Introduction. Metal exposure is an important factor for inducing antibiotic resistance in bacteria. Dandelion extracts have been used for centuries in traditional Chinese and Native American medicine.Aim. We assessed the effects of dandelion water extracts and taraxasterol on heavy metal-induced antibiotic resistance in Escherichia coli as well as the underlying mechanisms.Methodology. Dandelion extracts were obtained through 4 h of boiling in distilled water. Bacterial growth was monitored with a spectrophotometer. Biochemical assays were performed to assess the activities and gene transcriptions of β-lactamase and acetyltransferase. Oxidative stress was determined using an oxidation-sensitive probe, H2DCFDA.Results. The present study demonstrated that higher concentrations of nickel (>5 µg ml-1), cadmium (>0.1 µg ml-1), arsenic (>0.1 µg ml-1) and copper (>5 µg ml-1) significantly inhibited the growth of E. coli. Lower concentrations of nickel (0.5 µg ml-1), cadmium (0.05 µg ml-1) and arsenic (0.05 µg ml-1) had no effect on bacterial growth, but helped the bacteria become resistant to two antibiotics, kanamycin and ampicillin. The addition of dandelion root extracts and taraxasterol significantly reversed the antibiotic resistance induced by these heavy metals. The supplements of antibiotics and cadmium generated synergistic effects on the activities of β-lactamase and acetyltransferase (two antibiotic resistance-related proteins), which were significantly blocked by either dandelion root extract or taraxasterol. In contrast, oxidative stress was not involved in the preventative roles of dandelion root extracts and taraxasterol in heavy metal-induced antibiotic resistance.Conclusion. This study suggests that heavy metals induce bacterial antibiotic resistance and dandelion root extracts and taraxasterol could be used to help reverse bacterial resistance to antibiotics.

The objective of this study was to investigate whether leukocyte telomere length (LTL) predicts the risk for cancer mortality among American Indians participating in the Strong Heart Study (1989-1991). Participants (aged 45-74 years) were followed annually until December 2015 to collect information on morbidity/mortality. LTL was measured by qPCR using genomic DNA isolated from peripheral blood. The association between LTL and risk for cancer mortality was examined using a multivariable Cox proportional hazard model, adjusting for age, gender, education, study site, smoking, alcohol use, physical activity, systolic blood pressure, fasting blood glucose, obesity, and low- and high-density lipoprotein. Of 1945 participants (mean age 56.10 ± 8.17 at baseline, 57% women) followed for an average 20.5 years, 220 died of cancer. Results showed that longer LTL at baseline significantly predicts an increased risk of cancer death among females (HR 1.57, 95% CI 1.08-2.30), but not males (HR 0.74, 95% CI 0.49-1.12) (p for interaction 0.009). Specifically, compared with the women with the longest LTL (fourth quartile), those in the third, second, and first quartiles showed 53%, 41%, and 44% reduced risk for cancer death, respectively. The findings highlight the importance of sex-specific analysis in future telomere research.

Northeastern Siberia has been inhabited by humans for more than 40,000 years but its deep population history remains poorly understood. Here we investigate the late Pleistocene population history of northeastern Siberia through analyses of 34 newly recovered ancient genomes that date to between 31,000 and 600 years ago. We document complex population dynamics during this period, including at least three major migration events: an initial peopling by a previously unknown Palaeolithic population of \'Ancient North Siberians\' who are distantly related to early West Eurasian hunter-gatherers; the arrival of East Asian-related peoples, which gave rise to \'Ancient Palaeo-Siberians\' who are closely related to contemporary communities from far-northeastern Siberia (such as the Koryaks), as well as Native Americans; and a Holocene migration of other East Asian-related peoples, who we name \'Neo-Siberians\', and from whom many contemporary Siberians are descended. Each of these population expansions largely replaced the earlier inhabitants, and ultimately generated the mosaic genetic make-up of contemporary peoples who inhabit a vast area across northern Eurasia and the Americas.

