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Acute myocardial infarction (AMI) is a heart lesion, that endangers the life safety of patients. This study focused on exploring the clinical effect of miR-542-3p on AMI and no-reflow after percutaneous coronary intervention (PCI). Serum samples were collected from 100 AMI emergency inpatients. The expression of miR-542-3p was quantified by qPCR. The predictive role of miR-542-3p was disclosed by plotting ROC curve. In addition, AMI subjects were cataloged into a group of no-reflow and normal reflow group. The risk factors of no-reflow were estimated by logistic regression analysis. In the serum samples of AMI patients, the level of miR-542-3p showed a pattern of decreasing. MiR-542-3p expression represented a high sensitivity and specificity of the prediction of AMI. A decrease of miR-542-3p content was revealed in AMI patients without reflow after PCI. Logistic regression results reflected that miR-542-3p was an independent biomarker for no-reflow. The declined miR-542-3p expression was a predictive marker for AMI and no-reflow in AMI patients.

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Introduction: Rhodiola species have been utilized as functional foods in Asia and Europe for promoting health. Research has demonstrated that Rhodiola has the potential to alleviate inflammatory bowel disease (IBD) in animal models. However, the specific active components and the underlying mechanism for ameliorating intestinal damage remain unclear. This study aims to explore the relieving effect of Rosavin (Rov), a known active constituent of Rhodiola, in IBD and the regulatory mechanisms. Methods: The therapeutic effect of Rov was evaluated using a murine model of acute colitis induced by dextran sulfate sodium salt (DSS). Inflammatory cytokines and neutrophil activation markers were measured by corresponding kits. Immunohistochemistry, immunofluorescence, TUNEL, and EdU assays were applied to investigate the tight conjunction proteins expression, epithelial marker expression, number of apoptotic cells, and epithelial proliferation, respectively. The protection effect of Rov on gut epithelial injury was assessed using TNF-α-induced intestinal organoids. Additinally, RNA sequencing was applied to observe the genetic alteration profile in these intestinal organoids. Results: Oral administration of Rov significantly attenuated weight loss and restored colon length in mice. Notably, Rov treatment led to decreased levels of pro-inflammatory cytokines and neutrophil activation markers while increasing anti-inflammatory factors. Importantly, Rov restored intestinal despair by increasing the number of Lgr5+ stem cells, Lyz1+ Paneth cells and Muc2+ goblet cells in intestines of colitis mice, displaying reduced epithelial apoptosis and recovered barrier function. In TNF-α-induced intestinal organoids, Rov facilitated epithelial cell differentiation and protected against TNF-α-induced damage. RNA sequencing revealed upregulation in the gene expression associated with epithelial cells (including Lgr5+, Lyz1+ and Muc2+ cells) proliferation and defensin secretion, unveiling the protective mechanisms of Rov on the intestinal epithelial barrier. Discussion: Rov holds potential as a natural prophylactic agent against IBD, with its protective action on the intestinal epithelium being crucial for its therapeutic efficacy.

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Subsequently to the publication of the above paper, an interested reader drew to the authors' attention that the control western blots shown for Fig. 1A and B on p. 908 and Fig. 8A and C on p. 911 were apparently the same, where different experiments were intended to have been portrayed. After having re­examined their original data files, the authors realized that these figures had been published with the control western blots shown incorrectly for Fig. 1A and 8C. The  corrected versions of this pair of figures are shown on the next page. Note that the corrections made to these figures do not affect the overall conclusions reported in the paper. The authors are grateful to the Editor of Oncology Reports for allowing them the opportunity to publish this Corrigendum, and apologize to the readership for any inconvenience caused. [Oncology Reports 33: 905­912, 2015; DOI: 10.3892/or.2014.3656].

