A risk prediction model based on machine learning algorithm for parastomal hernia after permanent colostomy.

OBJECTIVE: To develop a machine learning-based risk prediction model for postoperative parastomal hernia (PSH) in colorectal cancer patients undergoing permanent colostomy, assisting nurses in identifying high-risk groups and devising preventive care strategies. METHODS: A case-control study was conducted on 495 colorectal cancer patients who underwent permanent colostomy at the Second Affiliated Hospital of Anhui Medical University from June 2017 to June 2023, with a 1-year follow-up period. Patients were categorized into PSH and non-PSH groups based on PSH occurrence within 1-year post-operation. Data were split into training (70%) and testing (30%) sets. Variable selection was performed using Least Absolute Shrinkage and Selection Operator (LASSO) regression, and binary classification prediction models were established using Logistic Regression (LR), Support Vector Classification (SVC), K Nearest Neighbor (KNN), Random Forest (RF), Light Gradient Boosting Machine (LGBM), and Extreme Gradient Boosting (XgBoost). The binary classification label denoted 1 for PSH occurrence and 0 for no PSH occurrence. Parameters were optimized via 5-fold cross-validation. Model performance was evaluated using Area Under Curve (AUC), specificity, sensitivity, accuracy, positive predictive value, negative predictive value, and F1-score. Clinical utility was evaluated using decision curve analysis (DCA), model explanation was enhanced using shapley additive explanation (SHAP), and model visualization was achieved using a nomogram. RESULTS: The incidence of PSH within 1 year was 29.1% (144 patients). Among the models tested, the RF model demonstrated the highest discrimination capability with an AUC of 0.888 (95% CI: 0.881-0.935), along with superior specificity, accuracy, sensitivity, and F1 score. It also showed the highest clinical net benefit on the DCA curve. SHAP analysis identified the top 10 influential variables associated with PSH risk: body mass index (BMI), operation duration, history and status of chronic obstructive pulmonary disease (COPD), prealbumin, tumor node metastasis (TNM) staging, stoma site, thickness of rectus abdominis muscle (TRAM), C-reactive protein CRP, american society of anesthesiologists physical status classification (ASA), and stoma diameter. These insights from SHAP plots illustrated how these factors influence individual PSH outcomes. The nomogram was used for model visualization. CONCLUSION: The Random Forest model demonstrated robust predictive performance and clinical relevance in forecasting colonic PSH. This model aids in early identification of high-risk patients and guides preventive care.

Applicability of Sniffin' Sticks Identification Test as a Screening Tool for Olfactory Dysfunction in Northeast China.

BACKGROUND Because most case of smell loss are unrecognized, a valid and reliable screening test for olfactory function is needed. The Sniffin' Sticks test is one of the most widely used olfactory tests. As olfaction can be affected by environment and social background, we investigated the regional applicability of Sniffin' Sticks identification subtest as a screening tool. MATERIAL AND METHODS Normosmic volunteers were recruited between May 2021 and August 2021. We collected data on participants' age, sex, and educational level. The Self-Reported Mini-Olfactory Questionnaire and identification test of Sniffin' Sticks test battery were used to assess their olfactory function. RESULTS A total of 688 subjects (316 male, 371 female) volunteered for the screening test. The mean age of participants was 30±7.69 years (range, 15-63 years), and the average score of all subjects was 12.7±0.81 points. The 3 least recognized items among all 16 tests were lemon (correct identification rate 5.4%), clove (correct identification rate 1.5%), and apple (correct identification rate 0.7%). For Self-Reported Mini-Olfactory Questionnaire, 48 of the 687 subjects (7%) stated that they could not recognize the smell of freshly mowed grass. CONCLUSIONS We investigated the applicability of using Sniffin' Sticks Identification test and Self-MOQ as a screening tool for olfactory dysfunction in northeast China. Most of the subjects enrolled in this study failed to reach the normative standard for their age groups in the Sniffin' Sticks test. We suggest the deletion or replacement of items with extremely low correct identification rates and that physicians who use the Sniffin's Sticks test in clinical practice test the applicability in advance to avoid misdiagnosis.

