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Background Acute kidney injury (AKI) has been associated with increased risks of new-onset and worsening proteinuria. However, the epidemiologic data of post-AKI proteinuria was still lacking. This study aimed to determine the incidence, risk factors and clinical correlations of post-AKI proteinuria among hospitalized patients. Methods This study conducted a multicenter cohort including patients aged 18–100 years with hospital-acquired AKI (HA-AKI) hospitalized at 19 medical centers throughout China. The primary outcome was the incidence of post-AKI proteinuria. Secondary outcomes included AKI recovery and kidney disease progression. The results of both quantitative and qualitative urinary protein tests were used to define post-AKI proteinuria. Cox proportional hazard model with stepwise regression was used to determine the risk factors for post-AKI proteinuria. Results Of 6,206 HA-AKI patients without proteinuria at baseline, 2,102 (33.9%) had new-onset proteinuria, whereas, of 5,137 HA-AKI with baseline proteinuria, 894 (17.4%) had worsening proteinuria after AKI. Higher AKI stage and preexisting CKD diagnosis were risk factors for new-onset proteinuria and worsening proteinuria, whereas treatment with RAS inhibitors was associated with an 11% lower risk of incident proteinuria. About 60% and 75% of patients with post-AKI new-onset and worsening proteinuria, respectively, recovered within 3 months. Worsening proteinuria was associated with a lower incidence of AKI recovery and a higher risk of kidney disease progression. Conclusions Post-AKI proteinuria is common and usually transient among hospitalized patients. The risk profiles for new-onset and worsening post-AKI proteinuria differed markedly. Worsening proteinuria after AKI was associated with adverse kidney outcomes, which emphasized the need for close monitoring of proteinuria after AKI.

Background In the general population, metabolic syndrome (MetS) is associated with increased risk of cognitive impairment, including global and specific cognitive domains. These associations are not well studied in patients undergoing hemodialysis and were the focus of the current investigation. Methods In this multicenter cross-sectional study, 5492 adult hemodialysis patients (3351 men; mean age: 54.4 ± 15.2 years) treated in twenty-two dialysis centers of Guizhou, China were included. The Mini-Mental State Examination (MMSE) was utilized to assess mild cognitive impairment (MCI). MetS was diagnosed with abdominal obesity, hypertension, hyperglycemia, and dyslipidemia. Multivariate logistic and linear regression models were used to examine the associations of MetS, its components, and metabolic scores with the risk of MCI. Restricted cubic spline analyses were performed to explore the dose–response associations. Results Hemodialysis patients had a high prevalence of MetS (62.3%) and MCI (34.3%). MetS was positively associated with MCI risk with adjusted ORs of 1.22 [95% confidence interval (CI) 1.08–1.37, P = 0.001]. Compared to no MetS, adjusted ORs for MCI were 2.03 (95% CI 1.04–3.98) for 22.51 (95% CI 1.28–4.90) for 3, 2.35 (95% CI 1.20–4.62) for 4, and 2.94 (95% CI 1.48–5.84) for 5 components. Metabolic syndrome score, cardiometabolic index, and metabolic syndrome severity score were associated with increased risk of MCI. Further analysis showed that MetS was negatively associated with MMSE score, orientation, registration, recall and language (P P for interaction = 0.012) on the MetS-MCI was observed. Conclusion Metabolic syndrome was associated with MCI in hemodialysis patients in a positive dose–response effect.

Background: Little is known about the impact of haemodialysis (HD) and peritoneal dialysis (PD) on health-related quality of life (HRQoL). We compared HRQoL between conventional in-centre HD and home-based PD in 1082 newly diagnosed kidney failure patients. Methods: This was an open-label, randomised, non-inferiority trial of adult patients with a diagnosis of end-stage kidney disease (estimated glomerular filtration rate ≤ 15 mL/min/1.73 m2) requiring maintenance dialysis from 36 sites in China randomised 1:1 to receive PD or conventional in-centre HD. The primary outcome was the ‘Burden of Kidney Disease’ assessed using the Kidney Disease Quality of Life-Short Form (KDQoL-SF) survey over 48 weeks and the main secondary outcomes were the remaining scales of KDQoL-SF and all-cause mortality. The effect of PD versus HD on the primary outcome was compared by their geometric mean (GM) ratio, and non-inferiority was defined by the lower bound of a one-sided 95% confidence interval (CI) >0.9. Results: A total of 725 subjects completed the trial per protocol (395 PD and 330 HD, mean age 49.8 (standard deviation (SD) 14.4) years, 41.4% women). For the primary outcome, the mean (SD) change in ‘Burden of Kidney Disease’ over 48 weeks was 2.61 (1.27) in PD group and 2.58 (1.35) in HD group, and the GM ratio (95% CI) was 1.059 (0.908–1.234), exceeding the limit for non-inferiority. For the secondary outcomes, the PD and HD groups were similar in all scales. There were 17 and 31 deaths in PD and HD groups, respectively. Patients receiving PD had more adverse events, adverse event leading to hospitalisation and serious adverse events compared to those allocated to HD, but adverse events leading to death and discontinuation of the trial were not different between PD and HD. Conclusions: In this trial, PD may be non-inferior to HD on the ‘Burden of Kidney Disease’ among Chinese kidney failure patients who are of younger age and have lower comorbidity after 48 weeks’ follow-up.

The association between muscle mass and cognitive impairment (CI) is conflicting. We aimed to evaluate and compare the associations of muscle strength, muscle mass and CI risk in maintenance hemodialysis (MHD) patients.We conducted a multicenter, cross-sectional study. Cognitive function was assessed with the Mini-Mental State Examination (MMSE) score. Muscle strength was assessed by hand grip strength (HGS), muscle mass was assessed by lean tissue mass (LTM). Education status was divided into two groups: lower education status (senior middle school and below) and higher education status (high school and above). Multivariable logistic regression models and subgroup analyses were performed. Receiver-operating characteristic (ROC) analyses were conducted to compare their predictive power in discriminating CI.2827 adult MHD patients were included in our final analysis. Patients in the lowest quartile of HGS was 2.82-fold as likely to have CI as compared to those in the highest quartile, while participants in the lowest quartile of LTM group were 1.52-fold as likely to have CI, when compared with the highest quartile group of LTM after adjusting for age, gender and education level. The association persisted in all subgroups except for women and well-educated participants. There was a significant interaction between HGS and education status on CI and age played an interactive role in the association between LTM and incident CI (P for interaction 0.05). The AUC value of the HGS was significantly higher than that of LTM (0.69 VS 0.63, P 0.001).Muscle strength performed better than muscle mass in identifying individuals at high risk of CI, particularly in male and less educated Chinese MHD patients.Level V, cross-sectional study.

Background: PM2.5, the particles with diameters no larger than 2.5 micrometers, are important contributors to air pollution and have been related to diabetes and kidney injury. The present study aims to investigate whether PM2.5 aggravates kidney conditions in the context of diabetes. Methods: Db/db mice were used to model diabetes and treated with escalating doses of PM2.5 particles. The treatments were performed through intratracheal instillation. Kidney conditions were assessed using a battery of histopathological staining and laboratory tests. Results: PM2.5 treatment led to more severe phenotypes of kidney injury characterized by altered histology and overall deteriorated kidney functions. Many biological processes were implicated in the injury including progression of renal interstitial fibrosis, increased monocyte infiltration and an exhausted antioxidative defense system. Conclusions: PM2.5 induces an additional detrimental effects on kidney conditions in diabetic mice, calling for focuses on the diabetes patients living at highly PM2.5-polluted environments.