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The incorporation of trinitrophenyl-modified 1,3,4-oxadiazole fragments is commonly observed in high-energy molecules with heat-resistant properties. This study explores the strategy of developing heat-resistant energetic materials by incorporating trinitrophenyl and an azo group into 1,3,4-oxadiazole, which involved the synthesis and characterization of (E)-1,2-bis(5-(2,4,6-trinitrophenyl)-1,3,4-oxadiazol-2-yl)diazene (2), N-(5-(2,4,6-trinitrophenyl)-1,3,4-oxadiazol-2-yl)nitramide (3), and the energetic salts of 3. Characterization techniques employed included 1H and 13C NMR, IR and elemental analysis. Additionally, the structures of 2 and 3 were validated using single crystal X-ray analysis. To further understand the physical and chemical characteristics of these novel energetic compounds, various calculations and measurements were performed. Compound 2 exhibits excellent thermostability (Td = 294 °C), which is comparable to that of traditional heat-resistant explosive HNS (Td = 318 °C). But 2 is insensitive towards impact (>40 J) and friction (>360 N), surpassing HNS (5 J, 240 N), suggesting that compound 2 deserves further investigation as a potential heat-resistant explosive.

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PURPOSE: To compare outcomes of radical (RN) and partial nephrectomy (PN) in Sarcomatoid Renal Cell Carcinoma (sRCC) utilizing a large national cohort. As RN is the reference standard for localized RCC with clinically aggressive features, PN in sRCC has been seldom studied. METHODS: We performed a retrospective cohort analysis of the National Cancer Database from 2004 to 2019 for patients who underwent PN and RN for sRCC (T1-T3N0-N1M0). We performed multivariable analyses (MVA) to determine factors associated with PN and all-cause mortality (ACM), and Kaplan-Meier Analysis (KMA) for overall survival (OS) in Charlson 0 patients who underwent PN vs. RN according to clinical stage. RESULTS: The cohort consisted of 5,265 patients [RN 4,582 (87.0%)/PN 683 (13.0%)]. Increased odds of receiving PN was associated with papillary RCC (OR = 1.69, p = 0.015); inversely with increasing age (OR = 0.99, p = 0.004), cT2-cT3 (OR = 0.23, p < 0.001), and cN1 (OR = 0.2, p < 0.001). Worsened ACM was associated with positive margins (HR = 1.59, p < 0.001), male (HR = 1.1, p = 0.044), Charlson [Formula: see text]2 (HR = 1.47, p < 0.001), cT2-cT3 (HR 1.17-1.39, p < 0.001-0.035), and cN1 (HR = 1.59, p < 0.001). Improved ACM was noted with PN (HR = 0.64, p < 0.001), increasing household income (HR = 0.77-0.79, p < 0.001), and private insurance (HR = 0.80, p = 0.018). KMA showed PN had improved 5-year OS compared to RN in cT1 (86.5% vs. 63.2%, p < 0.001), and cT3 (61.0% vs. 44.0% p < 0.001), but not cT2 (p = 0.67). CONCLUSION: In select patients, PN with negative margins may not compromise outcomes and may provide benefit when indicated. Patients with private insurance and highest income experienced improved survival suggesting disparity in care.

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To understand the effects of nitrogen deposition on element cycling and nutrient limitation status in forest ecosystems, we examined the effects of nitrogen deposition on the stoichiometric characteristics of forest soil-microbial-extracellular enzymes in Pinus yunnanensis forest. We conducted a field experiment with control (CK, 0 g N·m-2·a-1), low nitrogen (LN, 10 g N·m-2·a-1), medium nitrogen (MN, 20 g N·m-2·a-1) and high nitrogen (HN, 25 g N·m-2·a-1) since 2019. We collected soil samples (0-5 cm, 5-10 cm and 10-20 cm) at September 2022, and measured the contents of soil organic, total nitrogen, total phosphorus, microbial biomass carbon, nitrogen and phosphorus (MBC, MBN, MBP) and the activities of C, N, and P acquisition enzymes. The results showed that nitrogen deposition significantly reduced soil organic content, C:N and C:P by 6.9%-29.8%, 7.6%-45.2% and 6.5%-28.6%, and increased soil total N content and N:P by 10.0%-45.0% and 19.0%-46.0%, respectively. Nitrogen addition did not affect soil total P content. Except for soil C:N and C:P, soil nutrient content and stoichiometric ratio were highest in 0-5 cm soil layer. MN and HN treatments significantly decreased MBN by 11.0%-12.7%. MBC, MBP, and their stoichiometry did not change significantly under nitrogen deposition. Soil microbial nutrient content in 0-5 cm soil layer was significantly higher than that in other soil layers. Nitrogen deposition significantly decreased the activities of cellobiose hydrolase and leucine aminopeptidase (decreased by 14.5%-16.2% and 48.7%-66.3%). HN treatment promoted ß-1,4-glucosidase activity (increased by 68.0%), but inhibited soil enzyme stoichiometric carbon to nitrogen ratio and nitrogen to phosphorus ratio (decreased by 95.4% and 88.4%). LN and MN treatment promoted ß-1,4-N-acetylglucosaminidase activity (increased by 68.3%-116.6%), but inhibited enzyme stoichiometric carbon to phosphorus ratio (decreased by 14.9%-29.4%). Alkaline phosphatase activity had no significant change. Soil enzyme activities were significantly decreased with increasing soil depth. Soil total N and total P and microbial nutrients were negatively correlated with vector angle (representing microbial nitrogen or phosphorus limitation), while vector length (representing microbial carbon limitation) was consistently significantly positively correlated with vector angle, suggesting the synergistic promotion between microbial carbon limitation and phosphorus limitation. Nitrogen deposition gradually shifted to phosphorus limitation while alleviating microbial nitrogen limitation in P. yunnanensis forest. In addition, microbial activities in this region was limited by C availability, and the relationship between microbial C and P limitation was proportional.

