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Root hairs are considered important for rhizosphere formation, which affects root system functioning. Through interactions with soil microorganisms mediated by root exudation, root hairs may affect the phenotypes and growth of young plants. We tested this hypothesis by integrating results from two experiments: (1) a factorial greenhouse seedling experiment with Zea mays B73-wt and its root-hairless mutant, B73-rth3, grown in live and autoclaved soil, quantifying 15 phenotypic traits, seven growth rates, and soil microbiomes and (2) a semi-hydroponic system quantifying root exudation of maize genotypes. Possibly as compensation for lacking root hairs, B73-rth3 seedlings allocated more biomass to roots and grew slower than B73-wt seedlings in live soil, whereas B73-wt seedlings grew slowest in autoclaved soil, suggesting root hairs can be costly and their benefits were realized with more complete soil microbial assemblages. There were substantial differences in root exudation between genotypes and in rhizosphere versus non-rhizosphere microbiomes. The microbial taxa enriched in the presence of root hairs generally enhanced growth compared to taxa enriched in their absence. Our findings suggest the root hairs' adaptive value extends to plant-microbe interactions mediated by root exudates, affecting plant phenotypes, and ultimately, growth.
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Microbiota , Solo , Plântula , Zea mays , Raízes de Plantas , Rizosfera , Microbiologia do SoloRESUMO
Probiotic microorganisms have been used for therapeutic purposes for over a century, and recent advances in biotechnology and genetic engineering have opened up new possibilities for developing therapeutic approaches using indigenous probiotic microorganisms. Diseases are often related to metabolic and immunological factors, which play a critical role in their onset. With the help of advanced genetic tools, probiotics can be modified to produce or secrete important therapeutic peptides directly into mucosal sites, increasing their effectiveness. One potential approach to enhancing human health is through the use of designer probiotics, which possess immunogenic characteristics. These genetically engineered probiotics hold promise in providing novel therapeutic options. In addition to their immunogenic properties, designer probiotics can also be equipped with sensors and genetic circuits, enabling them to detect a range of diseases with remarkable precision. Such capabilities may significantly advance disease diagnosis and management. Furthermore, designer probiotics have the potential to be used in diagnostic applications, offering a less invasive and more cost-effective alternative to conventional diagnostic techniques. This review offers an overview of the different functional aspects of the designer probiotics and their effectiveness on different diseases and also, we have emphasized their limitations and future implications. A comprehensive understanding of these functional attributes may pave the way for new avenues of prevention and the development of effective therapies for a range of diseases.
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Probióticos , Humanos , Probióticos/uso terapêutico , Probióticos/metabolismo , Engenharia Genética , Biotecnologia , Redes Reguladoras de GenesRESUMO
8-Quinolinyl directed N-arylguanidines were subjected to cobalt(II) catalyzed C-H functionalization/1,3-diyne annulation under mild conditions to afford 40 alkynylated indole guanidines in 34% to 92% yields. The scope of the substrates was explored. The reported procedure is mostly regioselective and tolerates various functional groups in the substrates. The regioselectivity of the reactions was assessed with the aid of multinuclear NMR spectroscopy and X-ray crystallography. Competition and labeling experiments were carried out to support the proposed mechanism.
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Platelets are essential component of circulation that plays a major role in hemostasis and thrombosis. During activation and its demise, platelets release platelet-derived microvesicles, with lysophosphatidylcholine (LPC) being a prominent component in their lipid composition. LPC, an oxidized low-density lipoprotein, is involved in cellular metabolism, but its higher level is implicated in pathologies like atherosclerosis, diabetes, and inflammatory disorders. Despite this, its impact on platelet function remains relatively unexplored. To address this, we studied LPC's effects on washed human platelets. A multimode plate reader was employed to measure reactive oxygen species and intracellular calcium using H2DCF-DA and Fluo-4-AM, respectively. Flow cytometry was utilized to measure phosphatidylserine expression, mitochondrial membrane potential (ΔΨm), and mitochondrial permeability transition pore (mPTP) formation using FITC-Annexin V, JC-1, and CoCl2/calcein-AM, respectively. Additionally, platelet morphology and its ultrastructure were observed via phase contrast and electron microscopy. Sonoclot and light transmission aggregometry were employed to examine fibrin formation and platelet aggregation, respectively. The findings demonstrate that LPC induced oxidative stress and increased intracellular calcium in platelets, resulting in increased phosphatidylserine expression and reduced ΔΨm. LPC triggered caspase-independent platelet death and mPTP opening via cytosolic and mitochondrial calcium, along with microvesiculation and reduced platelet counts. LPC increased the platelet's size, adopting a balloon-shaped morphology, causing membrane fragmentation and releasing its cellular contents, while inducing a pro-coagulant phenotype with increased fibrin formation and reduced integrin αIIbß3 activation. Conclusively, this study reveals LPC-induced oxidative stress and calcium-mediated platelet death, necrotic in nature with pro-coagulant properties, potentially impacting inflammation and repair mechanisms during vascular injury.
