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Abstract Soil organic matter (SOM) plays key roles in sloping land erosion control. This study explores SOM content across Hubei Province, China, focusing on four soil types under various conservation strategies. Field samples (n = 243) were collected under 27 monitoring sites employing diverse conservation strategies in runoff plots. Results indicated substantial variability in SOM content among soil types, with calcareous soils exhibiting the highest levels (12.63 g kg−1). Conversely, red soils displayed the lowest SOM content (6.32 g kg−1). However, short‐term conservation strategies and their interaction with soil type did not significantly influence SOM. The findings underscore the intricate relationship between soil types and SOM dynamics. This study contributes to the understanding of SOM dynamics in diverse landscapes, offering valuable guidance for policymakers and land managers to apply practices in mitigating erosion and enhancing soil health. Core Ideas Soil organic matter (SOM) characteristics focusing on four soil types under various conservation strategies were studied in Hubei Province. Calcareous soils exhibited the highest levels of SOM. Short‐term conservation strategies have no significant effect on SOM for each soil type. Land managers need proper practices to retain soil organic matter in mitigating erosion and enhancing soil health.

Abstract Background Eukaryotic genes contain introns that are removed by the spliceosomal machinery during mRNA maturation. Introns impose a huge energetic burden on a cell; therefore, they must play an essential role in maintaining genome stability and/or regulating gene expression. Many genes (> 50%) in Plasmodium parasites contain predicted introns, including introns in 5′ and 3′ untranslated regions (UTR). However, the roles of UTR introns in the gene expression of malaria parasites remain unknown. Methods In this study, an episomal dual-luciferase assay was developed to evaluate gene expression driven by promoters with or without a 5′UTR intron from four Plasmodium yoelii genes. To investigate the effect of the 5′UTR intron on endogenous gene expression, the pytctp gene was tagged with 3xHA at the N-terminal of the coding region, and parasites with or without the 5′UTR intron were generated using the CRISPR/Cas9 system. Results We showed that promoters with 5′UTR introns had higher activities in driving gene expression than those without 5′UTR introns. The results were confirmed in recombinant parasites expressing an HA-tagged gene (pytctp) driven by promoter with or without 5′UTR intron. The enhancement of gene expression was intron size dependent, but not the DNA sequence, e.g. the longer the intron, the higher levels of expression. Similar results were observed when a promoter from one strain of P. yoelii was introduced into different parasite strains. Finally, the 5′UTR introns were alternatively spliced in different parasite development stages, suggesting an active mechanism employed by the parasites to regulate gene expression in various developmental stages. Conclusions Plasmodium 5′UTR introns enhance gene expression in a size-dependent manner; the presence of alternatively spliced mRNAs in different parasite developmental stages suggests that alternative slicing of 5′UTR introns is one of the key mechanisms in regulating parasite gene expression and differentiation. Graphical Abstract

The determination of soil saturated hydraulic conductivity (Ks) is crucial in environmental and engineering fields. However, the current direct measurement methods of Ks are time-consuming and labor-intensive. As an alternative method, many researchers have developed a series of pedotransfer functions (PTFs) that estimate Ks based on easily accessible soil properties. Unfortunately, most existing PTFs of Ks focus on temperate and tropical regions in the United States and Europe. There is a lack of research discussing the applicability of Ks models in subtropical areas. To resolve this issue, we conduct a study using 515 subtropical soil samples to test the performance of existing PTFs of Ks. The Ks values of investigated soils range from 1.4 × 10-4 to 290 cm h−1. Among the affecting factors, soil bulk density (ρb) and effective porosity (φe) are found to be the most important variables. Current PTFs considering soil pore structural property (i.e., φe) or soil texture solely are not effective in assessing Ks of subtropical soils. To address this limitation, we integrate soil pore structural and textural properties and develop a new PTF based on the Kozeny-Carman equation. The performance and reliability of the new PTF are evaluated using independent Ks datasets from various regions. The results show a significant positive correlation between the measured Ks and the predicted Ks from the new PTF for subtropical soils with an R2 of 0.69, an average RMSE in log10Ks (cm h−1) of 0.496, and a mean bias value of 0.070. Besides, the new PTF is found to perform as well as widely used machine learning tools.

