Historical epidemiology of hepatitis C virus in select countries-volume 4.

Due to the introduction of newer, more efficacious treatment options, there is a pressing need for policy makers and public health officials to develop or adapt national hepatitis C virus (HCV) control strategies to the changing epidemiological landscape. To do so, detailed, country-specific data are needed to characterize the burden of chronic HCV infection. In this study of 17 countries, a literature review of published and unpublished data on HCV prevalence, viraemia, genotype, age and gender distribution, liver transplants and diagnosis and treatment rates was conducted, and inputs were validated by expert consensus in each country. Viraemic prevalence in this study ranged from 0.2% in Hong Kong to 2.4% in Taiwan, while the largest viraemic populations were in Nigeria (2 597 000 cases) and Taiwan (569 000 cases). Diagnosis, treatment and liver transplant rates varied widely across the countries included in this analysis, as did the availability of reliable data. Addressing data gaps will be critical for the development of future strategies to manage and minimize the disease burden of hepatitis C.

Strategies to manage hepatitis C virus infection disease burden-Volume 4.

The hepatitis C virus (HCV) epidemic was forecasted through 2030 for 17 countries in Africa, Asia, Europe, Latin America and the Middle East, and interventions for achieving the Global Health Sector Strategy on viral hepatitis targets-"WHO Targets" (65% reduction in HCV-related deaths, 90% reduction in new infections and 90% of infections diagnosed by 2030) were considered. Scaling up treatment and diagnosis rates over time would be required to achieve these targets in all but one country, even with the introduction of high SVR therapies. The scenarios developed to achieve the WHO Targets in all countries studied assumed the implementation of national policies to prevent new infections and to diagnose current infections through screening.

The present and future disease burden of hepatitis C virus infections with today's treatment paradigm: Volume 4.

Factors influencing the morbidity and mortality associated with viremic hepatitis C virus (HCV) infection change over time and place, making it difficult to compare reported estimates. Models were developed for 17 countries (Bahrain, Bulgaria, Cameroon, Colombia, Croatia, Dominican Republic, Ethiopia, Ghana, Hong Kong, Jordan, Kazakhstan, Malaysia, Morocco, Nigeria, Qatar and Taiwan) to quantify and characterize the viremic population as well as forecast the changes in the infected population and the corresponding disease burden from 2015 to 2030. Model inputs were agreed upon through expert consensus, and a standardized methodology was followed to allow for comparison across countries. The viremic prevalence is expected to remain constant or decline in all but four countries (Ethiopia, Ghana, Jordan and Oman); however, HCV-related morbidity and mortality will increase in all countries except Qatar and Taiwan. In Qatar, the high-treatment rate will contribute to a reduction in total cases and HCV-related morbidity by 2030. In the remaining countries, however, the current treatment paradigm will be insufficient to achieve large reductions in HCV-related morbidity and mortality.

The macrophagic activity of patients affected by pneumonia or chronic obstructive pulmonary disease.

The function of alveolar macrophages (AMS) in patients with pneumonia (n = 7) (Group A) and chronic obstructive pulmonary disease (COPD) (n = 11) (Group B) was investigated by evaluating the rate of phagocytosis and of the intracellular killing. A control group of healthy subjects (n = 8) was also included. Phagocytosis frequency (PHF), phagocytosis index (PHI) and intracellular killing towards Candida albicans were then evaluated. PHF and PHI were found to be significantly (p < 0.05) lower in Group B patients than in the control group, while intracellular killing showed a behaviour similar to controls. PHF and PHI values observed in the patients of Group A and in the control group did not show any significant difference; the intracellular killing rate proved on the contrary to be significantly (p < 0.05) lower than that observed in the controls.

Cisplatin plus epirubicin and etoposide followed by irradiation plus lonidamine in stage III nonsmall cell lung cancer.

Forty-seven patients with stage III nonsmall cell lung cancer (NSCLC) were treated with the sequential administration of combination chemotherapy consisting of cisplatin, epirubicin and etoposide and of irradiation plus lonidamine. The response rate was 49% after chemotherapy with an improvement of 14% after radiation therapy and lonidamine. The median survival was around 15 months for responders and 9 months for nonresponders. Toxicity was moderate and acceptable. It is concluded that this schedule is active in the treatment of NSCLC.

Immunomodulating activities associated with the cytosol fraction of a 3-methylcholanthrene-induced rat fibrosarcoma.

Cytosol fraction(s) from McFiFi2(s) fibrosarcoma cells (Fcc), isolated from either cultured cells or solid tumors induced in F344 rats, produced a dose-related inhibition of lymphoproliferative responses to several mitogens, whatever the lymphoid organ or the animal species used as the source of lymphocytes. Only stimulated human lymphocytes were not Fcc inhibited; instead, Fcc was a potent stimulator of their spontaneous proliferation. Fcc cytostatic activity was not effective in various cycling cell lines and was restricted to mitogen-stimulated lymphocytes. Fcc, a primary tumor product, did not induce suppressive cells and was unable to prevent mitogen cell surface binding. However, expression of its modulating effect was accelerated by the simultaneous presence of the mitogen. Moreover, Fcc produced its suppression by interrupting lymphocyte activation at some point within the G0-G1-phase transition. Molecular sieving showed that Fcc contains at least two factors with suppressive (mol wt, approximately 3,000) and stimulatory (mol wt, greater than 5,000) activities, respectively.

Increase in lipolysis and decrease in plasma-heparin lipoprotein lipase activity and alpha 1 lipoprotein level after aminophylline in man.

Intravenous aminophylline 0.48 g produced a sharp increase in plasma free fatty acids. After three days of treatment with aminophylline 0.96 g/day i.v., plasma post-heparin lipoprotein lipase was significantly reduced, and post-heparin hepatic triglyceridase remained unchanged. alpha 1 lipoprotein was reduced by treatment, in parallel with lipoprotein lipase, while other lipoprotein fractions, serum cholesterol and triglycerides were unaffected.

Evidence for suppressor cells in Lewis rats' experimental allergic encephalomyelitis.

In this work we demonstrate a suppressive activity on the induction of experimental allergic encephalomyelitis (EAE) in Lewis rats, transferable to syngeneic animals, challenged with encephalitogenic mixture (myelin basic protein, complete Freud's adjuvant plus Bordetella pertussis organisms) 24 h later. This activity is probably effected by T cells and not by (an) inhibitory serum factor(s). The induction of this specific protection could be due to the penetration of the myelin basic protein antigen into the thymus where we first found suppressive cells. From the thymus, suppressor cells could then emigrate to spleen (on day 15) and to nondraining lymph nodes (on day 17). In the course of normal EAE in Lewis rats and especially at the time of self cure, this suppression is not demonstrated, but possible.

[Suppressor cells in allergic encephalomyelitis]. / Rôle de cellules suppressives dans l'encéphalomyélite allergique expérimentale (EAE) des rats Lewis

The induction of EAE in Lewis rats by basic protein (BP) is suppressed by the transfer of non-draining lymphnode cells from cured animals. The activation of draining lymphnode cells of these cured animals by BP, PHA or ConA is decreased with the addition of non-draining lymph node cells from the same rats.