Diagnostic and prognostic significance of apelin-13, APJ for sepsis in the emergency department: A prospective study.

Objectives: This study aimed to assess the diagnostic, risk stratification, and prognostic capabilities of apelin-13 and APJ in comparison to procalcitonin (PCT) for septic patients presenting to the emergency department (ED). Methods: Two hundred and thirty-eight patients meeting the Third International Consensus Definition (Sepsis-3) criteria were enrolled from Beijing Chaoyang Hospital's ED, along with a control group of forty healthy individuals. Patients were categorized into two groups based on disease severity: those with sepsis or septic shock. Plasma levels of apelin-13, CD4+ Th cells, and PCT were measured. The expression levels of plasma APJ mRNA were quantified using real-time fluorescence quantitative PCR (RT-qPCR) methodology. The Sequential Organ Failure Assessment (SOFA) score was determined at the time of enrollment. The prognostic values of apelin-13 and APJ was evaluated in comparison to that of PCT and the SOFA score. All patients were followed up for a duration of 28 days. Results: The plasma concentrations of apelin-13 and APJ exhibited a positive correlation with the severity of sepsis, while the number of CD4+ T cells decreased in septic patients. The areas under the receiver operating characteristic (AUC) curves for apelin-13 and APJ in the diagnosis and prediction of 28-day mortality were greater than that of PCT. In non-survivors at the 28-day follow-up, the plasma levels of apelin-13 and APJ were significantly higher compared to survivors. Furthermore, apelin-13 levels were notably higher in cases of sepsis-induced cardiomyopathy (SICM) than in those without SICM. Apelin-13 and APJ emerged as independent predictors of 28-day mortality among septic patients. Conclusions: Apelin-13 and APJ demonstrate value in the assessment of risk stratification, early diagnosis, and prognosis of sepsis in the ED. Apelin-13 also proves to be an effective biomarker for assessing the prognosis of SICM in the ED. Sepsis may lead to immune function suppression.

Persistent high sepsis-induced coagulopathy and sequential organ failure assessment scores can predict the 28-day mortality of patients with sepsis: A prospective study.

BACKGROUND: The performance of the sepsis-induced coagulopathy (SIC) and sequential organ failure assessment (SOFA) scores in predicting the prognoses of patients with sepsis has been validated. This study aimed to investigate the time course of SIC and SOFA scores and their association with outcomes in patients with sepsis. METHODS: This prospective study enrolled 209 patients with sepsis admitted to the emergency department. The SIC and SOFA scores of the patients were assessed on days 1, 2, and 4. Patients were categorized into survivor or non-survivor groups based on their 28-day survival. We conducted a generalized estimating equation analysis to evaluate the time course of SIC and SOFA scores and the corresponding differences between the two groups. The predictive value of SIC and SOFA scores at different time points for sepsis prognosis was evaluated. RESULTS: In the non-survivor group, SIC and SOFA scores gradually increased during the first 4 days (P < 0.05). In the survivor group, the SIC and SOFA scores on day 2 were significantly higher than those on day 1 (P < 0.05); however, they decreased on day 4, dropping below the levels observed on day 1 (P < 0.05). The non-survivors showed higher SIC scores on days 2 (P < 0.05) and 4 (P < 0.001) than the survivors, whereas no significant differences were found between the two groups on day 1 (P > 0.05). The performance of SIC scores on day 4 for predicting mortality was more accurate than that on day 2, with areas under the curve of 0.749 (95% confidence interval [CI]: 0.674-0.823), and 0.601 (95% CI: 0.524-0.679), respectively. The SIC scores demonstrated comparable predictive accuracy for 28-day mortality to the SOFA scores on days 2 and 4. Cox proportional hazards models indicated that SIC on day 4 (hazard ratio [HR] = 3.736; 95% CI: 2.025-6.891) was an independent risk factor for 28-day mortality. CONCLUSIONS: The time course of SIC and SOFA scores differed between surviving and non-surviving patients with sepsis, and persistent high SIC and SOFA scores can predict 28-day mortality.