Gouty arthritis, often referred to simply as gout, is a disorder of purine metabolism characterized by the deposition of monosodium urate monohydrate (MSU) crystals in multiple systems and organs, especially in joints and their surrounding soft tissue. Gout is a treatable chronic disease, and the main strategy for effective management is to reverse the deposition of MSU crystals by uric acid reduction, and to prevent gout attacks, tophi deposition and complications, and thereby improve the quality of life. However, the frequent association of gout with other conditions such as hypertension, obesity, cardiovascular disease, diabetes, dyslipidemia, chronic kidney disease (CKD) and kidney stones can complicate the treatment of gout and lead to premature death. Here, we review the use of medical imaging techniques for studying gouty arthritis with special interest in the potential role of single photon emission computed tomography (SPECT)/computed tomography (CT) in the clinical management of gout and complications (e.g., chronic kidney disease and cardiovascular disease).

Objectives: This study involved a multi-omics analysis of glioblastoma (GBM) samples to elaborate the potential mechanism of drug treatment.Methods: The GBM cells treated with or without orexin A were acquired from sequencing analysis. Differentially expressed genes/proteins/metabolites (DEGs/ DEPs/ DEMs) were screened. Next, combination analyses were conducted to investigate the common pathways and correlations between the two groups. Lastly, transcriptome-proteome-metabolome association analysis was carried out to determine the common pathways, and the genes in these pathways were analyzed through Kaplan-Meier (K-M) survival analysis in public databases. Cell and animal experiments were performed to investigate the anti-glioma activity of orexin A.Results: A total of 1,527 DEGs, 52 DEPs, and 153 DEMs were found. Moreover, the combination analyses revealed that 6, 4, and 1 common pathways were present in the transcriptome-proteome, proteome-metabolome, and transcriptome-metabolome, respectively. Certain correlations were observed between the two data sets. Finally, 11 common pathways were discovered in association analysis, and 138 common genes were screened out in these common pathways. Six genes showed significant differences in terms of survival in both TCGA and CGGA. In addition, orexin A inhibited the proliferation, migration, and invasion of glioma in vitro and in vivo.Conclusion: Eleven common KEGG pathways with six common genes were found among different omics participations, revealing the underlying mechanisms in different omics and providing theoretical basis and reference for multi-omics research on drug treatment.

Diabetic kidney disease (DKD) is a major health burden closely related to lipid metabolism disorders. Leptin has lipid-lowering efficacy, but the specific mechanism of its local effects on kidney is still unclear. This study aims to investigate the role of ectopic lipid deposition (ELD) in DKD and evaluate the lipid-lowering efficacy of leptin in the palmitic acid (PA)-induced renal tubular epithelial cells (NRK-52E). DKD model was established in Sprague-Dawley (SD) rats by giving single intraperitoneal injection of streptozotocin (STZ, 30 mg/kg) after high-fat diet for 8 weeks. Then, the expression changes of lipid metabolism-related markers were observed. At week 12, the protein expression level of lipid-deposited marker adipose differentiation-related protein (ADRP) was significantly increased. Besides, the lipid synthesis marker sterol regulatory element-binding protein 1c (SREBP 1c) was highly expressed while the expression of insulin-induced gene 1 (Insig-1), a key molecular of inhibiting SREBP 1c, was decreased. Leptin and compound c were incubated with the PA-induced NRK-52E cells to investigate the lipid-lowering effects and whether this effect was mediated by the AMPK/Insig-1/SREBP 1c signaling pathways. mRNA and protein of ADRP and SREBP 1c were reduced after leptin treatment, while Insig-1 and phosphorylated AMP-activated protein kinase (AMPK) were increased. Conversely, inhibition of AMPK phosphorylation by compound c mostly eliminated lipid-lowering efficacy of leptin in PA-induced cells. Collectively, these results suggested that there was ELD of renal tubular epithelial cells in DKD rats. Leptin upregulated the expression level of Insig-1 by activating AMPK to attenuate ELD in PA-induced NRK-52E cells.

Background: Lung adenocarcinoma (LUAD) and squamous cell carcinoma (LUSC) are two major subtypes of Non-Small Cell Lung Cancer (NSCLC). Studies have shown that abnormal expression of glucose transport type 1 (GLUT1) in NSCLC patients has been associated with cancer progression, aggressiveness, and poor clinical outcome. However, the clinical effect of GLUT1 expression on LUAD and LUSC is unclear. Objective: This study aims to learn more about the character of GLUT1 in LUAD and LUSC. Methods: A meta-analysis was performed to evaluate the GLUT1 protein level, and the bioinformatics analysis was used to detect the GLUT1 mRNA expression level, survival differences, and the infiltration abundance of immune cells in samples from TCGA. Meanwhile, functional and network analysis was conducted to detect important signaling pathways and key genes with the Gene Expression Omnibus (GEO) dataset. Results: Our results showed that GLUT1 was over-expressed both in LUAD and LUSC. LUAD patients with high GLUT1 expression had a poor prognosis. Additionally, GLUT1 was related to B cell and neutrophil infiltration of LUAD. In LUSC, GLUT1 was correlated with tumor purity, B cell, CD8+ T cell, CD4+ T cell, macrophage, neutrophil, and dendritic cell infiltration. The GEO dataset analysis results suggested GLUT1 potentially participated in the p53 signaling pathway and metabolism of xenobiotics through cytochrome P450 and was associated with KDR, TOX3, AGR2, FOXA1, ERBB3, ANGPT1, and COL4A3 gene in LUAD and LUSC. Conclusion: GLUT1 might be a potential biomarker for aggressive progression and poor prognosis in LUAD, and a therapeutic biomarker in LUSC.

Introduction: Cognitive impairment is prevalent in patients undergoing hemodialysis (HD), which is related to the nutritional and inflammatory status of this population. Malnutrition-inflammation score (MIS) has been identified as a useful tool to evaluate nutrition and inflammation status. The aim of this study is to investigate the association between MIS and cognitive impairment in HD patients. Methods: This was a multicenter observational cohort study with 1,591 patients undergoing HD. Nutritional and inflammatory status was evaluated with MIS, anthropometric measurements, and body composition assessments. Cognitive function was evaluated with the Mini Mental State Examination (MMSE). The associations between MIS and cognitive impairment were analyzed by multivariable logistic regression models. Results: Among 1,591 HD patients, the mean MIS was 6.0 ± 2.6. Patients with higher MIS had significantly lower MMSE scores. 311 patients had cognitive impairment. After adjusting clinical confounders, higher MIS was independently associated with increased rate of cognitive impairment both as a categorized variable (OR, 1.358; 95% CI, 1.010–1.825; p = 0.045) and as a continuous variable (OR, 1.113; 95% CI, 1.053–1.178; p < 0.001). Subgroup analysis showed a stronger association between MIS and cognitive impairment in males, the population with age 41–60 years, and 61–80 years, no smoker, living by oneself, HD combined with or without hemoperfusion as dialysis modality. ROC curve analysis of MIS showed 60.1% sensitivity and 52.0% specificity in predicting cognitive impairment (AUC 0.604; 95% CI 0.567–0.640, p < 0.001). Conclusions: MIS was independently associated with cognitive impairment in HD patients.

