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CCN1 is a matricellular protein highly expressed in esophageal squamous cell carcinoma (ESCC) but hardly detectable in esophageal adenocarcinoma (EAC). Expression of CCN1 in EAC cells leads to TRAIL-mediated apoptosis. Unlike TRAIL, which primarily triggers cell death, APRIL and BAFF promote cell growth via NFκB signaling. They become active ligands by Furin cleavage. This study found that CCN1 upregulated APRIL and BAFF expression in both ESCC and EAC cells but attenuated their signaling in the latter. CCN1 kept Furin stable in ESCC allowing APRIL/BAFF to signal through their common receptor BCMA properly. In EAC cells, however, expression of CCN1 lowered Furin activity and thus limited APRIL/BAFF cleavage. As a result, ESCC cells benefited from CCN1 while EAC cell viability was attenuated by it.

Introduction: Obesity is a major risk factor for metabolic disorders in children. Therefore, it is particularly important to study the abnormal regulation of circulating miR-24-3p in obese children and its predictive value for metabolic syndrome. Methods: Serum samples were obtained from children with obesity (n = 45), obese children with metabolic syndrome (n = 52), and healthy controls (n = 50). The expression levels of miR-24-3p were detected by reverse transcription quantitative PCR. The ROC curve was used to evaluate the diagnostic value of miR-24-3p. Pearson’s correlation analysis was performed to evaluate the relationship between serum miR-24-3p and different clinical parameters. Logistic regression analysis was used to evaluate the relationship between miR-24-3p and obesity with metabolic syndrome in children. Results: The expression of miR-24-3p was the highest in obese children with metabolic syndrome. ROC results showed that miR-24-3p had the ability to distinguish healthy individuals from obese children (area under the curve [AUC] = 0.951) and can predict the occurrence of metabolic syndrome for obese children (AUC = 0.890). The expression level of miR-24-3p was positively correlated with body mass index (r = 0.817, p < 0.001), fasting blood glucose (r = 0.798, p < 0.001), triglycerides (r = 0.773, p < 0.001), systolic blood pressure (r = 0.746, p < 0.001), and diastolic blood pressure (r = 0.623, p < 0.001), respectively. Logistic regression analysis showed that miR-24-3p was an independent influence factor for the occurrence of metabolic syndrome in obese children. Discussion/Conclusion: MiR-24-3p is a potential noninvasive marker for children with obesity and has predictive value for the occurrence of metabolic syndrome.

Background Ureteral obstruction causes injury of the renal tissues and can irreversibly progress to renal fibrosis, with atrophy and apoptosis of tubular cells. The goal of the current study was to examine the effects of rhein on the apoptosis o renal tubular cells as well as renal fibrosis using a rodent model of unilateral ureteral obstruction (UUO). Methods UUO was induced through ureteral ligation, then animals received treatments with rhein or vehicle. The control rats only received sham operation. The renal tissue was harvested 1 week after surgery for assessment of kidney fibrosis. Results The expressions of collagen I and α-smooth muscle actin (α-SMA), as well as the severity of renal tubular apoptosis and fibrosis were time-dependently increased following UUO. Treatments with rhein partially inhibited such responses. Renal interstitial fibrosis was associated with STAT3 (signal transducer and activator of transcription 3) phosphorylation as well as altered expressions of Bax and Bcl2, both apoptosis-related proteins. Treatment with rhein also partly blocked these responses. Conclusion These findings demonstrated that rhein mitigated apoptosis of renal tubular cell as well as renal fibrosis in a UUO rodent model. This curative effect is likely mediated via suppression of STAT3 phosphorylation.

To evaluate the clinical performance of noninvasive prenatal screening (NIPS) for fetal sex chromosome aneuploidies (SCAs), pregnant women were recruited in this retrospective observational study. The NIPS test was undertaken using high-throughput gene sequencing. In total,50,301 pregnant women were analysed for demographic characteristics and medical history. Of them, 308 women (0.61%) had high risk for fetal SCAs, including 138 for 45,X, 111 for 47,XXY, 42 for 47,XXX, and 17 for 47,XYY. After the pre-test counselling, 182 participants chose to undergo invasive prenatal diagnosis, confirming 59 positive cases. The combined positive predictive value of NIPS was 32.42% (59/182), 18.39% (16/87), 44.4% (12/27), 39.29% (22/56), and 75% (9/12) for detecting SCAs, 45,X, 47,XXX, 47,XXY, and 47,XYY, respectively. NIPS can be a useful method to detect the fetal SCAs using high-throughput gene sequencing, though accuracy can still be improved, especially for 45,X. Although the value of NIPS compare favorably with those seen in traditional screening approaches for SCAs, it is important to highlight the limitations of NIPS while educating clinicians and patients.

Renal tubular injury plays a critical role in the progression of lupus nephritis (LN); however, the underlying mechanisms remain poorly understood. In this study, we found that CDO1 expression was significantly positively correlated with the degree of renal tubular injury in renal tissues from LN patients. Using in vitro HK-2 and TCMK-1 cells as well as an in vivo MRL/lpr mouse model, we confirmed that knockdown of CDO1 alleviated renal tubular epithelial cell injury and lipid deposition. Mechanistic studies revealed that CDO1 inhibits lipid metabolism by negatively regulating the expression of ACSM3; notably, downregulation of ACSM3 reversed the ameliorative effects of CDO1 knockdown on lipid deposition and cellular injury. Further investigation demonstrated that ACSM3 deficiency mediates lipid deposition by inducing mitochondrial morphological abnormalities and dysfunction. In summary, this study uncovers a novel mechanism by which the CDO1–ACSM3 axis mediates renal tubular lipid deposition and injury in LN through the regulation of mitochondrial function, offering a potential therapeutic target for this disease.