ABSTRACT Aims/Introduction The coronary physiology and prognosis of patients with different hemoglobin A1c (HbA1c) levels after percutaneous coronary intervention (PCI) are currently unknown. The aim of this study was to assess the effect of different levels of HbA1c control on coronary physiology in patients who underwent PCI for coronary heart disease combined with type 2 diabetes mellitus by quantitative flow ratio (QFR). Materials and Methods Patients who successfully underwent PCI and completed 1‐year coronary angiographic follow up were enrolled, clinical data were collected, and QFR at immediate and 1‐year follow up after PCI was retrospectively analyzed. A total of 257 patients (361 vessels) were finally enrolled and divided into the hemoglobin A1c (HbA1c)‐compliance group (103 patients, 138 vessels) and non‐HbA1c‐compliance group (154 patients, 223 vessels) according to the HbA1c cut‐off value of 7%. We compared the results of QFR analysis and clinical outcomes between the two groups. Results At 1‐year follow up after PCI, the QFR was significantly higher (0.94 ± 0.07 vs 0.92 ± 0.10, P = 0.019) and declined less (0.014 ± 0.066 vs 0.033 ± 0.095, P = 0.029) in the HbA1c‐compliance group. Meanwhile, the incidence of physiological restenosis was lower in the HbA1c‐compliance group (2.9% vs 8.5%, P = 0.034). Additionally, the target vessel revascularization rate was lower in the HbA1c‐compliance group (6.8% vs 16.9%, P = 0.018). Furthermore, HbA1c ≥7% (OR 2.113, 95% confidence interval 1.081–4.128, P = 0.029) and QFR decline (OR 2.215, 95% confidence interval 1.147–4.277, P = 0.018) were independent risk factors for target vessel revascularization. Conclusion Patients with well‐controlled HbA1c levels have better coronary physiological benefits and the incidence of adverse clinical outcome events might be reduced.

Abstract Mutations in a Plasmodium de-ubiquitinase UBP1 have been linked to antimalarial drug resistance. However, the UBP1-mediated drug-resistant mechanism remains unknown. Through drug selection, genetic mapping, allelic exchange, and functional characterization, here we show that simultaneous mutations of two amino acids (I1560N and P2874T) in the Plasmodium yoelii UBP1 can mediate high-level resistance to mefloquine, lumefantrine, and piperaquine. Mechanistically, the double mutations are shown to impair UBP1 cytoplasmic aggregation and de-ubiquitinating activity, leading to increased ubiquitination levels and altered protein localization, from the parasite digestive vacuole to the plasma membrane, of the P. yoelii multidrug resistance transporter 1 (MDR1). The MDR1 on the plasma membrane enhances the efflux of substrates/drugs out of the parasite cytoplasm to confer multidrug resistance, which can be reversed by inhibition of MDR1 transport. This study reveals a previously unknown drug-resistant mechanism mediated by UBP1 through altered MDR1 localization and substrate transport direction in a mouse model, providing a new malaria treatment strategy.

Metabolic syndrome (MetS) is a group of conditions characterized by hypertension (HTN), hyperglycaemia or insulin resistance (IR), hyperlipidaemia, and abdominal obesity. MetS is associated with a high incidence of cardiovascular events and mortality and is an independent risk factor for chronic kidney disease (CKD). MetS can cause CKD or accelerate the progression of kidney disease. Recent studies have found that MetS and kidney disease have a cause-and-effect relationship. Patients with CKD, those undergoing kidney transplantation, or kidney donors have a significantly higher risk of developing MetS than normal people. The present study reviewed the possible mechanisms of MetS in patients with CKD, including the disorders of glucose and fat metabolism after kidney injury, IR, HTN and the administration of glucocorticoid and calcineurin inhibitors. In addition, this study reviewed the effect of MetS in patients with CKD on important target organs such as the kidney, heart, brain and blood vessels, and the treatment and prevention of CKD combined with MetS. The study aims to provide strategies for the diagnosis, treatment and prevention of CKD in patients with MetS.