Disheveled-associated antagonist of β-catenin (DACT), which ubiquitously expressed in human tissue, is critical for regulating cell proliferation and several developmental processes in different cellular contexts. In addition, DACT is essential for some other cellular processes, such as cell apoptosis, migration and differentiation. Given the importance of DACT in these cellular processes, many scientists are gradually interested in studying the role of DACT in tumorigenesis and cancer progression. This review article focuses on the latest research regarding the essential functions and potential DACT mechanisms in the occurrence and progression of tumors. Our study indicates that DACT may act as a tumor biomarker for cancer diagnosis and prognosis, as well as a promising therapeutic target in cancers.

Background: Sepsis-associated encephalopathy (SAE) is a diffuse cerebral dysfunction resulting from a systemic inflammatory response to infection, but the pathophysiological mechanism remains unclear. Sepsis-induced neuroinflammation and blood-brain barrier (BBB)disruption have been demonstrated as the crucial factors in the brain functional disturbance in SAE. Mast cells (MCs) activation has been reported to play an important role in several neuroinflammation models. However, the role of MCs in SAE has not been comprehensively investigated. Methods: We first established a SAE model by cecal ligation puncture (CLP) surgery and checked the activation of MCs. We further analyzed the effects of MCs on neuroinflammation response, BBB permeability, cognitive function, and the underlying molecular mechanism in both tissue samples and cellular co-culture system. MCs activation was measured using immumohistochemical staining and 1% Toluidine Blue (TB) staining. We administrated a MC stabilizer, Cromolyn (10mg/ml), to rescue the septic mice. Brain cytokines levels were measured using biochemical assays. BBB disruption was assessed by measuring levels of key tight-junction (TJ) proteins. Cognitive function of mice was analyzed by Y maze and open field test. Transwell cultures of brain microvascular endothelial cells (BMVECs) co-cultured with MCs were used to assess the effect of LPS (1mg/ml) on expression of TJ proteins. The expression of TJ and TLR2/4-MAPK signaling pathway proteins were measured by immunoblotting and/or immunofluorescence. Results: The results showed that MCs were seriously overactivated in the hippocampus of CLP-induced SAE mice. The inhibition of MCs by Cromolyn i.c.v injection significantly inhibited the inflammation responses, ameliorated the impairment of the BBB, improved the survival rate, and alleviated cognitive dysfunction. In vitro experiments, we revealed that MCs activation increased the sensitivity of brain microvascular endothelial cells (BMVECs) against to lipopolysaccharide (LPS) challenge. Furthermore, we found that histamine-H1R mediates the interaction between MCs and BMVECs, and amplifies the LPS induced inflammation response in BMVECs by modulating the TLR2/4-MAPKsignaling pathway. Conclusions: The activation of MCs mediates BBB impairment and cognitive dysfunction of septic mice in a histamine dependent pathway.

Acute kidney injury (AKI) is a complex and common set of multifactorial clinical syndromes, and associated with increased in-hospital mortality. There is increasing evidence that Hyperhomocysteinemia (HHcy) is highly associated with the development of a variety of kidney diseases, including AKI. However, the pathogenesis of HHcy in AKI remains unclear. In this study, we investigated the effect and mechanism of HHcy on cisplatin-induced AKI in mice and NRK-52E cells cultured with HHcy. We confirmed that mice with HHcy had higher serum levels of creatinine and more severe renal tubule injury after cisplatin injection. We found that HHcy aggravated renal mitochondrial damage, mainly manifested as decreased ATP β, significantly increased cytoplasmic Cyt C expression and the ADP/ATP ratio, and a significantly decreased mitochondrial DNA (mtDNA) copy number. In addition, we found that HHcy accelerated cisplatin-induced renal DNA damage; culturing NRK-52E cells with homocysteine (Hcy) could significantly increase apoptosis and mitochondrial damage. Interestingly, we found that Mdivi-1 reduced Hcy-induced mitochondrial damage, thereby reducing the level of apoptosis. In conclusion, these results suggest that HHcy might aggravate the development of AKI by increasing mitochondrial damage and that reducing Hcy levels or inhibiting mitochondrial damage may be a potential therapeutic strategy to delay the development of AKI.

Heavy metal-containing atmospheric particulate matter (PM) and acid rain (AR) trigger molecular alteration in plants, perturbing metabolites and damaging plant growth. However, the molecular mechanisms of plants under AR along with Cd-containing atmospheric fine particulate matter (PM2.5-Cd) stress remain unknown. In this study, integrated transcriptomics and metabolomics analyses of pak choi (Brassica pekinensis (Lour.) Rupr) exposed to AR (pH3.5) and PM2.5-Cd (500 μg·m−3) stress were performed. Metabolomics analyses revealed that AR-Cd stress mainly affected 42 metabolic pathways, including 451 differentially expressed metabolites (DEMs). RNA-seq identified 735 common differentially expressed genes (DEGs: 557 upregulated and 178 downregulated). Further analysis found several important DEGs (transcription factors, metabolic pathways genes, and signal transduction genes), including WRKY11, WRKY53, WRKY41, MYB73, NAC062, NAC046, HSFA4A, ABCC3, CAXs, GSTs, AZFs, PODs, PME41, CYP707A2, and CDPK32 implying that Cd chelate sequestration into the vacuoles, the antioxidant system, cell wall biosynthesis pathway, and calcium signaling play a critical role in AR damage and Cd detoxification. Conjoint revealed phenylpropanoid and flavonoid biosynthesis pathways with different metabolism patterns, including the key DEM, chlorogenic acids. The results obtained using multiple approaches provide a molecular-scale perspective on plant response to AR-Cd stress.

Kidney functions, including electrolyte and water reabsorption and secretion, could be influenced by circulating hormones. The pituitary gland produces a variety of hormones and cytokines; however, the influence of these factors on the kidney has not been well explained and explored. To provide more in-depth information and insights to support the pituitary–kidney axis connection, we used mouse pituitary and kidney single-cell transcriptomics data from the GEO database for further analysis. Based on a ligand–receptor pair analysis, cell–cell interaction patterns between the pituitary and kidney cell types were described. Key ligand–receptor pairs, such as GH-GHR, PTN-SDC2, PTN-SDC4, and DLK1-NOTCH3, were relatively active in the pituitary–kidney axis. These ligand–receptor pairs mainly target proximal tubule cells, principal cells, the loop of Henle, intercalated cells, pericytes, mesangial cells, and fibroblasts, and these cells are related to physiological processes, such as substance reabsorption, angiogenesis, and tissue repair. Our results suggested that the pituitary gland might directly regulate kidney function by secreting multiple hormones or cytokines and indicated that the above ligand–receptor pairs might represent a new research focus for studies on kidney function or kidney disease.

