Association between albumin corrected anion gap and all-cause mortality in critically ill patients with acute kidney injury: a retrospective study based on MIMIC-IV database.

BACKGROUND: The early identification of patients at high risk for acute kidney injury (AKI) with a poor prognosis is crucial to prevent complications and minimize mortality. This study sought to investigate the association between albumin-corrected anion gap (ACAG) and all-cause mortality among critically ill patients with AKI. METHODS: All eligible AKI patients from the Medical Information Mart for Intensive Care IV (MIMIC-IV version 2.0) database were considered for participation in this study. We employed Kaplan-Meier curves to assess the 30-d and 360-d cumulative survival rates among various groups. Flexibly visualizing the connection between ACAG and mortality, we utilize restricted cubic splines (RCS) and multivariate Cox regression models. Result robustness underwent assessment through subgroup analyses and sensitivity analyses. Receiver-operating characteristic (ROC) curves were generated to evaluate the predictive performance of ACAG. RESULTS: The study included 9625 AKI participants, of whom 58.60% were male, and the 360-d all-cause mortality rate was 39.89%. According to Kaplan-Meier analysis, the 30-d and 360-d cumulative survival rates for AKI patients were significantly lower in the high ACAG group than in the normal ACAG group. RCS analysis indicated that ACAG levels had a non-linear correlation with the risk of 30-d and 360-d mortality for AKI patients. Cox regression analysis demonstrated that ACAG is an independent risk indicator for 30-d and 360-d prognosis in AKI patients in the ICU. CONCLUSIONS: Elevated ACAG levels (> 20 mmol/L) at ICU admission were associated with 30-d and 360-d all-cause mortality in critically ill patients with AKI.

Effect of a 630 nm light on vasculogenic mimicry in A549 lung adenocarcinoma cells in vitro.

OBJECTIVE: The objective of this study was to investigate the effect of photodynamic therapy (PDT) on the formation of vasculogenic mimicry (VM) in the human lung adenocarcinoma A549 cell line in vitro. METHODS: The participants were divided into a blank control group, a photosensitizer group, a light group, and a PDT group. Cells from each group were cultured in three dimensions using Matrigel, and vasculogenic mimicry generation was observed microscopically. Periodic Acid-Schiff (PAS) staining was used to verify the vasculogenic mimicry structure. Reverse Transcription-Polymerase Chain Reaction (RT-PCR) was used to detect the expression levels of cellular osteopontin (OPN) and vascular endothelial growth factor (VEGF) mRNA. Western blotting was used to detect the expression levels of cellular OPN and VEGF protein. RESULTS: A549 cells cultured on Matrigel for about six hours revealed VM on PAS staining, and the number of formations was significantly reduced in the PDT group compared with other groups (P < 0.05). The RT-PCR results showed that the PDT group downregulated OPN and VEGF mRNA expression compared with each control group (P < 0.05). Western blot results showed that OPN and VEGF protein expression was downregulated in the PDT group compared with each control group (P < 0.05). The results of RT-PCR showed that the expression of OPN and VEGF mRNA was downregulated in the PDT group compared with each control group (P < 0.05). The results of Western blotting showed that the expression of OPN and VEGF was downregulated in the protein PDT group compared with each control group (P < 0.001). CONCLUSION: Photodynamic therapy significantly inhibited the formation of vasculogenic mimicry in human lung adenocarcinoma A549 cells in vitro and downregulated the expression of OPN, VEGF mRNA, and protein levels.

[Application of noninvasive brain-edema dynamic monitoring in critically ill patients with traumatic brain injury].

Brain edema could be secondary to cerebral lesion caused by a variety of reasons, severe cases may result in brain herniation or even death. Accurate real-time monitoring of cerebral edema, rational application of dehydrating drugs, and timely treatment of cerebral edema were very important for patients. However, there were defects in the monitoring methods commonly used in clinical practice. Noninvasive brain-edema monitoring was a new method, which can quantify the degree of brain edema by electromagnetic disturbance and directly reflect the state of brain edema. This article reviews the application of noninvasive brain-edema monitoring in the treatment of in critically ill patients with traumatic brain injury.

lncRNA LINC00473 promotes proliferation, migration, invasion and inhibition of apoptosis of non-small cell lung cancer cells by acting as a sponge of miR-497-5p.

Lung cancer is the leading cause of cancer-associated death worldwide and exhibits a poor prognosis. The present study aimed to determine the effect of long non-coding (lnc)RNA-LINC00473 on the development of non-small cell lung cancer (NSCLC) cells by regulating the expression of microRNA (miR)-497-5p. Reverse transcription-quantitative PCR was conducted to detect the level of LINC00473 and miR-497-5p. An MTT assay, flow cytometry and Transwell tests were performed to evaluate the proliferation, apoptosis, migration and invasion of NSCLC cells. Western blotting was performed to detect the expression of apoptosis- and migration-related proteins. RNA immunoprecipitation and a luciferase reporter assay were performed to verify the regulatory relationship between lncRNA-LINC00473 and miR-497-5p. LINC00473 expression was upregulated in lung cancer tissues and NSCLC cells (A549 and H1299) when compared with adjacent tissues or human bronchial epithelial cell lines and the 5-year survival rate was lower in patients with high LINC00473 expression compared with in patients with low LINC00473 expression. A negative correlation between LINC00473 and miR-497-5p was observed in lung cancer tissues. Proliferation, migration and invasion as well as the related protein levels were increased in A549 and H1299 transfected with pcDNA3.1-LINC00473, while the opposite results were obtained in A549 and H1299 transfected with small interfering (si)-LINC00473. Notably, it was demonstrated that LINC00473 could bind directly with miR-497-5p and inhibit its expression. miR-497-5p inhibitors reversed the effect of si-LINC00473. Furthermore, the present study demonstrated that LINC00473 promoted the malignant behaviour of NSCLC cells via regulating the ERK/p38 and MAPK signalling pathways and the expression of miR-497-5p.

