Atomic pseudospin resonance.

A new type of resonance is discovered in Rydberg atoms placed in a constant magnetic field -->B and a transient electric field that rotates at the constant frequency -->omega in a plane perpendicular to -->B. The dynamics is explained in terms of two pseudoparticles with spin 1 / 2 in two generalized magnetic fields. The resonance frequency is predicted and found at -->omega = (e/2m)-->B, where -e/m is the electron's charge-to-(reduced)mass ratio. We discuss the applicability of the resonance to accurate magnetic field measurements and the prospects for determining e/m with improved precision.

Diseases associated with asbestos exposure. Diagnostic perspectives in forensic pathology.

Asbestos, a fibrous mineral, has unique physical and chemical properties, including resistance to heat, acids, and other chemicals; flexibility; and great tensile strength. The fibers subdivide into unit fibrils of molecular dimensions, resulting in a vast mineral surface area which has a direct bearing on its unusual features and its numerous applications. Its biological effects, which include fibrogenesis and carcinogenesis, may be related to the cellular reaction, to its large specific surface, or to the size and shape of the fibers. Its oncogenic action may be multiplied by other carcinogens, principally cigarette smoking. There is clinical, pathologic, and epidemiologic evidence that exposure to asbestos, following a long latent period, constitutes an important health hazard. Direct occupational exposure, followed by a long lapsed period after the initial exposure, is associated with pleural plaques and pleural effusion, pulmonary parenchymal fibrosis (asbestosis), pulmonary carcinoma, pleural and peritoneal mesothelioma, and other neoplasms. Indirect exposure may also entail an increased risk of lung disease or mesothelioma or both. Medicolegal investigation of suspected cases includes a lifetime occupational history, clinical history including smoking habits, radiological findings, clinical evidence of asbestosis, and may require detection of asbestos tissue burden.

Asbestos-related diseases. Algorithm for forensic pathological diagnosis.

The pathological diagnosis and proof of asbestos causation in environmental-occupational diseases is based on a spectrum of increasingly sophisticated determinations with greater confidence in detection of asbestos bodies and fibers. These include the following: pathology (histology) and/or thick smears of lung, microincineration, bulk chemical digestion, and electron beam instruments. The requisites of medical and forensic asbestos causation differ, and do not always require the full range of these analytical techniques. The need and significance of some of these determinations, as expressed in number of asbestos bodies and fibers, may be related in many cases to the evidence of asbestosis; to the gross and microscopic pathological findings (asbestosis, lung carcinoma, mesothelioma); the exposure history (type, duration, intensity, and period of latency); and nature of the asbestos mineral. An algorithm for the forensic pathological diagnosis of asbestosis and of asbestos-related diseases is proposed.

Asbestos fibers in human lung: forensic significance.

Asbestos is a fibrous mineral which, because of its unique properties, has innumerable applications in many industries and is used in a large variety of consumer products. It has become ubiquitous and is woven, literally and figuratively, into the fabric of our present-day civilization. However, its presence is sometimes unknown and unsuspected by those who are exposed to asbestos by virtue of occupation or environment and inhale its fibers. Exposed workers and even urban dwellers may have a variable lung burden of asbestos fibers. There is indisputable clinical, pathological, experimental and epidemiological proof that, after varying periods of latency, asbestos may cause benign and malignant disease often leading to disability or death. Forensic investigation of suspected asbestos-related deaths includes a life-time occupational history, a complete autopsy, and identification of the asbestos fiber tissue burden. The latter usually requires special procedures.

In vitro gamma irradiation of leukemic cells in mice, rats, and guinea pigs.

