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Osteoprotegerin (OPG) is supposed to participate in the development of atherosclerosis and cardio-cerebrovascular disease. However, the results of research on relationship between OPG and ischemic stroke (IS) are controversial. Therefore, we carried out the first systematic review and meta-analysis to evaluate prognostic effect of osteoprotegerin in patients with IS. We comprehensively searched databases of PubMed, Embase, and the Cochrane Library through 21 August 2023 to identify observational studies that evaluated effect of OPG on poor functional outcome (modified Rankin Scale [mRS] Score of 3-6) and mortality in patients with IS. Adjusted odds ratios (aOR) with a 95% confidence interval (CI) of each included study were used as much as possible to assess the pooled effect. Five studies that enrolled 4,506 patients in total fulfilled our inclusion criteria. Three studies were included in the pooled analysis for each endpoint since one of the included studies had provided data on poor functional outcome as well as mortality. OPG was neither associated with poor functional outcome (aOR 1.29, 95% CI 0.90-1.85) nor with mortality (aOR 1.57, 95% CI 0.90-2.74) in patients with IS. There is insufficient evidence to demonstrate the correlation between OPG and mortality or poor functional outcome in IS patients. OPG cannot be applied to predict worse neurological function in IS patients based on the current evidence.

Streptococcus suis is one of the most common zoonotic pathogens, in humans and can cause meningitis, endocarditis, arthritis and sepsis. Human cases of Streptococcus suis infection have been reported worldwide, and most of those cases occurred in Asia. Hearing loss is the most common sequela of Streptococcus suis meningitis. Streptococcus suis infection complicated with acute cerebral infarction has rarely been reported. Therefore, to provide a reference for this disease, we reported a case of acute multiple brain infarctions associated with Streptococcus suis infection. In our report, a 69yearold male patient had Streptococcus suis meningitis and sepsis, which were associated with multiple acute cerebral infarctions in the pons and bilateral frontotemporal parietal occipital lobes. After treatment, the patient exhibited cognitive impairment, dyspraxia and irritability. There are limited case reports of cerebral infarction associated with Streptococcus suis infection, and further research is needed to determine the best treatment method.

Powdery mildew is a devastating disease that affects wheat yield and quality globally. Here, we identify a powdery mildew resistance locus MlIW39 from wild emmer wheat through map-based cloning, mutagenesis, and stable genetic transformation. Unlike many other cloned Pm genes, the MlIW39 -mediated resistance is conferred by the combined effect of two complementary nucleotide-binding and leucine-rich repeat (NLR) genes, encoding a canonical coiled-coil (CC) type NLR protein ( MlIW39-R1 ) and an atypical NLR protein ( MlIW39-R2 ) with an unknown domain (CC-like), respectively. Overexpression of the NLR pair induces cell death in Nicotiana benthamiana , whereas MlIW39-R1 or MlIW39-R2 alone does not. The MlIW39-R1 and MlIW39-R2 proteins physically interact with each other. MlIW39-R1 and MlIW39-R2 likely originate independently and become neighborly located during evolution. Our findings shed light on the significance of NLR pairs in plant immunity and can facilitate wheat disease-resistance breeding using the developed MlIW39 introgression lines and functional marker. Powdery mildew is a devasting disease for both common wheat and durum wheat. Here, the authors report the powdery mildew resistance locus derived from wild emmer wheat is conferred by the combined effect of two complementary nucleotide-binding and leucine-rich repeat genes.

Wheat leaf rust (also known as brown rust), caused by the fungal pathogen Puccinia triticina Erikss. (Pt), is one by far the most troublesome wheat disease worldwide. The exploitation of resistance genes has long been considered as the most effective and sustainable method to control leaf rust in wheat production. Previously the leaf rust resistance gene Lr65 has been mapped to the distal end of chromosome arm 2AS linked to molecular marker Xbarc212 . In this study, Lr65 was delimited to a 0.8 cM interval between flanking markers Alt-64 and AltID-11 , by employing two larger segregating populations obtained from crosses of the resistant parent Altgold Rotkorn (ARK) with the susceptible parents Xuezao and Chinese Spring (CS), respectively. 24 individuals from 622 F 2 plants of crosses between ARK and CS were obtained that showed the recombination between Lr65 gene and the flanking markers Alt-64 and AltID-11 . With the aid of the CS reference genome sequence (IWGSC RefSeq v1.0), one SSR marker was developed between the interval matched to the Lr65 -flanking marker and a high-resolution genetic linkage map was constructed. The Lr65 was finally located to a region corresponding to 60.11 Kb of the CS reference genome. The high-resolution genetic linkage map founded a solid foundation for the map-based cloning of Lr65 and the co-segregating marker will facilitate the marker-assisted selection (MAS) of the target gene.

