Effect of acidic vaginal pH on the efficacy of dinoprostone (PGE2) vaginal tablet for labor induction in full term pregnant women: a randomized controlled trial.

OBJECTIVES: There is controversial evidence that acidification of vaginal pH may increase the efficacy of vaginal prostaglandins in labor induction, with research being mainly focused on misoprostol. This study aims to evaluate the impact of this intervention on the progress of labor induction with dinoprostone (PGE2) vaginal tablet. METHODS: This double-blind, parallel-group, randomized study was conducted between October 2021 and December 2022 at Alexandra General Hospital, Athens, Greece. A total of 230 women with singleton, full term pregnancy that were scheduled for labor induction were randomly divided into two groups: Group A, who received acidic vaginal wash (5 % acetic acid) and Group B, who received a normal saline vaginal wash. Afterwards, participants received a vaginal tablet of 3 mg dinoprostone every 6 h (maximum two doses). RESULTS: There were no statistically significant differences in mode of delivery, duration of different labor stages, Bishop score changes and possible complications. Participants in the acidification group needed less often labor augmentation with oxytocin and epidural anesthesia (p=0.03). CONCLUSIONS: Vaginal acidification seems to have no effect on the efficacy of the dinoprostone vaginal tablet. Even though it may reduce the need for oxytocin augmentation, there is no apparent benefit on clinical outcomes, such as reduction in cesarean section rates or shorter labor duration. Future research is necessary in order to validate these findings.

Differential regulation of mitochondrial uncoupling protein 2 in cancer cells.

The persistent growth of cancer cells is underscored by complex metabolic reprogramming, with mitochondria playing a key role in the transition to aerobic glycolysis and representing new therapeutic targets. Mitochondrial uncoupling protein 2 (UCP2) has attracted interest because of its abundance in rapidly proliferating cells, including cancer cells, and its involvement in cellular metabolism. However, the specific contributions of UCP2 to cancer biology remain poorly defined. Our investigation of UCP2 expression in various human and mouse cancer cell lines aimed to elucidate its links to metabolic states, proliferation, and adaptation to environmental stresses such as hypoxia and nutrient deprivation. We observed significant variability in UCP2 expression across cancer types, with no direct correlation to their metabolic activity or proliferation rates. UCP2 abundance was also differentially affected by nutrient availability in different cancer cells, but UCP2 was generally downregulated under hypoxia. These findings challenge the notion that UCP2 is a marker of malignant potential and suggest its more complex involvement in the metabolic landscape of cancer.

Long-term Trends of Dissolved Organic Carbon Dynamics in a Subtropical Forest Responding to Environmental Changes.

Dissolved organic carbon (DOC) dynamics are critical to carbon cycling in forest ecosystems and sensitive to global change. Our study, spanning from 2001 to 2020 in a headwater catchment in subtropical China, analyzed DOC and water chemistry of throughfall, litter leachate, soil waters at various depths, and streamwater. We focused on DOC transport through hydrological pathways and assessed the long-term trends in DOC dynamics amidst environmental and climatic changes. Our results showed that the annual DOC deposition via throughfall and stream outflow was 14.2 ± 2.2 and 1.87 ± 0.83 g C m-2 year-1, respectively. Notably, there was a long-term declining trend in DOC deposition via throughfall (-0.195 mg C L-1 year-1), attributed to reduced organic carbon emissions from clean air actions. Conversely, DOC concentrations in soil waters and stream waters showed increasing trends, primarily due to mitigated acid deposition. Moreover, elevated temperature and precipitation could partly explain the long-term rise in DOC leaching. These trends in DOC dynamics have significant implications for the stability of carbon sink in terrestrial, aquatic, and even oceanic ecosystems at regional scales.

Dmxl1 Is an Essential Mammalian Gene that Is Required for V-ATPase Assembly and Function In Vivo.

