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Biomedical subjects

L Tomatis

Publications and source records attributed to L Tomatis.

At least 19 recordsLinked to original sources
PubMed2005

Modulation of leg muscle activity and gait kinematics by walking speed and bodyweight unloading.

During rehabilitation, many patient groups are being trained using bodyweight-supported treadmill training. However, little is known about modulation of time and distance parameters, joint movements and leg muscle EMG patterns by very low walking speeds or partial bodyweight unloading. We collected data from 20 healthy young volunteers who walked on a treadmill at walking speeds varying between 0.5 and 5.0 km h(-1) (0.14-1.39 ms(-1)) and with 0%, 25%, 50% and 75% bodyweight unloading. We found that cadence and stride length were largely influenced by walking speed, while bodyweight unloading influenced these measures only at 75%. However, the relative duration of the gait phases changed largely only at walking speeds less than 2.5 km h(-1), but was influenced by all different bodyweight unloading conditions. Joint trajectories of knee and ankle joint, as well as leg muscle EMG activity patterns changed largely at walking speeds slower than 2.5 km h(-1) and with 75% bodyweight unloading. We concluded that the parameters we investigated changed minimally at walking speeds faster than 2.5 km h(-1) and bodyweight unloading conditions less than 50%. Therefore, standards for EMG activity and joint angle trajectories should only be compared when the training is done with velocities higher than 2.5 km h(-1) and less than 50% body weight unloading.

Adult↗
PubMed2001

Inequalities in cancer risks.

Inequalities in health reflect social inequalities in society. The incapacity of our society to eliminate poverty is indeed one of the most blatant examples of failure in prevention. Every individual's health history is characterized by life-long influences and superimposed short-term factors, but health biographies of the rich and the poor show divergences that are the result of the accumulation and interaction of a series of events that may be quantitatively and qualitatively different. Schematically this could, for example, mean that certain individuals, or certain segments of the populations, are exposed more frequently and to more hazardous agents than others and/or less frequently to protective agents. Sanitary conditions are worse, mortality higher, survival rates of cancer patients lower, and life expectancy shorter in developing countries than in industrialized countries. The projection of the total number of cancer cases in the next decades indicates a general increase, proportionally greater in developing than in industrialized countries. Semin Oncol 28:207-209.

Developing Countries↗
PubMed2001

Carcinogenesis bioassays: study duration and biological relevance.

Criticisms of the scientific value of rodent carcinogenicity bioassays have focused on the arguments that the studies are too long and that most organ-specific carcinogenic effects observed in experimental animals have little or no relevance to humans. For example, Davies et al. (Davies, T.S., Lynch, B.S., Monro, A.M., Munro, I.C., Nestmann, E.R., 2000. Rodent carcinogenicity tests need be no longer than 18 months: an analysis based on 210 chemicals in the IARC Monographs. Food and Chemical Toxicology 38, 219-235) concluded that the duration of rodent bioassays should be no more than 18 months, based on their analysis of 210 International Agency for Research on Cancer (IARC) rodent carcinogens in which they report that most chemicals showed "tumorigenic effects" at or before 12 months. However, many of these "tumorigenic effects" reflect the occurrence of a single neoplasm, with most tumors occurring much later in the study. Reliance on a single tumor at an early time point as providing definitive evidence of rodent carcinogenicity is a dangerous practice that could produce both false positive and false negative outcomes. An extensive evaluation of the NTP database reveals that many rodent carcinogens produce later-appearing tumors that would not be detected as statistically significant in a 12-18 month study. Such a shortened duration study would be roughly equivalent to evaluating human cancer in subjects 30-50 years of age, which would result in markedly reduced study sensitivity. In fact, many investigators recommend extending the duration of rodent studies to 30 months or to a true lifetime to increase study sensitivity. We also do not agree with the second conclusion of Davies et al. (2000) that the mode of action of rodent carcinogenesis is sufficiently well understood to justify discounting the majority of organ-specific carcinogenic effects found in these studies. The consequences of performing rodent carcinogenicity studies with inadequate sensitivity, and then discounting most of the carcinogenic effects that are observed will be that potential human carcinogens will not be detected, thus forcing near total reliance on human studies for this purpose. This is not prudent public health policy.