Background Portal vein tumor thrombosis (PVTT) in hepatocellular carcinoma (HCC) is a sign of advanced stage disease, which is associated with poor prognosis. Liver resection (LR) may provide better prognosis in selected patients. In the present study, we aimed to assess information from HCC patients with PVTT who died within 3 months or 2 years after LR in order to identify preoperative factors correlated to short-term or long-term survival, by which inappropriate selection of patients for LR might be avoided in the future. Methods A retrospective cohort study consisting of 487 consecutive cases of HCC patients with PVTT was performed from 2008 to 2010 at Eastern Hepatobiliary Surgery Hospital. Medical records, including laboratory values, imaging results and treatment information, were obtained from participants. Study endpoints were survival at 3 months and 2 years post-hepatectomy. Logistic regression analysis was utilized to determine the significant pre-operative factors influencing short-term or long-term survival. Results In multivariable analysis, α-fetoprotein, total bilirubin and radiologic ascites were significantly associated with short-term survival, while α-fetoprotein level, clinical significant portal hypertension, extent of PVTT and tumor differentiation were factors significantly associated with long-term survival. Conclusions The independent risk factors of poor short-term survival were the liver function-associated, such as factors radiologic ascites and total bilirubin, while tumor differentiation indicating the tumor biology was associated with longer-term survival. In addition, α-fetoprotein was a risk factor associated with both short-term and longer-term survivals.

Powdery mildew (PM), caused by Blumeria graminis f. sp. tritici (Bgt), is one of the destructive wheat diseases worldwide. Wild emmer wheat (Triticum turgidum ssp. dicoccoides, WEW), a tetraploid progenitor of common wheat, is a valuable genetic resource for wheat disease resistance breeding programs. We developed three hexaploid pre-breeding lines with PM resistance genes derived from three WEW accessions. These resistant pre-breeding lines were crossed with susceptible common wheat accessions. Segregations in the F2 populations were 3 resistant : 1 susceptible, suggesting a single dominant allele in each resistant parent. Mapping of the resistance gene in each line indicated a single locus on the long arm of chromosome 7A, at the approximate location of previously cloned Pm60 from T. urartu. Sanger sequencing revealed three different Pm60 haplotypes (Hap 3, Hap 5, and Hap 6). Co-segregating diagnostic markers were developed for identification and selection of each haplotype. The resistance function of each haplotype was verified by the virus-induced gene silencing (VIGS). Common wheat lines carrying each of these Pm60 haplotypes were resistant to most Bgt isolates and differences in the response arrays suggested allelic variation in response.

Early diagnosis and clear differentiation of pancreatic ductal adenocarcinoma (PDAC) from chronic pancreatitis (CP) is clinically challenging. A machine learning model is developed for the diagnosis of PDAC. The model is induced using a dataset of 13  987 participants, of which 12  402 are used for training the model and the remaining 1585 for testing purposes. One thousand sixty‐six laboratory variables are reduced to 18 measures using standard filtering and feature importance methods. Then, five machine learning classifiers are evaluated for the study. Hyperparameter optimization for each classifier is carried out, and the optimal algorithm is established using a tenfold cross validation on the training data. Finally, gradient boosting decision tree‐based ternary classifier composed of 18 routine laboratory variables (GBDT‐TC18) is established. In the test cohort, GBDT‐TC18 differentiates PDAC from CP and healthy control (HC) with an accuracy better than carbohydrate antigen 19‐9 (CA19‐9)‐based diagnosis. It also maintains a high diagnostic accuracy for stages I, IIA, and IIB PDAC, small‐sized PDAC, body and tail adenocarcinoma, CA19‐9‐negative PDAC, and nonjaundice PDAC. What's more, GBDT‐TC18 shows a higher accuracy than CA19‐9 in distinguishing PDAC from CP. GBDT‐TC18 can be used to augment the capability of doctors for early and differential diagnosis of PDAC. A machine learning model is developed for the diagnosis of pancreatic ductal adenocarcinoma (PDAC). The model is created using a dataset of 13 987 participants, of which 12 402 are used for training the model and the remaining 1585 for testing purposes. Compared with carbohydrate antigen 19‐9 (CA19‐9), this model can better distinguish PDAC, chronic pancreatitis (CP), and healthy people.

