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Background and Aims Eating habits may contribute to longevity. We characterized the eating habits and cardiovascular risk (CVR) biomarkers in Portuguese centenarians (CENT) compared to controls. Methods and Results Centenarians (n = 253), 100.26 ± 1.98 years, were compared with 268 controls (67.51 ± 3.25), low (LCR) and high (HCR) CVR (QRISK®2-2016). Anthropometric and body composition were evaluated by bioimpedance. Abdominal obesity, BMI, and fat mass (FM) cut-offs were according to the WHO. Sarcopenia was defined by muscle mass index cut-off ≤ 16.7 kg/m2. Daily red meat intake, adjusted for age and gender, was sarcopenia protective (OR = 0.25, 95% CI = 0.096–0.670, P = 0.006); however, it contributes for FM excess (OR = 4.946, 95% CI = 1.471–16.626, P = 0.01), overweight, and obesity (OR = 4.804, 95% CI = 1.666–13.851, P = 0.004). This centenarian eating habit (2%) contrasts to HCR (64.3%). The history of red meat (P < 0.0001) and canned/industrialized food intakes (P < 0.0001) was associated with HCR. Basal metabolism was lower in centenarians versus LCR/HCR (CENT = 1176.78 ± 201.98; LCR = 1356.54 ± 170.65; HCR = 1561.33 ± 267.85; P < 0.0001), BMI (CENT = 21.06 ± 3.68; LCR = 28.49 ± 4.69; HCR = 29.56 ± 5.26; P < 0.0001), waist circumference (CENT = 85.29 ± 10.83; LCR = 96.02 ± 11.71; HCR = 104.50 ± 11.84; P < 0.0001), and waist-hip ratio (CENT = 0.88 ± 0.07; LCR = 0.92 ± 0.08; HCR = 1.01 ± 0.08; P < 0.0001). CENT had lower total cholesterol, LDL cholesterol, non-HDL cholesterol, and cholesterol/HDL ratio than controls. Conclusions Frequent consumption of red meat, cholesterol, and heme iron rich may contribute to obesity and increased CVR. The low frequency of this consumption, observed in centenarians, although associated with sarcopenia, may be one of the keys to longevity.

The relationship between human cytomegalovirus (HCMV) and tumours has been extensively investigated, mainly in glioblastoma multiforme (GBM), a malignant tumour of the central nervous system with low overall survival rates. Several reports have demonstrated the presence of HCMV in GBM, although typically restricted to a low number of cells, and studies have indicated that viral proteins have the ability to dysregulate cellular processes and increase tumour malignancy. Treatment of GBM involves the use of the chemotherapeutic agents temozolomide (TMZ) and carmustine (bis-chloroethylnitrosourea, BCNU), which lead to the attachment of adducts to the DNA backbone, causing errors during replication and consequent cell death. It is known that HCMV infection can modulate DNA repair pathways, but what effects the virus may exhibit during chemotherapy are unknown. Here we approach this question by analysing HCMV infection and viral protein accumulation in GBM cell lines with different genotypes and their response to TMZ and BCNU in the presence of the virus. We demonstrate that A172, TP365MG and U251MG GBM cells are efficiently infected by both low-passage (TB40E) and high-passage (AD169) HCMV strains. However, the GBM cell lines vary widely in their permissiveness to viral gene expression and exhibit very different patterns of immediate early, early and late protein accumulation. HCMV reduces the viability of permissive GBM cells in a multiplicity-dependent manner in both the absence and presence of TMZ or BNCU. In sum, we demonstrate that GBM cell lines are equally susceptible but differentially permissive to infection by both low- and high-passage strains of HCMV. This observation not only indicates that viral replication is largely controlled by cellular factors in this system, but also provides a possible explanation for why viral gene products are only found in a subset of cells in GBM tumours. Furthermore, we conclude that the virus does not confer increased resistance to chemotherapeutic drugs in various GBM cell lines, but instead reduces tumour cell viability. These results highlight that the oncomodulatory potential of HCMV is not limited to cancer-promoting activities, but also includes adverse effects on tumour cell proliferation or survival.

Psoriasis is a multifactorial disease, with many genetic risk factors, one of which seems to be the angiotensin-converting enzyme (ACE) insertion/deletion (I/D) polymorphism. ACE activity has been shown to be higher in psoriatic patients and it suggests an oxidative stress state, as seen in many cardiovascular disorders. We aimed to explore the association between ACE activity and polymorphisms and cardiovascular risk amongst psoriatic patients. We included 64 psoriatic patients and 1091 controls and compared ACE I/D polymorphism genotype and serum activity for both groups. ACE genotypes were similar in psoriatic patients and controls. Notably, serum ACE activity was higher in psoriatic patients (19.09 ± 2.86 U/mL) compared to controls (11.85 ± 0.40 U/mL), p = 0.015. Non-HDL cholesterol was significantly lower in II polymorphism (p = 0.037). Psoriatic activity (PASI) was associated with a higher cardiovascular risk estimated by lower HDL concentrations (r = −0.496, p = 0.007), and higher triglyceride levels (r = 0.421, p = 0.020) and TC/HDL and LDL/HDL ratios (r = 0.612, p < 0.001 and r = 0.437, p = 0.023, respectively). Patients with psoriasis have higher ACE activity levels, independent of ACE genotype. Moreover, disease activity correlated with cardiovascular risk. This could support the eventual role of ACE as a possible biomarker for disease severity and cardiovascular risk in psoriasis patients.

