There is a lack of early specific diagnosis and effective evaluation of sepsis, and the clinical treatment is not timely. As a result, the mortality is high, which seriously threatens the health of the people. Data were collected from the human blood samples of the hospital by gas chromatography mass spectrometry. Thirty-five healthy controls and 42 sepsis patients were enrolled. Machine-learning techniques were used to diagnose the sepsis. Using the metabolic data from the sepsis patients, the proposed method has got 81.6% recognition rate, 89.57% sensitivity, and 65.77% specificity. A new learning strategy was proposed to boost the performance of the kernel extreme learning machine, known as, chaotic fruit fly optimization, and two new mechanisms were introduced into the original a fruit fly optimization, including the chaotic population initialization and the chaotic local search strategy. To further enhance the diagnosis accuracy and identify the most important biomarkers, we performed the feature selection using the random forest before the construction of the classification model. The final established model, random forest-improved fruit fly optimization algorithm-kernel extreme learning machine, was used to effectively diagnose the sepsis. Experimental results demonstrate that the proposed method obtains better results than other methods across four performance metrics. We screened out five biomarkers and performed statistical analysis on these five substances. The level of acetic acid increased (p < 0.05) in the sepsis group, while the level of linoleic acid and cholesterol decreased (p < 0.05). The promising results suggest that the developed methodology can be a useful diagnostic tool for clinical decision support.

A New Effective Machine Learning Framework for Sepsis Diagnosis

Breast cancer is the most common cancer in women and a leading cause of cancer-associated mortalities in the world. Epithelial-to-mesenchymal transition (EMT) serves an important role in the process of metastasis and invasive ability in cancer cells, and transforming growth factor β1 (TGF-β1) have been investigated for promoting EMT. However, in the present study, the role of the sphingomyelin synthase 1 (SMS1) in TGF-β1-induced EMT development was investigated. Firstly, bioinformatics analysis demonstrated that the overexpression of SMS1 negatively regulated the TGFβ receptor I (TβRI) level of expression. Subsequently, the expression of SMS1 was decreased, whereas, SMS2 had no significant difference when MDA-MB-231 cells were treated by TGF-β1 for 72 h. Furthermore, the present study constructed an overexpression cells model of SMS1 and these cells were treated by TGF-β1. These results demonstrated that overexpression of SMS1 inhibited TGF-β1-induced EMT and the migration and invasion of MDA-MB-231 cells, increasing the expression of E-cadherin while decreasing the expression of vimentin. Furthermore, the present study further confirmed that SMS1 overexpression could decrease TβRI expression levels and blocked smad family member 2 phosphorylation. Overall, the present results suggested that SMS1 could inhibit EMT and the migration and invasion of MDA-MB-231 cells via TGF-β/Smad signaling pathway.

/pdf/sphingomyelin-synthase-1-regulates-the-epithelial-to-433a8zwysq.pdf

Sphingomyelin synthase 1 regulates the epithelial‑to‑mesenchymal transition mediated by the TGF‑β/Smad pathway in MDA‑MB‑231 cells.

Sphingomylin participates in sperm function in animals, and also regulates the Akt and ERK signaling pathways, both of which are associated with the asthenospermia. Sphingomyelin synthase 2 (SMS2) is involved in the biosynthesis of sphingomylin. To determine the relationship between SMS2 and human sperm function, we analyzed the distribution of SMS2 in human sperm and testes, and SMS2 expression in patients with asthenospermia and normozoospermia; human sperm were treated with anti-SMS2, and the sperm motility, penetration ability into methylcellulose, capacitation and acrosome reaction, and sperm [Ca2+]i imaging were evaluated, while the Akt and ERK pathway and cleaved caspase 3 were also analyzed. Results showed that SMS2 was localized in the testis and human sperm, and the protein levels of normozoospermia were higher than asthenospermia. Inhibition of SMS2 activity significantly decreased sperm motility and penetration ability into methylcellulose, but had no influence on capacitation and acrosome reaction, or on intracellular [Ca2+]i compared to IgG-treated control groups. Moreover, the phosphorylation level of Akt was decreased, whereas the phosphorylation of ERK and cleaved-caspase 3 levels were significantly increased. Taken together, SMS2 can affect sperm motility and penetration ability into methylcellulose, and participate in apoptosis associated with the Akt and ERK signaling pathways.

https://www.mdpi.com/1420-3049/25/18/4231/pdf

Sphingomyelin Synthase 2 Participate in the Regulation of Sperm Motility and Apoptosis.

