The maize single-nucleus transcriptome comprehensively describes signaling networks governing movement and development of grass stomata.

The unique morphology of grass stomata enables rapid responses to environmental changes. Deciphering the basis for these responses is critical for improving food security. We have developed a planta platform of single-nucleus RNA-sequencing by combined fluorescence-activated nuclei flow sorting, and used it to identify cell types in mature and developing stomata from 33,098 nuclei of the maize epidermis-enriched tissues. Guard cells (GCs) and subsidiary cells (SCs) displayed differential expression of genes, besides those encoding transporters, involved in the abscisic acid, CO2, Ca2+, starch metabolism, and blue light signaling pathways, implicating coordinated signal integration in speedy stomatal responses, and of genes affecting cell wall plasticity, implying a more sophisticated relationship between GCs and SCs in stomatal development and dumbbell-shaped guard cell formation. The trajectory of stomatal development identified in young tissues, and by comparison to the bulk RNA-seq data of the MUTE defective mutant in stomatal development, confirmed known features, and shed light on key participants in stomatal development. Our study provides a valuable, comprehensive, and fundamental foundation for further insights into grass stomatal function.

Function analysis of transcription factor OSR1 regulating osmotic stress resistance in maize.

BACKGROUND: Maize is a major cereal crop world widely, however, the yield of maize is frequently limited by dehydration and even death of plants, which resulted from osmotic stress such as drought and salinity. Dissection of molecular mechanisms controlling stress tolerance will enable plant scientists and breeders to increase crops yield by manipulating key regulatory components. METHODS: The candidate OSR1 gene was identified by map-based cloning. The expression level of OSR1 was verified by qRT-PCR and digital PCR in WT and osr1 mutant. Electrophoretic mobility shift assay, transactivation activity assay, subcellular localization, transcriptome analysis and physiological characters measurements were conducted to analyze the function of OSR1 in osmotic stress resistance in maize. RESULTS: The osr1 mutant was significantly less sensitive to osmotic stress than the WT plants and displayed stronger water-holding capacity, and the OSR1 homologous mutant in Arabidopsis showed a phenotype similar with maize osr1 mutant. Differentially expressed genes (DEGs) were identified between WT and osr1 under osmotic stress by transcriptome analysis, the expression levels of many genes, such as LEA, auxin-related factors, PPR family members, and TPR family members, changed notably, which may primarily involve in osmotic stress or promote root development. CONCLUSIONS: OSR1 may serve as a negative regulatory factor in response to osmotic stress in maize. The present study sheds new light on the molecular mechanisms of osmotic stress in maize.

Trade-offs between the accumulation of cuticular wax and jasmonic acid-mediated herbivory resistance in maize.

Plants have evolved complex physical and chemical defense systems that allow them to withstand herbivory infestation. Composed of a complex mixture of very-long-chain fatty acids (VLCFAs) and their derivatives, cuticular wax constitutes the first physical line of defense against herbivores. Here, we report the function of Glossy 8 (ZmGL8), which encodes a 3-ketoacyl reductase belonging to the fatty acid elongase complex, in orchestrating wax production and jasmonic acid (JA)-mediated defenses against herbivores in maize (Zea mays). The mutation of GL8 enhanced chemical defenses by activating the JA-dependent pathway. We observed a trade-off between wax accumulation and JA levels across maize glossy mutants and 24 globally collected maize inbred lines. In addition, we demonstrated that mutants defective in cuticular wax biosynthesis in Arabidopsis thaliana and maize exhibit enhanced chemical defenses. Comprehensive transcriptomic and lipidomic analyses indicated that the gl8 mutant confers chemical resistance to herbivores by remodeling VLCFA-related lipid metabolism and subsequent JA biosynthesis and signaling. These results suggest that VLCFA-related lipid metabolism has a critical role in regulating the trade-offs between cuticular wax and JA-mediated chemical defenses.

MRI-based automatic identification and segmentation of extrahepatic cholangiocarcinoma using deep learning network.

