CLCF1 signaling restrains thermogenesis and disrupts metabolic homeostasis by inhibiting mitochondrial biogenesis in brown adipocytes.

Great progress has been made in identifying positive regulators that activate adipocyte thermogenesis, but negative regulatory signaling of thermogenesis remains poorly understood. Here, we found that cardiotrophin-like cytokine factor 1 (CLCF1) signaling led to loss of brown fat identity, which impaired thermogenic capacity. CLCF1 levels decreased during thermogenic stimulation but were considerably increased in obesity. Adipocyte-specific CLCF1 transgenic (CLCF1-ATG) mice showed impaired energy expenditure and severe cold intolerance. Elevated CLCF1 triggered whitening of brown adipose tissue by suppressing mitochondrial biogenesis. Mechanistically, CLCF1 bound and activated ciliary neurotrophic factor receptor (CNTFR) and augmented signal transducer and activator of transcription 3 (STAT3) signaling. STAT3 transcriptionally inhibited both peroxisome proliferator-activated receptor-γ coactivator (PGC) 1α and 1ß, which thereafter restrained mitochondrial biogenesis in adipocytes. Inhibition of CNTFR or STAT3 could diminish the inhibitory effects of CLCF1 on mitochondrial biogenesis and thermogenesis. As a result, CLCF1-TG mice were predisposed to develop metabolic dysfunction even without external metabolic stress. Our findings revealed a brake signal on nonshivering thermogenesis and suggested that targeting this pathway could be used to restore brown fat activity and systemic metabolic homeostasis in obesity.

Osthole exhibits the remedial potential for polycystic ovary syndrome mice through Nrf2-Foxo1-GSH-NF-κB pathway.

Polycystic ovary syndrome (PCOS) is the primary cause of female infertility with a lack of universal therapeutic regimen. Although osthole exhibits numerous pharmacological activities in treating various diseases, its therapeutic effect on PCOS is undiscovered. The present study found that application of osthole improved the symptoms of PCOS mice through preventing ovarian granulosa cells (GCs) production of more estrogen and alleviating the liberation of pro-inflammatory cytokine interleukin (IL)-1ß, IL-6, and tumor necrosis factor alpha. Meanwhile, osthole enhanced ovarian antioxidant capacity and alleviated intracellular reactive oxygen species (ROS) accumulation with a concurrent attenuation for oxidative stress, while intervention of antioxidant enzymic activity and glutathione (GSH) synthesis neutralized the salvation of osthole on GCs secretory disorder and chronic inflammation. Further analysis revealed that osthole restored the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and forkhead box O 1 (Foxo1) whose repression antagonized the amelioration of osthole on the insufficiency of antioxidant capacity and accumulation of ROS. Moreover, Nrf2 served as an intermedium to mediate the regulation of osthole on Foxo1. Additionally, osthole restricted the phosphorylation of IκBα and nuclear factor kappa B (NF-κB) subunit p65 by DHEA and weakened the transcriptional activity of NF-κB, but this effectiveness was abrogated by the obstruction of Nrf2 and Foxo1, whereas adjunction of GSH renewed the redemptive effect of osthole on NF-κB whose activation caused an invalidation of osthole in rescuing the aberration of GCs secretory function and inflammation response. Collectively, osthole might relieve the symptoms of PCOS mice via Nrf2-Foxo1-GSH-NF-κB pathway.

Enhanced autophagy reversed aflatoxin B1-induced decrease in lactate secretion of dairy goat Sertoli cells.

The deleterious effects of aflatoxins, especially aflatoxin B1 (AFB1) which are widespread at all stages of food production, on the reproductive system have been widely reported in males. However, it is still far from fully understood about the toxic effect and molecular mechanism after exposure to AFB1 in various testicular cells, especially Sertoli cells (SCs) which provide various energy materials and support to the developing germ cells as nurse cells. In this work, we examined the effects of AFB1 in dairy goat SCs on lactate production and autophagy, and the role of autophagy on AFB1-induced reduction in lactate production. Mechanistically, AFB1 destroyed the energy balance and reduced the secretion of lactate in dairy goat SCs (P < 0.01), resulting in a reduced level of ATP (P < 0.01) and phosphorylation of AMPK (P < 0.01). Subsequently, activated AMPK triggers autophagy by directly phosphorylating ULK1 (P < 0.05). The enhancement of autophagy partially reversed the AFB1-induced decrease in lactate secretion by promoting glucose utilization (P < 0.01) and increasing the expression of proteins related to lactate secretion in dairy goat SCs (P < 0.05) such as GLUT1, GLUT3, LDHA, and MCT4. Collectively, our study suggests that AFB1 inhibits the secretion of lactate which supply for germ cell development by damaging the "Warburg-like" metabolism of dairy goat SCs. Moreover, autophagy contributes to the resistance of glucose metabolism damage induced by AFB1. DATA AVAILABILITY: All data generated or analyzed in this study are available from the corresponding authors upon request.

