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PubMed1999

Are low income countries targets of the tobacco industry? Plenary lecture given during the Conference on Global Lung Health and 1997 Annual Meeting of the International Union Against Tuberculosis and Lung Disease, Palais des Congrès, Paris, France, 1-4 October 1997.

Estimations show that tobacco consumption is steadily increasing in low income countries already deprived of basic human needs, such as adequate food and water supplies and education. Among the many factors affecting this, the most significant is the aggressive marketing strategies of the tobacco industry. The tobacco industry operates by denying health evidence, sponsoring scientific research that diverts attention to other fields, investing heavily in promotion and advertising, interfering with national public health laws, forming joint ventures with national monopolies, and persuading governments on the risks of smuggling. Turkey, a tobacco-growing country, opened its markets to the multinational tobacco industry after 1984. This paper presents examples of the marketing strategies used by the tobacco industry in the last two decades, and shows the consequences for Turkey in the hope that this information can help other low income countries that are not yet targets of the invasion of the tobacco industry.

Agriculture↗
PubMed1998

[Rudolf-Virchow Prize 1998. Award lecture. Toxoplasmosis: a model infection for studying systemic and intracerebral immune reactions].

Toxoplasmosis has gained particular attention in the AIDS era as the most common opportunistic encephalitis in HIV-infected patients. Since there are important parallels between the human and rodent infection, experimental murine toxoplasmosis is widely used to study the immune reactions to this protozoal parasite. Oral application of low-virulent Toxoplasma (T.) gondii cysts leads to a biphasic disease characterized by an acute, generalized phase followed by a chronic stage confined to the brain, where an encephalitis with persistence of the parasite develops. Immunity to T. gondii is T cell mediated, and there is increasing evidence for a critical role of cytokines for an effective immune response. In order to address the functional role of interferon (IFN)-gamma in toxoplasmosis, we took advantage of mice lacking the IFN-gamma-receptor. Inactivation of the IFN-gamma-receptor rendered mice highly susceptible to T. gondii, and they died of a fulminant acute toxoplasmosis. Among the various organs affected, hepatitis was severe enough to cause death. In contrast to wild type animals, IFN-gamma-receptor-deficient mice were unable to activate their macrophages as evidenced by a lack of major histocompatibility complex (MHC) class II antigen induction and the absence of an upregulation of tumor necrosis factor (TNF)-alpha and inducible nitric oxide synthase (iNOS) mRNA transcripts, two macrophage effector molecules. These observations prompted the investigation of TNF- and TNF-receptor-mediated effects in toxoplasmosis by use of mice deficient in either the TNF-receptor type 1 (TNFR1) and/or the TNF-receptor type 2 (TNFR2). The lethal outcome of T. gondii-infected TNFR1/2- and TNFR1-deficient mice, but not of TNFR2-deficient and wild type animals, illustrated the important role of TNF-alpha and TNFR1-mediated signalling, respectively, in this infection. Histopathology attributed death of TNFR1- and TNFR1/2-deficient mice to a severe, necrotizing encephalitis. Unrestricted intracerebral parasite replication in these strains was associated with reduced numbers of iNOS+ leukocytes and a lack of iNOS mRNA induction in their brains as compared to resistant wild type and TNFR2-deficient mice. To precisely identify the cellular sources of cytokines in the brain, flow cytometry of leukocytes isolated from the brain, in situ hybridization, immunohistochemistry and RT-PCR analysis of cytokine mRNA transcripts of magnetically purified leukocyte populations were performed. These studies disclosed that both CD4+, CD8+ T lymphocytes and macrophages recruited to the brain as well as resident cell populations of the CNS including neurons, astrocytes and microglia contributed to the intracerebral cytokine synthesis. Each population was characterized by a specific cytokine pattern. Interestingly, activation of brain cells is a hallmark of Toxoplasma encephalitis. The marked induction of a variety of immunologically important cell surface molecules as MHC class I and II antigens, cell adhesion molecules and their ligands on microglia points to a particular important role of this cell type for the immune response to T. gondii, since the expression of these molecules is a prerequisite for cellular interactions with T cells. The observation of a prominent interleukin (IL)-10 production in the T. gondii-infected brain initiated studies addressing the function of this powerful immunosuppressive mediator in chronic Toxoplasma encephalitis. Neutralization experiments revealed that IL-10 facilitates persistence of the parasite in the brain by downregulating the intracerebral immune response. On the other hand, IL-10 may exert a regulatory role and may be necessary to prevent immunopathological effects of an uncontrolled immune response. In conclusion, these studies demonstrate the important role of the cytokines IFN-gamma and TNF-alpha and their receptors, respectively, for an effective control of T. gondii. In the CNS, the target organ of the parasite, a

Animals↗
PubMed1996

Implementation of non-smoking policies in hospitals--Tom Hurst Memorial Lecture.

The paper draws upon the experience of the Preston Acute Hospitals NHS Trust in being a member of the European Network of Health Promoting Hospitals and, in so doing, places the health promoting activities of the Trust in its widest context. There is a discussion on the advice issued by the Department of Health towards making hospitals smoke free, which concludes that the advice is not helpful. It is suggested that successful attempts to eradicate smoking in hospitals must be part of a wider health promoting strategy. This, in turn, can be linked to the changing role of hospitals where there is an increasing emphasis on primary care services and a push towards rationalisation of district general hospitals.

Health Promotion↗
PubMed1999

The Emanuel Miller Memorial Lecture 1998. Autism: two-way interplay between research and clinical work.

