Research on Human Posture Estimation Algorithm Based on YOLO-Pose.

In response to the numerous challenges faced by traditional human pose recognition methods in practical applications, such as dense targets, severe edge occlusion, limited application scenarios, complex backgrounds, and poor recognition accuracy when targets are occluded, this paper proposes a YOLO-Pose algorithm for human pose estimation. The specific improvements are divided into four parts. Firstly, in the Backbone section of the YOLO-Pose model, lightweight GhostNet modules are introduced to reduce the model's parameter count and computational requirements, making it suitable for deployment on unmanned aerial vehicles (UAVs). Secondly, the ACmix attention mechanism is integrated into the Neck section to improve detection speed during object judgment and localization. Furthermore, in the Head section, key points are optimized using coordinate attention mechanisms, significantly enhancing key point localization accuracy. Lastly, the paper improves the loss function and confidence function to enhance the model's robustness. Experimental results demonstrate that the improved model achieves a 95.58% improvement in mAP50 and a 69.54% improvement in mAP50-95 compared to the original model, with a reduction of 14.6 M parameters. The model achieves a detection speed of 19.9 ms per image, optimized by 30% and 39.5% compared to the original model. Comparisons with other algorithms such as Faster R-CNN, SSD, YOLOv4, and YOLOv7 demonstrate varying degrees of performance improvement.

Variation characteristics of climatic potential yield and resources utilization efficiency of maize under the background of climate change in agro-pastoral transitional zone of Gansu, China.

To evaluate the effects of changes in radiation, accumulative temperature, precipitation and climate resources on climate resource utilization efficiency in the agro-pastoral transitional zone of Gansu Province, we analyzed the variations of climate potential yield loss rate, light, heat, precipitation and comprehensive utilization efficiency of climate resources in the agro-pastoral transitional zone of Gansu Province by the step-by-step correction and indexation method, with the 1971-2020 weather data from 45 meteorological sites and the maize phenology data. The results showed that solar radiation showed fluctuating downward trend at a rate of -22.03 MJ·m-2·(10 a)-1, the accumulative ≥11 ℃ temperature showed significant upward trend at a rate of 60.89 ℃·(10 a)-1, the precipitation showed slow upward trend at a rate of 2.05 mm·(10 a)-1 during the study period. The climate potential yield loss rate due to temperature and precipitation limitations was relatively high in Gannan and the northern part of Longzhong, while it was relatively low in the most areas of Longdong. Except for the central part of the study area and part of Longdong, the climate potential yield loss rate due to temperature and precipitation limitations in other regions of the study area showed decreased trend at the rate of -2.0%·(10 a)-1 and -0.6%·(10 a)-1. The low-value areas of light and heat utilization efficiency distributed in the northern and southern parts of Longzhong and part of Gannan, the low-value area of precipitation utilization efficiency distributed in Gannan, and the low value of comprehensive utilization efficiency distributed in Lanzhou and Baiyin which were 0.41 and 0.47, respectively. Longdong was the most suitable for maize planting, where the climate resources utilization efficiency of maize was highest, followed by Gannan and Longzhong. The average tendency rate of light, heat, precipitation and climate resources comprehensive utilization efficiency in the study area showed increased trend, which were 0.1%·(10 a)-1, 0.07 kg·hm-2·â„ƒ-1·d-1·(10 a)-1, 1.17 kg·hm-2·mm-1·(10 a)-1 and 0.05 ·(10 a)-1, respectively, showing a good potential to increase maize yield.

Circ_0136474 promotes the progression of osteoarthritis by sponging mir-140-3p and upregulating MECP2.