BACKGROUND: Accurate identification of extrahepatic cholangiocarcinoma (ECC) from an image is challenging because of the small size and complex background structure. Therefore, considering the limitation of manual delineation, it's necessary to develop automated identification and segmentation methods for ECC. The aim of this study was to develop a deep learning approach for automatic identification and segmentation of ECC using MRI. METHODS: We recruited 137 ECC patients from our hospital as the main dataset (C1) and an additional 40 patients from other hospitals as the external validation set (C2). All patients underwent axial T1-weighted imaging (T1WI), T2-weighted imaging (T2WI), and diffusion-weighted imaging (DWI). Manual delineations were performed and served as the ground truth. Next, we used 3D VB-Net to establish single-mode automatic identification and segmentation models based on T1WI (model 1), T2WI (model 2), and DWI (model 3) in the training cohort (80% of C1), and compared them with the combined model (model 4). Subsequently, the generalization capability of the best models was evaluated using the testing set (20% of C1) and the external validation set (C2). Finally, the performance of the developed models was further evaluated. RESULTS: Model 3 showed the best identification performance in the training, testing, and external validation cohorts with success rates of 0.980, 0.786, and 0.725, respectively. Furthermore, model 3 yielded an average Dice similarity coefficient (DSC) of 0.922, 0.495, and 0.466 to segment ECC automatically in the training, testing, and external validation cohorts, respectively. CONCLUSION: The DWI-based model performed better in automatically identifying and segmenting ECC compared to T1WI and T2WI, which may guide clinical decisions and help determine prognosis.

All-cause mortality risk with different metabolic abdominal obesity phenotypes: the Rural Chinese Cohort Study.

We aimed to investigate the association of metabolic obesity phenotypes with all-cause mortality risk in a rural Chinese population. This prospective cohort study enrolled 15 704 Chinese adults (38·86 % men) with a median age of 51·00 (interquartile range: 41·00-60·00) at baseline (2007-2008) and followed up during 2013-2014. Obesity was defined by waist circumference (WC: ≥ 90 cm for men and ≥ 80 cm for women) or waist-to-height ratio (WHtR: ≥ 0·5). The hazard ratio (HR) and 95 % CI for the risk of all-cause mortality related to metabolic obesity phenotypes were calculated using the Cox hazards regression model. During a median follow-up of 6·01 years, 864 deaths were identified. When obesity was defined by WC, the prevalence of participants with metabolically healthy non-obesity (MHNO), metabolically healthy obesity (MHO), metabolically unhealthy non-obesity (MUNO) and metabolically unhealthy obesity (MUO) at baseline was 12·12 %, 2·80 %, 41·93 % and 43·15 %, respectively. After adjusting for age, sex, alcohol drinking, smoking, physical activity and education, the risk of all-cause mortality was higher with both MUNO (HR = 1·20, 95 % CI 1·14, 1·26) and MUO (HR = 1·20, 95 % CI 1·13, 1·27) v. MHNO, but the risk was not statistically significant with MHO (HR = 0·99, 95 % CI 0·89, 1·10). This result remained consistent when stratified by sex. Defining obesity by WHtR gave similar results. MHO does not suggest a greater risk of all-cause mortality compared to MHNO, but participants with metabolic abnormality, with or without obesity, have a higher risk of all-cause mortality. These results should be cautiously interpreted as the representation of MHO is small.

Long-Term Exposure to Traffic Noise and Risk of Incident Cardiovascular Diseases: a Systematic Review and Dose-Response Meta-Analysis.

While noise pollution from transportation has become an important public health problem, the relationships between different sources of traffic noise and cardiovascular diseases (CVDs) remain inconclusive. A comprehensive meta-analysis was therefore conducted to quantitatively assess the effects of long-term exposure to road traffic, railway, and aircraft noise on CVDs and relevant subtypes. We systematically retrieved PubMed, Embase, and Web of Science for articles published before April 4, 2022. Summary relative risks (RRs) and 95% confidence intervals (CIs) were estimated by the fixed- or random-effects models. In total, 23 articles were included in our meta-analysis. The risk of CVDs increased by 2% (RR 1.020, 95% CI 1.006-1.035) and 1.6% (RR 1.016, 95% CI 1.000-1.032) for every 10 dB increment of road traffic and aircraft noise. For CVD subtypes, the risk increased by 3.4% (1.034, 1.026-1.043) for stroke and 5% (1.050, 1.006-1.096) for heart failure with each 10 dB increment of road traffic noise; the risk of atrial fibrillation increased by 1.1% (1.011, 1.002-1.021) with each 10 dB increment of railway noise; and the risk increased by 1% (1.010, 1.003-1.017) for myocardial infarction, 2.7% (1.027, 1.004-1.050) for atrial fibrillation, and 2.3% (1.023, 1.016-1.030) for heart failure with each 10 dB increment in aircraft noise. Further, effects from road traffic, railway, and aircraft noise all followed positive linear trends with CVDs. Long-term exposure to traffic noise is positively related to the incidence risk of cardiovascular events, especially road traffic noise which significantly increases the risk of CVDs, stroke, and heart failure.