Both pregestational and gestational diabetes mellitus (PGDM, GDM) occur more frequently in First Nations (North American Indians) pregnant women than their non-Indigenous counterparts in Canada. We assessed whether the impacts of PGDM and GDM on perinatal and postneonatal mortality may differ in First Nations versus non-Indigenous populations.
A population-based linked birth cohort study.
17 090 First Nations and 217 760 non-Indigenous singleton births in 1996-2010, Quebec, Canada.
Relative risks (RR) of perinatal and postneonatal death. Perinatal deaths included stillbirths and neonatal (0-27 days of postnatal life) deaths; postneonatal deaths included infant deaths during 28-364 days of life.
PGDM and GDM occurred much more frequently in First Nations (3.9% and 10.7%, respectively) versus non-Indigenous (1.1% and 4.8%, respectively) pregnant women. PGDM was associated with an increased risk of perinatal death to a much greater extent in First Nations (RR=5.08[95% CI 2.99 to 8.62], p<0.001; absolute risk (AR)=21.6 [8.6-34.6] per 1000) than in non-Indigenous populations (RR=1.76[1.17, 2.66], p=0.003; AR=4.2[0.2, 8.1] per 1000). PGDM was associated with an increased risk of postneonatal death in non-Indigenous (RR=3.46[1.71, 6.99], p<0.001; AR=2.4[0.1, 4.8] per 1000) but not First Nations (RR=1.16[0.28, 4.77], p=0.35) infants. Adjusting for maternal and pregnancy characteristics, the associations were similar. GDM was not associated with perinatal or postneonatal death in both groups.
The study is the first to reveal that PGDM may increase the risk of perinatal death to a much greater extent in First Nations versus non-Indigenous populations, but may substantially increase the risk of postneonatal death in non-Indigenous infants only. The underlying causes are unclear and deserve further studies. We speculate that population differences in the quality of glycaemic control in diabetic pregnancies and/or genetic vulnerability to hyperglycaemia\'s fetal toxicity may be contributing factors.

Historical records and genetic analyses indicate that Latin Americans trace their ancestry mainly to the intermixing (admixture) of Native Americans, Europeans and Sub-Saharan Africans. Using novel haplotype-based methods, here we infer sub-continental ancestry in over 6,500 Latin Americans and evaluate the impact of regional ancestry variation on physical appearance. We find that Native American ancestry components in Latin Americans correspond geographically to the present-day genetic structure of Native groups, and that sources of non-Native ancestry, and admixture timings, match documented migratory flows. We also detect South/East Mediterranean ancestry across Latin America, probably stemming mostly from the clandestine colonial migration of Christian converts of non-European origin (Conversos). Furthermore, we find that ancestry related to highland (Central Andean) versus lowland (Mapuche) Natives is associated with variation in facial features, particularly nose morphology, and detect significant differences in allele frequencies between these groups at loci previously associated with nose morphology in this sample.

The expansion of modern humans to the American continent after the Last Glacial Maximum led the way to the present-day distribution of American aborigines. Recent advances in autosomal DNA research and expanded testing of mtDNA lineages has provided a clearer picture of the number and timing of founding lineages. However, both autosomal DNA and mtDNA research have provided unresolved competing theories between the short-term and the long-term models of the Beringian standstill hypothesis. Further, the source of founding paternal lineages of American aborigines and their relationship with ancient Siberia populations remains ambiguous. In this study, we reanalyzed a 7.0 Mbp region of 132 paternal Y-chromosome sequences, including 39 newly reported ones, of male samples from American aborigines and Eurasian populations. Among Eurasian samples, we identified Y-chromosome branches that are most closely related to known American aborigine founding lineages, that is, Q1-L804 links to Q1-M3, Q1-L330 links to Q1-Z780, Q1-M120 links to Q1-B143, and C2-F1756 links to C2-P39. The revised phylogenetic tree and age estimates indicate a narrow timeframe (~15.3-14.3 kya) for the upper time limit of human entry to the American continent. Our analysis suggests that the in situ differentiation of Q-M242 in Central Eurasia and South Siberia region gave rise to numerous sub-lineages older than 15.3 kya, and the founding of Paleo-Indian paternal lineages is part of the great Q1-L53 diffusion throughout the Eurasia after the Last Glacial Maximum. The results of our study will assist in future studies of the history of modern populations in Eurasia and the Americas.

Relying on a national stratified random sample of Indigenous peoples aged 19 years old and above in Canada, this study investigates the correlates of illicit drug use among Indigenous peoples, paying special attention to the association between social support measures and illegal drug use. Results from multivariate logistical regression show that measures of social support, such as residential mobility, strength of ties within communities, and lack of timely counseling, are statistically significant correlates of illicit drug use. Those identifying as Christian are significantly less likely to use illegal drugs. This is the first nationwide analysis of the illicit drug usage of Indigenous peoples in Canada. The results are robust because we have controlled for a range of comorbidity variables as well as a series of sociodemographic variables. Policy implications from these findings are discussed.

