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Biomedical subjects

L Hammarström

Publications and source records attributed to L Hammarström.

At least 379 records · Page 21Linked to original sources
PubMed1978

In vitro interaction between 99Tcm-labeled pyrophosphate, 32P-labeled pyrophosphate and rat tissues.

Whole-body sections from young rats were incubated with solutions containing 32P-labeled pyrophosphate, 99Tcm-labeled pyrophosphate and 99Tcm-pertechnetate, respectively, at pH 7.6 or pH 8.6. After incubation, the sections were used for autoradiography and/or staining in order to visualize tissue affinity for 99 Tcm and areas of pyrophosphatase activity. At pH 7.6, the distribution patterns of 99Tcm-labeled pyrophosphate and 32P-labeled pyrophosphate were similar. When pH was raised to 8.6, 99Tcm-labeled pyrophosphate was degraded before reaching the tissues and their enzymes. The distribution pattern of 99Tcm-labeled pyrophosphate at pH 8.6 was similar to that of 99Tcm-pertechnetate. 32P-labeled pyrophosphate could serve as a substrate for alkaline pyrophosphatase and the enzyme activity was demonstrated autoradiographically.

Animals↗
PubMed1978

B-cell activating properties of polymyxin B.

Polymyxins are known to be inhibitors of certain polyclonal B cell activators such as lipopolysaccharide and dextransulphate. However, increased specific responses to hapten-coupled mitogens have been reported after the addition of polymyxins to superoptimal conjugate doses. In this paper we have studied the effect of polymyxin B on superoptimal polyclonal doses of lipopolysaccharide. Results similar to those reported for hapten-lipopolysaccharide conjugates were obtained. Polymyxin B was also found to exert adjuvant properties for a primary immune response to sheep erythrocytes and to be a thymus-independent antigen.

Animals↗
PubMed1978

Role of suppressor T cells in autoimmune responses induced by polyclonal B cell activators.

In order to investigate a possible role of suppressor T cells in the maintenance of self tolerance, we compared the autoimmune response induced by LPS in cultures of untreated spleen cells with the one of anti-theta treated spleen lymphocytes. It was constantly found that T cell depletion never resulted in an increase in the number of plaques directed against autologous albumin coupled SRBC. The same finding was also apparent when the autoimmune response given by spleen cells of old, normal or thymectomized and young untreated animals was compared. In order to exclude the possibility that lack of increase of the autoimmune response in animals with T cells deficiency was due to long-lived suppressor functions, cells or factors, we compared the response to autologous albumin, as induced by LPS, in spleen cells of nude mice with the one given by their normal littermates. Since even in this instance no significant increase could be detected, we conclude that suppressor cells do not play an active role in the maintenance of self tolerance.

Animals↗
PubMed1978

Functional characterization of lanatoside-C-responsive cells.

Lanatoside C, a digitalis glycoside previously shown to be a polyclonal B-cell activator (PBA), was found to stimulate immature cells residing in fetal liver, bone marrow and spleen but also to activate cells from peripheral lymph nodes and peripheral blood. The proliferative response obtained in spleen cells was not affected by macrophage removal, whereas anti-Ig or anti-Ia antiserum pretreatment partially inhibited the responses. Removal of T cells by a pretreatment with anti-Thy 1.2 antiserum plus complement caused a marked increase in the proliferative response of the remaining cells, suggesting the existence of a naturally occurring suppressor T cell for glycoside-induced mitogenesis. Synergy experiments with 'classical' PBAs and lanatoside C, given simultaneously or subsequently, suggest an overlap between the lanatoside-C-responding cell population and the dextran sulphate (DxS)- and lipopolysaccharide (LPS)-sensitive cells. Since DxS-induced activation of B cells is dependent on macrophages, it is suggested that lanatoside C may be used as a functional marker for direct activation of immature B cells.

Animals↗
PubMed1978

HLA-A, -B, -C and -D antigens in male patients with myasthenia gravis.