Transcriptome analysis of long non-coding RNAs reveals NR_015556 lncRNA is a novel regulator for adipocyte differentiation.

Long non-coding RNAs (lncRNAs) have gained extensive attentions due to their significant roles in diverse biological process. However, the potential functions of lncRNAs participation in adipocyte differentiation have not been fully explored. In the present study, we globally profiled lncRNA expression using lncRNA microarray and identified 1745 lncRNA probes with differential expression on day 0 and day 4 post-induction in both C3H10T1/2 mesenchymal stem cells and 3T3-L1 preadipocytes. Furthermore, we showed that stable shRNA knockdown (KD) of NR_015556, a novel lncRNA that was significantly down-regulated in adipocyte differentiation, promoted adipocyte differentiation by increasing the number of lipid droplets and adipocyte markers such as Fabp4, Adipsin and Fasn. Mechanistically, NR_015556 KD attenuated the expression of Wnt signaling components Wnt10b and non-phospho (active) ß-catenin, and elevated adipocyte master factors Ppar-γ and C/EBPα levels. Conversely, pharmacological activation of Wnt10b-ß-catenin signaling by LiCl suppressed NR_015556 KD-induced enhancement of adipocyte differentiation and Ppar-γ and C/EBPα expression levels. Taken together, these results indicate that down-regulation of NR_015556 promotes adipocyte differentiation through inhibiting Wnt10b-ß-catenin signaling pathway and then elevating Ppar-γ and C/EBPα triggered transcriptional cascades.

Long non-coding RNA lnc-OAD is required for adipocyte differentiation in 3T3-L1 preadipocytes.

Long non-coding RNAs (lncRNAs) have gained extensive attentions due to their significant roles in diverse biological process. However, the potential functions of lncRNAs participation in adipocyte differentiation have not been fully explored. Here we identified a long non-coding RNA called lnc-OAD (lncRNA associated with osteoblast and adipocyte differentiation, transcribed from 1700018A04Rik gene), which modulated 3T3-L1 adipocyte differentiation. Lnc-OAD was up-regulated expression during 3T3-L1 differentiation and stable knockdown of lnc-OAD inhibited adipocyte differentiation in 3T3-L1 cells. Further mechanisms study revealed that silencing of lnc-OAD strongly elevated the protein expression of ß-catenin, and then decreased expression of adipocyte master transcription factors PPAR-γ and C/EBPα. The addition of IWR-1 up-regulated the expression of PPAR-γ and C/EBPα and rescued the impairment of adipocyte differentiation caused by lnc-OAD knockdown. Meanwhile, we also found mitotic clonal expansion (MCE) during the early stage of adipocyte differentiation was inhibited in lnc-OAD-knockdown cells. Taken together, our study reveals a novel function of lnc-OAD in modulating adipogenesis via influencing mitotic clonal expansion and regulating WNT/ß-catenin signaling pathway.

Identification of Pyrvinium, an Anthelmintic Drug, as a Novel Anti-Adipogenic Compound Based on the Gene Expression Microarray and Connectivity Map.

Obesity is a serious health problem, while the current anti-obesity drugs are not very effective. The Connectivity Map (C-Map), an in-silico drug screening approach based on gene expression profiles, has recently been indicated as a promising strategy for drug repositioning. In this study, we performed mRNA expression profile analysis using microarray technology and identified 435 differentially expressed genes (DEG) during adipogenesis in both C3H10T1/2 and 3T3-L1 cells. Then, DEG signature was uploaded into C-Map, and using pattern-matching methods we discovered that pyrvinium, a classical anthelminthic, is a novel anti-adipogenic differentiation agent. Pyrvinium suppressed adipogenic differentiation in a dose-dependent manner, as evidenced by Oil Red O staining and the mRNA levels of adipogenic markers. Furthermore, we identified that the inhibitory effect of pyrvinium was resulted primarily from the early stage of adipogenesis. Molecular studies showed that pyrvinium downregulated the expression of key transcription factors C/EBPa and PPARγ. The mRNA levels of notch target genes Hes1 and Hey1 were obviously reduced after pyrvinium treatment. Taken together, this study identified many differentially expressed genes involved in adipogenesis and demonstrated for the first time that pyrvinium is a novel anti-adipogenic compound for obesity therapy. Meanwhile, we provided a new strategy to explore potential anti-obesity drugs.

