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Mitigation of low stream pH and its effects on salmonids.

Crushed limestone (200 tonnes) was spread in bars on the bed of an acidic brook (mean pH 5.0) in Nova Scotia, Canada. A seasonally variable but significant increase in pH of running water resulted, and a longitudinal pH gradient over the limed section extended to the mouth of the brook. The effectiveness persisted after 3 years, during which pH downstream of the limestone increased an average of 0.4 pH units (range < 0.1-1.3 pH units) along with significantly increased Ca, Mg and acid neutralizing capacity. Total and exchangeable Al were not altered by the limestone and non-exchangeable forms dominated. The interstitial water was nearly neutral (mean pH 7.1) in limestone beds but it was acidic (mean pH 5.4) in gravel beds of the control section upstream. Spawning Atlantic salmon (Salmo salar) dug three times more redds in gravel of the limed section than in the control. Salmon fry survived and they were significantly more abundant in the limed section than in the control. The density of juvenile salmon increased over time, indicating a recovery of the population. The density of brook trout (Salvelinus fontinalis) also increased and trout fry were usually more abundant in the limed section than in the control. The observed benefits for salmonids suggest that small-scale application of limestone to stream beds and spawning sites can be used to mitigate the effects of low stream pH.

Journal Article↗

Alpha-tocopherol succinate does not mitigate nitrofurantoin-induced changes in the glutathione and protein thiol status of the isolated perfused rat liver.

Because it had been suggested that alpha-tocopherol might protect protein thiols (PSH) from oxidation, we were interested in determining if alpha-tocopherol could prevent or mitigate nitrofurantoin-induced changes in the glutathione (GSH) or PSH status of the liver. Isolated rat livers were perfused in the single pass mode for 310 min with Krebs-Henseleit buffer or the same buffer containing 25 nmol/ml of alpha-tocopherol succinate. Treated livers were exposed to 1200 nmol/ml of nitrofurantoin from 30 to 90 min. In control (no nitrofurantoin or alpha-tocopherol) livers, tissue levels of GSH and PSH were maintained at 78 +/- 6% and 94 +/- 6% of their initial values, but alpha-tocopherol levels declined from 34.9 +/- 0.6 nmol/g to 26 +/- 1.5 nmol/g. In the nitrofurantoin-only livers, GSH and PSH tissue levels fell to 17 +/- 10% and 49 +/- 6% of their initial levels (P less than 0.05, vs. controls), alpha-Tocopherol levels fell from 31.7 +/- 4.8 nmol/g to 17.0 +/- 2.8 nmol/g. In the alpha-tocopherol-supplemented, nitrofurantoin-treated livers, initial tissue levels of alpha-tocopherol were elevated to 43.8 +/- 1.4 nmol/g (P less than 0.05), but fell to 26.1 +/- 4.2 nmol/g. Their GSH and PSH tissue levels also declined to 7 +/- 3% and 56 +/- 8% of their initial values (P less than 0.05, vs. controls). Thus, it appeared that alpha-tocopherol supplementation was unable to prevent nitrofurantoin-induced changes in the GSH or PSH status of the liver.

Animals↗

Blockade of nitric oxide formation by N omega-nitro-L-arginine mitigates ischemic brain edema and subsequent cerebral infarction in rats.

In order to investigate whether or not nitric oxide (NO) formation underlies the cellular mechanisms of ischemic brain damage, we examined the effects of N omega-nitro-L-arginine (L-NNA), a NO synthase inhibitor, on ischemic brain edema and subsequent infarction in rats with middle cerebral artery occlusion (MCAo). For this purpose, administrations of L-NNA (1 mg/kg, i.p.) to each animal were done at the time of 5 min, 3, 6 and 24 h after MCAo, respectively. It was shown from this study that L-NNA significantly mitigated ischemic cerebral edema, and histological examinations revealed that this compound markedly reduced infarction size that occurred following MCAo. These results strongly suggest that NO formation is at least partly involved in the pathogenetic mechanisms of ischemic brain edema and subsequent cerebral infarction.

Animals↗

Can stock rotation effectively mitigate EMS medication exposure to excessive heat and cold?