Assisted reproductive technology induces different secondary sex ratio: parental and embryonic impacts.

BACKGROUND: Assisted reproduction technology (ART) has advanced significantly, raising concerns regarding its impact on the secondary sex ratio (SSR), which is the sex ratio at birth in offspring. This study aimed to explore factors affecting SSR in singletons, singletons from twin gestation, and twins from twin gestation within the context of ART. METHODS: A retrospective analysis was conducted on data from 8335 births involving 6,223 couples undergoing ART. Binary logistic regression assessed relationships between parental and embryonic factors and SSR in singletons and singletons from twin gestation. Multinomial logistic regression models were utilized to identify factors influencing SSR in twins from twin gestation. RESULTS: Secondary infertility (OR = 1.164, 95% CI: 1.009-1.342), advanced paternal age (OR = 1.261, 95% CI: 1.038-1.534), and blastocyst embryo transfer (OR = 1.339, 95% CI: 1.030-1.742) were associated with an increased SSR, while frozen embryo transfer (FET) showed a negative association with SSR (OR = 0.738, 95% CI: 0.597-0.912) in singletons. A longer duration of gonadotropin (Gn) usage reduced SSR in singletons (OR = 0.961, 95% CI: 0.932-0.990) and singletons from twin gestation (OR = 0.906, 95% CI: 0.838-0.980). In singletons from twin gestation, male-induced infertility (OR = 2.208, 95% CI: 1.120-4.348) and higher Gn dosage (OR = 1.250, 95% CI: 1.010-1.548) were significantly associated with an increased SSR. Women aged > 35 years and intracytoplasmic sperm injection (ICSI) were associated with lower SSR (OR = 0.539, 95% CI: 0.293-0.990 and OR = 0.331, 95% CI: 0.158-0.690, respectively). In twins from twin gestation, paternal age exceeded maternal age (OR = 0.682, 95% CI: 0.492-0.945) and higher Gn dosage (OR = 0.837, 95% CI: 0.715-0.980) were associated with a higher proportion of male twins. Cleavage stage transfer (OR = 1.754, 95% CI: 1.133-2.716) resulted in a higher percentage of boy-girl twins compared to blastocyst transfer. CONCLUSION: This study demonstrates the complex interplay of various factors in determining the SSR in ART, highlighting the importance of considering infertility type, paternal age, fertilization method, embryo transfer stage, and Gn use duration when assessing SSR. Nevertheless, further research with a large sample size is necessary to confirm and expand upon the findings of this study.

Protective Effect of Topiroxostat on Myocardial Injury Induced by Lipopolysaccharide.

BACKGROUND: Myocardial injury induced by sepsis is the most common cause of death. Topiroxostat has been found to have organ protective effects, but its role in septic shock-related cardiomyocyte damage is still unclear and needs further study. MATERIAL AND METHODS: An endotoxemic shock model in rats was constructed. After topiroxostat treatment, hemodynamic parameters, myocardial injury marker enzymes, oxidative stress, myocardial injury, and apoptosis were measured by polyphysiograph, enzyme-linked immunosorbent assay, hematoxylin and eosin staining, TUNEL staining, and western blot. During in vitro experiments, the effect of topiroxostat on cell vitality, oxidative stress, inflammatory factors, apoptosis-related markers, phosphorylated-p65 (p-p65) and p65 expressions were measured by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), flow cytometry, enzyme-linked immunosorbent assay, quantitative real-time polymerase chain reaction, and western blot. RESULTS: Topiroxostat improved myocardial dysfunction and superoxide dismutase activity while suppressing levels of creatine kinase, lactate dehydrogenase and malondialdehyde in serum of endotoxemic shock rats. Additionally, topiroxostat augmented dry-wet weight ratios of the hearts in rats. Meanwhile, topiroxostat was proved to alleviate interstitial edema and apoptosis in myocardial tissues of endotoxemic shock rats. During in vitro experiments, topiroxostat pretreatment elevated lipopolysaccharide (LPS)-induced H9c2 cell vitality, and alleviated oxidative stress and inflammation. Moreover, topiroxostat pretreatment downregulated apoptosis-related markers, p-p65, and p-p65/p65 levels in LPS-induced H9c2 cells. CONCLUSIONS: Topiroxostat attenuated LPS-induced myocardial injury via repressing apoptosis and oxidative stress.

