High Monocyte-to-Lymphocyte Ratio is Associated with Obstructive Sleep Apnea Hypopnea Syndrome.

Objective: This study aims to explore the correlation between serum monocyte-to-lymphocyte ratio (MLR) and other inflammatory parameters with the occurrence of obstructive sleep apnea-hypopnea syndrome (OSAHS) in patients. Methods: This study included 310 patients who underwent polysomnography monitoring at our hospital between January 2021 and January 2023. Routine blood inflammatory parameters and polysomnography (PSG) results were also evaluated. The differences in inflammatory markers between the OSAHS and normal groups were compared, and OSAHS independent related factors were screened. Results: The MLR of OSAHS group was significantly higher than that of control group, and the difference was statistically significant. Multivariate logistic regression analysis suggested that MLR is an independent risk factor for OSAHS. Conclusion: High MLR was correlated with OSAHS. The diagnostic value of MLR was better than that of the other inflammatory parameters.

Unraveling the hierarchical structure of posture and muscle activity changes during mating of Caenorhabditis elegans.

One goal of neurobiology is to explain how decision-making in neuromuscular circuits produces behaviors. However, two obstacles complicate such efforts: individual behavioral variability and the challenge of simultaneously assessing multiple neuronal activities during behavior. Here, we circumvent these obstacles by analyzing whole animal behavior from a library of Caenorhabditis elegans male mating recordings. The copulating males express the GCaMP calcium sensor in the muscles, allowing simultaneous recording of posture and muscle activities. Our library contains wild type and males with selective neuronal desensitization in serotonergic neurons, which include male-specific posterior cord motor/interneurons and sensory ray neurons that modulate mating behavior. Incorporating deep learning-enabled computer vision, we developed a software to automatically quantify posture and muscle activities. By modeling, the posture and muscle activity data are classified into stereotyped modules, with the behaviors represented by serial executions and transitions among the modules. Detailed analysis of the modules reveals previously unidentified subtypes of the male's copulatory spicule prodding behavior. We find that wild-type and serotonergic neurons-suppressed males had different usage preferences for those module subtypes, highlighting the requirement of serotonergic neurons in the coordinated function of some muscles. In the structure of the behavior, bi-module repeats coincide with most of the previously described copulation steps, suggesting a recursive "repeat until success/give up" program is used for each step during mating. On the other hand, the transition orders of the bi-module repeats reveal the sub-behavioral hierarchy males employ to locate and inseminate hermaphrodites.

Retrospective comparison of endoscopic transoral and bilateral areolar approaches for thyroglossal cyst resection: a single-centre experience.

PURPOSE: Our study aimed to compare the efficacy, safety, and clinical effect of the transoral approach and the bilateral areolar approach (BAA) for endoscopic thyroglossal duct cyst (TGDC) resection. METHODS: In total, 42 patients who received an endoscopic TGDC resection between January 2019 and May 2022 via a transoral (n = 22) or bilateral areolar (n = 20) approach by a single surgeon were retrospectively enrolled. We collected and compared the following data: patients' demographic data, complication events, operative time, bleeding volume, drainage volume, 6-h postoperative pain scores, length of hospitalisation, resected TGDC size, and cosmetic satisfaction. RESULTS: There were no cases of conversion to a transcervical approach in the two groups. No significant differences were found between the two groups in terms of age, sex, body mass index, complication, bleeding volume, 6-h postoperative pain scores, and TGDC size (all p > 0.05). However, the operative time and patients' cosmetic satisfaction were higher in the transoral group than in the BAA group (all p < 0.05). In addition, the drainage volume and length of hospitalisation in the transoral group were less than those in the BAA group (all p < 0.05). CONCLUSIONS: Both the transoral approach and BAA are safe and reliable; however, the transoral approach is more complex than the BAA and offers better cosmetic satisfaction. Doctors should choose the appropriate surgical procedure based on the patient's condition and preferences.

Cryptotanshinone Reverses Corticosteroid Insensitivity by Inhibition of Phosphoinositide-3-Kinase-δ in Chronic Obstructive Pulmonary Disease.

