Silicon a key player to mitigate chromium toxicity in plants: Mechanisms and future prospective.

Chromium is a serious heavy metal (HM) and its concentration in plant-soil interface is soaring due to anthropogenic activities, unregulated disposals, and lack of efficient treatments. High concentration of Cr is toxic to ecosystems and human health. Cr stress also diminishes the plant performance by changing the plant's vegetative and reproductive development that ultimately affects sustainable crop production. Silicon (Si) is the second-most prevalent element in the crust of the planet, and has demonstrated a remarkable potential to minimize the HM toxicity. Amending soils with Si mitigates adverse effects of Cr by improving plant physiological, biochemical, and molecular functioning and ensuring better Cr immobilization, compartmentation, and co-precipitation. However, there is no comprehensive review on the role of Si to mitigate Cr toxicity in plants. Thus, in this present review; the discussion has been carried on; 1) the source of Cr, 2) underlying mechanisms of Cr uptake by plants, 3) how Si affects the plant functioning to reduce Cr toxicity, 4) how Si can cause immobilization, compartmentation, and co-precipitation 5) strategies to improve Si accumulation in plants to counter Cr toxicity. We also discussed the knowledge gaps and future research needs. The present review reports up-to-date knowledge about the role of Si to mitigate Cr toxicity and it will help to get better crop productivity in Cr-contaminated soils. The findings of the current review will educate the readers on Si functions in reducing Cr toxicity and will offer new ideas to develop Cr tolerance in plants through the use of Si.

Linear brain measurement: a new screening method for cognitive impairment in elderly patients with cerebral small vessel disease.

Background: The old adults have high incidence of cognitive impairment, especially in patients with cerebral small vessel disease (CSVD). Cognitive impairment is not easy to be detected in such populations. We aimed to develop clinical prediction models for different degrees of cognitive impairments in elderly CSVD patients based on conventional imaging and clinical data to determine the better indicators for assessing cognitive function in the CSVD elderly. Methods: 210 CSVD patients were screened out by the evaluation of Magnetic Resonance Imaging (MRI). Then, participants were divided into the following three groups according to the cognitive assessment results: control, mild cognitive impairment (MCI), and dementia groups. Clinical data were collected from all patients, including demographic data, biochemical indicators, carotid ultrasound, transcranial Doppler (TCD) indicators, and linear measurement parameters based on MRI. Results: Our results showed that the brain atrophy and vascular lesions developed progressive worsening with increased degree of cognitive impairment. Crouse score and Interuncal distance/Bitemporal distance (IUD/BTD) were independent risk factors for MCI in CSVD patients, and independent risk factors for dementia in CSVD were Crouse Score, the pulsatility index of the middle cerebral artery (MCAPI), IUD/BTD, and Sylvian fissure ratio (SFR). Overall, the parameters with high performance were the IUD/BTD (OR 2.28; 95% CI 1.26-4.10) and SFR (OR 3.28; 95% CI 1.54-6.91), and the AUC (area under the curve) in distinguishing between CSVD older adults with MCI and with dementia was 0.675 and 0.724, respectively. Linear brain measurement parameters had larger observed effect than other indexes to identify cognitive impairments in CSVD patients. Conclusion: This study shows that IUD/BTD and SFR are good predictors of cognitive impairments in CSVD elderly. Linear brain measurement showed a good predictive power for identifying MCI and dementia in elderly subjects with CSVD. Linear brain measurement could be a more suitable and novel method for screening cognitive impairment in aged CSVD patients in primary healthcare facilities, and worth further promotion among the rural population.

Diffusion MRI marks progressive alterations in fiber integrity in the zQ175DN mouse model of Huntington's disease.