Clinicopathologic and prognostic significance of VEGF, JAK2 and STAT3 in patients with nasopharyngeal carcinoma.

BACKGROUND: The aim of the study was to investigate the effect associated with the protein expression of VEGF, JAK2 and STAT3 on the clinicopathologic characteristics and prognosis in the development and progression of nasopharyngeal carcinoma (NPC). METHODS: Fifty NPC patients in addition to 20 patients with chronic nasopharyngitis (CNP) were recruited for the purposes of the study. Western blotting and immunohistochemistry methods were employed to evaluate the protein expressions of JAK2, STAT3 and VEGF in the NPC and CNP tissues, with their respective correlations with the clinicopathologic characteristics of NPC patients subsequently analyzed. Spearman's rank correlation coefficient and Kaplan-Meier method were conducted to evaluate the respective correlations of JAK2, STAT3 and VEGF with NPC as well as the survival rates of patients with NPC. Cox regression analyses was performed in determine the prognostic NPC factors. RESULTS: Compared with the CNP tissues, the NPC tissues exhibited elevated levels of JAK2, STAT3 and VEGF which were subsequently determined to share a positive correlation with T stages, lymph node metastasis (LNM), N stages and clinical stages, while a negative correlation with survival rates were observed in the NPC patients. Positive correlations between the expressions of JAK2, STAT3 and VEGF were detected among the NPC tissues. NPC patients survival time with negative expressions of JAK2, STAT3 and VEGF were observed to be longer than that of NPC patients with positive expressions of JAK2, STAT3 and VEGF. T stage, LNM, N stage, clinical stage. The expressions of JAK2, STAT3 and VEGF were discovered to be independent risk factors associated with the prognosis of patients with NPC. CONCLUSION: The results obtained from the present study support the notion that higher expressions of JAK2, STAT3 and VEGF may be correlated with the clinicopathologic characteristics and prognosis of patients suffering from NPC.

E3 ubiquitin ligase DTX4 is required for adipogenic differentiation in 3T3-L1 preadipocytes cell line.

Deltex4 (DTX4) is a member of the Deltex family of proteins. To date several lines of evidences suggest that Deltex family of proteins is closely linked to cell development and cell differentiation. However, little is known about the role of DTX4 in adipogenic differentiation. In this study, we assessed the impact of DTX4 on adipogenic differentiation in vitro, we found that DTX4 protein expression gradually increased during adipogenic differentiation of 3T3-L1 preadipocytes cell line. While DTX4 stable knockdown by recombinant shRNA lentivirus (sh-DTX4) notably reduced the number of lipid droplets and down-regulated the expression of adipogenic transcription factors C/EBPα and PPARγ and adipogenic markers gene FABP4 and Adipsin. Besides, cell numbers and incorporation of 5-Ethynyl-2'-deoxyuridine (EdU) into cells were significantly decreased during mitotic clonal expansion (MCE) in sh-DTX4 cells postinduction. Furthermore, compared to recombinant shRNA lentivirus control group (sh-CON), the mRNA levels of Wnt signaling genes such as Wnt6, Wnt10b and ß-catenin, were obviously elevated in sh-DTX4 group at day 3 of postinduction. Taken together, our results indicate that DTX4 stable knockdown inhibits adipogenesis of 3T3-L1 cells through inhibiting C/EBPα and PPARγ, arresting mitotic clonal expansion and regulating Wnt signaling pathway.

High quality in vitro expansion of human endothelial progenitor cells of human umbilical vein origin.