BACKGROUND: Circular RNAs (circRNAs) have pivotal roles in the progression of many diseases, including osteoarthritis (OA). The detained function and regulatory mechanism of circ_0136474 in OA are still largely unknown. METHODS: The chondrocytes (CHON-001 cells) were exposed to interleukin-1 beta (IL-1ß) to mimic the injury in OA. The expression levels of circ_0136474, microRNA-140-3p (miR-140-3p), methyl-CpG-binding protein 2 (MECP2) mRNA were measured by qRT-PCR. Cell proliferation was assessed using CCK-8 assay. Flow cytometry was employed for measuring cell apoptosis. All protein levels were evaluated via western blot analysis. ELISA was used for detecting the concentrations of the inflammatory cytokines. Dual-luciferase reporter analysis and RNA Immunoprecipitation analysis were conducted for confirming the association between miR-140-3p and circ_0136474 or MECP2. RESULTS: Circ_0136474 was upregulated in IL-1ß-induced CHON-001 cells and OA cartilage tissues. Circ_0136474 deficiency alleviated IL-1ß-stimulated CHON-001 cell damage via enhancing cell proliferation and reducing extracellular matrix (ECM) degradation, apoptosis, and inflammation. Circ_0136474 was a sponge of miR-140-3p, and miR-140-3p inhibition reversed the roles of circ_0136474 knockdown in IL-1ß-treated CHON-001 cells. Moreover, miR-140-3p directly targeted MECP2, and upregulation of miR-140-3p attenuated L-1ß-triggered CHON-001 cell injury via targeting MECP2. Additionally, circ_0136474 regulated MECP2 level via sponging miR-140-3p. CONCLUSION: Circ_0136474 knockdown alleviated IL-1ß-triggered CHON-001 cell damage through modulation of miR-140-3p/MECP2 axis, indicating a new target for treatment of OA.

Evaluating the effects of different sowing dates and tillage methods on dry-land wheat grain dry matter accumulation based on the APSIM model.

Accurate simulation of dry matter accumulation in wheat grains can provide important technical support for regulating wheat production in hilly areas of Loess Plateau. Using the APSIM model, we analyzed dryland wheat grain dry matter accumulation and distribution using the meteorological data from 1971 to 2017 in Anding District, and the field test data from 2016 to 2017 in Anjiagou Village, Fengxiang Town, Anding District, Dingxi City, Gansu Province. Furthermore, the influence of sowing date and tillage method on dry matter accumulation of wheat grain was quantitatively analyzed on the basis of model validation. The results showed that the root mean square error (RMSE) between the simulated and measured values of grain dry matter was 57.5-143.1 kg·hm-2 and the normalized root mean square error (NRMSE) was 1.4%-9.9% under the three sowing dates and four tillage methods, respectively. The precision of the APSIM model was satisfactory. Under different sowing dates, the order for beneficial degree of tillage treatment to dry matter accumulation in wheat grains was no tillage with straw cover > conventional tillage with straw cover > no tillage > conventional tillage. The treatment of no tillage with straw covered was the most favora-ble to dry matter accumulation in wheat grains, with no significant difference between no tillage and conventional tillage treatments. Under different farming methods, early sowing was better than normal sowing and late sowing for the dry matter accumulation process of wheat. Late sowing had stronger impacts on dry matter accumulation, with the least ideal accumulation process.

Glucocorticoids induce femoral head necrosis in rats through the ROS/JNK/c-Jun pathway.

Osteonecrosis of the femoral head (ONFH) is a common clinical disease with a high disability rate. Apoptosis of osteoblasts caused by high-dose short-term or low-dose long-term glucocorticoid (GC) administration is the biological basis of steroid-induced avascular necrosis of the femoral head (SANFH). The pathogenesis of SANFH has not yet been fully elucidated, and there is currently a lack of effective clinical treatments. Here, we investigated the role of the reactive oxygen species (ROS)/JNK/c-Jun signaling pathway in SANFH. Dexamethasone (Dex) was used to induce apoptosis in osteoblasts, and this resulted in a significant increase in levels of p-JNK, p-c-Jun, Bax, caspase-3, caspase-9, cytochrome C, Beclin-1, and LC3, and a decrease in levels of P62 and Bcl-2. In addition, intracellular ROS levels were increased and mitochondrial membrane potential was decreased. Administration of 3-MA, an autophagy inhibitor, attenuated Dex-mediated changes in autophagy and apoptosis. A rat model of ONFH exhibited severe bone trabecular hollow bone pits along with a significant increase in femoral head cell apoptosis compared with the control group. Additionally, micro-CT analysis showed that both bone tissue content and femoral head integrity were significantly reduced in the ONFH group. Furthermore, 3-MA treatment decreased the effect of Dex on GC-induced ONFH and osteoblast apoptosis in rats and could counteract microstructure destruction due to femoral head necrosis. In summary, our data suggest that GC can induce osteoblast apoptosis and autophagy through the ROS/JNK/c-Jun signaling pathway, which contributes to ONFH.

