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Post-stroke depression (PSD) is one of common and serious sequelae of stroke. Approximately, one in three stroke survivors suffered from depression after stroke. It heavily affected functional rehabilitation, which leaded to poor quality of life. What is worse, it is strongly associated with high mortality. In this review, we aimed to derive a comprehensive and integrated understanding of PSD according to recently published papers and previous classic articles. Based on the considerable number of studies, we found that within 2 years incidence of PSD has a range from 11 to 41%. Many factors contribute to the occurrence of PSD, including the history of depression, stroke severity, lesion location, and so on. Currently, the diagnosis of PSD is mainly based on the DSM guidelines and combined with various depression scales. Unfortunately, we lack a unified mechanism to explain PSD which mechanisms now involve dysregulation of hypothalamic–pituitary–adrenal (HPA) axis, increased inflammatory factors, decreased levels of monoamines, glutamate-mediated excitotoxicity, and abnormal neurotrophic response. At present, both pharmacotherapy and psychological therapies are employed in treating PSD. Although great advance has been made by researchers, there are still a lot of issues need to be addressed. Especially, the mechanism of PSD is not completely clear.

Banana is a key staple crop in the world, but its yield is very desperately affected by the leaf diseases like Sigatoka, Fusarium Wilt, and Cordana, which bring serious losses of yield and economy. The manual disease detection methods deployed in the past are time and labor-intensive and cannot be effective in the field, so powerful automated solutions are sought. In this paper, we have presented a hybrid deep learning architecture which combines MobileNetV2 and ResNet101 with attention, dilated convolutions, multi-scale feature pooling and PCA-based feature fusion to classify banana leaf disease accurately and efficiently. The Banana and Banana Leaf, Banana Disease Recognition, and Banana LSD three benchmark datasets have been trained and evaluated following an innovative preprocessing pipeline that consists of illumination correction, background suppression, denoising, and hi-tech data augmentation. The experimental findings have shown that the presented hybrid model is always better than ten state-of-the-art deep learning models, such as VGG16, ResNet50, DenseNet121, EfficientNet-B0, and Vision Transformer (ViT). It has reached an optimal accuracy of 98.28, precision of 98.18, recall of 98.77 and F1-score of 98.43, with only 12.7 M trainable parameters and convergence rate of only 15 epochs, which makes the model both high-accuracy and computationally efficient.

Background Pancreatic cancer is the 12th most common type of cancer, and the sixth leading cause of cancer-related mortality, worldwide. Up-to-date statistics on pancreatic cancer would provide us with a better understanding of epidemiology and identify the causative risk factors for the prevention of this disease. Methods The degree and change patterns of exposure as well as the attributable cancer burden, including incidence, mortality, disability-adjusted life years (DALYs), and prevalence in global and regional, by sex, age, year, for pancreatic cancer, with the data extracted from the Global Burden of Diseases Study (GBD) 2021. All data analyses were conducted using linear regression analysis and the Joinpoint software (version 5.0.1). Results In 2021, 508,533 new cases of pancreatic cancer have been reported; the mortality and prevalence rate increased to 5.95, and 5.12 respectively; and the global DALYs rate increased to 130.33 this year. Besides, the pancreatic cancer-associated rates of incidence, mortality, DALYs, and prevalence were higher in males than in females. In addition, these indicators in the high SDI (Sociodemographic index) region were higher than the global mean. To date, the high fasting plasma glucose remained the major risk factor that influenced the incidence, mortality, DALYs, and prevalence of pancreatic cancer, followed by tobacco and high body mass index (BMI). Conclusions Results of this study suggest that the burden of pancreatic cancer is increasing generally, therefore, more attention and measures should be taken to cope with this situation.

