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Terrestrial and aquatic ecosystems have specific carbon fingerprints and sequestration potential, due to the intrinsic properties of the organic matter (OM), mineral content, environmental conditions, and microbial community composition and functions. A small variation in the OM pool can imbalance the carbon dynamics that ultimately affect the climate and functionality of each ecosystem, at regional and global scales. Here, we review the factors that continuously contribute to carbon stability and lability, with particular attention to the OM formation and nature, as well as the microbial activities that drive OM aggregation, degradation and eventually greenhouse gas emissions. We identified that in both aquatic and terrestrial ecosystems, microbial attributes (i.e., carbon metabolism, carbon use efficiency, necromass, enzymatic activities) play a pivotal role in transforming the carbon stock and yet they are far from being completely characterised and not often included in carbon estimations. Therefore, future research must focus on the integration of microbial components into carbon mapping and models, as well as on translating molecular-scaled studies into practical approaches. These strategies will improve carbon management and restoration across ecosystems and contribute to overcome current climate challenges., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier B.V. All rights reserved.)

Digitalization provides access to an integrated network of unexploited big data with potential benefits for society and the environment. The development of smart systems connected to the internet of things can generate unique opportunities to strategically address challenges associated with the United Nations Sustainable Development Goals (SDGs) to ensure an equitable, environmentally sustainable, and healthy society. This perspective describes the opportunities that digitalization can provide towards building the sustainable society of the future. Smart technologies are envisioned as game-changing tools, whereby their integration will benefit the three essential elements of the food-water-energy nexus: (i) sustainable food production; (ii) access to clean and safe potable water; and (iii) green energy generation and usage. It then discusses the benefits of digitalization to catalyze the transition towards sustainable manufacturing practices and enhance citizens' health wellbeing by providing digital access to care, particularly for the underserved communities. Finally, the perspective englobes digitalization benefits by providing a holistic view on how it can contribute to address the serious challenges of endangered planet biodiversity and climate change., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2021 Elsevier B.V. All rights reserved.)

Early secretory antigenic target protein (ESAT-6) is an important virulent factor which plays a crucial role in Mycobacterium tuberculosis (MTB) pathogenesis. Here, we demonstrate the role of ESAT-6 in phagocytosis and intracellular survival of mycobacteria through a mechanism mediated by regulation of a host protein; Peroxiredoxin-1 (Prdx-1). Prdx-1 is an anti-apoptotic and stress response protein which protects cells from damage by ROS and H 2 O 2 . The J774 A.1 cells infected with MTB or over-expressing ESAT-6 through eukaryotic promoter vector showed elevated expression of Prdx-1. Further investigation revealed that the up-regulation of Prdx-1 is mediated through the activation of one of the MAP kinases, p38. The NRF-2, a transcriptional activator of Prdx-1 is translocated to the nucleus upon phosphorylation by p38 and subsequently, regulates expression of Prdx-1. Inhibition of the p38 MAPK by a specific inhibitor, SB203580, abrogates the ESAT-6 mediated induction of Prdx-1 expression as well as the phosphorylation of NRF-2 in a time-dependent manner. The inhibition of Prdx-1 expression by specific siRNA in J774 A.1 cells resulted in the reduced bacterial uptake and intracellular survival of the mycobacteria. This is the first report proclaiming that the ESAT-6 regulates Prdx-1 which is involved in the increase of mycobacterial uptake and survival. The intermediate mechanisms involve the increased Prdx-1 production in macrophages through the activation of p38 and NRF-2 dependent signaling., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Remediation and management of organochlorine pesticide (OCPs) contaminated soil is becoming a global priority as they are listed in the Stockholm list of persistent organic pollutants (POPs) for global elimination. Lindane is a OCPs candidate recently included in the Stockholm list. However, India has an exemption to produce lindane for malaria control. Because of its widespread use during the last few decades, lindane contaminated soils are found in almost all parts of India. Since phytoremediation is widely acknowledged as an innovative strategy for the clean-up of contaminated soils; the present study was aimed to evaluate the phytoextraction and dissipation of lindane by a leafy vegetable Spinacia oleracea L (Spinach). The test plant was grown in different concentrations of lindane (5, 10, 15 and 20 mg kg(-1)) and harvested at 10, 30 and 45 days. At 45 days, the concentrations of lindane in root and leaf of Spinach growing in four different concentrations were reached up to 3.5, 5.4, 7.6 and 12.3 mg kg(-1) and 1.8, 2.2, 3 and 4.9 mg kg(-1), respectively. There was a significant difference (p<0.01) in the dissipation of lindane in vegetated and non-vegetated soil. Moreover, the residual lindane in four experiments was reduced to 81, 76, 69 and 61 percent, respectively. The experimental results indicate that Spinach can be used for the phytoremediation of lindane. However, more studies are required to prevent the toxicity of harvested parts., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Objective: The current study sought to investigate the effect of the estrogen metabolite 2-methoxyestradiol (2-MeOHE(2)) on apoptosis, cell proliferation, and collagen synthesis in human and rat leiomyoma cells., Methods: [(3)H] thymidine and [(3)H] proline incorporation studies were conducted. The expression of vascular endothelial growth factor (VEGF), cyclin D1, Bcl-2, and Bax were evaluated by Western blot. Flow cytometry analysis was used to study the effect of 2-MeOHE(2) on apoptosis and the cell cycle., Results: Compared with untreated controls, treatment of rat leiomyoma (ELT3) cells with 2-MeOHE(2) (0.1, 1, 2, 5, or 10 muM) reduced cell proliferation by 17%, 52%, 61%, 73%, and 79%, respectively (P <.05). Similarly, in human uterine leiomyoma cell line (huLM) cells, proliferation was reduced by 4%, 18%, 37%, 41%, and 51%, respectively. 2-MeOHE(2) also caused a concentration-dependent inhibition of collagen synthesis by 4%, 16%, 23%, 51%, and 70%, respectively, in huLM cells (P <.05). Cell cycle analysis indicated that 2-MeOHE(2) treatment (1 to 5 muM) in huLM cells resulted in G(2)/M cell cycle arrest and a 45% increase in apoptosis compared with untreated control (P <.05). Western immunoblotting analysis indicated that 2-MeOHE(2) induces a concentration-dependent reduction in the expression of cyclin D1, Bcl-2, and VEGF proteins in both rat and human leiomyoma cell lines., Conclusions: This study provides the first evidence that 2-MeOHE(2) is a potent antiproliferative/apoptotic and collagen synthesis inhibiting agent in human and rat leiomyoma cells. To the best of our knowledge, this is the first report showing the potential use of 2-methoxyestradiol as a nonsurgical alternative therapy for uterine leiomyomas.