Huntington's disease (HD) is a progressive neurodegenerative disease affecting motor and cognitive abilities. Multiple studies have found white matter anomalies in HD-affected humans and animal models of HD. The identification of sensitive white-matter-based biomarkers in HD animal models will be important in understanding disease mechanisms and testing the efficacy of therapeutic interventions. Here we investigated the progression of white matter deficits in the knock-in zQ175DN heterozygous (HET) mouse model of HD at 3, 6 and 11 months of age (M), reflecting different states of phenotypic progression. We compared findings from traditional diffusion tensor imaging (DTI) and advanced fixel-based analysis (FBA) diffusion metrics for their sensitivity in detecting white matter anomalies in the striatum, motor cortex, and segments of the corpus callosum. FBA metrics revealed progressive and widespread reductions of fiber cross-section and fiber density in myelinated bundles of HET mice. The corpus callosum genu was the most affected structure in HET mice at 6 and 11 M based on the DTI and FBA metrics, while the striatum showed the earliest progressive differences starting at 3 M based on the FBA metrics. Overall, FBA metrics detected earlier and more prominent alterations in myelinated fiber bundles compared to the DTI metrics. Luxol fast blue staining showed no loss in myelin density, indicating that diffusion anomalies could not be explained by myelin reduction but diffusion anomalies in HET mice were accompanied by increased levels of neurofilament light chain protein at 11 M. Altogether, our findings reveal progressive alterations in myelinated fiber bundles that can be measured using diffusion MRI, representing a candidate noninvasive imaging biomarker to study phenotype progression and the efficacy of therapeutic interventions in zQ175DN mice. Moreover, our study exposed higher sensitivity of FBA than DTI metrics, suggesting a potential benefit of adopting these advanced metrics in other contexts, including biomarker development in humans.

Overexpression of OsACL5 triggers environmentally-dependent leaf rolling and reduces grain size in rice.

Major polyamines include putrescine, spermidine, spermine and thermospermine, which play vital roles in growth and adaptation against environmental changes in plants. Thermospermine (T-Spm) is synthetised by ACL5. The function of ACL5 in rice is still unknown. In this study, we used a reverse genetic strategy to investigate the biological function of OsACL5. We generated several knockout mutants by pYLCRISPR/Cas9 system and overexpressing (OE) lines of OsACL5. Interestingly, the OE plants exhibited environmentally-dependent leaf rolling, smaller grains, lighter 1000-grain weight and reduction in yield per plot. The area of metaxylem vessels of roots and leaves of OE plants were significantly smaller than those of WT, which possibly caused reduction in leaf water potential, resulting in leaf rolling with rise in the environmental temperature and light intensity and decrease in humidity. Additionally, the T-Spm contents were markedly increased by over ninefold whereas the ethylene evolution was reduced in OE plants, suggesting that T-Spm signalling pathway interacts with ethylene pathway to regulate multiple agronomic characters. Moreover, the osacl5 exhibited an increase in grain length, 1000-grain weight, and yield per plot. OsACL5 may affect grain size via mediating the expression of OsDEP1, OsGS3 and OsGW2. Furthermore, haplotypes analysis indicated that OsACL5 plays a conserved function on regulating T-Spm levels during the domestication of rice. Our data demonstrated that identification of OsACL5 provides a theoretical basis for understanding the physiological mechanism of T-Spm which may play roles in triggering environmentally dependent leaf rolling; OsACL5 will be an important gene resource for molecular breeding for higher yield.

The effect of winter crop incorporation on greenhouse gas emissions from double rice-green manure rotation in South China.

Chemical fertilizer plays a vital role in increasing crop yield. However, the environmental risk and the adverse effect on soil caused by excessive chemical fertilizer can be mitigated by using organic fertilizer (green manure Chinese milk vetch) and straw returning. Therefore, this field study was conducted to determine the impact of winter crop incorporation with mineral fertilizers on methane (CH4) and nitrous oxide (N2O) emissions and the related genes (mcrA, pmoA, AOA, AOB, nirS, nirK, and nosZ) as well as the relationship among greenhouse gas (GHG) emissions, related genes, and soil properties. The study comprised winter crop incorporation with mineral fertilizer at the reduced rate of 0% (MRN1), 12.5% (MRN2), and 25% (MRN3). The results indicated that the early and late rice yield from treatments MRN2 and MRN3 increased by 25% and 4% compared with control CK (winter fallow, without green manure incorporation, and conventional nitrogen fertilizer amount). CH4 annual cumulative emission increased by 34% resulting from increased abundance of mcrA genes of methanogens. Furthermore, N2O annual cumulative emission increased due to soil microbial biomass nitrogen, AOA (amoA), AOB(amoA), nirK, and nirS abundance. The global warming potential (GWP) increased by 34%; however, there was no significant difference on the GHGI from all the treatments resulting from the increased yield. Therefore, winter crop incorporation with different rate of reduced mineral fertilizer significantly increased the crop yield and increased the SOC and MBC content. Meanwhile, winter crop incorporation increased CH4 and N2O annual cumulative emission mainly resulting from the increased abundance of mcrA genes of methanogens, soil microbial biomass nitrogen, AOA(amoA), AOB(amoA), nosZ, nirK, and nirS abundance.