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Background: The demand for fertility-sparing surgery (FSS) is increasing among patients with early-stage cervical cancer (CC). This study aimed to evaluate the feasibility of local excision as an alternative to hysterectomy in stage I CC patients aged 15-39 years-commonly referred to as adolescents and young adults (AYAs)-with varying clinicopathological characteristics. Methods: Using the Surveillance, Epidemiology, and End Results (SEER) database, we identified patients diagnosed between 2000 and 2020. We examined treatment interventions across different age groups, degrees of histological types, tumor differentiation, and tumor stages. The effect of local excision vs. hysterectomy was assessed by comparing overall survival (OS) and disease-specific survival (DSS) rates. Results: A total of 10,629 stage I AYA cervical cancer patients were included in this study. Among these patients, 24.5% underwent local excision for fertility preservation, while 67.3% underwent radical hysterectomy. For patients with cervical squamous cell carcinoma (SCC), long-term outcomes favored local excision over hysterectomy, and a similar trend was observed in those with adenosquamous cell carcinoma (ASCC). However, the prognosis was comparable among patients with cervical adenocarcinoma (AC). In patients with well- and moderate- differentiated tumors, local excision demonstrated superior OS compared to hysterectomy. No significant differences in prognosis were found between the two surgical interventions for patients with poorly differentiated and undifferentiated tumors. In stage IA patients, local excision was considered a viable alternative to hysterectomy. In stage IB1-IB2, FSS yielded prognostic outcomes comparable to those of hysterectomy. Conversely, patients with stage IB3 exhibited significantly shorter 5-year OS and DSS following local excision than those who underwent hysterectomy. Conclusion: In stage IA-IB2 (diameter ≤4 cm) AYA patients, local excision may serve as a viable option for fertility preservation. The histological type of SCC, AC, and ASCC, along with differentiation, should not serve as restrictive factors in determining fertility preservation strategies for these patients. Patients with early-stage, well- or moderately-differentiated SCC may benefit from local excision surgery, even when fertility preservation is not the primary objective.

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Background: Ocular comorbidities of hidradenitis suppurativa (HS) has been widely evaluated; however real-world evidence was scarce. Moreover, risk of glaucoma in HS patients remained unclear. This study aimed to evaluate the 5-year glaucoma risk in HS patients. Methods: This retrospective cohort study used the TriNetX database covering 2005-2017. In total, 53,281 HS patients were propensity score matched 1:1 to controls based on demographics, including comorbidities, medications, healthcare utilization, etc. Patients were followed for 5 years post-index date. Glaucoma risks were calculated based on hazard ratios and 95% confidence intervals (95% CI). Stratified analyses by sex and age were performed. Results: After matching, baseline characteristics were similar between groups. HS was associated with a 1.25 times higher 5-year glaucoma risk (95% CI, 1.10-1.42). The risk was significant within 1 year (HR=1.37; 95% CI, 1.03-1.82), 3 years (HR=1.31; 95% CI, 1.12-1.54), and 5 years post-index. In subgroup analysis, women had a 1.28 times higher risk (95% CI, 1.10-1.49). Patients aged 18-64 years (HR=1.33; 95% CI, 1.14-1.55) and ≥65 years (HR=1.33; 95% CI, 1.05-1.67) also presented elevated glaucoma risks. Conclusion: This real-world data analysis demonstrated a significantly increased 5-year glaucoma risk in HS patients versus matched controls. Ocular complications should be concerned while managing HS patients.