Crocin protects against dexamethasone­induced osteoblast apoptosis by inhibiting the ROS/Ca2+­mediated mitochondrial pathway.

Osteoblast apoptosis has been identified as an important event in the development of glucocorticoid (GC)­induced osteoporosis and osteonecrosis of the femoral head. Crocin, a bioactive ingredient of saffron, has been demonstrated to induce antiapoptotic effects on numerous types of cell in vitro; however, the effects of crocin on the dexamethasone (Dex)­induced apoptosis of osteoblasts remain unclear. In the present study, the protective effects of crocin during Dex­induced apoptosis of MC3T3­E1 osteoblasts, and the underlying mechanisms, were investigated. MTT and Annexin V­FITC/PI flow cytometry assays were performed to evaluate the viability and apoptosis of cells, respectively. The mitochondrial transmembrane potential, reactive oxygen species (ROS), intracellular Ca2+ levels and apoptosis­associated protein expression were assessed via flow cytometry, fluorescence microscopy and western blotting. It was demonstrated that crocin pretreatment inhibited Dex­induced apoptosis of osteoblasts in a dose­dependent manner. Crocin reversed Dex­induced decreases in the mitochondrial transmembrane potential, and increases in ROS and intracellular Ca2+ levels. Furthermore, crocin upregulated the expression levels of B­cell lymphoma-2 (Bcl­2) and mitochondrial cytochrome c (Cyt C), and downregulated those of cleaved caspase­9, cleaved caspase­3, Bcl­2­associated X protein and cytoplasmic Cyt C. N­acetylcysteine, a ROS inhibitor, and 1,2­bis(2­aminophenoxy)ethane­N,N,N',N'­tetraacetic acid, a calcium chelator, attenuated Dex­induced osteoblast apoptosis, whereas H2O2 and ionomycin, a calcium ionophore that increases intracellular calcium levels, reversed the antiapoptotic effects of crocin on Dex­treated osteoblasts. These results indicated that crocin may protect osteoblasts from Dex­induced apoptosis by inhibiting the ROS/Ca2+­mediated mitochondrial pathway, thus suggesting that crocin has potential value as a treatment for GC­induced bone diseases.

Decrease of GSK3ß Ser-9 Phosphorylation Induced Osteoblast Apoptosis in Rat Osteoarthritis Model.

Nowadays, the cumulative intake of glucocorticoids has become the most common pathogenic factor for non-traumatic osteonecrosis of the femoral head (ONFH). Apoptosis of osteoblasts is considered as the main reason of ONFH at the molecular level. Glycogen synthase kinase 3ß (GSK3ß) is an important regulator of cellular differentiation and apoptosis pathway, which can modulate the balance between osteoblasts and osteoclasts. Several studies have reported about its function in osteoporosis, but little is known about it in osteonecrosis. In our study, lipopolysaccharide and methylprednisolone were utilized to establish a rat ONFH model. The phosphorylation of GSK3ß Ser-9 was decreased in the model. Western blotting examination of ß-catenin, Bcl-2, Bax and caspase-3 revealed that the osteoblasts were apoptotic. In dexamethasone (Dex)-incubated primary osteoblasts, the expression profile of GSK3ß phosphorylation and apoptotic factors were consistent with those in the rat ONFH model. To further investigate the regulation of osteonecrosis caused by GSK3ß, the expression and function of GSK3ß were inhibited in Dex-incubated primary osteoblasts. The knockdown of GSK3ß by siRNA decreased the expression of Bax and cleaved caspase-3, but increased Bcl-2 and ß-catenin. On the other hand, selective inhibition of GSK3ß function by LiCl counteracted the activation of caspase-3 induced by Dex. Our work is the first study about the GSK3ß phosphorylation in ONFH, and provides evidence for further therapeutic methods.