In vitro gamma irradiation of virus-induced (Gross) mouse leukemia cells at doses of 350-1600 rads (1 rad = 0.01 gray) had no effect on their ability to induce leukemia, usually within 2 weeks, after transplantation into syngeneic mice. However, when cells irradiated at doses of 2000-20,000 rads were transplanted, they induced leukemia after a latency period exceeding 2.5 months, similar to the results observed in mice inoculated with filtered mouse leukemia extracts. Similar results were also obtained after irradiation of leukemic cells derived from rats in which leukemia had been induced by rat-adapted mouse leukemia virus. Apparently, gamma irradiation at a dose of, or exceeding, 2000 rads, inhibits the ability of mouse and rat leukemic cells to induce leukemia after transplantation into syngeneic hosts; however, it does not inactivate the virus carried by such cells nor prevent it from inducing leukemia. [In previous experiments, doses of more than 4,500,000 rads were needed to inactivate the passage A (Gross) leukemia virus carried in either mouse or rat leukemic cells.] In vitro gamma irradiation of L2C guinea pig leukemic cells at doses of 750-2500 rads had no apparent effect on their ability to induce leukemia after transplantation effect on their ability to induce leukemia after transplantation into strain 2 guinea pigs. However, irradiation at doses of 3250-20,000 rads inactivated their ability to do so. The morphology of mouse, rat, and guinea pig leukemic cells and the virus particles present in such cells was not affected by irradiation at doses of 20,000 rads.

Renal disease from exposure to solvents.

Exposure to a variety of solvents may result in renal disease. Tubular renal disease with anuria occurring fairly promptly after exposure is most commonly seen. There is evidence that some cases of glomerular disease, such as extra-capillary glomerulonephritis and membranous nephropathy, may be causally related to chronic solvent exposure. Their detection may be impeded by the prolonged latent period between exposure and onset of disease, the non-specificity of the glomerular lesions and the non-availability of a history of exposure.

Treatment of idiopathic membranous nephropathy.

In a retrospective study of the effect of treatment in biopsy-proved idiopathic membranous nephropathy, 91 adults and 12 children were followed for periods up to 29 years after clinical onset (mean, 6.5 years). Forty-four were treated with corticosteroids, 15 with corticosteroids and immunosuppressants; 44 had no treatment and served as a control group. Clinical cure and improvement were significantly greater in the treated than in the nontreated group (P less than 0.01). The recurrence rate, occurrence of renal failure and probability of death were significantly greater in the nontreated group, although some of these patients eventually showed improvement. Prognosis was better in patients who responded to therapy. These data strongly suggest that steroid therapy is beneficial in patients with membranous nephropathy.

Electrocardiographic and pathological studies of the heart in experimental guinea pig leukemia.

Electrocardiographic tracings were performed on 26 strain 2 guinea pigs in which leukemia was induced by inoculation of L2C leukemic cells. All inoculated animals developed leukemia. In terminal phases of this disease significant electrocardiographic changes were observed in 20 of the 26 animals; in 5 animals the electrocardiograms were normal and in 1 guinea pig the changes were borderline. The most significant changes consisted of the onset of a Q-wave or a T-wave inversion or both. Pathological examination of the heart removed in the terminal phase of the disease revealed infiltration of the endocardium and epicardium and in the capillaries of the myocardium. Such areas of infiltration, when viewed with the electron microscope, revealed the presence of leukemic cells within the lumen of capillaries and in areas immediately surrounding the capillaries. Infiltration of myocardial fibers was not observed. The electrocardiographic changes observed in guinea pig leukemia may be related to the leukemic infiltration of myocardial capillaries and the resulting anoxia.

C-type virus particles in urethan-induced pulmonary and renal carcinomas, in cell-graft-transmitted carcinosarcomas, and in filtrate-induced lymphomas in mice.

Repeated injections of urethan into suckling BALB/c mice induced multiple papillary adenocarcinomas in the lungs and kidneys. When the pulmonary tumors were transplanted i.p. by cell graft into 6 suckling BALB/c mice, they induced disseminated carcinosarcomas within the peritoneal cavity in all inoculated animals. Tumors resulting from the transplantation of tumor cells were used for preparation of filtered extracts. The filtrates were inoculated into 6 suckling BALB/c mice and induced generalized malignant lymphomas in all animals. The primary urethan-induced pulmonary and renal tumors, the carcinosarcomas that resulted from i.p. cell transfer, and also the generalized malignant lymphomas induced by inoculation of filtered extracts contained C-type virus particles. Theoretically, it could be assumed that both the primary urethan-induced pulmonary and renal tumors, as well as the cell-graft-induced peritoneal carcinosarcomas, contained the C-type virus particles as passengers, not necessarily related etiologically to the tumors in which they were found. It is quite likely, however, that these virus particles were etiologically related to the filtrate-induced malignant lymphomas in which they were also found.