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Plaquetas , Cálcio , Morte Celular , Lisofosfatidilcolinas , Estresse Oxidativo , Espécies Reativas de Oxigênio , Humanos , Estresse Oxidativo/efeitos dos fármacos , Lisofosfatidilcolinas/farmacologia , Lisofosfatidilcolinas/metabolismo , Cálcio/metabolismo , Plaquetas/metabolismo , Plaquetas/efeitos dos fármacos , Espécies Reativas de Oxigênio/metabolismo , Morte Celular/efeitos dos fármacos , Potencial da Membrana Mitocondrial/efeitos dos fármacos , Mitocôndrias/metabolismo , Mitocôndrias/efeitos dos fármacos , Agregação Plaquetária/efeitos dos fármacos , Poro de Transição de Permeabilidade Mitocondrial/metabolismoRESUMO
Attaching a dipolar molecule in a symmetric system induces a major change in the electronic structure, which may be reflected as the enhancement of the optical and charge-transfer properties of the combined system as compared to the pristine ones. Furthermore, the orientation of the dipolar molecule may also affect the said properties. This idea is explored in this work by taking porphyrinoid molecules as the pristine systems. We attached azulene, a dipolar molecule, at various positions of five porphyrinoid cores and studied the effect on charge-transfer and one- and two-photon absorption properties using the state-of-the-art RICC2 method. The attachment of azulene produces two major effects - firstly it introduces asymmetry in the system and, secondly, being dipolar, it makes the resultant molecule dipolar/quadrupolar. Porphyrin, N-confused porphyrin, sub-porphyrin, sapphyrin, and hexaphyrin are used as core porphyrinoid systems. The change in charge-transfer has been studied using the orbital analysis and charge-transfer distance parameter for the first five singlet states of the systems. The effect of orientation of azulene on the said properties is also explored. The insights gained from our observations are explored further at the dipole and transition dipole moment levels using a three-state model.
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Parkinson's disease (PD) is a predominant neuromotor disorder characterized by the selective death of dopaminergic neurons in the midbrain. The majority of PD cases are sporadic or idiopathic, with environmental toxins and pollutants potentially contributing to its development or exacerbation. However, clinical PD patients are often associated with a reduced stroke frequency, where circulating blood platelets are indispensable. Although platelet structural impairment is evident in PD, the platelet functional alterations and their underlying molecular mechanisms are still obscure. Therefore, we investigated rotenone (ROT), an environmental neurotoxin that selectively destroys dopaminergic neurons mimicking PD, on human blood platelets to explore its impact on platelet functions, thus replicating PD conditions in vitro. Our study deciphered that ROT decreased thrombin-induced platelet functions, including adhesion, activation, secretion, and aggregation in human blood platelets. As ROT is primarily responsible for generating intracellular reactive oxygen species (ROS), and ROS is a key player regulating the platelet functional parameters, we went on to check the effect of ROT on platelet ROS production. In our investigation, it became evident that ROT treatment resulted in the stimulation of ROS production in human blood platelets. Additionally, we discovered that ROT induced ROS production by augmenting Ca2+ mobilization from inositol 1,4,5-trisphosphate receptor. Apart from this, the treatment of ROT triggers protein kinase C associated NADPH oxidase-mediated ROS production in platelets. In summary, this research, for the first time, highlights ROT-induced abnormal platelet functions and may provide a mechanistic insight into the altered platelet activities observed in PD patients.
