Ginsenoside Rg3 attenuates the osimertinib resistance by reducing the stemness of non-small cell lung cancer cells.

PMID: 

Environ Toxicol. 2020 Jan 9. Epub 2020 Jan 9. PMID: 31916386

Abstract Title: 

Ginsenoside Rg3 attenuates the osimertinib resistance by reducing the stemness of non-small cell lung cancer cells.

Abstract: 

In the present study, we found that Ginsenoside Rg3 attenuated the stemness of non-small cell lung cancer (NSCLC) cells, evident by decreasing spheroid formation ability, ALDH1 activity and stemness marker expression. Furthermore, osimertinib-resistant NSCLC cells displayed a stronger stemness than the parental cells. Ginsenoside Rg3 reduced the stemness and osimertinib resistance of osimertinib-resistant cells. RNA-sequencing revealed that Hippo signaling was shown on the top of the most upregulated pathways regulated by Ginsenoside Rg3 in NSCLC cells, and YAP/TAZ expression was suppressed by Ginsenoside Rg3. Notably, the inhibitor of Hippo signaling attenuated the effects of Ginsenoside Rg3 on the stemness of NSCLC cells. Therefore, Ginsenoside Rg3 attenuates the osimertinib resistance of NSCLC cells via suppressing the stemness, which is dependent on Hippo pathway.

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Ginsenoside Rg3 can inhibit expression of HIF-1α and VEGF in human gastric cancer cells

PMID: 

J Cancer Res Ther. 2019 ;15(7):1642-1646. PMID: 31939450

Abstract Title: 

Inhibition of the hypoxia-induced factor-1α and vascular endothelial growth factor expression through ginsenoside Rg3 in human gastric cancer cells.

Abstract: 

Objective: The aim of this study is to probe in the inhibitory effects of ginsenoside Rg3 on the expression of hypoxia-induced factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF) in human gastric cancer cells.Materials and Methods: Human gastric cancer BGC823 cells were divided into the control group and experiment group, and expression levels of HIF-1α and VEGF were detected by immunocytochemistry and Western blot after cells were cultured under hypoxia for different durations.Results: Under hypoxia, expression of HIF-1α and VEGF in human gastric cancer BGC823 cells showed an increasing trend, and that was remarkably lower in experiment group than in the control group after applying Rg3, which was obvious at 12 and 24 h (P

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Ginsenoside Rg5 could be a potential therapeutic agent for breast cancer treatment.

PMID: 

Nutrients. 2020 Jan 18 ;12(1). Epub 2020 Jan 18. PMID: 31963684

Abstract Title: 

The Preparation of Ginsenoside Rg5, Its Antitumor Activity against Breast Cancer Cells and Its Targeting of PI3K.

Abstract: 

Ginsenosides have been reported to possess various pharmacological effects, including anticancer effects. Nevertheless, there are few reports about the antitumor activity and mechanisms of ginsenoside Rg5 against breast cancer cells. In the present study, the major ginsenoside Rb1 was transformed into the rare ginsenoside Rg5 through enzymatic bioconversion and successive acid-assisted high temperature and pressure processing. Ginsenosides Rb1, Rg3, and Rg5 were investigated for their antitumor effects against five human cancer cell lines via the MTT assay. Among them, Rg5 exhibited the greatest cytotoxicity against breast cancer. Moreover, Rg5 remarkably suppressed breast cancer cell proliferation through mitochondria-mediated apoptosis and autophagic cell death. LC3B-GFP/Lysotracker and mRFP-EGFP-LC3B were utilized to show that Rg5 induced autophagosome-lysosome fusion. Western blot assays further illustrated that Rg5 decreased the phosphorylation levels of PI3K, Akt, mTOR, and Bad and suppressed the PI3K/Akt signaling pathway in breast cancer. Moreover, Rg5-induced apoptosis and autophagy could be dramatically strengthened by the PI3K/Akt inhibitor LY294002. Finally, a molecular docking study demonstrated that Rg5 could bind to the active pocket of PI3K. Collectively, our results revealed that Rg5 could be a potential therapeutic agent for breast cancer treatment.

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Acute effects of air pollutants on daily mortality and hospitalizations due to cardiovascular and respiratory diseases.

PMID: 

J Thorac Dis. 2019 Jul ;11(7):3070-3083. PMID: 31463136

Abstract Title: 

Acute effects of air pollutants on daily mortality and hospitalizations due to cardiovascular and respiratory diseases.

