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Sex identification of ancient individuals is important to understand aspects of the culture, demographic structure, religious practices, disease association, and the history of the ancient civilizations. Sex identification is performed using anthropometric measurements and molecular genetics techniques, including quantification of the X and Y chromosomes. These approaches are not always reliable in subadult, or fragmented, incomplete skeletons or when the DNA is highly degraded. Most of the methods include the identification of the male and female sexes, but the absence of a specific marker for the males does not mean that the sample obtained was from a female. This study aims (1) to identify new male-specific regions that allow male identification; (2) to contrast the effectiveness of these markers against AMELX/AMELY and anthropometric measurement procedures; and (3) to test the efficacy of these markers in archaeological samples. For the first two aims, we used known sex samples, and for the third aim, we used samples from different archaeological sites. A novel molecular technique to identify male-specific regions by amplification of TTTY7, TSPY3, TTTY2, and TTTY22 genes of the human Y chromosome was developed. The results showed amplification of the specific DNA regions of Y chromosome in male individuals, with no amplification being observed in any of the female samples, confirming their specificity for male individuals. This approach complements the current procedures, such as the AMELX/AMELY test and anthropometric principle.

Dengue virus (DENV) evolution has had a significant impact on disease pathogenesis, virulence, and epidemiology in Mexico. Novel genotypic variation in DENV serotypes and genotypes may influence the magnitude and severity of dengue epidemics, as evidenced by 2009 data from Veracruz State. The data presented herein is related to the publication entitled "Epidemiological Implications of the Genetic Diversification of Dengue Virus (DENV) Serotypes and Genotypes in Mexico" [1]. Raw data and trees provide epidemiological data on DENV prevalence and a comprehensive phylogeny of both representative sequences collected from an NCBI repository, and 28 additional isolates from acute-phase plasma samples diagnosed with dengue fever or severe dengue (Raw sequencing data is hosted in the public repository Mendeley Data (http://dx.doi.org/10.17632/bf2kdhhf6x.2). Phylogenetic trees for each DENV serotype (DENV-1, -2, -3 and -4) were constructed using these sequences by a maximum likelihood methodology as well as a Bayesian Markov chain Monte Carlo (MCMC) integration approach. Phylogenetic trees exhibited: (1) DENV-1, genotype V, (2) the DENV-2 Asian/American and Asian II genotypes, (3) DENV-3, genotype III, and (4) DENV-4, genotype I. This data can be beneficial for future analyses on DENV serotype and genotype structure and the introduction of novel DENV genotype sequences in the Americas, for the further elucidation of dengue etiology.

Variation and clade shifts in dengue virus (DENV) genotypes are responsible for numerous dengue fever outbreaks throughout Latin America in the past decade. Molecular analyses of dengue serotypes have revealed extensive genetic diversification and the emergence of new genotypes in Brazil (DENV-4 genotype I) and elsewhere in tropical and subtropical America. The goal of the present study is to assess the extent to which the adventitious introduction of DENV genotypes and their increasing genetic diversity affects dengue epidemiology in Mexico. A nuanced sequence inspection and phylogenetic analysis of the C-prM nucleotide region of DENV was performed for specimens collecting in 2009 from the Veracruz State, Mexico. Findings were contrasted with specimens collected in adjacent years and analysed based on the epidemiological patterns reported between 1990 and 2019. Additionally, the identification process of various DENV genotypes was assessed, including: (1) DENV-1, genotype V, (2) the DENV-2 Asian/American and Asian II genotypes (3) DENV-3, genotype III, and (4) DENV-4, genotype I. This resulted in the discovery of a distinct genetic cladistic pattern for serotype DENV-2. Lastly, study findings suggest that a correlation exists between the emergence of novel genotypes and genetic diversification, with the increasing incidence of DENV infections in Mexico in 2009.

Mitochondrial DNA (mtDNA) copy number and mitochondrial DNA haplogroups have been associated with different types of cancer, including breast cancer, because they alter cellular energy metabolism. However, whether mtDNA copy number or haplogroups are predictors of oxidative stress-related risks in human breast cancer tissue in Mexican patients remains to be determined. Using quantitative real-time PCR assays and sequencing of the mtDNA hypervariable region, analysis of mtDNA copy numbers in 82 breast cancer tissues (BCT) and matched normal adjacent tissues (NAT) was performed to determine if copy number correlated with clinical features and Amerindian haplogroups (A2, B2, B4, C1 and D1) . The results showed that the mtDNA copy number was significantly decreased in BCT compared with NAT (p = 0.010); it was significantly decreased in BCT and NAT in women 50 years of age, compared with NAT in women 50 years of age (p = 0.032 and p = 0.037, respectively); it was significantly decreased in NAT and BCT in the postmenopausal group and in BCT in the premenopausal group compared with NAT in the premenopausal group (p = 0.011, p = 0.010 and, p = 0.018; respectively); and it was also significantly decrease in members of the BCT group classified as having invasive ductal carcinoma I-III (IDC-I, IDC-II and IDC-III) and IDC-II for NAT compared to IDC-I of NAT (p = 0.025, p = 0.022 and p = 0.031 and p = 0.020; respectively). The mtDNA copy number for BCT from patients with haplogroup B2 was decreased compared to patients with haplogroup D1 (p = 0.01); for BCT from patients with haplogroup C1 was also decreased compare with their NAT counterpart (p = 0.006) and with BCT patients belonging to haplogroups A2 and D1 (p = 0.01 and p = 0.03; respectively). In addition, the mtDNA copy number was decrease in the sequences with three deletions relative to the rCRS at nucleotide positions A249del, A290del and A291del, or C16327T polymorphism with the same p = 0.019 for all four variants. Contrary, the copy number increased in sequences containing C16111T, G16319A or T16362C polymorphisms (p = 0.021, =0.048, and = 0.001; respectively). In conclusion, a decrease in the copy number of mtDNA in BCT compared with NAT was shown by the results, which suggests an imbalance in oxidative phosphorylation (OXPHOS) that can affect the apoptosis pathway and cancer progression. It was also observed an increase of the copy number in samples with specific polymorphisms, which may be a good sign of favourable prognosis.