The effect of an ICU liaison nurse-led family-centred transition intervention program in an adult ICU.

BACKGROUND: ICUs follow a restrictive companionship policy, especially after the COVID-19 outbreak. This strategy often limits the time families spend with patients, hinders their knowledge and skills in caregiving, and the sudden transfer of ICU patients to assist with disease monitoring and daily care can be very stressful for families. It is beneficial to use the transition period of transferring ICU patients to help families adjust to the role of caregiver. AIM: To develop and implement a patient- and family-centered transitional care intervention plan for patients transferred to the ICU. DESIGN: Prospective, pretest and posttest design. METHODS: The experimental group received an individualized family-centered transition plan led by the ICU liaison nurse that included 1) communication with health care professionals; distribution of a transfer booklet; 2) identification of nursing issues and communication with the ward nurse; invitation of family members to participate in the patient's rehabilitation; 3) follow-up instruction on bedside range of motion exercises; and provision of a patient rehabilitation diary. Patients in the control group received only routine care. Data were collected using the General Information Questionnaire, Family Satisfaction with ICU Patients (FS-ICU), the Family Relocation Stress Scale (FRSS), and the Stanford Acute Stress Response Questionnaire (SASRQR). RESULTS: After the intervention, the total family satisfaction score of ICU patients in the experimental group was significantly higher than that of the control group (87.18 ± 8.38 vs 78.74 ± 10.63, p<0.001), and the satisfaction with the care and information provided was significantly higher in the experimental group compared to the control group (p < 0.001), with no significant difference between the two groups in terms of satisfaction with decision making (p>0.001). The level of relocation stress of patients' families was significantly lower in the experimental group compared to the control group after the intervention (p < 0.001). And there was no statistically significant difference between the two groups in terms of patients' acute stress disorder scores (p>0.001). CONCLUSION: The implementation of a family-involved transition care programme significantly improved the satisfaction of ICU patients' families and reduced the stress of relocation for patients' families. RELEVANCE TO CLINICAL PRACTICE: Focusing on the transition of ICU patients to ensure continuity of critical care and improve the quality of care for ICU patient transfers can be accomplished through a family-centered transition care plan led by the ICU liaison nurse.

Generation and transmission of phase-stable coherent multi-band linear frequency modulated signals.

We present a coherent multi-band linear frequency modulated (LFM) signal generation and transmission system based on dual optical frequency combs (OFCs). In the proposed scheme, the two OFCs are phase-locked to ensure high coherence of the generated multi-band LFM signals. A round-trip phase correction is adopted to stabilize the time delay of the fiber transmission and enable the system to resist temperature variation. In the demonstration experiment, the generated multi-band LFM signals across L, S, and C frequency bands has a bandwidth of 200 MHz in each band. The root-mean-square (RMS) phase deviation of the multi-band signal is below 4×10-3rad after 1.2 km fiber transmission. During 1°C temperature variation, the RMS phase drift is suppressed from 1 rad to 0.1 rad. The high signal coherence between different bands and the capability of resisting temperature variation are highly desired for a multi-band distributed radar system.

Histone demethylase KDM5A is transactivated by the transcription factor C/EBPß and promotes preadipocyte differentiation by inhibiting Wnt/ß-catenin signaling.

