YOLO-Drone:Airborne real-time detection of dense small objects from high-altitude perspective

Unmanned Aerial Vehicles (UAVs), specifically drones equipped with remote sensing object detection technology, have rapidly gained a broad spectrum of applications and emerged as one of the primary research focuses in the field of computer vision. Although UAV remote sensing systems have the ability to detect various objects, small-scale objects can be challenging to detect reliably due to factors such as object size, image degradation, and real-time limitations. To tackle these issues, a real-time object detection algorithm (YOLO-Drone) is proposed and applied to two new UAV platforms as well as a specific light source (silicon-based golden LED). YOLO-Drone presents several novelties: 1) including a new backbone Darknet59; 2) a new complex feature aggregation module MSPP-FPN that incorporated one spatial pyramid pooling and three atrous spatial pyramid pooling modules; 3) and the use of Generalized Intersection over Union (GIoU) as the loss function. To evaluate performance, two benchmark datasets, UAVDT and VisDrone, along with one homemade dataset acquired at night under silicon-based golden LEDs, are utilized. The experimental results show that, in both UAVDT and VisDrone, the proposed YOLO-Drone outperforms state-of-the-art (SOTA) object detection methods by improving the mAP of 10.13% and 8.59%, respectively. With regards to UAVDT, the YOLO-Drone exhibits both high real-time inference speed of 53 FPS and a maximum mAP of 34.04%. Notably, YOLO-Drone achieves high performance under the silicon-based golden LEDs, with a mAP of up to 87.71%, surpassing the performance of YOLO series under ordinary light sources. To conclude, the proposed YOLO-Drone is a highly effective solution for object detection in UAV applications, particularly for night detection tasks where silicon-based golden light LED technology exhibits significant superiority

Extraction optimization of Eucommia ulmoides Oliver and its effect on bone quality in OVX rats

Purpose: To maximize the yield of extract from Eucommia ulmoides Oliver and its effect on bone quality. Methods: Different extraction indices were optimized with response surface methodology (RSM) for maximization of extract yield from Eucommia ulmoides Oliver. Box–Behnken design (BBD) was used to identify the effects of temperature, time, and liquid to solid ratio on extract yield from Eucommia ulmoides Oliver. After 4-week acclimatization, thiry-two rats were randomly assigned to 4 groups (n = 8): group 1 (sham) given vehicle only; group 2 (OVX rats given Eucommia ulmoides Oliver extract at a dose of 4 g/kg; group 3 (OVX + vehicle); group 4 (OVX + EUOE), i.e., OVX rats given Eucommia ulmoides Oliver extract (4 g/kg). Sham rats had intact ovaries. After surgery, the rats received gentamicin intramuscularly for 3 successive days. Two months after surgery, blood and trabecular bones was taken for analysis. Results: Temperature and liquid-to-solid ratio had marked impact on extract yield from Eucommia ulmoides Oliver, with the best conditions being temperature of 88 °C, time of 137 min, and liquid to solid ratio 16:1. Using these optimized conditions, the maximum yield of extract obtained experimentally (2.53%) was very close to the predicted value of 2.49 %. There was a good fit between the mathematical model evolved and the data on extract yield. The extract significantly (p < 0.01) increased the Ca and P and Cr levels in OVX + EUOE group compared to those in OVX control. Moreover, the extract significantly (p < 0.01) increased macro-mechanical indices of trabecular bone in OVX+EUOE group, relative to those in OVX control. Conclusion: The yield of Eucommia ulmoides Oliver extract has been successfully optimized using RSM. The extract exhibited strong effects on bone quality. Keywords: Optimization, Eucommia ulmoides, Box–Behnken design, Response surface methodology, Bone loss, Gen

A Novel Derivative of the Natural Product Danshensu Suppresses Inflammatory Responses to Alleviate Caerulein-Induced Acute Pancreatitis