HLA-A, -B, -C and -D antigens were determined in 54 male Myasthenia Gravis patients. A significant increase of the B8 antigen frequency was found among patients with an onset of the disease before the age of 35. No significant increase was found among the D antigens. In a combined male and female material with an early age at onset, thymic hyperplasia was correlated to the presence of HLA-B8.

Adult↗
PubMed1978

No significant correlation of HLA-B8 and amount of antibodies directed to acetylcholine receptor protein in patients with myasthenia gravis.

Forty patients with myasthenia gravis were HLA tissue typed and the amount of anti-acetylcholine receptor protein antibody determined. Sera from seven patients were tested for antibody titer by repeated determinations and the serum concentration was found to be stable. Patients with thymoma had higher titers than patients with normal thymus histology or hyperplasia. Individuals with thymoma lacking HLA-B8 were found to have a higher concentration of antibodies than HLA-B8 negative individuals with hyperplasia. No statistically significant differences were obtained when comparing the amount of antibody in HLA-B8 positive and negative individuals. Titers in patients subjected to thymectomy more than 8 years before sampling did not deviate from those in non-thymectomized myasthenics.

Acetylcholine↗
PubMed1978

Morphologic changes in the rat enamel organ following a single intraperitoneal injection of sodium fluoride.

Enamel organs in developing teeth of young rats were studied after single intraperitoneal injections of a high dose of sodium fluoride (60 mg NaF/kg body wt.). The study employed primarily light microscopy, but electron microscopy was used to clarify some of the light microscopic findings. The pathogenesis of the fluoride-induced changes was followed during 72 h. Cellular changes were consistently found in the molars, but were never seen in the incisors. In the maxillary molars, ameloblastic injury was most commonly seen on the mesial surfaces of the cusps. One hour after injection, the most prominent findings were swollen mitochondria in the secretory ameloblasts and cleft formations between the ameloblasts and the enamel matrix. The clefts were filled with a stippled material. Some of the clefts gradually expanded to cystic cavities. The stippled material began to calcify after 24 h and formed small, darkly stained globules. After 72 h dearranged ameloblasts were found as islands intermingled with calcified rounded structures in the stellate reticulum. In stratum intermedium numerous atypic autophagic vacuoles appeared 2 h after injection. No light microscopic changes were observed in the postsecretory ameloblasts.

Ameloblasts↗
PubMed1978

Role of virus for the induction of myasthenia gravis.

Virus has been suggested as an etiological agent in myasthenia gravis. In this investigation 36 patients with the clinical diagnosis of myasthenia gravis were tested for antibodies against ornithosis, mycoplasma pneumoniae and 16 viral antigens. Rabbits with experimentally induced autoimmune myasthenia gravis were similarly tested. There was no overall correlation to any microorganism, which might have suggested the involvement of a viral infection in the pathogenesis of the disease. Neither was there any difference in incidence of antibodies in female patients carrying the HLA B8 antigen, an antigen which is associated with myasthenia gravis, as compared to HLA B8 negative individuals.

Adolescent↗
PubMed1978

In vivo and in vitro study of 59Fe uptake in developing rat molars.

Autoradiographic methods were used to study 59Fe uptake in vivo in mineralizing tissues of young rats. Localization of 59Fe was observed in the ameloblastic layers of molars. In vitro studies were performed which demonstrated that 59Fe uptake in developing rat molar enamel was limited by the metabolic activity of the cells of the enamel organ.

Animals↗
PubMed1978

Sodium polyanethole sulfonate: a new macrophage-dependent polymyxin-inhibitable, polyclonal B cell activator.

The anionic detergent sodium polyanethole sulfonate was found to activate mouse B lymphocytes to increased cell division and formation of plaque-forming cells, possibly by an indirect mechanism. An increased cell division was also obtained in guinea pig and in rabbit lymphooid cell cultures. A strong similarity was found when comparing the dextran sulfate- and the sodium polyanethole sulfonate-sensitive cell population. Thus, the responding mouse cells resided in spleen and lymph node and also in fetal liver and bone marrow. The sensitive lymphocytes were dependent on the presence of macrophages or macrophage-replacing factors, since depletion of phagocytic cells resulted in loss of response. Addition of polymyxin B inhibited the stimulation, possibly through a direct interaction with the polyanion. In potency sodium polyanethole sulfonate was found to surpass dextran sulfate, making this benzene sulfonate a useful tool when studying lymphocyte responses.

