HRST: An Improved HRNet for Detecting Joint Points of Pigs.

The body size of pigs is a vital evaluation indicator for growth monitoring and selective breeding. The detection of joint points is critical for accurately estimating pig body size. However, most joint point detection methods focus on improving detection accuracy while neglecting detection speed and model parameters. In this study, we propose an HRNet with Swin Transformer block (HRST) based on HRNet for detecting the joint points of pigs. It can improve model accuracy while significantly reducing model parameters by replacing the fourth stage of parameter redundancy in HRNet with a Swin Transformer block. Moreover, we implemented joint point detection for multiple pigs following two steps: first, CenterNet was used to detect pig posture (lying or standing); then, HRST was used for joint point detection for standing pigs. The results indicated that CenterNet achieved an average precision (AP) of 86.5%, and HRST achieved an AP of 77.4% and a real-time detection speed of 40 images per second. Compared with HRNet, the AP of HRST improved by 6.8%, while the number of model parameters and the calculated amount reduced by 72.8% and 41.7%, respectively. The study provides technical support for the accurate and rapid detection of pig joint points, which can be used for contact-free body size estimation of pigs.

Th17, rather than Th1 cell proportion, is closely correlated with elevated disease severity, higher inflammation level, and worse prognosis in sepsis patients.

OBJECTIVE: The current study aimed to investigate the prognostic value of T helper (Th) 1 and Th17 proportions in sepsis patients. METHODS: Th1 and Th17 cells in blood CD4+ T cells were detected by flow cytometry in 210 sepsis patients and 100 healthy controls (HCs). Besides, serum interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α), and interleukin-17 (IL-17) levels in the enrolled sepsis patients were determined with enzyme-linked immunosorbent assay. RESULTS: Compared with HCs, Th1 and Th17 proportions were elevated in sepsis patients (both p < .001). Meanwhile, Th1 proportion was strongly correlated with IFN-γ (p < .001, r = .484) but weakly correlated with TNF-α (p = .024, r = .156) and IL-17 (p = .002, r = .212), while Th17 proportion showed faint correlation with IFN-γ (p = .015, r = .168), but strong correlations with TNF-α (p < .001, r = .602) and IL-17 (p < .001, r = .498) in sepsis patients. Besides, Th1 proportion was weakly associated with APACHE II score (p = .030, r = .150), but Th17 proportion was closely associated with APACHE II score (p < .001, r = .322) and SOFA score (p < .001, r = .337) in sepsis patients. Regarding their prognostic value, Th1 proportion (p = .042) was slightly, while Th17 proportion (p < .001) was dramatically, increased in septic deaths compared with survivors, and Th17 possessed good predictive value for 28-day mortality risk (AUC: 0.748, 95% CI: 0.659-0.836). CONCLUSION: Th1 and Th17 proportions are elevated in sepsis patients compared with HCs, and Th17 proportion is correlated with increased disease severity, higher inflammation level, and worse prognosis in sepsis patients.

Clinical Course and Mortality of Stroke Patients With Coronavirus Disease 2019 in Wuhan, China.

BACKGROUND AND PURPOSE: No studies have reported the effect of the coronavirus disease 2019 (COVID-19) epidemic on patients with preexisting stroke. We aim to study the clinical course of COVID-19 patients with preexisting stroke and to investigate death-related risk factors. METHODS: We consecutively included 651 adult inpatients with COVID-19 from the Central Hospital of Wuhan between January 2 and February 15, 2020. Data on the demography, comorbidities, clinical manifestations, laboratory findings, treatments, complications, and outcomes (ie, discharged or death) of the participants were extracted from electronic medical records and compared between patients with and without preexisting stroke. The association between risk factors and mortality was estimated using a Cox proportional hazards regression model for stroke patients infected with severe acute respiratory syndrome coronavirus 2. RESULTS: Of the 651 patients with COVID-19, 49 with preexisting stroke tended to be elderly, male, had more underlying comorbidities and greater severity of illness, prolonged length of hospital stay, and greater hospitalization expenses than those without preexisting stroke. Cox regression analysis indicated that the patients with stroke had a higher risk of developing critical pneumonia (adjusted hazard ratio, 2.01 [95% CI, 1.27-3.16]) and subsequent mortality (adjusted hazard ratio, 1.73 [95% CI, 1.00-2.98]) than the patients without stroke. Among the 49 stroke patients, older age and higher score of Glasgow Coma Scale or Sequential Organ Failure Assessment were independent risk factors associated with in-hospital mortality. CONCLUSIONS: Preexisting stroke patients infected with severe acute respiratory syndrome coronavirus 2 were readily predisposed to death, providing an important message to individuals and health care workers that preventive measures must be implemented to protect and reduce transmission in stroke patients in this COVID-19 crisis.

Co-expression of Mcl-1 and Bak induces mitochondrial swelling.

We here used fluorescence imaging to explore the effect of co-overexpression of Mcl-1 and Bak/BH3-only proteins on mitochondrial morphology. The cells co-expressing CFP-Mcl-1 and YFP-Bak/BimL/Puma/tBid showed co-localization of Mcl-1 with Bak/Puma/BimL/tBid and also showed the inhibitory action of Mcl-1 on the Bak-, BimL-, Puma- or tBid-mediated cell death. Co-expression of Mcl-1 and Bak but not BH3-only proteins induced time-dependent mitochondrial swelling. Fluorescence resonance energy transfer (FRET) imaging proved the direct binding of Mcl-1 to Bak, BimL, Puma and tBid, respectively. In addition, Mcl-1 prevented Bak oligomerization by retrotranslocating Bak from mitochondria into cytoplasm. Moreover, Mcl-1-Bak complex exhibited a good co-localization with mitochondria, and co-expression of Mcl-1 and Bak for more than 24 h not only induced mitochondrial swelling but also impaired mitochondrial membrane potential. Collectively, co-expression of Mcl-1 and Bak but not BH3-only proteins significantly induced mitochondrial swelling and subsequent loss of mitochondrial membrane potential.