The Role of AGGF1 in the Classification and Evaluating Prognosis of Adult Septic Patients: An Observational Study.

Purpose: Angiogenic factor with G patch and FHA domains 1 (AGGF1) is a crucial angiogenic factor that is involved in a variety of diseases and in the regulation of inflammatory responses. However, its role in sepsis is poorly understood. We have investigated the role of AGGF1 in the classification and prognostic evaluation of adult septic patients in a clinical context. Patients and Methods: A total of 126 septic patients who visited the Emergency Department of Beijing Chao-Yang Hospital and 76 non-sepsis patients visiting the Physical Examination Center of Beijing Chao-Yang Hospital were enrolled. AGGF1 levels in plasma were detected by enzyme-linked immunosorbent assay. Spearman correlation analysis was used to determine correlations between plasma AGGF1 and Sequential Organ Failure Assessment (SOFA) score, Acute Pathology and Chronic Health Evaluation II (APACHE II) score, procalcitonin and lactate. We evaluated the classification significance of AGGF1 in sepsis using receiver operating characteristic (ROC) curves. We also assessed the predictive significance of AGGF1 for 28-day mortality in sepsis using ROC curves and Kaplan-Meier analyses. Results: Plasma AGGF1 levels were higher in sepsis patients than in non-sepsis patients (P < 0.001). Among sepsis patients, plasma AGGF1 levels were higher in non-survivors than in survivors (P < 0.001). Increased plasma AGGF1 levels were positively correlated with SOFA score, APACHE II score, procalcitonin and lactate. Plasma AGGF1 levels could distinguish sepsis patients from non-sepsis patients (area under the curve [AUC] = 0.777). AGGF1 had a higher predictive value than SOFA score, APACHE II score, lactate, procalcitonin, and white blood cell count for 28-day mortality in patients with sepsis (AUC = 0.876). Furthermore, Kaplan-Meier analysis indicated that lower plasma AGGF1 levels were associated with lower 28-day mortality compared with higher plasma AGGF1 levels (log rank P < 0.001). Conclusion: AGGF1 is useful for the classification and evaluating prognosis of adult septic patients.

ACE2 Rescues Sepsis-Associated Encephalopathy by Reducing Inflammation, Oxidative Stress, and Neuronal Apoptosis via the Nrf2/Sestrin2 Signaling Pathway.

Neuroinflammation and oxidative stress contribute to the progression of sepsis-associated encephalopathy (SAE). Angiotensin-converting enzyme 2 (ACE2) is considered to be a neuroprotective factor due to its anti-inflammatory and antioxidant properties. However, the role of ACE2 on myeloid cells in regulating SAE and the underlying mechanism warrants further exploration. SAE was induced in ACE2 transgenic (TG), knockout (KO), and bone marrow (BM) chimeric mice by cecal ligation and puncture (CLP). The expression levels of apoptosis-, oxidation- and neuroinflammation-associated mediators and morphological changes were monitored by quantitative real-time PCR analyses and histological examinations in the cortex of septic mice. The contents of angiotensin (Ang) II and Ang-(1-7) along with the activity of ACE2 were examined with commercial kits. The expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and Sestrin2 was detected by immunoblotting analysis. Our results indicated that the expression of cortical ACE2 was significantly reduced in the early phase of CLP-induced sepsis. Moreover, ACE2 overexpression in TG mice conferred neuroprotection against sepsis, as evidenced by alleviated neuronal apoptosis, oxidative stress, and proinflammatory M1-like microglial polarization, accompanied by upregulation of the Ang-(1-7), Nrf2, and Sestrin2 protein levels. Conversely, ACE2 deficiency in KO mice exacerbated SAE. The neuroprotective effects of ACE2 were further confirmed in wild-type mice transplanted with ACE2-TG and KO BM cells. Therefore, our data suggest that myeloid ACE2 exerts a protective role in the pathogenesis of SAE, potentially by activating Ang-(1-7)-Nrf2/sestrin2 signaling pathway, and highlight that upregulating ACE2 expression and activity may represent a promising approach for the treatment of SAE in patients with sepsis.