The United States Pharmacopeia recently published a general chapter specifically addressing on-ambulance storage of medications, including a suggestion for stock rotation. This study describes the effectiveness of a simple stock rotation strategy in mitigating EMS medication exposure to excessive heat and cold. Previously collected on-ambulance temperature data from 5 US cities were randomly resampled to generate model exposures of 2 days to 6 months duration. The temperature measurements for every other 24-hour period were then set at 20 degrees C to model the rotation of medications into a controlled environment. For each model, we then determined consistency with the official United States Pharmacopeia definition of controlled room temperature. Without stock rotation, excessive heat occurred in 39.9% of the model exposures. With stock rotation, exposures to excessive heat occurred in less than 1% of northern city models and in 2.9% of the central US models. Stock rotation did not reduce heat exposures in the models for southern cities.

Ambulances↗

Mitochondrially targeted vitamin E and vitamin E mitigate ethanol-mediated effects on cerebellar granule cell antioxidant defense systems.

Ethanol (EtOH) disrupts the structure and function of the developing nervous system, sometimes leading to birth defects associated with fetal alcohol syndrome (FAS). Animal FAS models indicate that cellular membrane peroxidation, intracellular oxidant accumulation, and suppression of endogenous antioxidant enzymes contribute to the toxic effects of EtOH. Mitochondrially targeted vitamin E (MitoVit E), a chemically engineered form of vitamin E (VE) designed to accumulate in the mitochondria, has been shown to inhibit intracellular oxidant accumulation and cell death more effectively than VE. In previous investigations, we have shown that, in vivo, VE reduces neuronal death in the developing cerebellum of EtOH-exposed animals, and, in vitro, VE prevents apoptotic and necrotic death of EtOH-exposed cerebellar granule cells (CGCs). The present investigation shows that, in a FAS CGC model, 1 nM MitoVit E renders significant neuroprotection against EtOH concentrations as high as 1600 mg/dL. The present study also demonstrates that, in this same model, MitoVit E mitigates EtOH-induced accumulation of intracellular oxidants and counteracts suppression of glutathione peroxidase/glutathione reductase (GSH-Px/GSSG-R) functions, protein expression of gamma-glutamylcysteine synthetase (gamma-GCS), and total cellular glutathione (GSH) levels. In the presence and absence of EtOH, VE amplifies the protein expression levels of gamma-GCS, an enzyme that performs the rate-limiting step for GSH synthesis, and total GSH levels. These results suggest that MitoVit E and VE ameliorate EtOH toxicity through non-oxidant mechanisms-modulations of endogenous cellular proteins-and antioxidant means.

Animals↗

Motherhood mitigates aging-related decrements in learning and memory and positively affects brain aging in the rat.

The current work examined spatial learning and memory (i.e., latencies to find a baited food well) in age-matched nulliparous, primiparous and multiparous (NULL, PRIM and MULT, zero, one or two pregnancies and lactations, respectively). We tested at 6, 12, 18 and 24 months of age in a dry land version of the Morris water maze (Main task), and at 12, 18 and 24 months in the same task in which the original location of the baited well was changed (Reversal task). We show that PRIM/MULT rats, compared to the age-matched NULL females, learned the spatial tasks significantly better and exhibited attenuated memory decline, up to 24 months of age. Furthermore, at the conclusion of behavioral testing, we investigated levels of these animals' hippocampal (CA1 and dentate gyrus) immunoreactive amyloid precursor protein (APP), a marker of neurodegeneration and age-related cognitive loss. MULTs had significantly reduced APP in both CA1 and DG, relative to PRIMs and NULLs, and PRIMs had a trend (p<0.06) toward a reduction in APP compared to NULLs in DG. Further, level of APP was negatively correlated with performance in the two tasks (viz., more APP, worse maze performance). Reproduction, therefore, with its attendant natural endocrine and postpartum sensory experiences, may facilitate lifelong learning and memory, and may mitigate markers of neural aging, in the rat. Combining natural hormonal exposure with subsequent substantial experience with stimuli from the offspring may preserve the aged parous female brain relative to that of NULL females.

Age Factors↗

Dietary high protein and vitamin C mitigate stress due to chelate claw ablation in Macrobrachium rosenbergii males.