We have developed a gas chromatography/mass spectrometry (GC/MS) assay to measure 17beta-estradiol (E) and its biologically active metabolites 2-hydroxyestradiol (2OHE) and 4-hydroxyestradiol (4OHE), and 2-methoxyestradiol (2MEOE) and 4-methoxyestradiol (4MEOE) in rat plasma. All analytes are well separated and show a linear relationship between concentration (0.25-5 pg/microl) and signal, and coefficients of variation (CVs) are low. Intra-assay CV for the lowest quality control samples (QCs) (0.375 pg/microl) were on average for 17beta-estradiol 20.5%, for 2-hydroxyestradiol 15.6%, for 4-hydroxyestradiol 16.5%, for 2-methoxyestradiol 16.5%, and for 4-methoxyestradiol 11.5%. The inter-assay CVs for the lowest QCs were for 17beta-estradiol 12.1%, for 2-hydroxyestradiol 7.1%, for 4-hydroxyestradiol 15.5%, for 2-methoxyestradiol 16.7%, and for 4-methoxyestradiol 9.7%. The highest sensitivity for this assay was observed for hydroxyestradiols followed by the methoxyestradiols and 17beta-estradiol. In summary, we describe a convenient, sensitive, and specific assay to measure 17beta-estradiol and its biologically active metabolites.

The aim of this prospective cross-over study was to investigate the effect of two low-dosed oral contraceptives on markers of endothelial function and plasma lipids. Twelve healthy, nonsmoking women (mean age: 21.7 years) were recruited from the family planning clinic of the university hospital Zurich. For 6 months the participants received a treatment with two contraceptive pills containing 30 microg ethinyl estradiol/150 microg levonorgestrel (three cycles) and 30 microg ethinyl estradiol/75 microg gestodene (three cycles). Plasma levels of endothelin-1, nitric oxide, cholesterol, and HDL were measurement before and during treatment with both oral contraceptive treatments. No significant changes in the plasma levels of nitric oxide and endothelin-1, both important regulators of the vascular tone, were observed during oral contraceptive use. A significant negative correlation was found between nitric oxide and endothelin-1 and nitric oxide and cholesterol. There was a positive correlation between endothelin-1 and cholesterol. In conclusion, the investigated contraceptive pills did not cause major changes in circulating nitric oxide and endothelin-1 plasma levels.

Estrogen receptors (ERs) are widely held to mediate the ability of 17 beta-estradiol (estradiol) to attenuate injury-induced proliferation of vascular smooth muscle cells (VSMCs) leading to vascular lesions. However, recent findings that estradiol prevents injury-induced vascular lesion formation in knock-out mice lacking either ER alpha or ER beta seriously challenge this concept. Here we report that the local metabolism of estradiol to methoxyestradiols, endogenous metabolites of estradiol with no affinity for ERs, is responsible for the ER-independent inhibitory effects of locally applied estradiol on rat VSMC growth. These finding imply that local vascular estradiol metabolism may be an important determinant of the cardiovascular protective effects of circulating estradiol. Thus, interindividual differences, either genetic or acquired, in the vascular metabolism of estradiol may define a given female's risk of cardiovascular disease and influence the cardiovascular benefit she receives from estradiol replacement therapy in the postmenopausal state. These findings also imply that nonfeminizing estradiol metabolites may confer cardiovascular protection in both women and men., (Copyright 2000 Academic Press.)