A continuous GPS array across the southern segment of the Longmenshan fault zone recorded the deformation during the process of the Lushan MS7.0 earthquake that occurred on April 20, 2013. Such data can provide meaningful information regarding the dynamic evolution of crustal deformation in the seismogenic zone. Our studies have shown that the occurrence of the Wenchuan earthquake led to the loading of compressive and sinistral shearing strain on the southern segment of the Maoxian-Wenchuan fault, whereby the extrusion strain accumulated at a greater rate than before the Wenchuan earthquake. The strain time series in the seismogenic zone revealed that the principal compression strain rates decreased from west to east in the direction of N30°–45°W. Furthermore, the area to the east of Beichuan-Yingxiu fault behaved as a zone of compressive deformation with obvious sinistral shearing deformation. The surface strain and the first shearing strain time series decreased with time, while the area to the west of the Beichuan-Yingxiu fault behaved as a zone of dextral shear deformation that increased with time. Furthermore, the regional deformation field before the Lushan earthquake showed that the rate of extrusion strain accumulation in the southern segment of the Longmenshan fault zone was obviously larger than before the Wenchuan earthquake. Moreover, the sinistral shearing strain accumulated in the area of the southern segment of the Maoxian-Wenchuan fault. Based on the above analysis, we consider that the eastward movement of the Bayan Har block increased considerably following the Wenchuan earthquake, which enhanced the accumulation of compression strain in the southern segment of the Longmenshan fault zone.

Background: Only a small proportion of patients with compensated advanced chronic liver disease (cACLD) had varices needing treatment (VNT) after recommended esophagogastroduodenoscopy (EGD) screening. We aimed to create a non-invasive nomogram based on routine tests to detect VNT in cACLD patients. Methods: The training cohort included 162 cACLD patients undergoing EGD in a university hospital, between January 2014 and September 2019. A nomogram was developed based on the independent predictors of VNT, selected using a multivariate logistic regression analysis. Thirty-three patients from eight university hospitals were prospectively enrolled as validation cohort between December 2018 and December 2019. Results: The prevalence of VNT was 32.7% (53/162) and 39.4% (13/33) in training and validation cohorts, respectively. The univariate analysis identified six risk factors for VNT. On the multivariate analysis, four of them, i.e., gallbladder wall thickness (odds ratio [OR]: 1.23; 95% confidence interval [CI]: 0.98-1.56), spleen diameter (OR: 1.02; 95% CI: 1.00-1.04), platelet count (OR: 0.98; 95% CI: 0.97-0.99), and international normalized ratio (OR: 0.58; 95% CI: 0.06-5.84) were independently associated with VNT. Thus, a nomogram based on the four above - mentioned variables was developed, and showed a favorable performance for detecting VNT, with an area under receiver operating characteristic curve of 0.848 (95% CI: 0.769-0.927) in training cohort. By applying a cut-off value of 105 in validation cohort, 31.0% of EGD were safely spared with 3.4% of missed VNT. Conclusion: A nomogram based on routine clinical parameters was developed for detecting VNT and avoiding unnecessary EGD in cACLD patients.

Fibrosis is a typical aging-related pathological process involving almost all organs, including the heart, kidney, liver, lung, and skin. Fibrogenesis is a highly orchestrated process defined by sequences of cellular response and molecular signals mechanisms underlying the disease. In pathophysiologic conditions associated with organ fibrosis, a variety of injurious stimuli such as metabolic disorders, epigenetic changes, and aging may induce the progression of fibrosis. Sirtuins protein is a kind of deacetylase which can regulate cell metabolism and participate in a variety of cell physiological functions. In this review, we outline our current understanding of common principles of fibrogenic mechanisms and the functional role of SIRT3/6 in aging-related fibrosis. In addition, sequences of novel protective strategies have been identified directly or indirectly according to these mechanisms. Here, we highlight the role and biological function of SIRT3/6 focus on aging fibrosis, as well as their inhibitors and activators as novel preventative or therapeutic interventions for aging-related tissue fibrosis. Graphical abstract