Animals↗
PubMed2001

Between the body and the mind: the involvement of psychological factors in the development of multifactorial diseases.

A possible aetiological role for psychological factors has been propounded in particular in relation to diseases of which the causes are only partially known and which are in most cases multifactorial, such as cancer. The long period between a possible first event and the point of no return, gives appeal to the belief that life events other than "material" causes may play a role in cancer. The evidence that the immune and the nervous system may produce the same substances has opened the way to a new area of research. However, a lack of standardised instruments and the difficulty of conducting systematic and adequate analyses of potential confounding variables have discouraged most qualified scientists from devoting time and effort to investigating the possible role of psychological factors in the aetiology of human diseases. A few studies have reported a positive association between severe life events and breast cancer, but the prevailing view of the medical establishment is that there is no true association between stress and the onset of breast cancer. Although many criticisms of the studies reporting a positive association are definitely based on solid arguments, at least some of the criticisms cling to the requirement for absolute certainty in establishing a cause-effect relationship, which epidemiological studies can rarely, if ever, provide. A challenge for the future of research will be to investigate and better understand the role of subjective factors on the course and outcome of various pathologies, and in modulating the risk of developing a pathology.

Humans↗
PubMed2001

Alleged misconceptions' distort perceptions of environmental cancer risks.

In a series of papers, Ames and colleagues allege that the scientific and public health communities have perpetuated a series of 'misconceptions' that resulted in inaccurate identification of chemicals that pose potential human cancer risks, and misguided cancer prevention strategies and regulatory policies. They conclude that exposures to industrial and synthetic chemicals represent negligible cancer risks and that animal studies have little or no scientific value for assessing human risks. Their conclusions are based on flawed and untested assumptions. For instance, they claim that synthetic residues on food can be ignored because 99.99% of pesticides humans eat are natural, chemicals in plants are pesticides, and their potential to cause cancer equals that of synthetic pesticides. Similarly, Ames does not offer any convincing scientific evidence to justify discrediting bioassays for identifying human carcinogens. Ironically, their arguments center on a ranking procedure that relies on the same experimental data and extrapolation methods they criticize as being unreliable for evaluating cancer risks. We address their inconsistencies and flaws, and present scientific facts and our perspectives surrounding Ames' nine alleged misconceptions. Our conclusions agree with the International Agency for Research on Cancer, the National Toxicology Program, and other respected scientific organizations: in the absence of human data, animal studies are the most definitive for assessing human cancer risks. Animal data should not be ignored, and precautions should be taken to lessen human exposures. Dismissing animal carcinogenicity findings would lead to human cancer cases as the only means of demonstrating carcinogenicity of environmental agents. This is unacceptable public health policy.

Animals↗
PubMed2000

The identification of human carcinogens and primary prevention of cancer.

Primary prevention is based on the incontrovertible logic that a most efficient way to decrease the risk for a disease is to avoid, or reduce to minimal attainable levels, exposures to agents that can cause the disease or contribute to an increase in risk for the disease. This notwithstanding, the adoption of primary prevention measures has often encountered serious obstacles and unjustifiable delays. The success of primary prevention has also been limited by the combined effect of: (a) the inefficient and/or incomplete use of the cumulated etiological knowledge: (b) the spectrum of target organs for human carcinogens which does not include some of the most common cancer sites, a limitation that may be related to a disregard of epidemiological results and case reports that provide evidence that is less than sufficient of a causal relationship between an exposure and human cancer: (c) the pressure that powerful economic interests may have exerted in a variegated way to interfere or delay implementation of preventive measures that could have decreased their profit, and (d) the decreased acceptance of the ability of experimental results to predict similar effects in humans, in spite of the evidence that positive carcinogenicity results in experimental animals have often preceded and could indeed have predicted similar results in humans.

Carcinogens↗
PubMed2000

Etiologic evidence and primary prevention of cancer.