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Plaquetas , Doença de Parkinson , Espécies Reativas de Oxigênio , Rotenona , Humanos , Rotenona/farmacologia , Plaquetas/metabolismo , Plaquetas/efeitos dos fármacos , Doença de Parkinson/metabolismo , Doença de Parkinson/sangue , Espécies Reativas de Oxigênio/metabolismoRESUMO
BACKGROUND: Infection risk was significant for front-line nurses during the Covid-19 outbreak. The pandemic presented several ethical difficulties and sapped nurses' drive to labor harder for longer periods. This study evaluates registered nurses' perceptions of Covid-19 infection risk, ethical dilemmas, and motivating factors. MATERIALS AND METHODS: During March and April 2022, 400 registered nurses from a newly established tertiary care hospital participated in this cross-sectional exploratory survey. The risk assessment scale, motivation to work scale, and ethical dilemma scale were used to assess the perceived risk of infection, motivational factors and ethical challenges experienced by the nurses. Appropriate descriptive and inferential statistics were applied to compute the results. RESULTS: 76.4% of nurses feared working as a nurse put them at higher risk of infection. Besides the fear of contracting infection, nurses believed they were the source of infection to family members (70.8%) and people around (67.5%). 63.3% of nurses agree that they do not have the right to refuse treatment and every patient has the right to receive optimal care, regardless of age, gender, and medical conditions. Professional obligation to treat patients (72.3%) and sound professional knowledge and experience (83.5%) are important motivating factors to work during the pandemic. Multilinear regression analysis revealed that professional education (95% CI, 3.845 - 0.694, p = 0.005), Covid-19 positive status (95% CI,0.455-2.756, p = 0.006), and post-Covid-19 hospitalization (95% CI, 1.395-6.978, p = 0.003) and duration of hospitalization (95% CI, 0.754-0.058, p = 0.022) are independent predictors of higher perceived risk of infection among nurses. CONCLUSIONS: During the pandemic, nurses were afraid to work and faced personal and family risks of contracting the virus. Despite these challenges, they still feel a strong sense of commitment and dedication to providing the best possible care. Nurse administrators need to create a supportive environment that follows ethical principles and meets the needs of nurses to boost their motivation and encourage them to continue working for longer periods.
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The blood platelet plays an important role but often remains under-recognized in several vascular complications and associated diseases. Surprisingly, platelet hyperactivity and hyperaggregability have often been considered the critical risk factors for developing vascular dysfunctions in several neurodegenerative diseases (NDDs) like Alzheimer's disease, Parkinson's disease, Huntington's disease, and multiple sclerosis. In addition, platelet structural and functional impairments promote prothrombotic and proinflammatory environment that can aggravate the progression of several NDDs. These findings provide the rationale for using antiplatelet agents not only to prevent morbidity but also to reduce mortality caused by NDDs. Therefore, we thoroughly review the evidence supporting the potential pleiotropic effects of several novel classes of synthetic antiplatelet drugs, that is, cyclooxygenase inhibitors, adenosine diphosphate receptor antagonists, protease-activated receptor blockers, and glycoprotein IIb/IIIa receptor inhibitors in NDDs. Apart from this, the review also emphasizes the recent developments of selected natural antiplatelet phytochemicals belonging to key classes of plant-based bioactive compounds, including polyphenols, alkaloids, terpenoids, and flavonoids as potential therapeutic candidates in NDDs. We believe that the broad analysis of contemporary strategies and specific approaches for plausible therapeutic treatment for NDDs presented in this review could be helpful for further successful research in this area.
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Doença de Alzheimer , Doença de Huntington , Doenças Neurodegenerativas , Doença de Parkinson , Humanos , Doenças Neurodegenerativas/tratamento farmacológico , Inibidores da Agregação Plaquetária/farmacologia , Inibidores da Agregação Plaquetária/uso terapêuticoRESUMO
The unobtrusive cold environmental temperature can be linked to the development of cancer. This study, for the first time, envisaged cold stress-mediated induction of a zinc finger protein 726 (ZNF726) in breast cancer. However, the role of ZNF726 in tumorigenesis has not been defined. This study investigated the putative role of ZNF726 in breast cancer tumorigenic potency. Gene expression analysis using multifactorial cancer databases predicted overexpression of ZNF726 in various cancers, including breast cancer. Experimental observations found that malignant breast tissues and highly aggressive MDA-MB-231 cells showed an elevated ZNF726 expression as compared to benign and luminal A type (MCF-7), respectively. Furthermore, ZNF726 silencing decreased breast cancer cell proliferation, epithelial-mesenchymal transition, and invasion accompanied by the inhibition of colony-forming ability. Concordantly, ZNF726 overexpression significantly demonstrated opposite outcomes than ZNF726 knockdown. Taken together, our findings propose cold-inducible ZNF726 as a functional oncogene demonstrating its prominent role in facilitating breast tumorigenesis. An inverse correlation between environmental temperature and total serum cholesterol was observed in the previous study. Furthermore, experimental outcomes illustrate that cold stress elevated cholesterol content hinting at the involvement of the cholesterol regulatory pathway in cold-induced ZNF726 gene regulation. This observation was bolstered by a positive correlation between the expression of cholesterol-regulatory genes and ZNF726. Exogenous cholesterol treatment elevated ZNF726 transcript levels while knockdown of ZNF726 decreased the cholesterol content via downregulating various cholesterol regulatory gene expressions (e.g., SREBF1/2, HMGCoR, LDLR). Moreover, an underlying mechanism supporting cold-driven tumorigenesis is proposed through interdependent regulation of cholesterol regulatory pathway and cold-inducible ZNF726 expression.