Stress due to claw ablation was tested in Macrobrachium rosenbergii males. Dietary high protein and vitamin C were supplemented for amelioration of stress. We used four different treatments: fed with 25% protein and a normal dose (0.12%) of vitamin C (T(1)); 35% protein and a normal dose (0.12%) of vitamin C (T(2)); 25% protein and a high dose (0.24%) of vitamin C (T(3)); and high protein 35% and a high dose (0.24%) of vitamin C (T(4)) for 30 days. All test prawns (T(1) to T(4)) were subjected to ablation of their second chelate legs after the 15th day of the feeding trial. A control treatment was maintained without claw ablation and fed with 25% protein. Haemolymph glucose, hepatopancreatic glycogen, muscle ascorbate and enzyme activities (glucose 6 phosphatase (G6Pase), fructose-1,6-bisphosphatase (FBPase), lactate dehydrogenase (LDH), Alanine aminotransferase (ALT) in hepatopancreas) were tested at different recovery periods (0, 6, 24 h, 7 and 14 days). Results indicate a high glucose level immediately after claw ablation and a concomitant increase in gluconeogenic enzymes (G6Pase and FBPase). However, glycogen reserves were regained in the treatments due to claw ablation stress after 24 h. LDH and ALT activity decreased in the hepatopancreas of M. rosenbergii up to 24 h after claw ablation. Overall results indicate that claw ablation is stressful to M. rosenbergii and high protein and vitamin C diet may mitigate stress due to claw ablation.

Alanine Transaminase↗

Androgen ablation mitigates tolerance to a prostate/prostate cancer-restricted antigen.

To understand the T cell response to prostate cancer, we created transgenic mice that express a model antigen in a prostate-restricted pattern and crossed these animals to TRAMP mice that develop spontaneous prostate cancer. Adoptive transfer of prostate-specific CD4 T cells shows that, in the absence of prostate cancer, the prostate gland is mostly ignored. Tumorigenesis allows T cell recognition of the prostate gland--but this recognition is tolerogenic, resulting in abortive proliferation and ultimately in hyporesponsiveness at the systemic level. Androgen ablation (the most common treatment for metastatic prostate cancer) was able to mitigate this tolerance--allowing prostate-specific T cells to expand and develop effector function after vaccination. These results suggest that immunotherapy for prostate cancer may be most efficacious when administered after androgen ablation.

Adoptive Transfer↗

Foam formation and mitigation in a three-phase gas-liquid-particulate system.

Foaming is of great concern in a number of industrial processes involving three-phase gas-liquid-finely divided solid systems such as those encountered in the vitrification of highly radioactive nuclear waste slurries and sludges. Recent work has clearly shown that the surface properties of the particles such as hydrophilicity, hydrophobicity or biphilicity (i.e. partially wetted by water) are the cause of foamability and foam stability. The literature data on particles causing foaminess and foam stability in the absence of any surfactant are rather scarce. This paper presents experimental observations on aqueous foams with polyhedral structures containing over 90% air generated due to the presence of irregularly-shaped fine crystalline particles of sodium chloride which were modified into amphiphilic particles by physical adsorption of a cationic surfactant. Cross-polarized light microscopy was used to visualize the physical adsorption of the surfactant on the crystal surface. It is shown that these biphilic or amphiphilic particles attach to the air bubble surface and prevent the coalescence of bubbles, thereby extending the life of the foam. The foaming power of solid particles increases with an increase in the concentration of amphiphilic particles, and a maximum in foaminess is observed which is due to two competing effects. Amphiphilic particles promote foamability by attachment to the bubble surfaces as individual particles and foam inhibition due to the clustering or flocculation of particles in the bulk at high particle concentrations. We studied the adsorption of amphiphilic particles at a planar air-water surface and found that the degree of foamability correlates well with the particle coverage (i.e. adsorption density) at the air-liquid surface. An exploratory study was also conducted using an antifoam recently developed by IIT researchers to mitigate foaming in particle-laden gas-liquid systems.

Colloids↗

Work experience mitigated age-related differences in balance and mobility during surface accommodation.