ACE2 Expressed on Myeloid Cells Alleviates Sepsis-Induced Acute Liver Injury via the Ang-(1-7)-Mas Receptor Axis.

Sepsis-induced acute liver injury (ALI) is common in intensive care units. Angiotensin-converting enzyme 2 (ACE2) plays a vital role in hepatic fibrosis and steatosis; however, its role in sepsis-induced ALI remains unclear. This study found that hepatic ACE2 expression in cecal ligation and puncture (CLP)-treated mice significantly decreased 24 h after CLP. ACE2-transgenic (TG) mice exhibited a significant improvement in CLP-induced ALI, accompanied by the inhibition of hepatocyte apoptosis, oxidative stress, and inflammation, while ACE2-knockout mice demonstrated an opposite trend. During sepsis-induced ALI, ACE2-TG could also elevate the Ang-(1-7) and Mas receptor (MasR) levels in liver tissues. Interestingly, the MasR inhibitor A779 abrogated the favorable effects of ACE2 on CLP-induced ALI. In a bone marrow transplantation experiment, the ACE2-TG transplantation group showed significantly improved inflammation and liver dysfunction, less hepatocyte apoptosis, and reduced oxidative stress after CLP compared with the wild-type transplantation group. In contrast, the ACE2-knockout group showed poor inflammatory response and liver dysfunction, significantly more hepatocyte apoptosis, and elevated oxidative stress than the wild-type transplantation group after CLP. ACE2 protects against sepsis-induced ALI by inhibiting hepatocyte apoptosis, oxidative stress, and inflammation via the Ang-(1-7)-Mas receptor axis. Thus, targeting ACE2 may be a promising novel strategy for preventing and treating sepsis-induced ALI.

Acute muscle wasting is associated with poor prognosis in older adults with severe community-acquired pneumonia.

PURPOSE: To investigate the impact of acute muscle wasting on 90-day mortality in older patients with severe pneumonia using ultrasound and chest computed tomography (CT). METHODS: Quadriceps muscle layer thickness was measured via ultrasound on days 1, 7, and 14, and cross-sectional area of the erector spinae muscle was assessed using chest CT on days 1 and 14 in patients aged ≥ 65 years old. The primary outcome was all-cause 90-day mortality. Receiver operating characteristic curves were conducted for muscle loss to predict 90-day mortality. Cox proportional hazard models and Kaplan-Meier survival curves were employed to evaluate the association between muscle loss and 90-day mortality. RESULTS: Sixty-two patients were enrolled with median age of 80.2 years, 29 (46.8%) were men and 28 (45.2%) patients died. Muscle mass measured using ultrasound and CT decreased significantly from baseline to day 14 in the non-survivor group. Muscle loss assessed by ultrasound (with minimum and maximum pressure) and CT independently predicted all-cause 90-day mortality (adjusted hazard ratios = 1.497, 1.400 and 1.082; P < 0.001, P = 0.002, and P = 0.004; respectively), and cutoff values of muscle loss were 0.34 cm, 0.11 cm and 4.92 cm2, correspondingly. A higher muscle loss had an increased risk of 90-day mortality. CONCLUSIONS: Acute muscle wasting assessed by ultrasound and chest CT persisted for 14 days and was an independent predictor of adverse outcomes in older patients with severe pneumonia. A greater decline in muscle mass was associated with a higher 90-day mortality risk.

PD-L1 Blockade Improves Survival in Sepsis by Reversing Monocyte Dysfunction and Immune Disorder.

