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To establish a tumor prognostic risk assessment model related to target genes of the miR-34 family. Methods Target genes of the miR-34 family were screened, and the scores of miR-34 target genes were assessed in 16 tumor types. Univariate Cox regression analysis was used to identify the tumor type with the strongest correlation between miR-34 target gene scores and overall survival (OS). Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were performed to elucidate the functional roles and signaling pathways of miR-34 target genes. A prognostic risk model based on the miR-34 target genes was constructed using univariate Cox and LASSO regression analyses. Quantitative real-time PCR (qPCR) and dual-luciferase reporter assays were conducted to validate whether the target genes bind to miR-34 and measure their RNA expression levels in the relevant tumors. Additionally, the risk score was integrated with other clinical indicators to develop a nomogram prediction model for patient survival. Results A total of 65 target genes of the miR-34 family were screened. The cancer type exhibiting stronger correlation between the target gene scores and OS was lung adenocarcinoma (P = 0.003, HR= 5.150). Furthermore, miR-34 target genes were predominantly enriched in oxidative stress pathways and various tumor-related processes. Three genes, LDHA, GALNT7, and SATB2, were identified as core components of the prognostic analysis model for lung adenocarcinoma. Additionally, the constructed nomogram model demonstrated robust predictive performance. Conclusion The risk model and prognosis model oflung adenocarcinoma constructed based on the key target genes of miR-34 have good predictive performance.

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To investigate the mechanism of Dipeptidyl peptidase 7 (DPP7) in hepatocellular carcinoma (HCC). Methods The expression of DPP7 protein in hepatocellular carcinoma tissues and liver benign tissues was detected by UALCAN and GEPIA database, immunohistochemical, and Western blot, and its relationship with clinicopathological characteristics was analyzed. The expression of DPP7 was silenced by siRNA and the protein expression of DPP7 in MHCC97H cells was detected by Western blot and qPCR. MTTassay, colony formation assay and wound healing assay were used to detect cell proliferation. Transwell assay was used to detect the invasion and migration ability of cells. Western blot was used to detect the changes of protein markers related to Epithelial-mesenchymal transition (EMT). Results In UALCAN, GEPIA and clinical liver tissue samples, DPP7 expression was upregulated and it was closely related to TNM stage (P=0.002), lymph node metastasis (P=0.038) and depth of tumor invasion (P=0.027). The downregulation of DPP7 protein expression in MHCC97H cells was detected after transfection of siRNA in the experimental group (P < 0.01); Furthermore, the results of the MTT, colony formation, wound healing and Transwell assay demonstrated that knockdown of DPP7 expression in the MHCC97H cell line significantly inhibited the proliferative and metastatic capabilities of these cells. Consistent with this phenotypic change, analysis of epithelial-mesenchymal transition (EMT) related proteins revealed a significant upregulation of the epithelial marker E-cadherin (P<0.001) and downregulation of the mesenchymal markers Vimentin and N-cadherin (P<0.01).