[Prevention strategies for traumatic cardiac arrest].

The fatality rate of traumatic cardiac arrest (TCA) is extremely high, and it is very different from that of non-traumatic cardiac arrest (NTCA) in resuscitation strategy. Only when the standard resuscitation process is combined with rapid treatment of various reversible causes can the mortality rate of patients be decreased. In this paper, the key factors leading to TCA are reviewed, such as hypovolemic shock, asphyxia, tension pneumothorax, pericardial tamponade, crush syndrome, craniocerebral injury, cerebral hernia, and the control measures are elaborated respectively, so as to provide references for clinical treatment of patients with severe trauma, and reduce TCA incidence and mortality.

Fetal Dermal Mesenchymal Stem Cell-Derived Exosomes Accelerate Cutaneous Wound Healing by Activating Notch Signaling.

Fetal dermal mesenchymal stem cells (FDMSCs), isolated from fetal skin, are serving as a novel MSC candidate with great potential in regenerative medicine. More recently, the paracrine actions, especially MSC-derived exosomes, are being focused on the vital role in MSC-based cellular therapy. This study was to evaluate the therapeutic potential of exosomes secreted by FDMSCs in normal wound healing. First, the in vivo study indicated that FDMSC exosomes could accelerate wound closure in a mouse full-thickness skin wound model. Then, we investigated the role of FDMSC-derived exosomes on adult dermal fibroblast (ADFs). The results demonstrated that FDMSC exosomes could induce the proliferation, migration, and secretion of ADFs. We discovered that after treatment of exosomes, the Notch signaling pathway was activated. Then, we found that in FDMSC exosomes, the ligands of the Notch pathway were undetectable expect for Jagged 1, and the results of Jagged 1 mimic by peptide and knockdown by siRNA suggested that Jagged 1 may lead the activation of the Notch signal in ADFs. Collectively, our findings indicated that the FDMSC exosomes may promote wound healing by activating the ADF cell motility and secretion ability via the Notch signaling pathway, providing new aspects for the therapeutic strategy of FDMSC-derived exosomes for the treatment of skin wounds.

The oncogenic role of CB2 in the progression of non-small-cell lung cancer.

BACKGROUND: Several studies have verified the important role of cannabinoid and cannabinoid receptor agonists in tumor progression. However, little is known about the precise role of CB2 expression level in the progression of non-small-cell lung cancer (NSCLC). METHODS: The expression of CB2 in NSCLC tissues and corresponding paracancerous tissues was examined using immunohistochemical staining assay. The expression of CB2 was silenced by siRNA interference and loss-of-function assays were performed to investigate the biological function of CB2 in the proliferation, migration, invasion, and apoptosis of NSCLC cells. The expression of related proteins was detected using western blot analysis. RESULTS: In this study, we observed that CB2 was up-regulated in NSCLC tissues and the up-regulation was correlated with tumor size and advanced NSCLC pathological grading. Moreover, compared with the control group, silencing of CB2 decreased the proliferation, migration and invasion abilities of A549 and H1299 cells, and induced apoptosis by regulation of Bcl-2/Bax axis and active Caspase3. Furthermore, CB2 knockdown inactivated the Akt/mTOR/P70S6K pathway by decreasing the level of p-Akt, p-mTOR and expression of P70S6K in A549 and H1299 cells. CONCLUSION: Our data suggested that targeting CB2 may inhibit the growth and survival of NSCLC cells, which the Akt/mTOR/P70S6K pathway may be involved in. These results confer the pro-oncogenic role of CB2 in the progression of NSCLC, thus improving our understanding of CB2 in tumor progression.

[Research on morbidity and relative factors of cough variant asthma among patients with chronic cough syndrome].

OBJECTIVE: To study the morbidity of cough variant asthma (CVA) among patients with chronic cough syndrome and its relative risk factors. METHODS: Patients were recruited with detailed history on their illness. Data were collected on physical examination, chest X-ray, eosinophil cell counts, pulmonary ventilation with histamine stimulating test and bronchi dilation test. According to available data, diagnosis of CVA was confirmed and the relative factors Questionnaire form was completed for each patient. RESULTS: Among 473 patients with chronic cough, 95 (44 male and 51 female) were confirmed to be CVA (20.08%). Analysis of the relative factors suggested that CVA was associated with multiple factors. Morbidity of CVA was associated with season, personal histories on allergy and family history on asthma. CVA could be induced by upper respiratory tract infection, inhale of oil vapor, acrimony air, over-burdened physical exercises etc. CONCLUSION: For patients with chronic cough symptom, clear diagnosis of CVA, avoid of passable risk factors and timely medical intervention when necessary, would be helpful in controlling clinical courses and improving the prognosis of the disease.