Serum uric acid and outcome in hospitalized elderly patients with chronic heart failure through the whole spectrum of ejection fraction phenotypes.

INTRODUCTION: Elevated serum uric acid (SUA) levels have been associated with poor outcome in patients with heart failure (HF). Uric acid is associated with inflammation and microvascular dysfunction, which may differentially affect left ventricular ejection fraction (EF) phenotypes. We aimed to identify the role of SUA across EF phenotypes in hospitalized elderly patients with chronic HF. METHODS: We analyzed 1355 elderly patients who were diagnosed with chronic HF. All patients had SUA levels measured within the first 24 h following admission. Patients with left ventricle EF were categorized as having HF with reduced EF (HFrEF, EF < 40%), HF with mid-range EF (HFmrEF, 40%≦LVEF ≦ 49%) or HF with preserved EF (HFpEF, LVEF ≥ 50%). Endpoints were cardiovascular death, HF rehospitalization, and their composite. The median follow-up period was 18 months. RESULTS: Compared with the lowest SUA quartile, the highest SUA quartile was significantly associated with the endpoints (adjusted HR: 2.404, 95% CI: 1.178-4.906, P = 0.016; HR: 1.418, 95% CI: 1.021-1.971, P = 0.037; HR: 1.439, 95% CI: 1.049-1.972, P = 0.024, respectively). After model adjustment, a significant association of SUA with cardiovascular death and the composite endpoint persisted among HFrEF and HFmrEF patients in the highest SUA quartile (P < 0.05 for all). CONCLUSIONS: In hospitalized elderly patients with chronic HF, SUA is an independent predictor of adverse outcomes, which can be seen in HFrEF and HFmrEF patients.

The impact of obstructive sleep apnea on nonalcoholic fatty liver disease.

Obstructive sleep apnea (OSA) is characterized by episodic sleep state-dependent collapse of the upper airway, with consequent hypoxia, hypercapnia, and arousal from sleep. OSA contributes to multisystem damage; in severe cases, sudden cardiac death might occur. In addition to causing respiratory, cardiovascular and endocrine metabolic diseases, OSA is also closely associated with nonalcoholic fatty liver disease (NAFLD). As the prevalence of OSA and NAFLD increases rapidly, they significantly exert adverse effects on the health of human beings. The authors retrieved relevant documents on OSA and NAFLD from PubMed and Medline. This narrative review elaborates on the current knowledge of OSA and NAFLD, demonstrates the impact of OSA on NAFLD, and clarifies the underlying mechanisms of OSA in the progression of NAFLD. Although there is a lack of sufficient high-quality clinical studies to prove the causal or concomitant relationship between OSA and NAFLD, existing evidence has confirmed the effect of OSA on NAFLD. Elucidating the underlying mechanisms through which OSA impacts NAFLD would hold considerable importance in terms of both prevention and the identification of potential therapeutic targets for NAFLD.

A review on sources of soil antimony pollution and recent progress on remediation of antimony polluted soils.