ß-Catenin signaling is triggered by WNT proteins and is an important pathway that negatively regulates adipogenesis. However, the mechanisms controlling the expression of WNT proteins during adipogenesis remain incompletely understood. Lysine demethylase 5A (KDM5A) is a histone demethylase that removes trimethyl (me3) marks from lysine 4 of histone 3 (H3K4) and serves as a general transcriptional corepressor. Here, using the murine 3T3-L1 preadipocyte differentiation model and an array of biochemical approaches, including ChIP, immunoprecipitation, RT-qPCR, and immunoblotting assays, we show that Kdm5a is a target gene of CCAAT/enhancer-binding protein ß (C/EBPß), an important early transcription factor required for adipogenesis. We found that C/EBPß binds to the Kdm5a gene promoter and transactivates its expression. We also found that siRNA-mediated KDM5A down-regulation inhibits 3T3-L1 preadipocyte differentiation. The KDM5A knockdown significantly up-regulates the negative regulator of adipogenesis Wnt6, having increased levels of the H3K4me3 mark on its promoter. We further observed that WNT6 knockdown significantly rescues adipogenesis inhibited by the KDM5A knockdown. Moreover, we noted that C/EBPß negatively regulates Wnt6 expression by binding to the Wnt6 gene promoter and repressing Wnt6 transcription. Further experiments indicated that KDM5A interacts with C/EBPß and that their interaction cooperatively inhibits Wnt6 transcription. Of note, C/EBPß knockdown impaired the recruitment of KDM5A to the Wnt6 promoter, which had higher H3K4me3 levels. Our results suggest a mechanism involving C/EBPß and KDM5A activities that down-regulates the Wnt/ß-catenin pathway during 3T3-L1 preadipocyte differentiation.

Taurine-mediated browning of white adipose tissue is involved in its anti-obesity effect in mice.

Taurine, a nonprotein amino acid, is widely distributed in almost all animal tissues. Ingestion of taurine helps to improve obesity and its related metabolic disorders. However, the molecular mechanism underlying the protective role of taurine against obesity is not completely understood. In this study, it was found that intraperitoneal treatment of mice with taurine alleviated high-fat diet (HFD)-induced obesity, improved insulin sensitivity, and increased energy expenditure and adaptive thermogenesis of the mice. Meanwhile, administration of the mice with taurine markedly induced the browning of inguinal white adipose tissue (iWAT) with significantly elevated expression of PGC1α, UCP1, and other thermogenic genes in iWAT. In vitro studies indicated that taurine also induced the development of brown-like adipocytes in C3H10T1/2 white adipocytes. Knockdown of PGC1α blunted the role of taurine in promoting the brown-like adipocyte phenotypes in C3H10T1/2 cells. Moreover, taurine treatment enhanced AMPK phosphorylation in vitro and in vivo, and knockdown of AMPKα1 prevented taurine-mediated induction of PGC1α in C3H10T1/2 cells. Consistently, specific knockdown of PGC1α in iWAT of the HFD-fed mice inhibited taurine-induced browning of iWAT, with the role of taurine in the enhancement of adaptive thermogenesis, the prevention of obesity, and the improvement of insulin sensitivity being partially impaired. These results reveal a functional role of taurine in facilitating the browning of white adipose tissue, which depends on the induction of PGC1α. Our studies also suggest a potential mechanism for the protective role of taurine against obesity, which involves taurine-mediated browning of white adipose tissue.

Enhanced acetylation of ATP-citrate lyase promotes the progression of nonalcoholic fatty liver disease.

Hepatic steatosis is a hallmark of nonalcoholic fatty liver disease (NAFLD) and is promoted by dysregulated de novo lipogenesis. ATP-citrate lyase (ACLY) is a crucial lipogenic enzyme that is up-regulated in individuals with NAFLD. A previous study has shown that acetylation of ACLY at Lys-540, Lys-546, and Lys-554 (ACLY-3K) increases ACLY protein stability by antagonizing its ubiquitylation, thereby promoting lipid synthesis and cell proliferation in lung cancer cells. But the functional importance of this regulatory mechanism in other cellular or tissue contexts or under other pathophysiological conditions awaits further investigation. Here, we show that ACLY-3K acetylation also promotes ACLY protein stability in AML12 cells, a mouse hepatocyte cell line, and found that the deacetylase sirtuin 2 (SIRT2) deacetylates ACLY-3K and destabilizes ACLY in these cells. Of note, the livers of mice and humans with NAFLD had increased ACLY protein and ACLY-3K acetylation levels and decreased SIRT2 protein levels. Mimicking ACLY-3K acetylation by replacing the three lysines with three glutamines (ACLY-3KQ variant) promoted lipid accumulation both in high glucose-treated AML12 cells and in the livers of high-fat/high-sucrose (HF/HS) diet-fed mice. Moreover, overexpressing SIRT2 in AML12 cells inhibited lipid accumulation, which was more efficiently reversed by overexpressing the ACLY-3KQ variant than by overexpressing WT ACLY. Additionally, hepatic SIRT2 overexpression decreased ACLY-3K acetylation and its protein level and alleviated hepatic steatosis in HF/HS diet-fed mice. Our findings reveal a posttranscriptional mechanism underlying the up-regulation of hepatic ACLY in NAFLD and suggest that the SIRT2/ACLY axis is involved in NAFLD progression.