Acute pancreatitis (AP), a common abdominal inflammatory disorder, is characterized by premature intracellular activation of digestive proteases within pancreatic acini and a consecutive systemic inflammatory response. Although the mechanism remains to be fully understood, inflammation is the main cause of pancreatic damage in AP. A novel compound [4-(2-acetoxy-3-((R)-3-(benzylthio)-1-methoxy-1-oxopropan-2-ylamino)-3-oxopropyl)-1,2-phenylene diacetate (DSC)], derived from danshensu, exhibits anti-inflammatory and anti-apoptotic properties in vitro. However, its potential beneficial effect in AP has not been demonstrated. This study aimed to investigate the effects and underlying mechanisms of DSC in experimental AP in mice. We found that DSC suppressed inflammatory responses in AP by inhibiting the activation of nuclear factor-κB (NF-κB), signal transducer and activator of transcription 3 (STAT3) and nucleotide-binding domain leucine-rich repeat containing family, pyrin domain-containing 3 (NLRP3) inflammasome. Furthermore, treatment with DSC modulated the infiltration of neutrophils and the phenotypes of macrophages in mice induced with AP. Interestingly, we found that the expression of nuclear factor-erythroid 2 related factor 2 (Nrf2) and its regulated antioxidant enzyme heme oxygenase-1 (HO-1), which modulate inflammatory activities, was significantly increased in DSC-treated groups. Together, our findings demonstrate that DSC alleviates pancreatic inflammation and damage in AP by inhibiting the activation of NF-κB, STAT3, and NLRP3 inflammasome and modulating immune cell responses

PRMT2 promotes dextran sulfate sodium-induced colitis by inhibiting SOCS3 via histone H3R8 asymmetric dimethylation

BACKGROUND AND PURPOSE: There is emerging evidence for critical roles of epigenetic modifiers in development of inflammatory bowel disease (IBD). Protein arginine methyltransferase 2 (PRMT2) is responsible for methylation of arginine residues on histones and targets transcription factors critically involved in many cellular processes, including gene transcription, mRNA splicing, cell proliferation and differentiation. However, its role in colitis remains unknown. In this study, the role and underlying mechanisms of PRMT2 in colitis was studied. EXPERIMENTAL APPROACH: A mouse dextran sulfate sodium (DSS)-induced experimental colitis model was applied to study PRMT2 in colitis. Lentivirus induced PRMT2 silencing or overexpression in vivo was applied to address the role of PRMT2 in colitis. Detailed western blot and expression analysis was done to understand epigenetic changes induced by PRMT2 in colitis. KEY RESULTS: PRMT2 is highly expressed in patients with IBD, inflamed colon of mice and TNF-α stimulated mice gut epithelial cells. PRMT2 overexpression aggravates while knockdown alleviates DSS-induced colitis in mice, suggesting that PRMT2 is a pivotal mediator of colitis development. Mechanistically, PRMT2 mediates colitis by increasing repressive histone mark H3R8 asymmetric methylation (H3R8me2a) at the promoter region of the suppressor of cytokine signaling 3 (SOCS3) promoter. Resultant inhibition of SOCS3 expression and SOCS3-mediated degradation of TNF receptor associated factor 5 (TRAF5) via ubiquitination led to elevated TRAF5 expression and TRAF5-mediated downstream NF-κB/MAPK activation. CONCLUSION AND IMPLICATIONS: Our study demonstrates that PRMT2 acts as a transcriptional co-activator for proinflammatory genes during colitis. Hence targeting PRMT2 may provide a novel therapeutic approach for colitis

Identification of key genes responsible for green and white colored spathes in Anthurium andraeanum (Hort.)

Modern anthuriums, Anthurium andraeanum (Hort.) are among the most popular flowering plants and widely used for interior decoration. Their popularity is largely attributed to the exotic spathes with different colors. Previous studies have reported color development in red spathe cultivars, but limited information is available on key genes regulating white and green colored spathes. This study analyzed anthocyanin, chlorophyll, and carotenoid contents as well as transcript differences in spathes of eight cultivars that differed in spathe colors ranging from red to white and green. Results showed that increased expression of a transcription factor AaMYB2 was associated with elevated levels of anthocyanin in spathes, but decreased expression of AaMYB2 and increased expression of AaLAR (leucoanthocyanidin reductase) and AaANR (anthocyanidin reductase) were accompanied with the accumulation of colorless proanthocyanidin, thus the white spathe. As to the green colored spathe, chlorophyll content in the green spathe cultivar was substantially higher than the other cultivars. Correspondingly, transcripts of chlorophyll biosynthesis-related genes AaHemB (porphobilinogen synthase) and AaPor (protochlorophyllide oxidoreductase) were highly upregulated but almost undetectable in white and red spathes. The increased expression of AaHemB and AaPor was correlated with the expression of transcription factor AaMYB124. Subsequently, qRT-PCR analysis confirmed their expression levels in nine additional cultivars with red, white, and green spathes. A working model for the formation of white and green spathes was proposed. White colored spathes are likely due to the decreased expression of AaMYB2 which results in increased expression of AaLAR and AaANR, and the green spathes are attributed to AaMYB124 enhanced expression of AaHemB and AaPor. Further research is warranted to test this working model

