Lie Algebras Represented as a Sum of Two Subalgebras

Let L be a Lie algebra represented as a sum of two subalgebras A and B. We prove that if L belongs to a subclass of the class of locally finite Lie algebras over a field of characteristic &#8800; 2 and both A and B are locally nilpotent, then L is locally soluble. We also prove that if L is a serially finite Lie algebra over a field of characteristic zero, then any common serial subalgebra of A and B is serial in L.</p

SERIALLY COALESCENT CLASSES OF LIE ALGEBRAS

We introduce the concept of serially coalescent classes of Lie algebras corresponding to those of coalescent classes and ascendantly coalescent classes. We show that the class of finite-dimensional and nilpotent, the class of finite-dimensional and the class of finite-dimensional and soluble Lie algebras, are serially coalescent classes for locally finite Lie algebras over any field of characteristic zero. We also introduce the concept of locally serially coalescent classes of Lie algebras and find some locally serially coalescent classes for locally finite Lie algebras.</p

Is the Comet Assay a Sensitive Procedure for Detecting Genotoxicity?

Although the Comet assay, a procedure for quantitating DNA damage in mammalian cells, is considered sensitive, it has never been ascertained that its sensitivity is higher than the sensitivity of other genotoxicity assays in mammalian cells. To determine whether the power of the Comet assay to detect a low level of genotoxic potential is superior to those of other genotoxicity assays in mammalian cells, we compared the results of Comet assay with those of micronucleus test (MN test). WTK1 human lymphoblastoid cells were exposed to methyl nitrosourea (MNU), ethyl nitrosourea (ENU), methyl methanesulfonate (MMS), ethyl methanesulfonate (EMS), bleomycin (BLM), or UVC. In Comet assay, cells were exposed to each mutagen with (Comet assay/araC) and without (Comet assay) DNA repair inhibitors (araC and hydroxyurea). Furthermore, acellular Comet assay (acellular assay) was performed to determine how single-strand breaks (SSBs) as the initial damage contributes to DNA migration and/or to micronucleus formation. The lowest genotoxic dose (LGD), which is defined as the lowest dose at which each mutagen causes a positive response on each genotoxicity assay, was used to compare the power of the Comet assay to detect a low level of genotoxic potential and that of MN test; that is, a low LGD indicates a high power. Results are summarized as follows: (1) for all mutagens studied, LGDs were MN test ≦ Comet assay; (2) except for BLM, LGDs were Comet assay/araC ≦ MN test; (3) except for UVC and MNU, LGDs were acellular assay ≦ Comet assay/araC ≦ MN test ≦ Comet assay. The following is suggested by the present findings: (1) LGD in the Comet assay is higher than that in MN test, which suggests that the power of the MN test to detect a low level of genotoxic potential is superior to that of the Comet assay; (2) for the studied mutagens, all assays were able to detect all mutagens correctly, which suggests that the sensitivity of the Comet assay and that of the MN test were exactly identical; (3) the power of the Comet assay to detect a low level of genotoxic potential can be elevated to a level higher than that of MN test by using DNA resynthesis inhibitors, such as araC and HU

Systematic review protocol of the effectiveness of HIV prevention interventions for reducing risky sexual behaviour among youth globally

INTRODUCTION: Human immunodeficiency virus (HIV) prevention interventions focused at reducing risky sexual behaviours are an important strategy for preventing HIV infection among youth (15-24 years) who continue to be vulnerable to the disease. This systematic review aims to synthesise current global evidence on the effectiveness of HIV prevention interventions for reducing risky sexual behaviour among youth in the last decade. METHODS AND ANALYSIS: MEDLINE/PubMed, EMBASE, PsychINFO, ProQuest Central, CINAHL and Web of Science databases, ClinicalTrials.gov and the WHO International Clinical Trials Registry Platform and reference lists of included studies and systematic reviews on effectiveness of HIV prevention interventions for reducing risky sexual behaviour among youth will be searched for articles published from August 2011 to August 2021. Eligible studies will be longitudinal studies including randomised controlled trials and quasi-experimental studies that examined the effectiveness of HIV prevention interventions among youth populations (15-24 years) with risky sexual behaviour as a primary or secondary outcome. Study selection and quality assessment will be undertaken independently by three reviewers and disagreements will be resolved through consensus. Data analysis will be undertaken using RevMan software V.5.3.3. A random effects meta-analysis will be conducted to report heterogeneous data where statistical pooling is achievable. We will use I2 statistics to test for heterogeneity. Where appropriate, a funnel plot will be generated to assess publication bias. Where statistical pooling is unachievable, the findings will be reported in a narrative form, together with tables and figures to assist in data presentation if required. Reporting of the systematic review will be informed by Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. ETHICS AND DISSEMINATION: Ethical approval is not required. Findings of the systematic review will be published in a peer-reviewed journal. The findings will be of interest to researchers, healthcare practitioners and policymakers. PROSPERO REGISTRATION NUMBER: CRD42021271774

