A comparison of online versus offline gambling harm in Portuguese pathological gamblers: an empirical study

Over the past decade, gambling has become a very popular activity across Europe including the growth of Internet gambling. Portugal is one of the few European countries where little research has been carried out. Given the lack of studies, a Portuguese sample (N = 1,599) was surveyed concerning their online and offline gambling habits. More specifically, the aim of this study was to identify and compare from the total sample, online pathological gamblers (PGON) (n = 171) and offline pathological gamblers' (PGOF) (n = 171) characteristics, and eventual risk factors for the development of problem gambling. Results demonstrated that PGON had different profiles compared to PGOF, although there were also similarities. Situational characteristics were much more significant for PGON than PGOF (e.g., availability, accessibility, affordability), but PGOF had higher scores than PGON on factors concerning individual characteristics (e.g., intensity of feelings while gambling, depression, suicidal ideation, etc.). Findings also showed differences concerning attitudes toward responsible gambling measures. The fact that situational characteristics are more attractive to online gamblers confirms differences between PGON and PGOF and suggests that this preferred attractiveness may enhance problem gambling potential. Further research is needed to better understand the interaction between Internet situational characteristics and the individual characteristics of gamblers, as well as the profile of the growing population of gamblers that uses both online and offline modes to gamble

Lymphocyte subsets in human immunodeficiency virus-unexposed Brazilian individuals from birth to adulthood

Ethnic origin, genetics, gender and environmental factors have been shown to influence some immunologic indices, so that development of reference values for populations of different backgrounds may be necessary. We have determined the distribution of lymphocyte subsets in healthy Brazilian individuals from birth to adulthood. Lymphocyte subsets were determined using four-colour cytometry in a cross-sectional study of 463 human immunodeficiency virus-unexposed children and adults from birth through 49 years of age. Lymphocyte subsets varied according to age, as previously observed in other studies. However, total CD4+ T cell numbers were lower than what was described in the Pediatric AIDS Clinical Trials Group P1009 (PACTG P1009), which assessed an American population of predominantly African and Hispanic backgrounds until the 12-18 year age range, when values were comparable. Naïve percentages and absolute values of CD8+ T cells, as assessed by CD45RA expression, were also lower than the PACTG P1009 data for all analysed age ranges. CD38 expression on both CD4+ and CD8+ T cells was lower than the PACTG P1009 values, with a widening gap between the two studies at older age ranges. Different patterns of cell differentiation seem to occur in different settings and may have characteristic expression within each population.Universidade Federal de São Paulo (UNIFESP) Departamento de MedicinaCentro Assistencial Cruz de MaltaUniversidade Federal de São Paulo (UNIFESP) Departamento de PediatriaUNIFESP, Depto. de MedicinaUNIFESP, Depto. de PediatriaSciEL

A revision of the status of Lepadogaster lepadogaster (Teleostei : Gobiesocidae): sympatric subspecies or a long misunderstood blend of species?

Molecular (partial mitochondrial 12S ribosomal DNA sequences), morphological and meristic analysis of Lepadogaster lepadogaster lepadogaster, L. l. purpurea and L. zebrina were performed to investigate the relationships between these taxa. On the western shore of mainland Portugal, where the two subspecies of L. lepadogaster occur sympatrically, they differ in microhabitat preferences and their breeding seasons are largely out of phase. This information, combined with data on distribution patterns, led to the following conclusions: Lepadogaster l. purpurea is considered to be a valid species, L. purpurea (Bonnaterre, 1788), different from L. l. lepadogaster, now designated L. lepadogaster (Bonnaterre, 1788). L. zebrina was found to be a synonym of L. lepadogaster. The two newly defined species were found to be in sympatry at Madeira and the Canary islands, the Atlantic coast of the Iberian Peninsula, and the Mediterranean at least as far as Genoa (Italy). Diagnostic characters and a list of synonyms are provided. (C) 2002 The Linnean Society of London, Biological Journal of the Linnean Society, 2002, 76, 327-338

Sexual dimorphism in cancer.