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To investigate the mechanism through which miR‑21 improves chronic renal fibrosis in mice via targeted modulation of the phosphatase and tensin homolog (PTEN)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway. Methods Thirty‑two chronic kidney disease model mice were randomly divided into four groups (n=8 each group): model group, miR‑21 overexpression group, miR‑21 inhibition group, and miR‑21 inhibition + MK‑2206 group. Eight healthy mice were included as the control group. The miR‑21 overexpression, miR‑21 inhibition, and miR‑21 inhibition + MK‑2206 groups received tail‑vein injections of lentivirus (50 μL, 1×10⁸ TU per mouse) once weekly for three weeks. The control and model groups were injected with an equal volume of empty vector (LV‑NC). The miR‑21 inhibition + MK‑2206 group additionally received gavage of the AKT/mTOR pathway inhibitor MK‑2206 (480 mg/kg) once weekly for three weeks. The expressions of miR‑21, 24‑h urinary protein, serum creatinine (Scr), blood urea nitrogen (BUN), and renal tissue levels of collagen I, collagen III, α‑smooth muscle actin (α‑SMA), and PTEN protein, as well as p‑AKT/AKT and p‑mTOR/mTOR ratios, were compared among groups. HE staining was used to observe pathological changes in renal tissue, and Masson staining was used to observe the degree of renal fibrosis. A dual‑luciferase assay was performed to verify the targeting relationship between miR‑21 and PTEN. Results Compared with the model group, miR‑21 expression in renal tissue increased in the miR‑21 overexpression group (P<0.05) and decreased in the miR‑21 inhibition group (P<0.05). Compared with the model group, the miR‑21 overexpression group showed increased 24‑h urinary protein, Scr, BUN, and renal tissue expression of collagen I, collagen III, and α‑SMA (all P<0.05), while these indicators decreased in the miR‑21 inhibition group (all P<0.05). Compared with the miR‑21 inhibition group, the miR‑21 inhibition + MK‑2206 group exhibited lower 24‑h urinary protein, Scr, BUN, and renal tissue expression of collagen I, collagen III, and α‑SMA (all P<0.05). Compared with the model group, the miR‑21 overexpression group showed decreased PTEN protein expression (P<0.05) and increased p‑AKT/AKT and p‑mTOR/mTOR ratios (P<0.05), while the miR‑21 inhibition group showed increased PTEN expression (P<0.05) and decreased p‑AKT/AKT and p‑mTOR/mTOR ratios (P<0.05). Compared with the miR‑21 inhibition group, the miR‑21 inhibition + MK‑2206 group had lower p‑AKT/AKT and p‑mTOR/mTOR ratios (P<0.05), with no significant difference in PTEN protein expression (P>0.05). HE and Masson staining showed normal kidney structure and almost no fibrosis in the control group. The model group exhibited glomerular enlargement, capillary loop adhesion, and focal fibrosis. The miR-21 overexpression group showed severe destruction of glomerular structure, accompanied by extensive fibrosis and renal tubular atrophy. The pathological changes and degree of fibrosis were alleviated in the miR-21 inhibition group. The miR-21 inhibition + MK-2206 group showed only mild pathological changes and mild fibrosis, with the interstitium being largely normal. Compared with PTEN-WT + NC mimics 1, the relative luciferase activity in the PTEN-WT + miR-21 mimics group decreased (P<0.001). There was no statistically significant difference in relative luciferase activity between PTEN-WT + NC mimics group and PTEN-MUT + miR-21 mimics group (P>0.05). Conclusion miR‑21 may improve renal function indicators and alleviate renal fibrosis in chronic kidney disease mice via targeted modulation of PTEN and subsequently inhibiting theAKT/mTOR pathway.

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To investigate the incidence and influencing factors of posttraumatic stress disorder (PTSD) three months after a traffic accident, and to explore the role of social support and coping strategies. Methods A total of 117 individuals exposed to trauma following road traffic accidents were recruited. General demographic and clinical information was collected within one week, and the hamilton anxiety rating scale (HAMA), the hamilton depression rating scale-24 (HAMD-24), the social support rating scale (SSRS), and the simplified coping style questionnaire (SCSQ) were administered. A 3-month follow-up was subsequently conducted, during which PTSD symptoms were assessed using the post-traumatic stress disorder checklist for DSM-5 (PCL-5). Participants were divided into a PTSD group and a non-PTSD group according to whether PTSD occurred. Between-group comparisons were performed using the Mann-Whitney U non-parametric test or the χ2 test, as appropriate. Spearman’s correlation analysis was used to examine the associations between general characteristics and PCL-5 scores. Binary logistic regression was applied to identify factors influencing PTSD, and receiver operating characteristic (ROC) curve analysis was conducted to evaluate the diagnostic value of the SCSQ and SSRS. Results During the 3-month follow-up of the 117 trauma-exposed individuals, 17 cases developed PTSD, with a higher proportion of females (70.59%). Between-group comparisons showed that, compared with the PTSD group, the non-PTSD group had higher scores for positive coping, objective support, and subjective support (P<0.05), and lower scores for negative coping, HAMA, HAMD, and PCL-5 (P<0.05). Correlation analysis indicated that female gender, negative coping, and higher HAMA and HAMD scores were associated with greater PTSD severity. Logistic regression analysis demonstrated that educational level (OR=1.715, 95% CI: 1.020-2.883, P=0.042) and negative coping (OR=1.590, 95% CI: 1.003-2.522, P=0.048) were risk factors for PTSD, whereas objective support (OR=0.646, 95% CI: 0.451-0.925, P=0.017) was a protective factor. The ROC analysis showed that the total SCSQ score and its negative and positive coping dimensions, the total SSRS score and its subjective and objective support dimensions, as well as their combined use, all demonstrated good discriminative ability in distinguishing between the PTSD and non-PTSD groups. Conclusion The results suggest that individuals who are female, with higher HAMA and HAMD scores after a motor vehicle accident, and those with lower social support and negative coping strategies, should be given particular attention. Early interventions for these individuals may reduce the incidence of PTSD.