BACKGROUND: Locomotor behavior at the roofing worksite is challenged by factors such as sloped surfaces, wind gusts and handling loads. Chronic exposure to this environment may result in enhanced locomotor strategies that are resistant to aging effects. The purpose of this study was to determine if roofers demonstrated enhanced locomotor strategies and if the strategies were maintained with age. METHODS: The gait of ten younger roofers (mean age 27.2 years), eight older roofers (55.4 years), ten younger controls (25.4 years) and nine older controls (57.6 years) was examined during level gait and stepping up onto a wooden surface (0.15m high). Subjects either carried no load, an empty box or the same box loaded to the equivalent of 5% body mass. FINDINGS: Work by age interactions were observed for toe clearance, step width, net angular momentum of the head, arms and trunk segment and gait speed (P<0.0001). Younger roofers demonstrated the greatest toe clearance; older roofers had a smaller lead clearance but decreased variability. Older control groups had the greatest risk of tripping due to low lead toe clearance and high variability, and were least likely to recover if they did trip due to faster gait speed and increased net angular momentum. Work experience resulted in enhanced changes in lead toe clearance and mitigated age-related changes in step width and net angular momentum. INTERPRETATION: Challenging environments show promise for maintaining balance skills in older adults; however care should be taken when introducing inexperienced older adults to a challenging environment.

Adaptation, Physiological↗

Eucalyptol mitigates isoproterenol-induced myocardial injury in rats via activation of p38 MAPK/JNK signaling, suppression of ER stress, and modulation of apoptotic pathway.

BACKGROUND: Myocardial injury (MI), a subset of cardiovascular diseases, remains a leading cause of deaths globally, driven by pathological inflammation, oxidative stress, and apoptosis. Despite advances in interventional cardiology, high relapse rates and therapeutic limitations underscore the urgent need for novel pharmacological agents. Phytochemicals, with their multi-target approach and favorable safety profiles, offer promising alternatives for mitigating ischemic injury. METHODS: The cardioprotective effects of 1,8-cineole, a monoterpene derived from Eucalyptus species, was investigated in a rat model of isoproterenol-induced myocardial injury. Serum levels of cardiac enzymes (creatine kinase (CK), lactate dehydrogenase (LDH)) and pro-inflammatory cytokines (TNF-&#x3b1;, IL-6, IL-1&#x3b2;) were quantified. Preliminary histopathological analysis was performed to assess the extent of myocardial damage. Key molecular mechanisms were evaluated via western blotting and immunohistochemistry, examining pathways related to inflammation (NF-&#x3ba;B), apoptosis (Bcl-2/Bax, caspase-3), endoplasmic reticulum (ER) stress (GRP78, CHOP, PERK-eIF2&#x3b1;), and antioxidant defense (GSH, SOD, CAT). RESULTS: Our results demonstrate that 1,8-cineole significantly reduced the levels of serum cardiac enzymes (CK-MB, LDH), and histopathological damage. Mechanistically, 1,8-cineole also suppressed pro-inflammatory cytokine release (TNF-&#x3b1;, IL-6, and IL-1&#x3b2;) via inhibition of the NF-&#x3ba;B pathway. Furthermore, it attenuated cardiomyocyte apoptosis by modulating Bcl-2/Bax expression and inhibiting caspase-3 activation. Additionally, 1,8-cineole alleviated ER stress by downregulating GRP78, CHOP, and PERK-eIF2&#x3b1; signaling. Importantly, we identified enhanced Nrf2 nuclear translocation and subsequent upregulation of antioxidant enzymes (GSH, SOD, CAT) as key contributors to its cytoprotective effects. CONCLUSIONS: 1,8-Cineole exhibits potent cardio-protection in experimental myocardial injury by targetinginflammation, apoptosis, ER stress, and oxidative stress through modulation of p38 MAPK/JNK, suppression of inflammatory markers (TNF-&#x3b1;, IL-6, IL-1&#x3b2;) and apoptotic markers (Bax, p53). Its natural origin, bioavailability, and multi-mechanistic effectiveness make it a promising candidate for translational development as an adjunct therapy for myocardial injury.

Animals↗

Cyclosporine mitigates graft coronary artery disease in murine cardiac allografts: description and validation of a novel fully allogeneic model.