Sweet sorghum ( Sorghum bicolor Moench) seedling emergence and growth are significantly impeded by physical soil crusts (PSCs) in saline-alkaline soils. Abscisic acid (ABA) is a potent seed priming agent known for modulating plant physiological and metabolic responses under salinity stress. However, the influence of ABA priming on seedling emergence in PSCs remains unclear. This study conducted both pot and field experiment to examine the effects of ABA priming on enhancing seedling emergence under PSC conditions. ABA priming altered the balance of at least 24 endogenous phytohormones, including abscisic acid, jasmonic acid, gibberellins, ethylene, auxins, and cytokinins. Additionally, it reprogrammed starch and sucrose metabolism, resulting in the differential expression of genes encoding key enzymes such as AMY, BAM, and INV, which are crucial for converting complex sugars into readily available energy sources, thereby supporting seedling growth. Furthermore, 52 differentially expressed metabolites (DEMs) of flavonoids were identified in germinating seedlings, including 15 anthocyanins, 3 flavones, 7 flavonols, 6 isoflavones, 7 flavanones, and 14 other flavonoids. Genetic and metabolic co-expression network analysis, along with flavonoid biosynthesis pathway exploration, revealed that the biosynthesis of 17 key DEMs—including liquiritigenin, apigenin, kaempferide, syringetin, phloretin, formononetin, dihydrokaempferol, and xanthohumol—was regulated by 10 differentially expressed genes (DEGs) associated with flavonoid biosynthesis. These DEGs encoded 7 enzymes critical for this pathway, including chalcone synthase, shikimate O-hydroxycinnamoyltransferase, bifunctional dihydroflavonol 4-reductase, naringenin 7-O-methyltransferase, and anthocyanidin reductase. This regulation, along with reduced levels of superoxide anion (O 2 − ) and malondialdehyde and increased antioxidant enzyme activities, suggested that flavonoids played a vital role in mitigating oxidative stress. These findings demonstrate that ABA priming can effectively enhance sweet sorghum seedling emergence in PSCs by accelerating emergence and boosting stress resistance.

Background Amoebiasis is caused by the protozoan Entamoeba histolytica , which is a rare infectious disease in developed countries. If the trophozoites enter the blood, it can spread through the body, such as brain, and lungs. Cases of simultaneous infection of multiple organs are extremely rare. Case presentation Here we report a case of simultaneous infection of amoeba in pulmonary pleura, urinary system and central nervous system. Although the patient received anti amoeba treatment, the prognosis of the patient was poor. Conclusions In this patient, multiple extraintestinal amebic infections in the absence of clinically confirmed intestinal amebiasis or amebic liver abscess are rare and pose diagnostic challenges. The disseminated amebiasis has significantly increased the mortality. Early diagnosis and appropriate treatment may reduce the mortality of disseminated amebiasis.