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To explore the role of the histone deacetylase Sirtuin-1 (SIRT1)/p53 signaling pathway in promoting apoptosis of non-small cell lung cancer cells (NSCLC) induced by the co- stimulatory molecule B7-H3. Methods The GEPIA 2 platform was used for survival analysis of NSCLC patients based on B7-H3 gene expression levels. The Gene Enrichment Analysis (GSEA) method was used to analyze the enrichment characteristics of B7-H3 molecules in the gene set of cell apoptosis. In the non-small cell lung cancer A549 cell line, B7-H3 was knocked down, and the protein expression levels of SIRT1 and p53 were detected by Western blot. B7-H3 was overexpressed in A549 cells and the apoptosis rate was analyzed by flow cytometry after Annexin V/PI double staining. Overexpression of B7-H3 and knockdown ofSIRT1 were performed inA549 cell line. The expression levels of p53 and apoptosis-related proteins B-cell lymphoma/leukemia-2 (Bcl-2) and Bcl-2-associated X protein (Bax) were detected respectively by Western blot. Cell apoptosis rate was analyzed by flow cytometry after Annexin V/PI double staining. Results The overall survival of the B7-H3 high-expression group was significantly lower than that of the low- expression group (P<0.01). B7-H3 was significantly enriched in the cell apoptosis signaling pathway and the p53 signaling pathway (P<0.05). Compared with the control group, the expression of SIRT1 was significantly downregulated, and p53 was significantly upregulated in the B7-H3 knockdown group (both P<0.001). Overexpression of B7-H3 significantly up-regulated SIRT1 protein expression (P<0.05), down-regulated p53 expression (P<0.01), and markedly increased the Bcl-2/Bax ratio of apoptosis-related proteins (P<0.001). The results of Annexin V/PI double staining showed that the apoptosis rate of A549 cells with overexpressed B7-H3 decreased (the apoptosis rate of the control group was 26.72%±4.13%, while that of the B7-H3 overexpression group was 13.87%±0.82%; P<0.01). In B7-H3-overexpressing cell lines, SIRT1 knockdown significantly reversed apoptosis (P<0.05), up-regulated p53 protein expression (P<0.001), and markedly reduced the Bcl-2/Bax ratio (P<0.001). Conclusion B7-H3 molecule inhibits the apoptosis of non-small cell lung cancer cells via the SIRT1/p53 signaling pathway.

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To investigate the diagnostic value of coagulation function indicators and proteinuria in preeclampsia and its severity assessment. Methods A total of 239 pregnant women who visited our hospital from January 2022 to December 2023 were selected as research subjects. They were divided into healthy control group (n=50), non-gestational hypertension group (n=39), and gestational hypertension group (n=150) based on clinical diagnosis. The gestational hypertension group was further subdivided into three subgroups: simple hypertension group (n=50), mild preeclampsia group (n=50), and severe preeclampsia group (n=50). The study compared differences in plasma protein S (PS), plasma protein C (PC), fibrin degradation products (FDP), fibrin monomer (FM), and proteinuria levels among different groups. The correlation between proteinuria and coagulation function indicators in patients with gestational hypertension was analyzed, and ROC curves were used to analyze the diagnostic efficacy of coagulation indicators and proteinuria for gestational hypertension and different stages of preeclampsia. Results The gestational hypertension group showed lower PS and PC values compared to the non- gestational hypertension group and healthy control group, while FDP, FM values, and proteinuria levels were higher than those in the non-gestational hypertension group and healthy control group (P<0.05). Significant differences in coagulation indicators and proteinuria levels were observed among pregnant women with different degrees of gestational hypertension (P<0.05). The AUC values for diagnosing gestational hypertension using PS, PC, FDP, FM, and proteinuria were 0.927, 0.957, 0.967, 0.947, and 0.932 respectively (P<0.000 1). For diagnosing simple hypertension and mild preeclampsia, the AUC values were 0.875, 0.777, 0.830, 0.678, and 0.935 respectively (P<0.000 1). For diagnosing mild and severe preeclampsia, the AUC values were 0.900, 0.776, 0.779, 0.806, and 0.847 respectively (P<0.000 1). Conclusion Coagulation function indicators and proteinuria show significant differences between healthy pregnant women and those with gestational hypertension. PS, PC, FDP, FM, and proteinuria levels vary among pregnant women with different stages of preeclampsia. The aforementioned indicators exhibit certain diagnostic efficacy for gestational hypertension and preeclampsia.