Monocyte dysfunction is critical to sepsis-induced immunosuppression. Programmed death ligand-1 (PD-L1) has shown a close relationship with inflammatory disorder among animal models and patients. We aimed to investigate the potential beneficial immunologic mechanisms of anti-PD-L1 on monocyte dysfunction of mice with sepsis. Firstly, we assessed the potential association between PD-L1 expression on monocyte subsets and sepsis severity as well as 28-day mortality. In this study, 52 septic patients, 28 septic shock patients, and 40 healthy controls were enrolled and their peripheral whole blood was examined by flow cytometry. Then, cecal ligation and puncture (CLP) were performed for establishing the mouse sepsis model. Subsequently, effects of anti-PD-L1 antibody on monocyte subset, major histocompatibility complex II (MHC II) expression, cytokine production, and survival were investigated. PD-L1 expression on the classical monocytes (CD14 + + CD16 -) was significantly upregulated among septic shock patients and the 28-day death group than non-septic shock group and 28-day survival group (P < 0.05). Compared to septic mice, anti-PD-L1-treated mice had significantly elevated percentages of major histocompatibility complex (MHC) II on peripheral Ly6chi monocyte at 24 h after CLP. Our results showed that the anti-PD-L1 antibody markedly decreased the level of serum inflammatory cytokines interleukin (IL)-6, tumor necrosis factor (TNF)-α, and IL-10 in sepsis mice at 24 h, 48 h, and 72 h, respectively (P < 0.05). The survival rate of CLP mice was significantly improved by anti-PD-L1 antibody treatment. Classical monocytes with high expression of PD-L1 were thought to be connected with sepsis progression. The PD-L1 blockade protects from sepsis, at least partially by inhibiting the reversal of monocyte dysfunction.

ACE2 activation alleviates sepsis-induced cardiomyopathy by promoting MasR-Sirt1-mediated mitochondrial biogenesis.

Sepsis-induced cardiomyopathy (SIC), caused by a dysregulated host response to infection, is a major contributor to high mortality. Angiotensin-converting enzyme 2 (ACE2), a crucial component of the renin-angiotensin system (RAS), has protective effects against several cardiovascular diseases, such as myocardial infarction and heart failure. However, the role of ACE2 in the pathogenesis of SIC and underlying mechanisms remain unknown. The present study was designed to examine the effects of ACE2 activation or inhibition on SIC in C57BL/6 mice. The ACE2 activator diminazene aceturate (DIZE) and ACE2 inhibitor MLN-4760 were applied for treatment. Myocardial function, inflammatory response, oxidative stress, apoptosis and mitochondrial biogenesis were investigated. Major assays were echocardiography, H&E staining, immunofluorescence staining, DHE staining, TUNEL staining, Western blot, qPCR analysis, ELISA and corresponding kits. We confirmed that ACE2 was markedly downregulated in septic heart tissues. Pharmacological activation of ACE2 by DIZE ameliorated cecal ligation puncture (CLP)-induced mortality, cardiac dysfunction, inflammatory response, oxidative stress and the cardiomyocyte apoptosis by promoting MasR-Sirt1-mediated mitochondrial biogenesis. In contrast, SIC was aggravated via inhibiting MasR-Sirt1-mediated mitochondrial biogenesis by the use of ACE2 inhibitor MLN-4760. Consequently, activation of ACE2 may protect against SIC by promoting MasR-Sirt1-mediated mitochondrial biogenesis.

Reduced IgG2 with thrombocytopenia predicts mortality in patients with influenza pneumonia.