The proton pumping V-ATPase drives essential biological processes, such as acidification of intracellular organelles. Critically, the V-ATPase domains, V1 and VO, must assemble to produce a functional holoenzyme. V-ATPase dysfunction results in cancer, neurodegeneration, and diabetes, as well as systemic acidosis caused by reduced activity of proton-secreting kidney intercalated cells (ICs). However, little is known about the molecular regulation of V-ATPase in mammals. We identified a novel interactor of the mammalian V-ATPase, Drosophila melanogaster X chromosomal gene-like 1 (Dmxl1), aka Rabconnectin-3A. The yeast homologue of Dmxl1, Rav1p, is part of a complex that catalyzes the reversible assembly of the domains. We, therefore,hypothesized that Dmxl1 is a mammalian V-ATPase assembly factor. Here, we generated kidney IC-specific Dmxl1 knockout (KO) mice, which had high urine pH, like B1 V-ATPase KO mice, suggesting impaired V-ATPase function. Western blotting showed decreased B1 expression and B1 (V1) and a4 (VO) subunits were more intracellular and less colocalized in Dmxl1 KO ICs. In parallel, subcellular fractionation revealed less V1 associated B1 in the membrane fraction of KO cells relative to the cytosol. Furthermore, a proximity ligation assay performed using probes against B1 and a4 V-ATPase subunits also revealed decreased association. We propose that loss of Dmxl1 reduces V-ATPase holoenzyme assembly, thereby inhibiting proton pumping function. Dmxl1 may recruit the V1 domain to the membrane and facilitate assembly with the VO domain and in its absence V1 may be targeted for degradation. We conclude that Dmxl1 is a bona fide mammalian V-ATPase assembly factor.

Nitrogen input modulates the effects of coastal acidification on nitrification and associated N2O emission.

Acidification of coastal waters, synergistically driven by increasing atmospheric carbon dioxide (CO2) and intensive land-derived nutrient inputs, exerts significant stresses on the biogeochemical cycles of coastal ecosystem. However, the combined effects of anthropogenic nitrogen (N) inputs and aquatic acidification on nitrification, a critical process of N cycling, remains unclear in estuarine and coastal ecosystems. Here, we showed that increased loading of ammonium (NH4+) in estuarine and coastal waters alleviated the inhibitory effect of acidification on nitrification rates but intensified the production of the potent greenhouse gas nitrous oxide (N2O), thus accelerating global climate change. Metatranscriptomes and natural N2O isotopic signatures further suggested that the enhanced emission of N2O may mainly source from hydroxylamine (NH2OH) oxidation rather than from nitrite (NO2-) reduction pathway of nitrifying microbes. This study elucidates how anthropogenic N inputs regulate the effects of coastal acidification on nitrification and associated N2O emissions, thereby enhancing our ability to predict the feedbacks of estuarine and coastal ecosystems to climate change and human perturbations.

Mechanisms of biodiversity loss under nitrogen enrichment: unveiling a shift from light competition to cation toxicity.

The primary mechanisms contributing to nitrogen (N) addition induced grassland biodiversity loss, namely light competition and soil cation toxicity, are often examined separately in various studies. However, their relative significance in governing biodiversity loss along N addition gradient remains unclear. We conducted a 4-yr field experiment with five N addition rates (0, 2, 10, 20, and 50 g N m-2 yr-1) and performed a meta-analysis using global data from 239 observations in N-fertilized grassland ecosystems. Results from our field experiment and meta-analysis indicate that both light competition and soil cation (e.g. Mn2+ and Al3+) toxicity contribute to plant diversity loss under N enrichment. The relative importance of these mechanisms varied with N enrichment intensity. Light competition played a more significant role in influencing species richness under low N addition (≤ 10 g m-2 yr-1), while cation toxicity became increasingly dominant in reducing biodiversity under high N addition (>10 g m-2 yr-1). Therefore, a transition from light competition to cation toxicity occurs with increasing N availability. These findings imply that the biodiversity loss along the N gradient is regulated by distinct mechanisms, necessitating the adoption of differential management strategies to mitigate diversity loss under varying intensities of N enrichment.