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To establish an in vitro culture model ofrat corpora cavernous smooth muscle cells (CCSMCs) using a modified tissue block adherence method. Methods Corpus cavernosum smooth muscle tissue was digested with collagenase type I and subsequently cultured using an adherent method. Cells were purified via differential adhesion and identified through immunofluorescence and Western blotting. Results CCSMCs began to emerge from the tissue block after 3 days, increased significantly by day 7, and converged by day 12. Post-passage, CCSMCs exhibited strong proliferation and a “peak-to-valley” phenomenon. After purification, the cells tested positive for α-smooth muscle actin (α-SMA), confirming the successful establishment of the in vitro culture model. Conclusion The modified tissue block adherence method is a cost-effective and efficient way to obtain high-purity CCSMCs.

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To investigate the effects of hypoxia-treated mesenchymal stem cell (MSCs) exosomes (Exo) and their loading with curcumin on microglial inflammatory responses, and to explore the enhancing effect of hypoxia treatment on the function of MSCs Exo. Methods The supernatants of hUC-MSCs cultured under normal and hypoxic conditions were collected, and Exo were isolated using ultracentrifugation. After identification by transmission electron microscopy and Western blot, curcumin was loaded using the co-incubation method. The lipopolysaccharide (LPS)-induced microglial inflammation model was treated with dimethyl sulfoxide (DMSO), curcumin, normoxia Exo, hypoxia Exo, normoxic Exo loaded with curcumin, and hypoxic Exo loaded with curcumin, respectively. The expression of the M1-type marker inducible nitric oxide synthase (iNOS) in BV2 cells was detected by immunofluorescence (IF). Western blot and enzyme-linked immunosorbent assay (ELISA) were used to measure the expression and secretion levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and IL-6 in the cells and their culture supernatants. Results Normoxia Exo, hypoxia Exo, normoxic Exo loaded with curcumin, and hypoxic Exo loaded with curcumin exhibited a "saucer-like" shape with a diameter ranging from 30~150 nm, and the expression of exosomal markers CD9, CD81, and TSG101 were positive. After treating the BV2 cell inflammation model, IF results showed that, compared with the normoxia Exo group, treatment with hypoxic Exo significantly reduced the expression of iNOS. Moreover, when compared with the curcumin group and the normoxic Exo loaded with curcumin group, the expression level of iNOS significantly decreased after treatment with hypoxic Exo loaded with curcumin. The results of Western blot and ELISA indicated that, in comparison with the normoxia Exo group, treatment with hypoxic Exo significantly reduced the expression and secretion of the inflammatory cytokines TNF-α, IL-1β, and IL-6. Additionally, when compared with the curcumin group and the normoxic Exo loaded with curcumin group, both the expression and secretion of TNF-α, IL-1β, and IL-6 significantly decreased after treatment with hypoxic Exo loaded with curcumin. Conclusion Hypoxia preconditioning can enhance the ability of hUC-MSCs-Exo in the inhibition of microglial polarization and inflammatory factors, secretion. Additionally, using Hypoxia-MSCs-Exo as a drug-delivery carrier of curcumin can improve its solubility and stability, facilitating its absorption by cells and exerting the therapeutic effect of combination therapy.