BACKGROUND: Thrombocytopenia is a common disorder during influenza that is related to high mortality. OBJECTIVES: A prospective study was performed to investigate the association of immunoglobulin subclass changes accompanying incident thrombocytopenia with clinical outcomes in patients with severe influenza. METHODS: 96 influenza patients were recruited and divided into two groups, patients with thrombocytopenia (n = 30) and patients without thrombocytopenia (n = 66). Plasma microarrays were used for quantitative analysis of immunoglobulins. The endpoint was 28-day mortality. Continuous platelet count, d-dimer, level of each Ig subclass and other variables were compared between the two groups. Kaplan-Meier curve was taken to analyze the 28-day survival rate of the two groups and Cox regression analysis was performed to identify variables independently associated with 28-day mortality. RESULTS: Patients with thrombocytopenia had significantly high values of d-dimer at admission and when platelet lowest with high SOFA score. Their IgA2, IgG2, and IgG4 values were also lower than those without thrombocytopenia. Patients without thrombocytopenia had a higher 28-day survival rate than those in the thrombocytopenia group. In the multivariate Cox regression model, age (HR = 1.036, 95%CI = 1.011-1.062), IgG2 (HR = 0.990, 95%CI = 0.982-0.998), platelet minimum within 28 days (HR = 0.991, 95%CI = 0.982-0.999) and d-dimer when platelet lowest (HR = 1.091, 95%CI = 1.047-1.137) were independently related to 28-day mortality. CONCLUSION: Decreased IgG2 may be associated with thrombocytopenia. A coexistence of thrombocytopenia, IgG2 reduction and d-dimer elevation may improve the accuracy of mortality prediction in patients with influenza pneumonia.

Machine learning-based prediction model of acute kidney injury in patients with acute respiratory distress syndrome.

BACKGROUND: Acute kidney injury (AKI) can make cases of acute respiratory distress syndrome (ARDS) more complex, and the combination of the two can significantly worsen the prognosis. Our objective is to utilize machine learning (ML) techniques to construct models that can promptly identify the risk of AKI in ARDS patients. METHOD: We obtained data regarding ARDS patients from the Medical Information Mart for Intensive Care III (MIMIC-III) and MIMIC-IV databases. Within the MIMIC-III dataset, we developed 11 ML prediction models. By evaluating various metrics, we visualized the importance of its features using Shapley additive explanations (SHAP). We then created a more concise model using fewer variables, and optimized it using hyperparameter optimization (HPO). The model was validated using the MIMIC-IV dataset. RESULT: A total of 928 ARDS patients without AKI were included in the analysis from the MIMIC-III dataset, and among them, 179 (19.3%) developed AKI after admission to the intensive care unit (ICU). In the MIMIC-IV dataset, there were 653 ARDS patients included in the analysis, and among them, 237 (36.3%) developed AKI. A total of 43 features were used to build the model. Among all models, eXtreme gradient boosting (XGBoost) performed the best. We used the top 10 features to build a compact model with an area under the curve (AUC) of 0.850, which improved to an AUC of 0.865 after the HPO. In extra validation set, XGBoost_HPO achieved an AUC of 0.854. The accuracy, sensitivity, specificity, positive prediction value (PPV), negative prediction value (NPV), and F1 score of the XGBoost_HPO model on the test set are 0.865, 0.813, 0.877, 0.578, 0.957 and 0.675, respectively. On extra validation set, they are 0.724, 0.789, 0.688, 0.590, 0.851, and 0.675, respectively. CONCLUSION: ML algorithms, especially XGBoost, are reliable for predicting AKI in ARDS patients. The compact model maintains excellent predictive ability, and the web-based calculator improves clinical convenience. This provides valuable guidance in identifying AKI in ARDS, leading to improved patient outcomes.

Anisodamine hydrobromide in the treatment of critically ill patients with septic shock: a multicenter randomized controlled trial.

BACKGROUND: Septic shock is the development of sepsis to refractory circulatory collapse and metabolic derangements, characterized by persistent hypotension and increased lactate levels. Anisodamine hydrobromide (Ani HBr) is a Chinese medicine used to improve blood flow in circulatory disorders. The purpose of this study was to determine the therapeutic efficacy of Ani HBr in the treatment of patients with septic shock. METHODS: This was a prospective, multicenter, randomized controlled trial focusing on patients with septic shock in 16 hospitals in China. Patients were randomly assigned in a 1:1 ratio to either the treatment group or the control group. The primary endpoint was 28-day mortality. The secondary outcomes included 7-day mortality, hospital mortality, hospital length of stay, vasopressor-free days within 7 days, etc. These indicators were measured and collected at 0, 6h, 24h, 48h, 72h and 7d after the diagnosis. RESULTS: Between September 2017 and March 2021, 404 subjects were enrolled. 203 subjects received Ani HBr and 201 subjects were assigned to the control group. The treated group showed lower 28-day mortality than the control group. Stratified analysis further showed significant differences in 28-day mortality between the two groups for patients with a high level of illness severity. We also observed significant differences in 7-day mortality, hospital mortality and some other clinical indicators between the two groups. CONCLUSION: Ani HBr might be an important adjuvant to conventional treatment to reduce 28-day mortality in patients with septic shock. A large-scale prospective randomized multicenter trial is warranted to confirm our results.