Acidification state and interannual variability in marginal sea: A case study of the Bohai and the Yellow Seas surface waters in April 2023.

The acidification of the marginal seawater was a more intricate process than the ocean. Although some studies have been done on seasonal acidification in the bottom water of Chinese marginal seas, research on surface water acidification has still been insufficient. We analyzed the acidification properties and controlling factors in the Bohai Sea (BS) and Yellow Sea (YS) surface water during April 2023. The observation showed that the average surface water pH of the BS, North Yellow Sea (NYS), and South Yellow Sea (SYS) were 8.09 ± 0.06, 8.13 ± 0.05, and 8.15 ± 0.05. Phytoplankton significantly impacted pH and Ωarag, while riverine inputs and biological activity played a vital role in controlling DIC and TA. The Yellow River significantly impacted the BS. The North Yellow Sea Cold Water Mass had a limited impact on acidification, while the South Yellow Sea Cold Water Mass significantly affected the SYS. Regarding seasonal fluctuations, Ωarag was significantly higher in summer than in other seasons. DIC and TA showed different patterns in both the BS and YS, with a minimal fluctuation in pH. Over the last two decades, the pH in the BS showed a slight annual decline, and the rate of change was (-1.45 ± 2.19) × 10-5 yr-1. In contrast, the NYS and SYS have slightly risen, with rates of change of (2.39 ± 1.24) × 10-5 and (1.23 ± 0.76) × 10-5 yr-1. We believed that surface water acidification in the BS and YS did not follow the expected trend of significant acidification observed in open oceanic regions. Instead, the acidification process in these marginal seas was dominated by local factors such as riverine inputs, biological activity, and cold water masses, resulting in minimal pH changes over the last two decades.

Blockade of endolysosomal acidification suppresses TLR3-mediated pro-inflammatory signaling in airway epithelial cells.

BACKGROUND: Endolysosomal compartments are acidic and contain low pH-dependent proteases, and these conditions are exploited by respiratory viruses, such as SARS-CoV-2 and influenza virus, for escaping into the cytosol. Moreover, endolysosomes contain various pattern recognition receptors (PRRs), which respond to virus-derived pathogen-associated molecular patterns (PAMPs) by production of pro-inflammatory cytokines/chemokines. However, excessive pro-inflammatory responses can lead to a potentially lethal cytokine storm. OBJECTIVES: Here we investigated the endosomal PRR expression profile in primary human small airway epithelial cells (HSAECs), and whether blockade of endolysosomal acidification affects their cytokine/chemokine production after challenge with virus-derived stimulants. METHODS: HSAECs were exposed to stimulants mimicking virus-derived PAMPs, either in the absence or presence of compounds causing blockade of endolysosomal acidification, followed by measurement of cytokine expression and release. RESULTS: We show that toll-like receptor 3 (TLR3) is the major endosomal PRR expressed by HSAECs, and that TLR3 expression is strongly induced by TLR3 agonists, but not by a range of other PRR agonists. We also demonstrate that TLR3 engagement with its agonists elicits a robust pro-inflammatory cytokine/chemokine response, which is profoundly suppressed through blockade of endolysosomal acidification, by bafilomycin A1, monensin, or niclosamide. Using TLR3 reporter cells, it was confirmed that TLR3 signaling is strongly induced by Poly(I:C) and that blockade of endolysosomal acidification efficiently blocked TLR3 signaling. Finally, we show that blockade of endolysosomal acidification causes a reduction in the levels of TLR3 mRNA and protein. CONCLUSION: These findings show that blockade of endolysosomal acidification suppresses TLR3-dependent cytokine and chemokine production in HSAECs. CLINICAL IMPLICATION: These findings may be exploited for therapeutic strategies aiming to ameliorate the cytokine storm in response to respiratory virus infection.