Purpose: Corticosteroid insensitivity has become a major barrier in the treatment of chronic obstructive pulmonary disease (COPD). It is known that oxidative stress reduces the expression and activity of histone deacetylase (HDAC)-2 by activating phosphoinositide-3-kinase-δ(PI3Kδ)/Akt pathway, which is a common mechanism. The aim of this study was to investigate whether cryptotanshinone (CPT) can improve corticosteroid sensitivity and to investigate the molecular mechanisms by which this occurs. Patients and Methods: Corticosteroid sensitivity in peripheral blood mononuclear cells (PBMCs) collected from COPD patients, or in human monocytic U937 monocytic cells exposed to cigarette smoke extract (CSE), was quantified as the dexamethasone concentration required to achieve 30% inhibition of tumor necrosis factor-α (TNFα)-induced interleukin 8 (IL-8) production in the presence or absence of cryptotanshinone. PI3K/Akt activity (measured as the relative ratio of phosphorylated Akt at Ser-473 to total Akt) and HDAC2 expression levels were determined by western blotting. HDAC activity was evaluated by a Fluo-Lys HDAC activity assay kit in U937 monocytic cells. Results: Both PBMCs in patients with COPD and U937 cells exposed to CSE were found to be insensitive to dexamethasone, accompanied by increased phosphorylated Akt (pAkt) and decreased HDAC2 protein expression. The pretreatment of cryptotanshinone restored their sensitivity to dexamethasone, and simultaneously downregulated the level of phosphorylated Akt and upregulated the level of HDAC2 protein. Pretreatment with cryptotanshinone or IC87114 reversed the decrease in HDAC activity in CSE-stimulated U937 cells. Conclusion: Cryptotanshinone restores corticosteroid sensitivity induced by oxidative stress via inhibition of PI3Kδ and is a potential treatment for corticosteroid-insensitive diseases such as COPD.

Sparcl1 and Atherosclerosis.

Atherosclerosis and its complications constitute some of the major diseases affecting humans worldwide. A core component of atherogenesis is endothelial cell damage and dysfunction, which also includes factors such as adhesion and proliferation of various cells. Multiple studies have shown that atherosclerosis and cancer share a common pathophysiological process and exhibit a degree of similarity. Sparcl-1 is a cysteine-rich secretory stromal cell protein present in the extracellular matrix and belongs to the Sparc family of proteins. Its role in tumor development has been widely investigated; however, its role in cardiovascular diseases has rarely been studied. Sparcl-1 is considered an oncogene correlated with the regulation of cell adhesion, migration, and proliferation and is also related to blood vessel integrity. In this review, the potential link between Sparcl-1 and atherosclerosis development is investigated, and recommendations on future research on the role of Sparcl-1 in atherogenesis are provided.

Association between adult food insecurity and self-reported asthma in the United States: NHANES 2003-2018.

OBJECTIVE: Asthma is a chronic disease of the lungs. The development of asthma is related to various risk factors. Food insecurity is a critical social determinant of health, although there is little information on the association between adult food insecurity and asthma. The purpose of this study is to explore the potential correlation in US adults. METHODS: The study population data were extracted from NHANES 2003-2018. Food insecurity was measured using the USDA FSSM and categorized as full, marginal, low, or very low food security. The assessment of self-reported asthma was determined by self-report questionnaires. The self-reported positive outcomes were that participants had asthma and a history of asthma attacks and asthma-related ER visits in the past year. We developed two multivariate logistic regression models. Stratified analyses were performed by gender and age. RESULTS: A total of 38,077 participants were considered in our final analysis. Compared to participants with FFS, the ORs (95% CIs) for asthma were 1.16 (1.00-1.33), 1.42 (1.23-1.64), and 1.56 (1.34-1.80) for participants with MFS, LFS, and VLFS, respectively (Model II). Additionally, after full adjustment, individuals with VLFS had 49% greater risks of asthma attacks (OR = 1.49; 95% CI 1.13-1.97). The ORs (95% CIs) for asthma-related ER visits were 1.59 (1.14-2.23) and 1.98 (1.36-2.87) for participants with LFS and VLFS, respectively (Model II). The positive correlations remained robust when stratified by gender and age. CONCLUSION: Our research showed that food insecurity among US adults was associated with asthma, asthma attacks, and asthma-related ER visits.

USP9X expression is functionally related to laryngeal cancer.