BACKGROUND: The effect of cyclosporine (CsA) on the development of graft coronary artery disease (GCAD) is controversial. We developed a novel allogeneic mouse model of heart transplantation and investigated the effect of CsA on acute rejection and GCAD. METHODS: Hearts of FVB mice (H-2(q)) were heterotopically transplanted into 60 C57BL/6 mice (H-2(b)). CsA was administered to recipients at 10, 20 or 30 mg/kg/day for 10 or 30 days after transplantation. Untreated recipients as well as isograft recipients served as controls. Viability of the grafts was assessed daily by palpation. Parenchymal rejection was scored in grafts surviving 30 days in the 30-day treatment groups. GCAD was evaluated by the percentage of luminal narrowing, intima/media ratio and percentage of diseased vessels. Blood CsA and creatinine levels were also evaluated. Results were evaluated statistically. RESULTS: All groups except the untreated control group and the allograft groups treated with 10 or 20 mg for 10 days showed significant graft survival (>/=33% survival for 30 days). An inverse correlation was observed between CsA treatment dose, parenchymal rejection score and degree of GCAD in the 30-day treatment groups. However, graft survival in the 20-mg/kg/day group was significantly better than that in the 30-mg/kg/day group. Serum creatine levels showed no nephrotoxicity. CONCLUSIONS: Relatively high-dose CsA mitigated parenchymal rejection and GCAD of the mouse cardiac allografts. In addition, a valuable mouse model mimicking the clinical course of GCAD was achieved with CsA treatment of 20 mg/kg/day for 30 days.

Animals↗

Beta-blockade mitigates exercise blood pressure in hypertensive male patients.

OBJECTIVES: The purpose of this study was to determine the antihypertensive agent(s) more likely to mitigate an exaggerated rise in exercise blood pressure (BP) in hypertensive patients. BACKGROUND: An exaggerated rise in exercise BP is associated with increased cardiovascular risk. There are no recommendations for treating such response. METHODS: Participants were hypertensive men (n = 2,318; age 60 +/- 10 years), undergoing a routine exercise test at the Veterans Affairs Medical Center, Washington, DC. Antihypertensive therapy included angiotensin-converting enzyme inhibitors (n = 437), calcium-channel blockers (n = 223), diuretics (n = 226), and combinations (n = 1,442), beta-blockers alone (n = 201) or in combination with other antihypertensive agents (n = 467), and none (n = 208). Exercise BP, heart rate (HR) and rate-pressure product (RPP) at maximal and submaximal workloads were assessed. RESULTS: After adjusting for covariates, patients treated with beta-blockers or beta-blocker-based therapy had significantly lower BP, HR, and RPP at 5 and 7 metabolic equivalents (METs) and peak exercise than those treated with any other antihypertensive agent or combination (p < 0.05). The likelihood of achieving an exercise systolic BP of >/=210 mm Hg was 68% lower (odds ratio = 0.32, 96% confidence interval 0.2 to 0.53) in the beta-blocker-based therapy versus other medications. African Americans exhibited higher BP and HR than Caucasians at all exercise workloads regardless of antihypertensive therapy and had over a 90% higher likelihood for an abnormal exercise BP response. This risk was attenuated by 35% with a beta-blocker-based therapy. CONCLUSIONS: Significantly lower exercise BP, HR, and RPP levels are achieved with beta-blocker-based therapy than with other antihypertensive agents regardless of race. However, BP was better controlled in Caucasians than in African Americans regardless of antihypertensive therapy.

Adrenergic beta-Antagonists↗

Parabacteroides goldsteinii mitigates parkinsonism in LRRK2 mutant mice by reducing neuroinflammation through Gut-Brain axis.