The incidence of many types of cancer arising in organs with non-reproductive functions is significantly higher in male populations than in female populations, with associated differences in survival. Occupational and/or behavioural factors are well-known underlying determinants. However, cellular and molecular differences between the two sexes are also likely to be important. In this Opinion article, we focus on the complex interplay that sex hormones and sex chromosomes can have in intrinsic control of cancer-initiating cell populations, the tumour microenvironment and systemic determinants of cancer development, such as the immune system and metabolism. A better appreciation of these differences between the two sexes could be of substantial value for cancer prevention as well as treatment

Telomere Lengths, Pulmonary Fibrosis and Telomerase (TERT) Mutations

mutations. mutation carriers demonstrate reduced life expectancy, with a mean age of death of 58 and 67 years for males and females, respectively. mutation have shorter telomere lengths than controls, demonstrating epigenetic inheritance of a shortened parental telomere length set-point

Diminished Telomeric 3′ Overhangs Are Associated with Telomere Dysfunction in Hoyeraal-Hreidarsson Syndrome

BACKGROUND:Eukaryotic chromosomes end with telomeres, which in most organisms are composed of tandem DNA repeats associated with telomeric proteins. These DNA repeats are synthesized by the enzyme telomerase, whose activity in most human tissues is tightly regulated, leading to gradual telomere shortening with cell divisions. Shortening beyond a critical length causes telomere uncapping, manifested by the activation of a DNA damage response (DDR) and consequently cell cycle arrest. Thus, telomere length limits the number of cell divisions and provides a tumor-suppressing mechanism. However, not only telomere shortening, but also damaged telomere structure, can cause telomere uncapping. Dyskeratosis Congenita (DC) and its severe form Hoyeraal-Hreidarsson Syndrome (HHS) are genetic disorders mainly characterized by telomerase deficiency, accelerated telomere shortening, impaired cell proliferation, bone marrow failure, and immunodeficiency. METHODOLOGY/PRINCIPAL FINDINGS:We studied the telomere phenotypes in a family affected with HHS, in which the genes implicated in other cases of DC and HHS have been excluded, and telomerase expression and activity appears to be normal. Telomeres in blood leukocytes derived from the patients were severely short, but in primary fibroblasts they were normal in length. Nevertheless, a significant fraction of telomeres in these fibroblasts activated DDR, an indication of their uncapped state. In addition, the telomeric 3' overhangs are diminished in blood cells and fibroblasts derived from the patients, consistent with a defect in telomere structure common to both cell types. CONCLUSIONS/SIGNIFICANCE:Altogether, these results suggest that the primary defect in these patients lies in the telomere structure, rather than length. We postulate that this defect hinders the access of telomerase to telomeres, thus causing accelerated telomere shortening in blood cells that rely on telomerase to replenish their telomeres. In addition, it activates the DDR and impairs cell proliferation, even in cells with normal telomere length such as fibroblasts. This work demonstrates a telomere length-independent pathway that contributes to a telomere dysfunction disease

Genetic Anticipation Is Associated with Telomere Shortening in Hereditary Breast Cancer

There is increasing evidence suggesting that short telomeres and subsequent genomic instability contribute to malignant transformation. Telomere shortening has been described as a mechanism to explain genetic anticipation in dyskeratosis congenita and Li-Fraumeni syndrome. Since genetic anticipation has been observed in familial breast cancer, we aimed to study telomere length in familial breast cancer patients and hypothesized that genetic defects causing this disease would affect telomere maintenance resulting in shortened telomeres. Here, we first investigated age anticipation in mother-daughter pairs with breast cancer in 623 breast cancer families, classified as BRCA1, BRCA2, and BRCAX. Moreover, we analyzed telomere length in DNA from peripheral blood leukocytes by quantitative PCR in a set of 198 hereditary breast cancer patients, and compared them with 267 control samples and 71 sporadic breast cancer patients. Changes in telomere length in mother-daughter pairs from breast cancer families and controls were also evaluated to address differences through generations. We demonstrated that short telomeres characterize hereditary but not sporadic breast cancer. We have defined a group of BRCAX families with short telomeres, suggesting that telomere maintenance genes might be susceptibility genes for breast cancer. Significantly, we described that progressive telomere shortening is associated with earlier onset of breast cancer in successive generations of affected families. Our results provide evidence that telomere shortening is associated with earlier age of cancer onset in successive generations, suggesting that it might be a mechanism of genetic anticipation in hereditary breast cancer