Glucocorticoid induces osteonecrosis of the femoral head in rats through GSK3ß-mediated osteoblast apoptosis.

OBJECTIVE: One of the important causes of glucocorticoids (GCs)-induced osteonecrosis of the femoral head (ONFH) is osteoblast apoptosis. Glycogen synthase kinase 3ß (GSK3ß) has been reported to be related to dexamethasone (Dex)-induced osteoblast apoptosis. This study aimed to determine whether GSK3ß plays role in GC-induced ONFH and investigate the underlying mechanism. METHODS: 18 male Sprague-Dawley rats were divided into 3 groups. Rats from ONFH group underwent lipopolysaccharide and methylprednisolone injection. Lithium chloride (LiCl, a GSK3ß inhibitor) group were fed with LiCl solution. The control group were untreated. Osteonecrosis, apoptosis and bone loss were evaluated by HE staining, TUNEL staining and micro-CT respectively. Protein expressions were examined by western blotting. In addition, primary osteoblast cells were transfected by GSK3ß-siRNA and related signaling pathway and proteins were examined. RESULTS: ONFH group showed a relative high percentage of empty lacunae and apoptotic cells, whilst LiCl treatment markedly decreased the percentage. LiCl treatment decreased GC-induced bone loss. Immunoblot analysis for GSK3ß showed decreased level of Ser9-phosphorylated GSK3ß in ONFH group compared with control group. Knockdown of GSK3ß by siRNA in primary osteoblast cells attenuated DEX-induced apoptosis and loss of mitochondrial transmembrane potential (Δψm). GSK3ß knockdown also reversed the release of cytochrome C (Cyt C) from mitochondria to the cytosol. GSK3ß decreased apoptosis-related protein expression both in vitro and in vivo. CONCLUSION: Our findings suggest that GC induces ONFH in rats through GSK3ß-mediated osteoblast apoptosis, with involvement of mitochondrial apoptotic pathway.

Dexamethasone induces osteoblast apoptosis through ROS-PI3K/AKT/GSK3ß signaling pathway.

BACKGROUND: Osteoblasts play important roles in the process of osteogenesis and prevention of osteonecrosis. Dexamethasone (Dex), a type of glucocorticoids (GCs), induces apoptosis of osteoblasts and leads to the occurrence of non-traumatic osteonecrosis. This study aimed to explore the effects of phosphatidylinositol 3-kinase/Protein kinase 3 (PI3K/AKT) and glycogen synthase kinase 3ß (GSK3ß) on Dex-induced osteoblasts apoptosis. METHODS: Viabilities, proliferation, and apoptosis of primary osteoblasts and pre-osteoblast MC3T3-E1 cells after Dex treatment were detected using cell counting kit-8 (CCK-8) assay, 5-bromo-2'-deoxyuridine (BrdU) incorporation assay, FITC-Annexin V/PI staining and western blotting, respectively. 2',7'-Dichlorodihydrofluorescein diacetate (DCFH-DA) staining was performed to measure the intracellular reactive oxygen species (ROS) levels after Dex treatment. N-acetyl-l-cysteine (NAC) was used as ROS scavenger in this research. The expressions of PI3K/AKT and GSK3ß in osteoblasts and MC3T3-E1 cells after Dex treatment were analyzed using western blotting and qRT-PCR, respectively. Then the effects of GSK3ß knockdown on Dex-induced apoptosis of osteoblasts were explored. Alkaline phosphatase (ALP) activity assay was used to detect the role of Dex in regulating ALP activity. RESULTS: Dex remarkably inhibited proliferation and induced apoptosis of osteoblasts and MC3T3-E1 cells. Dex potentially attenuated the osteoblast differentiation. The intracellular ROS levels were significantly increased after Dex treatment. Dex suppressed the activation of PI3K/AKT pathway in osteoblasts and MC3T3-E1 cells by down-regulating the expressions of p-PI3K and p-AKT. The expressions of GSK3ß in osteoblasts and MC3T3-E1 cells were obviously up-regulated after Dex treatment. Knockdown of GSK3ß alleviated Dex-induced osteoblast and MC3T3-E1 cell apoptosis by decreasing the expressions of Bax, cleaved-caspase 3, cleaved-caspase 9 and increasing the expression of Bcl-2. CONCLUSION: Our research verified that Dex induced osteoblasts apoptosis by ROS-PI3K/AKT/GSK3ß signaling pathway.