Abstract: 

Background: Chiang Dao is one of the districts in Chiang Mai, Thailand facing high level of seasonal air pollution every year, the exposure of community dwellers to outdoor air pollutants 24 hours a day during seasonal smog period because of their open-air housing style, and agricultural occupational hazard. In addition, Chiang Dao hospital is the only available hospital serving the community with open-air wards; therefore we could certainly to identify the association between air pollution and mortality of hospitalized patients. Thus, the aim of this study was to determine the association between daily average seasonal air pollutants and daily mortality of hospitalized patients and community dwellers as well as emergency and hospitalization visits for serious respiratory, cardiovascular, and cerebrovascular diseases.Methods: This time series study was conducted between 1 March 2016 and 31 March 2017. The association of various air pollutant concentrations including particulate matter diameter less than 10 and 2.5 microns (PMand PM), sulfur dioxide (SO), nitrogen dioxide (NO), carbon monoxide (CO), ozone (O) and daily mortality of hospitalized patients and community dwellers as well as relationship with frequencies of serious respiratory, cardiovascular, and cerebrovascular diseases were analyzed using a general linear model with Poisson distribution.Results: Only PMwas found to be associated with increased daily mortality of hospitalized patients (lag day 6, adjusted RR =1.153, 95% CI: 1.001-1.329), whereas PM, PM, NO, and Owere associated with increased daily non-accidental mortality of community dwellers (lag day 0-7, adjusted RR =1.006-1.040, 95% CI: 1.000-1.074). For acute serious respiratory events; PMand PMwere associated with acute exacerbation of chronic obstructive pulmonary disease (AECOPD), while SO, CO, and Owere associated with emergency visits for community-acquired pneumonia (CAP). Owas associated with emergency visits for heart failure (HF), NOwith emergency visits for myocardial infarction (MI), and SOwith hospitalized visits for cerebrovascular accident (CVA).Conclusions: Seasonal air pollutants were found to be associated with higher mortality among hospitalized patients and community dwellers with varying effects on severe acute respiratory, cardiovascular, and cerebrovascular diseases.

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Particulate air pollution in Ho Chi Minh city and risk of hospital admission for acute lower respiratory infection among young children.

PMID: 

Environ Pollut. 2020 Feb ;257:113424. Epub 2019 Oct 18. PMID: 31672367

Abstract Title: 

Particulate air pollution in Ho Chi Minh city and risk of hospital admission for acute lower respiratory infection (ALRI) among young children.

Abstract: 

High levels of air pollutants in Vietnam, especially particulate matters including PM, can be important risk factors for respiratory diseases among children of the country. However, few studies on the effects of ambient air pollution on human health have been conducted in Vietnam so far. The aim of this study is to examine the association between PMand hospital admission due to acute lower respiratory infection (ALRI) among children aged 

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The association of childhood pneumonia with household air pollution in Nepal.

PMID: 

Matern Child Health J. 2020 Jan 24. Epub 2020 Jan 24. PMID: 31981064

Abstract Title: 

The Association of Childhood Pneumonia with Household Air Pollution in Nepal: Evidence from Nepal Demographic Health Surveys.

Abstract: 

INTRODUCTION: Childhood pneumonia is a major cause of mortality worldwide while household air pollution (HAP) is a major contributor to childhood pneumonia in low and middle-income countries. This paper presents the prevalence trend of childhood pneumonia in Nepal and assesses its association with household air pollution.METHODS: The study analysed data from the 2006, 2011 and 2016 Nepal Demographic Health Surveys (NDHS). It calculated the prevalence of childhood pneumonia and the factors that cause household air pollution. The association of childhood pneumonia and HAP was assessed using univariate and multi-variate analysis. The population attributable fraction (PAF) of indoor pollution for causing pneumonia was calculated using 2016 NDHS data to assess the burden of pneumonia attributable to HAP factors.RESULTS: The prevalence of childhood pneumonia decreased in Nepal between 2006 and 2016 and was higher among households using polluting cooking fuels. There was a higher risk of childhood pneumonia among children who lived in households with no separate kitchens in 2011 [Adjusted risk ratio (ARR) 1.40, 95% CI 1.01-1.97] and in 2016 (ARR 1.93, 95% CI 1.14-3.28). In 2016, the risk of children contracting pneumonia in households using polluting fuels was double (ARR 1.98, 95% CI 1.01-3.92) that of children from households using clean fuels. Based on the 2016 data, the PAF for pneumonia was calculated as 30.9% for not having a separate kitchen room and 39.8% for using polluting cooking fuel.DISCUSSION FOR PRACTICE: Although the occurrence of childhood pneumonia in Nepal has decreased, the level of its association with HAP remained high.

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Emerging role of air pollution in autoimmune diseases.

PMID: 

Autoimmun Rev. 2019 Jun ;18(6):607-614. Epub 2019 Apr 5. PMID: 30959217

Abstract Title: 

Emerging role of air pollution in autoimmune diseases.