The limited availability of qualified endothelial progenitor cells (EPCs) is a major challenge for regenerative medicine. In the present study, we isolated human EPCs from human umbilical vein endothelial cells (HUVECs) by using magnetic micro-beads coated with an antibody against human CD34. Flow cytometric assay showed that majority of these cells expressed VEGFR2 (KDR), CD34 and CD133, three molecular markers for early EPCs. It was also found that a bioreactor micro-carrier cell culture system (bio-MCCS) was superior to dish culture for in vitro expansion of EPCs. It expanded more EPCs which were in the early stage, as shown by the expression of characteristic molecular markers and had better angiogenic potential, as shown by matrix-gel based in vitro angiogenesis assay. These results suggest that HUVECs might be a novel promising resource of EPCs for regenerative medicine and that a bio-MCCS cell culture system might be broadly used for in vitro expansion of EPCs.

Resection of Adenoid Cystic Carcinoma Originating From the Cavernous Sinus Via Endoscopic Endonasal Approach.

A 50-year-old woman presented with gradually increasing right-sided facial numbness. Neuroimaging revealed a lesion in the right cavernous sinus mimicking meningioma. The resection of the right cavernous sinus neoplasm was implemented via endoscopic endonasal approach under general anesthesia. Histological examination of the surgical specimen revealed adenoid cystic carcinoma. Adenoid cystic carcinoma in the cavernous sinus is extremely rare as a primary lesion and challenging to manage. Little data exist to guide treatment when this tumor extends to involve the structure of cavernous sinus. Our study illustrates that endoscopic endonasal approach is a good choice for resection of the tumor in the cavernous sinus.

Arsenic Trioxide Activate Transcription of Heme Oxygenase-1 by Promoting Nuclear Translocation of NFE2L2.

In a previous study, we found that induced expression of Heme Oxygenase-1 (HO-1) is responsible for the resistance of human osteosarcoma MG63 cells to the chemotherapeutic agent arsenic trioxide (ATO). The present study was aimed at investigating the molecular mechanisms underlying the induction of HO-1 that occurs after exposure of MG63 cells to ATO. First, using RT-QPCT and Western-blot, we found that ATO strongly induced the expression of heme oxygenase-1 (HO-1) in these human osteosarcoma cells. Then by analyzing HO-1 mRNA of MG63 cells exposed to ATO in the presence and absence of a transcription inhibitor Actinomycin-D (Act-D), we demonstrated that ATO activates HO-1 expression in MG63 cells by regulating the transcription of the gene. Finally, through the analysis of the NFE2L2 protein levels among the total cellular and nuclear proteins by Western-blot and Immunocytochemical staning, we determined that ATO enhanced the nuclear translocation of nuclear factor erythroid 2-like 2 (NFE2L2), also known as Nrf2. From these results we have concluded that transcription activation of HO-1 resulting from the nuclear translocation of NFE2L2 is the underlying molecular mechanism for its high induction, which, in turn, is responsible for the resistance of human osteosarcoma cells to ATO treatment.

Silencing SATB1 inhibits the malignant phenotype and increases sensitivity of human osteosarcoma U2OS cells to arsenic trioxide.

In a previous study, we found that the global genome organizer Special AT-rich binding protein 1 (SATB1) is highly expressed in mesenchymal-derived human osteosarcoma U2OS cells and that the knock-down of SATB1 results in the inhibition of cell proliferation. The present study was aimed at investigating the effect of silencing SATB1 on cell migration, invasion, apoptosis and resistance to the chemotherapeutic drug arsenic trioxide. Cell migration and invasion were detected by wound-healing assays and trans-well invasion assays, respectively. Cell apoptosis was analyzed by an in situ Cell Death Detection POD Kit, based on terminal deoxynucleotydyl transferase mediated dUTP nick-end labeling (TUNEL) staining and mRNAs were analyzed by real time qRT-PCR. We found that cell migration and invasion were inhibited and that the proportion of apoptotic cells and sensitivities to the chemotherapeutic drug arsenic trioxide were enhanced by knockdown of SATB1 in U2OS cells. Furthermore, mRNA of ABCC1 and ABCG2 were decreased strikingly after SATB1 silencing. It was concluded that the elevated expression of SATB1 in U2OS cells contributes to maintenance of the malignant phenotype and resistance to chemotherapeutic drugs ATO, suggesting that silencing SATB1 in the cells might improve the effects of arsenic trioxides in the treatment of osteosarcoma in which SATB1 is over-expressed and that ABCC1 and ABCG2 were involved in SATB1 mediated resistance of U2OS cells to ATO.