Based on Gibson's concept of affordance and its methodological application in the design and the subject and object elements of "demand affordance, " ANP was used to solve the horizontal ties among the aspects of affordance, judge the research elements, SPSS correlation analysis was used to construct the judgment matrix, and a consistency test was conducted, establish a study on community function and behavior space design of elderly population under the dual coupling elements of functional needs and behavioral needs.

Objective To explore the changes of proopiomelanocortin (POMC) and Agouti-Related Peptide (AgRP) expression in brain and kidney tissues under insulin intervention at different stages of diabetic nephropathy (DN) rats. Methods The male Sprague-Dawley (SD) rats of DN were treated with high-fat diet for 8 weeks and induced by intraperitoneally injection of streptozotocin (30 mg/kg) for one time. Then DN rats were also injected insulin subcutaneously at 2–5 U/(kg·24 h) from initiation of the streptozotocin. Kidney tissue, blood sample, and 24 h-urine were collected to detect the ratio of kidney/body weight, blood glucose and 24-h urinary albumin excretion rate at different stages (4, 8, 12, and 16 weeks). Immunohistochemistry assay was used to measure the expression of POMC and AgRP at different stages of DN rats. Results The DN rats were established successfully. With the progression of DN, blood glucose, 24-h urinary albumin excretion rate and kidney body weight ratio increased significantly, while decreased when insulin was injected. Immunohistochemistry showed that the expression levels of POMC were decreased gradually in brain and kidney tissues. Conversely, the expression of AgRP in kidney was highest at week 8 and then decreased gradually. The effect of insulin on normalizing POMC and AgRP expression in brain and renal tissues was also observed in DKD rats. Conclusion With the progression of DN, the expression of POMC and AgRP in kidney tissues was observed at different stages of disease, and their expressions were significantly normalized by insulin. The mechanism of in situ expression of POMC and AGRP in kidney to the progression of DN needs further investigations.

Summary Observational studies on dietary or circulating magnesium and risk of cardiovascular disease (CVD) in Chronic Kidney Disease (CKD) stage 1–4 have reported no-to-modest inverse associations. 24 h Urinary magnesium concentration (24 h UMg), an indicator of intestinal magnesium absorption, may provide better insight into the connection of CKD progression. We examined 3179 participants aged 18–74 years with CKD stage 1–4 in the Chinese Cohort Study of Chronic Kidney Disease (C-STRIDE) study, a prospective population-based cohort study. Data were analysed using Spearman rank-order correlation coefficients for all comparisons. We also performed a time-to-event analysis of the data using the Kaplan–Meier survival model, Cox proportional hazard model and competing risk Fine and Gray subdistribution hazard model. During a median follow-up of 4.19 years (interquartile range, 3.43–5.09 years), when modelling end-stage renal disease (ESRD), CVD and death, 24 h UMg was associated with risk of CVD (HR, 1.612 (95% CI, 1.056–2.460)), while no significant association with ESRD and death endpoints could be detected. 24 h UMg risk variants display a modest association with CVD in CKD stage 1–4 patients. Trial registration ClinicalTrials.gov Identifier NCT03041987. Registered January 1, 2012. (retrospectively registered) ( https://www.clinicaltrials.gov/ct2/show/NCT03041987?term=Chinese+Cohort+Study+of+Chronic+Kidney+Disease+%28C-STRIDE%29&rank=1 ).

BACKGROUND A flare, or flare-up, of systematic lupus erythematosus (SLE) is diagnosed by an increase in disease activity in one or more organs, new symptoms, or changes in laboratory measurements. A hematoma can occur in the sheath of the rectus abdominis following muscle trauma or rupture of an epigastric vessel, or it can occur spontaneously. This report is of a 28-year-old woman who presented with a clinical flare of SLE and abdominal pain due to rectus sheath hematoma. CASE REPORT A 28-year-old woman had been suspected of having SLE 9 years ago and had received glucocorticoid therapy combined with hydroxychloroquine. However, lupus flared after she discontinued glucocorticoids, and she was admitted with a 1-month history of marked generalized edema, abdominal distension, frothy urine, and massive ascites. During hospitalization, she abruptly developed a continuous, stabbing abdominal pain and a bulge over the right abdomen as a result of straining during a bowel movement. On examination, a well-demarcated round mass that measured 121 mm × 96 mm was detected in the right quadrant. Abdominal emergency computed tomography revealed a right rectus sheath hematoma (21.4×4.7 cm). After her condition improved, the patient underwent an ultrasound-guided renal biopsy and was diagnosed with class III (A/C) and class V lupus nephritis. CONCLUSIONS This case has shown that spontaneous rectus sheath hematoma can occur without a history of trauma in a patient with an exacerbation of SLE. This association appears to be rare, and the cause is unknown.

Acute kidney injury (AKI) is a complex and common set of multifactorial clinical syndromes, and associated with increased in-hospital mortality. There is increasing evidence that Hyperhomocysteinemia (HHcy) is highly associated with the development of a variety of kidney diseases, including AKI. However, the pathogenesis of HHcy in AKI remains unclear. In this study, we investigated the effect and mechanism of HHcy on cisplatin-induced AKI in mice and NRK-52E cells cultured with HHcy. We confirmed that mice with HHcy had higher serum levels of creatinine and more severe renal tubule injury after cisplatin injection. We found that HHcy aggravated renal mitochondrial damage, mainly manifested as decreased ATP β, significantly increased cytoplasmic Cyt C expression and the ADP/ATP ratio, and a significantly decreased mitochondrial DNA (mtDNA) copy number. In addition, we found that HHcy accelerated cisplatin-induced renal DNA damage; culturing NRK-52E cells with homocysteine (Hcy) could significantly increase apoptosis and mitochondrial damage. Interestingly, we found that Mdivi-1 reduced Hcy-induced mitochondrial damage, thereby reducing the level of apoptosis. In conclusion, these results suggest that HHcy might aggravate the development of AKI by increasing mitochondrial damage and that reducing Hcy levels or inhibiting mitochondrial damage may be a potential therapeutic strategy to delay the development of AKI.

Long-term exposure to particulate air pollutants can lead to an increase in mortality of hemodialysis patients, but evidence of mortality risk with short-term exposure to ambient particulate matter is lacking. This study aimed to estimate the association of short-term exposure to ambient particulate matter across a wide range of concentrations with hemodialysis patients mortality.We performed a time-stratified case-crossover study to estimate the association between short-term exposures to PMDuring the study period, there were 18,114 case days and 61,726 control days. Of all case and control days, average PMThis study confirms that short-term exposure to particulate matter leads to increased mortality in hemodialysis patients. Policy makers and public health practices have a clear and urgent opportunity to pass air quality control policies that care for hemodialysis populations and incorporate air quality into the daily medical management of hemodialysis patients.