Animals↗
PubMed1978

Genetic control of lymphocyte suppression. I. Lack of suppression in aged NZB mice is due to a B cell defect.

Con A-activated cells from old NZB mice were found capable of inhibiting the polyclonal response of cells from young NZB and BALB/c animals. Furthermore, Con A-preactivated spleen cells from young NZB and BALB/c mice did not significantly affect the response of spleen cells from old NZB mice. These results suggest that the defective suppressive activity in old NZB mice may be traced to a defect at the B cell level.

Aging↗
PubMed1977

Genetic control of lymphocyte activation: lack of response to low doses of concanavalin A in lipopolysaccharide-nonresponder mice.

C3H/HeJ mice do not respond to the polyclonal B-cell activator lipopolysaccharide (LPS) from Escherichia coli; this was first described by Sultzer who observed that mice of this strain did not respond to an intraperitoneal (i.p.) injection of LPS as measured by the accumulation of leukocytes in the peritoneal cavity. Neither were C3H/HeJ mice as susceptible to LPS toxcitiy (1). It was later reported that LPS-induced mitogenesis (2,3), adjuvanticity (4), and the appearance of Ia antigens on B lymphocytes as induced by LPS, (5) was also absent in C3H/HeJ mice. However, lymphocytes from these mice respond normally to the polyclonal B-cell activators purified protein derivative of tuberculin (2,6) and dextran sulfate and have also been reported to respond normally to concanavalin A (Con A) (2). Furthermore, the immune responses to sheep erythrocytes (7) and soluble thymus-dependent antigens (4) are normal in C3H/HeJ mice. Unresponsiveness to LPS in C3H/HeJ mice has been found to Be due to a defect in a single gene or a set of linked genes (3,8) which has been mapped between the major urinary protein locus and the locus coding for polysyndactyly on chromosome 4. (1) We have reported that injection of LPS into mice of an LPS-responsive strain causes a shift in the Con A dose-response curve of cultured spleen cells, suppressing the low does response (9). Therefore, we tested the Con A proliferative response in cultures of normal or LPS-activated spleen cells from LPS-responder (C3H/Tif) and LPS-nonresponder (C3H/HeJ) mice. We report here that C3H/HeJ spleen cells respond poorly to low concentrations of Con A (0.05-0.1 mug/ml). Injection of LPS 2 days before culture inhibits the response to low doses of Con A in cultures of C3H/Tif spleen cells but has no inhibitory effect on the dose response profile of C3H/HeJ spleen cells. Furthermore, the low dose Con A response of spleen cells is dependent upon the presence of an Ia-positive cell. (2) The role of Ia-positive cells in the Con A response of C3H/Tif and C3H/HeJ spleen cells is described.

Animals↗
PubMed1977

Characterization of self-reactive B cells by polyclonal B-cell activators.

The existence of autoreactive B cells was predicted by theoretical considerations and, recently, confirmed by direct experiments. The aim of the present work was to investigate if the capacity of self-reactive B cells to be activated with different polyclonal B-cell activators (PBA) reflects the heterogeneity of the response as seen in all the Ig-positive cells. We injected mice with dextran sulfate, lipopolysaccharide from Escherichia coli 055:B5, and purified protein derivate of turbercle bacteria RT32 and studied the complement-dependent cytotoxicity against syngeneic spleen cells caused by the sera from injected mice with regard to the different parameters used for characterization of B-cell subpopulations. It was found that the capacity of self-reactive B cells to secrete antibodies reflects the polyclonal-activating capacity of the PBA used. The implications of these findings for the understanding of the triggering mechanism of B lymphocytes and for self-nonself discrimination are discussed.

Animals↗