Identification of core gene in chronic rhinosinusitis with nasal polyps and correlations with inflammation-related genes.

OBJECTIVE: Our aim in this study is to identify the core genes of chronic rhinosinusitis with nasal polyps and analyze the correlations between it and inflammation-related genes. METHODS: GSE72713 dataset containing gene expression data of ECRSwNP, nonECRSwNP and healthy samples was obtained from Gene Expression Omnibus (GEO) and filtered by limma to identify DEGs among three groups, then the functions and correlated pathways of DEGs were analyzed using GO and KEGG. The core DEGs were selected by the intersection of DEGs and the PPI network was constructed via STRING. The correlations between the expression levels of CRSwNP core gene and inflammation-related genes were analyzed via the Mann-Whitney U test. RESULTS: The DEGs among ECRSwNP, nonECRSwNP, and CTRL were filtered respectively, and enrichment analysis showed they were associated with olfaction and/or immune responses. The PPI network was constructed by 7 core DEGs obtained via the intersection among three groups, and ALOX15 was confirmed as the core gene in the network. Subsequently, the correlations between the expression levels of ALOX15 and inflammation-related genes were illustrated. CONCLUSION: In this study, the core gene ALOX15 was selected from the DEGs among ECRSwNP, nonECRSwNP, and CTRL. IL5, IL1RL1, and IL1RAP were found to exhibit a significant positive correlation with ALOX15. LEVEL OF EVIDENCE: Level 3.

Silencing SATB1 inhibits proliferation of human osteosarcoma U2OS cells.

It has been shown that over-expression of Special AT-rich binding protein 1 (SATB1) in breast cancer predicts a poor prognosis. This study was aimed at investigating the effects of silencing SATB1 on mesenchymal derived human osteosarcoma U2OS cells and the underlying mechanisms. The expressions of SATB1 and the related genes in the cells were detected by qRT-PCR and/or Western Blotting. SATB1 silencing was achieved by stable transfection with the vectors expressing small hairpin RNA versus SATB1. Cell proliferation was detected in a microplate reader with Cell Counting Kit-8 and the cell cycle was analyzed by flow cytometry using a cell cycle detection kit. The study found that SATB1 was particularly over-expressed in human osteosarcoma U2OS. Silencing SATB1 inhibited the proliferation of U2OS. It was found that inhibition of cell proliferation resulted from cell cycle arrest due to down-regulated expression of CFGF and JunB. The over-expression of SATB1 is responsible for abnormal proliferation of mesenchymal derived human Osteosatcoma U2OS cells, indicating that silencing SATB1 expression in the cells might be developed as an efficient osteosarcoma therapy. CTGF and JunB were involved in SATB1-mediated proliferation of U2OS cells.

Lactobacillus plantarum strains as potential probiotic cultures with cholesterol-lowering activity.