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To investigate the effect and mechanism of simvastatin pretreatment on kidney ischemia reperfusion injury (IRI) in mice. Methods Fifteen male C57BL/6 mice aged 6-8 weeks were divided into three groups: Sham operation group (Sham group), kidney IRI group (IR group), and simvastatin pretreatment+kidney IRI group (SIM group). Hematoxylin-eosin (HE) staining of kidney tissue and detection of serum creatinine (SCr) and lactate dehydrogenase (LDH) were used to evaluate kidney injury. The levels of superoxide dismutase (SOD), reduced glutathione (GSH), malondialdehyde (MDA) and reactive oxygen species (ROS) were detected to evaluate oxidative stress. The contents of ferrous iron (Fe2+) and ferric iron (Fe3+) in kidney tissue were detected, and the morphological changes of mitochondria were observed by transmission electron microscope. The relative expression levels of Kruppel-like factor 2 (KLF2), glutathione peroxidase 4 (GPX4), solute carrier family 7 member 11 (SLC7A11), and acyl-coa synthetase long chain family member 4 (ACSL4) protein in kidney tissue were detected to evaluate ferroptosis. Results Compared with the IR group, the SIM group had significantly reduced renal tubular injury and decreased contents of Scr and LDH in serum (P < 0.001). It also showed increased expression of SOD and GSH and decreased expression of MDA and ROS (P < 0.01). Simvastatin pretreatment reduced the contents of Fe2+ and Fe3+ in the tissues (P < 0.01) and alleviated mitochondrial damage. It also promoted the expression of KLF2 (P < 0.01), up- regulated the expression of ferroptosis-related protective proteins GPX4 and SLC7A11, and down-regulated the expression of ferroptosis-related damage protein ACSL4 (P < 0.05).

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To systematically evaluate the association between serum indirect bilirubin (IBIL) levels and the risk of stroke incidence in patients with cardiovascular-kidney-metabolic (CKM) syndrome stages 0-3. Methods A total of 48,301 participants with CKM syndrome stages 0-3 were included, during which 2,904 stroke events were recorded. A prospective cohort study design was employed. Cox proportional hazards regression models were used to analyze the relationship between IBIL and stroke risk, and restricted cubic spline (RCS) regression was applied to examine the dose-response relationship. Threshold effect analysis was conducted to identify potential inflection points in nonlinear relationships. Results Multivariable Cox regression analysis showed that in the overall population, each 1 μmol/L increase in IBIL level was associated with approximately a 1.2% reduction in stroke risk (HR = 0.988, 95% CI: 0.979–0.996, P < 0.05). A significant interaction was observed between IBIL and CKM stages in relation to stroke risk (P-interaction < 0.05). In individuals with stages 0–2 of CKM syndrome, higher IBIL levels showed a significant inverse association with stroke risk (P-trend < 0.05); however, no such association was observed in stage 3 patients. RCS regression and threshold effect analysis further revealed a nonlinear relationship between IBIL levels and stroke risk in stage 3 CKM patients (P-log-likelihood ratio < 0.05). When serum IBIL exceeded 10.980 μmol/L, each 1 μmol/L increase was associated with approximately 5.7% increase in stroke risk (HR = 1.057, 95% CI: 1.009–1.107, P < 0.05). Conclusion The protective effect of serum IBIL against stroke exhibits a significant CKM stage-dependent pattern, with its predictive value varying based on individual metabolic status.

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As a functional anatomical marker of cellular activity and neural circuitry, c-Fos protein has been extensively utilized in studies which investigate neuroendocrine regulation, autonomic nervous system activity, and behavioral responses to stress. Recent research in ophthalmology has revealed that dynamic c-Fos expression is closely associated with pathophysiological processes such as retinal ganglion cell apoptosis, visual cortical plasticity, photodamage repair, and angiogenesis. This review aims to summarize the mechanistic roles of c-Fos protein in ocular diseases including glaucoma, amblyopia, and retinopathy, as well as exploring potential therapeutic approaches targeting c-Fos modulation. The studies have shown that the activation ofc-Fos protein can promote the development of neurons in the visual cortex, and the inhibition ofc-Fos can delay the apoptosis of retinal ganglion cells, neuroglia and photoreceptors in retinal and optic nerve diseases.