Remote broadband RF signal down-conversion with stable phase and high efficiency using a sideband optical phase-locked loop.

We propose a phase-stable high-efficiency down-conversion approach for broadband radio frequency signals transmitted from a remote site. A high power coherent optical local oscillator signal is used at the local site to increase the conversion gain and the spurious-free dynamic range (SFDR) at the same time. A sideband optical phase-locked loop ensures the suppression of the phase noise induced by the fiber transmission and the relative frequency drift of the remote and local lasers, which are essential for the signal transmission and the down-conversion. We first experimentally demonstrate the down-conversion of a single frequency signal at 16.45 GHz to a 250 MHz intermediate frequency (IF) signal with 3 dB gain and 103 dB/Hz2/3 SFDR after 10 km fiber transmission. Then we show the broadband down-conversion capability by down-converting a 1 GHz wide linear frequency modulated pulse signal centered at 11 GHz to 1 GHz with 3 dB gain. Along with a positive gain, the SFDR of the IF signal down-converted from 5 GHz to 40 GHz has reached 97.6 dB/Hz2/3 on average. This approach is suitable for weak broadband remote signal down-conversion with a simple-structured remote end.

Transient Palatal Tremor and Action Induced Foot and Leg Dystonia due to Hypertrophic Olivary Degeneration: a Case Report.

Hypertrophic olivary degeneration (HOD) is a rare phenomenon that occurs after various insults to the Guillain-mollaret triangle (GMT). HOD is unique because the degeneration of inferior olivary nucleus becomes hypertrophic rather than atrophic. In this study, a 31-year-old woman developed HOD after pontine cavernoma surgery had been performed. The clinical manifestation was involuntary intorsion of right lower extremity during walking, which has not been reported in the literature. The woman also presented with palatal tremor, the most classic symptom of HOD. HOD's imaging trait include olive hypertrophy with increased T2 signal intensity on MRI, which are corresponding to the pathological findings. HOD is a self-limiting disease and excessive treatments are unnecessary.

Photonic generation of phase-stable and wideband chirped microwave signals based on phase-locked dual optical frequency combs.

A photonics-based scheme is presented for generating wideband and phase-stable chirped microwave signals based on two phase-locked combs with fixed and agile repetition rates. By tuning the difference of the two combs' repetition rates and extracting different order comb tones, a wideband linearly frequency-chirped microwave signal with flexible carrier frequency and chirped range is obtained. Owing to the scheme of dual-heterodyne phase transfer and phase-locked loop, extrinsic phase drift and noise induced by the separated optical paths is detected and suppressed efficiently. Linearly frequency-chirped microwave signals from 5 to 15 GHz and 237 to 247 GHz with 30 ms duration are achieved, respectively, contributing to the time-bandwidth product of 3×108. And less than 1.3×10-5 linearity errors (RMS) are also obtained.

Aquatic risk assessment of a novel strobilurin fungicide: A microcosm study compared with the species sensitivity distribution approach.

