrocnemius) of cigarette smoke-exposed mice weighed significantly less than sham-exposed mice (P<0.05) and the HFD had no protective effect. For the first time we report that cigarette smoke exposure significantly decreased insulin-like growth factor-1 (IGF-1) mRNA expression in the gastrocnemius and tibialis anterior and IGF-1 protein in the gastrocnemius (P<0.05). We have also shown that cigarette smoke exposure reduced circulating IGF-1 levels. IL-6 mRNA expression was significantly elevated in all three skeletal muscles of chow fed smoke-exposed mice (P<0.05). In conclusion, these findings suggest that a downregulation in local IGF-1 may be responsible for the loss of skeletal muscle mass following cigarette smoke exposure in mice. Ā© 2013 Hansen et al

    Glucose challenge increases circulating progenitor cells in Asian Indian male subjects with normal glucose tolerance which is compromised in subjects with pre-diabetes: A pilot study

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    <p>Abstract</p> <p>Background</p> <p>Haematopoietic stem cells undergo mobilization from bone marrow to blood in response to physiological stimuli such as ischemia and tissue injury. The aim of study was to determine the kinetics of circulating CD34<sup>+ </sup>and CD133<sup>+</sup>CD34<sup>+ </sup>progenitor cells in response to 75 g glucose load in subjects with normal and impaired glucose metabolism.</p> <p>Methods</p> <p>Asian Indian male subjects (n = 50) with no prior history of glucose imbalance were subjected to 2 hour oral glucose tolerance test (OGTT). 24 subjects had normal glucose tolerance (NGT), 17 subjects had impaired glucose tolerance (IGT) and 9 had impaired fasting glucose (IFG). The IGT and IFG subjects were grouped together as pre-diabetes group (n = 26). Progenitor cell counts in peripheral circulation at fasting and 2 hour post glucose challenge were measured using direct two-color flow cytometry.</p> <p>Results</p> <p>The pre-diabetes group was more insulin resistant (p < 0.0001) as measured by homeostasis assessment model (HOMA-IR) compared to NGT group. A 2.5-fold increase in CD34<sup>+ </sup>cells (p = 0.003) and CD133<sup>+</sup>CD34<sup>+ </sup>(p = 0.019) cells was seen 2 hours post glucose challenge in the NGT group. This increase for both the cell types was attenuated in subjects with IGT. CD34<sup>+ </sup>cell counts in response to glucose challenge inversely correlated with neutrophil counts (Ļ = -0.330, p = 0.019), while post load counts of CD133<sup>+</sup>CD34<sup>+ </sup>cells inversely correlated with serum creatinine (Ļ = -0.312, p = 0.023).</p> <p>Conclusion</p> <p>There is a 2.5-fold increase in the circulating levels of haematopoietic stem cells in response to glucose challenge in healthy Asian Indian male subjects which is attenuated in subjects with pre-diabetes.</p

    Pregnancy is associated with elevation of liver enzymes in HIV-positive women on antiretroviral therapy.

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    The objective of this study is to assess whether pregnancy is associated with an increased risk of liver enzyme elevation (LEE) and severe LEE in HIV-positive women on antiretroviral therapy (ART)

    Prediction of the Caspian Sea level using ECMWF seasonal forecasts and reanalysis

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    This article is made available through the Brunel Open Access Publishing Fund. This article is distributed under the terms of the Creative Commons Attribution License which permits any use, distribution, and reproduction in any medium, provided the original author(s) and the source are credited.The hydrological budget of the Caspian Sea (CS) is investigated using the European Centre for Medium-Range Weather Forecasts interim reanalysis (ERAi) and seasonal forecast (FCST) data with the aim of predicting the Caspian Sea Level (CSL) some months ahead. Precipitation and evaporation are used. After precipitation events over the Volga River, the discharge (Volga River discharge (VRD)) follows with delays, which are parameterized. The components of the water budget from ERAi and FCSTs are integrated to obtain time series of the CSL. Observations of the CSL and the VRD are used for comparison and tuning. The quality of ERAi data is sufficiently good to calculate the time variability of the CSL with a satisfactory accuracy. Already the storage of water within the Volga Basin allows forecasts of the CSL a few months ahead, and using the FCSTs of precipitation improves the CSL forecasts. The evaporation in the seasonal forecasts is deficient due to unrealistic sea surface temperatures over the CS. Impacts of different water budget terms on the CSL variability are shown by a variety of validation tools. The importance of precipitation anomalies over the catchment of the Volga River is confirmed, but also impacts from the two southern rivers (Sefidrud and Kura River) and the evaporation over the CS become obvious for some periods. When pushing the FCSTs beyond the limits of the seasonal FCSTs to 1 year, considerable forecast skill can still be found. Validating only FCSTs by the present approach, which show the same trend as one based on a statistical method, significantly enhances the skill scores