Prognostic factors for patients with chondrosarcoma: A survival analysis based on the Surveillance, Epidemiology, and End Results (SEER) database (1973-2012).

Current reports on prognostic factors for chondrosarcoma mainly involve patients in treatment centers. Few are based on multicenter or multi-eras. We analyzed existing data from the Surveillance, Epidemiology, and End Results (SEER) database to investigate the risk factors for survival outcomes. All patients with chondrosarcoma from 1973 to 2012 were identified. 3737 patients were eligible and included. In survival analysis, patient had good survival outcome if the patient was female, young, with localized stage, well grade, small tumor size, treated with surgery, while patient was male, old, with distant stage, undifferentiated grade, tumor size <50 mm, located in vertebral or pelvic bones, underwent radiation had bad survival outcome. Surgery types from having best survival outcomes to worst were local excision, radical excision, amputation, no surgery. 'Well' and 'moderately' grade seems to be suitable for local excision, but 'poorly' and 'undifferentiated' grade suitable for wide local excision. Multivariate COX regression analysis showed year of diagnosis, sex, age of diagnosis, stage, grade, tumor site, surgery, radiation were independent risk factors. Year of diagnosis, sex, age of diagnosis, stage, grade, tumor site, surgery, radiation were independent risk factors. Excision is a better treatment than amputation. Doctors can use wide local excision to treat chondrosarcoma, especially when encountering high grade chondrosarcoma or pelvic chondrosarcoma.

Osteosarcoma in patients below 25 years of age: An observational study of incidence, metastasis, treatment and outcomes.

Only few systematic and comprehensive studies have focused on osteosarcoma in children and adolescents. In the present study, 3,085 patients with osteosarcoma were identified in the Surveillance, Epidemiology and End Results Program database. The patients were <25 years of age and diagnosed between 1973 to 2012. A retrospective study was performed to investigate the factors associated with tumor incidence, metastasis, treatment and survival. The results indicated that the incidence of osteosarcoma was higher in male patients compared with female patients. In addition, the incidence rate of osteosarcoma was higher among male and female patients between the ages of 10 and 19. Osteosarcoma located in the chest and pelvic bones was associated with metastatic disease; however, metastasis in two histological types, parosteal and periosteal, was infrequent. Survival analysis revealed the following were associated with poor outcomes: Sex, patients diagnosed between 1973 and 1982, distant metastasis, treatment without surgery or with radiation, a tumor with a poorly differentiated or undifferentiated grade, tumor size ≥100 mm, and a tumor in the pelvic bones. Patient's whose histologic type was parosteal osteosarcoma and whose tumor was located in one of the limbs, or who underwent local or radical excision, exhibited a good survival outcome. Survival outcomes were ranked according to the type of surgery, from best to worst, as follows: Local excision, radical excision, amputation and no surgery. In summary, the incidence of osteosarcoma is higher in male patients compared with female patients. Furthermore, individuals between the ages of 10 and 19 have a higher risk of osteosarcoma. Osteosarcoma located in the chest and pelvic bones has a high risk of metastasis. Limb-salvage surgery may be the optimal treatment approach for non-metastatic osteosarcoma.

