Type-specific human papillomavirus detection in cervical smears in Romania

Abstract

To study type 1 diabetes (T1D), excellent animal models exist, both spontaneously diabetic and virus-induced. Based on knowledge from these, this review focuses on the environmental factors leading to T1D, concentrated into four areas which are: (1) The thymus-dependent immune system: T1D is a T cell driven disease and the beta cells are destroyed in an inflammatory insulitis process. Autoimmunity is breakdown of self-tolerance and the balance between regulator T cells and aggressive effector T cells is disturbed. Inhibition of the T cells (by e.g. anti-CD3 antibody or cyclosporine) will stop the T1D process, even if initiated by virus. Theoretically, the risk from immunotherapy elicits a higher frequency of malignancy. (2) The activity of the beta cells: Resting beta cells display less antigenicity and are less sensitive to immune destruction. Beta-cell rest can be induced by giving insulin externally in metabolic doses or by administering potassium-channel openers. Both procedures prevent T1D in animal models, whereas no good human data exist due to the risk of hypoglycemia. (3) NKT cells: According to the hygiene hypothesis, stimulation of NKT cells by non-pathogen microbes gives rise to less T cell reaction and less autoimmunity. Glycolipids presented by CD1 molecules are central in this stimulation. (4) Importance of the intestine and gliadin intake: Gluten-free diet dramatically inhibits T1D in animal models, and epidemiological data are supportive of such an effect in humans. The mechanisms include less subclinical intestinal inflammation and permeability, and changed composition of bacterial flora, which can also be obtained by intake of probiotics. Gluten-free diet is difficult to implement, and short-term intake has no effect. Regarding the onset of the T1D disease process, slow-acting enterovirus and gliadin deposits are speculated to be etiological in genetically susceptible individuals, followed by the mentioned four pathogenetic factors acting in concert. Neutralization of any one of these factors is capable of stopping T1D development, as lessons are learned from the animal models.

High prevalence of human papillomavirus infection in Eastern European and West African women immigrants in South Italy

“…The proportion of Eastern European migrants with normal cytology and with HPV infection (56.1%) is much higher than that reported in Russian Federation (29.1%) (15) or in the former Soviet Union states (27.4%) (16). Recent studies, however, conducted in Romania and in Estonia showed that HPV rates among women negative for intra-epithelial lesions and malignancy were 43.5% and 36.8%, respectively (29,30). In both countries, the high prevalence of HPV infection in the general population correlates with a very high incidence of invasive cervical cancer (31 new cases ⁄ 100 000 women in Romania and 21.5 new cases ⁄ 100 000 women in Estonia) (31).…”

Prevalence of abnormal Pap smears in a consecutive and previously unscreened population in Romania

“…The high prevalence of HSIL in the present study draws attention to the fact that the prevalence of high-risk HPV subtypes is probably much higher in Romania than in other countries [22][23][24][25][26], although these data are from only small study samples. Another explanation might be the unequal distribution of cases by age group in the present study (Table 4): 38.7% of abnormal samples were in the age group 30-39 years; 20.0% in the age group 40-49 years (the incidence of HSIL peaked at approximately 40 years of age); 17.8% in the age group 25-29 years; and 14.0% in the age group 24 years and younger (the incidence of LSIL peaked a decade earlier than that of HSIL).…”

Toll-Like Receptor 4 Deficiency Accelerates the Development of Insulin-Deficient Diabetes in Non-Obese Diabetic Mice

“…In order to study the possible role of TLR4 in diabetes development, we generated a TLR4-deficient strain of the NOD mouse, the currently best characterized model of human type 1 diabetes [27] and analysed diabetes progression by in vivo and in vitro approaches.…”