Carbon export from submarine groundwater discharge in a semi-enclosed bay: Impact for the buffering capacity against coastal ocean acidification.

Submarine groundwater discharge (SGD) serves as an important pathway for the transport of dissolved carbon from land to ocean, significantly affecting the coastal biogeochemical cycles. However, the impact of SGD-derived dissolved carbon on the coastal carbon budget remains poorly understood. This study first quantified SGD and associated dissolved organic carbon (DOC), dissolved inorganic carbon (DIC) and total alkalinity (TA) fluxes in Daya Bay using mass balance models based on radium isotopes (223Ra, 224Ra, 226Ra and 228Ra). We then constructed carbon mass balance models to evaluate the impact of SGD-derived carbon on the buffering capacity against coastal ocean acidification. The estimated SGD fluxes ranged from 0.80 × 107 to 2.64 × 107 m3d-1. The DIC, DOC and TA fluxes from SGD were 17.90-36.44 mmol m-2d-1, 0.93-2.13 mmol m-2d-1, and 21.19-28.47 mmol m-2d-1, respectively. Based on carbon mass balances, the DIC flux from SGD was 19-39 times the riverine input, accounting for 27.16 % ∼ 37.64 % of the total carbon source. These results suggest that SGD is a major contributor to DIC, significantly affecting the coastal carbon budget. Furthermore, the average TA:DIC ratio of groundwater discharging into Daya Bay was approximately 1.13. High TA exports enhance the buffering capacity of the coastal ocean and contribute bicarbonate to the ocean, playing a significant role in the ocean carbon sequestration process. This study demonstrates the importance of SGD-derived dissolved carbon in the assessment of coastal carbon budgets.

Rubble persistence under ocean acidification threatened by accelerated bioerosion and lower-density coral skeletons.

As the balance between erosional and constructive processes on coral reefs tilts in favor of framework loss under human-induced local and global change, many reef habitats worldwide degrade and flatten. The resultant generation of coral rubble and the beds they form can have lasting effects on reef communities and structural complexity, threatening the continuity of reef ecological functions and the services they provide. To comprehensively capture changing framework processes and predict their evolution in the context of climate change, heavily colonized rubble fragments were exposed to ocean acidification (OA) conditions for 55 days. Controlled diurnal pH oscillations were incorporated in the treatments to account for the known impact of diel carbonate chemistry fluctuations on calcification and dissolution response to OA. Scenarios included contemporary pH (8.05 ± 0.025 diel fluctuation), elevated OA (7.90 ± 0.025), and high OA (7.70 ± 0.025). We used a multifaceted approach, combining chemical flux analyses, mass alteration measurements, and computed tomography scanning images to measure total and chemical bioerosion, as well as chemically driven secondary calcification. Rates of net carbonate loss measured in the contemporary conditions (1.36 kg m-2 year-1) were high compared to literature and increased in OA scenarios (elevated: 1.84 kg m-2 year-1 and high: 1.59 kg m-2 year-1). The acceleration of these rates was driven by enhanced chemical dissolution and reduced secondary calcification. Further analysis revealed that the extent of these changes was contingent on the density of the coral skeleton, in which the micro- and macroborer communities reside. Findings indicated that increased mechanical bioerosion rates occurred in rubble with lower skeletal density, which is of note considering that corals form lower-density skeletons under OA. These direct and indirect effects of OA on chemical and mechanical framework-altering processes will influence the permanence of this crucial habitat, carrying implications for biodiversity and reef ecosystem function.

How water acidification influences the organism antioxidant capacity and gill structure of Mediterranean mussel (Mytilus galloprovincialis, Lamarck, 1819) at normoxia and hypoxia.