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Neoplasias da Mama , Humanos , Feminino , Neoplasias da Mama/metabolismo , Linhagem Celular Tumoral , Carcinogênese/genética , Colesterol/metabolismo , Dedos de Zinco , Transição Epitelial-Mesenquimal/genética , Movimento Celular , Regulação Neoplásica da Expressão Gênica , Proliferação de Células/genética , Células MCF-7RESUMO
Entamoeba histolytica causes amoebiasis which is a major health concern in developing countries. E. histolytica pathogenicity has been implicated to a large repertoire of small GTPases which switch between the inactive GDP bound state and the active GTP bound state with the help of guanine nucleotide exchange factors (GEFs) and GTPase activating protein (GAPs). Rho family of small GTPases are well known to modulate the actin cytoskeletal dynamics which plays a major role in E. histolytica pathogenicity. Here, we report an atypical amoebic RhoGEF, and its preferred substrate EhRho6, which, upon overexpression abrogated the pathogenic behavior of the amoeba such as adhesion to host cell, monolayer destruction, erythrophagocytosis, and formation of actin dots. A causative immunoblot analysis revealed actin degradation in the EhRho6 overexpressing trophozoites that could be inhibited by blocking the amoebic proteasomal pathway. A careful analysis of the results from a previously published transcriptomics study, in conjunction with our observations, led to the identification of a clade of Rho GTPases in this pathogenic amoeba which we hypothesize to have implications during the amoebic encystation.
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Amoeba , Entamoeba histolytica , Proteínas Monoméricas de Ligação ao GTP , Actinas/metabolismo , Animais , Entamoeba histolytica/metabolismo , Proteínas Monoméricas de Ligação ao GTP/metabolismo , Trofozoítos/metabolismo , VirulênciaRESUMO
Neighboring adipocytes of tumor cells/cancer associated adipocytes supply many factors and fatty acids as fuel to cancer cells for inducing cancer progression and development. Epithelial breast cancer cells also differentiate into several cell types to meet various demands. This study reports that breast cancer cells exhibit inherent adipocyte-like property which is further enhanced in presence of BMP2. Antidiabetic metformin inhibits BMP2 induced adipocyte-like potential in breast cancer cells. Interestingly, breast cancer cells not only show lipid accumulation but also have ability to release lipid content. Thus, this study centers around the presence of the adipocyte cell-like property in breast cancer cells, the significance of BMP2 and metformin that may be explored in designing therapeutics against breast cancer.
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Neoplasias da Mama , Metformina , Humanos , Feminino , Neoplasias da Mama/patologia , Metformina/farmacologia , Ácidos Graxos/metabolismo , Adipócitos/metabolismo , Proteína Morfogenética Óssea 2/metabolismoRESUMO
Platelet-derived microvesicles (PMVs) are the most abundant microvesicles in circulation, originating from blood platelets via membrane blebbing. PMVs act as biological cargo carrying key molecules from platelets, including immunomodulatory molecules, growth factors, clotting molecules, and miRNAs that can regulate recipient cellular functions. Formation and release of PMVs play an essential role in the pathophysiology of vascular diseases such as hemostasis, inflammation, and thrombosis. Platelet activation is considered the critical event in thrombosis, and a growing number of evidence suggests that oxidative stress-mediated signaling plays a significant role in platelet activation. Ca2+ is a notable player in the generation of ROS in platelets. Reports have established that microvesicles exhibit dual nature in redox mechanisms as they possess both pro-oxidant and antioxidant machinery. However, the impact of PMVs and their ROS machinery on platelets is still a limited explored area. Here, we have demonstrated that PMVs mediate platelet activation via intracellular ROS generation. PMVs interacted with platelets and induced calcium-mediated intracellular ROS production via NADPH oxidase (NOX), leading to platelet activation. Our findings will open up new insights into the tangible relationship of PMVs with platelets and will further contribute to the therapeutic aspects of PMVs in vascular injury and tissue remodeling.