A case of early relapsed multiple lung metastases after esophagectomy successfully treated with S-1/cisplatin therapy after docetaxel/5-fluorouracil/cisplatin therapy

A 55-year-old-male patient underwent subtotal esophagectomy for esophageal cancer (pT1b, N0, M0, stage II) in April 2005. The patient received postoperative chemotherapy (docetaxel 40 mg/body, 5-fluorouracil 750 mg/body, cisplatin 10 mg/body : administered every 4 weeks) for 3 months. Six months postoperatively, routine follow up CT demonstrated multiple metastatic tumors in the bilateral lungs. Under the diagnosis of multiple lung metastases, the patient was hospitalized and received intensive chemotherapy with docetaxel 40 mg/ week (day 1), 5-fluorouracil 500 mg/ day (days 1-5), cisplatin 10 mg/ day (days 1-5). After two weeks administration, the patient eagerly hoped for outpatient treatment. The treatment was changed to outpatient chemotherapy with S-1 100 mg/ day (continuous administration for 3 weeks followed by rest for 1 week) and cisplatin 20 mg/ every week. The treatment enabled the patient to keep working. Follow up CT showed disappearance of all tumors two months after TS-1/cisplatin chemotherapy. There were no obvious signs of recurrence 5 months after chemotherapy. The S-1/cisplatin therapy in the outpatient was thought to be one of the effective treatments in maintaining quality of life for the patient

The obesity paradox is not observed in chronic heart failure patients with metabolic syndrome

Although being overweight or obese is a risk factor for cardiovascular disease, obese subjects often live longer than their lean peers, and this is known as the obesity paradox. We investigated the impact of obesity on cardiac prognosis in chronic heart failure (CHF) patients, with or without metabolic syndrome. Design and Methods: We divided 374 consecutive CHF patients into two groups according to their mean body mass index (BMI) and prospectively followed them for 2 years. Results: There were 126 cardiac events, including 32 cardiac deaths and 94 re-hospitalizations. Kaplan-Meier analysis revealed a significantly lower cardiac event rate in the higher BMI group (log-rank test P < 0.001) in all patients and those patients without metabolic syndrome. There was no association between BMI and cardiac prognosis in patients with metabolic syndrome. Cox hazard analysis revealed that a higher BMI was associated with favorable cardiac outcomes in all patients and patients without metabolic syndrome, after adjusting for confounding factors. However, this finding did not extend to patients with metabolic syndrome. Conclusions: The advantages of obesity are not found in CHF patients with metabolic syndrome

Clarithromycin expands CD11b+Gr-1+ MDSC-like cells

Macrolides are used to treat various inflammatory diseases owing to their immunomodulatory properties; however, little is known about their precise mechanism of action. In this study, we investigated the functional significance of the expansion of myeloid-derived suppressor cell (MDSC)-like CD11b+Gr-1+ cells in response to the macrolide antibiotic clarithromycin (CAM) in mouse models of shock and post-influenza pneumococcal pneumonia as well as in humans. Intraperitoneal administration of CAM markedly expanded splenic and lung CD11b+Gr-1+ cell populations in naïve mice. Notably, CAM pretreatment enhanced survival in a mouse model of lipopolysaccharide (LPS)-induced shock. In addition, adoptive transfer of CAM-treated CD11b+Gr-1+ cells protected mice against LPS-induced lethality via increased IL-10 expression. CAM also improved survival in post-influenza, CAM-resistant pneumococcal pneumonia, with improved lung pathology as well as decreased interferon (IFN)-γ and increased IL-10 levels. Adoptive transfer of CAM-treated CD11b+Gr-1+ cells protected mice from post-influenza pneumococcal pneumonia. Further analysis revealed that the CAM-induced CD11b+Gr-1+ cell expansion was dependent on STAT3-mediated Bv8 production and may be facilitated by the presence of gut commensal microbiota. Lastly, an analysis of peripheral blood obtained from healthy volunteers following oral CAM administration showed a trend toward the expansion of human MDSC-like cells (Lineage−HLA-DR−CD11b+CD33+) with increased arginase 1 mRNA expression. Thus, CAM promoted the expansion of a unique population of immunosuppressive CD11b+Gr-1+ cells essential for the immunomodulatory properties of macrolides

Association of plasma thioredoxin-1 with renal tubular damage and cardiac prognosis in patients with chronic heart failure

