PMID: 

Am J Chin Med. 2019 ;47(8):1885-1899. PMID: 31838869

Abstract Title: 

Leaves Prevent NMU-Induced Mammary Tumor through Downregulation of Fatty Acid Synthase, Estrogen Receptor-α and Her2 Expression.

Abstract: 

Diet polyphenol can reportedly prevent the formation of breast-cancer cells. Nelumbo nucifera leaf extract (NLE) is enriched with polyphenols and has several cellular functions, such as anti-atherosclerosis, anti-inflammation, and antitumor. In this study, we investigated the role of NLE in the prevention of N-methyl-N-nitrosourea (NMU)-induced mammary tumor formation. Cotreatment with NLE significantly reduced the NMU-induced tumor incidence, number, and volume. NLE administration significantly repressed the tumor growth and weight of nude mice upon inoculation with BT-474 cancer cells. Immunohistochemical staining indicated that fatty acid synthetase, estrogen receptor (ER)-, and phosphorylated ER-were obviously reduced in the cancer part of BT-474 inoculated nude mice upon administration of 2% NLE. Western blot analysis revealed that NLE and NLPE (polyphenol-rich NLE) repressed ER-expression and phosphorylation and decreased the phosphorylation of Her-2 without affecting their expression. Overall, NLE and NLPE exhibited more effective antitumor abilities in NMU-induced mammary cancer formation than with tamoxifen and Herceptin.

read more

PMID: 

Sci Rep. 2019 Dec 27 ;9(1):20034. Epub 2019 Dec 27. PMID: 31882989

Abstract Title: 

Neferine induces autophagy-dependent cell death in apoptosis-resistant cancers via ryanodine receptor and Ca-dependent mechanism.

Abstract: 

Resistance of cancer cells to chemotherapy is a significant clinical concern and mechanisms regulating cell death in cancer therapy, including apoptosis, autophagy or necrosis, have been extensively investigated over the last decade. Accordingly, the identification of medicinal compounds against chemoresistant cancer cells via new mechanism of action is highly desired. Autophagy is important in inducing cell death or survival in cancer therapy. Recently, novel autophagy activators isolated from natural products were shown to induce autophagic cell death in apoptosis-resistant cancer cells in a calcium-dependent manner. Therefore, enhancement of autophagy may serve as additional therapeutic strategy against these resistant cancers. By computational docking analysis, biochemical assays, and advanced live-cell imaging, we identified that neferine, a natural alkaloid from Nelumbo nucifera, induces autophagy by activating the ryanodine receptor and calcium release. With well-known apoptotic agents, such as staurosporine, taxol, doxorubicin, cisplatin and etoposide, utilized as controls, neferine was shown to induce autophagic cell death in a panel of cancer cells, including apoptosis-defective and -resistant cancer cells or isogenic cancer cells, via calcium mobilization through the activation of ryanodine receptor and Ulk-1-PERK and AMPK-mTOR signaling cascades. Taken together, this study provides insights into the cytotoxic mechanism of neferine-induced autophagy through ryanodine receptor activation in resistant cancers.

read more

PMID: 

Kidney Int. 2019 Nov 2. Epub 2019 Nov 2. PMID: 31866113

Abstract Title: 

Magnesium prevents vascular calcification in Klotho deficiency.

Abstract: 

Klotho knock-out mice are an important model for vascular calcification, which is associated with chronic kidney disease. In chronic kidney disease, serum magnesium inversely correlates with vascular calcification. Here we determine the effects of serum magnesium on aortic calcification in Klotho knock-out mice treated with a minimal or a high magnesium diet from birth. After eight weeks, serum biochemistry and aorta and bone tissues were studied. Protective effects of magnesium were characterized by RNA-sequencing of the aorta and micro-CT analysis was performed to study bone integrity. A high magnesium diet prevented vascular calcification and aortic gene expression of Runx2 and matrix Gla protein found in such mice on the minimal magnesium diet. Differential expression of inflammation and extracellular matrix remodeling genes accompanied the beneficial effects of magnesium on calcification. High dietary magnesium did not affect serum parathyroid hormone, 1,25-dihydroxyvitamin Dor calcium. High magnesium intake prevented vascular calcification despite increased fibroblast growth factor-23 and phosphate concentration in the knock-out mice. Compared to mice on the minimal magnesium diet, the high magnesium diet reduced femoral bone mineral density by 20% and caused excessive osteoid formation indicating osteomalacia. Osteoclast activity was unaffected by the high magnesium diet. In Saos-2 osteoblasts, magnesium supplementation reduced mineralization independent of osteoblast function. Thus, high dietary magnesium prevents calcification in Klotho knock-out mice. These effects are potentially mediated by reduction of inflammatory and extracellular matrix remodeling pathways within the aorta. Hence magnesium treatment may be promising to prevent vascular calcification, but the risk for osteomalacia should be considered.

read more

PMID: 

Environ Int. 2019 Dec 26 ;135:105410. Epub 2019 Dec 26. PMID: 31884132

Abstract Title: 

Ambient air pollution and markers of fetal growth: A retrospective population-based cohort study of 2.57 million term singleton births in China.