Serum Cystatin C and Coronavirus Disease 2019: A Potential Inflammatory Biomarker in Predicting Critical Illness and Mortality for Adult Patients.

This study aimed at determining the relationship between baseline cystatin C levels and coronavirus disease 2019 (COVID-19) and investigating the potential prognostic value of serum cystatin C in adult patients with COVID-19. 481 patients with COVID-19 were consecutively included in this study from January 2, 2020, and followed up to April 15, 2020. All clinical and laboratory data of COVID-19 patients with definite outcomes were reviewed. For every measure, COVID-19 patients were grouped into quartiles according to the baseline levels of serum cystatin C. The highest cystatin C level was significantly related to more severe inflammatory conditions, worse organ dysfunction, and worse outcomes among patients with COVID-19 (P values < 0.05). In the adjusted logistic regression analyses, the highest cystatin C level and ln-transformed cystatin C levels were independently associated with the risks of developing critically ill COVID-19 and all-cause death either in overall patients or in patients without chronic kidney disease (P values < 0.05). As a potential inflammatory marker, increasing baseline levels of serum cystatin C might independently predict adverse outcomes for COVID-19 patients. Serum cystatin C could be routinely monitored during hospitalization, which showed clinical importance in prognosticating for adult patients with COVID-19.

Clinical analysis of central venous catheter-related infections in patients in the emergency ICU.

BACKGROUND: Catheter-related infection (CRI) of the central vein is a common cause of nosocomial infection. This study was undertaken to investigate the pathogen culturing and risk factors of CRI in emergency intensive care unit (EICU) in order to provide the beneficial reference. METHODS: From January 2008 to December 2010, a total of 1 363 patients were subjected to catheterization. In these patients, the peak CRI rate of the patients was determined by bacterial cultivation and blood bacterial cultivation. RESULTS: CRI happened in 147 of the 1 363 patients using the central venous catheter. The peak rate of CRI was 10.79%, with an incidence of 3.05 episodes per 1 000 catheter days. Of the 147 patients, 46.94% had gram-negative bacilli, 40.14% had gram-positive cocci, and 12.92% had fungi. Unconditional logistic regression analysis suggests that multiple catheterization, femoral vein catheterization, the application of multicavity catheter, and the duration of catheterization were the independent risk factors for CRI. CONCLUSION: The risk factors for catheter-related infections should be controlled to prevent the occurrence of nosocomial infection.

Rosiglitazone enhances the proliferation of neural progenitor cells and inhibits inflammation response after spinal cord injury.

It has been previously shown that peroxisome proliferators-activated receptor gamma (PPAR-γ) is beneficial for nervous system injury. In present study, we examined the effect of rosiglitazone, a PPAR-γ agonist, on spinal cord injury (SCI) in rats. SCI was induced by dropping a 10g weight rod at a height of 25mm. The animals were randomly divided into vehicle group, rosiglitazone treated group, and G3335 treated group. Locomotor function recovery was evaluated by the Basso-Beattie-Bresnahan locomotor rating scale (BBB scale), NF-κB expression and endogenous neural progenitor cells (NPCs) proliferation and differentiation was assessed by flow cytometry and immunohistochemistry. Compared with the vehicle groups, we found that the rosiglitazone could significantly ameliorate locomotor recovery, reduce NF-κB expression, and increase the proliferation of endogenous NPCs. when the PPAR-γ antagonist was use, these effects were abolished. However, neurons differentiating from endogenous NPCs were inhibited when PPAR-γ was activated. Our results suggest that the activation of PPAR-γ may be a potential alternative treatment for spinal cord injury.

[Arsenite removal performance by modified GAC].

Two kinds of Fe-Mn oxide impregnated GAC (FM-GAC-1, FM-GAC-2) were prepared and their arsenite removal performance were studied. The adsorption isotherm and reaction kinetic models of arsenite on the two kinds of modified GAC and influence of solution pH, temperature and co-exist anions were investigated in the study. The results showed FM-GAC-1 and FM-GAC-2 can adsorb arsenite effectively, the adsorption capacities were 32.37 mg x g(-1) and 26.67 mg x g(-1) respectively. The adsorb velocity could be predicted well by applying pseudosecond order rate equation and the chemistry reaction process was the limitation of the reaction for both modified GAC. The lower solution pH was benefit to the removal of arsenite. The adsorption capacity of FM-GAC-1 and FM-GAC-2 decreased with temperature increasing. The adsorption processes were spontaneous heat-discharge processes. Some co-exist anions can influence arsenite adsorption on modified GAC when their concentration were 200 times of arsenite. It was found that SiO3(2-), PO3(2-), NO3(-) had a significant negative influence on arsenite removal by FM-GAC-1 and SiO3(2-), CO3(2-) can markedly decrease arsenite adsorption on FM-GAC-2. As a whole, FM-GAC-1 had better arsenite removal performance than FM-GAC-2.