Estimations of changes of the Sun's mass and the gravitation constant from the modern observations of planets and spacecraft

More than 635 000 positional observations (mostly radiotechnical) of planets and spacecraft (1961-2010), have been used for estimating possible changes of the gravitation constant, the solar mass, and semi-major axes of planets, as well as the value of the astronomical unit, related to them. The analysis of the observations has been performed on the basis of the EPM2010 ephemerides of IAA RAS in post-newtonian approximation. The obtained results indicate on decrease in the heliocentric gravitation constant per year at the level $\dot {GM_{Sun}}/GM_{Sun} = (-5.0 \pm 4.1) 10^{-14} (3\sigma).$ The positive secular changes of semi-major axes $\dot a_i/a_i$ have been obtained simultaneously for the planets Mercury, Venus, Mars, Jupiter, Saturn, as expected if the geliocentric gravitation constant is decreasing in century wise. The change of the mass of the Sun $M_{Sun}$ due to the solar radiation and the solar wind and the matter dropping on the Sun (comets, meteors, asteroids and dust) was estimated. Taking into account the maximal limits of the possible $M_{Sun}$ change, the value $\dot G/G$ falls within the interval $-4.2\cdot10^{-14} < \dot G/G < +7.5\cdot10^{-14}$ in year with the 95% probability. The astronomical unit (au) is only connected with the geliocentric gravitation constant by its definition. In the future, the connection between $GM_{Sun}$ and au should be fixed at the certain time moment, as it is inconvenient highly to have the changing value of the astronomical unit.Comment: 20 pages, 4 tables, accepted for publication in Solar System Research, 2011 (Astronomicheskii vestnik

Application of Time Transfer Function to McVittie Spacetime: Gravitational Time Delay and Secular Increase in Astronomical Unit

We attempt to calculate the gravitational time delay in a time-dependent gravitational field, especially in McVittie spacetime, which can be considered as the spacetime around a gravitating body such as the Sun, embedded in the FLRW (Friedmann-Lema\^itre-Robertson-Walker) cosmological background metric. To this end, we adopt the time transfer function method proposed by Le Poncin-Lafitte {\it et al.} (Class. Quant. Grav. 21:4463, 2004) and Teyssandier and Le Poncin-Lafitte (Class. Quant. Grav. 25:145020, 2008), which is originally related to Synge's world function $\Omega(x_A, x_B)$ and enables to circumvent the integration of the null geodesic equation. We re-examine the global cosmological effect on light propagation in the solar system. The round-trip time of a light ray/signal is given by the functions of not only the spacial coordinates but also the emission time or reception time of light ray/signal, which characterize the time-dependency of solutions. We also apply the obtained results to the secular increase in the astronomical unit, reported by Krasinsky and Brumberg (Celest. Mech. Dyn. Astron. 90:267, 2004), and we show that the leading order terms of the time-dependent component due to cosmological expansion is 9 orders of magnitude smaller than the observed value of $d{\rm AU}/dt$, i.e., $15 \pm 4$ ~[m/century]. Therefore, it is not possible to explain the secular increase in the astronomical unit in terms of cosmological expansion.Comment: 13 pages, 2 figures, accepted for publication in General Relativity and Gravitatio

Biosorption of zinc(II) ions from aqueous solution using msasa tree (brachystegia spiciformis) leaf powder

The purpose of this study was to explore the effectiveness of the Brachystegia spiciformis leaf powder for the removal of zinc (II) ions from aqueous solution. Batch experiments for the effect of pH, contact time, biomass dose and initial metal ion concentration were carried out in the laboratory. The adsorbent was characterized before and after biosorption of zinc ions by Fourier Transform-Infrared Spectroscopy (FT-IR). The investigation showed that the highest metal uptake was at solution pH 6, contact time of 120 mins and biomass dose of 2.0 g. The experimental data for the biosorption zinc (II) ions by Brachystegia spiciformis leaf powder was modelled to the Langmuir and Freundlich isotherms. The biosorption of zinc (II) ions fits better to the Langmuir than to the Freundlich model having correlation coefficients of 0.9902 and 0.9569 respectively. The maximum adsorption capacity Qmax was found to be 1.85 mg/g indicating the ability of the biosorbent to remove zinc from aqueous solution

Elevated T-helper 2 cytokine levels in high fat diet-fed C57BL/6 mice are attenuated by short-term 6-week treatment with a combination of low-dose aspirin and metformin