The effect of water acidification in combination with normoxia or hypoxia on the antioxidant capacity and oxidative stress markers in gills and hemolymph of the Mediterranean mussel (Mytilus galloprovincialis), as well as on gill microstructure, has been evaluated through an in vivo experiment. Mussels were exposed to a low pH (7.3) under normal dissolved oxygen (DO) conditions (8 mg/L), and hypoxia (2 mg/L) for 8 days, and samples were collected on days 1, 3, 6, and 8 to evaluate dynamic changes of physiological responses. Cytoplasmic concentrations of reactive oxygen species (ROS) and levels of DNA damage were measured in hemocytes, while the activity of catalase (CAT) and superoxide dismutase (SOD) and histopathological changes were assessed in gills. The results revealed that while water acidification did not significantly affect the activity of SOD and CAT in gills under normoxic and hypoxic conditions, there was a trend towards suppression of CAT activity at the end of the experimental period (day 8). Similarly, we did not observe increased formation of ROS in hemocytes or changes in the levels of DNA damage during the experimental period. These results strongly suggest that the oxidative stress response system in mussels is relatively stable to experimental conditions of acidification and hypoxia. Experimental acidification under normoxia and hypoxia caused changes to the structure of the gills, leading to various histopathological alterations, including dilation, hemocyte infiltration into the hemal sinuses, intercellular edema, vacuolization of epithelial cells in gill filaments, lipofuscin accumulation, changes in the shape and adjacent gill filaments, hyperplasia, exfoliation of the epithelial layer, necrosis, swelling, and destruction of chitinous layers (chitinous rods). Most of these alterations were reversible, non-specific changes that represent a general inflammatory response and changes in the morphology of the gill filaments. The dynamics of histopathological alterations suggests an active adaptive response of gills to environmental stresses. Taken together, our data indicate that Mediterranean mussels have a relative tolerance to water acidification and hypoxia at tissue and cellular levels.

Freezing-induced acidification of sea ice brine.

The acidity of sea ice and snow plays a key role in the chemistry of the cryosphere; an important example lies in the photochemical catalytic release of reactive bromine in polar regions, facilitated at pHs below 6.5. We apply in-situ acid-base indicators to probe the microscopic acidity of the brine within the ice matrix in artificial sea water at a range of concentrations (0.35-70 PPT) and initial pHs (6-9). The results are supported by analogous measurements of the most abundant salts in seawater: NaCl, Na2SO4, and CaCO3. In the research herein, the acidity is expressed in terms of the Hammett acidity function, H2-. The obtained results show a pronounced acidity increase in sea water after freezing at -15 °C and during the subsequent cooling down to -50 °C. Importantly, we did not observe any significant hysteresis; the values of acidity upon warming markedly resembled those at the corresponding temperatures at cooling. The acidity increase is attributed to the minerals' crystallization, which is accompanied by a loss of the buffering capacity. Our observations show that lower salinity sea water samples (≤ 3.5 PPT) reach pH values below 6.5 at the temperature of -15 °C, whereas higher salinity ices attain such values only at -30 °C. The ensuing implications for polar chemistry and the relevance to the field measurements are discussed.

Gain-of-function variants in CLCN7 cause hypopigmentation and lysosomal storage disease.

Together with its ß-subunit OSTM1, ClC-7 performs 2Cl-/H+ exchange across lysosomal membranes. Pathogenic variants in either gene cause lysosome-related pathologies, including osteopetrosis and lysosomal storage. CLCN7 variants can cause recessive or dominant disease. Different variants entail different sets of symptoms. Loss of ClC-7 causes osteopetrosis and mostly neuronal lysosomal storage. A recently reported de novo CLCN7 mutation (p.Tyr715Cys) causes widespread severe lysosome pathology (hypopigmentation, organomegaly, and delayed myelination and development, "HOD syndrome"), but no osteopetrosis. We now describe two additional HOD individuals with the previously described p.Tyr715Cys and a novel p.Lys285Thr mutation, respectively. Both mutations decreased ClC-7 inhibition by PI(3,5)P2 and affected residues lining its binding pocket, and shifted voltage-dependent gating to less positive potentials, an effect partially conferred to WT subunits in WT/mutant heteromers. This shift predicts augmented pH gradient-driven Cl- uptake into vesicles. Overexpressing either mutant induced large lysosome-related vacuoles. This effect depended on Cl-/H+-exchange, as shown using mutants carrying uncoupling mutations. Fibroblasts from the p.Y715C patient also displayed giant vacuoles. This was not observed with p.K285T fibroblasts probably due to residual PI(3,5)P2 sensitivity. The gain of function caused by the shifted voltage-dependence of either mutant likely is the main pathogenic factor. Loss of PI(3,5)P2 inhibition will further increase current amplitudes, but may not be a general feature of HOD. Overactivity of ClC-7 induces pathologically enlarged vacuoles in many tissues, which is distinct from lysosomal storage observed with the loss of ClC-7 function. Osteopetrosis results from a loss of ClC-7, but osteoclasts remain resilient to increased ClC-7 activity.