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Optical coherence tomography (OCT) can be used to image microstructures of human kidneys. However, current OCT probes exhibit inadequate field-of-view, leading to potentially biased kidney assessment. Here we present a robotic OCT system where the probe is integrated to a robot manipulator, enabling wider area (covers an area of 106.39 mm by 37.70 mm) spatially-resolved imaging. Our system comprehensively scans the kidney surface at the optimal altitude with preoperative path planning and OCT image-based feedback control scheme. It further parameterizes and visualizes microstructures of large area. We verified the system positioning accuracy on a phantom as 0.0762 ± 0.0727 mm and showed the clinical feasibility by scanning ex vivo kidneys. The parameterization reveals vasculatures beneath the kidney surface. Quantification on the proximal convoluted tubule of a human kidney yields clinical-relevant information. The system promises to assess kidney viability for transplantation after collecting a vast amount of whole-organ parameterization and patient outcomes data.

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BACKGROUND: The 15q11.2 BP1-BP2 microdeletion syndrome is associated with developmental delays, language impairments, neurobehavioral disorders, and psychiatric complications. The aim of the present study was to provide prenatal and postnatal clinical data for 16 additional fetuses diagnosed with the 15q11.2 BP1-BP2 microdeletion syndrome in the Chinese population. METHODS: A total of 5,789 pregnancy women that underwent amniocentesis were enrolled in the present study. Both karyotype analysis and chromosomal microarray analysis (CMA) were conducted on these subjects to detect chromosomal abnormalities and copy number variants (CNVs). Whole exome sequencing (WES) was performed to investigate sequence variants in subjects with clinical abnormalities after birth. RESULTS: Sixteen fetuses with 15q11.2 BP1-BP2 microdeletion were identified in the present study, with a detection rate of 0.28% (16/5,789). The 15q11.2 BP1-BP2 microdeletion fragments ranged from 311.8 kb to 849.7 kb, encompassing the NIPA1, NIPA2, CYFIP1, and TUBGCP5 genes. The follow-up results regarding pregnancy outcomes showed that five cases opted for pregnancy termination, while the remaining cases continued with their pregnancies. Subsequent postnatal follow-up indicated that only one case with the 15q11.2 BP1-BP2 microdeletion displayed neurodevelopmental disorders, demonstrating an incomplete penetrance rate of 9.09% (1/11). CONCLUSION: The majority of fetuses with the 15q11.2 microdeletion exhibit typical features during early childhood, indicating a low penetrance and mild impact. Nonetheless, pregnancies involving fetuses with the 15q11.2 microdeletion require thorough prenatal counseling. Additionally, enhanced supervision and extended postnatal monitoring are warranted for those who choose to proceed with their pregnancies.

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The majority of acromegaly and gigantism are caused by growth hormone-secreting pituitary neuroendocrine tumors (PitNETs). Most cases can be cured or controlled by surgery, medical therapy, and/or radiotherapy. However, a few of these tumors are resistant to traditional therapy and always have a poor prognosis. The title aggressive/refractory is used to differentiate them from pituitary carcinomas. To date, there is no definitive conclusion on how to diagnose aggressive/refractory growth hormone-secreting PitNETs, which may have slowed the process of exploring new therapeutical strategies. We summarized the literature described diagnosis and treatment of the disease. Potential disease markers and prospective therapies were also included.