The ecotoxicological effects of pyraoxystrobin, a novel strobilurin fungicide, were studied using outdoor freshwater microcosms and the species sensitivity distribution approach. The microcosms were treated with pyraoxystrobin at concentrations of 0, 1.0, 3.0, 10, 30 and 100µg/L. Species sensitivity distribution (SSD) curves were constructed by means of acute toxicity data using the BurrliOZ model for fourteen representatives of sensitive invertebrates, algae and fish and eleven taxa of invertebrates and algae, respectively. The responses of zooplankton, phytoplankton and physical and chemical endpoints in microcosms were studied. Zooplankton, especially Sinodiaptomus sarsi was the most sensitive to pyraoxystrobin exposure in the microcosms. Short-term toxic effects (<8 weeks) on zooplankton occurred in 1µg/L treatment group. The duration of toxic effects on S. sarsi could not be evaluated within the initial 56 days. Significant long-term toxic effects were observed at 10, 30 and 100µg/L (>281 days) for S. sarsi and the zooplankton community. Based on the results obtained from the organisms in the microcosm system, 1µg/L was recommended as the NOEAEC (no observed ecologically adverse effect concentration). Also, 0.33µg/L was derived as the Regulatory Acceptable Concentration based on the ecological recovery option (ERO-RAC) of pyraoxystrobin. For all fourteen tested species, the median HC5 (hazardous concentration affecting 5% of species) was 0.86µg/L, and the lower limit HC5 (LL-HC5) was 0.39µg/L. For the eleven taxa of invertebrates and algae tested, the median HC5 was 1.1µg/L, and the LL-HC5 was 0.26µg/L. The present study positively contributes to the suggestion of adequately using acute L(E)C50-based HC5/ LL-HC5 for deriving protective concentrations for strobilurin fungicides, and it should be valuable for full comprehension of the potential toxicity of pyraoxystrobin in aquatic ecosystems.

The effectiveness of a modified Manchester Triage System for geriatric patients: A retrospective quantitative study.

AIM: Geriatric patients are increasingly dominating the daily routine in emergency department (ED). The atypical clinical presentation of disease, multimorbidity, frailty and cognitive impairment of geriatric patients pose particular challenges for triage in the ED. Efficient and accurate emergency triage plays a key role in differentiating between geriatric patients who need timely treatment and those who can wait safely. The purpose of this study was to evaluate the performance of the modified Manchester Triage System (mMTS) in classifying geriatric patients. DESIGN: An observational retrospective study. METHODS: A retrospective study of 18,796 geriatric patients (≥65 years) attending the ED of a tertiary care hospital in Zhejiang province between 1 June 2020 and 30 June 2022. Baseline information on patients was collected and divided into two different study groups according to triage level: high priority (red/orange) and low priority (yellow/green). The sensitivity and specificity of the mMTS were estimated by verifying the triage classification received by the emergency geriatric patients and their survival at 7 days or the need for acute surgery within 72 h. RESULTS: The study included a total of 17,764 geriatric patients with a median age of 72 years in ED. 10.7% (1896/17,764) of the geriatric patients were assigned to the high priority code group (red/orange) and 89.3% (15,868/17,764) were in the low priority code group (yellow/green). The sensitivity of the mMTS associated with death within 7 days was 85.7% (77.5-91.4), specificity was 89.8% (89.3-90.2), and accuracy was 89.8% (89.3-90.2). 1.8% of patients required surgery within 72 h. The sensitivity was 62.6% (57.0-67.9), specificity was 90.3% (89.8-90.7), and negative predictive value was 99.2% (99.0-99.4). CONCLUSIONS: The mMTS has good specificity, accuracy and negative predictive value for geriatric patients. However, its incorrect prediction of triage in high-priority code patients results in lower sensitivity, which may serve as a protective strategy for these individuals. The current emergency triage system does not completely screen geriatric patients with severe acute illness who present to the ED, and it is necessary to add comprehensive assessment tools that match the characteristics of geriatric patients to improve triage outcomes.

Hexavalent chromium damages intestinal cells and coelomocytes and impairs immune function in the echiuran worm Urechis unicinctus by causing oxidative stress and apoptosis.