An increasing number of studies have shown that USP9X is closely related to cancer. However, its role in carcinogenesis and progression of laryngeal cancer has not yet been investigated. In this study, we found that USP9X was upregulated in laryngeal cancer tissues. The expression of USP9X was significantly correlated with degree of laryngeal cancer differentiation and lymphatic metastasis. USP9X knockdown led to a decrease in the ability of proliferation, migration, and invasion of FaDu cells. The proportion of FaDu apoptotic cells increased by interfering with the endogenous expression of USP9X. We speculated that inhibiting USP9X might induce apoptosis in FaDu cells by downregulating Mcl-1 and upregulating Bax protein expression. Our findings for the first time suggest the expression level and trend of USP9X in laryngeal cancer tissue and USP9X may plays an important role in promoting the occurrence and progression of laryngeal cancer. USP9X may be a potential target for intervention in treatment of laryngeal cancer.

Identification of immunocell infiltrates and effective diagnostic biomarkers in laryngeal carcinoma.

Laryngeal cancer (LC) is a malignant tumor that occurs in the head and neck. Laryngeal cancer is one of the most common cancers of the neck and head, and its prognosis has always been poor. The incidence of LC increased gradually and showed an early rising trend. Laryngeal cancer is rarely studied in relation to immunity, Malignant tumors will change the state of the human body in various ways to adapt to their own survival and avoid the immune system. This study aims to explore the immune molecular mechanism of laryngeal cancer through bioinformatics analysis. The gene expression data was downloaded for 3 microarray datasets: GSE27020, GSE59102, and GSE51985. CIBERSORT algorithm was performed to evaluate immune cell infiltration in tissues between LC and healthy control (HC). Differentially expressed genes (DEGs) were screened. Functional correlation of DEGs were analyzed by Gene Ontology, Gene Set Enrichment Analysis and Kyoto encyclopedia of genes and genomes. Candidate biomarkers were identified by cytoHubba of Cytoscape. Spearman correlations between the above biomarkers and infiltrating immune cells were explored using R software analysis. The immune cell types of LC and HC were significantly different. Twenty-one DEGs were obtained by cross-screening. The function of DEGs is closely related to the number of immune cells. Five central genes (TNNT3, TNNI2, Desmin, matrix metallopeptidase 9 and cytotoxic T lymphocyte antigen 4) were screened. The HUB gene was demonstrated to have the ability to diagnose LC and HC with good specificity and sensitivity. The correlation between immune cells and biomarkers showed that hub gene was positively correlated with macrophages and dendritic cells, and negatively correlated with CD4 + T cell. TNNT3, TNNI2, Desmin, matrix metallopeptidase 9 and cytotoxic T lymphocyte antigen 4 can be used as diagnostic biomarker for LC. Macrophages, dendritic cells and CD4 + T cell may participate in the occurrence and development of LC.

RING finger 138 deregulation distorts NF-кB signaling and facilities colitis switch to aggressive malignancy.

Prolonged activation of nuclear factor (NF)-кB signaling significantly contributes to the development of colorectal cancer (CRC). New therapeutic opportunities are emerging from targeting this distorted cell signaling transduction. Here, we discovered the critical role of RING finger 138 (RNF138) in CRC tumorigenesis through regulating the NF-кB signaling, which is independent of its Ubiquitin-E3 ligase activity involved in DNA damage response. RNF138-/- mice were hyper-susceptible to the switch from colitis to aggressive malignancy, which coincided with sustained aberrant NF-кB signaling in the colonic cells. Furthermore, RNF138 suppresses the activation of NF-кB signaling pathway through preventing the translocation of NIK and IKK-Beta Binding Protein (NIBP) to the cytoplasm, which requires the ubiquitin interaction motif (UIM) domain. More importantly, we uncovered a significant correlation between poor prognosis and the downregulation of RNF138 associated with reinforced NF-кB signaling in clinical settings, raising the possibility of RNF138 dysregulation as an indicator for the therapeutic intervention targeting NF-кB signaling. Using the xenograft models built upon either RNF138-dificient CRC cells or the cells derived from the RNF138-dysregulated CRC patients, we demonstrated that the inhibition of NF-кB signaling effectively hampered tumor growth. Overall, our work defined the pathogenic role of aberrant NF-кB signaling due to RNF138 downregulation in the cascade events from the colitis switch to colonic neoplastic transformation and progression, and also highlights the possibility of targeting the NF-кB signaling in treating specific subtypes of CRC indicated by RNF138-ablation.

Stearoyl-CoA desaturases sustain cholinergic excitation and copulatory robustness in metabolically aging C. elegansmales.