The anti-microbial peptide LL-37/CRAMP levels are associated with acute heart failure and can attenuate cardiac dysfunction in multiple preclinical models of heart failure

Rationale: Biomarkers for the diagnosis of heart failure (HF) are clinically essential. Circulating antimicrobial peptides LL-37 has emerged as a novel biomarker in cardiovascular disease, however, its relevance as a biomarker for acute HF are undetermined. Methods: Acute HF patients were enrolled in this study and the serum levels of LL-37/CRAMP (cathelicidin-related antimicrobial peptide) were measured by ELISA. The receiver-operator characteristic (ROC) curve was used to determine if serum LL-37 could be a biomarker for acute HF. Mouse CRAMP (mCRAMP, mouse homolog for human LL-37) was also determined in both heart and serum samples of, transverse aortic constriction (TAC)- and isoproterenol (ISO)-induced HF mice models, and phenylephrine (PE) and angiotensin II (AngII)-induced neonatal mouse cardiomyocytes (NMCMs) hypertrophic models, both intracellular and secreted, by ELISA. The protective effects of mCRAMP were determined in TAC, ISO, and AngII-induced HF in mice while whether HF was exacerbated in AngII-infused animals were checked in mCRAMP knockout mice. The underlying mechanism for protective effects of CARMP in pathological hypertrophy was determined by using a NF-κB agonist together with rCRAMP (rat homolog for human LL-37) in AngII or PE treated neonatal rat cardiomyocytes (NRCMs). Results: Serum levels of LL-37 were significantly decreased in acute HF patients (area under the curve (AUC) of 0.616), and negatively correlated with NT-proBNP. We further confirmed that mCRAMP was decreased in both heart and serum samples of TAC- and ISO-induced HF mice models. Moreover, in PE and AngII-induced NMCMs hypertrophic models, both intracellular and secreted mCRAMP levels were reduced. Functionally, mCRAMP could attenuate TAC, ISO, and AngII-induced HF in mice while CRAMP deficiency exacerbated HF. Mechanistically, the anti-hypertrophy effects of CRAMP were mediated by NF-κB signaling. Conclusions: Collectively, serum LL-37 is associated with acute HF and increasing CRAMP is protective against deleterious NF-κB signaling in the rodent

The association between a body shape index and elevated urinary albumin–creatinine ratio in Chinese community adults

BackgroundObesity, especially visceral obesity, seems to be one of the most decisive risk factors for chronic kidney disease. A Body Shape Index (ABSI) is an emerging body size measurement marker of visceral obesity. This study aimed to explore whether ABSI is associated with albuminuria in Chinese community adults.MethodsThis cross-sectional study enrolled 40,726 participants aged 40 or older from seven provinces across China through a cluster random sampling method. ABSI was calculated by body mass index, waist circumference, and height. Increased albuminuria was defined as urinary albumin–creatinine ratio (UACR) ≥ 30 mg/g, indicating kidney injury. For ABSI, we divided it by quartile cutoff points and tried to determine the association between ABSI levels and UACR by multiple regression analysis. DAG (Directed Acyclic Graph) was plotted using literature and expert consensus to identify potential confounding factors.ResultsThe average age of subjects with elevated UACR was 61.43 ± 10.07, and 26% were men. The average age of subjects with normal UACR was 57.70 ± 9.02, and 30.5% were men. Multiple logistic regression analysis was conducted and demonstrated that the ABSI quartiles were related to elevated UACR positively (OR [95% CI] Q2 vs. Q1: 1.094 [1.004, 1.197]; OR [95% CI] Q3 vs. Q1: 1.126 [1.030, 1.231]; OR [95% CI] Q4 vs. Q1: 1.183 [1.080, 1.295], p for trend < 0.001) after adjustments for confounding factors. The stratified analysis further showed that with the mounting for ABSI levels, elevated UACR more easily occurred in the people characterized by the elderly, men, and hypertension.ConclusionsIn Chinese community adults, people with higher ABSI levels can be deemed as high-risk individuals with UACR elevation, and it will be beneficial for them to lose weight and significantly reduce visceral fat

Solid Tumor-Targeted Infiltrating Cytotoxic T Lymphocytes Retained by a Superantigen Fusion Protein

