Deterministic direct design method for a spherical-aberration-free singlet lens with reduced coma.

It is still challenging to find a spherical-aberration-free singlet lens with well corrected coma due to an undesired and complicated residual high-order coma. In this paper, we present a spherical-aberration-free singlet lens with reduced coma containing high-order coma contribution. This design algorithm is to deduce the front aspherical surface parameters from the back spherical surface using meridional ray tracing to find the proper values of the back focal length and the back spherical radius to reduce the coma. The exemplary lens demonstrates an excellent well-balanced and diffraction-limited performance at the field angle ranging from 0.0° to 2.5° with a working F# equal to 1.65.

Association between serum magnesium concentrations and the risk of developing acute kidney injury in patients with cirrhosis: a retrospective cohort study based on the MIMIC-IV database.

BACKGROUND: In various disease contexts, magnesium abnormalities are associated with acute kidney injury (AKI) incidence. However, this association remains unclear and has not been systematically investigated in patients with cirrhosis. Hence, we aimed to elucidate the association between admission serum magnesium levels and AKI incidence in intensive care unit (ICU)-admitted cirrhotic patients. METHODS: A retrospective cohort study was conducted using MIMIC-IV2.2 data, focusing on critically ill patients with cirrhosis. We employed univariable and multivariable logistic regression and restricted cubic spline analyses to robustly address our research objectives. To further substantiate the findings, subgroup and sensitivity analyses were also conducted. RESULTS: Among the 3,228 enrolled ICU-admitted cirrhotic patients, 34.4% were female, and the overall AKI incidence was 68.6% (2,213/3,228). Multivariable logistic regression analysis revealed an independent relationship between elevated serum magnesium levels and increased AKI risk (OR = 1.55 [95% CI = 1.15-2.09], p = 0.004). Compared with individuals with serum magnesium levels < 1.6 mg/dL, individuals with serum magnesium levels in Q2 (1.6-2.6 mg/dL) and Q3 (≥2.6 mg/dL) had adjusted ORs for AKI of 1.89 (95% CI = 1.34-2.65, p < 0.001) and 2.19 (95% CI = 1.27-3.75, p = 0.005), respectively. The restricted cubic spline analysis revealed that AKI risk increased linearly with increasing serum magnesium levels. Subgroup analysis revealed that the association between serum magnesium levels and AKI incidence was remarkably stable in subgroup analysis (all Pinteraction >0.05). CONCLUSIONS: High serum magnesium concentrations were significantly associated with an increased AKI risk in ICU-admitted patients with cirrhosis. Further randomized trials are needed to confirm this association.

Minimally Invasive Treatment of Pelvic Fractures with Titanium Elastic Nailing: An Innovative Technology.

BACKGROUND: Minimally invasive treatment has become the most popular and effective treatment for pelvic fractures. This study aimed to evaluate the safety and efficacy of a new technique, titanium elastic nailing (TEN), for the minimally invasive treatment of pelvic fractures. METHOD: Twenty-four patients with pelvic fractures were referred to us between January 2020 to January 2022, including sixteen males and 8 females. Pelvic fractures were temporarily fixed by pelvic fixation belt accompanied by traction from the lower limb bone. Anterior pelvic ring injuries (superior ramus of pubis) and ilium fractures were treated with closed reduction and intramedullary fixation with minimally invasive TEN. Intraoperative C-arm, including pelvic anteroposterior, pelvic outlet, inlet and ilium oblique views, and O-arm fluoroscopy (intraoperative CT) were employed to assess fractures reduction and determine the location of the elastic titanium nail within the bone channel. RESULTS: By adopting closed reduction and minimally invasive incision techniques, pelvic fractures could be safely fixed by placing an elastic titanium nail in the osseous medullary cavity channels of the pelvis. Postoperative investigation indicated that the wounds of all patients were healed in the first stage without any occurrence of complications, such as injuries to the nerves, blood vessels, and important tissue structures. Patients are essential quickly after the operation and could perform the functional exercise in the early stages of the recovery. CONCLUSION: TEN can be used for minimally invasive treatment of pelvic fractures. This novel technique has no obvious complications and is worthwhile in clinical practice.