Regulated metabolism is required for behaviors as adults age. To understand how lipid usage affects motor coordination, we studied male Caenorhabditis elegans copulation as a model of energy-intensive behavior. Copulation performance drops after 48 h of adulthood. We found that 12-24 h before behavioral decline, males prioritize exploring and copulation behavior over feeding, suggesting that catabolizing stored metabolites, such as lipids, occurs during this period. Because fat-6/7-encoded stearoyl-CoA desaturases are essential for converting the ingested fatty acids to lipid storage, we examined the copulation behavior and neural calcium transients of fat-6(lf); fat-7(lf) mutants. In wild-type males, intestinal and epithelial fat-6/7 expression increases during the first 48 h of adulthood. The fat-6(lf); fat-7(lf) behavioral and metabolic defects indicate that in aging wild-type males, the increased expression of stearoyl-CoA desaturases in the epidermis may indirectly modulate the levels of EAG-family K+ channels in the reproductive cholinergic neurons and muscles.

Promising novel biomarkers and candidate small-molecule drugs for lung adenocarcinoma: Evidence from bioinformatics analysis of high-throughput data.

Lung adenocarcinoma (LUAD) is the most common subtype of non-small cell lung cancer associated with an unstable prognosis. Thus, there is an urgent demand for the identification of novel diagnostic and prognostic biomarkers as well as targeted drugs for LUAD. The present study aimed to identify potential new biomarkers associated with the pathogenesis and prognosis of LUAD. Three microarray datasets (GSE10072, GSE31210, and GSE40791) from the Gene Expression Omnibus database were integrated to identify the differentially expressed genes (DEGs) in normal and LUAD samples using the limma package. Bioinformatics tools were used to perform functional and signaling pathway enrichment analyses for the DEGs. The expression and prognostic values of the hub genes were further evaluated by Gene Expression Profiling Interactive Analysis and real-time quantitative polymerase chain reaction. Furthermore, we mined the "Connectivity Map" (CMap) to explore candidate small molecules that can reverse the tumoral of LUAD based on the DEGs. A total of 505 DEGs were identified, which included 337 downregulated and 168 upregulated genes. The PPI network was established with 1,860 interactions and 373 nodes. The most significant pathway and functional enrichment associated with the genes were cell adhesion and extracellular matrix-receptor interaction, respectively. Seven DEGs with high connectivity degrees (ZWINT, RRM2, NDC80, KIF4A, CEP55, CENPU, and CENPF) that were significantly associated with worse survival were chosen as hub genes. Lastly, top 20 most important small molecules which reverses the LUAD gene expressions were identified. The findings contribute to revealing the molecular mechanisms of the initiation and progression of LUAD and provide new insights for integrating multiple biomarkers in clinical practice.

The expression of NLK is functionally associated with colorectal cancers (CRC).

The regulatory mechanism of NLK in the carcinomagenesis and progression of colorectal cancer (CRC) remains unclear. Here, we identified a single nucleotide polymorphism (SNP) site of NLK (rs2125846) as a new susceptibility locus for CRC risk located within an intron of the human NLK gene in a Chinese population. NLK downregulation led to a decrease in the ability of proliferation and migration of RKO cells in vitro. The proportion of RKO apoptotic cells increased by interfering with the endogenous expression of NLK. We speculate that LncRNA XIST may upregulate NLK expression by downregulating miR-92b-3p, thereby promote the development of CRC. These results provide important information for the identification of novel potential targets for the prevention or treatment of CRC.

Inhibition of Kelch-like epichlorohydrin-related protein 1 promotes the progression and drug resistance of lung adenocarcinoma.