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To explore the effects of serine hydroxymethyltransferase 1 (SHMT1) rs1979277 polymorphisms on pharmacokinetic characteristics and clinical prognosis of methotrexate (MTX) in children with acute lymphoblastic leukemia (ALL). Methods Matrix- assisted laser desorption/ionization time of flight mass spectrometry was used for SHMT1 rs1979277 genotyping. Clinical data including serum MTX concentrations, incidences of adverse events, and ALL relapse after chemotherapy with MTX were collected. The associations of SHMT1 rs1979277 G>A genotypes with dose-adjusted serum concentrations (C/D ratios), adverse events of MTX, and relapse were analyzed. The associations between rs1979277 genotypes and SHMT1 expression were explored based on Bioinformatics methods. Results Among the 146 children with ALL included, the rs1979277 GG homozygous genotype accounted for 85.62% (125/146), while the GA heterozygous genotype accounted for 14.38% (21/146). The frequency of the G allele was 92.81% (271/292), while theA allele was only 7.19% (21/292). Children with the GG homozygous genotype had higher median C/D ratios of MTX in 24 h [12.06 (μmol·m2)/(L·g)] and higher relapse rates (12.80%) than those in GA heterozygous genotype carriers [10.96 (μmol·m2)/(L·g), and 9.52%, respectively]. However, none of the above differences were statistically significant (all P>0.05). The incidences of respiratory (19.05%) and liver disorders (33.33%) in children with the GA heterozygous genotype were significantly higher than those in GG homozygous genotype carriers (4.00% and 12.00%, respectively, P<0.05). There were no statistically significant differences in the incidences of other adverse events. Bioinformatics analysis showed that the rs1979277 A allele was significantly associated with higher SHMT1 expression in multiple tissues, such as the tibial artery, pancreas, and adrenal gland (P<0.05).

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Robotic telesurgery is a technology that doctors use advanced surgical robots and network communication technology to carry out surgery on patients in different places. Robotic telesurgery can sink high-quality medical resources to serve patients in remote areas, and can also be used for emergency rescue, disaster relief, battlefield and other special occasions to provide patients with timely, effective and high-quality surgical treatment, as well as reducing medical costs and patient transport risks. With the rapid development of the fifth generation wireless network, low latency and high broadband communication are provided for robotic telesurgery, and faster and more accurate real-time data transmission makes it possible to carry out complex surgery remotely. In this review, the current situation of robotic telesurgery at home and abroad is described, and the future of robotic telesurgery is prospected.

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To investigate somatization symptoms in adolescents during frequent earthquakes in Hefei, and to explore their correlation with earthquake experiences. Methods A cross-sectional survey was used to select 324 adolescents in Hefei as the survey objects. The self-rating scale of somatization symptoms (SSS) and the exhaustion scale (FIS) were used to evaluate the somatization symptoms and fatigue degree of middle school students, and multivariate logistic regression analysis was used to explore the related factors of somatization symptoms and fatigue among middle school students. Results A total of 324 adolescents were included The overall detection rate of somatization symptoms was 6.5%, and the detection rate of moderate or above fatigue was 20.1%. The results of regression analysis showed that adolescents who were concerned about the earthquake for a longer time (≥1 h) had a higher risk of somatization symptoms (OR=5.430, 95%CI: 1.547-19.058), and adolescents who received pre-earthquake training had a lower degree of fatigue (OR=0.473, 95%CI: 0.270-0.829) (P<0.05).

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To explore the effect of transcription factor ZNF174 on the stemness of non-small cell lung cancer (NSCLC) . Methods StemChecker online analysis was employed to assess the impact of ZNF174 on tumor stemness markers . The ZNF174 knockdown plasmid was constructed via restriction enzyme digestion and enzyme- linked assembly , while the ZNF174 overexpression plasmid was generated through homologous recombination . Lentiviral infection established stable cell lines with ZNF174 knockdown or overexpression . Tumor stem cell sphe- roid formation assays were conducted to evaluate stemness maintenance capacity. RNA-seq and quantitative real- time polymerase chain reaction (qPCR) were utilized to detect effects on key stemness gene expression . Results The transcription factor ZNF174 promoted cellular stemness in non-small cell lung cancer (NSCLC) . It promoted the expression of key stemness genes : B-cell-specific moloney murine leukemia virus insertion site 1 (BMI1) , ac- etaldehyde dehydrogenase 2 (ALDH2) , SRY-box transcription factor 2 (SOX2) , recombinant high mobility group AT hook protein 2 (HMGA2) , and snail family transcriptional repressor 1 (Snail1) and enhanced tumor spheroid formation in NSCLC stem cells . Conclusion ZNF174 promotes the expression of tumor stemness genes in NSCLC and may become a novel therapeutic and prognostic target for NSCLC .