ABSTRACTCerebral malaria (CM) is a severe neurological complication of Plasmodium falciparum infection with acute brain lesions. Genetic variations in both host and parasite have been associated with susceptibility to CM, but the underlying molecular mechanism remains unclear. Here, we demonstrate that variants of human apolipoprotein E (hApoE) impact the outcome of Plasmodium berghei ANKA (PbA)-induced experimental cerebral malaria (ECM). Mice carrying the hApoE2 isoform have fewer intracerebral hemorrhages and are more resistant to ECM than mice bearing the hApoE3, hApoE4, or endogenous murine ApoE (mApoE). hApoE2 mice infected with PbA showed increased splenomegaly and IFN-γ levels in serum but reduced cerebral cell apoptosis that correlated with the survival advantage against ECM. In addition, upregulated expression of genes associated with lipid metabolism and downregulated expression of genes linked to immune responses were observed in the brain tissue of hApoE2 mice relative to ECM-susceptible mice after PbA infection. Notably, serum cholesterol and the cholesterol content of brain-infiltrating CD8+ T cells are significantly higher in infected hApoE2 mice, which might contribute to a significant reduction in the sequestration of brain CD8+ T cells. Consistent with the finding that fewer brain lesions occurred in infected hApoE2 mice, fewer behavioral deficits were observed in the hApoE2 mice. Finally, a meta-analysis of publicly available data also showed an increased hApoE2 allele in the malaria-endemic African population, suggesting malaria selection. This study shows that hApoE2 protects mice from ECM through suppression of CD8+ T cell activation and migration to the brain and enhanced cholesterol metabolism.IMPORTANCECerebral malaria (CM) is the deadliest complication of malaria infection with an estimated 15%–25% mortality. Even with timely and effective treatment with antimalarial drugs such as quinine and artemisinin derivatives, survivors of CM may suffer long-term cognitive and neurological impairment. Here, we show that human apolipoprotein E variant 2 (hApoE2) protects mice from experimental CM (ECM) via suppression of CD8+ T cell activation and infiltration to the brain, enhanced cholesterol metabolism, and increased IFN-γ production, leading to reduced endothelial cell apoptosis, BBB disruption, and ECM symptoms. Our results suggest that hApoE can be an important factor for risk assessment and treatment of CM in humans.

A 68-year-old male, who was undergoing XELOX plus trastuzumab therapy for gastric cancer, developed proteinuria, hematuria, and progressive increase in creatinine after 3 months. Subsequently, the patient also experienced hemoptysis, nasal bleeding. Chest CT examination shown pulmonary hemorrhage. The MRI of the nasopharynx ruled out nasopharyngeal cancer recurrence. The MPO and PR3 were elevated, and renal biopsy confirmed ANCA-related vasculitis, which affected the lungs, kidneys, and nasopharynx. Based on the review of the patient’’s medical history and medication, it is believed that ANCA-related vasculitis was caused by XELOX plus trastuzumab chemotherapy, but it is difficult to confirm which specific drug caused it. After stopping XELOX plus trastuzumab chemotherapy, glucocorticoids and cyclophosphamide was given, the patient’’s pulmonary hemorrhage and nasal bleeding stopped, and the lung lesions were absorbed. The renal function also improved. The patient later experienced pulmonary infection again, and tNGS indicated Legionella pneumophila and pulmonary tuberculosis infection. Despite anti-infection treatment, steroid dose was rapidly reduced. Ultimately, the patient gave up on treatment and eventually died.

Podocytes form a key component of the glomerular filtration barrier. Damage to podocytes is referred to as “podocyte disease.” There are many causes of podocyte injury, including primary injury, secondary injury, and gene mutations. Primary podocytosis mostly manifests as nephrotic syndrome. At present, first-line treatment is based on glucocorticoid administration combined with immunosuppressive therapy, but some patients still progress to end-stage renal disease. In Asia, especially in China, traditional Chinese medicine (TCM) still plays an important role in the treatment of kidney diseases. This study summarizes the potential mechanism of TCM and its active components in protecting podocytes, such as repairing podocyte injury, inhibiting podocyte proliferation, reducing podocyte apoptosis and excretion, maintaining podocyte skeleton structure, and upregulating podocyte-related protein expression. At the same time, the clinical efficacy of TCM in the treatment of primary podocytosis (including idiopathic membranous nephropathy, minimal change disease, and focal segmental glomerulosclerosis) is summarized to support the development of new treatment strategies for primary podocytosis.

A growing number of studies have confirmed that immune cells play various key roles in the pathophysiology of acute kidney injury (AKI) development. After the resident immune cells and intrinsic renal cells are damaged by ischemia and hypoxia, drugs and toxins, more immune cells will be recruited to infiltrate through the release of chemokines, while the intrinsic cells promote macrophage polarity conversion, and the immune cells will promote various programmed deaths, phenotypic conversion and cycle arrest of the intrinsic cells, ultimately leading to renal impairment and fibrosis. In the complex and dynamic immune microenvironment of AKI, the bidirectional interaction between immune cells and intrinsic renal cells affects the prognosis of the kidney and the progression of fibrosis, and determines the ultimate fate of the kidney.