BACKGROUND: Lung cancer is a common malignant carcinoma of respiratory system with high morbidity and mortality. Kelch-like epichlorohydrin-related protein 1 (Keap1), a member of the BTB-Kelch protein family, has been reported as an important molecule in several cancers. However, its potential role in tumor is still controversial. Here we aim to clarify the effect of Keap1 on the biological characteristics and chemotherapy resistance in lung adenocarcinoma (LUAD). METHODS: Immunohistochemistry was conducted to compare Keap1 expression in lung adenocarcinoma tissues and matched non-cancerous tissues, and the correlation between Keap1 expression and clinicopathological features was analyzed. Subsequently, the stable A549 and H1299 cell lines with Keap1 knockdown or overexpression were constructed using lentivirus. The roles of Keap1 on the cell proliferation, migration, invasion and drug resistance were investigated by colony formation assay, cell proliferation assay, wound scratch test, transwell invasion assay and drug sensitivity assay, respectively. RESULTS: Keap1 was lowly expressed in tumor tissues compared to matched non-cancerous tissues, and its expression was correlated with TNM stage and lymph node metastasis. Early stage (I) tumors without lymph node metastasis had higher levels of Keap1 expression compared with late-stage tumors (II, III) with the presence of lymphatic metastasis. Colony formation assays showed that Keap1 knockdown promoted the proliferation of A549 and H1299 cells, and the cell growth curves further confirmed this feature. In contrast, wound scratch and transwell invasion experiments showed that Keap1 overexpression inhibited cell migration and invasive malignancy. The IC50 for cisplatin and paclitaxel were significantly increased by Keap1 knockdown in A549 and H1299 cell lines. CONCLUSION: Keap1 knockdown promotes tumor cell growth, proliferation, invasion, metastasis and chemotherapy resistance in LUAD. It may be a potential tumor marker to guide the staging and treatment of lung cancer.

Hsa_circ_0001073 targets miR-626/LIFR axis to inhibit lung cancer progression.

Circular RNAs (circRNAs) are associated with lung cancer progression. However, it is unclear whether and how circRNA hsa_circ_0001073 (circ_0001073) are involved in lung cancer progression. circ_0001073, microRNA (miR)-626, and leukemia inhibitory factor receptor (LIFR) abundances were determined via quantitative reverse transcription polymerase chain reaction or western blot. Cell viability, invasion, and apoptosis were analyzed by cell counting kit-8, transwell analysis and flow cytometry, respectively. The target correlation was tested by dual-luciferase reporter analysis or RNA immunoprecipitation. Results showed that circ_0001073 abundance was down-regulated in lung cancer cells. circ_0001073 constrained cell viability and invasion and facilitated apoptosis in lung cancer cells. miR-626 was targeted via circ_0001073, and circ_0001073 inhibited lung cancer progression via reducing miR-626 expression. LIFR was targeted via miR-626, and miR-626 knockdown constrained cell viability and invasion and facilitated apoptosis in lung cancer cells via up-regulating LIFR. circ_0001073 increased LIFR expression via miR-626 in lung cancer cells. In conclusion, circ_0001073 represses lung cancer progression via miR-626/LIFR axis, indicating the potential value of circ_0001073 in lung cancer treatment.

Identification of biomarkers associated with clinical severity of chronic obstructive pulmonary disease.

We sought to identify the biomarkers related to the clinical severity of stage I to stage IV chronic obstructive pulmonary disease (COPD). Gene expression profiles from the blood samples of COPD patients at each of the four stages were acquired from the Gene Expression Omnibus Database (GEO, accession number: GSE54837). Genes showing expression changes among the different stages were sorted by soft clustering. We performed functional enrichment, protein-protein interaction (PPI), and miRNA regulatory network analyses for the differentially expressed genes. The biomarkers associated with the clinical classification of COPD were selected from logistic regression models and the relationships between TLR2 and inflammatory factors were verified in clinical blood samples by qPCR and ELISA. Gene clusters demonstrating continuously rising or falling changes in expression (clusters 1, 2, and 7 and clusters 5, 6, and 8, respectively) from stage I to IV were defined as upregulated and downregulated genes, respectively, and further analyzed. The upregulated genes were enriched in functions associated with defense, inflammatory, or immune responses. The downregulated genes were associated with lymphocyte activation and cell activation. TLR2, HMOX1, and CD79A were hub proteins in the integrated network of PPI and miRNA regulatory networks. TLR2 and CD79A were significantly correlated with clinical classifications. TLR2 was closely associated with inflammatory responses during COPD progression. Functions associated with inflammatory and immune responses as well as lymphocyte activation may play important roles in the progression of COPD from stage I to IV. TLR2 and CD79A may serve as potential biomarkers for the clinical severity of COPD. TLR2 and CD79A may also serve as independent biomarkers in the clinical classification in COPD. TLR2 may play an important role in the inflammatory responses of COPD.

miRNA-486-5p Promotes COPD Progression by Targeting HAT1 to Regulate the TLR4-Triggered Inflammatory Response of Alveolar Macrophages.

