Medical Hypotheses

Our medical research library holds 13 studies published in Medical Hypotheses (1978–2014). Each entry links to the study's record on PubMed and, where there is one, to the publisher's page and a free full text. 12 have an abstract, the authors' own summary as PubMed records it: open "Abstract" to read it.

About the journal

• Publisher: Eden Press
• Published: 1975 to the present, United States
• Language: English
• ISSN: 0306-9877 (print), 1532-2777 (electronic)
• Its record in the NLM Catalog

2010s

• Airways microbiota: Hidden Trojan horses in asbestos exposed individuals?. D.E. Magouliotis, V.S. Tasiopoulou, P.A. Molyvdas, et al. 2014;83(5):537-40. PubMed · Publisher

  Abstract

  Malignant pleura mesothelioma (MPM) is a rare type of cancer with devastating prognosis, which develops in the pleural cavity from transformed mesothelium. MPM has been directly associated with asbestos exposure however there are aspects of the pathophysiology involved in the translocation of asbestos fibers in the pleura that remain unclear. Here, we propose and discuss that certain proteins secreted by airways symbiotic microbiota create membrane pores to the airway epithelial cells, through which asbestos fibers can penetrate the lung parenchyma and reach the sub-pleural areas. We evaluate this hypothesis using data from the published literature regarding the airways microbiota toxins such as cholesterol-dependent cytolysins (CDCs).

  Copyright © 2014 Elsevier Ltd. All rights reserved.

• Are oestrogens and genetic predisposition etiologic factors in the development of clear cell carcinoma of the peritoneum?. R. Wuntakal, A. Lawrence. 2013;80(2):167-71. PubMed · Publisher

  Abstract

  A literature search was carried out for clinical observations that could explain the possible aetiology of primary peritoneal clear cell carcinoma (CCC) including diagnostic dilemmas, various theories of origin, oestrogen dependence and genetic association. It was found to be an extremely rare tumour (CCC) arising in the peritoneum and is often misdiagnosed as mesothelioma or serous carcinoma or metastatic adenocarcinoma due to overlapping morphological features. The awareness of such dilemmas is important even before making a diagnosis. Clinicopathological features and immunohistochemical studies like WT1, CK20 and calretinin are usually helpful in differentiating CCC from serous carcinoma, metastatic carcinoma from bowel and mesothelioma. (CK7 is common to all epithelial tumours, CEA can be expressed in clear cell carcinoma, WT1 is normally expressed in serous carcinoma, calretinin is expressed in mesothelioma and CK20 in colon carcinoma). The distinction between the above tumours is important as correct diagnosis is required in initiating appropriate treatment. Less than ten cases have been reported in the English language medical literature. Mullerian metaplasia and malignant transformation in endometriosis are two theories proposed for its existence. Peritoneal CCC can be oestrogen dependent in view of association with oestrogen dependent conditions which include endometriosis, adenomyosis and endometrial carcinoma. A genetic ascertain is difficult to be associated and needs further evaluation in a research setting in the familial cancer genetic clinics.

  Copyright © 2012 Elsevier Ltd. All rights reserved.

2000s

• Asbestos fibres in drinking water: are they carcinogenic or not?. C. Varga. 2000;55(3):225-6. PubMed · Publisher

  Abstract

  The paper discusses the possibility of a carcinogenic effect of consuming drinking water contaminated by asbestos fibres.

• Health effects of respirator use at low airborne concentrations. J.H. Lange. 2000;54(6):1005-7. PubMed · Publisher

  Abstract

  Respirators are considered a personal protective mechanism for preventing occupational disease because of inhaling toxic and hazardous substances. Engineering and work practice controls, in today's industrial environment, often maintain airborne contaminants below occupational hazardous levels. However, even at low concentrations, workers are often required to use respirators. Inappropriate use of respirators, during low exposure concentrations, may result in increased incidence and prevalence of disease from respirator use caused by physiological and psychological stress. This paper examines the hypothetical aspect of increased disease from using respirators at low exposure concentrations, with specific reference to the asbestos abatement industry.