The two-way interplay between research and clinical practice in relation to autism is reviewed with respect to: (1) diagnosis and syndrome delineation; (2) the nature of the disorder: (3) intervention studies; and (4) aetiology, as manifest during four time periods; (a) the 1950s and 1960s; (b) the 1970s into the mid 1980s; (c) the late 1980s and early 1990s; and (d) the late 1990s. It is concluded that clinical practice has changed out of all recognition during the last 50 years and that research findings have been crucial in bringing about that change. It has not, however, been a one-way traffic. Many key advances were prompted by astute clinical observations and some extravagant research claims were given a more balanced perspective through the light of clinical experience. Crucial research and clinical tasks remain but the means to meet them are there if the opportunities are taken and attention is paid to the lessons of the past.

Autistic Disorder↗
PubMed1997

The 22nd Kellersberger Memorial Lecture, 1997. Preventing loss of sight from leprosy.

Multidrug treatment of leprosy is being dramatically successful in sterilising the infection. However complications are still occurring, spoiling the result in some patients by residual damage, including to the eye. Prevention of this damage is imperative. It is stressed that eye complications will only lead to loss of sight if they are neglected. The lesions caused by leprosy in the eye are briefly described. The dangerous lesions are lagophthalmos causing corneal exposure, and iritis causing pupil block glaucoma. Frequency of the lesions were very common in the past, but seem to be becoming much less so, though good epidemiological studies are sparse. Cataract, mostly not caused by leprosy, is the commonest cause of loss of vision. Prediction of complications would facilitate prompt treatment, but despite some clues, prediction is at present inadequate and all cases must be watched. The management of complications is discussed: studies of the indications and outcome of surgery for lagophthalmos, and of intraocular lens implantation for cataract are priorities. If knowledge is to be put into practice to prevent blindness, training of front line staff and organisation of the service is central. Experience of these practical aspects in Uganda in recent years is described.

Africa↗
PubMed1999

Memorial lecture. Megakaryocytic growth factors: is there a new approach for management of thrombocytopenia in patients with malignancies?

C-mpl ligand acts primarily as a lineage-specific hematopoietic growth factor by promoting proliferation of megakaryocyte precursors and their differentiation into megakaryocytes and platelets. In addition to the ability of c-mpl ligand to support megakaryocytic development from CD34+ precursor cells, several lines of evidence also point to a stimulatory effect on hematopoietic stem cells. When recombinant thrombopoietin or pegylated megakaryocyte growth and development factor is administered to normal animals or humans, there is a dose-dependent increase in the platelet count. When administered following chemotherapy in animal models or humans, c-mpl ligands reduce the duration and sometimes the degree of thrombocytopenia. The issue of whether clinically relevant thrombocytopenia can be ameliorated has so far been more difficult to resolve. Because severe thrombocytopenia is not commonly seen with standard chemotherapy regimens, clinical studies examining c-mpl ligands for their ability to ameliorate chemotherapy-induced thrombocytopenia will focus on treatment of acute leukemias and bone marrow transplantation. The potential utility of c-mpl ligands for treatment of myelodysplastic syndromes, aplastic anemias, or in HIV infection, will have to be evaluated in the future. Possibly the greatest potential of thrombopoietic growth factors in the near future may be in transfusion medicine, to collect and to store platelets from healthy donors or in autologous settings.

Anemia, Aplastic↗
PubMed1999

The Fifth Carlos E. Rubio Memorial Lecture. Sclerosing cholangitis: pathogenesis, pathology, and practice.

Primary sclerosing cholangitis is a generally progressive, sometimes fatal, chronic hepatobiliary disorder for which no effective medical or surgical therapy now exists. The syndrome occurs most frequently in young men and is characterized by chronic cholestasis, frequent association with CUC, a paucity of serologic markers, hepatic copper overload, and characteristic abnormalities in some liver biopsy specimens and in virtually all cholangiograms. The natural history of the syndrome is still somewhat unclear; the disease likely progresses slowly and relentlessly over a decade or longer from an asymptomatic stage to a condition characterized by symptoms of cholestasis and complicated by cirrhosis and portal hypertension and carcinoma of the bile ducts. Management should first involve a thoughtful decision to observe, which is reasonable in the asymptomatic patient with early disease, or to intervene, particularly in patients with symptoms. Therapeutic goals should be defined and should concentrate on either alleviating symptoms, dealing with complications, or attempting to affect the underlying hepatobiliary disease. Symptomatic treatment and therapy for complications is similar to that employed in other chronic liver diseases, but also involves balloon dilatation of dominant strictures in appropriately selected symptomatic patients. Biliary tract reconstructive surgery may alleviate symptoms in selected patients with PSC, but its effect on the natural history of the syndrome has not been determined. Proctocolectomy for CUC in a patient with CUC and PSC does not beneficially affect the progression of the underlying hepatobiliary disease. In contrast, orthotopic liver transplantation may be life-saving for patients with advanced disease. Medical therapy directed at arresting the progression of the underlying hepatobiliary disease is currently experimental and includes cupruretic, immunosuppressive, antifibrogenic, and choleretic agents. Although a single recently completed controlled trial makes it unlikely that cupruretic agents will be helpful in this syndrome, immunosuppressive (i.e. cyclosporin A and methotrexate) and choleretic (i.e. ursodeoxycholic acid) agents alone or in combination are currently undergoing evaluation in randomized trials.

Adrenal Cortex Hormones↗