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H Folch

Publications and source records attributed to H Folch.

At least 37 records · Page 2Linked to original sources

Neuroendocrine regulation of thymus hormones: hypothalamic dependence of "facteur thymique serique" level.

The influence of the hypothalamus extract (HE) on the blood level of the "facteur thymique serique" (FTS) was studied. Hypothalami collected from young mice were pooled, homogenated in saline, and centrifuged; finally, the supernatant injected in old or thymectomized mice with no detectable levels of FTS. In the old mice the treatment results in a reappearance of this circulating thymic hormone; in contrast, in adult thymectomized animals, the HE injection was not able to induce FTS activity. When HE donors were pretreated with thymosin fraction 3, known to contain FTS among other active peptides, the capacity of such a hypothalamus preparation to induce reappearance of FTS in old animals is greatly diminished. The data presented here suggest that the capacity of the thymus to secrete FTS depends on a hypothalamic factor, and therefore the absence of this thymic hormone in the aged reflects a failure of the thymus linked to its impaired neurologic control. On the other hand it seems evident that a feedback system operates in order to regulate the release of this hypothalamus stimulatory factor.

Animals↗

Cytoplasmic requirements for the radio-induced modulation of IgG receptors on B-cells.

The effect of X-ray irradiation on IgG membrane receptors of B murine lymphocytes was studied. Cells were obtained from peripheral lymph nodes of RK mice and teased in Hank's solution. The cells were irradiated or kept as control samples, incubated at 37 degrees C, with or without drugs with known biochemical action at metabolic or structural levels, and labelled with fluorescein-conjugated anti-IgG antisera. The results show that X-ray irradiation results in a modulation of IgG receptor molecules on B-cells. The disappearance phase which takes only 10 min, is temperature dependent, and is prevented with metabolic inhibitors, microtubular disruptors, db-cAMP and local anesthetics. The re-appearance phase is also temperature dependent but apparently does not have either energy or cytoskeleton participation. The phenomenon is interpreted as partial and transient internalization of IgG molecules in the membrane.

2,4-Dinitrophenol↗

Autoimmune thyroiditis in young and old mice: differential effect of high doses of PHA.

Experimental autoimmune thyroiditis (EAT) was used to study the effect of age and PHA in the autoimmune response. EAT was induced in mice by two injections 7 days apart of soluble syngeneic mouse thyroglobulin (MTg) and lipopolysaccharide (LPS) as adjuvant. Thereafter the antibody titre to MTg was determined in the serum and the degree of cellular infiltration estimated in thyroid sections. The results show that in old mice the humoral response is low and no cellular infiltration is found in the thyroid; young mice showed both types of immune response. Phytohaemagglutinin (PHA) was shown to inhibit antibody production when given before the first and second antigen injection, and to suppress completely the cellular immunity against thyroid tissue. When given to old mice a reduction in anti-MTg titre is also seen, but no effect on infiltration is found. However when PHA is only given before the second dose of antigen a stimulation of cellular immunity is seen in contrast to young mice where there is no effect.

Aging↗

Modification of radiation response by agents that elevate the intracellular c-AMP level.

A study has been made of the effects of drugs known to elevate c-AMP level on radiation-induced damage in thymocytes. The test used was the ability of the cells to exclude dye, beta-receptor stimulation and phosphodiesterase inhibition were found to induce radioresistance. The possible importance of the plasma membrane in connection with cytoplasmic factors is briefly discussed.

Aminophylline↗

The immune response in cirrhotic rats. Antigen distribution, humoral immunity, cell-mediated immunity and splenic suppressor cell activity.

The immunological disturbances occurring as a result of liver disease have been studied in an animal model of cirrhosis. The mononuclear phagocytic cells of the normal liver phagocytose large amounts of antigen irrespective of whether that antigen is injected directly into the portal or into the systemic circulations. The liver therefore acts as a filter 'in series' and 'in parallel' with the spleen and reduces the immunogenicity of antigens entering the organism by either of these routes. In rats with hepatic cirrhosis, there is a reduction in the capacity of the liver to phagocytose the flagellar antigen of Salmonella adelaide. This results in increased stimulation of splenic lymphoid tissue and in an increased antibody response to this thymus-independent antigen. The increased antigenic stimulus to the spleen may also be responsible for the increased suppressor-cell activity which has been demonstrated in these rats, and may be the mechanism of the diminished cell-mediated immune response both in this animal model of cirrhosis and in the human disease state. These studies suggest that many of the immunological disturbances associated with chronic liver disease may be the result of maldistribution of antigen occurring because of impaired hepatic phagocytic capacity.

Animals↗