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Plaquetas , Trombose , Humanos , Plaquetas/metabolismo , Espécies Reativas de Oxigênio/metabolismo , Cálcio/metabolismo , Ativação Plaquetária , Trombose/metabolismoRESUMO
It is a public health imperative to have safe food and water across the population. Foodborne infections are one of the primary causes of sickness and mortality in both developed and developing countries. An estimated 100 million foodborne diseases and 120 000 foodborne illness-related fatalities occur each year in India. Several factors affect foodborne illness, such as improper farming methods, poor sanitary and hygienic conditions at all levels of the food supply chain, the lack of preventative measures in the food processing industry, the misuse of food additives, as well as improper storage and handling. In addition, chemical and microbiological combinations also play a key role in disease development. But recent disease outbreaks indicated that microbial pathogens played a major role in the development of foodborne diseases. Therefore, prompt, rapid, and accurate detection of high-risk food pathogens is extremely vital to warrant the safety of the food items. Conventional approaches for identifying foodborne pathogens are labor-intensive and cumbersome. As a result, a range of technologies for the rapid detection of foodborne bacterial pathogens have been developed. Presently, many methods are available for the instantaneous detection, identification, and monitoring of foodborne pathogens, such as nucleic acid-based methods, biosensor-based methods, and immunological-based methods. The goal of this review is to provide a complete evaluation of several existing and emerging strategies for detecting food-borne pathogens. Furthermore, this review outlines innovative methodologies and their uses in food testing, along with their existing limits and future possibilities in the detection of live pathogens in food.
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Ulcerative colitis (UC) is an idiopathic, chronic and relapsing colonic inflammatory disease. Despite the involvement of diverse intricate mechanisms, COX mediated inflammatory pathway is crucial in the pathophysiology of colitis. Thus, COX inhibition is imperative for managing colitis-associated inflammation. However, the use of COX inhibitory classical non-steroidal anti-inflammatory drugs (NSAIDs) for inflammation resolution has been linked to sudden increased flare-ups. Therefore, considering the anti-inflammatory and pro-resolution effects of antioxidant and essential trace element Selenium (Se), a Seleno-derivative of Celecoxib called Selenocoxib-3 was characterized and evaluated for its favourable pharmacokinetics, safety margins and anti-inflammatory therapeutic potential in DSS-induced experimental colitis. The serum pharmacokinetic profiling [elimination rate constant (K) and clearance (Cl) and toxicity profiling suggested enhanced efficacy, therapeutic potential and lesser toxicity of Selenocoxib-3 as compared to its parent NSAID Celecoxib. In vivo studies demonstrated that Selenocoxib-3 efficiently resolves the gross morphological signs of DSS-induced colitis such as diarrhoea, bloody stools, weight loss and colon shortening. Further, intestinal damage evaluated by H & E staining and MPO activity suggested of histopathological disruptions, such as neutrophil infiltration, mucodepletion and cryptitis, by Selenocoxib-3. The expression profiles of COX-1/2 demonstrated mitigation of pro-inflammatory mediators thereby promoting anti-inflammatory efficacy of Selenocoxib-3 when compared with Celecoxib. The current study suggests translational applicability of Se-containing novel class of COX inhibitors for efficiently managing inflammatory disorders such as UC.