AbstractBackgroundThioredoxin-1 (Trx-1) is an abundant 12.5kDa redox protein expressed in almost all eukaryotic cells that protect against the development of heart failure and kidney dysfunction. Plasma Trx-1 levels are considered as a reliable marker for oxidative stress. However, it remains to be determined whether plasma Trx-1 levels can predict cardiac prognosis in patients with chronic heart failure (CHF).Methods and resultsWe measured plasma Trx-1 levels and urinary β2-microglobulin–creatinine ratio (UBCR), a marker for renal tubular damage, in 156 consecutive patients with CHF and 17 control subjects. The patients were prospectively followed for a median follow-up period of 627 days and 46 cardiac events were observed. The patients with cardiac events had significantly higher plasma Trx-1 levels and UBCR levels than the cardiac event-free patients. Multivariate Cox proportional hazard analysis revealed that an elevated Trx-1 level was independently associated with poor outcome in patients with CHF after adjustment for confounding factors (hazard ratio, 1.74; 95% confidence interval, 1.33–2.29; p<0.0001). UBCR was increased with higher plasma Trx-1 levels. Kaplan–Meier analysis demonstrated that the highest Trx-1 tertile was associated with the highest risk of cardiac events.ConclusionPlasma Trx-1 level was associated with renal tubular damage and cardiac prognosis, suggesting that it could be a useful marker to identify patients at high risk for comorbid heart failure and renal tubular damage

High-mobility group box 1-mediated heat shock protein beta 1 expression attenuates mitochondrial dysfunction and apoptosis

AbstractAimsApoptosis of cardiomyocytes is thought to account for doxorubicin cardiotoxicity as it contributes to loss of myocardial tissue and contractile dysfunction. Given that high-mobility group box 1 (HMGB1) is a nuclear DNA-binding protein capable of inhibiting apoptosis, we aimed to clarify the role of HMGB1 in heat shock protein beta 1 (HSPB1) expression during doxorubicin-induced cardiomyopathy.Methods and resultsMitochondrial damage, cardiomyocyte apoptosis, and cardiac dysfunction after doxorubicin administration were significantly attenuated in mice with cardiac-specific overexpression of HMGB1 (HMGB1-Tg) compared with wild type (WT) -mice. HSPB1 levels after doxorubicin administration were significantly higher in HMGB1-Tg mice than in WT mice. Transfection with HMGB1 increased the expression of HSPB1 at both the protein and mRNA levels, and HMGB1 inhibited mitochondrial dysfunction and apoptosis after exposure of cardiomyocytes to doxorubicin. HSPB1 silencing abrogated the inhibitory effect of HMGB1 on cardiomyocyte apoptosis. Doxorubicin increased the binding of HMGB1 to heat shock factor 2 and enhanced heat shock element promoter activity. Moreover, HMGB1 overexpression greatly enhanced heat shock element promoter activity. Silencing of heat shock factor 2 attenuated HMGB1-dependent HSPB1 expression and abrogated the ability of HMGB1 to suppress cleaved caspase-3 accumulation after doxorubicin stimulation.ConclusionsWe report the first in vivo and in vitro evidence that cardiac HMGB1 increases HSPB1 expression and attenuates cardiomyocyte apoptosis associated with doxorubicin-induced cardiomyopathy. Cardiac HMGB1 increases HSPB1 expression in cardiomyocytes in a heat shock factor 2-dependent manner

Conditioned medium from stem cells derived from human exfoliated deciduous teeth ameliorates NASH via the Gut-Liver axis

Non-alcoholic steatohepatitis (NASH) occurrence has been increasing and is becoming a major cause of liver cirrhosis and liver cancer. However, effective treatments for NASH are still lacking. We examined the benefits of serum-free conditioned medium from stem cells derived from human exfoliated deciduous teeth (SHED-CM) on a murine non-alcoholic steatohepatitis (NASH) model induced by a combination of Western diet (WD) and repeated administration of low doses of carbon tetrachloride intraperitoneally, focusing on the gut-liver axis. We showed that repeated intravenous administration of SHED-CM significantly ameliorated histological liver fibrosis and inflammation in a murine NASH model. SHED-CM inhibited parenchymal cell apoptosis and reduced the activation of inflammatory macrophages. Gene expression of pro-inflammatory and pro-fibrotic mediators (such as Tnf-α, Tgf-β, and Ccl-2) in the liver was reduced in mice treated with SHED-CM. Furthermore, SHED-CM protected intestinal tight junctions and maintained intestinal barrier function, while suppressing gene expression of the receptor for endotoxin, Toll-like receptor 4, in the liver. SHED-CM promoted the recovery of Caco-2 monolayer dysfunction induced by IFN-γ and TNF-α in vitro. Our findings suggest that SHED-CM may inhibit NASH fibrosis via the gut-liver axis, in addition to its protective effect on hepatocytes and the induction of macrophages with unique anti-inflammatory phenotypes