To explore the molecular mechanism of Astragaloside IV (AS-IV) in alleviating renal fibrosis by inhibiting Urotensin II-induced pyroptosis and epithelial-mesenchymal transition of renal tubular epithelial cells. Forty SD rats were randomly divided into control group without operation: gavage with 5ml/kg/d water for injection and UUO model group: gavage with 5ml/kg/d water for injection; UUO+ AS-IV group (gavage with AS-IV 20mg/kg/d; and UUO+ losartan potassium group (gavage with losartan potassium 10.3mg/kg/d, with 10 rats in each group. After 2 weeks, Kidney pathology, serum Urotensin II, and cAMP concentration were detected, and the expressions of NLRP3, GSDMD-N, Caspase-1, and IL-1β were detected by immunohistochemistry. Rat renal tubular epithelial cells were cultured in vitro, and different concentrations of Urotensin II were used to intervene for 24h and 48h. Cell proliferation activity was detected using the CCK8 assay. Suitable concentrations of Urotensin II and intervention time were selected, and Urotensin II receptor antagonist (SB-611812), inhibitor of PKA(H-89), and AS-IV (15ug/ml) were simultaneously administered. After 24 hours, cells and cell supernatants from each group were collected. The cAMP concentration was detected using the ELISA kit, and the expression of PKA, α-SMA, FN, IL-1β, NLRP3, GSDMD-N, and Caspase-1 was detected using cell immunofluorescence, Western blotting, and RT-PCR. Renal tissue of UUO rats showed renal interstitial infiltration, tubule dilation and atrophy, renal interstitial collagen fiber hyperplasia, and serum Urotensin II and cAMP concentrations were significantly higher than those in the sham operation group (p <0.05). AS-IV and losartan potassium intervention could alleviate renal pathological changes, and decrease serum Urotensin II, cAMP concentration levels, and the expressions of NLRP3, GSDMD-N, Caspase-1, and IL-1β in renal tissues (p <0.05). Urotensin II at a concentration of 10-8 mol/L could lead to the decrease of cell proliferation, (p<0.05). Compared with the normal group, the cAMP level and the PKA expression were significantly increased (p<0.05). After intervention with AS-IV and Urotensin II receptor antagonist, the cAMP level and the expression of PKA were remarkably decreased (p<0.05). Compared with the normal group, the expression of IL-1β, NLRP3, GSDMD-N, and Caspase-1 in the Urotensin II group was increased (p<0.05), which decreased in the AS-IV and H-89 groups. AS-IV can alleviate renal fibrosis by inhibiting Urotensin II-induced pyroptosis of renal tubular epithelial cells by regulating the cAMP/PKA signaling pathway.

How FTO targets obesity The fat mass and obesity-associated ( FTO ) gene is associated with increased body weight and obesity risk. FTO protein is a DNA/RNA demethylase, and mice lacking it are abnormally lean. Now the crystal structure of human FTO in complex with the mononucleotide 3-meT has been determined. The structure reveals a novel mechanism by which the protein can discriminate between single- and double-stranded DNA. In addition, biochemical assays show that the C-terminal domain of FTO, previously of unknown function, is required for FTO catalytic activity via interactions with the N-terminal catalytic domain. These results provide a structural basis for understanding FTO substrate specificity, and serve as a foundation for the rational design of FTO inhibitors as potential anti-obesity agents. The fat mass and obesity-associated ( FTO ) gene has been associated with increased body weight. The FTO protein has DNA/RNA demethylase activity. Here, the crystal structure of human FTO in complex with the mononucleotide 3-methylthymidine is presented. The structure provides a basis for understanding the substrate specificity of FTO, and should serve as a foundation for the design of FTO inhibitors. Recent studies 1 , 2 , 3 , 4 , 5 have unequivocally associated the fat mass and obesity-associated ( FTO ) gene with the risk of obesity. In vitro FTO protein is an AlkB-like DNA/RNA demethylase with a strong preference for 3-methylthymidine (3-meT) in single-stranded DNA or 3-methyluracil (3-meU) in single-stranded RNA 6 , 7 , 8 . Here we report the crystal structure of FTO in complex with the mononucleotide 3-meT. FTO comprises an amino-terminal AlkB-like domain and a carboxy-terminal domain with a novel fold. Biochemical assays show that these two domains interact with each other, which is required for FTO catalytic activity. In contrast with the structures of other AlkB members, FTO possesses an extra loop covering one side of the conserved jelly-roll motif. Structural comparison shows that this loop selectively competes with the unmethylated strand of the DNA duplex for binding to FTO, suggesting that it has an important role in FTO selection against double-stranded nucleic acids. The ability of FTO to distinguish 3-meT or 3-meU from other nucleotides is conferred by its hydrogen-bonding interaction with the two carbonyl oxygen atoms in 3-meT or 3-meU. Taken together, these results provide a structural basis for understanding FTO substrate-specificity, and serve as a foundation for the rational design of FTO inhibitors.