1990s

• Could development of malignant mesothelioma be induced by Yersinia enterocolitica infection?. A. Saebø, K. Elgjo, J. Lassen. 1993;40(5):275-7. Case report PubMed · Publisher

  Abstract

  Two out of 458 hospitalized patients with Yersinia enterocolitica infection developed malignant mesothelioma of pleura viz. pericard; both died after a few months. Malignant mesothelioma of the pleura is commonly related to asbestos exposure, whereas pericardiac mesothelioma is an extremely uncommon neoplasm. The possible promotion of malignant mesothelioma by the Yersinia enterocolitica infection should not be disregarded, as the infection may launch chronic immunological reactions resembling those observed among asbestos workers.

• Cell proliferation and carcinogenesis may share a common basis of permeable plasma membrane clusters. J.A. Beech. 1992;38(3):208-14. PubMed · Publisher

  Abstract

  Wound potentials increase the surface potential of exposed areas of nearby cells. In these cells, soluble cytoplasmic bases are assumed gradually to move nearer the exposed area. Acidic molecules on the cell surface migrate to points opposite the bases. The image-charged species are mutually attracted to form transmembrane clusters. At clusters, membrane permeability increases and the cell is stimulated to cycle. When the wound heals, its clusters disperse, leaving a small 'permanent' residuum. Permanent clusters initiate cells to malignancy. They have (or develop) lipophilic molecules on both surfaces that help fix them in the membrane. Exposed cells contaminated with polycyclic aromatic hydrocarbon carcinogens (PAH) readily form permanent clusters. At mitosis, clusters on parental plasma membrane pass with that membrane to a daughter cell. Promotion results from many short-term or a single long-term exposure of initiated membranes to abnormal surface charge. Permanent clusters increase on the membrane after repeated wounding, proximity of charged foreign bodies like plastic film or asbestos, or oxidation of surface molecules. Progression requires acceleration of cluster growth so the daughter cell membranes become as leaky at maturity as was the parent membrane. One mechanism suggested involves reversible phosphorylation by membrane-bound kinases; another involves attraction of a basic protein (p36) to the membrane.

• A suggested air standard for lead to protect the public during lead abatement activities. J.H. Lange. 1991;36(3):211-2. PubMed · Publisher

  Abstract

  Lead abatement is developing as a new industry in a manner similar to asbestos abatement. Recent standards and guidelines have been established by various governmental agencies to ensure worker and public protection during lead abatement. An air concentration standard of 3.0 ug/m3 for lead is suggested in non-work locations based on hypothetical body burden calculations and sampling results during lead abatement activities. Adverse health effects to the general public resulting from exposure to lead from abatement activities at this concentration should not be observed.

• Asbestos and stomach cancer in Japan--a connection?. E.W. Kiritani. 1990;33(3):159-60. PubMed · Publisher

1980s

• Identification of environmental carcinogens utilizing T-cell mediated immunity. R.H. Stevens, D.A. Cole, P.A. Lindholm, et al. 1986;19(3):267-85. PubMed · Publisher

  Abstract

  There now exists a very large body of information that directly links the exposure to certain environmental factors with the ultimate development of specific types of human cancer. For this reason, a number of tests possessing varying degrees of biological complexity have been devised with the intent to first identify, and then ultimately reduce the risk of exposure to tumor causing agents. The presently employed chronic whole animal tests generally accepted as measures of human carcinogenicity have certain limitations in that they are lengthy to perform, very expensive, and require complicated pathological examinations of the various tissues. Consequently, there exists a need for short-term whole animal bioassays that can serve to complement such lengthy chronic studies; we are proposing that one such a test can be developed through utilizing procedures that have been designed for evaluating T-cell immunological responses.

• Laryngeal cancer: an explanation for the apparent occupational association. A. Chovil. 1981;7(7):951-6. PubMed · Publisher

  Abstract

  The apparent association of laryngeal cancer with asbestos and possibly other occupational exposures can be accounted for by the hypothesis that chronic vocal abuse peculiar to certain working conditions will act as a promoting factor for active carcinogens found mainly in tobacco smoke.