Objective: To evaluate T-helper cytokine responses in a short-term high fat diet (HFD) induced impaired glucose metabolism. To further evaluate the modulation of T-helper 1 (Th1) and T-helper 2 (Th2) cytokines using short-term low-dose aspirin in combination with metformin. Design: Two experiments were carried out in this study in order to evaluate the T-helper cytokine profiles in a state of impaired glucose metabolism. A total of 28 six-week-old male C57BL/6 mice were used in this study. In the first experiment, mice were fed either a high fat diet or low fat diet for a duration of 10 weeks. We then determined the Th1, Th2 and T-helper 17 (Th17) cytokine profiles. In the second experiment, we evaluated whether the short term 6-week treatment with low-dose aspirin in combination with metformin modulates T-helper cytokine profiles of the HFD-fed mice. Measurements: In the first experiment, we measured the body weights, blood glucose levels, insulin levels, lipid profiles and haematological parameters. We further performed oral glucose tolerance testing following an 8-hour fast and serum Th1, Th2 and Th17 cytokine levels were also determined following short-term 8-week diet-feeding and 6-week low-dose aspirin and combined metformin with low-dose aspirin treatment. Results: High fat diet-feeding caused a marked increase in circulating peripheral blood lymphocytes, which was attenuated by short-term low-dose aspirin treatment. Moreover, the HFD feeding resulted in 2-fold increase in total cholesterol and a 4-fold increase in low-density lipoprotein cholesterol when compared to the low-fat diet-fed group (p 0.05). While the combination of low-dose aspirin with metformin considerably reduced the levels of serum IFN-Ƴ (P < 0.05). Furthermore low-dose aspirin treatment showed the modest attenuation of the selected Th2 cytokines, IL-10 and IL-13 when compared to low-dose aspirin with metformin (P < 0.01). Conclusion: The early immunological and metabolic changes that occur in a state impaired glucose tolerance are accompanied by the increased production of Th2 cell cytokines. The short-term treatment using low-dose aspirin combined with metformin may provide therapeutic benefits in preventing complications associated with dysregulated Th2 cell responses

The impact of metformin and aspirin on T-cell mediated inflammation: A systematic review of in vitro and in vivo findings

Chronic inflammation and hyperglycaemia are well-established aspects in the pathogenesis of type 2 diabetes mellitus (T2D), including the progression of its associated complications such as cardiovascular diseases (CVDs). In fact, emerging evidence shows that dysfunctional immune responses due to dysregulated T-cell function aggravates CVD-related complications in T2D. However, there is a lack of specific therapeutic interventions that protect patients with diabetes who are at risk of heart failure. Metformin and aspirin are among the leading therapies being used to protect or at the very least slow the progression of CVD-related complications. The current review made use of major electronic databases to identify and systematically synthesise emerging experimental data on the impact of these pharmacological drugs on T-cell responses. The quality and risk of bias of include evidence were independently assessed by two reviewers. Overwhelming evidence showed that both metformin and aspirin can ameliorate T-cell mediated inflammation by inducing regulatory T-cells (Tregs) polarisation, inhibiting T-cell trafficking and activation as well as signal transducer and activator of transcription (STAT)3 signalling. As a plausible mechanism to mediate T-cell function, metformin showed enhanced potential to regulate mechanistic targets of rapamycin (mTOR), STAT5 and adenosine-monophosphate-activated protein kinase (AMPK) signalling pathways. Whilst aspirin modulated nuclear factor kappa-light-chain-enhancer of activated B-cells (NF-kB) and co-stimulatory signalling pathways and induced T-cell anergy. Overall, synthesised data prompt further investigation into the combinational effect of metformin and aspirin for the management of T2D-related cardiovascular complications

A systematic review on the functional role of Th1/Th2 cytokines in type 2 diabetes and related metabolic complications

The T-helper (Th1/Th2) paradigm is widely studied for its role in modulating an adaptive immune response, especially in relation to the onset of various autoimmune diseases. In fact, emerging evidence clearly shows an inverse relationship between Th1/Th2 cytokines and the development of type 2 diabetes (T2D) complications, which is accelerated by an exacerbated inflammatory state. Here, relevant studies reporting on any association between the levels of Th1/Th2 cytokines and the development of T2D were retrieved through major electronic databases such as The Cochrane Library, Embase and PubMed. Extracted evidence which mostly involved animal models and human subjects with T2D or metabolic syndrome was assessed for quality and risk of bias using the Downs and Black checklist and Animal Research: Reporting of In Vivo Experiments (ARRIVE) guidelines. Results strongly correlated raised Th1/Th2 cytokines such as interferon-gamma (IFN-γ)/interleukin (IL)-5 and IL-2/IL-5 ratios to T2D, and this was positively linked with the other complications including retinopathy and cardiovascular complications. Further, logistic regression analysis demonstrated that the Th1/Th2 ratios were significantly associated with impaired glucose homeostasis, abnormally enhanced lipid profiles, and insulin resistance. Although more studies making use of a larger sample size are required, current data suggest that optimal modulation of Th1/Th2 cytokines may be an important aspect in the management of T2D and its associated complications