Objective To explore the effect of low serum phosphorus and parathyroid hormone (PTH) levels on protein-energy wasting (PEW) in patients on maintenance hemodialysis (MHD) and provide a new method of nutritional monitoring and intervention in patients on MHD. Methods Four hundred end-stage renal disease (ESRD) patients on MHD for at least 3 months were selected from 17 dialysis units. Logistic regression analysis was used to analyze the relationship between serum phosphorus and PTH levels and PEW risk. Receiver operating characteristic (ROC) analysis was used to compare the predictive value of these two indices for PEW. We used the survival curve to analyze the effects of low serum phosphorus and PTH levels on mortality. Results In the unadjusted model, The PEW risk in group Q1 was 16.4 times higher than that in group Q4. Compared with group Q4 of PTH, the PEW risk in groups Q1 and Q2 of PTH was 2.817 times higher and 2.087 times higher, respectively, after adjusting. However, serum phosphorus and PTH levels were associated with PEW risk. PEW risk in the serum phosphorus Q1 group was 7.305 times higher than that in the Q4 group, and PEW risk in the PTH Q1 group was 2.75 times higher than that in the Q4 group. ROC analysis showed that the areas under the curve of serum phosphorus and PTH predicting PEW in MHD patients were 0.862 and 0.695, respectively, while the cut-off values of ROC curve were 1.36 mmol/L and 212.5 ng/L, respectively. The survival rate was significantly lower in patients with serum phosphorus ≤ 1.36 mmol/L of ≤ 212.5 ng/L. Conclusion Low serum phosphorus and PTH levels increased the incidence of PEW and death and seriously affected the prognosis of patients on hemodialysis. Therefore, The nutritional status of patients on MHD can be monitored and evaluated by integrating serum phosphorus, PTH, albumin, and body mass index.

Craniofacial microsomia (CFM, OMIM%164 210) is one of the most common congenital facial abnormalities worldwide, but it’s genetic risk factors and environmental threats are poorly investigated, as well as their interaction, making the diagnosis and prenatal screening of CFM impossible. We perform a comprehensive association study on the largest CFM cohort of 6074 samples. We identify 15 significant (P

Purpose Acteoside (Act), a phenylethanoid compound that was first isolated from mullein, has been widely used for the investigation of anti-inflammatory and anti-fibrotic effect. However, the mechanism of Act against unilateral ureteral obstruction (UUO)-mediated renal injury is largely unknown. Therefore, this study aimed to explore the effects of Act on UUO rats and possible mechanisms. Methods A total of 20 Sprague-Dawley (SD) rats were divided randomly into three groups (n ≥ 6): (i) sham-operated group (Sham); (ii) UUO group (UUO+Saline); and (iii) UUO + Act 40 mg/kg/day, (UUO+Act); Continuous gavage administration for 2 weeks postoperatively, while the rats in Sham and UUO+saline groups were given equal amounts of saline. All rats were sacrificed after 14 days, the urine and blood samples were collected for biochemical analysis, the renal tissues were collected for pathological staining and immunohistochemistry. Correlations between individual proteins were analyzed by Pearson correlation analysis. Results The results of renal function indexes and histopathological staining showed that Act could improve renal function by reducing serum creatinine, blood urea nitrogen and urine protein at the same time, Act could alleviate renal inflammation and fibrosis. In addition, the results of immunohistochemistry showed that Act could reduce the expression of inflammation and kidney injury-related proteins F4/80, Mcp-1, KIM-1 proteins, as well as the expression of fibrosis-related protein α-SMA and β-catenin. More importantly, Act can also reduce the expression of HMGN1, TLR4 and TREM-1 proteins. Conclusion These data demonstrate that Act can ameliorate UUO-induced renal inflammation and fibrosis in rats probably through triggering HMGN1/TLR4/TREM-1 pathway.

There is uncertainty about whether piperacillin/tazobactam (PT) increases the risk of acute kidney injury (AKI) in patients without concomitant use of vancomycin. This study compared the risk of hospital-acquired AKI (HA-AKI) among adults treated with PT or antipseudomonal β-lactams (meropenem, ceftazidime) without concomitant use of vancomycin.This real-world study analysed the data from China Renal Data System and assessed the risk of HA-AKI in adults hospitalized with infection after exposure to PT, meropenem or ceftazidime in the absence of concomitant vancomycin. The primary outcome was any stage of HA-AKI according to the Kidney Disease Improving Global Outcomes guidelines. A multi-variable Cox regression model and different propensity score (PS) matching models were used.Among the 29,441 adults [mean (standard deviation) age 62.44 (16.84) years; 17,980 females (61.1%)] included in this study, 14,721 (50%) used PT, 9081 (31%) used meropenem and 5639 (19%) used ceftazidime. During a median follow-up period of 8 days, 2601 (8.8%) develped HA-AKI. The use of PT was not associated with significantly higher risk of HA-AKI compared with meropenem [adjusted hazard ratio (aHR) 1.07, 95% confidence interval (CI) 0.97-1.19], ceftazidime (aHR 1.09, 95% CI 0.92-1.30) or both agents (aHR 1.07, 95% CI 0.97-1.17) after adjusting for confounders. Results were consistent in stratified analyses, PS matching using logistic regression or random forest methods to generate a PS, and in an analysis restricting outcomes to AKI stage 2-3.Without concomitant use of vancomycin, the risk of AKI following PT therapy is comparable with that of meropenem or ceftazidime among adults hospitalized with infection.

Drug conjugates are conjugates comprising a tumor-homing carrier tethered to a cytotoxic agent via a linker that are designed to deliver an ultra-toxic payload directly to the target cancer cells. This strategy has been successfully used to increase the therapeutic efficacy of cytotoxic agents and reduce their toxic side effects. Drug conjugates are being developed worldwide, with the potential to revolutionize current cancer treatment strategies. Antibody-drug conjugates (ADCs) have developed rapidly, and 14 of them have received market approval since the first approval event by the Food and Drug Administration in 2000. However, there are some limitations in the use of antibodies as carriers. Other classes of drug conjugates are emerging, such as targeted drugs conjugated with peptides (peptide-drug conjugates, PDCs) and polymers (polymer-drug conjugates, PolyDCs) with the remaining constructs similar to those of ADCs. These novel drug conjugates are gaining attention because they overcome the limitations of ADCs. This review summarizes the current state and advancements in knowledge regarding the design, constructs, and clinical efficacy of different drug conjugates.

Background: Novel Coronavirus disease 2019 (COVID-19) was first detected in pneumonia patients in Wuhan, China in December 2019. Based on the current understanding, COVID-19 has become a global issue. Presumably, numerous studies have found that SARS-CoV-2 also transpires in kidney tissue with permanent viral loads. However, it is elusive as to whether SARS-CoV-2 can directly damage the kidney or induce acute renal failure. Hence, to comprehensively understand the impact of COVID-19 on kidney damage, we conducted a retrospective series of case studies to assess kidney functions. Additionally, ACE2 distribution in kidney tissue was analyzed through RNAseq data in open-access databases. Results: According to the findings from transcriptome analysis, we revealed higher ACE2 expression levels in females than males. Similar results were more noticeable in the elderly than in young adults. Furthermore, single-cell RNA sequencing data analysis showed high ACE2 expression in kidney tubule and collecting duct principal cells as well as glomerular parietal epithelial cells. On their admission, the patient's serum creatinine and blood urea nitrogen (BUN) were elevated to between 36.13% and 16.80%, respectively. The estimated glomerular filtration rate (EGFR) of < 60 ml/min per 1.73 m2 was reported in 10.92 % of the patients. Notably, at admission, increased BUN time varied linearly following the generalized additive mixed model. Thus, the hourly-increase of BUN in patients was 0.495 (95%CI: 0.263, 0.726). Conclusion: Based on clinical findings, it was ascertained that COVID-19 can damage renal function, but it seldom causes acute renal failure. Coronavirus may directly bind to ACE2-positive cells and damage kidney tissue in the analysis of scRNA-seq data in kidney tissue. Therefore, this evidence suggests that kidney tissue act as the SARS-CoV-2 infection site and the findings could provide insight into the pathophysiology of kidney damage. Methods: We systematically analyzed ACE2 expression profiles in organs based on open-access datasets for healthy individuals. Meanwhile, single-cell sequencing data for kidney samples were collected and analyzed. Assessments on kidney functions were conducted on 119 selected COVID-19 positive patients admitted from 10th February – 18th March 2020, in hospital in Wuhan City, Hubei Province. Consequently, their clinical records and laboratory findings, such as the estimated glomerular filtration rate (eGFR), Blood Urea Nitrogen (BUN), Creatinine, and Comorbidities, were collected.