INTRODUCTION: Alterations in the gut microbiota accompanied by intestinal inflammation are early features of Parkinson's disease (PD). Mutations in the leucine-rich repeat kinase 2 (LRRK2) gene represent a common genetic risk factor for PD and inflammatory bowel disease. Parabacteroides goldsteinii has been reported to alleviate intestinal and systemic inflammation. However, whether modulation of the gut microenvironment at early disease stage can attenuate PD progression remains unclear. OBJECTIVE: To investigate the impact of P. goldsteinii colonization prior to the onset of motor dysfunction on PD progression. METHODS: We established a germ-free PD mouse model carrying the LRRK2 G2019S mutation and administered P. goldsteinii orally at the pre-symptomatic stage to evaluate its effects on motor performance and PD-related neuropathology. Spatial and bulk RNA transcriptomic analyses of brain tissue, together with cytokine profiling, were conducted to assess central changes. To investigate gut immunomodulatory mechanisms, we performed intestinal bulk and single-cell RNA sequencing, spectral flow cytometry as well as cellular bioenergetic analyses. RESULTS: Germ-free conditions partially alleviated PD-like phenotypes in LRRK2 G2019S mice. Colonization with P. goldsteinii at 5-months of age, prior to motor symptom onset, further improved locomotor performance, reduced neuronal &#x3b1;-synuclein aggregations, and mitigated microglial activation and dopaminergic neurodegeneration. Neuroprotection was mediated through enhanced noncanonical neuronal IL-12 receptor-dependent neurotrophic support without activating the canonical STAT4 phosphorylation pathway, along with suppression of microglial activation and downregulation of LRRK2 kinase activity. At the intestinal level, P. goldsteinii suppressed TLR4-driven inflammation, expanded anti-inflammatory intraepithelial CD4+CD8&#x3b1;&#x3b1;+ T cells, promoted dendritic cell and macrophage differentiation, upregulated epithelial tight-junction genes, and improved mitochondrial bioenergetics in intestinal cells. CONCLUSION: P. goldsteinii colonization attenuates the progression of LRRK2-associated parkinsonism by restoring intestinal homeostasis and reducing neuroinflammation. These findings underscore the therapeutic potential of modulating the gut-immune-brain axis during the prodromal stage of PD.

Animals↗

Tofacitinib Mitigates the Increased SARS-CoV-2 Infection Susceptibility Caused by an IBD Risk Variant in the PTPN2 Gene.

BACKGROUND & AIMS: Coronavirus disease (COVID-19), caused by severe acquired respiratory syndrome-Coronavirus-2 (SARS-CoV-2), triggered a global pandemic with severe medical and socioeconomic consequences. Although fatality rates are higher among the elderly and those with underlying comorbidities, host factors that promote susceptibility to SARS-CoV-2 infection and severe disease are poorly understood. Although individuals with certain autoimmune/inflammatory disorders show increased susceptibility to viral infections, there is incomplete knowledge of SARS-CoV-2 susceptibility in these diseases. The aim of our study was to investigate whether the autoimmunity risk gene, PTPN2, which also confers elevated risk to develop inflammatory bowel disease, affects susceptibility to SARS-CoV-2 viral uptake. METHODS: Using samples from PTPN2 genotyped patients with inflammatory bowel disease, PTPN2-deficient mice, and human intestinal and lung epithelial cell lines, we investigated how PTPN2 affects expression of the SARS-CoV-2 receptor angiotensin converting enzyme 2 (ACE2), and uptake of virus-like particles expressing the SARS-CoV2 spike protein and live SARS-CoV-2 virus. RESULTS: We report that the autoimmune PTPN2 loss-of-function risk variant rs1893217 promotes expression of the SARS-CoV-2 receptor, ACE2, and increases cellular entry of SARS-CoV-2 spike protein and live virus. Elevated ACE2 expression and viral entry were mediated by increased Janus kinase-signal transducers and activators of transcription signaling and were reversed by the Janus kinase inhibitor, tofacitinib. CONCLUSION: Collectively, our findings uncover a novel risk biomarker for increased expression of the SARS-CoV-2 receptor and viral entry, and identify a clinically approved therapeutic agent to mitigate this risk.

Humans↗

Elevated water levels drive greenhouse gas mitigation in the riparian zone profile.