Successful immune-mediated regression of solid tumors is difficult because of the small number of cytotoxic T lymphocytes (CTLs) that were traffic to the tumor site. Here, the targeting of tumor-specific infiltrating CTLs was dependent on a fusion protein consisting of human epidermal growth factor (EGF) and staphylococcal enterotoxin A (SEA) with the D227A mutation. EGF-SEA strongly restrained the growth of murine solid sarcoma 180 (S180) tumors (control versus EGF-SEA, mean tumor weight: 1.013 versus 0.197 g, difference  = 0.816 g). In mice treated with EGF-SEA, CD4+, CD8+ and SEA-reactive T lymphocytes were enriched around the EGFR expressing tumor cells. The EGF receptors were potentially phosphorylated by EGF-SEA stimulation and the fusion protein promoted T cells to release the tumoricidal cytokines interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α). Intratumoral CTLs secreted cytolytic pore-forming perforins and granzyme B proteins near the surface of carcinomas, causing the death of many tumor cells. We additionally show that labeled EGF-SEA was directly targeted to the tumor tissue after intravenous (i.v.) injection. The findings demonstrate that antibody-like EGF-SEA plays an important role in arresting CTLs in the solid tumor site and has therapeutic potential as a tumor-targeting agent

Modification effect of changes in cardiometabolic traits in association between kidney stones and cardiovascular events

BackgroundsWhether longitudinal changes in metabolic status influence the effect of kidney stones on cardiovascular disease (CVD) remains unclarified. We investigated the modification effect of status changes in metabolic syndrome (MetS) in the association of kidney stones with risk of incident CVD events.MethodsWe performed a prospective association and interaction study in a nationwide cohort including 129,172 participants aged ≥ 40 years without CVDs at baseline and followed up for an average of 3.8 years. Kidney stones information was collected by using a questionnaire and validated by medical records. The repeated biochemical measurements were performed to ascertain the metabolic status at both baseline and follow-up.Results4,017 incident total CVDs, 1,413 coronary heart diseases (CHDs) and 2,682 strokes were documented and ascertained during follow-up. Kidney stones presence was significantly associated with 44%, 70% and 31% higher risk of CVDs, CHDs and stroke, respectively. The stratified analysis showed significant associations were found in the incident and sustained MetS patients, while no significant associations were found in the non-MetS at both baseline and follow-up subjects or the MetS remission ones, especially in women. For the change status of each single component of the MetS, though the trends were not always the same, the associations with CVD were consistently significant in those with sustained metabolic disorders, except for the sustained high blood glucose group, while the associations were consistently significant in those with incident metabolic disorders except for the incident blood pressure group. We also found a significant association of kidney stone and CVD or CHD risk in the remain normal glucose or triglycerides groups; while the associations were consistently significant in those with incident metabolic disorders except for the incident blood pressure group. We also found a significant association of kidney stone and CVD or CHD risk in the remain normal glucose or triglycerides groups.ConclusionsA history of kidney stones in women with newly developed MetS or long-standing MetS associated with increased risk of CVD. The mechanisms link kidney stones and CVD risk in the metabolic and non-metabolic pathways were warranted for further studies

The Relative Body Weight Gain From Early to Middle Life Adulthood Associated With Later Life Risk of Diabetes: A Nationwide Cohort Study

AimTo determine the effect of decade-based body weight gain from 20 to 50 years of age on later life diabetes risk.Methods35,611 non-diabetic participants aged ≥ 50 years from a well-defined nationwide cohort were followed up for average of 3.6 years, with cardiovascular diseases and cancers at baseline were excluded. Body weight at 20, 30, 40, and 50 years was reported. The overall 30 years and each 10-year weight gain were calculated from the early and middle life. Cox regression models were used to estimate risks of incident diabetes.ResultsAfter 127,745.26 person-years of follow-up, 2,789 incident diabetes were identified (incidence rate, 2.18%) in 25,289 women (mean weight gain 20-50 years, 7.60 kg) and 10,322 men (7.93 kg). Each 10-kg weight gain over the 30 years was significantly associated with a 39.7% increased risk of incident diabetes (95% confidence interval [CI], 1.33-1.47); weight gain from 20-30 years showed a more prominent effect on the risk of developing diabetes before 60 years than that of after 60 years (Hazard ratio, HR = 1.084, 95% CI [1.049-1.121], P <0.0001 vs. 1.015 [0.975-1.056], P = 0.4643; PInteraction=0.0293). It showed a stable effect of the three 10-year intervals weight gain on risk of diabetes after 60 years (HR=1.055, 1.038, 1.043, respectively, all P < 0.0036).ConclusionsThe early life weight gain showed a more prominent effect on developing diabetes before 60 years than after 60 years; however, each-decade weight gain from 20 to 50 years showed a similar effect on risk developing diabetes after 60 years