Abstract: 

BACKGROUNDS: Evidence is scarce on the relation between maternal exposure to ambient air pollution during pregnancy and fetal growth in developing countries. Moreover, the current evidence is inconsistent. We aimed to investigate the association of trimester-specific exposure to air pollution with risk of being born small for gestational age (SGA) and birth weight-markers of fetal growth-among Chinese term births.METHODS: This retrospective population-based cohort study consisted of 2,567,457 singleton term live-births from January 1, 2014 to December 31, 2017 across 123 Chinese districts and counties. Personal exposure to ambient air pollutants including carbon monoxide (CO), sulfur dioxide (SO), nitrogen dioxide (NO), ozone (O), particulate matter with aerodynamic diameter 

read more

PMID: 

Oxid Med Cell Longev. 2019 ;2019:2492368. Epub 2019 Dec 7. PMID: 31885780

Abstract Title: 

Fine Particulate Matter Leads to Unfolded Protein Response and Shortened Lifespan by Inducing Oxidative Stress in.

Abstract: 

Oxidative stress has been proven as one of the most critical regulatory mechanisms involved in fine Particulate Matter- (PM-) mediated toxicity. For a better understanding of the underlying mechanisms that enable oxidative stress to participate in PM-induced toxic effects, the current study explored the effects of oxidative stress induced by PMon UPR and lifespan in. The results implicated that PMexposure induced oxidative stress response, enhanced metabolic enzyme activity, activated UPR, and shortened the lifespan of. Antioxidant N-acetylcysteine (NAC) could suppress the UPR through reducing the oxidative stress; both the antioxidant NAC and UPR inhibitor 4-phenylbutyric acid (4-PBA) could rescue the lifespan attenuation caused by PM, indicating that the antioxidant and moderate proteostasis contribute to the homeostasis and adaptation to oxidative stress induced by PM.

read more

PMID: 

Thorax. 2020 Jan ;75(1):85-87. Epub 2019 Nov 14. PMID: 31727788

Abstract Title: 

Association between particulate matter air pollution and lung cancer.

Abstract: 

Long-term exposure to particulate matter 2.5μm (PM) air pollution is associated with an increased risk of lung cancer. However, the evidence is limited in low-income and middle-income countries. We estimated the association between the incidence of lung cancer and PMair pollution exposure in the Urban Employee Basic Medical Insurance (UEBMI) beneficiaries in China. A total of 16 483 new lung cancer cases diagnosed from 12 966 137 UEBMI beneficiaries from 36 cities between 2013 and 2016. The relative risk for lung cancer associated with a 10 µg/mincrease in 3-year PMexposure was 1.12 (95% CI 1.00 to 1.26). The population attributable risk estimated for a reduction in PMconcentration to 35 µg/mcorresponded to a decrease of 14% in cases of lung cancer. Reducing PMair pollution has a significant public health benefit.

read more

PMID: 

Clin Rheumatol. 2019 Nov 15. Epub 2019 Nov 15. PMID: 31729679

Abstract Title: 

Exposure to ambient air pollution and autoantibody status in rheumatoid arthritis.

Abstract: 

OBJECTIVE: To evaluate the relationship between air pollutant (AP) exposure and rheumatoid arthritis (RA) autoantibody status METHODS: We performed a cross sectional study utilizing enrollment data from participants in the Veterans Affairs rheumatoid arthritis registry. HLA-DRB1 shared epitope (SE), smoking, rheumatoid factor (RF), and anti-cyclic citrullinated peptide antibody (ACPA) status were collected. Mean exposure levels were obtained for AP (NO, SO, particulate matter [PM, PM], and ozone) from air quality monitoring stations at patients' residential zip codes in the year prior to enrollment. Multivariable logistic and ordinary least squares regression models were used to determine independent associations of AP with RA seropositivity and autoantibody concentration.RESULTS: The cohort included 557 veterans (90% male, 76% Caucasian), with mean age of 70 years and mean disease duration of 13 years. The majority were HLA-DRB1 SE, RF, and ACPA positive (73%, 79%, and 76%, respectively). In univariate models, PMexposure was associated with higher ACPA concentration (p = 0.009). Similarly, in multivariable regression models, PMexposure was independently associated with higher ACPA concentration (p = 0.037). Current smoking independently predicted RF and ACPA positivity and titers, while HLA-DRB1 SE alleles were associated with RF positivity and ACPA positivity and titers.CONCLUSIONS: In an elderly cohort of RA patients, fine particulate matter (PM) exposure independently predicted higher ACPA concentration. Further study of fine particulate matter in the pathogenesis of RA is warranted. Key Points• A study that integrates both genetic and environmental exposure data, relative to RA autoantibody status. • Of different air pollutants measures, exposure to fine particulate matter (PM) appears to be most closely linked to ACPA titers.

read more

When the seasons change, especially into the cold, snowy days of winter, sometimes our bodies let us know by getting sick, developing dry skin, increased aches and pains, and more.