Processed food has become an indispensable part of the human food chain. It provides rich nutrition for human health and satisfies various other requirements for food consumption. However, establishing traceability systems for processed food faces a different set of challenges compared to primary agro-food, because of the variety of raw materials, batch mixing, and resource transformation. In this paper, progress in the traceability of processed food is reviewed. Based on an analysis of the food supply chain and processing stage, the problem of traceability in food processing results from the transformations that the resources go through. Methods to implement traceability in food processing, including physical separation in different lots, defining and associating batches, isotope analysis and DNA tracking, statistical data models, internal traceability system development, artificial intelligence (AI), and blockchain-based approaches are summarized. Traceability is evaluated based on recall effects, TRUs (traceable resource units), and comprehensive granularity. Different methods have different advantages and disadvantages. The combined application of different methods should consider the specific application scenarios in food processing to improve granularity. On the other hand, novel technologies, including batch mixing optimization with AI, quality forecasting with big data, and credible traceability with blockchain, are presented in the context of improving traceability performance in food processing.

Tumor-associated macrophages (TAMs) exert integrated effects in all aspects of tumor progression, including tumor cell proliferation, angiogenesis, invasion, and metastasis. Recently, considerable preclinical and clinical trials have demonstrated that TAM-targeted therapy is an effective antitumor therapeutic approach, especially as a complementary strategy in combination with conventional chemotherapy, radiotherapy, or emerging immunotherapy. Here, we review all of the current clinical trials targeting TAMs worldwide up to May 2021 and highlight instances of the synergetic therapeutic efficacy of TAM-targeted combined therapeutic strategies. In total, 606 clinical trials were conducted, including 143 tested products. There has been explosive growth in macrophage-targeted therapy around the world during the past decade. Most trials were at early phase, and two-thirds used macrophage-targeting therapy as part of a combination approach. The most common combination is that of traditional chemotherapy with TAM-targeted therapy, followed by immune checkpoint inhibitors and targeted drugs. TAM-targeted therapeutic approaches are a newly emerging but rapidly developing area of anticancer therapy, especially as a combinatorial therapeutic approach. Further investigation of promising combination strategies will pave the way to more effective anticancer therapies.

Neural crest cells (NCCs) are multipotent progenitor cells unique to vertebrates, and they have the ability to differentiate into a variety of cells, such as chondrocytes, neurons, and melanocytes. The formation, migration, and differentiation of NCCs are tightly regulated, and the disruption of NCC development results in abnormal embryo development. Neurocristopathies (NCPs) refer to a group of diseases that develop in response to abnormal development of NCCs. NCPs are of various types and exhibit complex phenotypes, which can affect many parts of the human body, such as the craniofacial structure, heart, intestine, and skin. NCPs negatively impact the physical function and mental health of the affected patients. NCPs account for one third of the defects in children with birth defects. Genetic factors are the main risk factors for NCPs, but environmental factors and abnormal gene-environment interactions can also lead to the development of NCPs. In this review, we introduce NCCs, NCPs, and their pathogenesis, so as to provide a reference point for a systematic understanding of NCPs and NCC development, and to provide scientific support for understanding the etiology of NCPs and their effective prevention and control.神经嵴细胞(neural crest cells,NCCs)是一类脊椎动物特有的可迁移的多能干细胞,其可分化为软骨细胞、神经元和黑色素细胞等多种类型细胞。NCCs的形成、迁移和分化受到严格调控,任何扰乱NCCs发育的因素都可导致胚胎发育畸形。由神经嵴细胞发育异常所导致的一系列疾病统称为神经嵴病(neurocristopathies,NCPs)。NCPs种类繁多且表型复杂,可累及人体多个部位(颅面部、心脏、肠胃和皮肤等),严重危害患者的身体机能和心理健康。NCPs占所有出生缺陷患儿的1/3,遗传因素是导致NCPs的主要风险因素,但环境风险因子以及基因-环境交互作用异常也可导致NCPs。本文对神经嵴细胞和神经嵴病及其致病机制进行综述,为系统认知神经嵴细胞发育以及神经嵴病提供参考,为了解神经嵴病的病因以及开展有效防控提供科学支撑。.

We reported 20 cases of discharged COVID‐19 patients whose RT‐PCR test results showed “re‐positive”. After finding “re‐positive ”, these patients were admitted to hospital for the second time and were followed up until the end of May 2020. Methods: Record detailed treatment and follow‐up process, and collect relevant data. The possible causes and potential clinical significance of this phenomenon are discussed. This article is protected by copyright. All rights reserved.

Background Previous studies on the pneumonia outbreak caused by the 2019 novel coronavirus disease (COVID-19) were mainly based on information from adult populations. Limited data are available for children with COVID-19, especially for infected infants. Methods We report a 55-day-old case with COVID-19 confirmed in China and describe the identification, diagnosis, clinical course, and treatment of the patient, including the disease progression from day 7 to day 11 of illness. Results This case highlights that children with COVID-19 can also present with multiple organ damage and rapid disease changes. Conclusions When managing such infant patients with COVID-19, frequent and careful clinical monitoring is essential., Data about infants infected with novel coronavirus disease (COVID-19) are scarce. Herein, we report a 55-day-old case who presented with COVID-19 pneumonia. The exposure, symptoms, laboratory indicators, and hospitalization are described in detail.

Background: The lack of consensus criteria of acute on chronic kidney injury (ACKI) affects the judgment for its clinical prognosis. Methods: In this study, we analyzed the data from 711,615 hospitalized adults who had at least 2 serum creatinine (SCr) tests within 30 days. We estimated the reference change value (RCV) of SCr given initial SCr level in adults without known risks of acute kidney injury other than chronic kidney disease (CKD). We proposed a criterion for ACKI based on the RCV of SCr (cROCK), which defined ACKI as a ≥25% increase in SCr in 7 days. We validated cROCK by its association with the risks of in-hospital mortality, death after discharge, and CKD progression in a large cohort of patients with CKD stage 3. Results: In 21,661 patients with CKD stage 3, a total of 3,145 (14.5%), 1,512 (7.0%), and 221 (1.0%) ACKI events were detected by both cROCK and Kidney Disease Improving Global Outcomes (KDIGO), cROCK only, and KDIGO only, respectively. cROCK detected 40% more ACKI events than KDIGO. Compared with patients without ACKI by both definitions, those with cROCK- but not KDIGO-defined ACKI had a significantly increased risk of in-hospital mortality (hazard ratio [HR] 5.53; 95% CI 3.75–8.16), death after discharge (HR 1.51; 95% CI 1.21–1.83), and CKD progression (OR 5.65; 95% CI 3.05–10.48). Conclusions: RCV-based criterion (cROCK) for ACKI is clinically valid in that it has a substantially improved sensitivity in identifying patients with high risk of adverse outcomes.