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Parkinson's disease (PD) is characterized by the accumulation of misfolded α-synuclein protein and the loss of dopaminergic neurons in the substantia nigra. Abnormal α-synuclein aggregates form toxic Lewy bodies, ultimately inducing neuronal injury. Mitochondrial dysfunction was reported to be involved in the neurotoxicity of α-synuclein aggregates in PD. However, the specific mechanism by which abnormal α-synuclein aggregates cause mitochondrial disorders remains poorly defined. Previously, we found that cofilin-1, a member of the actin-binding protein, regulates α-synuclein pathogenicity by promoting its aggregation and spreading in vitro and in vivo. In this study, we further investigated the effect of cofilin-1 on α-synuclein induced mitochondrial damage. We discovered that α-synuclein aggregates accelerate the translocation of cofilin-1 to mitochondria, promote its combination with the mitochondrial outer membrane receptor Tom 20, and ultimately activate the oxidative damage and apoptosis pathway in mitochondria. All these results demonstrate the important regulatory role of cofilin-1 in the mitochondrial neurotoxicity of pathological α-synuclein during the progression of PD.

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Utilizing deep features from electroencephalography (EEG) data for emotional music composition provides a novel approach for creating personalized and emotionally rich music. Compared to textual data, converting continuous EEG and music data into discrete units presents significant challenges, particularly the lack of a clear and fixed vocabulary for standardizing EEG and audio data. The lack of this standard makes the mapping relationship between EEG signals and musical elements (such as rhythm, melody, and emotion) blurry and complex. Therefore, we propose a method of using clustering to create discrete representations and using the Transformer model to reverse mapping relationships. Specifically, the model uses clustering labels to segment signals and independently encodes EEG and emotional music data to construct a vocabulary, thereby achieving discrete representation. A time series dictionary was developed using clustering algorithms, which more effectively captures and utilizes the temporal and structural relationships between EEG and audio data. In response to the insensitivity to temporal information in heterogeneous data, we adopted a multi head attention mechanism and positional encoding technology to enable the model to focus on information in different subspaces, thereby enhancing the understanding of the complex internal structure of EEG and audio data. In addition, to address the mismatch between local and global information in emotion driven music generation, we introduce an audio masking prediction loss learning method. Our method generates music that Hits@20 On the indicator, a performance of 68.19% was achieved, which improved the score by 4.9% compared to other methods, indicating the effectiveness of this method.

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The therapeutic efficacy of vaccines for treating cancers in clinics remains limited. Here, a rationally designed cancer vaccine by placing immunogenically differential and clinically approved aluminum (Al) or manganese (Mn) in a 2D nanosheet (NS) architecture together with antigens is reported. Structurally optimal NS with a high molar ratio of Mn to Al (MANS-H) features distinctive immune modulation, markedly promoting the influx of heterogeneous innate immune cells at the injection site. Stimulation of multiple subsets of dendritic cells (DCs) significantly increases the levels, subtypes, and functionalities of antigen-specific T cells. MANS-H demonstrates even greater effectiveness in the production of antigen-specific antibodies than the commercial adjuvant (Alhydrogel) by priming T helper (Th)2 cells rather than T follicular helper (Tfh) cells. Beyond humoral immunity, MANS-H evokes high frequencies of antigen-specific Th1 and CD8+ cell immunity, which are comparable with Quil-A that is widely used in veterinary vaccines. Immunized mice with MANS-H adjuvanted vaccines exert strong potency in tumor regression by promoting effector T cells infiltrating at tumor and overcoming tumor resistance in multiple highly aggressive tumor models. The engineered immunogen with an intriguing NS architecture and safe immunopotentiators offers the next clinical advance in cancer immunotherapy.

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Addressing the inefficiency of current therapeutic approaches for hepatocellular carcinoma is an urgent and pressing challenge. PANoptosis, a form of inflammatory programmed cell death, presents a dependable strategy for combating cancer by engaging multiple cell death pathways (apoptosis, pyroptosis, and necroptosis). In this study, an ultrasmall Bi2Sn2O7 nanozyme with ultrasound-magnified multienzyme-mimicking properties is designed and engineered as a PANoptosis inducer through destroying the mitochondrial function of tumor cells and enhancing the intracellular accumulation of toxic reactive oxygen species, finally triggering the activation of PANoptosis process. The role of PANoptosis inducer has been verified by the expression of related proteins, including cleaved Caspase 3, NLRP3, N-GSDMD, cleaved Caspase 1, p-MLKL, and RIPK3. The inclusion of external ultrasonic irradiation significantly augments the enzyodynamic therapeutic efficiency. In vitro and in vivo antineoplastic efficacy, along with inhibition of lung metastasis, validate the benefits of the Bi2Sn2O7-mediated PANoptosis pathway. This study not only elucidates the intricate mechanisms underlying Bi2Sn2O7 as a PANoptosis inducer, but also offers a novel perspective for the treatment of hepatocellular carcinoma.