Mowing aggravates the adverse effects of nitrogen addition on soil acid neutralizing capacity in a meadow steppe.

Soil acidification induced by reactive nitrogen (N) inputs is a major environmental issue in grasslands, as it lowers the acid neutralizing capacity (ANC). The specific impacts of different N compound forms on ANC remain unclear. Grassland management practices like mowing and grazing can remove a considerable amount of soil N and other nutrients, potentially mitigating soil acidification by removing N from the ecosystem or aggravating it by removing base cations. However, empirical evidence regarding the joint effects of adding different forms of N compounds and mowing on ANC changes in different-sized soil aggregates is still lacking. This study aimed to address this knowledge gap by examining the effects of three N compounds (urea, ammonium nitrate, and ammonium sulfate) combined with mowing (mown vs. unmown) on soil ANC in different soil aggregate sizes (>2000 µm, 250-2000 µm, and <250 µm) through a 6-year field experiment in Inner Mongolia grasslands. We found that the average decline in soil ANC caused by ammonium sulfate (AS) addition (-78.9%) was much greater than that by urea (-25.0%) and ammonium nitrate (AN) (-52.1%) as compared to control. This decline was attributed to increased proton (H+) release from nitrification and the leaching of exchangeable Ca2+ and Mg2+. Mowing aggravated the adverse effects of urea and AN on ANC, primarily due to the reduction in soil organic matter (SOM) contents and the removal of exchangeable Ca2+, K+, and Na + via plant biomass harvest. This pattern was consistent across all aggregate fractions. The lack of variation in soil ANC among different soil aggregate fractions is likely due to the contrasting trend in the distribution of exchangeable Ca2+ and Mg2+. Specifically, the concentration of exchangeable Ca2+ increased with increasing aggregate size, while the opposite was true for that of exchangeable Mg2+. These findings underscore the importance of considering the forms of N compounds when assessing the declines of ANC induced by N inputs, which also calls for an urgent need to reduce N emissions to ensure the sustainable development of the meadow ecosystems.

Pathological and ultrastructural changes of Bellamya bengalensis under chronic carboxylic acid exposure at environmentally relevant levels: Inferences from general unified threshold model for survival (GUTS) predictions and hepatopancreatic integrity assessment.

This study aimed to understand the effects of freshwater acidification, driven by industrial runoff, agricultural activities, and atmospheric deposition, on the freshwater mollusk Bellamya bengalensis. By systematically investigating the impact of two common carboxylic acids, acetic acid (AA) and benzoic acid (BA), this research employed diverse toxicological, pathological, and ecological assessments. We explored survival predictions through the generic unified threshold model of survival (GUTS-SD), examined oxidative stress responses, and investigated hepatopancreatic alterations. In the experimental design, Bellamya bengalensis were subjected to environmentally relevant sublethal concentrations (10%, 20% LC50) of AA (39.77 and 79.54 mg/l) and BA (31.41 and 62.82 mg/l) over 28 days. Acute toxicity tests revealed increased LC50 values, indicating heightened toxicity with prolonged exposure, particularly due to the greater potency of benzoic acid compared to acetic acid. The GUTS-SD model provided accurate predictions of time-specific effects on populations, presenting long-term exposure (100 days) LC50 values for AA (263.7 mg/l) and BA (330.9 mg/l). Sequentially, the integrated biomarker response (IBR) analysis across study intervals highlighted the 28-day interval as the most sensitive, with GST emerging as the most responsive enzyme to oxidative stress induced by AA and BA. Histopathological and ultrastructural assessments of the hepatopancreas showed severe alterations, including necrosis, vacuolation and disrupted micro-villi, which were especially pronounced in higher BA exposure concentrations. These findings highlight the health and survival impacts of carboxylic acid toxicity on Bellamya bengalensis, emphasizing the need for proactive measures to mitigate acidification in aquatic ecosystems. The broader ecological implications underscore the importance of effective management and conservation strategies to address ongoing environmental challenges.