Elevated blood cholesterol is an important risk factor associated with atherosclerosis and coronary heart disease. The search for mediators that fine-tune cholesterol homeostasis has revealed lactic acid bacteria (LAB) to be potentially beneficial. The aim of the present study was to identify and characterize probiotic strains with bile salt hydrolase activity from kefir grains and evaluate their potential use as cholesterol-reducing probiotics in rats. Two isolates, Lp09 and Lp45, obtained from kefir grains were identified as Lactobacillus plantarum via molecular typing methods. Lactobacillus plantarum Lp09 and Lp45 exhibited excellent tolerance to low pH levels and high bile salt concentrations and showed potential bile salt hydrolase activity, bile salt deconjugation activity, and cholesterol coprecipitation ability. Additionally, the potential effect of Lb. plantarum Lp09 and Lp45 on plasma cholesterol levels was evaluated in Sprague-Dawley rats. Rats in 3 treatment groups were fed different experimental diets: a high-cholesterol diet, a high-cholesterol diet plus Lb. plantarum Lp09, or a high-cholesterol diet plus Lb. plantarum Lp45 for 4 wk. Total cholesterol, triglyceride, and low-density lipoprotein cholesterol levels in serum as well as cholesterol and triglyceride levels in liver were significantly decreased in the LAB-treated rats compared with rats fed a high-cholesterol diet without LAB supplementation. Also, both fecal cholesterol and bile acid levels were significantly increased after LAB administration. No significant changes were detected in high-density lipoprotein cholesterol levels. These results suggest that the Lb. plantarum Lp09 and Lp45 strains present the potential to be explored as probiotic agents for the management of hypercholesterolemia.

Immunoglobulin G4-related disease presenting with hypertrophy and sclerosis of the inferior turbinate.

Immunoglobulin G4-related disease (IgG4-RD) is a novel clinical disease entity characterized by elevated serum IgG4 concentration and tumefaction or tissue infiltration by IgG4+ plasma cells.1 We report the case of a 56-year-old man who presented with nasal obstruction for 5 years. Rhinoscopy revealed hypertrophy and sclerosis of the inferior turbinate, whereas computed tomography revealed inflammation of the anterior ethmoid sinus and frontal sinuses. An endoscopic inferior turbinectomy was performed, and IgG4-RD was definitively diagnosed based on the histopathological features of the turbinate tissue. Prednisolone was administered postoperatively. IgG4-RD presenting with hypertrophy and sclerosis of the inferior turbinate is rare. Awareness of IgG4-RD originating in the sinonasal cavity is essential to avoid delayed diagnosis.

N'-(2-Bromo-5-hy-droxy-4-meth-oxy-benzyl-idene)-3,5-dihy-droxy-benzo-hydrazide methanol monosolvate.

In the crystal structure of the title compound, C(15)H(13)BrN(2)O(5)·CH(3)OH, the methanol solvent mol-ecule links symmetry-related mol-ecules through O-H⋯O and N-H⋯O hydrogen bonds. Further inter-molecular O-H⋯O hydrogen bonds link symmetry-related mol-ecules, leading to the formation of a three-dimensional network. Two of the H atoms involved in hydrogen bonding are disordered. The dihedral angle between the rings is 5.64 (14)°.

[Analysis of allergen distribution and clinical characteristics of autumn allergic rhinitis in Changchun and surrounding areas].

Objective:To investigate the allergen characteristics, allergen distribution and clinical symptoms of autumn allergic rhinitis in Changchun and surrounding areas. Methods:The allergen test results of 1080 allergic rhinitis（AR） suspected patients from Changchun and surrounding areas were collected, from August to October 2019 and August to October 2020 in the Department of Otorhinolaryngology Head and Neck Surgery, the Second Hospital of Jilin University. The positive rates of major allergens and their differences in gender, age, different years and clinical symptom were compared and analyzed. Results:①Among the 1080 suspected AR patients, 804 patients（74.44%） had positive allergens. ②The top 3 allergens of autumn AR in Changchun and surrounding areas were Artemisia（36.20%）, Dwarf ragweed（33.24%） and Candida/Penicillium notarum/Cladosporium/Alternaria/Aspergillus niger（19.81%）. The positive rates of Artemisia and Dwarf ragweed were higher in men than in women（P<0.05）. ③Artemisia was the major allergen of autumn AR in juvenile group, youth group and middle-aged group. ④The positive rate of two or more allergens was 2.39 times that of single allergen. ⑤Patients with positive autumn pollen allergens had more severe symptoms of nasal congestion, red eye/eye itching and epiphora than those in other groups. Conclusion:Seasonal AR had typical clinical symptom characteristics. Major allergens in autumn AR in Changchun and surrounding areas are autumn pollen allergens（Artemisia, Dwarf ragweed, Humulus）. The distribution of those allergens was different in gender, age, and different years.