A highly selective, sensitive, and fairly rapid and economical differential pulse polarographic (DPP) method has been reported for the determination of trace amounts of vanadium and molybdenum in standard alloys and various environmental samples. The morpholine-4-carbodithioates of these metals were retained (>99% recovery) quantitatively on microcrystalline naphthalene in the pH range 4.5-6.9 for vanadium and 1.5-4.5 for molybdenum. These metals were determined by DPP after desorption with 10 ml of 1 M HCl. Vanadium and molybdenum may also be preconcentrated by passing their aqueous solutions under similar conditions on morpholine-4-dithiocarbamate CTMAB-naphthalene adsorbent packed in a column at a flow rate of 1-5 ml min(-1) and determined similarly. The detection limits are 0.20 ppm for vanadium and 0.04 ppm for molybdenum at minimum instrumental settings (signal to noise ratio=2). The linearity is maintained in the following concentration ranges, vanadium 0.50-10.0 and molybdenum 0.10-9.0 ppm, with a correlation factor of 0.9996 (confidence interval of 95%, slopes 0.0196 and 0.01497 muA mug(-1), intercepts 3.65x10(-3) and -1.92x10(-3) respectively) and relative standard deviation of 1.1% in the microcrystalline method, while in the column method, the linearity is maintained in the concentration ranges, 0.50-6.5 for vanadium and 0.10-5.5 ppm for molybdenum with correlation factor of 0.9994 (with confidence interval of 95%, slopes 0.0194, 0.015 muA mug(-1), intercepts 3.60x10(-3) and -1.90x10(-3) respectively) and relative standard deviation of 1.4%. Various parameters such as the effect of pH, reagent, naphthalene and CTMAB concentrations, volume of aqueous phase and interference of a large number of metal ions on the estimation of vanadium and molybdenum have been studied in detail to optimize the conditions for their voltammetric determination at trace level in various standard alloys and environmental samples.

A highly selective, sensitive and rapid differential pulse polarographic method (DPP) has been developed for the simultaneous estimation of trace amounts of lead and cadmium in standard alloys, biological and environmental samples. The morpholine-4-carbodithioates of the samples were absorbed on microcrystalline naphthalene in the pH range of 5-10 for lead and 3.4-11 for cadmium. The metal complexes were desorbed with 10 ml of 1M HCl and determined simultaneously with a differential pulse polarograph. These metals can alternatively be quantitatively adsorbed on morpholine-4-dithiocarbamate-cetyltrimethylammonium bromide-naphthalene adsorbent packed in a column and determined similarly. The detection limits are 0.14 ppm for Pb and 0.014 ppm for Cd at minimum instrumental settings (signal-to-noise ratio = 2). The linearity is maintained in the concentration ranges of Pb, 0.7-15 ppm and Cd, 0.07-10 ppm with a correlation factor of 0.9997 and relative standard deviations of 0.95 and 0.81%, respectively. Various parameters such as the effect of pH, volume of aqueous phase, and interference of a number of metal ions on the estimation of lead and cadmium have been studied in detail to optimize the conditions for their simultaneous estimation in various biological and environmental samples.

Ovarian dysfunction as well as impaired release of endothelium-derived nitric oxide (NO) is associated with increased incidence of cardiovascular disease in postmenopausal women. Estrogen replacement therapy in postmenopausal women has a cardioprotective effect. Hence, using follicular development (FD) phase of the menstrual cycle of normal women (n = 7) and of patients undergoing in vitro fertilization (n = 16), we tested whether ovarian/sex hormones modulate NO-release. Levels of nitrite/nitrate (stable metabolites of NO), 17 beta-estradiol (E), progesterone (P), follicle-stimulating hormone (FSH) and luteinizing hormone (LH) were measured in serum collected during FD-phase. Serum nitrite/nitrate levels increased (p < .01) with the normal, as well as hormonally-induced FD and correlated with increases in serum E levels (r2 = 0.67; p < .01), but not with P, FSH and LH (p > .05). Post-ovulatory increase in P and LH levels decreased serum nitrite/nitrate levels (p < .05), even in presence of high E levels. In conclusion, nitrite/nitrate increase with follicular development, an effect that is potentially mediated by E induced NO release.

We recently reported that oviduct epithelial cells in culture produce endothelin (ET) and postulated that ET could play an important role in the contraction of the oviduct. In the present study using an organ chamber myograph system, we evaluated the contractile effects of ET-1 on bovine oviduct ampullary-isthmus segments. Additionally, the possibility whether the basal release/synthesis of nitric-oxide (N(O)) and/or prostacyclin modulates the contractile effect of ET-1 was investigated. ET-1 (10(-10) to 10(-7) M) contracted oviduct rings in a concentration dependent manner (P < 0.05). ET-1 (10(-7) M) induced contractions were significantly enhanced in presence of nitric oxide synthase inhibitor N-nitro-L-arginine-methyl-ester (10(-4) M), but remained unaltered in the presence of indomethacin (10(-5) M), an inhibitor for prostacyclin synthesis. In conclusion, ET-1 induced contraction of the oviduct is reduced/modulated by endogenous basal release/synthesis of N(O).