Alpha-Hederin induces incomplete autophagic injury in non-small cell lung cancer by interfering with the lysosomal acidification.

Lung cancer is the most common oncological disease worldwide, with non-small cell lung cancer accounting for approximately 85% of lung cancer cases. α-Hederin is a monodesmosidic triterpenoid saponin isolated from the leaves of Hedera helix L. or Nigella sativa and has been extensively studied for its antitumor activity against a variety of tumor cells. It has been suggested that α-Hederin is a potential regulator of autophagy and has high promise for application. However, the specific mechanism and characteristics of α-Hederin in regulating autophagy are not well understood. In this study, we confirmed the potential of α-Hederin application in lung cancer treatment and comprehensively explored the mechanism and characteristics of α-Hederin in regulating autophagy in lung cancer cells. Our results suggest that α-Hederin is an incomplete autophagy inducer that targets mTOR to activate the classical autophagic pathway, inhibits lysosomal acidification without significantly affecting the processes of autophagosome transport, lysosome biogenesis, autophagosome and lysosome fusion, and finally leads to impaired autophagic flux and triggers autophagic damage in NSCLC.

Soil organic matter priming: The pH effects.

Priming of soil organic matter (SOM) decomposition by microorganisms is a key phenomenon of global carbon (C) cycling. Soil pH is a main factor defining priming effects (PEs) because it (i) controls microbial community composition and activities, including enzyme activities, (ii) defines SOM stabilization and destabilization mechanisms, and (iii) regulates intensities of many biogeochemical processes. In this critical review, we focus on prerequisites and mechanisms of PE depending on pH and assess the global change consequences for PE. The highest PEs were common in soils with pH between 5.5 and 7.5, whereas low molecular weight organic compounds triggered PE mainly in slightly acidic soils. Positive PEs up to 20 times of SOM decomposition before C input were common at pH around 6.5. Negative PEs were common at soil pH below 4.5 or above 7 reflecting a suboptimal environment for microorganisms and specific SOM stabilization mechanisms at low and high pH. Short-term soil acidification (in rhizosphere, after fertilizer application) affects PE by: mineral-SOM complexation, SOM oxidation by iron reduction, enzymatic depolymerization, and pH-dependent changes in nutrient availability. Biological processes of microbial metabolism shift over the short-term, whereas long-term microbial community adaptations to slow acidification are common. The nitrogen fertilization induced soil acidification and land use intensification strongly decrease pH and thus boost the PE. Concluding, soil pH is one of the strongest but up to now disregarded factors of PE, defining SOM decomposition through short-term metabolic adaptation of microbial groups and long-term shift of microbial communities.

Soil organic matter and total nitrogen as key driving factors promoting the assessment of acid-base buffering characteristics in a tea (Camellia sinensis) plantation habitat.