Actively implementing an evidence-based feeding guideline for critically ill patients (NEED): a multicenter, cluster-randomized, controlled trial.

BACKGROUND: Previous cluster-randomized controlled trials evaluating the impact of implementing evidence-based guidelines for nutrition therapy in critical illness do not consistently demonstrate patient benefits. A large-scale, sufficiently powered study is therefore warranted to ascertain the effects of guideline implementation on patient-centered outcomes. METHODS: We conducted a multicenter, cluster-randomized, parallel-controlled trial in intensive care units (ICUs) across China. We developed an evidence-based feeding guideline. ICUs randomly allocated to the guideline group formed a local "intervention team", which actively implemented the guideline using standardized educational materials, a graphical feeding protocol, and live online education outreach meetings conducted by members of the study management committee. ICUs assigned to the control group remained unaware of the guideline content. All ICUs enrolled patients who were expected to stay in the ICU longer than seven days. The primary outcome was all-cause mortality within 28 days of enrollment. RESULTS: Forty-eight ICUs were randomized to the guideline group and 49 to the control group. From March 2018 to July 2019, the guideline ICUs enrolled 1399 patients, and the control ICUs enrolled 1373 patients. Implementation of the guideline resulted in significantly earlier EN initiation (1.20 vs. 1.55 mean days to initiation of EN; difference - 0.40 [95% CI - 0.71 to - 0.09]; P = 0.01) and delayed PN initiation (1.29 vs. 0.80 mean days to start of PN; difference 1.06 [95% CI 0.44 to 1.67]; P = 0.001). There was no significant difference in 28-day mortality (14.2% vs. 15.2%; difference - 1.6% [95% CI - 4.3% to 1.2%]; P = 0.42) between groups. CONCLUSIONS: In this large-scale, multicenter trial, active implementation of an evidence-based feeding guideline reduced the time to commencement of EN and overall PN use but did not translate to a reduction in mortality from critical illness. TRIAL REGISTRATION: ISRCTN, ISRCTN12233792 . Registered November 20th, 2017.

Effect of oXiris-CVVH on the Clinical Outcomes of Patients with Septic Shock: An Inverse Probability of Treatment-Weighted Analysis.

BACKGROUND: Limited previous studies had proved that oXiris-continuous veno-venous hemofiltration (CVVH) could decrease endotoxins and inflammatory factors, thereby improving circulation's stability. However, conclusive data are lacking regarding the comparison between oXiris membrane (with the function of removing endotoxins and decreasing inflammatory factors) and AN69 filters (with the only function of decreasing inflammatory) on the mortality of patients with septic shock. The potential mechanisms of oXiris that might influence the mortality of septic shock patients remain unexplored. METHODS: This is a single-center, retrospective cohort study. The experimental group (30 patients with septic shock) was treated with oXiris-CVVH, and the control group (46 patients with septic shock) was treated with AN69 filter-CVVH. We employed the inverse probability of treatment-weighting method (IPTW), doubly robust estimation, and mediating effect analysis to analyze those clinical outcomes, with a special focus on the results of 28-day mortality, 72-h lactate, the need for norepinephrine (NE) in the next 72 h. RESULTS: A total of 76 patients with septic shock who received blood purification therapies were enrolled. After IPTW, differences in patient characteristics have been minimized. The 28-day mortality in the control group is higher than in the treatment group (73.3% vs. 47.3%, p < 0.001; median survival time: 10 vs. ≥28 days, log-rank p = 0.0366). And the 25% decrease and the 50% decrease in demand for NE in the next 72 h are different between the treatment and control groups (median time of 25% decrease in demand: 24 vs. >72 h, log-rank p = 0.0126; median time of 50% decrease in demand: 24 vs. >72 h, log-rank p = 0.0322). The 72-h lactic acid level and white blood cell (WBC) counts in the oXiris group are lower than in the control group. The 72-h lactate fully mediated the effects of oXiris on 28-day mortality after confounds adjustment. CONCLUSIONS: For septic shock patients, the use of oXiris-CVVH was associated with lower mortality and appeared to reduce lactate, NE dosage, PCT, and WBC counts, as compared to AN69-CVVH.