Purpose: The aim of this study was to investigate the role of miRNA-486-5p in chronic obstructive pulmonary disease (COPD) progression and the underlying molecular mechanisms. Materials and Methods: Aberrant miRNA expression profiles between smokers and nonsmokers, and those between COPD patients and normal subjects were analyzed using microarray datasets and reverse-transcriptase quantitative polymerase chain reaction (qPCR). Enzyme-linked immunosorbent assay was used to determine the levels of inflammatory cytokines in cell supernatants. Expression levels of inflammatory cytokines, HAT1, TLR4, and miR-486-5p, were determined using qPCR or Western blotting. Luciferase reporter assays and fluorescence in situ hybridization were used to confirm the regulatory interaction between miR-486-6p and HAT1. Results: miR-486-5p was significantly upregulated in the COPD and smoker groups compared to the control group, as demonstrated using bioinformatics analysis and validated using qPCR assay of alveolar macrophages and peripheral monocytes. Moreover, miR-486-5p expression was significantly correlated with the expression of IL-6, IL-8, TNF-α, and IFN-γ. Luciferase reporter assays confirmed that miR-486-5p directly targeted HAT1, and cellular localization showed that miR-486-5p and HAT1 were highly expressed in the cytoplasm. miR-486-5p overexpression led to a significant upregulation of TLR4 and a significant downregulation of HAT1. Inversely, miR-486-5p inhibition led to a significant downregulation of TLR4 and a significant upregulation of HAT1. HAT1 knockdown using siRNA significantly upregulated the expression of TLR4, IL-6, IL-8, TNF-α, and IFN-γ. Conclusion: miR-486-5p was differentially expressed in the alveolar macrophages of COPD patients. miR-486-5p overexpression may enhance the TLR4-triggered inflammatory response in COPD patients by targeting HAT1.

MicroRNA-421 Inhibits Apoptosis by Downregulating Caspase-3 in Human Colorectal Cancer.

PURPOSE: Dysregulated microRNAs (miRNAs/miRs) have been reported to play significant roles in pathogenesis of colorectal cancer (CRC). Previous studies have demonstrated that miR-421 regulates apoptosis in some cancers. Caspase-3 plays a key role in apoptosis, but the relationship between miR-421 and caspase-3 in CRC has not been determined. In this study, we investigated the role of miR-421 in CRC and the relationship between miR-421 and caspase-3. METHODS: Expression of miR-421 and caspase-3 were detected in human paired CRC cancer tissues and corresponding paracancerous tissues. In situ detection of tissue, apoptosis was performed via the TUNEL assay. HCT116 and SW480 cell lines were subjected to several in vitro experiments to explore the relationship between miRNA421 and caspase-3 during apoptosis using miR421 mimics/antagomir and luciferase reporter assay. Apoptosis was measured by determining the levels and activity of caspase-3 as well as DNA fragmentation. Luciferase reporter assay was performed to determine the potential interaction of miR-421 with caspase-3. RESULTS: The results showed that the expression of miR-421 in cancer tissues was higher than that in corresponding paracancerous tissues. Inhibition of miR-421 induced apoptosis, as shown by the upregulation of caspase-3 activity and expression as well as DNA fragmentation, which were attenuated by miR-421 mimic. We further showed that miR-421 targeted and inhibited CASP3 expression by targeting sites located in the 3'-untranslated region (3'-UTR) of CASP3 mRNA. CONCLUSION: This study demonstrated an anti-apoptotic role of miR-421 in CRC and identified caspase-3 gene as a direct target of miR-421. These findings provide a potential treatment strategy using miR-421 as a therapeutic target for CRC.

[Efficacy analysis of use of absorbable sinus drug stents in functional endoscopic sinus surgery].