Gene expression profiling of osteoblasts subjected to dexamethasone-induced apoptosis with/without GSK3ß-shRNA.

OBJECTIVE: Glucocorticoids (GCs)-induced osteoblast apoptosis has been identified as an important cause of GCs related osteonecrosis of the femoral head (ONFH). Glycogen synthase kinase 3ß (GSK3ß) has been proved to mediate dexamethasone (Dex)-induced osteoblast apoptosis. This study aimed to investigate the underlying mechanism of GSK3ß in Dex-induced osteoblast apoptosis. METHODS: Osteoblast cells were transfected with lentivirus expressing GSK3ß-shRNA, and a DNA microarray was performed to analyze gene expression after Dex treatment with or without GSK3ß-shRNA. Some differentially expressed genes were further validated by quantitative real-time-PCR (qRT-PCR). RESULTS: 460 genes were up-regulated (at least 2-fold) with Dex treatment but down-regulated (at least 2-fold) with GSK3ß-shRNA treatment. In addition, 315 genes were down-regulated (at least 2-fold) with Dex treatment but up-regulated (at least 2-fold) with GSK3ß-shRNA treatment. Among these genes, the apoptosis-related genes Hoxb8, Kif18a, Dock8, Dlk1, Tnfsf14, Casq2, Bcl2l14 and mechanosensation-related gene Piezo2 were selected for further qRT-PCR analysis. 7 of 8 genes (Piezo2, Hoxb8, Kif18a, Dlk1, Tnfsf14, Casq2, Bcl2l14) showed the same tendency between gene chip results and qRT-PCR results. The microarray data also showed that apoptotic pathway, MAPK pathway, TGFß pathway and Wnt pathway might be related to the mechanism of GSK3ß in Dex-induced osteoblast apoptosis. CONCLUSION: Our findings indicate that GSK3ß-shRNA treatment can alter various genes expression levels and change diverse signaling pathways involved in Dex-induced osteoblast apoptosis. Furthermore, Piezo2, Hoxb8, Kif18a, Dlk1, Tnfsf14, Casq2 and Bcl2l14 genes may play an important role in the GSK3ß-mediated osteoblast apoptosis process.

Sesamin Protects the Femoral Head From Osteonecrosis by Inhibiting ROS-Induced Osteoblast Apoptosis in Rat Model.

Glucocorticoids intake has become the most common pathogenic factor for osteonecrosis of the femoral head (ONFH). Annually, tens of millions of patients suffer from pain related to ONFH. Researchers have proposed several underlying mechanisms of ONFH, including osteocyte apoptosis, cell differentiation disorder, and angiogenesis hindrance. Sesamin, isolated from Sesamum indicum seeds, was reported could affect osteocyte inflammation and differentiation in osteoarthritis and osteoporosis. We investigated the underlying influence of sesamin on ONFH rat model. Fifteen male Sprague-Dawley rats were randomly divided into three groups. The ONFH model group only received the methylprednisolone (MPS) and lipopolysaccharide (LPS) injection to promote the development of ONFH. The sesamin treatment group was injected with sesamin, MPS, and LPS. The control group was untreated. Rats from above groups were sacrificed 4 weeks later. The effect of sesamin on ONFH rats was validated by H&E staining. TUNEL staining showed that femoral head necrosis was attenuated by sesamin. Furthermore, the phosphorylation of Akt was increased and the downstream cellular apoptosis signal pathway was inhibited. Intracellular ROS level was decreased after sesamin treatment. In conclusion, our findings suggest that sesamin protects the femoral head from osteonecrosis by inhibiting ROS-induced osteoblast apoptosis.