This study investigated the role of insulin-like growth factor-1/insulin-like growth factor-1 receptor (IGF-1/IGF-1R) in the genesis and progression of diabetic kidney disease (DKD) in a streptozotocin (STZ)-induced mouse diabetes model. We showed elevated IGF-1 expression in the DKD kidneys after 16 wk of diabetic onset. Intraperitoneal administration of IGF-1R inhibitor (glycogen synthase kinase-3β, GSK4529) from week 8 to week 16 postdiabetes induction ameliorated urinary albumin excretion and kidney histological changes due to diabetes, including amelioration of glomerulomegaly, inflammatory infiltration, and tubulointerstitial fibrosis. The GSK4529 treatment also attenuated alterations in renal tubular expression of E-cad and matrix protein fibronectin. Moreover, renal fibrosis in DKD (without treatment) was associated with Snail1 overexpression that was effectively prevented by IGF-1R inhibition. Further experiments in cultured renal epithelial cells (NRK) showed that IGF-1 silencing reproduced in vivo effects of IGF-1R inhibition with markedly attenuated Snail1 expression and near normalization of the Ecad1 and fibronectin expression pattern. Further Snail1 silencing prevented high-glucose-induced changes without affecting IGF-1 expression, consistent with Snail1 acting downstream to IGF-1. The antifibrotic effects were also shown with benazepril or insulin treatment but to a much lesser degree. In summary, in STZ-induced diabetic mice, activation of IGF-1 in diabetic kidneys induces fibrogenesis through Snail1 upregulation. The diabetes-related histological and functional changes, as well as fibrogenesis, can be attenuated by IGF-1/IGF-1R inhibition.

Objective. To investigate the relationship between body cell mass index (BCMI) and cognitive impairment in maintaining hemodialysis (MHD) patients. Methods. We collected the general materials, laboratory indexes, and physical measurement indexes of patients undergoing maintenance hemodialysis in hemodialysis centers of 20 tertiary and tertiary general hospitals in Guizhou Province from June to September 2020. The body composition was measured by bioelectrical impedance method, and the BCMI value was calculated. The subjects were divided into normal cognitive function group (score ≥27), mild cognitive impairment group (score 23–26), and severe cognitive impairment group (score P < 0.001 ). ROC curve analysis showed that the best threshold of BCMI for predicting cognitive impairment in MHD patients was 9.05, the sensitivity and specificity were 71.5% and 62.7%, respectively, and the area under the curve was 0.713 (95% CI: 0.678 ∼ 0.748, P < 0.001 ). Conclusions BCMI is related to cognitive impairment in MHD patients and has predictive value for the onset of cognitive impairment in MHD patients.

Background Normal-weight maintenance hemodialysis (MHD) patients with abdominal obesity exhibited a more proatherogenic profile than overweight and obesity patients with abdominal obesity, highlighting the importance of early identification of metabolically unhealthy nonobese (MUNO) in this population. Visceral fat accumulation plays a crucial role in the development of MUNO. Lipid accumulation product (LAP), visceral adiposity index (VAI) have been proved as reliable visceral obesity markers. The Chinese visceral adiposity index (CVAI) and a body shape index (ABSI) are newly discovered indexes of visceral obesity and have been reported to be associated with multiple metabolic disorders. There are limited studies investigating the associations between different visceral obesity indices and risk of MUNO, especially in hemodialysis patients. Moreover, no general agreement has been reached to date regarding which of these obesity indices performs best in identifying MUNO. We aimed to investigate the prevalence of MUNO in MHD patients and compare the associations between different adiposity indices (CVAI, ABSI,VAI, LAP, body mass index (BMI), waist circumference (WC) and waist-to-hip ratio (WHtR)) with MUNO risk in this population. Methods We conducted a multi-center cross-sectional study in Guizhou Province, Southwest China. 1302 nonobese adult MHD patients were included in our study. MUNO was defined as being nonobese and having the presence of > = 2 components of metabolic syndrome (MetS). Nonobese was defined as BMI less than 25 kg/m2. VAI, LAP, CVAI, ABSI, BMI, WC and WHtR were calculated. Logistic regression analyses and receiver operator curve (ROC) analyses were performed. Results 65.6% participants were metabolically unhealthy. The ROC curve analysis demonstrated that of the seven obesity indices tested, the VAI (AUC 0.84 for women and 0.79 for men) followed by LAP (AUC 0.78 for women and 0.72 for men) had the highest diagnostic accuracy for MUNO phenotype while ABSI exhibited the lowest AUC value for identifying MUNO phenotype Conclusions Metabolically unhealthy is highly prevalent in nonobese MHD patients. VAI and LAP outperformed CVAI in discriminating MUNO in MHD patients. Though ABSI could be a weak predictor of MUNO, it is not better than WHtR, WC and BMI.

Background: Endocrine system plays an important role in infectious disease prognosis. Our goal is to assess the value of radiomics features extracted from adrenal gland and periadrenal fat CT images in predicting disease prognosis in patients with COVID-19. Methods: A total of 1,325 patients (765 moderate and 560 severe patients) from three centers were enrolled in the retrospective study. We proposed a 3D cascade V-Net to automatically segment adrenal glands in onset CT images. Periadrenal fat areas were obtained using inflation operations. Then, the radiomics features were automatically extracted. Five models were established to predict the disease prognosis in patients with COVID-19: a clinical model (CM), three radiomics models (adrenal gland model [AM], periadrenal fat model [PM], fusion of adrenal gland and periadrenal fat model [FM]), and a radiomics nomogram model (RN).Data from one center (1,183 patients) were utilized as training and validation sets. The remaining two (36 and 106 patients) were used as 2 independent test sets to evaluate the models’ performance. Results: The auto-segmentation framework achieved an average dice of 0.79 in the test set. CM, AM, PM, FM, and RN obtained AUCs of 0.716, 0.755, 0.796, 0.828, and 0.825, respectively in the training set, and the mean AUCs of 0.754, 0.709, 0.672, 0.706 and 0.778 for 2 independent test sets. Decision curve analysis showed that if the threshold probability was more than 0.3, 0.5, and 0.1 in the validation set, the independent-test set 1 and the independent-test set 2 could gain more net benefits using RN than FM and CM, respectively. Conclusion: Radiomics features extracted from CT images of adrenal glands and periadrenal fat are related to disease prognosis in patients with COVID-19 and have great potential for predicting its severity.