Wetlands are critical for climate regulation, with their hyporheic zone serving as sensitive interfaces for groundwater-soil-atmosphere exchange. These zones are active hotspots for carbon-nitrogen cycling and greenhouse gas (GHG) emissions (CO2, CH4, N2O), yet the impact of water level fluctuations on these emissions and their microbial drivers in freshwater wetlands remains poorly understood. This study investigated the spatiotemporal dynamics of GHG emissions and carbon-nitrogen coupling processes along riparian soil profiles of Baiyangdian Lake during water level fluctuations. Employing static chamber measurements, microcosms, quantitative PCR, Metagenome-Assembled genome (MAG) analyses, and Structural Equation Modeling (SEM), we observed that GHG emissions were significantly affected by water level fluctuations. Specifically, CO2 and N2O fluxes, as well as CO2 production potential were significantly lower at high-water-level conditions. Water level also emerged as a key driver of microbial community structure, with Methylococcaceae and Methanosarcinaceae as key regulators of CH4 emission, and Anaeromyxobacteraceae as central to N2O dynamics. A high-quality Methylomirabilales-like MAG, possessing the complete pathway for coupled nitrate reduction and methane oxidation, was identified. Its abundance negatively correlated with water level, suggesting that these C-N coupling bacteria contribute to reducing GHG emissions. This study provides crucial theoretical insights and identifies microbial targets for mitigating wetland GHG emission through hydrological management.

Greenhouse Gases↗

Mov10 mitigates hematopoietic stem cell exhaustion under stress by modulating the Camp-mediated inflammatory pathway.

The integrity of hematopoietic stem cell (HSC) function is crucial for robust hematopoietic regeneration following stress. Inflammatory responses are pivotal drivers of HSC stress response, yet the precise modulation of inflammatory pathways remains incompletely defined. In this study, we identify the RNA helicase Mov10 as a negative regulator of stress-induced inflammatory pathways in HSC. Our study indicates that Mov10, which is critically required for HSC maintenance, is highly expressed in HSC, and its loss adversely affects HSC fitness and survival during hematopoietic stress induced by bone marrow transplantation and irradiation (IR). Mechanistically, Mov10 mitigates excessive inflammatory activation to sustain HSC functional integrity during hematopoietic stress, primarily by enhancing the translation of CAMP, which inhibits the interaction between TNF-&#x3b1; and its receptor TNFR1 and suppresses NF-&#x3ba;B activation. Overall, our results imply that Mov10 plays a critical role in averting functional failure of hematopoiesis under stress, presenting viable paths for the therapeutic intervention of relevant diseases.

Camp↗

Effect of organic additives on the mitigation of volatility of 1-nitro-3,3'-dinitroazetidine (TNAZ): next generation powerful melt cast able high energy material.

1-Nitro-3,3'-dinitroazetidine (TNAZ) was synthesized based on the lines of reported method. Thermolysis studies on synthesized and characterized TNAZ using differential scanning calorimetry (DSC) and hyphenated TG-FT-IR techniques were undertaken to generate data on decomposition pattern. FT-IR of decomposition products of TNAZ revealed the evolution of oxides of nitrogen and HCN containing species suggesting the cleavage of C/N-NO(2) bond accompanied with the collapse of ring structure. The effect of incorporation of 15% additives namely, 3-amino-1,2,4-triazole (AT), 3,5-diamino-1,2,4-triazole (DAT), carbohydrazide (CHZ), 5,7-dinitrobenzofuroxan (DNBF), bis (2,2-dinitropropyl) succinate (BNPS), triaminoguanidinium nitrate (TAGN), 2,4,6-trinitrobenzoic acid (TNBA) and nitroguanidine (NQ) on the volatility of TNAZ was investigated by undertaking thermogravimetric analysis. The TG pattern brings out the potential of BNPS and TAGN as additives to mitigate the volatility of TNAZ. The influence of additives on thermal decomposition of pattern of TNAZ was also investigated by DSC. The DSC results indicated that the additives did not have appreciable effect on the melting point of TNAZ. Scanning electron microscopic (SEM) studies were carried out to investigate the effect of additives on morphology of TNAZ. This paper also discusses the possible mechanism involved in between the TNAZ and TAGN and BNPS. It appears that the formation of charge transfer complex formation between the TNAZ and TAGN/BNPS. The effect of addition of high explosives such as CL-20, HMX and RDX on thermo-physical characteristics of TNAZ is also reported in this paper.

Azetidines↗