Exploring efficient and easily implementable prenatal screening strategies aims at birth defect prevention and control. However, there have been limited economic evaluations of non-invasive prenatal screening (NIPS) strategies in China. Furthermore, these studies were predominantly confined to local or geographically proximate provinces and lacked universality and representativeness. This study assesses the health economics of current prenatal screening strategies and NIPS as first-line screening programs, analyzing their efficacy to determine an optimal strategy. From the perspective of health economics, cost-effectiveness, cost-benefit, and single-factor sensitivity were conducted for five different screening strategies using a decision tree model. Among pregnant women aged < 35 years who underwent only one screening for foetal Down syndrome (DS), the detection rate, false positive rate and positive predictive value of NIPS for foetuses with DS were superior to those of the other four serological screening methods. Although applying NIPS as first-line screening method yields the highest efficacy and benefits, it currently lacks cost-effectiveness when compared to serological screening and sequential NIPS screening strategies.

Background Pathogenic (P) copy number variants (CNVs) may be associated with second-trimester ultrasound soft markers (USMs), and noninvasive prenatal screening (NIPS) can enable interrogate the entire fetal genome to screening of fetal CNVs. This study evaluated the clinical application of NIPS for detecting CNVs among fetuses with USMs in pregnant women not of advanced maternal age (AMA). Results Fetal aneuploidies and CNVs were identified in 6647 pregnant women using the Berry Genomics NIPS algorithm.Those with positive NIPS results underwent amniocentesis for prenatal diagnosis. The NIPS and prenatal diagnosis results were analyzed and compared among different USMs. A total of 96 pregnancies were scored positive for fetal chromosome anomalies, comprising 37 aneuploidies and 59 CNVs. Positive predictive values (PPVs) for trisomy 21, trisomy 18, trisomy 13, and sex chromosome aneuploidies were 66.67%, 80.00%, 0%, and 30.43%, respectively. NIPS sensitivity for aneuploidies was 100%. For CNVs, the PPVs were calculated as 35.59% and false positive rate of 0.57%. There were six P CNVs, two successfully identified by NIPS and four missed, of which three were below the NIPS resolution limit and one false negative. The incidence of aneuploidies was significantly higher in fetuses with absent or hypoplastic nasal bone, while that of P CNVs was significantly higher in fetuses with aberrant right subclavian artery (ARSA), compared with other groups. Conclusions NIPS yielded a moderate PPV for CNVs in non-AMA pregnant women with fetal USM. However, NIPS showed limited ability in identifying P CNVs. Positive NIPS results for CNVs emphasize the need for further prenatal diagnosis. We do not recommend the use of NIPS for CNVs screening in non-AMA pregnant women with fetal USM, especially in fetuses with ARSA.

Short-time oxidation behavior of nanocrystalline Ta coating is studied at 850 °C in comparison with that of the Ta sheet. Owing to the large PBR value and insufficient expansion space, the oxide scale on Ta sheet is dramatically cracked, delaminated and pulverized, resulting in rapid deterioration. For nanocrystalline Ta coatings with columnar structures and quantitative grain boundaries, a rapid oxygen diffusion rate causes no initial Ta 2 O 5 to form. The gap between columns provides spaces for bulk expansion, resulting in few opening cracks and delamination. Ta oxidation experiences a crystallization course from amorphous Ta oxide, leading to in situ temperature surging and thus pulverization.

Background Complex chromosomal rearrangements (CCRs) are associated with high reproductive risk, infertility, abnormalities in offspring, and recurrent miscarriage in women. It is essential to accurately characterize apparently balanced chromosome rearrangements in unaffected individuals. Methods A CCR young couple who suffered two spontaneous abortions and underwent labor induction due to fetal chromosomal abnormalities was studied using long‐read sequencing(LRS), single‐nucleotide polymorphism (SNP) array, G‐banding karyotype analysis (550‐band resolution), and Sanger sequencing. Results SNP analysis of the amniotic fluid cells during the third pregnancy revealed a 9.9‐Mb duplication at 7q21.11q21.2 and a 24.8‐Mb heterozygous deletion at 13q21.1q31.1. The unaffected female partner was a carrier of a three‐way CCR [46,XX,? ins(7;13)(q21.1;q21.1q22)t(2;13)(p23;q22)]. Subsequent LRS analysis revealed the exact breakpoint locations on the derivative chromosomes and the specific method of chromosome rearrangement, indicating that the CCR carrier was a more complex structural rearrangement comprising five breakpoints. Furthermore, LRS detected an inserted fragment of chromosome 13 in chromosome 7. Conclusions LRS is effective for analyzing the complex structural variations of the human genome and may be used to clarify the specific CCRs for effective genetic counseling and appropriate intervention. This study investigated a de novo case of complex chromosomal rearrangement (CRR) in a young couple visited our hospital for genetic counseling and fertility guidance due to the increased thickness of the fetal nuchal translucency. We successfully identified the female partner as a carrier of a three‐way CCR [46, XX, ? ins(7; 13)(q21.1;q21.1q22)t(2;13)(p23;q22)] using high‐resolution G‐banding karyotype analysis (550‐band resolution). Third‐generation sequencing (TGS) using PromethION platform revealed that the five breakpoints on chromosomes 2, 7, and 13 (2:18044504, 7:82511487, 7:92482297, 13:56958850, and 13:81861586) participated in the CCR.