For many decades, primary prevention of cancer was implemented on the basis of evidence for a causal relationship between exposure and human cancer that took into consideration biological plausibility, but did not depend on the degree of understanding of the underlying mechanisms. One of the credos of public health is that primary prevention can be implemented before reaching a complete understanding of mechanisms that could confirm/explain causality. Measures of primary prevention are taken on the basis of what is recognized as causative factors of human cancer. The most authoritative lists of recognized human carcinogens are those compiled from the evaluations of carcinogenic risk carried out by the International Agency for Research on Cancer (IARC) and the evaluations that the U.S. National Toxicology Program (NTP) publishes in its periodical Report on Carcinogens. Knowledge of mechanisms is accumulating at a fast pace, and although it has not yet led to the definition of an efficient strategy for primary prevention for the majority of cancer cases, it may drive the scientific establishment toward a high-risk approach to prevention. The most reasonable and socially acceptable development of primary prevention should be the blending of a population approach; that is, the shifting of the distribution of risk factors across an entire population in a favorable direction (e.g., a general decrease of the levels of exposure to environmental carcinogens) with the high-risk approach that will concern individuals with extreme values of genetically determined weaknesses in the interactions with the environment.

Carcinogens↗
PubMed1999

Results from a historical survey of the survival of cancer patients given Di Bella multitherapy.

BACKGROUND: The Italian media have given wide coverage to a number of successes in treating cancer patients with an alternative therapy developed by Dr. Luigi Di Bella, a physician in Modena, Italy. In 1998, the Ministry of Health, under considerable pressure from the public, decided to promote studies to evaluate its efficacy. METHODS: Follow-up was conducted for cancer patients previously treated during the years 1971-1997 by Dr. Di Bella and registered in his archive. Identified cases were searched in cancer registries for diagnostic confirmation, date of diagnosis, and follow-up. Survival was compared with that in individually matched cancer cases derived from a pool of Italian cancer registries (the ITACARE data base). Kaplan-Meier survival curves were produced for all adult cancer patients as well as for children with leukemia and, in the matched analysis, for patients with cancer at the major anatomic sites and for all cancer patients combined. The homogeneity of survival curves between the two groups was tested by means of the log rank test. RESULTS: After several exclusions, 314 patients were entered into the study. Follow-up was completed for 79%. Only four patients received Di Bella Multitherapy (MDB) as their only anticancer therapy. Of these, only 1 is still alive 2 years after diagnosis. Five-year survival rates for children with leukemia and adult cancer patients were both 29.4%. Five-year survival was significantly lower in comparison with ITACARE cases for patients with childhood leukemia, breast carcinoma, and adult leukemia, and for all cancer patients combined. Twenty-seven MDB patients survived 10 years or longer after diagnosis. In only three cases was this long survival unexpected. CONCLUSIONS: The results for this series did not give any evidence that MDB improved the survival of the cancer patients. [See editorial on pages 1887-9 and commentaries on pages 1900-2 and 1903-11 this issue.]

Adolescent↗
PubMed1999

Quality control of three methods for lung tumorigenesis studies.

Many variables influence experimental results obtained from laboratory animal studies. One of the variables is tissue sampling for the detection of lesions. The contribution of different levels of sampling to the variability in reported tumour rates was evaluated in a tumorigenesis study using 1872 CBA/J mice. The number of lung neoplasms was estimated by three methods and the results compared. These methods were: 1. counting the macroscopically visible nodules, 2. microscopical examination of macroscopically-detected nodules and one histological section of each lung lobe, cut at the level of the bronchi (common method) and 3. microscopical examination as in method number 2 and additional microscopic examination of step-sections (200 microm interval) of the remaining lung tissue beginning at the level of the bronchi. Analysis using only macroscopic examination (method 1) showed that 40% (747/1872) of the animals had single or multiple nodules (i.e. tumour suspicious areas) in the lungs. When combined with microscopic examination (method 2), primary lung tumours were diagnosed in only 586 animals (31%). Evaluation by gross examination alone therefore gave an apparent overestimation of lung tumours compared to microscopic evaluation of grossly visible nodules. This was found to be due to a significant number of mice having nodules formed by processes other than primary lung tumours (i.e. non-specific inflammation, alveolar histiocytosis, focal hyperplasia of the alveolar epithelium, lymphoma infiltration or tumour metastases). On the other hand, in the more thorough sectioning of the lungs (method 3), primary lung tumours were detected in 712/1872 animals (38%). Additionally, these three different methods influenced the results with regard to the tumour multiplicity in each tumour-bearing animal.

Adenoma↗
PubMed1999

Possible carcinogenic effects of X-rays in a transgenerational study with CBA mice.