Chlorpheniramine poisoning as a potential cause of rhabdomyolysis.

Chlorpheniramine is an H1 receptor antagonist of the alkylamine class. It is a widely used anti-allergy drug due to its strong antihistamine effect and mild adverse effects. In the case of chlorpheniramine overdose or poisoning, the primary manifestation is central nervous system symptoms. To date, no case of rhabdomyolysis induced by acute poisoning with chlorpheniramine has ever been reported. This study reports a case of acute chlorpheniramine poisoning at an oral dose of 4000 mg, which is the highest reported poisoning dose to date. The diagnosis of rhabdomyolysis (creatine kinase, 195,489 U/L) and acute kidney injury (serum creatinine, 150.1 umol/L) was confirmed based on laboratory results. After haemoperfusion and continuous renal replacement therapy, the patient's renal function fully recovered. This paper aims to analyse the clinical data of this patient and summarize its clinical characteristics. At the same time, the mechanism of chlorpheniramine-induced rhabdomyolysis is also explored in the context of the literature review.

Utilizing reclassification to explore characteristics and prognosis of KDIGOSCr AKI subgroups: a retrospective analysis of a multicenter prospective cohort study.

BACKGROUND: Acute kidney injury (AKI) is widespread in the intensive care unit (ICU) and affects patient prognosis. According to Kidney Disease: Improving Global Outcomes (KDIGO) guidelines, the absolute and relative increases of serum creatinine (Scr) are classified into the same stage. Whether the prognosis of the two types of patients is similar in the ICU remains unclear. METHODS: According to the absolute and relative increase of Scr, AKI stage 1 and stage 3 patients were divided into stage 1a and 1b, stage 3a and 3b groups, respectively. Their demographics, laboratory results, clinical characteristics, and outcomes were analyzed retrospectively. RESULTS: Of the 345 eligible cases, we analyzed stage 1 because stage 3a group had only one patient. Using 53 or 61.88 µmol/L as the reference Scr (Scrref), no significant differences were observed in ICU mortality (P53=0.076, P61.88=0.070) or renal replacement therapy (RRT) ratio, (P53=0.356, P61.88=0.471) between stage 1a and 1b, but stage 1b had longer ICU length of stay (LOS) than stage 1a (P53<0.001, P61.88=0.032). In the Kaplan-Meier survival analysis, no differences were observed in ICU mortality between stage 1a and 1b (P53=0.378, P61.88=0.255). In a multivariate analysis, respiratory failure [HR = 4.462 (95% CI 1.144-17.401), p = 0.031] and vasoactive drug therapy [HR = 4.023 (95% CI 1.584-10.216), p = 0.003] were found to be independently associated with increased risk of death. CONCLUSION: ICU LOS benefit was more prominent in KDIGOSCr AKI stage 1a patients than in stage 1 b. Further prospective studies with a larger sample size are necessary to confirm the effectiveness of reclassification.

Artesunate alleviates the inflammatory response of ulcerative colitis by regulating the expression of miR-155.

