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Biomedical subjects

M Rosenthal

Publications and source records attributed to M Rosenthal.

At least 325 records · Page 18Linked to original sources
PubMed1976

Suppression and stimulation of immunoglobulin synthesis by agents present in rheumatoid synovial effusions.

Synovial effusions from 14 patients with rheumatoid arthritis contain factors capable of enhancing and suppressing the production of immunoglobulin when added to normal peripheral lymphocyte cultures in vitro. Utilizing a radioactive immune coprecipitation technique it could be demonstrated that enhancement was observed upon addition of relatively small amounts of synovial fluid, while addition of higher amounts resulted in suppression of immunoglobulin synthesis. Nine of ten non-rheumatoid joint effusions showed neither enhancing nor suppressing activities. The possible relationship of these events to lymphokine production in the joint is discussed.

Arthritis, Rheumatoid↗
PubMed1976

Discordance of diabetic microangiopathy in identical twins.

In a pair of 19-year-old monozygotic twin girls, one developed insulin-dependent, ketosis-prone diabetes at the age of three and has required insulin for the past 16 years. Her identical twin has maintained normal oral and intravenous glucose tolerance with normal insulin release and glucagon suppression. An unequivocal hypertrophy of the muscle capillary basement membrane (1,800 +/- 148 A) was dound in the diabetic twin, while a normal thickness of 1,149 +/- 62 A was present in her nondiabetic sister. Follow-up of the present subjects and data from other discordant identical twins who have reached adulthood could determine whether muscle capillary basement membrane hypertrophy is an independent marker of genetic diabetes in adults. Discordance of diabetic microangiopathy in a pair of monozygotic twins has important implications regarding the influence of heredity and environment on diabetic microangiopathy.

Adult↗
PubMed1976

Immunotherapy with levamisole in rheumatic diseases.

The immuno-modulatory effect of Levamisole in the treatment of rheumatic diseases was studied in an open trial. Nine patients with theumatoid arthritis (RA), 13 with ankylosing spondylitis (AS) and one with Reiter's syndrome (RS) were treated initially with 150 mg Levmisole daily for 4 weeks, then intermittently 3 days a week. Significant clinical improvement was observed in 7 out of 9 patients with RA, in 4 out of 13 patients with AS, and in the one patient with RS. An increased skin sensitivity to a panel of antigens was noted in 3 out of 9 RA patients and in 6 out of 13 AS patients. A fall in rheumatoid factor titre was observed in 2 out of 5 patients with seropositive RA. No development of other auto-antibodies was observed. No significant changes in the absolute lymphocyte counts either of the total counts or of the T, B, and null cell counts, were noted. Drug-related adverse reactions were seen in 13 patients, mostly allergic skin rash which required a short interruption in therapy. Severe leucopenia was observed in 2 patients, whereupon therapy was definitely withdrawn. Levamisole seems to have a definite beneficial effect on RA and a possible effect on AS and RS. Severe adverse reactions, mostly on the haemopoietic system, demonstrated some potential hazardous complications of the drug and required physical and laboratory examinations at short intervals.

Adult↗
PubMed1976

The effect of Levamisole on peripheral blood lymphocyte subpopulations in patients with rheumatoid arthritis and ankylosing spondylitis.

Although Levamisole, an antihelmintic drug, has shown to have some modulatory effect on the immune response in clinical trials and experimental models, its mode of action remains obscure. In a group of fifteen patients with rheumatoid arthritis and ankylosing spondylitis receiving Levamisole on an intermittant regime, simultaneous determinations of the lymphocyte subpopulations were made prior to Levamisole administration and 3 months thereafter. No significant changes were observed either in the absolute or in the relative number of T- and B-cell populations, while a statistically significant reduction was found in the "null" cells. These findings suggest that the immune potentiating effect of Levamisole may at least partially be due to a maturation process of the "null" cells.

Arthritis, Rheumatoid↗
PubMed1976

The effect of levamisole on adjuvant arthritis in the rat.

Levamisole (LEV), an immunostimulatory agent, was studied for its effect on adjuvant disease of the rat. The drug was administered continuously according to three schedules: (a) seven days prior to immunization with complete Freund's adjuvant (CFA); (b) simultaneously with CFA; or (c) 14 days after CFA. Control animals received CFA alone, LEV alone, or were sham treated with saline. Three weekly evaluations were made, recording the general condition, weight curves, joint scores, and volume of hind paws. Whole body radiographs were made at the end of six weeks. In all experimental groups, LEV accentuated the severity of the disease as compared to animals receiving CFA alone. Within the experimental groups, an increased severity was observed with earlier administration of LEV, although the day of disease onset was not altered. Spinal involvement was less severe with each consecutive administration of LEV. These findings suggest that LEV is effective not only in restoring an impaired cellular immune response, but also in enhancing an already activated system. It seems however, that for this stimulation the timetable of LEV administration is crucial, and that continuous therapy may result in a loss of efficiency.

Animals↗
PubMed1975

[Possibilities of differentiation of antinuclear antibodies].

Antinuclear antibodies can give diagnostic informations according to their titre values, the belonging to different classes of immune globulins and on the basis of different patterns of immunofluorescence connection. The determination of granulocyte-specific antibodies which frequently appear in progressive chronic polyarthritis further contributes to the differential-diagnostic classification of diseases of the connective tissue. An antibody against extractable nuclear antigen is specific for the so-called mixed connective tissue disease, an antimitochondrial antibody for the pseudo-LE-syndrome. Moreover, the own examinations resulted in a particularly high and frequent ability of complement fixation of the antinuclear factors in systematic lupus erythematosus and sclerodermy. In contrast to this in the progressive chronic polyarthritis the complement fixation was clearly more insignificant.