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To construct a deep learning model based on convolutional neural network ( CNN)-long short term memory network (LSTM)-Attention to explore the correlation between meteorological and clinical factors and the incidence of ischemic stroke . Methods A fusion model CNN-LSTM-Attention based on CNN , LSTM , and Attention was constructed by incorporating clinical data and meteorological data of ischemic stroke inpatients . The predictive performance of the model was evaluated by maximum prediction error and root mean square error (RMSE) . The impact of different lag days on prediction performance was investigated by selecting lag periods ran- ging from 1 to 7 days . Results In both short-term and long-term predictions , the CNN-LSTM-Attention fusion model (short-term : 1 . 5 and 0. 6 ; long-term : 8. 3 and 2. 5) showed superior maximum prediction bias and RMSE compared to the LSTM model ( short-term : 2. 8 and 1 . 2 ; long-term : 19. 5 and 5 . 5) and the CNN-LSTM model (short-term : 2. 0 and 0. 8 ; long-term : 11 . 2 and 3 . 3) . After incorporating lag days , the maximum prediction devi- ation and RMSE for lags of 3 days (short-term : 0. 7 and 0. 4 ; long-term : 5 . 5 and 1 . 9) and 5 days (short-term : 0. 8 and 0. 3 ; long-term : 6. 5 and 2. 0) in both short-term and long-term forecasts were smaller than lags of 0 days (short-term : 1 . 5 and 0. 6 ; long-term : 8. 3 and 2. 5) . The maximum prediction deviation and RMSE with a lag of 1 day (short-term : 1 . 5 and 0. 8 ; long-term : 6. 8 and 2. 4) and 7 days (short-term : 1 . 9 and 0. 9 ; long-term : 7. 5 and 2. 7) were both greater than those with a lag of 0 days . Conclusion The established CNN-LSTM-Attention model demonstrates significant predictive value for the onset of ischemic stroke and can provide reference for the ra- tional allocation of medical resources .

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To investigate the regulatory relationship between long non-coding RNA LINC01578 and c - Myc , and to explore the effect of LINC01578 on the metabolic process of oral squamous cell carcinoma (OSCC) . Methods After c-Myc was knocked down in OSCC cell line CAL27 , LINC01578 , a long non-coding RNA that is positively regulated by c-Myc , was identified by high-throughput sequencing technology . qRT-PCR was employed to measure the expression levels of c-Myc and LINC01578 in OSCC tissues and adjacent normal tissues . Following overexpression or knockdown of c-Myc in CAL27 and HN6 cells , qRT-PCR was conducted to validate the consisten- cy with sequencing results . The binding of c-Myc to the LINC01578 promoter was confirmed using a dual luciferase reporter assay . Seahorse , ATP production and lactate production assays were utilized to examine the impact of c - Myc on glucose metabolism in OSCC via LINC01578 . Colony formation assays assessed the proliferative capacity of OSCC cell lines . Results qRT-PCR analysis revealed significantly higher expression levels of c-Myc and LINC01578 in OSCC tissues compared to adjacent tissues( P < 0. 05) , confirming that c-Myc positively regulates LINC01578 expression . Consistent with sequencing data , c-Myc overexpression markedly upregulated LINC01578 (P < 0. 001) , while c-Myc knockdown led to a significant decrease in LINC01578 levels(P < 0. 000 1) . Dual lu- ciferase reporter gene assays demonstrated that c-Myc directly targets and transcriptionally enhanced LINC01578 ex- pression(P < 0. 001) . Seahorse experiments indicated that c-Myc promoted glucose metabolism in OSCC through LINC01578 regulation(P < 0. 05) . Colony formation assays showed that LINC01578 overexpression enhanced OS- CC cell proliferation , whereas LINC01578 knockdown inhibited it. Conclusion c-Myc upregulates LINC01578 expression in OSCC cells , thereby modulating glycolysis and promoting cell proliferation .