CONTEXT: Ulcerative colitis (UC) is a recrudescent and chronic inflammatory disease. Artesunate (ART) has shown its anti-inflammatory and antioxidative properties in severe diseases, including UC. OBJECTIVE: The present study investigates the molecular mechanisms for effects of ART on UC, and the role of miR-155 in this process. MATERIALS AND METHODS: The in vitro UC model was established by using lipopolysaccharide (LPS)-induced RAW264.7 cells. For BALB/c mice model, different concentrations/doses of ART were treated once a day for 7 days. The apoptosis and viability were measured by CCK-8 and flow cytometry assay, respectively. The expressions and concentrations of inflammatory factors were detected by qRT-PCR and ELISA, respectively. Colon tissues of mice were used for detecting the activity of MPO, and the histological changes were observed by H&E staining. RESULTS: The IC50 of ART for RAW264.7 cells was 107.3 µg/mL. In LPS-induced cells, ART treatment inhibited the cell apoptosis and promoted cell viability compared with the model group. Besides, ART treatment also reduced the expressions of pro-inflammatory factors and miR-155. However, overexpression of miR-155 showed opposite effects and attenuated the effects of ART. Meanwhile, inhibiting miR-155 expression also improved the inflammatory response induced by LPS. In UC mice model, ART treatment also alleviated the mice's survival and alleviated the inflammatory response. In addition, the expression of p-NF-κB was suppressed by ART. CONCLUSION: ART reduced the inflammatory response by inhibiting the expression of miR-155 in UC to inhibit the NF-κB pathway. This research showed ART might have potential in UC treatment.

MiR-155 aggravated septic liver injury by oxidative stress-mediated ER stress and mitochondrial dysfunction via targeting Nrf-2.

OBJECTIVE: Liver is uniquely vulnerable during sepsis. MicroRNA-155 (miR-155) is confirmed to play crucial roles in septic liver injury. The present study aims to investigate the mechanisms of miR-155 in septic liver injury. METHODS: The sepsis model was established by intraperitoneal injection of lipopolysaccharide (LPS) in mice. Mice were divided into four groups: Vehicle, miR-155 antagomir, LPS, LPS+ miR-155 antagomir. The survival rate and body weight were monitored. Liver injury was assessed by H&E staining. The levels of serum ALT and inflammatory cytokines were determined by ELISA kits. Oxidative stress was detected by MDA and SOD detection kits. The miR-155, Nrf-2, and markers related to oxidative stress, endoplasmic reticulum (ER) stress, mitochondrial injury and apoptosis were detected by western blotting and qPCR. Apoptosis in liver tissues was detected by TUNELstaining. RESULTS: MiR-155 antagomir alleviated liver injury as evidenced by enhancing survival rate and body weight, inhibiting inflammatory cell infiltration, liver cells necrosis and decreasing ALT level. The productions of TNF-α, IL-6 were suppressed, while anti-inflammatory cytokine IL-10 was promoted by miR-155 antagomir. Oxidative stress was inhibited by miR-155 antagomir via enhancing nuclear factor, erythroid 2-like 2 (Nrf-2) expression. ER stress and Cytochrome C (Cyto-C) release were restrained by miR-155 antagomir. Sepsis-induced apoptosis was repressed by miR-155 antagomir as manifested by the decreased levels of Bax, cleaved caspase-12, 9 and 3, and increased levels of Bcl-2 and uncleaved PARP. CONCLUSION: MiR-155 antagomir relieved septic liver injury through inhibiting oxidative stress-mediated ER stress, mitochondrial dysfunction and apoptosis via targeting Nrf-2, suggesting miR-155 as a therapeutic target for septic liver injury.

PAI-1/PIAS3/Stat3/miR-34a forms a positive feedback loop to promote EMT-mediated metastasis through Stat3 signaling in Non-small cell lung cancer.