Background Appendiceal goblet cell adenocarcinoma (GCA) is a rare malignant tumor originating from the appendiceal mucosa, with an insidious onset. Its biological behavior lies between that of a carcinoid tumor and an adenocarcinoma, and it has a relatively favorable prognosis but a high risk of long-term recurrence and metastasis. The coexistence of primary cecal tubular adenocarcinoma and appendiceal GCA is extremely rare, and poses challenges in diagnosis and treatment. Case demonstration An 86-year-old male presented with a 2-month history of abdominal pain and diarrhea. Abdominal CT revealed thickening of the ascending colon wall, suggesting colon cancer. Laparoscopic right hemicolectomy was performed. Postoperative pathological examination confirmed primary cecal tubular adenocarcinoma combined with appendiceal goblet cell adenocarcinoma. Adjuvant chemotherapy was recommended, but the patient refused. Seven months later, lung metastasis was detected. Chemotherapy with “raltitrexed plus bevacizumab” was administered. During an 8-month follow-up, the patient remained in generally good condition. Conclusion Appendiceal GCA is more common in middle-aged and elderly women and is associated with a good overall survival rate but a high risk of long-term recurrence and metastasis, especially in patients with distant metastases. The coexistence of appendiceal GCA and cecal tubular adenocarcinoma is exceedingly rare. This case report analyzes the clinical features, histological morphology, immunohistochemistry, and differential diagnosis of this condition to enhance understanding of this rare disease.

Brassinosteroids are essential phytohormones that have crucial roles in plant growth and development. Perception of brassinosteroids requires an active complex of BRASSINOSTEROID-INSENSITIVE 1 (BRI1) and BRI1-ASSOCIATED KINASE 1 (BAK1). Recognized by the extracellular leucine-rich repeat (LRR) domain of BRI1, brassinosteroids induce a phosphorylation-mediated cascade to regulate gene expression. Here we present the crystal structures of BRI1(LRR) in free and brassinolide-bound forms. BRI1(LRR) exists as a monomer in crystals and solution independent of brassinolide. It comprises a helical solenoid structure that accommodates a separate insertion domain at its concave surface. Sandwiched between them, brassinolide binds to a hydrophobicity-dominating surface groove on BRI1(LRR). Brassinolide recognition by BRI1(LRR) is through an induced-fit mechanism involving stabilization of two interdomain loops that creates a pronounced non-polar surface groove for the hormone binding. Together, our results define the molecular mechanisms by which BRI1 recognizes brassinosteroids and provide insight into brassinosteroid-induced BRI1 activation. Steroid hormone recognition The brassinolides are potent steroid hormones that are central to plant growth and development. They bind to the plasma membrane receptor BRI1, a member of the leucine-rich repeat (LRR) receptor family that also includes the mammalian Toll-like receptors, which are important in innate immunity. Two independent studies now present the crystal structure of BRI1 from Arabidopsis thaliana , both in the free form and in complex with brassinolide. BRI1 is found to adopt a solenoid-like superhelical structure involving 25 leucine-rich repeats. The structure is strikingly different from that of Toll-like receptors and reveals a novel mechanism of steroid recognition. This work suggests synthetic routes to nonsteroidal mimetics of BRI1 that could have a possible use in agriculture.

Nonhuman animals, human infants, and human adults all share an Approximate Number System (ANS) that allows them to imprecisely represent number without counting. Among humans, people differ in the precision of their ANS representations, and these individual differences have been shown to correlate with symbolic mathematics performance in both children and adults. For example, children with specific math impairment (dyscalculia) have notably poor ANS precision. However, it remains unknown whether ANS precision contributes to individual differences only in populations of people with lower or average mathematical abilities, or whether this link also is present in people who excel in math. Here we tested non-symbolic numerical approximation in 13- to 16-year old gifted children enrolled in a program for talented adolescents (the Center for Talented Youth). We found that in this high achieving population, ANS precision significantly correlated with performance on the symbolic math portion of two common standardized tests (SAT and ACT) that typically are administered to much older students. This relationship was robust even when controlling for age, verbal performance, and reaction times in the approximate number task. These results suggest that the Approximate Number System is linked to symbolic math performance even at the top levels of math performance.