The issue of soil acidification in tea plantations has become a critical concern due to its potential impact on tea quality and plant health. Understanding the factors contributing to soil acidification is essential for implementing effective soil management strategies in tea-growing regions. In this study, a field study was conducted to investigate the effects of tea plantations on soil acidification and the associated acid-base buffering capacity (pHBC). We assessed acidification, pHBC, nutrient concentrations, and cation contents in the top 0-20 cm layer of soil across forty tea gardens of varying stand ages (0-5, 5-10, 10-20, and 20-40 years old) in Anji County, Zhejiang Province, China. The results revealed evident soil acidification due to tea plantation activities, with the lowest soil pH observed in tea gardens aged 10-20 and 20-40 years. Higher levels of soil organic matter (SOM), total nitrogen (TN), Olsen phosphorus (Olsen-P), available iron (Fe), and exchangeable hydrogen (H+) were notably recorded in 10-20 and 20-40 years old tea garden soils, suggesting an increased risk of soil acidification with prolonged tea cultivation. Furthermore, prolonged tea cultivation correlated with increased pHBC, which amplified with tea stand ages. The investigation of the relationship between soil pHBC and various parameters highlighted significant influences from soil pH, SOM, cation exchange capacity, TN, available potassium, Olsen-P, exchangeable acids (including H+ and aluminum), available Fe, and available zinc. Consequently, these findings underscore a substantial risk of soil acidification in tea gardens within the monitored region, with SOM and TN content being key driving factors influencing pHBC.

Connexin hemichannels drive lactation-induced osteocyte acidification and perilacunar-canalicular remodeling.

The maternal skeleton experiences significant bone loss during lactation, followed by rapid restoration post weaning. Parathyroid-related protein (PTHrP)-induced acidification of the perilacunar matrix by osteocytes is crucial in this process, yet its mechanism remains unclear. Here, we identify Cx43 hemichannels (HCs) as key mediators of osteocyte acidification and perilacunar-canalicular remodeling (PLR). Utilizing transgenic mouse models expressing dominant-negative Cx43 mutants, we show that mice with impaired Cx43 HCs exhibit attenuated lactation-induced responses compared to wild-type and only gap junction-impaired groups, including lacunar enlargement, upregulation of PLR genes, and bone loss with compromised mechanical properties. Furthermore, inhibition of HCs by a Cx43 antibody blunts PTHrP-induced calcium influx and protein kinase A activation, followed by impaired osteocyte acidification. Additionally, impeded HCs suppress bone recovery during the post-lactation period. Our findings highlight the pivotal role of Cx43 HCs in orchestrating dynamic bone changes during lactation and recovery by regulating acidification and remodeling enzyme expression.

Impacts of climate-related stressors on social group cohesion and individual sociability in fish.

Group-living in animals comes with a number of benefits associated with predator avoidance, foraging, and reproduction. A large proportion of fish species display grouping behaviour. Fish may also be particularly vulnerable to climate-related stressors including thermal variation, hypoxia, and acidification. As climate-related stressors are expected to increase in magnitude and frequency, any effects on fish behaviour may be increased and affect the ability of fish species to cope with changing conditions. Here we conduct a systematic review of the effects of temperature, hypoxia, and acidification on individual sociability and group cohesion in shoaling and schooling fishes. Searches of the published and grey literature were carried out, and studies were included or excluded based on selection criteria. Data from studies were then included in a meta-analysis to examine broad patterns of effects of climate-related stressors in the literature. Evidence was found for a reduction in group cohesion at low oxygen levels, which was stronger in smaller groups. While several studies reported effects of temperature and acidification, there was no consistent effect of either stressor on sociability or cohesion. There was some evidence that marine fishes are more strongly negatively affected by acidification compared with freshwater species, but results are similarly inconsistent and more studies are required. Additional studies of two or more stressors in combination are also needed, although one study found reduced sociability following exposure to acidification and high temperatures. Overall, there is some evidence that hypoxia, and potentially other climate-related environmental changes, impact sociability and group cohesion in fishes. This may reduce survival and adaptability in shoaling and schooling species and have further ecological implications for aquatic systems. However, this synthesis mainly highlights the need for more empirical studies examining the effects of climate-related factors on social behaviour in fishes.