AIM: This study intented to clarify the intracellular effect of PAI-1 on Non-small cell lung cancer (NSCLC) metastasis and the precise mechanism involved. METHODS: The metastatic properties of NSCLC cells were determined by transwell assays and wound-healing assay in vitro. The mRNA and protein expressions of genes were analyzed by Real-time qPCR and western blot, respectively. Pulmonary metastasis model of NSCLC cells was established to evaluate the pro-metastasis effect of PAI-1 and anti-metastatic effect of miR-34a in vivo. The gene targets of miR-34a were confirmed by luciferase reporter assays. Chromatin immunoprecipitation assay was employed to detect the transcriptional regulation of miR-34a. Co-immunoprecipitation assay was performed to observe the interaction of proteins. RESULTS: PAI-1, which was elevated in NSCLC patients with recurrence and metastasis, augmented NSCLC metastasis and was negatively related to the prognosis of NSCLC. miR-34a, which was decreased in NSCLC patients with metastasis, attenuated NSCLC metastasis and was positively correlated with the prognosis of NSCLC. Moreover, PAI-1 was identified as the target gene of miR-34a and activated the Stat3 signaling pathway to promote epithelial-mesenchymal transition (EMT) in NSCLC cells. PAI-1 interacted with PIAS3 to regulate Stat3-dependent gene expression and miR-34a was transcriptionally suppressed by Stat3 to form a positive regulatory loop through Stat3 signaling. CONCLUSION: Our findings suggest that PAI-1 and miR-34a, which can be clinically utilized as biomarkers for the clinical prognosis or diagnosis of NSCLC, are potential targets for the treatment of NSCLC.

Use of noninvasive ventilation in immunocompromised patients with acute respiratory failure: a systematic review and meta-analysis.

BACKGROUND: Acute respiratory failure (ARF) remains a common hazardous complication in immunocompromised patients and is associated with increased mortality rates when endotracheal intubation is needed. We aimed to evaluate the effect of early noninvasive ventilation (NIV) compared with oxygen therapy alone in this patient population. METHODS: We searched for relevant studies in MEDLINE, EMBASE, and the Cochrane database up to 25 July 2016. Randomized controlled trials (RCTs) were included if they reported data on any of the predefined outcomes in immunocompromised patients managed with NIV or oxygen therapy alone. Results were expressed as risk ratio (RR) and mean difference (MD) with accompanying 95% confidence interval (CI). RESULTS: Five RCTs with 592 patients were included. Early NIV significantly reduced short-term mortality (RR 0.62, 95% CI 0.40 to 0.97, p = 0.04) and intubation rate (RR 0.52, 95% CI 0.32 to 0.85, p = 0.01) when compared with oxygen therapy alone, with significant heterogeneity in these two outcomes between the pooled studies. In addition, early NIV was associated with a shorter length of ICU stay (MD -1.71 days, 95% CI -2.98 to 1.44, p = 0.008) but not long-term mortality (RR 0.92, 95% CI 0.74 to 1.15, p = 0.46). CONCLUSIONS: The limited evidence indicates that early use of NIV could reduce short-term mortality in selected immunocompromised patients with ARF. Further studies are needed to identify in which selected patients NIV could be more beneficial, before wider application of this ventilator strategy.

Does training improve diagnostic accuracy and inter-rater agreement in applying the Berlin radiographic definition of acute respiratory distress syndrome? A multicenter prospective study.