Curcumin supplementation improves biomarkers of oxidative stress and inflammation in conditions of obesity, type 2 diabetes and NAFLD: Updating the status of clinical evidence

Oxidative stress and inflammation remain the major complications implicated in the development and progression of metabolic complications, including obesity, type 2 diabetes (T2D) and nonalcoholic fatty liver disease (NAFLD). In fact, due to their abundant antioxidant and anti-inflammatory properties, there is a general interest in understanding the therapeutic effects of some major food-derived bioactive compounds like curcumin against diverse metabolic diseases. Hence, a systematic search, through prominent online databases such as MEDLINE, Scopus, and Google Scholar was done focusing on randomized controlled trials (RCTs) reporting on the impact of curcumin supplementation in individuals with diverse metabolic complications, including obesity, T2D and NAFLD. Summarized findings suggest that curcumin supplementation can significantly reduce blood glucose and triglycerides levels, including markers of liver function like alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in patients with T2D and NAFLD. Importantly, this effect was consistent with the reduction of predominant markers of oxidative stress and inflammation, such as the levels of malonaldehyde (MDA), tumor necrosis factor-alpha (TNF-α), high sensitivity C-reactive protein (hs-CRP) and monocyte chemoattractant protein-1 (MCP-1) in these patients. Although RCTs suggest that curcumin is beneficial in ameliorating some metabolic complications, future research is still necessary to enhance its absorption and bioavailability profile, while also optimizing the most effective therapeutic doses

Drug-Induced Liver Injury: Clinical Evidence of N-Acetyl Cysteine Protective Effects

Oxidative stress is a key pathological feature implicated in both acute and chronic liver diseases, including drug-induced liver injury (DILI). The latter describes hepatic injury arising as a direct toxic effect of administered drugs or their metabolites. Although still underreported, DILI remains a significant cause of liver failure, especially in developed nations. Currently, it is understood that mitochondrial-generated oxidative stress and abnormalities in phase I/II metabolism, leading to glutathione (GSH) suppression, drive the onset of DILI. N-Acetyl cysteine (NAC) has attracted a lot of interest as a therapeutic agent against DILI because of its strong antioxidant properties, especially in relation to enhancing endogenous GSH content to counteract oxidative stress. Thus, in addition to updating information on the pathophysiological mechanisms implicated in oxidative-induced hepatic injury, the current review critically discusses clinical evidence on the protective effects of NAC against DILI, including the reduction of patient mortality. Besides injury caused by paracetamol, NAC can also improve liver function in relation to other forms of liver injury such as those induced by excessive alcohol intake. The implicated therapeutic mechanisms of NAC extend from enhancing hepatic GSH levels to reducing biomarkers of paracetamol toxicity such as keratin-18 and circulating caspase-cleaved cytokeratin-18. However, there is still lack of evidence confirming the benefits of using NAC in combination with other therapies in patients with DILI

Adipokines as a therapeutic target by metformin to improve metabolic function: A systematic review of randomized controlled trials

Metformin is a widely used glucose-lowering drug, although its impact on adipose tissue function remains elusive. Adipose tissue-derived molecules regulate diverse physiological mechanisms, including energy metabolism, insulin sensitization, and inflammatory response. Alternatively, it has remained relevant to understand the therapeutic regulation of adipokines in efforts to alleviate inflammation in conditions associated with the metabolic syndrome. The current qualitative analysis of available literature focused on randomized clinical trials (RCTs) assessing the association between administration of metformin and adipokine regulation in individuals with metabolic syndrome. The major electronic databases such as MEDLINE, Cochrane Library, Scopus, and EMBASE were searched for eligible RCTs. Overall, 13 RCTs met the inclusion criteria, with a total of 4605 participants. Patients with metabolic syndrome were characterized by a state of obesity, impaired glucose tolerance, insulin resistance, and type 2 diabetes. Cumulative evidence from these RCTs supported the blood glucose lowering effects of metformin, in addition to promoting weight loss, ameliorating insulin resistance, and reducing pro-inflammatory markers such as interleukin-6 and tumor necrosis factor-α in patients with metabolic syndrome. Importantly, these therapeutic effects are associated with the upregulation of adiponectin and suppression of leptin and resistin