Hexavalent chromium (Cr(VI)) is a common pollutant in the marine environment, which impairs immunity and causes reproductive and heredity disorders in organisms. To clarify the immunotoxic effects of Cr (VI) on the marine worm Urechis unicinctus, we analyzed tissue damage and immune dysfunction caused by Cr (VI) in this organism at histopathologic, zymologic, apoptotic and molecular levels. The results indicated that the bioaccumulation of Cr (VI) bioaccumulation levels in coelomocytes was significantly higher than in the intestines and muscles. Pathological observation showed that Cr (VI) caused damage to the respiratory intestine, stomach and midgut. Cr (VI) also increased the replication of goblet cells and a reduction in the replication of epithelial cells. Meanwhile, Cr (VI) induced apoptosis of intestinal cells and coelomocytes, accompanied by an increase in the expression of Caspase-3, COX-2, and MyD88 in the intestine and coelomocytes. At the same time, Cr (VI) significantly affected the activities of antioxidant enzymes such as SOD, ACP, CAT, CAT, and GST, and increased H2O2 and MDA contents in U. unicinctus. Moreover, Cr (VI) exposure also up-regulated the transcription of hsc70, mt and jnk genes but decreased that of sod in the intestines. In contrast, Cr (VI) down-regulated the expression of sod, hsc70, mt, and jnk genes in coelomocytes. Collectively, Cr (VI) bioaccumulated in U. unicinctus cells and tissues, causing several histopathological changes, oxidative stress, and apoptosis of several cells in the organism, resulting in intestinal and coelomocyte damage and immune dysfunctioning.

Cure Kinetics and Thermal Decomposition Behavior of Novel Phenylacetylene-Capped Polyimide Resins.

Based on a novel phenylacetylene capped polyimide (PI) with unique high-temperature resistance, its curing kinetics and thermal decomposition behavior were investigated. The curing mechanism and kinetics were studied by differential scanning calorimetry (DSC), and the activation energy (Ea) and pre-exponential factor (A) of the curing reaction were calculated based on the Kissinger equation, Ozawa equation, and Crane equation. According to the curve of conversion rate changing with temperature, the relationship between the dynamic reaction Ea and conversion rate (α) was calculated by the Friedman equation, Starink equation, and Ozawa-Flynn-Wall (O-F-W) equation, and the reaction Ea in different stages was compared with the results of molecular dynamics. Thermogravimetric analysis (TGA) and a scanning electron microscope (SEM) were used to analyze the thermal decomposition behavior of PI resins before and after curing. Temperatures at 5% and 20% mass loss (T5%, T20%), peak decomposition temperature (Tmax), residual carbon rate (RW), and integral process decomposition temperature (IPDT) were used to compare the thermal stability of PI resins and cured PI resins. The results display that the cured PI has excellent thermal stability. The Ea of the thermal decomposition reaction was calculated by the Coats-Redfern method, and the thermal decomposition behavior was analyzed. The thermal decomposition reaction of PI resins at different temperatures was simulated by molecular dynamics, the initial thermal decomposition reaction was studied, and the pyrolysis mechanism was analyzed more comprehensively and intuitively.

Puerarin Ameliorated PCOS through Preventing Mitochondrial Dysfunction Dependent on the Maintenance of Intracellular Calcium Homeostasis.

Polycystic ovarian syndrome (PCOS) is the major cause of infertility in reproductive women, but no universal drug is feasible. Although puerarin clinically treats cerebrovascular and cardiovascular diseases, its curative effect on PCOS remains elusive. The present study discovered that administration of puerarin restored estrous cycle of PCOS mice and diminished the number of cystic follicles with the concomitant recovery for circulating testosterone, LH and FSH levels, and LH/FSH ratio, indicating the therapeutic role of puerarin in PCOS. KEGG analysis of differential genes between PCOS and control revealed the enrichment in MAPK and calcium signaling pathway. Application of puerarin restricted the phosphorylation of ERK1/2 and JNK, whose activation neutralized the improvement of puerarin on the secretory function and apoptosis of ovarian granulosa cells (GCs). Meanwhile, puerarin alleviated the accumulation of cytosolic Ca2+ through restricting the opening of Ryr and Itpr channels, but this effectiveness was counteracted by the activatory ERK1/2 and JNK. Attenuation of cytosolic Ca2+ counteracted the antagonistic effects of ERK1/2 and JNK activation on puerarin's role in rescuing the calcineurin and Nfatc. Further analysis manifested that Mcu had been authenticated as a direct downstream target of Nfatc to mediate the amelioration of puerarin on mitochondrial Ca2+ uptake. Moreover, puerarin prevented the disorder of ATP content, mitochondrial membrane potential, and mitochondrial permeability transition pore opening through maintaining mitochondrial Ca2+ homeostasis. Collectively, puerarin might ameliorate the symptoms of PCOS mice through preventing mitochondrial dysfunction that is dependent on the maintenance of intracellular Ca2+ homeostasis after inactivation of ERK1/2 and JNK.