High arsenic exposure has been related to diabetes, but at low-moderate levels the evidence is mixed. Arsenic metabolism, which is partly genetically controlled and may rely on certain B vitamins, plays a role in arsenic toxicity.
We evaluated the prospective association of arsenic exposure and metabolism with type 2 diabetes and insulin resistance.
We included 1,838 American Indian men and women free of diabetes (median age, 36 y). Arsenic exposure was assessed as the sum of inorganic arsenic (iAs), monomethylarsonate (MMA), and dimethylarsinate (DMA) urine concentrations (ΣAs). Arsenic metabolism was evaluated by the proportions of iAs, MMA, and DMA over their sum (iAs%, MMA%, and DMA%). Homeostasis model assessment for insulin resistance (HOMA2-IR) was measured at baseline and follow-up visits. Incident diabetes was evaluated at follow-up.
Median ΣAs, iAs%, MMA%, and DMA% was 4.4 μg/g creatinine, 9.5%, 14.4%, and 75.6%, respectively. Over 10,327 person-years of follow-up, 252 participants developed diabetes. Median HOMA2-IR at baseline was 1.5. The fully adjusted hazard ratio [95% confidence interval (CI)] for incident diabetes per an interquartile range increase in ΣAs was 1.57 (95% CI: 1.18, 2.08) in participants without prediabetes at baseline. Arsenic metabolism was not associated with incident diabetes. ΣAs was positively associated with HOMA2-IR at baseline but negatively with HOMA2-IR at follow-up. Increased MMA% was associated with lower HOMA2-IR when either iAs% or DMA% decreased. The association of arsenic metabolism with HOMA2-IR differed by B-vitamin intake and AS3MT genetics variants.
Among participants without baseline prediabetes, arsenic exposure was associated with incident diabetes. Low MMA% was cross-sectional and prospectively associated with higher HOMA2-IR. Research is needed to confirm possible interactions of arsenic metabolism with B vitamins and AS3MT variants on diabetes risk. https://doi.org/10.1289/EHP2566.

BACKGROUND: The authors have previously published the complete mitochondrial genome (mitogenome) sequences of two indigenous Mesoamerican populations, Mazahua (n = 25) and Zapotec (n = 88).
METHODS: This study determined the complete mitogenome sequences of nine unrelated individuals from the indigenous Maya population living in Mexico.
RESULTS: Their mitogenome sequences could be classified into either of the haplogroups A2 and C1. Surprisingly, there were no mitogenome sequences (haplotypes) that the Maya, Mazahua, and Zapotec people share in common.
CONCLUSIONS: This indicates that no genetic exchange, at least matrilineally, has occurred among them.

BACKGROUND: Infant mortality is higher in Indigenous than non-Indigenous populations, but comparable data on infant morbidity are lacking in Canada. We evaluated disparities in infant morbidities experienced by Indigenous populations in Canada.
METHODS: We used linked population-based birth and health administrative data from Quebec, Canada, to compare hospitalization rates, an indicator of severe morbidity, in First Nations, Inuit and non-Indigenous singleton infants (< 1 year) born between 1996 and 2010.
RESULTS: Our cohort included 19 770 First Nations, 3930 Inuit and 225 380 non-Indigenous infants. Compared with non-Indigenous infants, all-cause hospitalization rates were higher in First Nations infants (unadjusted risk ratio [RR] 2.05, 95% confidence interval [CI] 1.99-2.11; fully adjusted RR 1.43, 95% CI 1.37-1.50) and in Inuit infants (unadjusted RR 1.96, 95% CI 1.87-2.05; fully adjusted RR 1.37, 95% CI 1.24-1.52). Higher risks of hospitalization (accounting for multiple comparisons) were observed for First Nations infants in 12 of 16 disease categories and for Inuit infants in 7 of 16 disease categories. Maternal characteristics (age, education, marital status, parity, rural residence and Northern residence) partly explained the risk elevations, but maternal chronic illnesses and gestational complications had negligible influence overall. Acute bronchiolitis (risk difference v. non-Indigenous infants, First Nations 37.0 per 1000, Inuit 39.6 per 1000) and pneumonia (risk difference v. non-Indigenous infants, First Nations 41.2 per 1000, Inuit 61.3 per 1000) were the 2 leading causes of excess hospitalizations in Indigenous infants.
CONCLUSIONS: First Nations and Inuit infants had substantially elevated burdens of hospitalizations as a result of diseases of multiple systems. The findings identify substantial unmet needs in disease prevention and medical care for Indigenous infants.