Abstract: 

Autoimmune diseases (ADs) are a broad spectrum of disorders featured by the body's immune responses being directed against its own tissues, resulting in prolonged inflammation and subsequent tissue damage. Recently, the exposure to ambient air pollution has been implicated in the occurrence and development of ADs. Mechanisms linking air pollution exposures and ADs mainly include systemic inflammation, increased oxidative stress, epigenetic modifications induced by exposures and immune response caused by airway damage. The lung may be an autoimmunity initiation site in autoimmune diseases (ADs). Air pollutants can bind to the Aryl hydrocarbon receptor (AHR) to regulate Th17 and Treg cells. Oxidative stress and inducible bronchus associated lymphoid tissue caused by the pollutants can influence T, B cells, resulting in the production of proinflammatory cytokines. These cytokines stimulate B cell and dendritic cells, resulting in a lot of antibodies and self-reactive T lymphocytes. Moreover, air pollutants may induce epigenetic changes to contribute to ADs. In this review, we will concern the associations between air pollution and immune-inflammatory responses, as well as mechanisms linking air pollution exposure and autoimmunity. In addition, we focus on the potential roles of air pollution in major autoimmune diseases including systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), multiple sclerosis (MS), and type 1 diabetes mellitus (T1DM).

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Two case reports of life-threatening breakthrough varicella occurring despite vaccination prior to cancer diagnosis, with one resulting in death.

PMID: 

Pediatr Infect Dis J. 2015 Sep ;34(9):1027-9. PMID: 25955833

Abstract Title: 

Failure of a Single Varicella Vaccination to Protect Children With Cancer From Life-Threatening Breakthrough Varicella.

Abstract: 

We report 2 children with life-threatening breakthrough varicella. Both had received 1 varicella vaccination before onset of cancer. Despite treatment with intravenous acyclovir, 1 child died of disseminated varicella. Because similar fatal cases have been reported, high-risk immunocompromised children with 1 varicella vaccination may warrant the same varicella prophylaxis as immunocompromised children who have never been vaccinated.

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Parental PM2.5 exposure-promoted development of metabolic syndrome in offspring.

PMID: 

Toxicol Sci. 2019 Aug 1 ;170(2):415-426. PMID: 31086988

Abstract Title: 

Parental PM2.5 Exposure-Promoted Development of Metabolic Syndrome in Offspring Is Associated With the Changes of Immune Microenvironment.

Abstract: 

Parental exposure to ambient fine particulate matter (PM2.5) has been associated with some of adverse health outcomes in offspring. The association between parental PM2.5 exposure and the development of metabolic syndrome (MetS) in offspring, and the effects of parental PM2.5 exposure on the susceptibility of offspring mice to PM2.5, has not been evaluated. The C57BL/6 parental mice (male and female mice) were exposed to filtered air (FA) or concentrated PM2.5 (PM) using Shanghai-METAS for a total of 16 weeks. At week 12 during the exposure, we allowed the parental male and female mice to breed offspring mice. The male offspring mice were divided into 4 groups and exposed to PM and FA again. The results showed that whether the parental mice were exposed to PM2.5 or not, the offspring mice exposure to PM2.5 appeared the elevation of blood pressure, insulin resistance, impairment of glucose tolerance, and dyslipidemia when compared to the offspring mice exposure to FA. More importantly, no matter what the offspring mice were exposed to, parental PM exposure overwhelmingly impacted the fasting blood insulin, homeostasis model assessment-insulin resistance, serous low-density lipoprotein cholesterol, and total cholesterol, splenic T helper cell 17 (Th17) and Treg cells, serous interleukin (IL)-17A, IL-6, and IL-10 in offspring mice. The results suggested that the parental exposure to airpollution might induce the development of MetS in offspring and might enhance the susceptibility of offspring to environmental hazards. The effects of parental PM exposure on offspring might be related to the changes of immune microenvironment.

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There is not enough experience on vaccines in Europe to draw clear conclusions on benefits. It is also not clear what role varicella immunization may play in shingles incidence.

PMID: 

Vaccine. 2015 May 15 ;33(21):2406-13. Epub 2015 Apr 1. PMID: 25839105

Abstract Title: 

Varicella in Europe-A review of the epidemiology and experience with vaccination.

Abstract: 

There is no consensus as regards the European varicella immunisation policy; some countries have introduced varicella vaccination in their routine childhood immunisation programs whereas others have decided against or are debating. With the aim of providing an overview of the epidemiology of varicella in Europe and addressing the different strategies and the experiences so far, we performed a review of epidemiological studies done in Europe from 2004 to 2014. Varicella is mainly a disease of childhood, but sero-epidemiological studies show regional differences in the proportion of susceptible adults. Hospitalisation due to varicella is not common, but complications and hospitalisation mainly affect previously healthy children, which underlines the importance of not dismissing varicella as a disease of little importance. The experience with universal vaccination in Europe shows that vaccination leads to a rapid reduction of disease incidence. Vaccine effectiveness is high and a protective herd effect is obtained. Experience with vaccination in Europe has not been long enough, though, to draw conclusions on benefits and drawbacks with vaccination as well as the capacity for national programs in Europe to maintain a sufficiently high coverage to prevent a change in age group distribution to older children and young adults or on the impact that varicella immunisation may have on the epidemiology of shingles.

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