1970s

• Carcinogenicity of fibers and films: a theory. V.E. Archer. 1979;5(11):1257-62. PubMed · Publisher

  Abstract

  A theory based on frustrated phagocytosis is advanced to explain the carcinogenesis of fibers and films. Exocytosis combined with flexion of a foreign body permits the escape of superoxide radicals which, in a manner similar to that postulated for ionizing radiation, induces somatic mutations. The theory is subject to experimental verification, and offers hope for the development of preventive therapy which can be used to prevent some of the fibrosis and cancer resulting from asbestos inhalation.

• Biological autoxidation. I. Decontrolled iron: an ultimate carcinogen and toxicant: an hypothesis. S.H. Kon. 1978;4(5):445-71. PubMed · Publisher

  Abstract

  Ionic iron at physiological pH hydrolyzes into insoluble aggregates, which disperse on slight acidification. Uncontrolled ionic iron promotes autoxidation, which crosslinks biomolecules and produces destructive activated oxygen. Defenses against autoxidative crosslinking include: 1. ferritin, the macromolecular scavenger of iron; 2. metabolic turnover, which prevents irreversible crosslinking through early catabolic degradation and replacement; and 3. enzymatic deactivation of oxygen. I am proposing that the anticrosslinking defenses are defeated by transient actions of metabolic perturbations, toxicants, oxidants and "foreign bodies", which cause oxidative crosslinking of proteins and lipids into irreversible tissue imprint: indigestible bodies containing porous limited-access spaces (LASs). The pores exclude the macromolecular ferritin and the digestive and antiautoxidation enzymes but admit ionic iron which, sheltered from ferritin, accumulates into decontrolled-iron pathogen (DIP). DIP utilizes the energy of ambient pH fluctuations to erupt from the LAS, swamp the available ferritin, poison the surroundings, catalyze autoxidation and crosslink cell components into additional LAS carriers. With time and sufficient promotion by pH fluctuations or metal-complexing agents, DIP and LAS expand. DIP injures through heavy-metal inhibition of life processes and catalysis of autoxidation. Typically, carcinogenic initiators are protein denaturants, cell poisons, "foreign bodies" and autoxidation catalysts. These are DIP-initiating properties, and DIP may be a preneoplastic stage of carcinogenesis. A DIP-model interpretation is given for the growth of asbestos bodies. DIP is an inorganic parasite. It may envelope and attack phagocytized particles.

• Biological autoxidation. II. Cholesterol esters as inert barrier antioxidants. Self-assembly of porous membrane sacs. An hypothesis. S.H. Kon. 1978;4(6):559-80. PubMed · Publisher

  Abstract

  The antioxidation defenses recognized thus far appear too weak. Needed are inert barriers to encapsulate foci of activated oxygen (FAOs) and contain their spreading. These capsules must: 1. self-assemble nonenzymatically and spontaneously in face of adversity; 2. resist oxidation and dissolution in water; and 3. be moderately fluid and elastic enough to withstand flexing by tissues. Evidence shows activated oxygen: a. is produced by common cholesterolester (CE)-raising agents; b. boosts accumulation of CEs; and c. splits low-density lipoproteins (LDL), thus releasing CE-rich coalescence-prone lipid micelles. I am proposing that CEs, combined with polar lipids, are uniquely suited to form inert-lipid antioxidation barriers (ILABs). Porous ILAB capsules self-assemble from lipid micelles released by oxidatively degraded LDL. The capsules are thermodynamically unstable but elastic, durable and capable of self-repair through oxidation of ambient LDL. All capsules tend to contract into spheres. Enclosed needle-like "foreign bodies", such as asbestos, puncture the contracting capsules. Hence the odd bulbous architecture of asbestos bodies. ILABs protect from--and their failure initiates and promotes--carcinogenesis and atherosclerosis. ILABs may be mediators of membrane biogenesis. The loss of arterial flexibility in atherosclerosis protects ILAB capsules from breakage.

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