At present, there is no effective drug for the treatment of renal fibrosis; in particular, a safe and effective treatment for renal fibrosis should be established. Cordyceps has several medical effects, including immunoregulatory, antitumor, anti-inflammatory, and antioxidant effects, and may prevent kidney, liver, and heart diseases. Cordyceps has also been reported to be effective in the treatment of renal fibrosis. In this paper, we review the potential mechanisms of Cordyceps against renal fibrosis, focusing on the effects of Cordyceps on inflammation, oxidative stress, apoptosis, regulation of autophagy, reduction of extracellular matrix deposition, and fibroblast activation. We also discuss relevant published clinical trials and meta-analyses. Available clinical studies support the possibility that Cordyceps and related products provide benefits to patients with chronic kidney diseases as adjuvants to conventional drugs. However, the existing clinical studies are limited by low quality and significant heterogeneity. The use of Cordyceps and related products may be a potential strategy for the treatment of renal fibrosis. Randomized controlled trial studies with good methodological quality, favorable experimental design, and large sample size are needed to evaluate the efficacy and safety of Cordyceps.

Metabolic syndrome (MetS) includes visceral obesity, hyperglycemia, dyslipidemia, and hypertension. The prevalence of MetS is 20-25%, which is an important risk factor for chronic kidney disease (CKD). MetS causes effects on renal pathophysiology, including glomerular hyperfiltration, RAAS, microalbuminuria, profibrotic factors and podocyte injury. This review compares several criteria of MetS and analyzes their differences. MetS and the pathogenesis of CKD includes insulin resistance, obesity, dyslipidemia, inflammation, oxidative stress, and endothelial dysfunction. The intervention of MetS-related renal damage is the focus of this article and includes controlling body weight, hypertension, hyperglycemia, and hyperlipidemia, requiring all components to meet the criteria. In addition, interventions such as endoplasmic reticulum stress, oxidative stress, gut microbiota, body metabolism, appetite inhibition, podocyte apoptosis, and mesenchymal stem cells are reviewed.

Antineutrophil cytoplasmic antibody associated vasculitis includes granulomatosis with polyangiitis, eosinophilic granulomatosis with polyangiitis (EGPA), and microscopic polyangiitis. While EGPA has no specific symptoms, it usually presents as necrotizing vasculitis, eosinophil infiltration of the tissues and organs, and extravascular granuloma formation. Here, we report a patient who had a rare initial presentation of oral granuloma and had been previously misdiagnosed several times at other hospitals. He was finally diagnosed with EGPA and recovered after methylprednisolone and cyclophosphamide treatment. The disease EGPA can present with a rare initial presentation of oral granuloma, methylprednisolone, and cyclophosphamide can be a suitable choice of treatment.

Sepsis-associated acute kidney injury (SA-AKI) is common in patients with severe sepsis, and has a high incidence rate and high mortality rate in ICU patients. Most patients progress to AKI before drug treatment is initiated. Early studies suggest that the main mechanism of SA-AKI is that sepsis leads to vasodilation, hypotension and shock, resulting in insufficient renal blood perfusion, finally leading to renal tubular cell ischemia and necrosis. Research results in recent years have shown that programmed cell death such as apoptosis, necroptosis, pyroptosis and autophagy play important roles. In the early stage of sepsis-related AKI, autophagy bodies form and inhibit various types of programmed cell death. With the progress of disease, programmed cell death begins. Apoptosis promoter represents caspase-8-induced apoptosis and apoptosis effector represents caspase-3-induced apoptosis, however, caspase-11 and caspase-1 regulate gasdermin D-mediated pyroptosis. Caspase-8 and receptor interacting kinase 1 bodies mediate necroptosis. This review focuses on the pathophysiological mechanisms of various programmed cell death in sepsis-related AKI.

2024 marks the 20th anniversary of our research on the resolution and absolute asymmetric synthesis of cis-[CoBr(NH3)(en)2]Br2 in the department of chemistry at Xiamen University. It has been 113 years since the founder of coordination chemistry, Alfred Werner, successfully resoluted the two series of complexes cis-[CoX(NH3)(en)2]X2 (X = Br-, Cl-) in 1911. In order to commemorate Werner and his team's extraordinary contributions to the founding and development of coordination chemistry, this article for the first time elaborates on the initial exploration, subsequent progress, and related studies on the resolution (Alfred Werner with Victor Louis King and Ernst Scholze) of cis-[CoX(NH3)(en)2]X2 and the absolute asymmetric synthesis (Kouichi Asakura) of cis-[CoBr(NH3)(en)2]Br2. It elucidates the important role of coordination stereochemistry of chiral octahedral complexes in the history of scientific development, and the "electron transfer catalysis-crystallization induction" mechanism based on the basic principles of coordination chemistry is proposed for the absolute asymmetric synthesis of cis-[CoBr(NH3)(en)2]Br2. [ABSTRACT FROM AUTHOR]