Erector spinae muscle-based nomogram for predicting in-hospital mortality among older patients with severe community-acquired pneumonia.

BACKGROUND: No multivariable model incorporating erector spinae muscle (ESM) has been developed to predict clinical outcomes in older patients with severe community-acquired pneumonia (SCAP). This study aimed to construct a nomogram based on ESM to predict in-hospital mortality in patients with SCAP. METHODS: Patients aged ≥ 65 years with SCAP were enrolled in this prospective observational study. Least absolute selection and shrinkage operator and multivariable logistic regression analyses were used to identify risk factors for in-hospital mortality. A nomogram prediction model was constructed. The predictive performance was evaluated using the concordance index (C-index), calibration curve, net reclassification improvement (NRI), integrated discrimination improvement (IDI), and decision curve analysis. RESULTS: A total of 490 patients were included, and the in-hospital mortality rate was 36.1%. The nomogram included the following independent risk factors: mean arterial pressure, peripheral capillary oxygen saturation, Glasgow Coma Scale score (GCS), lactate, lactate dehydrogenase, blood urea nitrogen levels, and ESM cross-sectional area. Incorporating ESM into the base model with other risk factors significantly improved the C-index from 0.803 (95% confidence interval [CI], 0.761-0.845) to 0.836 (95% CI, 0.798-0.873), and these improvements were confirmed by category-free NRI and IDI. The ESM-based nomogram demonstrated a high level of discrimination, good calibration, and overall net benefits for predicting in-hospital mortality compared with the combination of confusion, urea, respiratory rate, blood pressure, and age ≥ 65 years (CURB-65), Pneumonia Severity Index (PSI), Acute Physiology and Chronic Health Evaluation II (APACHEII), and Sequential Organ Failure Assessment (SOFA). CONCLUSIONS: The proposed ESM-based nomogram for predicting in-hospital mortality among older patients with SCAP may help physicians to promptly identify patients prone to adverse outcomes. TRIAL REGISTRATION: This study was registered at www.chictr.org.cn (registration number Chi CTR-2300070377).

Predictive nomogram for in-hospital mortality among older patients with intra-abdominal sepsis incorporating skeletal muscle mass.

BACKGROUND: Studies on prognostic factors for older patients with intra-abdominal sepsis are scarce, and the association between skeletal muscle mass and prognosis among such patients remains unclear. AIMS: To develop a nomogram to predict in-hospital mortality among older patients with intra-abdominal sepsis. METHODS: Older patients with intra-abdominal sepsis were prospectively recruited. Their demographics, clinical features, laboratory results, abdominal computed tomography-derived muscle mass, and in-hospital mortality were recorded. The predictors of mortality were selected via least absolute shrinkage and selection operator and multivariable logistic regression analyses, and a nomogram was developed. The nomogram was assessed and compared with Sequential Organ Failure Assessment score, Acute Physiology and Chronic Health Evaluation II score, and Simplified Acute Physiology Score II. RESULTS: In total, 464 patients were included, of whom 104 (22.4%) died. Six independent risk factors (skeletal muscle index, cognitive impairment, frailty, heart rate, red blood cell distribution width, and blood urea nitrogen) were incorporated into the nomogram. The Hosmer-Lemeshow goodness-of-fit test and calibration plot revealed a good consistency between the predicted and observed probabilities. The area under the receiver operating characteristic curve was 0.875 (95% confidence interval = 0.838-0.912), which was significantly higher than those of commonly used scoring systems. The decision curve analysis indicated the nomogram had good predictive performance. DISCUSSION: Our nomogram, which is predictive of in-hospital mortality among older patients with intra-abdominal sepsis, incorporates muscle mass, a factor that warrants consideration by clinicians. The model has a high prognostic ability and might be applied in clinical practice after external validation.