BACKGROUND: Poor inter-rater reliability in chest radiograph interpretation has been reported in the context of acute respiratory distress syndrome (ARDS), although not for the Berlin definition of ARDS. We sought to examine the effect of training material on the accuracy and consistency of intensivists' chest radiograph interpretations for ARDS diagnosis. METHODS: We conducted a rater agreement study in which 286 intensivists (residents 41.3%, junior attending physicians 35.3%, and senior attending physician 23.4%) independently reviewed the same 12 chest radiographs developed by the ARDS Definition Task Force ("the panel") before and after training. Radiographic diagnoses by the panel were classified into the consistent (n = 4), equivocal (n = 4), and inconsistent (n = 4) categories and were used as a reference. The 1.5-hour training course attended by all 286 intensivists included introduction of the diagnostic rationale, and a subsequent in-depth discussion to reach consensus for all 12 radiographs. RESULTS: Overall diagnostic accuracy, which was defined as the percentage of chest radiographs that were interpreted correctly, improved but remained poor after training (42.0 ± 14.8% before training vs. 55.3 ± 23.4% after training, p < 0.001). Diagnostic sensitivity and specificity improved after training for all diagnostic categories (p < 0.001), with the exception of specificity for the equivocal category (p = 0.883). Diagnostic accuracy was higher for the consistent category than for the inconsistent and equivocal categories (p < 0.001). Comparisons of pre-training and post-training results revealed that inter-rater agreement was poor and did not improve after training, as assessed by overall agreement (0.450 ± 0.406 vs. 0.461 ± 0.575, p = 0.792), Fleiss's kappa (0.133 ± 0.575 vs. 0.178 ± 0.710, p = 0.405), and intraclass correlation coefficient (ICC; 0.219 vs. 0.276, p = 0.470). CONCLUSIONS: The radiographic diagnostic accuracy and inter-rater agreement were poor when the Berlin radiographic definition was used, and were not significantly improved by the training set of chest radiographs developed by the ARDS Definition Task Force. TRIAL REGISTRATION: The study was registered at ClinicalTrials.gov (registration number NCT01704066 ) on 6 October 2012.

Dehydrogenation of Formic Acid at Room Temperature: Boosting Palladium Nanoparticle Efficiency by Coupling with Pyridinic-Nitrogen-Doped Carbon.

The use of formic acid (FA) to produce molecular H2 is a promising means of efficient energy storage in a fuel-cell-based hydrogen economy. To date, there has been a lack of heterogeneous catalyst systems that are sufficiently active, selective, and stable for clean H2 production by FA decomposition at room temperature. For the first time, we report that flexible pyridinic-N-doped carbon hybrids as support materials can significantly boost the efficiency of palladium nanoparticle for H2 generation; this is due to prominent surface electronic modulation. Under mild conditions, the optimized engineered Pd/CN0.25 catalyst exhibited high performance in both FA dehydrogenation (achieving almost full conversion, and a turnover frequency of 5530 h(-1) at 25 °C) and the reversible process of CO2 hydrogenation into FA. This system can lead to a full carbon-neutral energy cycle.

An aqueous rechargeable formate-based hydrogen battery driven by heterogeneous Pd catalysis.

The formate-based rechargeable hydrogen battery (RHB) promises high reversible capacity to meet the need for safe, reliable, and sustainable H2 storage used in fuel cell applications. Described herein is an additive-free RHB which is based on repetitive cycles operated between aqueous formate dehydrogenation (discharging) and bicarbonate hydrogenation (charging). Key to this truly efficient and durable H2 handling system is the use of highly strained Pd nanoparticles anchored on graphite oxide nanosheets as a robust and efficient solid catalyst, which can facilitate both the discharging and charging processes in a reversible and highly facile manner. Up to six repeated discharging/charging cycles can be performed without noticeable degradation in the storage capacity.

Artesunate alleviates sepsis-induced liver injury by regulating macrophage polarization via the lncRNA MALAT1/PTBP1/IFIH1 axis.

BACKGROUND: The present study aimed to explore the regulatory effects of artesunate on macrophage polarization in sepsis. METHODS: Cell models and mice models were established using lipopolysaccharide (LPS), followed by treatment with various concentrations of artesunate. The phenotype of the macrophages was determined by flow cytometry. RNA immunoprecipitation was used to confirm the binding between MALAT1 and polypyrimidine tract-binding protein 1 (PTBP1), as well as between PTBP1 and interferon-induced helicase C domain-containing protein 1 (IFIH1). RESULTS: Treatment with artesunate inhibited M1 macrophage polarization in Kupffer cells subjected to LPS stimulation by downregulating MALAT1. Furthermore, MALAT1 abolished the inhibitory effect of artesunate on M1 macrophage polarization by recruiting PTBP1 to promote IFIH. In vivo experiments confirmed that artesunate alleviated septic liver injury by affecting macrophage polarization via MALAT1. CONCLUSION: The present study showed that artesunate alleviates LPS-induced sepsis in Kupffer cells by regulating macrophage polarization via the lncRNA MALAT1/PTBP1/IFIH1 axis.