Objective: The purpose of this paper is to promote the medical treatment of colorectal cancer in our country and to save the lives of patients with colorectal cancer by studying mammalian target of rapamycin (mTOR) and the biologic information analysis of colorectal cancer. Methods: We analyzed mTOR expression and survival differences using data from Coad & read from the TCGA public database and explored the coexpression regulatory network of mTOR. mTOR-regulated mirnas were screened using the Linked Omics database. In addition, we explored the association of mTOR with drug sensitivity, immune cell correlations, microsatellite deletions, tumor mutational burden, and mutational analysis. Results: The expression and survival of mTOR were significant different in colorectal cancer, and were related to the sensitivity of Bleomycin, Cisplatin and Gemcitabine. mTOR is associated with dendritic cell activation, NK cell dormancy, dendritic cell dormancy, and eosinophil granulocyte. mTOR is associated with microsatellite deletions, and tumor mutational load. Conclusions: Based on these findings, we consumer mTOR as a biomarker for the diagnosis and prognosis of colorectal cancer. [ABSTRACT FROM AUTHOR]

The preparation of coumarin-3-carboxylic acid is a classical chemistry experiment. In this experiment, the reactants, salicylaldehyde and diethyl malonate, as well as the piperidine catalyst are mixed under reflux for 2 h to obtain coumarin-3-carboxylic acid after base hydrolysis and acidification. We have made the following improvements and extensive designs to the experiment: 1) By substituting diethyl malonate with Meldrum's acid, coumarin-3-carboxylic acid can be obtained by heating at 90 °C for 30 min in water, and 7-(diethylamino)coumarin-3-carboxylic acid can be synthesized by changing the substrate; 2) Observing the fluorescence of the solution with Eu3+, coumarin-3-carboxylic acid, and 7-(diethylamino)coumarin-3-carboxylic acid and using computational chemistry can help verify the energy transfer property. The modified experiment, which involves a number of important multidisciplinary knowledge points, has strong modularity, comprehensiveness, interest, and teaching feasibility. Moreover, it is conducive to cultivating students' innovative and comprehensive application abilities. [ABSTRACT FROM AUTHOR]

Objective To establish an automated corneal nerve analysis system for corneal in vivo confocal microscopy (IVCM) images from both the whorl-like corneal nerves in the inferior whorl (IW) region and the straight ones in the central cornea and to characterise the geometric features of cornea nerves in dry eye disease (DED).Methods and analysis An encoder–decoder-based semi-supervised method was proposed for corneal nerve segmentation. This model’s performance was compared with the ground truth provided by experienced clinicians, using Dice similarity coefficient (DSC), mean intersection over union (mIoU), accuracy (Acc), sensitivity (Sen) and specificity (Spe). The corneal nerve total length (CNFL), tortuosity (CNTor), fractal dimension (CNDf) and number of branching points (CNBP) were used for further analysis in an independent DED dataset including 50 patients with DED and 30 healthy controls.Results The model achieved 95.72% Acc, 97.88% Spe, 80.61% Sen, 75.26% DSC, 77.57% mIoU and an area under the curve value of 0.98. For clinical evaluation, the CNFL, CNBP and CNDf for whorl-like and straight nerves showed a significant decrease in DED patients compared with healthy controls (p0.05).Conclusion The proposed method segments both whorl-like and straight corneal nerves in IVCM images with high accuracy and offered parameters to objectively quantify DED-induced corneal nerve injury. The IW is an effective region to detect alterations of multiple geometric indices in DED patients.

Objectives This study aims to evaluate the effect of congenital ectopia lentis (CEL) on functional vision and eye-related quality of life (ER-QOL) in children and their families using the Paediatric Eye Questionnaire (PedEyeQ).Design A questionnaire survey administered via in-person interviews of patients with CEL and their parents.Participants 51 children with CEL and 53 visually normal controls accompanied by 1 parent completed the survey questionnaires for the study from March 2022 to September 2022.Outcome measures PedEyeQ domain scores. Functional vision and ER-QOL of children and their families were evaluated by calculating and comparing the Rasch domain scores of the PedEyeQ.Results PedEyeQ domain scores were significantly worse with CEL compared with controls (p