Objective:To explore the efficacy of functional endoscopic sinus surgery（FESS） with an absorbable sinus drug stent in the treatment of chronic sinusitis. Method:107 patients with chronic sinusitis who underwent FESS were divided into two groups: 58 patients were set as stent group who were treated with sinus drug elution during surgery; 49 patients who did not receive a sinus drug stent were included in the non-stent group. The same postoperative treatment were used in the two groups. The patients were followed up for 1 month and reviewed 3 months after surgery. Efficacy is mainly evaluated by endoscopy. The evaluation indicators include whether the sinus mucosa is congested and edema, whether there is adhesion in the middle turbinate, whether vesicles or polyp-like mucosa are formed, whether the sinus mouth is stenosed or reoccluded, whether the sinus mucosa is epithelialized, and whether the patient had intervention after surgery. Result:Stents were successfully implanted in 58 patients in the stent group. The difference of the above six indexes between the stent group and the non-stent group was statistically significant at 1 month after operation. The postoperative complication rate and postoperative intervention rate were significantly lower in the stent group than in the control group（P<0.01）, the incidence of sinus mucosal epithelialization in the stent group was significantly higher than that in the non-stent group（P<0.01）. The sinus mucosal epithelialization were all completed in both groups after 3 months of surgery. The postoperative complication rate and postoperative intervention rate were significantly lower in the stent group than in the non-stent group（P<0.05 or P<0.01）. Conclusion:FESS combined with the absorption of sinus drug stents for the treatment of chronic sinusitis is safe and effective which can control the complications further after surgery while relieving the clinical symptoms of patients with sinusitis effectively.

Succinate Dehydrogenase-Regulated Phosphoenolpyruvate Carboxykinase Sustains Copulation Fitness in Aging C. elegans Males.

Dysregulated metabolism accelerates reduced decision-making and locomotor ability during aging. To identify mechanisms for delaying behavioral decline, we investigated how C. elegans males sustain their copulatory behavior during early to mid-adulthood. We found that in mid-aged males, gluco-/glyceroneogenesis, promoted by phosphoenolpyruvate carboxykinase (PEPCK), sustains competitive reproductive behavior. C. elegans' PEPCK paralogs, pck-1 and pck-2, increase in expression during the first 2 days of adulthood. Insufficient PEPCK expression correlates with reduced egl-2-encoded ether-a-go-go K+ channel expression and premature hyper-excitability of copulatory circuits. For copulation, pck-1 is required in neurons, whereas pck-2 is required in the epidermis. However, PCK-2 is more essential, because we found that epidermal PCK-2 likely supplements the copulation circuitry with fuel. We identified the subunit A of succinate dehydrogenase SDHA-1 as a potent modulator of PEPCK expression. We postulate that during mid-adulthood, reduction in mitochondrial physiology signals the upregulation of cytosolic PEPCK to sustain the male's energy demands.

A Novel Long Non-coding RNA, MSTRG.51053.2 Regulates Cisplatin Resistance by Sponging the miR-432-5p in Non-small Cell Lung Cancer Cells.

Objective: The aim of this study was to investigate the molecular mechanisms underlying cisplatin (DDP) resistance in non-small cell lung cancer (NSCLC) cells by constructing a competing endogenous RNA (ceRNA) network. Methods: The gene expression profiles of human lung adenocarcinoma DDP-resistant cell line (A549/DDP) and its progenitor (A549) were comparatively evaluated by whole-transcriptome sequencing. The differentially expressed genes (DEGs) were subjected to KEGG pathway analysis. The expression levels of mRNAs involved in several pathways associated with conferring DDP resistance to tumor cells were evaluated. The ceRNA network was constructed based on the mRNA expression levels and the sequencing data of miRNA and lncRNA. Several ceRNA regulatory relationships were validated. Results: We quantified the expression of 17 genes involved in the six pathways by quantitative real-time polymerase chain reaction (qRT-PCR). The differential protein expression levels of eight genes were quantified by western blotting. Western blot analysis revealed six differentially expressed proteins (MGST1, MGST3, ABCG2, FXYD2, ALDH3A1, and GST-ω1). Among the genes encoding these six proteins, ABCG2, ALDH3A1, MGST3, and FXYD2 exhibited interaction with 8 lncRNAs and 4 miRNAs in the ceRNA regulatory network. The expression levels of these lncRNAs and miRNAs were quantified in cells; among these, 6 lncRNAs and 4 miRNAs exhibited differential expression between A549/DDP and A549 groups, which were used to construct a ceRNA network. The ceRNA regulatory network of MSTRG51053.2-miR-432-5p-MGST3 was validated by luciferase reporter assay. Conclusion: The MSTRG51053.2 lncRNA may function as a ceRNA for miR-432-5p to regulate the DDP resistance in NSCLC. The MGST1, MGST3, GST-ω1, and ABCG2 mRNAs, miR-432-5p and miR-665 miRNAs, and MSTRG51053.2 and PPAN lncRNAs can serve as potential DDP drug targets to reverse DDP resistance in NSCLC.