Antimony (Sb) is a serious toxic and non-essential metalloid for animals, humans, and plants. The rapid increase in anthropogenic inputs from mining and industrial activities, vehicle emissions, and shoot activity increased the Sb concentration in the environment, which has become a serious concern across the globe. Hence, remediation of Sb-contaminated soils needs serious attention to provide safe and healthy foods to humans. Different techniques, including biochar (BC), compost, manures, plant additives, phyto-hormones, nano-particles (NPs), organic acids (OA), silicon (Si), microbial remediation techniques, and phytoremediation are being used globally to remediate the Sb polluted soils. In the present review, we described sources of soil Sb pollution, the environmental impact of antimony pollution, the multi-faceted nature of antimony pollution, recent progress in remediation techniques, and recommendations for the remediation of soil Sb-pollution. We also discussed the success stories and potential of different practices to remediate Sb-polluted soils. In particular, we discussed the various mechanisms, including bio-sorption, bio-accumulation, complexation, and electrostatic attraction, that can reduce the toxicity of Sb by converting Sb-V into Sb-III. Additionally, we also identified the research gaps that need to be filled in future studies. Therefore, the current review will help to develop appropriate and innovative strategies to limit Sb bioavailability and toxicity and sustainably manage Sb polluted soils hence reducing the toxic effects of Sb on the environment and human health.

Programmed Cell Death in Liver Fibrosis.

Programmed cell death (PCD) is a comprehensive term that encompasses various forms of cell death, such as apoptosis, necroptosis, pyroptosis, ferroptosis, and autophagy, which play a crucial role in the pathogenesis of liver fibrosis. PCD facilitates the elimination of aberrant cells, particularly activated hepatic stellate cells (HSCs), which are the primary producers of extracellular matrix (ECM). The removal of HSCs may impede ECM synthesis, thereby mitigating liver fibrosis. As such, PCD has emerged as a promising therapeutic target for the development of novel drugs to treat liver fibrosis. Numerous studies have been conducted to investigate the underlying mechanisms of PCD in the elimination of activated HSCs and other aberrant liver cells in fibrotic liver tissue, including hepatocytes, hepatic sinusoid endothelial cells (LSECs), and Kupffer cells (KCs). The induction of PCD, the interplay between different forms of PCD, and the potential harm or benefit of PCD in liver fibrosis are topics of ongoing research. Evidences suggest that PCD is a complex process with dual effects on liver fibrosis. The purpose of this review is to summarize the most recent advances in PCD and liver fibrosis research.

The impact and role of identified long noncoding RNAs in nonalcoholic fatty liver disease: A narrative review.

BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease worldwide, but its mechanism and pathophysiology remain unclear. Long noncoding RNAs (lncRNAs) may exert a vital influence on regulating various biological functions in NAFLD. METHODS: The databases such as Google Scholar, PubMed, and Medline were searched using the following keywords: nonalcoholic fatty liver disease, nonalcoholic fatty liver disease, NAFLD, nonalcoholic steatohepatitis, nonalcoholic steatohepatitis, NASH, long noncoding RNAs, and lncRNAs. Considering the titles and abstracts, unrelated studies were excluded. The authors evaluated the full texts of the remaining studies. RESULTS: We summarized the current knowledge of lncRNAs and the main signaling pathways of lncRNAs involved in NAFLD explored in recent years. As a heterogeneous group of noncoding RNAs (ncRNAs), lncRNAs play crucial roles in biological processes underlying the pathophysiology of NAFLD. The mechanisms, particularly those associated with the regulation of the expression and activities of lncRNAs, play important roles in NAFLD. CONCLUSION: A better comprehension of the mechanism controlled by lncRNAs in NAFLD is necessary for the identification of novel therapeutic targets for drug development and improved, noninvasive methods for diagnosis.

nirS and nosZII bacterial denitrifiers as well as fungal denitrifiers are coupled with N2O emissions in long-term fertilized soils.

Fertilizer application plays a critical role in soil fertility and crop yield and has been reported to significantly affect soil denitrification. However, the mechanisms by which denitrifying bacteria (nirK, nirS, nosZI, and nosZII) and fungi (nirK and p450nor) affect soil denitrification are poorly understood. Therefore, in this study, we investigated the effect of different fertilization treatments on the abundance, community structure, and function of soil denitrifying microorganisms in an agricultural ecosystem with long-term fertilization using mineral fertilizer or manure and their combination. The results showed that the application of organic fertilizer significantly increased the abundance of nirK-, nirS-, nosZI-, and nosZII-type denitrifying bacteria as the soil pH and phosphorus content increased. However, only the community structure of nirS- and nosZII-type denitrifying bacteria was influenced by the application of organic fertilizer, which led to a higher contribution of bacteria to nitrous oxide (N2O) emissions than that observed after inorganic fertilizer application. The increase in soil pH reduced the abundance of nirK-type denitrifying fungi, which may have presented a competitive disadvantage relative to bacteria, resulting in a lower contribution of fungi to N2O emissions than that observed after inorganic fertilizer application. The results demonstrated that organic fertilization had a significant impact on the community structure and activity of soil denitrifying bacteria and fungi. Our results also highlighted that after organic fertilizer application, nirS- and nosZII-denitrifying bacteria communities represent likely hot spots of bacterial soil N2O emissions while nirK-type denitrifying fungi represent hot spots for fungal soil N2O emissions.