Antibodies, Antinuclear↗
PubMed1975

Lymphokines in rheumatoid synovitis.

In antigen-induced experimental arthritis of rabbits, a macrophage migration inhibitory factor was released from the inflamed synovial tissues. A migration inhibitory factor, blastogenic factor, and B-cell-stimulating factor were also found in human rheumatoid synovial fluids and culture supernatants of rheumatoid tissue explants. Joint fluids from patients with inflammatory conditions other than RA sometimes also displayed these activities. OA fluids were usually inactive. At present, little is known of the origin or role in vivo of the lymphokine-like activities observed in the joints of rheumatoid patients. In related experiments, injection of lymphokine-rich antigen-free lymphocyte supernatants into normal rabbit knee joints produced a synovitis characterized by lining layer hyperplasia and infiltration of the sublining layer by macrophages. The lymphocytic and plasmacytic components seen in active antigen-induced synovitis were absent. It seems likely that some of the changes observed in active chronic synovitis are mediated by soluble factors of the lymphokine variety.

Animals↗
PubMed1975

Responses of electrical potential, potassium levels, and oxidative metabolic activity of the cerebral neocortex of cats.

We measured simultaneously the oxidative metabolic activity, monitored as the tissue fluorescence attribute to intramitochondrial NADH, the extracellular potassium level with ion-selective microelectrodes, and the focal extracellular electrical potential, of one site in intact cerebral cortex of cats. When the cerebral was stimulated by trains of repeated electric pulses applied either directly to its surface or to an afferent pathway, the corrected cortical fluorescence (F-R) declined indicating oxidation of NADH, the activity of extracellular potassium [K+]o increased, and the extracellular potential (Vec) shifted in the negative direction. When mild to moderate stimuli not exceeding 10-15 sec in duration were used, a 3-fold correlation was found between these three variables. The regression of F-R over either Vec, or over log [K+]o had a positive ordinal intercept. The results are in agreement with earlier suggestions 4,24,25,43,45,46 that (a) much but not all the oxidative metabolic response of cortex to electrical stimulation is expended in restoring disturbed ion balance; and (b) that sustained shifts of potential (SP) in response to repetitive electrical stimulation are generated by glia cells depolarized by excess potassium. The magnitude of SP shifts associated with a given elevation of [k+]o are smaller in cerebral cortex than in spinal cord48,49. The correlation of F-R with [K+]o breaks down when pathologic processes of either seizure activity or spreading depression set in. During paroxysmal activity [K+]o tends to remain confined below 10-12 mM, a level observed in non-convulsing cortex as well, but oxidation of NADH progresses beyond that seen in non-convulsing cortex as well, but oxidation of NADH progresses beyond that seen in non-convulsing tissue. This observation is hard to reconcile with the suggestion that excess potassium is a factor in the generation of seizures, at least of the type observed in this study. When [K+]o levels exceeded 10-12 mM, spreading depression invariably followed at least under the unanesthetized condition in these experiments. During spreading depression [K+]o levels rose to exceed 30 mM, sometimes 80 mM. NADH was oxidized during spreading depression to a level comparable to that seen in seizures. The observations are compatible with the suggestion13 that spreading depression occurs whenever the release of potassium into extracellular fluid is overloading its clearance therefrom.

Animals↗
PubMed1975

Maturation and differentiation of B16 melanoma cells induced by theophylline treatment.

Recent studies suggested that 3',5'-cyclic AMP (CAMP) may be involved in the regulation of cell proliferation and differentiation. Theophylline, an inhibitor of cyclic nucleotide phosphodiesterase, elevated intracellular cAMP. A melanotic clone of the B16 melanoma was treated with theophylline and studied in vitro and in vivo. With 12 hours after 1.0 mM theophylline was added to growing cultures, the number of cells incorporating tritiated thymidine (3-H-TDR) and the rate of uptake of 3-H-TDR into DNA were significantly reduced. After 7 days, the number of cells in the control cultures increased twenty-four times, whereas theophylline-treated cells increased only sixfold. Compared to the controls, the theophylline-treated cells contained ten times the melanin and an elevated cAMP content. Stimulation of melanogenesis and inhibition of proliferation increased progressively with duration of exposure to theophylline. After 5 days of culture with theophylline, cells were assayed for plating efficiency in theophylline-free medium. Although the number of colony-forming cells was unaffected by previous exposure to theophylline, the colonies were composed of fewer cells inoculated into syngeneic hosts were less tumorigenic than untreated cells. However, theophylline treatment of hosts bearing B16 tumors failed to reduce the tumor growth rate, and theophylline did not potentiate the growth inhibition resulting from treatment with the synthetic polyribonucleotide, polyinosinic-polycytidylic acid.

Animals↗
PubMed1975

Lymphocyte subpopulations in normals and patients with rheumatoid arthritis and ankylosing spondylitis.

Seventy-four normal persons, 48 patients with rheumatoid arthritis, and 25 patients with ankylosing spondylitis, were examined in respect to lymphocyte subpopulations in the peripheral blood. The simultaneous enumeration of T lymphocytes (E rosettes), B lymphocytes (surface immunoglobulin), as well as null cells and double marker cells was performed. No significant differences could be observed in the three examined groups in respect to the absolute or the relative lymphocyte counts, suggesting that possible immunological impairment assumed in rheumatoid arthritis and ankylosing spondylitis, is due not to reduced cell numbers, but to a possible functional disorder.

Arthritis, Rheumatoid↗