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Colite Ulcerativa , Colite , Animais , Celecoxib/efeitos adversos , Anti-Inflamatórios/farmacologia , Colite/metabolismo , Colite Ulcerativa/induzido quimicamente , Colite Ulcerativa/tratamento farmacológico , Colite Ulcerativa/patologia , Anti-Inflamatórios não Esteroides/farmacologia , Colo , Inflamação/metabolismo , Ciclo-Oxigenase 2/metabolismo , Sulfato de Dextrana/farmacologia , Modelos Animais de DoençasRESUMO
Platelet-derived microvesicles (PMVs) represent a significant proportion of microvesicles in circulation and have been linked to various pathophysiological complications. Recent research suggests that PMVs carry significant amounts of cargo that can affect cellular functions by influencing calcium oscillations in target cells. As calcium is involved in multiple cellular processes, including hemostasis and thrombosis, this study aimed to investigate the impact of PMVs on platelet calcium mobilization. The study found that PMVs increase platelet intracellular calcium levels via both intracellular storage and extracellular space in a dose-dependent manner. The study highlighted the critical role of the dense tubular system, acidic vacuoles, mitochondrial stores, and store-operated calcium entry (SOCE) in PMV-mediated calcium release in human platelets. Moreover, the study revealed that PMV-induced calcium rise in platelets does not occur via sarcoendoplasmic reticulum calcium ATPase, and extracellular calcium addition further increases the calcium level in platelets, demonstrating the involvement of SOCE. These findings provide insights into the platelet stimulation signaling mechanisms and contributes to our understanding of platelet and cell behavior when exposed to PMV-rich environments.
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Plaquetas , Cálcio , Humanos , Cálcio/metabolismo , Plaquetas/metabolismo , Sinalização do CálcioRESUMO
Groundwater uranium (U) concentrations have been measured above the U.S. EPA maximum contaminant level (30 µg/L) in many U.S. aquifers, including in areas not associated with anthropogenic contamination by milling or mining. In addition to carbonate, nitrate has been correlated to uranium groundwater concentrations in two major U.S. aquifers. However, to date, direct evidence that nitrate mobilizes naturally occurring U from aquifer sediments has not been presented. Here, we demonstrate that the influx of high-nitrate porewater through High Plains alluvial aquifer silt sediments bearing naturally occurring U(IV) can stimulate a nitrate-reducing microbial community capable of catalyzing the oxidation and mobilization of U into the porewater. Microbial reduction of nitrate yielded nitrite, a reactive intermediate, which was further demonstrated to abiotically mobilize U from the reduced alluvial aquifer sediments. These results indicate that microbial activity, specifically nitrate reduction to nitrite, is one mechanism driving U mobilization from aquifer sediments in addition to previously described bicarbonate-driven desorption from mineral surfaces, such as Fe(III) oxides.
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Água Subterrânea , Urânio , Poluentes Radioativos da Água , Nitratos , Compostos Férricos , Nitritos , Sedimentos Geológicos , Poluentes Radioativos da Água/análiseRESUMO
Environmental bacterial isolates play a very important role in bioremediation of metals and toxic metalloids. A bacterial strain with high selenite (SeO32-) tolerance and reducing capability was isolated from electronic waste dump site in Banaras Hindu University, Varanasi, India. Based on 16 S rRNA sequencing and BLAST search, this bacterial isolate was identified as Bacillus paramycoides and designated as strain MF-14. It tolerated Sodium selenite up to 110 mM when grown aerobically in LB broth and reduced selenite into elemental selenium (Se0) significantly within 24 h with concomitant biosynthesis of selenium nanoparticles as clearly revealed by brick red precipitate and specific surface plasmon resonance peak at 210 nm using UV-Visible spectrophotometer. Scanning electron microscopy (SEM) analysis of this bacterial strain exposed to 1mM and 5 mM selenite also demonstrated morphological alterations as cell enlargement due to accumulation and bioprecipitation of elemental selenium (Se0). The FTIR analysis clearly demonstrated that functional groups present on the surface of biogenic selenium nanoparticles (SeNPs) play a significant role in the stabilization and capping of SeNPs. Furthermore, these SeNPs were characterized using spectroscopic analysis involving Dynamic light scattering, zeta potential, XPS, FTIR, XRD and Raman spectroscopy which clearly revealed particle size 10-700 nm, amorphous nature, stability as well as it's oxidation state. The biochemical studies have demonstrated that membrane bound reductase enzyme may be responsible for significant reduction of selenite into elemental selenium. Therefore, we may employ Bacillus paramycoides strain MF-14 successfully for bioremediation of selenite contaminated environmental sites with concomitant green synthesis of SeNPs.