Role of PI3-Kinase in Angiotensin II-Induced Cardiac Hypertrophy: Class I Versus Class III.

Cardiac hypertrophy is an adaptive response to cardiac overload initially but turns into a decompensated condition chronically, leading to heart failure and sudden cardiac death. The molecular mechanisms involved in cardiac hypertrophy and the signaling pathways that contribute to the switch from compensation to decompensation are not fully clear. The aim of the current study was to examine the role of PI3-kinases Class I (PI3KC1) and Class III (PI3KC3) in angiotensin (Ang) II-induced cardiac hypertrophy. The results demonstrate that treatment of cardiomyocytes with Ang II caused dose-dependent increases in autophagy, with an increasing phase followed by a decreasing phase. Ang II-induced autophagic increases were potentiated by inhibition of PI3KC1 with LY294002, but were impaired by inhibition of PI3KC3 with 3-methyladenine (3-MA). In addition, blockade of PI3KC1 significantly attenuated Ang II-induced ROS production and cardiomyocyte hypertrophy. In contrast, blockade of PI3KC3 potentiated Ang II-induced ROS production and cardiac hypertrophy. Moreover, blockade of PI3KC1 by overexpression of dominant negative p85 subunit of PI3KC1 significantly attenuated Ang II-induced cardiac hypertrophy in normotensive rats. Taken together, these results demonstrate that both PI3KC1 and PI3KC3 are involved in Ang II-induced cardiac hypertrophy by different mechanisms. Activation of PI3KC1 impairs autophagy activity, leading to accumulation of mitochondrial ROS, and, hence, cardiac hypertrophy. In contrast, activation of PI3KC3 improves autophagy activity, thereby reducing mitochondrial ROS and leads to a protective effect on Ang II-induced cardiac hypertrophy.

A Novel Long Noncoding RNA, Lnc-OAD, Is Required for Bone Morphogenetic Protein 2- (BMP-2-) Induced Osteoblast Differentiation.

Long noncoding RNAs (lncRNAs) play very important roles in cell differentiation. Our recent study has demonstrated that a novel lncRNA named lnc-OAD modulated 3T3-L1 adipocyte differentiation. In the present study, we examined the roles of lnc-OAD in bone morphogenetic protein 2- (BMP-2-) induced osteoblast differentiation. Lnc-OAD expression was increased during BMP-2-induced osteoblast differentiation in C3H10T1/2 mesenchymal stem cells and MC3T3-E1 preosteoblast cells. Knockdown of lnc-OAD expression by specific siRNA remarkably decreased early osteoblast differentiation. In addition, stable knockdown of lnc-OAD by lentivirus vector also significantly inhibited late osteoblast differentiation and matrix mineralization in vitro. Conversely, stably overexpressed lnc-OAD with lentiviral vector accelerated osteoblast differentiation. Mechanistically, knockdown of lnc-OAD reduced significantly the phosphorylation of AKT and the expression of Osterix induced by BMP-2, while overexpression of lnc-OAD enhanced the phosphorylation of AKT and the expression of Osterix. Taken together, our study suggests that lnc-OAD plays an important role in modulating BMP-2-induced osteoblast differentiation via, at least in part, regulating the AKT-Osterix signaling axis.

2-Fluoro-N'-(2-hy-droxy-benzyl-idene)benzohydrazide.

In the title compound, C(14)H(11)FN(2)O(2), an intra-molecular O-H⋯N hydrogen bond influences the mol-ecular conformation; the two benzene rings form a dihedral angle of 18.4 (3)°. The F atom is disordered over two positions in a 0.717 (5):0.283 (5) ratio. In the crystal, inter-molecular N-H⋯O hydrogen bonds link the mol-ecules into chains extending along the c axis.