Complex dynamics in a Hopfield neural network under electromagnetic induction and electromagnetic radiation.

Due to the potential difference between two neurons and that between the inner and outer membranes of an individual neuron, the neural network is always exposed to complex electromagnetic environments. In this paper, we utilize a hyperbolic-type memristor and a quadratic nonlinear memristor to emulate the effects of electromagnetic induction and electromagnetic radiation on a simple Hopfield neural network (HNN), respectively. The investigations show that the system possesses an origin equilibrium point, which is always unstable. Numerical results uncover that the HNN can present complex dynamic behaviors, evolving from regular motions to chaotic motions and finally to regular motions, as the memristors' coupling strength changes. In particular, coexisting bifurcations will appear with respect to synaptic weights, which means bi-stable patterns. In addition, some physical results obtained from breadboard experiments confirm Matlab analyses and Multisim simulations.

Identification of WRKY transcription factors responding to abiotic stresses in Brassica napus L.

MAIN CONCLUSION: A total of 278 BnWRKYs were identified and analyzed. Ectopic expression of BnWRKY149 and BnWRKY217 suggests that they function in the ABA signaling pathway. WRKY transcription factors play an important role in plant development, however, their function in Brassica napus L. abiotic stress response is still unclear. In this study, a total of 278 BnWRKY transcription factors were identified from the B. napus genome data, and they were subsequently distributed in three main groups. The protein motifs and classification of BnWRKY transcription factors were analyzed, and the locations of their corresponding encoding genes were mapped on the chromosomes of B. napus. Transcriptome analysis of rapeseed seedlings exposed to drought, salt, heat, cold and abscisic acid treatment revealed that 99 BnWRKYs responded to at least one of these stresses. The expression profiles of 12 BnWRKYs were examined with qPCR and the result coincided with RNA-seq analysis. Two genes of interest, BnWRKY149 and BnWRKY217 (homologs of AtWRKY40), were overexpressed in Arabidopsis, and the corresponding proteins were located to the nucleus. Transgene plants of BnWRKY149 and BnWRKY217 were less sensitive to ABA than Arabidopsis Col-0 plants, suggesting they might play important roles in the responses of rapeseed to abiotic stress.

NORAD lentivirus shRNA mitigates fibrosis and inflammatory responses in diabetic cardiomyopathy via the ceRNA network of NORAD/miR-125a-3p/Fyn.

OBJECTIVE: Diabetic cardiomyopathy (DCM) is a serious complication of diabetes, but its pathogenesis is still unclear. This study investigated the mechanism of long noncoding RNA (lncRNA) NORAD in DCM. METHODS: Male leptin receptor-deficient (db/db) mice and leptin control mice (db/ +) were procured. DCM model was established by subcutaneous injection of angiotensin II (ATII) in db/db mice. NORAD lentivirus shRNA or Adv-miR-125a-3p was administered to analyze cardiac function, fibrosis, serum biochemical indexes, inflammation and fibrosis. Primary cardiomyocytes were extracted and transfected with miR-125a-3p mimic. The competing endogenous RNA (ceRNA) network of NORAD/miR-125a-3p/Fyn was verified. The levels of fibrosis- and inflammation-related factors were measured. RESULTS: In db/db mice treated with ATII, the body weight and serum biochemical indexes were increased, while the cardiac function was decreased, and inflammatory cell infiltration and fibrosis were induced. NORAD was upregulated in diabetic and DCM mice. The 4-week intravenous injection of NORAD lentivirus shRNA reduced body weight and serum biochemical indexes, improved cardiac function, and attenuated inflammation and fibrosis in DCM mice. NORAD acted as a sponge to adsorb miR-125a-3p, and miR-125a-3p targeted Fyn. Intravenous injection of miR-125a-3p adenovirus improved cardiac function and fibrosis and reduced inflammatory responses in DCM mice. Co-overexpression of miR-125-3p and Fyn partly reversed the improving effect of miR-125-3p overexpression on cardiac fibrosis in DCM mice. CONCLUSION: NORAD lentivirus shRNA improved cardiac function and fibrosis and reduced inflammatory responses in DCM mice via the ceRNA network of NORAD/miR-125a-3p/Fyn. These findings provide a valuable and promising therapeutic target for the treatment of DCM.