Background: Rare solid tumors have attracted much more attention due to the great unmet clinical need, limited treatment options, and poor prognosis. As the most thoroughly studied tumor marker, carcinoembryonic antigen (CEA) can not only overexpress in various common solid tumors but also in several rare solid tumors. Oncolytic virus therapy has achieved excellent anticancer effects in the past decades. Due to the specific high expression of CEA in certain tumor tissues but not in normal tissues, CEA has been applied to improve the tumor specificity of gene expression. Methods: The studies of CEA expression in rare solid tumors and CEA-regulated oncolytic virus therapy were reviewed. Results: We showed the types of rare solid tumors with the overexpression of CEA. Elevated serum CEA levels can indicate the diagnosis, response of surgery or system therapy, distal metastasis, recurrence, and survival. Due to high tumor specificity, CEA-regulated OA therapy has demonstrated a surprising antitumor effect for common CEA-positive tumors in preclinical trials. Conclusion: These data suggested that CEA could be a diagnostic and prognostic biomarker for several rare solid tumors. We proposed the hypothesis that CEA-regulated oncolytic virus therapy could be a promising therapeutic strategy for CEA-positive rare solid tumors.

To explore the association between fluid overload, evaluated by a new fluid overload indicator, the bioelectrical impedance analysis-derived whole-body extracellular to intracellular water ratio (ECW/ICW), and sarcopenia in maintenance hemodialysis (MHD) patients.A multicenter, cross-sectional study that included 3320 adult MHD patients was conducted in 20 hemodialysis centers of Guizhou Province, Southwest China from June 1, 2020, to September 30, 2020. The diagnosis of sarcopenia was based on the Asian Working Group's definition of sarcopenia. Multiple logistic regression models, stratified analyses, and interactive analyses were conducted.A total of 3196 participants were included in the final analysis. The prevalence of sarcopenia was 36.2% in the total population. The prevalence of sarcopenia was increased with increasing quartiles of ECW/ICW (18.1%, 33.3%, 37.8%, and 55.4% for the first, second, third, and fourth quartiles, respectively). Increased ECW/ICW was significantly associated with sarcopenia. The association remained statistically significant even after adjusting for age, sex, body mass index (BMI), dialysis vintage, C-reactive protein, and various medical histories. The odds ratios were 2.11 (1.41, 3.14), 1.83 (1.22, 2.76), and 3.45 (2.21, 5.39) for ECW/ICW quartiles 2-4, respectively (P for trend.001). The interaction analysis showed that history of diabetes had an interactive role in the association between ECW/ICW and sarcopenia (P for interaction = .034). The association stably existed across subgroups and was more prominent in older patients and those with higher BMI and a history of diabetes.Elevated ECW/ICW was associated with increased sarcopenia risk independent of BMI, prealbumin, C-reactive protein, and other potential confounders in MHD patients. The association was more prominent in older patients and those with higher BMI and a history of diabetes, suggesting that controlling volume balance may help to reduce the occurrence of sarcopenia in these populations.

Objective: A comparative analysis was performed to investigate the potential risk factors of Adverse Events Following Immunization (AEFI) after receiving different booster vaccines. Methods: From 18 January 2021 to 21 January 2022, the Health Care Workers (HCWs) of Guizhou Provincial Staff Hospital (Guizhou Province, China) who received a third Booster vaccine, that was either homologous (i.e., (i) a total of three doses of Vero cell vaccine or (ii) three doses of CHO cell vaccine) or (iii) heterologous with two first doses of Vero cell vaccine, being either CHO cell vaccine or adenovirus type-5 (Ad5) vectored COVID-19 vaccine, were asked to complete a self-report questionnaire form to provide information on any AEFI that may have occurred in the first 3 days after vaccination with the booster. The frequency of AEFI corresponding to the three different booster vaccines was compared, and the risk factors for predicting AEFI were determined by multivariate logistic regression analysis. Results: Of the 904 HCWs who completed the survey, 792 met the inclusion criteria. The rates of AEFI were 9.8% (62/635) in the homologous Vero cell booster group, 17.3% (13/75) in the homologous CHO cell booster group, and 20.7% (17/82) in the heterologous mixed vaccines booster group, and the rates were significantly different (χ2 = 11.5, p = 0.004) between the three groups of vaccines. Multivariate logistic regression analysis showed that: (1) compared to the homologous Vero cell booster group, the risk of AEFI was about 2.1 times higher (OR = 2.095, 95% CI: 1.056–4.157, p = 0.034) in the CHO cell booster group and 2.5 times higher (OR = 2.476, 95% CI: 1.352–4.533, p = 0.003) in the mixed vaccines group; (2) the odds for women experiencing AEFI were about 2.8 times higher (OR = 2.792, 95% CI: 1.407–5.543, p = 0.003) than men; and (3) compared to the non-frontline HCWs, the risk of AEFI was about 2.6 times higher (OR = 2.648, 95% CI: 1.473–4.760, p = 0.001) in the doctors. Conclusion: The AEFI in all three booster groups are acceptable, and serious adverse events are rare. The risk of AEFI was higher in doctors, which may be related to the high stress during the COVID-19 epidemic. Support from government and non-governmental agencies is important for ensuring the physical and mental health of HCWs.

Objective: Acteoside (ACT) has been reported to regulate the inflammation and immune response. The study aims to explore the effect of ACT on renal fibrosis in unilateral ureteral obstruction (UUO) rats. Methods: Eighteen Sprague-Dawley rats were randomly divided into 3 groups: sham group, opened the abdominal cavity and sutured abdominal; UUO group, performed UUO surgery; and ACT + UUO group, ACT (40 mg/kg) was given by gavage every day after UUO surgery. After 2 weeks of rat model construction, urine and blood samples were collected for biochemical analysis, while kidney tissues were harvested for hematoxylin and eosin (H&E), Masson's trichrome, and immunohistochemistry staining. The expression of connective tissue growth factor (CTGF), alpha smooth muscle actin (α-SMA), collagen III, heat shock protein 47 (HSP47), and β-catenin in the renal tissue was detected and the correlation between these proteins was analyzed. Results: ACT improved the parameters of renal function in UUO rats, including decreased creatinine and urea nitrogen, and declined urinary protein. Pathological analysis suggested that ACT improved the conditions of renal tubule lesion (including structure destruction, atrophy and lumen obstruction), renal interstitial fibrosis and inflammatory cell infiltration in UUO rats. It also down-regulated the expressions of fibrin-related proteins β-catenin, CTGF, α-SMA, collagen III, and HSP47. Correlation analysis found that β-catenin and CTGF were correlated with the expressions of α-SMA, collagen III, and HSP47. Conclusions: ACT could alleviate renal fibrosis in UUO rats probably via inhibiting β-catenin/CTGF signaling pathway.

Single-photon emission computed tomography (SPECT)/computed tomography (CT) imaging of the gouty spine is rare. We describe a 66-year-old man who presented with pain and numbness in the right lower leg; he reported a 2-month history of intermittent low back pain. Imaging revealed neoplastic lesions of the spine, which were initially regarded as tumors. Thus, the patient underwent surgical removal of the lumbar lesion. However, the postoperative pathological diagnosis was gout spondylitis. In this report, we show multimodal images of advanced gout spondylitis. The metabolic information provided by SPECT/CT, combined with the microscopic changes in bone structure revealed by dual-source thin-layer CT and the anatomical localization information provided by magnetic resonance imaging, can help clinicians to more fully understand the pathophysiological mechanisms and imaging manifestations of gout from multiple perspectives, thereby reducing the rate of misdiagnosis.