Background/aim Pulmonary microvascular endothelial cells (PMVECs) play a pivotal role in the process of acute lung injury (ALI), which can be induced by lipopolysaccharide (LPS). Numerous reports have indicated that both miR-33 and RIP140 are involved in the inflammatory response in macrophages. In this study, we sought to investigate whether miR-33 and RIP140 participate in ALI induced by LPS. Materials and methods First, we isolated and identified PMVECs from BALB/c mice. Subsequently, both PMVECs and BALB/c mice were treated with PBS, LPS, or pyrrolidine dithiocarbamate (PDTC) plus LPS and divided into three groups: control (PBS), LPS (LPS), and L+P (LPS plus PDTC) groups. We assessed pathology by hematoxylin and eosin staining, and miR-33 and RIP140 expression levels were examined using quantitative PCR and Western blot analyses. Results Our results demonstrated that LPS can induce PMVEC injury and ALI and that LPS treatment significantly decreased miR-33 expression compared with controls (P < 0.001, n = 5). On the contrary, RIP140 was markedly overexpressed by LPS treatment (P < 0.001, n = 5). However, this alteration can be inhibited by pretreatment with PDTC before LPS (P < 0.05, n = 5). Conclusion This study is the first to confirm that both miR-33 and RIP140 participate in LPS-induced PMVEC injury and ALI, which may help uncover the mechanism of ALI

/pdf/mir-33-and-rip140-participate-in-lps-induced-acute-lung-nqmx0l9yfz.pdf

miR-33 and RIP140 participate in LPS-induced acute lung injury

Abstract Context Plantamajoside (PMS) possesses rich pharmacological characteristics that have been applied to remedy dozens of diseases. However, the understanding of PMS in sepsis remains insufficient. Objective Role of PMS in sepsis-regulated organ dysfunction and potential mechanisms were investigated. Materials and methods Thirty C57BL/6 male mice were adaptive fed for three days and used to establish acute sepsis model by caecal ligation and perforation (CLP). These experimental mice were divided into Sham, CLP, CLP + 25 mg PMS/kg body weight (PMS/kg), CLP + 50 mg PMS/kg and CLP + 100 mg PMS/kg (n = 6). The pathological and apoptotic changes of lung, liver and heart tissues were observed via HE and TUNEL staining. The injury-related factors of lung, liver and heart were detected by corresponding kits. ELISA and qRT-PCR were applied to assess IL-6/TNF-α/IL-1β levels. Apoptosis-related and TRAF6/NF-κB-related proteins were determined using Western blotting. Results All doses of PMS enhanced the survival rates in the sepsis-induced mouse model. PMS remitted sepsis-mediated lung, liver and heart injury through prohibiting MPO/BALF (70.4%/85.6%), AST/ALT (74.7%/62.7%) and CK-MB/CK (62.3%/68.9%) levels. Moreover, the apoptosis index (lung 61.9%, liver 50.2%, heart 55.7% reduction) and IL-6/TNF-α/IL-1β levels were suppressed by PMS. Furthermore, PMS lowered TRAF6 and p-NF-κB p65 levels, whereas TRAF6 overexpression reversed the protective influences of PMS in organ injury, apoptosis and inflammation triggered by sepsis. Discussion and conclusions PMS suppressed sepsis-induced organ dysfunction by regulating the TRAF6/NF-κB axis, and PMS treatment may be considered as a novel strategy for sepsis-caused damage in future.

https://www.tandfonline.com/doi/pdf/10.1080/13880209.2023.2215849?needAccess=true&role=button

Plantamajoside alleviates acute sepsis-induced organ dysfunction through inhibiting the TRAF6/NF-κB axis

Sepsis is characterized by a severe inflammatory response to infection. With the spread of sepsis, various tissues, including the lungs, liver and kidney, may be damaged. This may finally develop into multiple organ dysfunction syndrome. Sphingomyelin and cholesterol are two main lipids involved in sepsis. The metabolism of sphingomyelin and cholesterol in the livers of mice with sepsis needs to be clarified. To achieve this, the present study intraperitoneally injected mice with PBS, lipopolysaccharide (LPS; 10 mg/kg) and LPS + pyrrolidine dithiocarbamate (PDTC; 30 mg/kg). Subsequently, sphingomyelin and cholesterol content were measured using kits, the sphingomyelin synthase (SMS) activity was measured using thin layer chromatography, and the expression levels of SMS1 and 2, hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR), ATP binding cassette subfamily A member 1 (ABCA1), scavenger receptor class B member 1 (SR-B1) and apolipoprotein A1 (Apo A1) were determined by western blotting in the livers of mice. Results demonstrated that, in the LPS group, sphingomyelin and cholesterol content was significantly increased (P 0.05; n=6), compared to the levels in the control group. However, PDTC was able to attenuate these alterations. These results indicated that sphingomyelin and cholesterol content may increase in the liver dysfunction of sepsis by increasing the expression of SMS2, HMGCR, SR-B1 and ABCA1, and downregulating Apo A1.

/pdf/effects-of-sepsis-on-the-metabolism-of-sphingomyelin-and-15zbp088jf.pdf

Effects of sepsis on the metabolism of sphingomyelin and cholesterol in mice with liver dysfunction.

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Effects of sepsis on the metabolism of sphingomyelin and cholesterol in mice with liver dysfunction.