Blockage of S100A8/A9 ameliorates septic nephropathy in mice.

Septic acute kidney injury (AKI) is the commonest cause of complication of sepsis in intensive care units, but its pathophysiology remains unclear. Calprotectin (S100A8/A9), which is a damage-associated molecular patterns (DAMPs) molecule, exerts a critical role in modulating leukocyte recruitment and inflammatory response during various diseases. However, role of S100A8/A9 in septic AKI is largely unknown. In this research, Septic AKI was triggered by cecal ligation and puncture (CLP) operation in wild-type mice, which treated with or without an S100A9 inhibitor, Paquinimod (Paq, 10 mg/kg) that prevents S100A8/A9 to bind to Toll-like receptor 4 (TLR4). Renal function, pathological changes, cell death, and oxidative stress were evaluated. Our research indicated that the mRNA and protein expression of S100A9 are time-dependently elevated in the kidney following CLP. Moreover, the administration of Paq for 24 h significantly improved CLP-induced renal dysfunction and pathological alterations compared with vehicle treatment in mice. These beneficial effects were associated with the inhibition of CLP-triggered renal tubular epithelial cell apoptosis, inflammation, superoxide production, and mitochondrial dynamic imbalance. What's more, we further confirmed the above findings by cell co-culture experiments. Our study demonstrates that S100A9 is a prominent protein to lead to septic AKI, and the selective inhibition of S100A9 could represent a new therapeutic approach which can treat septic AKI.

From coarse to fine: Two-stage deep residual attention generative adversarial network for repair of iris textures obscured by eyelids and eyelashes.

We propose a two-stage deep residual attention generative adversarial network (TSDRA-GAN) for inpainting iris textures obscured by eyelids. This two-stage generation approach ensures that the semantic and texture information of the generated images is preserved. In the second stage of the fine network, a modified residual block (MRB) is used to further extract features and mitigate the performance degradation caused by the deepening of the network, thus following the concept of using a residual structure as a component of the encoder. In addition, for the skip connection part of this phase, we propose a dual-attention computing connection (DACC) to computationally fuse the features of the encoder and decoder in both directions to achieve more effective information fusion for iris inpainting tasks. Under completely fair and equal experimental conditions, it is shown that the method presented in this paper can effectively restore original iris images and improve recognition accuracy.

Validation of heart failure algorithm for diagnosing heart failure with preserved ejection fraction: a meta-analysis.

The aim of the meta-analysis was to generate a more comprehensive understanding of the HFA-PEFF score in the diagnosis of heart failure with preserved ejection fraction (HFpEF) and to pose clues in the field of scientific and clinical practice. Electronic databases of PubMed, Web of Science, Cochrane Library, and Embase were systematically searched. Studies investigating the use of the HFA-PEFF score to diagnose HFpEF were included. Pooled sensitivity, specificity, positive likelihood ratio (PLR) and negative Likelihood Ratio (NLR), diagnostic odds ratio (DOR), area under the curve of summary receiver operating characteristic, and superiority index were calculated. Five studies with 1521 participants were included in this meta-analysis. In the pooled analysis of the 'Rule-out' approach, the pooled sensitivity, specificity, PLR, NLR, and DOR were 0.98 (0.94, 1.00), 0.33 (0.08, 0.73), 1.5 (0.8, 2.5), 0.05 (0.02, 0.17), and 28 (6, 127). In the pooled analysis of the 'Rule-in' approach, the pooled sensitivity and specificity, PLR, NLR, and DOR were 0.69 (0.62, 0.75), 0.87 (0.64, 0.96), 5.5 (1.8, 16.9), 0.35 (0.30, 0.41), and 16 (5, 50). This meta-analysis indicates that the HFA-PEFF algorithm showed acceptable specificity and sensitivity for the diagnosis and exclusion of HFpEF. More relevant studies on the diagnostic validity of the HFA-PEFF score are needed in the future.