A lifetime experiment using 4279 CBA/J mice was carried out to investigate whether the pre-conceptual exposure of sperm cells to X-ray radiation or urethane would result in an increased cancer risk in the untreated progeny, and/or increased susceptibility to cancer following exposure to a promoting agent. The study consisted of four main groups, namely a control group (saline), a urethane group (1 mg/g body wt) and two X-ray radiation groups (1 Gy, 2 Gy). At 1, 3 and 9 weeks after treatment, the males of these four parental groups were mated with untreated virgin females. The offspring of each parental group was divided into two subgroups: one received s.c. urethane (0.1 mg/g body wt once) as a promoter, the other saline, at the age of 6 weeks. All animals were evaluated for the occurrence of tumours. K-ras oncogene and p53 tumour suppressor gene mutations were investigated in frozen lung tumour samples. The female offspring of male parents exposed to X-rays 1 week before their mating showed a trend towards a higher tumour incidence of the haematopoietic system than the F1 controls. In addition, a higher percentage of bronchioloalveolar adenocarcinomas in male offspring born to irradiated paternals mated 1 week after X-ray treatment points to a plausible increased sensitivity of post-meiotic germ cell stages towards transgenerational carcinogenic effects. On the other hand, no increased tumour incidence and malignancy were observed in the offspring born to irradiated paternals mated 3 and 9 weeks after X-ray treatment. Paternal urethane treatment 1, 3 and 9 weeks prior to conception did not result in significantly altered incidence or malignancy of tumours of the lung, liver and haematopoietic tissue in the offspring. K-ras mutations increased during tumour progression from bronchioloalveolar hyperplasia to adenoma. Codon 61 K-ras mutations were more frequent in lung tumours of urethane-promoted progeny from irradiated parents than from control parents. P53 mutations were absent from these lung alterations.

Adenocarcinoma↗
PubMed1998

Ki-ras gene mutations and absence of p53 gene mutations in spontaneous and urethane-induced early lung lesions in CBA/J mice.

Ki-ras and p53 genes are involved in human lung carcinogenesis; however, the role of these genes in experimental lung tumors is not well known. In our study, the CBA/J mouse strain was used to investigate the presence of Ki-ras and p53 alterations in lung carcinogenesis of spontaneous tumors and tumors induced with high and low doses of urethane (ethyl carbamate). To study the presence of these alterations in the early stages of lung carcinogenesis and in very small lung tumors, restriction fragment length polymorphism and single-strand conformation polymorphism analyses were performed on polymerase chain reaction-amplified DNA from microdissected tumoral and normal lung samples. Ki-ras gene mutations in codons 12 and 61 were detected in all types of lung lesions, even in small and preneoplastic lesions, and their incidence increased with progression from lung hyperplasias (18%) to adenomas (75%) and to carcinomas (80%). Urethane exposure, in both high and low doses, increased the incidence of Ki-ras mutations in lung tumors, especially in adenomas. The presence of Ki-ras gene mutations in very small urethane-induced lung tumors and the absence of hyperplasias among the treated-group lesions may indicate that urethane accelerates tumoral progression. No p53 mutations were detected in exons 5-8 in any of the epithelium-derived lung tumors. Only one p53 mutation in exon 5 was found in a spontaneous lymphoma. Therefore, p53 mutations do not seem to cooperate with Ki-ras gene mutations or represent an alternative molecular pathway in murine carcinogenesis.

Adenoma↗
PubMed1997

Subcutaneous soft tissue tumours at the site of implanted microchips in mice.

An experiment using 4279 CBA/J mice of two generations was carried out to investigate the influence of parental preconceptual exposure to X-ray radiation or to chemical carcinogens. Microchips were implanted subcutaneously in the dorsolateral back for unique identification of each animal. The animals were kept for lifespan under standard laboratory conditions. In 36 mice a circumscribed neoplasm occurred in the area of the implanted microchip. Females were significantly more frequently affected than male mice. An influence of age or different treatment on the s.c. tumour incidence in two mice generations could not be observed. Macroscopically, firm, pale white nodules up to 25 mm in diameter with the microchip in its center were found. Microscopically, soft tissue tumours such as fibrosarcoma and malignant fibrous histiocytoma were detected.

Animal Identification Systems↗