Longitudinal investigation of changes in resting-state co-activation patterns and their predictive ability in the zQ175 DN mouse model of Huntington's disease.

Huntington's disease (HD) is a neurodegenerative disorder caused by expanded (≥ 40) glutamine-encoding CAG repeats in the huntingtin gene, which leads to dysfunction and death of predominantly striatal and cortical neurons. While the genetic profile and clinical signs and symptoms of the disease are better known, changes in the functional architecture of the brain, especially before the clinical expression becomes apparent, are not fully and consistently characterized. In this study, we sought to uncover functional changes in the brain in the heterozygous (HET) zQ175 delta-neo (DN) mouse model at 3, 6, and 10 months of age, using resting-state functional magnetic resonance imaging (RS-fMRI). This mouse model shows molecular, cellular and circuitry alterations that worsen through age. Motor function disturbances are manifested in this model at 6 and 10 months of age. Specifically, we investigated, longitudinally, changes in co-activation patterns (CAPs) that are the transient states of brain activity constituting the resting-state networks (RSNs). Most robust changes in the temporal properties of CAPs occurred at the 10-months time point; the durations of two anti-correlated CAPs, characterized by simultaneous co-activation of default-mode like network (DMLN) and co-deactivation of lateral-cortical network (LCN) and vice-versa, were reduced in the zQ175 DN HET animals compared to the wild-type mice. Changes in the spatial properties, measured in terms of activation levels of different brain regions, during CAPs were found at all three ages and became progressively more pronounced at 6-, and 10 months of age. We then assessed the cross-validated predictive power of CAP metrics to distinguish HET animals from controls. Spatial properties of CAPs performed significantly better than the chance level at all three ages with 80% classification accuracy at 6 and 10 months of age.

A novel digital biomarker of sarcopenia in frail elderly: New combination of gait parameters under dual-task walking.

Background: Frailty caused by deterioration in multiple physiological systems has led to a significant increase in adverse events such as falls, disability, and death in frail older people. Similar to frailty, sarcopenia, defined as loss of skeletal muscle mass and strength, is tightly related to mobility disorders, falls, and fractures. With population aging, co-occurrences of frailty and sarcopenia are increasingly common in the elderly, which are more deleterious for the health and independence of older adults. But the high similarity and overlap between the frailty and sarcopenia increase the difficulty of early recognition of frailty with sarcopenia. The purpose of this study is to use detailed gait assessment to determine the more convenient and sensitive digital biomarker of sarcopenia in the frail population. Methods: Ninety-five frail elderly people (age = 86 ± 7 years old, BMI, and body mass index = 23.21 ± 3.40 kg/m2) were screened out by the evaluation of Fried criteria. Then, 41 participants (46%) were identified with sarcopenia, and 51 participants (54%) were identified without sarcopenia. Using a validated wearable platform, participants' gait performance was evaluated under single-task and dual-task (DT). Participants walked back and forth on the 7-m-long trail for 2 min at a habitual speed. Gait parameters of interest include cadence, gait cycle duration, step duration, gait speed, variability of gait speed, stride length, turn duration, and steps in turn. Results: Our results showed that compared with the frail elderly without sarcopenia, the gait performance of the sarcopenic group in single-task and dual-task walking was worse. Overall, the parameters with high performance were the gait speed (DT) (OR 0.914; 95% CI 0.868-0.962) and turn duration (DT) (OR 7.907; 95% CI 2.401-26.039) under dual-task conditions, and the AUC in distinguishing between frail older adults with and without sarcopenia was 0.688 and 0.736, respectively. Turn duration in dual-task testing had larger observed effect than gait speed to identify sarcopenia in the frail population, this result remained significant even after controlling for potential confounds. When gait speed (DT) and turn duration (DT) were combined in the model, AUC increased from 0.688 to 0.763. Conclusion: This study shows that gait speed and turn duration under dual-task are good predictors of sarcopenia in frail elderly, and turn duration (DT) has a better predictive ability. The gait speed (DT) combined with turn duration (DT) is a potential gait digital Biomarker of sarcopenia in the frail elderly. Dual-task gait assessment and detailed gait indexes provide important value for identification of sarcopenia in frail elderly people.