Early human albumin administration is associated with reduced mortality in septic shock patients with acute respiratory distress syndrome: A retrospective study from the MIMIC-III database.

Background: Sepsis-induced acute respiratory distress syndrome (ARDS) was associated with higher mortality. It is unclear whether albumin supplementation early in the course of ARDS can affect the prognostic outcomes of septic shock (SS) patients with ARDS. Methods: The MIMIC-III database was employed to identify SS patients with ARDS. The effect of early application (<24 h after ICU admission) of human albumin on 28-day mortality in SS patients with ARDS was explored. The propensity score matching was used to minimize the bias between the non-albumin and early albumin treatment groups. Results: The analysis for all eligible patients who received human albumin showed significantly lower 28-hospital mortality rates than the non-albumin group (37% versus 47%, p = 0.018). After propensity matching, the difference between the two groups also significantly (34.8% versus 48.1%, p = 0.031). Moreover, we found that the relationship between albumin use and reduced 28-day mortality was inconsistent across SOFA score subgroups (Pinteraction = 0.004, non-adjustment for multiple testing). Conclusion: Early human albumin administration in SS patients with ARDS was independently associated with a reduction of 28-day mortality. Furthermore, the benefit of human albumin treatment appeared to be more pronounced in patients with a SOFA score of ≤ 10.

Peripheral blood monocyte status is a predictor for judging occurrence and development on sepsis in older adult population: a case control study.

BACKGROUND: Peripheral blood monocytes are important immune modulatory cells that change during aging. Previous studies on sepsis and monocytes did not distinguish between age groups, especially in the older adult population. The mechanisms of monocyte subsets and function are not well-understood in the aging context with sepsis. METHODS: Monocyte subsets were measured using flow cytometry in 80 sepsis patients and 40 healthy controls. Plasma cytokine levels were measured using cytokine antibody arrays. RESULTS: The percentage of MO3 (CD14 + CD16 + +)/monocytes was higher in sepsis patients than in controls (P = 0.011), whereas the percentage of MO1 (CD14 + + CD16 -)/monocytes was higher in septic shock patients and 28-day death group than in those without shock and 28-day survival group (P = 0.034, 0.038). Logistic regression analysis showed that the percentage of MO3/monocytes (OR = 1.120, P = 0.046) and plasma level of monocyte chemoattractant protein (MCP)-1 (OR = 1.006, P = 0.023) were independently associated with the occurrence of sepsis, whereas the percentage of MO1/monocytes (OR = 1.255, P = 0.048) was independently associated with septic shock. The receiver operating characteristic (ROC) curve showed that the area under the curve (AUC) of MO3/monocyte percentage in combination with MCP-1 plasma level (AUC = 0.799) for predicting sepsis was higher than that of each parameter alone (P < 0.001). The AUC of MO1/monocyte percentage with the value 0.706 (P = 0.003) was lower than the AUC of SOFA (sequential organ failure assessment) score with the value 0.966 (P < 0.001) for predicting septic shock, but the value of the two AUCs were similar for predicting 28-day mortality (AUC = 0.705, 0.827; P = 0.020, P < 0.001). The AUC of MO1/monocytes percentage in combination with SOFA score for predicting 28-day mortality was higher than that of each parameter alone (AUC = 0.867, P < 0.001). Using a cut-off of 58.5% (for MO1/monocytes determined by ROC) could discriminate between survivors and non-survivors on Kaplan-Meier curves for 28-day mortality with a positive predictive value of 77.4%. CONCLUSION: The MO3/monocyte percentage and plasma MCP-1 level were independent predictors of sepsis occurrence, whereas the percentage of MO1/monocytes was an independent predictor of prognosis in the Chinese Han older adult population. TRIAL REGISTRATION: Registration number: ChiCTR2200061490, date of registration: 2022-6-26 (retrospectively registered).