USP31 promotes the inflammatory response of human lung organoids to lipopolysaccharide treatment.

BACKGROUND: Acute lung injury (ALI) is a severe condition characterized by a high mortality rate, driven by an uncontrolled inflammatory response. Emerging evidence has underscored the crucial role of the ubiquitin system in ALI. However, due to their vast number, the specific functions of individual ubiquitination regulators remain unclear. MATERIALS AND METHODS: In this study, we established human lung organoids (HLOs) derived from human embryonic stem cells and subjected them to lipopolysaccharide (LPS) treatment to induce an inflammatory response, mimicking ALI. Subsequently, we detected the expression of inflammatory cytokines, including tumour necrosis factor alpha (TNF-α), interleukin 6, interleukin 18 (IL-18), and interleukin-1ß (IL-1ß), by qPCR experiments. We also detected changes in the mRNA expression of several USPs before and after HLOs treatment and thus screened for USPs that had significant changes in HLOs after LPS stimulation. After screening for USP, we silenced the USP in HLOs and then subjected them to LPS treatment, and TNF-α, IL-6, IL-18, and IL-1ß expressions were detected using qPCR assays. Meanwhile, Western blot was used to detect changes in NOD-, LRR- and pyrin domain-containing 3 (NLRP3) and apoptosis-associated Speck-like protein containing a CARD (ASC) protein level in HLOs. RESULTS: Through screening the expression of 40 ubiquitin-specific proteases (USPs), which are responsible for removing ubiquitination, we identified several USPs that exhibited differential expression in LPS-treated HLOs compared to untreated HLOs. Notably, USP31 emerged as the most significantly upregulated USP, and the knockdown of USP31 markedly attenuated the inflammatory response of HLOs to LPS treatment. CONCLUSIONS: USP31 may play a facilitating role in the inflammatory response during ALI.

Development of a nomogram for predicting in-hospital mortality in patients with liver cirrhosis and sepsis.

In this study, we aimed to investigate the risk factors associated with in-hospital mortality in patients with cirrhosis and sepsis, establish and validate the nomogram. This retrospective study included patients diagnosed with liver cirrhosis and sepsis in the Medical Information Mart for Intensive Care IV (MIMIC-IV). Models were compared by the area under the curve (AUC), integrated discriminant improvement (IDI), net reclassification index (NRI) and decision curve analysis (DCA). A total of 1,696 patients with cirrhosis and sepsis were included in the final cohort. Our final model included the following 9 variables: age, heartrate, total bilirubin (TBIL), glucose, sodium, anion gap (AG), fungal infections, mechanical ventilation, and vasopressin. The nomogram were constructed based on these variables. The AUC values of the nomograms were 0.805 (95% CI 0.776-0.833), which provided significantly higher discrimination compared to that of SOFA score [0.684 (95% CI 0.647-0.720)], MELD-Na [0.672 (95% CI 0.636-0.709)] and ABIC [0.674(95% CI 0.638-0.710)]. We established the first nomogram for predicting in-hospital mortality in patients with liver cirrhosis and sepsis based on these factors. This nomogram can performs well and facilitates clinicians to identify people at high risk of in-hospital mortality.

An unusual case of traumatic injury to the first metatarsal a case report.

A 44-year-old male sustained trauma to his foot leading to a 5-cm defect of the first metatarsal bone and infection of the bone by Staphylococcus aureus. Osteotomy is the most suitable method for treating large metatarsal defects complicated with osteomyelitis, however few reports have been published on this challenging approach. In this case, osteotomy and external fixation for distraction were performed. Finally, the osteomyelitis of the patient was well controlled, the bone length was restored, and the patient could carry weight completely, and the treatment effect was satisfactory.