Resting-state fMRI reveals longitudinal alterations in brain network connectivity in the zQ175DN mouse model of Huntington's disease.

Huntington's disease is an autosomal, dominantly inherited neurodegenerative disease caused by an expansion of the CAG repeats in exon 1 of the huntingtin gene. Neuronal degeneration and dysfunction that precedes regional atrophy result in the impairment of striatal and cortical circuits that affect the brain's large-scale network functionality. However, the evolution of these disease-driven, large-scale connectivity alterations is still poorly understood. Here we used resting-state fMRI to investigate functional connectivity changes in a mouse model of Huntington's disease in several relevant brain networks and how they are affected at different ages that follow a disease-like phenotypic progression. Towards this, we used the heterozygous (HET) form of the zQ175DN Huntington's disease mouse model that recapitulates aspects of human disease pathology. Seed- and Region-based analyses were performed at different ages, on 3-, 6-, 10-, and 12-month-old HET and age-matched wild-type mice. Our results demonstrate decreased connectivity starting at 6 months of age, most prominently in regions such as the retrosplenial and cingulate cortices, pertaining to the default mode-like network and auditory and visual cortices, part of the associative cortical network. At 12 months, we observe a shift towards decreased connectivity in regions such as the somatosensory cortices, pertaining to the lateral cortical network, and the caudate putamen, a constituent of the subcortical network. Moreover, we assessed the impact of distinct Huntington's Disease-like pathology of the zQ175DN HET mice on age-dependent connectivity between different brain regions and networks where we demonstrate that connectivity strength follows a non-linear, inverted U-shape pattern, a well-known phenomenon of development and normal aging. Conversely, the neuropathologically driven alteration of connectivity, especially in the default mode and associative cortical networks, showed diminished age-dependent evolution of functional connectivity. These findings reveal that in this Huntington's disease model, altered connectivity starts with cortical network aberrations which precede striatal connectivity changes, that appear only at a later age. Taken together, these results suggest that the age-dependent cortical network dysfunction seen in rodents could represent a relevant pathological process in Huntington's disease progression.

MiR-155-5p-SOCS1/JAK1/STAT1 participates in hepatic lymphangiogenesis in liver fibrosis and cirrhosis by regulating M1 macrophage polarization.

BACKGROUND: The role and underlying mechanism of liver macrophages and their derived miR-155-5p in hepatic lymphangiogenesis in liver fibrosis remain unclear. Here, we investigated the mechanism by which macrophages and miR-155-5p were involved in lymphangiogenesis during liver fibrosis and cirrhosis. METHODS: In vivo, hepatic lymphatic vessel expansion was evaluated; the liver macrophage subsets, proportion of peripherally-derived macrophages and expressions of CCL25, MCP-1, VAP-1 and MAdCAM-1 were documented; and miR-155-5p in the peripheral blood and liver was detected. In vitro, macrophages with miR-155-5p overexpression and inhibition were used to clarify the effect of miR-155-5p on regulation of macrophage polarization and the possible signalling pathway. RESULTS: Hepatic lymphangiogenesis was observed in mice with liver fibrosis and cirrhosis challenged with carbon tetrachloride (CCl4). In the liver, the number of M1 macrophages was associated with lymphangiogenesis and the degree of fibrosis. The liver recruitment of peripherally-derived macrophages occurred during liver fibrosis. The levels of miR-155-5p in the liver and peripheral blood gradually increased with aggravation of liver fibrosis. In vitro, SOCS1, a target of miR-155-5p, regulated macrophage polarization into the M1 phenotype through the JAK1/STAT1 pathway. CONCLUSION: MiR-155-5p-SOCS1/JAK1/STAT1 pathway participates in hepatic lymphangiogenesis in mice with liver fibrosis and cirrhosis induced by CCl4 by regulating the polarization of macrophages into the M1 phenotype.