Digestive system manifestations and clinical significance of coronavirus disease 2019: A systematic literature review.

BACKGROUND AND AIM: A worldwide outbreak of coronavirus disease 2019 (COVID-19) has drawn global attention. Several reports have described the gastrointestinal (GI) manifestations in the infected patients. The systematic review was designed to highlight the gaps in our knowledge about the prevalence and clinical significance of GI symptoms in patients with COVID-19. METHODS: We searched PubMed database and Google articles published in both English and Chinese up to June 3, 2020, using search terms "clinical features," "2019 novel coronavirus," "2019-nCoV," "COVID-19," or "SARS-Cov-2." Observational studies, case reports, or letters describing the clinical features or observational studies regarding the detection and/or isolation of severe acute respiratory syndrome coronavirus 2 viruses in stools were included. RESULTS: A total of 22 publications were finally selected. It was reported that GI symptoms occurred in about 3-40.7% of patients. GI manifestations included nausea, diarrhea, anorexia, vomiting, abdominal pain, belching, abdominal distension, and GI hemorrhage. Diarrhea was the most common GI symptom. Infected patients had various degrees of liver dysfunction, and the severity of liver dysfunction was significantly associated with the severity of the disease. Therapy focusing on digestive system like liver supportive therapy or nutrition support or probiotics has been demonstrated to be effective interventions, which greatly improve prognosis. Fecal-oral transmission route is a potential risk for transmission. CONCLUSIONS: GI symptoms are common in COVID-19. Strengthening the recognition on abnormalities in digestive system of patients with COVID-19 is crucial for early identification and timely treatment, especially for those atypical patients. Hygiene protection and keeping the drainpipe free flowing are necessary for everyone.

Consensus on eradication of Helicobacter pylori and prevention and control of gastric cancer in China (2019, Shanghai).

BACKGROUND AND AIM: China is a country with high prevalence of Helicobacter pylori (H. pylori) infection, which in turn is closely related to the occurrence of gastric cancer. Therefore, the risks of H. pylori infection and gastric cancer are highly overlapping, and the prevention and treatment of H. pylori infection are necessary to prevent gastric cancer. METHODS: Based on evidence-based medicine and the Delphi method, the National Clinical Medical Research Center for Digestive Disease along with the National Early Gastrointestinal Cancer Prevention and Treatment Center Alliance organized dozens of experts in the fields of digestive diseases, H. pylori research, gastric cancer surgery, epidemiology, health economics, and health management to discuss the relationship between H. pylori eradication and prevention and the treatment of gastric cancer. RESULTS: A preliminary consensus on the relationship between H. pylori infection and gastric cancer, H. pylori eradication and gastric cancer prevention, and H. pylori screening and eradication strategy was reached. The consensus further clarified the relationship between H. pylori and gastric cancer and how to formulate future prevention and control strategies for gastric cancer. CONCLUSIONS: This consensus could provide guidance on early detection, diagnosis, and treatment of H. pylori to reduce the occurrence of gastric cancer in China.

Comparison of the short-term and long-term outcomes of surgical treatment versus endoscopic treatment for early esophageal squamous cell neoplasia larger than 2 cm: a retrospective study.