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To explore the microbiological characteristics of Staphylococcus epidermidis with hemolytic phenotype (SEHP). Methods Hemolytic phenotype was detected using the three-point inoculation method, involving a total of 5 strains of SEHP and 5 strains of S.epidermidis with non-hemolytic phenotype (SENHP) . Bacterial species were identified using the Microflex LT MALDI-TOF mass spectrometer, and a phylogenetic tree was constructed through 16S rRNA sequence alignment. Antimicrobial susceptibility testing of SEHP and SENHP against commonly used antibiotics was performed using a VITEK 2 GP639 test kit. Antagonistic effects of SEHP and SENHP against Staphylococcus aureus and Corynebacterium striatum were evaluated by the Oxford cup inhibition assay. Red blood cell toxicity was detected using the microplate method. Biofilm formation ability was assessed by microplate crystal violet staining. Growth curves were monitored through the microcultivation assay. Results Compared with SENHP, SEHP had lower resistance rates to levofloxacin and moxifloxacin. Additionally, SEHP could antagonize S. aureus and C. striatum, exhibiting significant hemolytic toxicity, as well as a marked decrease in growth rate during the late logarithmic phase. Conclusion The microbiological characteristics of SEHP differ from those of SENHP in that SEHP demonstrates antagonistic effects against S. aureus and C. striatum, warranting further investigation.

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To investigate the effect of HQJND on acute liver injury in severely scalded rats and its possible molecular mechanism by animal experiments and modern pharmacological tools. Methods Firstly, the rat model of sepsis was established and randomly divided into 4 groups. The normal saline group was given 1 mL of normal saline twice a day, and the traditional Chinese medicine group was given 1 mL of concentrated Huangqi Jiuni decoction twice a day. After 72 hours of shock, the samples were sacrificed, and then the serum liver function and (+)-haematoxylin eosin staining were performed to verify the efficacy of the drug. Sham Operation Group and sepsis group were fed normally without any special treatment. Then, network pharmacology was used to screen the targets of drugs and drug responses and predict the signaling pathways that might play a role in the treatment of diseases. Finally, fluorescence quantitative PCR (RT-qPCR) was performed to detect gene expression, Western blot (WB) was performed to detect Tumor necrosis factor (TNFα), P65, phosphorylated P65 (P-P65), and immunohistochemical (IHC) were performed assays to verify drug efficacy and explore the mechanism of drug treatment. Results Serum liver function and histopathology in rats showed that HQJND significantly improved liver function in severely burned rats. Network pharmacology screening was used to identify 353 disease-related marker genes and 286 drug targets. It was predicted that tumor necrosis/NF-NF-κB pathway (TNF/NF-NF-κB pathway) might be a key pathway for HQJND to treat acute liver injury after severe burns. The results of immunohistochemistry (IHC) showed that the staining of TNF-α in the liver of the sepsis group was more than that of the Sham Operation Group and the traditional Chinese medicine group. The results of fluorescence quantitative PCR (RT-qPCR) and Western blot (WB) showed that the expression of TNF-α, TNFR1 and P65 proteins in the liver of rats in the sepsis group was significantly higher than that in the Sham Operation Group and the traditional Chinese medicine group; on the contrary, the expression of TNF-α, TNFR1 and P65 proteins in the liver of rats in the sepsis group was significantly higher than that in the Sham Operation Group and the traditional Chinese medicine group. The expression level of IKBα was higher in the Sham Operation Group and the traditional Chinese medicine group, indicating that drug treatment effectively inhibited the activation of the TNF/NF-κb signaling pathway and alleviated the inflammatory response, thereby alleviating tissue damage. Conclusion Animal experiments and network pharmacology results confirm that HQJND has a protective effect on acute liver injury in severely burned rats, which may be related to the inhibition of TNF/NF-κB signaling pathway.