Toxic effects of antimony in plants: Reasons and remediation possibilities-A review and future prospects.

Antimony (Sb) is a dangerous heavy metal (HM) that poses a serious threat to the health of plants, animals, and humans. Leaching from mining wastes and weathering of sulfide ores are the major ways of introducing Sb into our soils and aquatic environments. Crops grown on Sb-contaminated soils are a major reason of Sb entry into humans by eating Sb-contaminated foods. Sb toxicity in plants reduces seed germination and root and shoot growth, and causes substantial reduction in plant growth and final productions. Moreover, Sb also induces chlorosis, causes damage to the photosynthetic apparatus, reduces membrane stability and nutrient uptake, and increases oxidative stress by increasing reactive oxygen species, thereby reducing plant growth and development. The threats induced by Sb toxicity and Sb concentration in soils are increasing day by day, which would be a major risk to crop production and human health. Additionally, the lack of appropriate measures regarding the remediation of Sb-contaminated soils will further intensify the current situation. Therefore, future research must be aimed at devising appropriate measures to mitigate the hazardous impacts of Sb toxicity on plants, humans, and the environment and to prevent the entry of Sb into our ecosystem. We have also described the various strategies to remediate Sb-contaminated soils to prevent its entry into the human food chain. Additionally, we also identified the various research gaps that must be addressed in future research programs. We believe that this review will help readers to develop the appropriate measures to minimize the toxic effects of Sb and its entry into our ecosystem. This will ensure the proper food production on Sb-contaminated soils.

Association between Dietary Carbohydrate Intake and Control of Blood Pressure in Patients with Essential Hypertension.

BACKGROUND: Both high and low percentages of carbohydrate diets were associated with increased mortality and new-onset hypertension. However, few studies have aggregated to explore the association between carbohydrate intake and blood pressure (BP) control in patients with hypertension. This study aimed to explore the association between carbohydrate-to-energy proportion (CEP) and the rate of poorly controlled BP in patients with hypertension. METHODS: A cross-sectional survey was conducted in one comprehensive hospital and one community clinic in China. Dietary CEP was obtained through two-24 h dietary recalls. According to the quintiles of CEP, the participants were divided into Q1-Q5 groups. The average of two BP values was adopted as the final BP value, and poorly controlled BP was defined as systolic BP (SBP) ≥140 mmHg and/or diastolic BP (DBP) ≥ 90 mmHg. RESULTS: A total of 459 hypertensive patients were recruited. In univariate analyses, CEP was associated with the control of SBP and DBP. After the covariates were adjusted for, fewer CEPs in Q1 (OR, 4.335; 95% CI, 1.663, 11.299) and Q2 (OR, 2.482; 95% CI, 1.234, 4.989) were significantly associated with higher rates of poor SBP control. CONCLUSIONS: A lower dietary CEP is a risk factor for SBP control, whereas an appropriate CEP of 56% to 66% is beneficial for BP control in patients with essential hypertension.

A multi-omics approach based on 1H-NMR metabonomics combined with target protein analysis to reveal the mechanism of RIAISs on cervical carcinoma patients.

Cervical carcinoma (CC) is the fourth most common cancer in females and radiotherapy is always as the definitive therapy for cervical cancer patients who are not suitable for surgery. Radiation-induced acute intestinal symptoms (RIAISs) occur in 50-80% of cervical cancer patients. Some research shows that RIAISs may relate to inflammatory reaction by radiotherapy but the action mechanism is also not clearly and the details of the molecular mechanism are still urgently needed. In this paper, basing on 1H-NMR metabonomic and bioinformatics analysis, an integrated multi-omics analysis including metabonomics and bioinformatics was performed. We propose a hypothesis about pathogenic mechanism on RIAISs and proofed it through western-blot. Our results indicated significant dysregulation of metabolic pathways in RIAIS patients. Most importantly, we found that RIAISs were associated p53 and PI3K-AKT pathway.