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As a nonenzymatic DNA signal amplification technique, localized hybridization chain reaction (LHCR) was designed to improve the limitations in response speed and low sensitivity of conventional free diffusional HCR (hybridization chain reaction). However, it is still confronted with the challenges of complicated DNA scaffolds with low loading capacity and a time-consuming process of diffusion. Herein, we introduced modular assembly of a DNA minimal scaffold for coassembly of DNA hairpins for amplified fluorescence imaging of mRNA in situ. DNA hairpins were spatially bound to two Y-shaped modules to form H-shaped DNA modules, and then multiple H-shaped DNA modules can further assemble into an H-module-based hairpin scaffold (HHS). Benefiting from highly spatial localization and high loading capacity, the HHS system showed higher sensitivity and faster speed. It has also been proven to work perfectly in vitro and in vivo, which could provide a promising bioanalysis system for low abundance biomolecule detection.

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Background: Hospital-acquired pneumonia is one of the most important causes of recurrent illness, disease progression, and even death during hospitalization. Patients with schizophrenia have the special characteristics of their disease, and at the same time, the occurrence of hospital-acquired pneumonia is more common among patients with schizophrenia due to the prolonged stay in closed wards, accompanied by various factors such as age, gender, and nutritional status. Methods: The PubMed, Web of Science, Cochrane Library, China National Knowledge Infrastructure (CNKI), and China Biomedical Literature Database (CBM) databases were searched with a timeframe of build to February 2024 to collect studies on factors influencing hospital-acquired pneumonia in patients with schizophrenia. Two researchers independently screened the literature, extracted data, and analyzed them. Results: A total of 5 papers including 85246 patients were included in the literature, which suggested that benzodiazepines (especially the use of clozapine), combination of antipsychotics, mood stabilizers, modified electroconvulsive therapy (MECT), duration of hospitalization, underlying diseases, hyperglycemia, and salivation/dysphagia were important risk factors for hospital-acquired pneumonia in schizophrenia patients, and that advanced age, smoking and alcohol drinking Older age, smoking and drinking habits, malnutrition, and underlying diseases are also risk factors for hospital-acquired pneumonia. Conclusions: Patients with schizophrenia are at a higher risk of developing hospital-acquired pneumonia, so identifying the risk factors associated with hospital-acquired pneumonia and evaluating them comprehensively and promptly during hospitalization facilitates the development of early interventions, which are essential for improving the prognosis of patients with schizophrenia.

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Dysregulated calcium (Ca2+) signaling pathways are associated with tumor cell death and drug resistance. In non-excitable cells, such as hepatocellular carcinoma (HCC) cells, the primary pathway for Ca2+ influx is through stromal interaction molecule 1 (STIM1)-mediated store-operated calcium entry (SOCE). Previous studies have demonstrated the involvement of STIM1-mediated SOCE in processes such as genesis, metastasis, and stem cell self-renewal of HCC. However, it remains unclear whether STIM1-mediated SOCE plays a role in developing acquired resistance to sorafenib in HCC patients. In this study, we established acquired sorafenib-resistant (SR) HCC cell lines by intermittently exposing them to increasing concentrations of sorafenib. Our results showed higher levels of STIM1 and stronger SOCE in SR cells compared with parental cells. Deleting STIM1 significantly enhanced sensitivity to sorafenib in SR cells, while overexpressing STIM1 promoted SR by activating SOCE. Mechanistically, STIM1 increased the transcription of SLC7A11 through the SOCE-CaN-NFAT pathway. Subsequently, up-regulated SLC7A11 increased glutathione synthesis, resulting in ferroptosis insensitivity and SR. Furthermore, combining the SOCE inhibitor SKF96365 with sorafenib significantly improved the sensitivity of SR cells to sorafenib both in vitro and in vivo. These findings suggest a potential strategy to overcome acquired resistance to sorafenib in HCC cells.