Volleyball Movement Standardization Recognition Model Based on Convolutional Neural Network.

Artificial intelligence and deep learning have attracted much attention from researchers in industry and academia. The volleyball movement standardization and recognition model involve the application of artificial intelligence and deep learning. In order to solve the problem that human action in volleyball video is continuous and effective spatial and temporal features need to be extracted from the video stream, the Inception module is decoupled and heterogeneous, replacing the original 5 × 5 convolutional structures with two 3 × 3 convolutional structures, as well as replacing the 3 × 3 convolutional structures with 1 × 3 and a 3 × 1 convolutional structure with internal parameter optimization to ensure the accuracy of recognition. The model uses the input motion video RGB map as the spatial input and the optical flow map as the temporal input, and the two are weighted 1 : 1 for feature fusion. Experiments are conducted on the volleyball action video and homemade dataset in UCF101, and the experimental data show that the accuracy of the DNet volleyball action standardization recognition model proposed in this paper is 94.12%, which proves that the method improves the recognition ability of the model while speeding up the training speed. The research presented in this paper provides important theoretical guidance for artificial intelligence and deep learning.

Expression analysis of human glioma susceptibility gene and P53 in human glioma and its clinical significance based on bioinformatics.

Background: The exact mechanism of glioblastoma multiforme (GBM) remains unclear. This study was to clarify the expression of P53 in glioma and its molecular mechanism, and to explore the possibility of P53 as a potential therapeutic target of glioma and its clinical application value, so as to provide a new theoretical basis for the treatment of glioma. Methods: Firstly, a dataset was established to analyze the expression of P53 in different stages of glioma and its relationship with prognosis by using The Cancer Genome Atlas (TCGA) database, RNA-seq data, and survival data of glioma and normal control samples in gene expression profiling and interactive analysis (GEPIA). The genes co-expressed with P53 were screened out, their differential expression between glioma and normal control group was analyzed, and their functions were analyzed by enrichment analysis. The TGGA database was used for data verification and analysis. The correlation between P53 expression and clinicopathological parameters was analyzed. Kaplan-Meier survival analysis was used to analyze the relationship between P53 expression and overall survival (OS) and progression-free survival (PFS) of glioma patients, and Cox regression analysis was used to analyze the independent factors affecting OS and PFS of glioma patients. Results: The results of TCGA data analysis were as follows: The expression level of P53 was different from that of different stages of glioma, namely, the expression level of P53 between grade II and grade III, grade III and grade IV, and grade II and grade IV were significantly different (P<0.05). The results of P53 gene-related survival analysis showed that KNL1 high expression and low expression were significantly different in OS, and the high expression group was associated with poor prognosis (P<0.05). Conclusions: The P53 expression can be an effective biological indicator of poor prognosis of glioma.

HIGD1A links SIRT1 activity to adipose browning by inhibiting the ROS/DNA damage pathway.

Energy-dissipating adipocytes have the potential to improve metabolic health. Here, we identify hypoxia-induced gene domain protein-1a (HIGD1A), a mitochondrial inner membrane protein, as a positive regulator of adipose browning. HIGD1A is induced in thermogenic fats by cold exposure. Peroxisome proliferator-activated receptor gamma (PPARγ) transactivates HIGD1A expression synergistically with peroxisome proliferators-activated receptor γ coactivator α (PGC1α). HIGD1A knockdown inhibits adipocyte browning, whereas HIGD1A upregulation promotes the browning process. Mechanistically, HIGD1A deficiency impairs mitochondrial respiration to increase reactive oxygen species (ROS) level. This increases NAD+ consumption for DNA damage repair and curtails the NAD+/NADH ratio, which inhibits sirtuin1 (SIRT1) activity, thereby compromising adipocyte browning. Conversely, overexpression of HIGD1A blunts the above process to promote adaptive thermogenesis. Furthermore, mice with HIGD1A knockdown in inguinal and brown fat have impaired thermogenesis and are prone to diet-induced obesity (DIO). Overexpression of HIGD1A favors adipose tissue browning, ultimately preventing DIO and metabolic disorders. Thus, the mitochondrial protein HIGD1A links SIRT1 activity to adipocyte browning by inhibiting ROS levels.