MicroRNA-30a inhibits cell proliferation in a sepsis-induced acute kidney injury model by targeting the YAP-TEAD complex.

Background: Acute kidney injury (AKI) is a primary feature of renal complications in patients with sepsis. MicroRNA (miRNA/miR)-30a is an essential regulator of cardiovascular diseases, tumors, phagocytosis, and other physical processes, but whether it participates in sepsis-induced AKI (sepsis-AKI) is unknown. We aimed to elucidate the functions and molecular mechanism underlying miR-30a activity in sepsis-AKI. Methods: The classical cecal ligation and puncture (CLP) method and lipopolysaccharide (LPS)-induced Human Kidney 2 (HK-2) cells were used to establish in vivo and in vitro sepsis-AKI models. Specific pathogen-free and mature male Sprague-Dawley (SD) rats, aged 6-8 weeks (weight 200-250 g), were randomly divided into five-time phase subgroups. Fluid resuscitation with 30 mL/kg 37 °C saline was administered after the operation, without antibiotics. Formalin-fixed, paraffin-embedded kidney sections were stained with hematoxylin and eosin. SD rat kidney tissue samples were collected for analysis by real-time quantitative polymerase chain reaction and enzyme-linked immunosorbent assay. HK-2 cells were transfected with hsa-miR-30a-3p mimics or inhibitors, and compared with untreated normal controls. RNA, protein, and cell viability were evaluated by quantitative reverse transcription-polymerase chain reaction (qRT-PCR), western blot, and cell counting kit-8 methods. A Dual-Luciferase Assay Kit (Promega) was used to measure luciferase activity 48 h after transfection with miR-30a-3p mimics. Results: Expression levels of miR-30a-3p and miR-30a-5p in renal tissues of the sepsis group were significantly reduced at 12 h and 24 h (P <0.05). Tumor necrosis factor-α (TNF-α) and interleukin-1ß (IL-1ß) were significantly increased in renal tissue 3 h after the operation in rats (P <0.05), and gradually decreased 6 h, 12 h, and 24 h after CLP. Levels of miR-30a-5p and miR-30a-3p were significantly down-regulated at 3 h after LPS treatment (P <0.05), and gradually decreased in HK-2 cells. One hour after LPS (10 µg/mL) treatment, TNF-α and IL-1ß levels in HK-2 cells were significantly up-regulated (P < 0.05), and they were markedly down-regulated after 3 h (P <0.05). IL-6 expression levels began to rise after LPS treatment of cells, peaked at 6 h (P <0.05), and then decreased to the initial level within a few hours. Stimulation with 10 µg/mL LPS promoted HK-2 cells proliferation, which was inhibited after miR-30a-3p-mimic transfection. Bioinformatics prediction identified 37 potential miR-30a-3p target genes, including transcriptional enhanced associate domain 1 (TEAD1). After transfection of HK-2 cells with miR-30a-3p mimics and miR-30a-3p inhibitor, TEAD1 transcript was significantly up- and down-regulated, respectively (both P <0.05). After LPS treatment (24 h), expression of TEAD1 in the inhibitors group was significantly increased (P <0.01), while that in the mimics group was significantly suppressed (P <0.01). In the dual luciferase reporter experiment, miR-30a-3p overexpression decreased fluorescence intensity (P <0.01) from TEAD1-wt-containing plasmids, but did not influence fluorescence intensity from TEAD1-muta-containing plasmids. LPS may promote HK-2 cells proliferation through the miR-30a-3p/TEAD1 pathway. Conclusion: In a background of expression of inflammatory factors, including TNF-α, IL-1ß, and IL-6, which were transiently increased in the sepsis-AKI model, miR-30a was down-regulated. Down-regulated miR-30a-3p may promote cell proliferation by targeting TEAD1 in LPS-induced HK-2 cells, demonstrating its potential as a biomarker for early sepsis-AKI diagnosis.