Here are a few ways CBD might help you this winter.

Winter Blues

When the days get shorter and the sun disappears for what seems like months, many develop Seasonal Affective Disorder, or SAD. This is a common condition that impacts more than 300 million yearly. Symptoms include depressed mood, anxiety, general unhappiness, hopelessness, fatigue, and social withdrawal.

CBD may help with SAD by increasing mood and decreasing anxiety.

Boost Immunity

During cold and flu season, our immune systems can take a beating. CBD might be able to help fight back. The cannabinoid receptors (CB1 and CB2) in the central, peripheral nervous system, and endocannabinoid system reacts with CBD by improving your immune system by possibly reducing the body’s inflammatory immune response.

Moisturize Skin

The dry, cold winter air depletes your skin from moisture. CBD has shown promise in possibly reliving your dry, scaly winter skin. Along with moisturizing, CBD can possibly help with excessive sebum production.

Muscle Soreness/Stiffness

The cold temperatures can restrict blood flow causing stiff and sore muscles. This is even more pronounced when performing physical activities outdoors. CBD can possibly help reduce muscle soreness and inflammation.

Ease Cold and Flu Symptoms

It’s difficult to make it through winter without a runny nose or worst case, the flu. The anti-inflammatory properties show promise in helping fight cold and flu symptoms, mainly inflammation from stuffy noses and aches and pains.

PMID: 

Sci Total Environ. 2019 Nov 2 ;703:134985. Epub 2019 Nov 2. PMID: 31731170

Abstract Title: 

The correlation between PMexposure and hypertensive disorders in pregnancy: A Meta-analysis.

Abstract: 

OBJECTIVE: To find the correlation between exposure to PM(fine particulate matter) and hypertensive disorders in pregnancy (HDP), and provide medical evidence for decreasing the incidence of hypertensive disorders in pregnancy.METHOD: A combination of computer and manual retrieval was used to search for keywords in PubMed (385 records), Cochrane Library (20 records), Web of Science (419 records) and Embase (325 records). Finally, ten epidemiological articles were considered in this meta-analysis. Stata 13.0 was used to examine the heterogeneity among the studies and to calculate the combined effect value (OR, odds ratio) by selecting the corresponding models. Sensitivity analysis and publication bias test were also performed.RESULTS: Meta-analysis indicated that there was an association between PMexposure (per 10 µg/mincrease) and hypertensive disorders in pregnancy (OR = 1.52, 95% CI: 1.24-1.87). Exposure to PM(per 10 µg/mincrease) enhanced the risk of pre-eclampsia (OR = 1.31, 95% CI: 1.07-1.61), but there was no evidence relating exposure to PMto gestational hypertension (OR = 1.35, 95% CI: 0.98-1.87).CONCLUSION: There is a significant link between exposure to PMand hypertensive disorders in pregnancy. The first and the third trimester were more susceptible to PMexposure. It is recommended to further strengthen protective measures against PMduring pregnancy.

read more

PMID: 

Int J Environ Res Public Health. 2019 10 25 ;16(21). Epub 2019 Oct 25. PMID: 31731429

Abstract Title: 

Urban Air Pollution Particulates Suppress Human T-Cell Responses to.

Abstract: 

Tuberculosis (TB) and air pollution both contribute significantly to the global burden of disease. Epidemiological studies show that exposure to household and urban air pollution increase the risk of new infections with(M.tb) and the development of TB in persons infected withand alter treatment outcomes. There is increasing evidence that particulate matter (PM) exposure weakens protective antimycobacterial host immunity. Mechanisms by which exposure to urban PM may adversely affect-specific human T cell functions have not been studied. We, therefore, explored the effects of urban air pollution(aerodynamic diameters≤2.5µm) on M.tb-specific T cell functions in human peripheral blood mononuclear cells (PBMC).exposure decreased the capacity of PBMC to control the growth of M.tb and the M.tb-induced expression of CD69, an early surface activation marker expressed on CD3T cells.exposure also decreased the production of IFN-γ in CD3, TNF-α in CD3and CD14M.tb-infected PBMC, and the M.tb-induced expression of T-box transcription factor TBX21 (T-bet). In contrast,exposure increased the expression of anti-inflammatory cytokine IL-10 in CD3and CD14PBMC. Taken together,exposure of PBMC prior to infection with M.tb impairs critical antimycobacterial T cell immune functions.

read more