BACKGROUND: NCCN Guidelines of esophageal cancer recommend that endoscopic therapy is considered "preferred" for patients with limited early-stage disease less than or equal to 2 cm. However, there is currently no definite evidence to support either endoscopic therapy or esophagectomy for early esophageal cancer larger than 2 cm. We aimed to explore the optimal treatment for this condition. METHODS: From January 2010 to June 2016, 116 patients with early esophageal neoplasia [high-grade dysplasia (HGD), lamina propria and muscularis mucosae (T1a) cancer, selected superficial submucosa (T1b) cancer without lymph node metastases] larger than 2 cm and treated either surgically or endoscopically were included. RESULTS: Endoscopic therapy was performed in 69 patients and esophagectomy in 47 patients, respectively. The median follow-up time was 43.8 months in the endoscopic cohort and 49.4 months in the surgical cohort. The overall survival was similar between the two cohorts (97.1% vs. 91.5%, P = 0.18). Survival without readmission for treatment-related complicates was also similar. Minor and severe procedure-related complications occurred more often in the surgical cohort than in the endoscopic cohort (63.8% vs. 43.5% and 8.5% vs. 0 respectively, P < 0.05 for both). Four patients in the endoscopic cohort had to undergo additional esophagectomy and were alive during follow-up. There were no procedure-related deaths in the endoscopic cohort, whereas two deaths occurred in the surgical cohort. Recurrence occurred in nine patients in the endoscopic group (13%): six with local recurrence, one with residual neoplasia and two with metachronous neoplasia. None of them died after repeated endoscopic treatments. CONCLUSIONS: Efficacy was similar between endoscopic therapy and esophagectomy in the treatment of early esophageal squamous cell neoplasia larger than 2 cm and endoscopic therapy was associated with fewer and manageable complications. We recommend endoscopic treatment should be preferred selected for early esophageal neoplasia larger than 2 cm.

Clinical Features and Prognosis of Crohn's Disease with Upper Gastrointestinal Tract Phenotype in Chinese Patients.

BACKGROUND: The epidemiology of upper gastrointestinal (L4) Crohn's disease in China remains poorly characterized. AIMS: We aimed to identify the clinical characteristics of L4 disease and clarify the relationship between disease characteristics at diagnosis and early outcomes. METHODS: We retrospectively enrolled 246 patients diagnosed between 2013 and 2017 and followed up for > 1 year post-diagnosis. Primary outcomes included the 1-year rates of hospitalization and abdominal surgery according to disease location and behavior. RESULTS: Of 80 patients with L4 disease (61, 25, and 18 with esophagogastroduodenal, jejunal, and proximal ileal involvement, respectively), none had granuloma, whereas 66.7%, 50%, 46.9%, 75%, and 70% had disease-specific endoscopic lesions in the esophagus, stomach, duodenum, jejunum, and proximal ileum, respectively. Compared to non-L4 disease, L4 disease was associated with higher rates of abdominal surgery (41.3% vs. 11.4%, P < 0.001) but similar rates of hospitalization within 1 year post-diagnosis. In L4 disease, jejunal and proximal ileal involvement was associated with stricturing behavior (P = 0.034, P < 0.001) and higher abdominal surgery rate (both: P < 0.001). Risk factors for abdominal surgery within 1 year post-diagnosis included age ≥ 40 years (OR 1.920; 95% CI 1.095-3.367), L4 phenotype (OR 6.335; 95% CI 3.862-10.390), stricturing disease (OR 3.162; 95% CI 1.103-9.866), and penetrating disease (OR 11.504; 95% CI 3.409-38.825), whereas the protective factor was female sex (OR 0.214; 95% CI 0.123-0.373). CONCLUSIONS: Early outcomes are worse for L4 than for non-L4 disease. Jejunoileum involvement predicts stricturing disease and early surgery. More aggressive initial therapy is needed to improve L4-disease prognosis.

MiR-21-3p modulates lipopolysaccharide-induced inflammation and apoptosis via targeting TGS4 in retinal pigment epithelial cells.

Age-related macular degeneration (AMD) is a major reason of blindness in the elderly. MicroRNAs are implicated in various pathological processes, including inflammation and apoptosis. In this study, we aim to investigate the biological functions of miR-21-3p in inflammation and apoptosis caused by lipopolysaccharide (LPS) in human retinal pigment epithelial (ARPE-19) cells. The miR-21-3p inhibitor and mimic were transfected into ARPE-19 cells for 48 hours, followed by exposed to LPS (10 µg/mL) for 24 hours. The mRNA and protein expression of IL-6 and MCP-1 were measured using real-time PCR (RT-PCR) and enzyme-linked immunosorbent assays. Cell viability, apoptosis, caspase 3 activity, cleaved caspase-3 and cleaved-PARP protein levels were detected to evaluate the effects of miR-21-3p on apoptosis. Additionally, the target relationship between miR-21-3p and regulator of G-protein signalling 4 (RGS4) was verified by dual luciferase reporter assay. RT-PCR analysis demonstrated that LPS induced miR-21-3p expression. Inhibition of miR-21-3p reduced the mRNA and protein levels of IL-6 and MCP-1. Apoptosis, caspase-3 activity, and cleaved-caspase 3 and cleaved PARP protein levels were repressed by the miR-21-3p inhibitor. However, overexpression of miR-21-3p showed the opposite results. Furthermore, we identified that miR-21-3p directly targeted the 3' untranslated region of RGS4. MiR-21-3p negatively regulated the expression of RGS4 both in mRNA and protein levels. Silencing RGS4 reduced the anti-inflammatory and anti-apoptotic effects of miR-21-3p inhibitor. Our results revealed that miR-21-3p inhibition targeted RGS4 to attenuate inflammatory responses and apoptosis caused by LPS in ARPE-19 cells.