The extracellular matrix (ECM) is the non-cellular component of the tissues of our organism. It is the dynamic element that maintains a biochemical structure capable of supporting the organization and architecture of the tissue constituents. The diversity of ECM’s constituents gives it the biochemical and biophysical properties necessary to regulate its behavior and differentiation. ECM has an important role in the biology of cancer cell development and progression. Human papillomavirus infection (HPV) is the principal etiological agent of the most common sexually transmitted diseases. It is a virus that can cause lesions precursors of epithelial squamous and glandular tumors. Type 16 (HPV16) is the leading cause of pre-malignant lesions and invasive cancers in these tissues. This work will focus on HPV infection to understand the role of ECM in the invasion, spread, and pathogenesis of the lesions caused by this virus. Cancer is no longer considered a pathology explained only by uncontrolled proliferation and apoptosis but also by the deregulation of the microenvironment.

Purpose To evaluate complete blood count (CBC) parameters in the first week of life as predictive biomarkers for the development of retinopathy of prematurity (ROP). Methods Multicenter, prospective, observational study of a cohort of preterm infants born with gestational age (GA) < 32 weeks or birth weight < 1500 g in eight Portuguese neonatal intensive care units. All demographic, clinical, and laboratory data from the first week of life were collected. Univariate logistic regression was used to assess risk factors for ROP and then multivariate regression was performed. Results A total of 455 infants were included in the study. The median GA was 29.6 weeks, and the median birth weight was 1295 g. One hundred and seventy-two infants (37.8%) developed ROP. Median values of erythrocytes (p < 0.001), hemoglobin (p < 0.001), hematocrit (p < 0.001), mean corpuscular hemoglobin concentration (p < 0.001), lymphocytes (p = 0.035), and platelets (p = 0.003) of the group of infants diagnosed with ROP any stage were lower than those without ROP. Mean corpuscular volume (MCV) (p = 0.044), red blood cell distribution width (RDW) (p < 0.001), erythroblasts (p < 0.001), neutrophils (p = 0.030), neutrophils-lymphocytes ratio (p = 0.028), and basophils (p = 0.003) were higher in the ROP group. Higher values of MCV, erythroblasts, and basophils remained significantly associated with ROP after multivariate regression. Conclusion In our cohort, the increase in erythroblasts, MCV, and basophils in the first week of life was significantly and independently associated with the development of ROP. These CBC parameters may be early predictive biomarkers for ROP.

The gene TAS2R38 single nucleotide polymorphisms (SNPs-P49A, A262V and V296I) can condition bitter tasting by PAV (proline–alanine–valine) and non-bitter-tasting by AVI (alanine–valine–isoleucine) homozygosity. We evaluated this polymorphisms association with thyroid function, metabolism and anthropometry parameters determined by: Endpoint analysis (SNPs); DXA (fat mass-%, total fat mass—kg, lean mass—kg); Standard methods (lipid metabolism parameters, HbA1c-%, glycemia—mg/dL, insulinemia—µIU/mL, HOMA-IR, uricemia—mg/dL, calcemia—mg/dL and BMI—kg/m2); ELISA (leptinemia—ng/mL); Spectrophotometry (Angiotensin Converting Enzyme activity—UI/L). Statistics: SPSS program; OR [IC95%]; p < 0.05. Sample: 114 hypothyroid, 49 hyperthyroid, and 179 controls. An association between A262V-valine–valine and hypothyroidism/hyperthyroidism was verified (OR = 2.841; IC95% [1.726–4.676]), p < 0.001/OR = 8.915; IC95% [4.286–18.543]), p < 0.001). Protector effect from thyroid dysfunction: A262V-alanine–valine (OR = 0.467; IC95% [0.289–0.757], p = 0.002/OR = 0.132; IC95% [0.056–0.309], p < 0.001) and PAV (OR = 0.456; IC95% [0.282–0.737], p = 0.001/OR = 0.101; IC95% [0.041–0.250], p < 0.001). Higher parameter values associated with genotypes were: fat-mass-% (V296I-valine–isoleucine), lean-mass (P49A-proline–proline; PVI), leptin (AVI), HbA1c (A262V-alanine–valine) and lower values in lean-Mass (AVI; PVV), leptin (A262V-alanine–alanine), HbA1c (PVV), uricemia (V296I-valine–isoleucine), glycemia (A262V-alanine–alanine; AAV) and plasma triglycerides (PVV). In conclusion, TAS2R38 influences thyroid function, body composition and metabolism. Bitter taste perception (PAV) and the genotype A262V-alanine–valine can protect from thyroid dysfunction. AVV, PVV and genotype A262V-valine–valine may confer higher predisposition for thyroid dysfunction, particularly PVV for hyperthyroidism.

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