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Nanopartículas , Selênio , Humanos , Selênio/metabolismo , Ácido Selenioso/metabolismo , Sideróforos , Nanopartículas/químicaRESUMO
In spite of recent advances made in understanding its progression, cancer is still a leading cause of death across the nations. Molecular pathophysiology of these cancer cells largely differs depending on cancer types and even within the same tumor. Pathological mineralization/calcification is seen in various tissues including breast, prostate, and lung cancer. Osteoblast-like cells derived after trans-differentiation of mesenchymal cells usually drive calcium deposition in various tissues. This study aims to explore the presence of osteoblast-like potential in lung cancer cells and its prevention. ALP assay, ALP staining, nodule formation, RT-PCR, RT-qPCR, and western blot analysis experiments were carried out in lung cancer A549 cells to achieve said objective. Expressions of various osteoblast markers (e.g., ALP, OPN, RUNX2, and Osterix) along with osteoinducer genes (BMP-2 and BMP-4) were observed in A549 cells. Moreover, ALP activity and ability leading to nodule formation revealed the presence of osteoblast-like potential in lung cancer cells. Here, BMP-2 treatment increased expressions of osteoblast transcription factors such as RUNX2 and Osterix, enhanced ALP activity, and augmented calcification in this cell line. It was also observed that antidiabetic metformin inhibited BMP-2 mediated increase in osteoblast-like potential and calcification in these cancer cells. The current study noted that metformin blocked BMP-2 mediated increase in epithelial to mesenchymal transition (EMT) in A549 cells. The above findings for the first time unravel that A549 cells possess osteoblast-like potential which drives lung cancer calcification. Metformin might prevent BMP-2 induced osteoblast-like phenotype of the lung cancer cells with concomitant inhibition of EMT to inhibit lung cancer tissue calcification.
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Neoplasias Pulmonares , Metformina , Masculino , Humanos , Subunidade alfa 1 de Fator de Ligação ao Core/genética , Subunidade alfa 1 de Fator de Ligação ao Core/metabolismo , Neoplasias Pulmonares/metabolismo , Transição Epitelial-Mesenquimal , Metformina/farmacologia , Células A549 , Diferenciação Celular , Osteoblastos/metabolismo , OsteogêneseRESUMO
This study aimed to isolate and characterize probiotic Lactobacilli from human faecal samples of Jammu region of India and evaluation of their antioxidative properties. A total of 29 Lactobacillus strains were isolated and tested for their ability to withstand different pH levels, high concentrations of bile salt and lysozyme along with their adhesion ability to different hydrocarbons and auto-aggregation. Selected probiotic Lactobacillus isolates were further examined for their antioxidant potential using ABTS, DPPH methods, and the ability to scavenge superoxide and hydroxyl radicals. The results showed that Lactobacillus LpJ1 (7.93 ± 0.23) and LpJ5 (7.93 ± 0.59) had the highest cell viability at a pH of 2.5, while Lactobacillus LpJ16 (7.91 ± 0.48) had the highest resistance to bile salts. Many of the isolates also demonstrated good tolerance to lysozyme. The adhesion abilities of these isolates were characterized by cell surface hydrophobicity and auto aggregation which ranged between 50.32% to 77.8% and 51.02% to 78.95% respectively. In addition, Lactobacillus LpJ5 and LpJ8 showed excellent antioxidant activity. Based on these findings, the selected probiotic strains could be potential candidates for use in functional food to reduce oxidative stress.
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Microalgae are recognized as cell factories enriched with biochemicals suitable as feedstock for bio-energy, food, feed, pharmaceuticals, and nutraceuticals applications. The industrial application of microalgae is challenging due to hurdles associated with mass cultivation and biomass recovery. The scale-up production of microalgal biomass in freshwater is not a sustainable solution due to the projected increase of freshwater demands in the coming years. Microalgae cultivation in wastewater is encouraged in recent years for sustainable bioeconomy from biorefinery processes. Wastewater from the food industry is a less-toxic growth medium for microalgal biomass production. Traditional wastewater treatment and management processes are expensive; hence it is highly relevant to use low-cost wastewater treatment processes with revenue generation through different products. Microalgae are accepted as potential biocatalysts for the bioremediation of wastewater. Microalgae based purification of wastewater technology could be a universal alternative solution for the recovery of resources from wastewater for low-cost biomass feedstock for industry. This review highlights the importance of microalgal biomass production in food processing wastewater, their characteristics, and different microalgal cultivation methods, followed by nutrient absorption mechanisms. Towards the end of the review, different microalgae biomass harvesting processes with biorefinery products, and void gaps that tend to hinder the biomass production with future perspectives will be intended. Thus, the review could claim to be valuable for sustainable microalgae biomass production for eco-friendly bioproduct conversions.