Characterization of controlled cortical impact devices by high-speed image analysis.

As a consequence of their commercial availability, ease of use, and reproducibility, controlled cortical impact (CCI) devices have attained significant prevalence in preclinical traumatic brain injury research. With a CCI, the severity of injury is controlled by varying the impact depth, velocity, and duration, but the actual performance of the device is not well appreciated, partly because of the velocity and short travel distance to impact. This study used a high-speed video digital camera to investigate the performance of five electromagnetically driven CCI devices of the same model. Videography indicated that the impactor tip made a series of distinctive vertical advances and retractions before it attained the desired preset depth; this was also observed in male mouse CCI tests. The impactor tip was also observed to move in the horizontal direction by .8-1.6 mm. On the first advance, the tip extended a distance that was shorter than the preset depth and the velocity of impactor tip was slightly faster than the preset values for three of the five machines. One of the devices was evaluated on four separate occasions over a 14-month period and was found to operate consistently over time. Overall, differences in impact depth and velocity between the devices were modest, suggesting that comparisons of experimental results from different laboratories will generally be informative, particularly if reports provide relevant descriptions of neuropathology. However, the repetitive extension and retraction and horizontal movement of the tip suggests caution in modeling CCI as a single injurious event.

An attempt to treat Hoffa fractures under arthroscopy: A case report.

We treated a 15-year-old female patient with fracture of the post-lateral femoral condyle and the bone shifted in front of the knee. Considering that the traditional surgical approach has the shortcomings of significant trauma and poor prognosis, we designed an arthroscopic procedure, which achieved satisfactory short-term efficacy, effectively reduced and fixed the fractures, avoided damage to vascular nerves, and maximally reduced the trauma caused by surgery itself.

Inhibition of the SOCS1-JAK2-STAT3 Signaling Pathway Confers Neuroprotection in Rats with Ischemic Stroke.

BACKGROUND: The present study aims to investigate the protective effects of the SOCS1-JAK2-STAT3 signaling pathway on neurons in a rat model of ischemic stroke. METHODS: Our study was conducted using an ischemic stroke rat model. After the microglia were extracted, 40 neonatal Sprague-Dawley (SD) rats were assigned into the blank, AG490, model and negative control (NC) groups. The neurological function of all the rats was evaluated. Histopathological changes were observed. qRT-PCR and western blotting were applied to measure the expression of genes and proteins in the SOCS1-JAK2-STAT3 signaling pathway and related to apoptosis. The TUNEL assay was conducted to calculate the cellular morphology and apoptosis of neuronal cells. Cell viability was detected using the MTT assay. In addition, immunoassays were used to measure the content of superoxide dismutase (SOD), glutathione (GSH) and malondialdehyde (MDA) as well as the levels of oxidative stress. RESULTS: Compared with the blank group, the model and NC groups showed higher neurological function scores-the cytoplasm of the neurons were cavitated, the organelles were reduced with unclear margins, some of the neurons were necrotic, and apoptosis was increased. In addition, the NC and model groups exhibited decreased cell viability, lower mRNA and protein expression of SOCS1 SOCS3 and bcl-2 and reduced SOD and GSH levels but higher mRNA and protein expression levels of AK2, STAT3,Bax and caspase-3 as well as increased protein expression of P-JAK2, P-STAT3 and activated caspase-3 (c-caspase-3). Moreover, the MDA levels were up-regulated in the NC and model groups. In contrast, opposing trends were found in the AG490 group compared with the NC and model groups. CONCLUSION: These data demonstrate that inhibiting the SOCS1-JAK2-STAT3 signaling pathway can reduce the loss of nerve function and apoptosis of neuronal cells, which provides a new target for the clinical treatment of ischemic stroke.