    Electroacupuncture enhances spermatogenesis in rats after scrotal heat treatment

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    Spermatogenesis is regulated by a cascade of steroid regulated genes in the testis. Recent studies suggested that acupuncture may improve fertility in men with abnormal semen parameters. Yet, the underlying mechanisms in which acupuncture enhances spermatogenesis remain largely unknown. Here we used a scrotal heat-treated rat model to study the effect of electroacupuncture (EA) on recovery of spermatogenesis. In this model, spermatogenesis was disrupted by 30 min scrotal heat treatment at 43Ā°C. Ten sessions of EA were given at Baihui (GV20), Guanyuan (CV4), Zusanli (ST36) and Sanyinjiao (SP6) from day 9 to day 36 post-treatment. Sperm motility and production, morphology of the germinal epithelium by Johnsenā€™s scoring, germ cell apoptosis by TUNEL staining, proliferation by proliferating cell nuclear antigen (PCNA) staining, as well as serum testosterone and inhibin B levels by immunoassays were evaluated on day 0, 1, 9, 25, 37, 46, 56 and 79. When compared with the heat-treated (H) group, the heat-treated plus EA (H+EA) group showed a significant increase (p < 0.05) in PCNA-positive cells and inhibin B levels on days 37 and 46, and a higher Johnsenā€™s score till day 56. On day 79, motile spermatozoa could be found in the vas deferens of H+EA group only. Consistently, there was a trend of improved motility and increased number of motile epididymal spermatozoa in the H+EA group than the H group; while apoptosis of germ cells and serum testosterone levels were similar between the two groups. Taken together, EA enhanced germ cell proliferation through improvement of Sertoli cell functions. This may facilitate the recovery of spermatogenesis and may restore normal semen parameters in subfertile patients

    Key indicators to track current progress and future ambition of the Paris Agreement

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    Current emission pledges to the Paris Agreement appear insufficient to hold the global average temperature increase to well below 2 Ā°C above pre-industrial levels. Yet, details are missing on how to track progress towards the Ć¢ ā‚¬ Paris goal', inform the five-yearly Ć¢ ā‚¬ global stocktake', and increase the ambition of Nationally Determined Contributions (NDCs). We develop a nested structure of key indicators to track progress through time. Global emissions track aggregated progress, country-level decompositions track emerging trends that link directly to NDCs, and technology diffusion indicates future reductions. We find the recent slowdown in global emissions growth is due to reduced growth in coal use since 2011, primarily in China and secondarily in the United States. The slowdown is projected to continue in 2016, with global CO 2 emissions from fossil fuels and industry similar to the 2015 level of 36 GtCO 2. Explosive and policy-driven growth in wind and solar has contributed to the global emissions slowdown, but has been less important than economic factors and energy efficiency. We show that many key indicators are currently broadly consistent with emission scenarios that keep temperatures below 2 Ā°C, but the continued lack of large-scale carbon capture and storage threatens 2030 targets and the longer-term Paris ambition of net-zero emissions

    An Exactly Solvable Model for the Integrability-Chaos Transition in Rough Quantum Billiards

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    A central question of dynamics, largely open in the quantum case, is to what extent it erases a system's memory of its initial properties. Here we present a simple statistically solvable quantum model describing this memory loss across an integrability-chaos transition under a perturbation obeying no selection rules. From the perspective of quantum localization-delocalization on the lattice of quantum numbers, we are dealing with a situation where every lattice site is coupled to every other site with the same strength, on average. The model also rigorously justifies a similar set of relationships recently proposed in the context of two short-range-interacting ultracold atoms in a harmonic waveguide. Application of our model to an ensemble of uncorrelated impurities on a rectangular lattice gives good agreement with ab initio numerics.Comment: 29 pages, 5 figure
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