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Biomedical subjects

H Friedman

Publications and source records attributed to H Friedman.

At least 469 records · Page 26Linked to original sources
PubMed1976

[Colloid bodies. A cause of vascular complications (author's transl)].

Optic disc colloid bodies are more common than previously supposed. They were noted to occur in 2.04% of unselected globes obtained at autopsy. Hemorrhages of the disc and juxtapapillary fundus are not infrequently found in association with disc colloid bodies. Superficial hemorrhages may be due to erosion of existing disc blood vessels by enlarging colloid bodies, on the other hand, juxtapapillary hemorrhages may occur from neovascularization induced by the colloid bodies. Ultrasound examination may be useful as an aid in diagnosing disc colloid bodies.

Colloids↗
PubMed1975

Leukemia virus-induced immunosuppression: scanning electron microscopy of infected spleen cells.

Spleen cells from mice infected with Friend leukemia virus were examined by scanning electron microscopy. Whereas splenocytes from normal noninfected animals showed the expected morphologic classes of lymphocytes, including those with smooth surfaces and with numerous villous projections, an alteration of cell type was evident within a few days after infection. Friend leukemia virus caused a rapid decrease in the number of villous cells, with a concomitant increase in the number of cells with smoother surfaces. By the end of the first 1 to 12 weeks after infection the majority of cells were smooth, many showing distinct morphologic changes, including "holes" and a spongy appearance. Nearly all of the splenocytes were abnormal in appearance by days 17 to 30 after infection, with most showing a spongy topography. These changes paralleled the marked immunosuppression induced by Friend leukemia virus infection, as well as the appearance of virus-associated surface antigen on individual splenocytes. Topographic changes evident by examination with scanning electron microscopy were not readily apparent by either standard histology or transmission electron microscopy.

Animals↗
PubMed1975

Human brain in tissue culture. I. Acquisition, initial processing, and establishment of brain cell cultures.

This paper details the in vitro techniques used to establish cells in culture from the brains of 40 patients, most of whom had chronic neurologic disease. The clinical and pathologic features of these patients are given. The success in establihsing cell lines was dependent upon the origin of tissue (biopsy vs. autopsy), the site of removal from the brain, and various environmental and technical manipulations in vitro.

Adolescent↗
PubMed1975

Human brain in tissue culture. II. Studies of long-term cultures.

This paper describes the techniques used to maintain and reconstitute from storage adult human brain cells in culture. Growth characteristics, cell morphology, lifespan, and karyotypic analysis of cell lines derived from patients with multiple sclerosis (MS), non-MS neurologic diseases, and normal brains are compared.

Aging↗
PubMed1975

Viral hepatitis, type A. Identification by specific complement fixation and immune adherence tests.

Hepatitis A antibody was detected by specific immune adherence and complement-fixation tests in a study involving 473 serum specimens from 20 patients who had viral hepatitis, Type A. In all 20 patients who had no detectable immune adherence antibody (less than 1:5) before onset of hepatitis high levels (greater than or equal to 1:1024) developed one to four weeks later, occasionally reaching peak levels exceeding greater than or equal to 1:81,920 several months thereafter. Five to 10 years later the immune adherence antibody levels ranged between 1:640 and 1:20,480. In general, the complement-fixation test was not as sensitive or as specific as the immune adherence test. These findings indicate that the immune adherence test should be a valuable tool for diagnosis, for epidemiologic surveys, for identification of susceptible and immune persons, for quantitative assays of gamma globulin and for identification of hepatitis A virus in attempts to propagate the virus in cell culture.

Animals↗
PubMed1975

Involvement of T- and B-lymphocytes in the immune response to the protein exotoxin and the lipopolysaccharide antigens of Vibrio cholerae.

The immune response at the level of individual immunocytes to the somatic lipopolysaccharide antigen derived from whole Vibrio cholerae and to the purified protein exotoxin from this organism were studied in terms of the role of T- and B-lymphocytes. By adoptive cell transfer studies with irradiated recipient mice, it was shown that normal spleen cells from normal syngeneic mice could readily transfer the capability of responding to both types of cholera antigens. However, when the spleen cells were depleted of T-cells with anti-theta serum and complement, antibody responsiveness to the LPS antigen, but not to exotoxin, could be achieved in recipients. Furthermore, by appropriate transfer of either bone marrow, thymus, or thymus-marrow cell mixtures to irradiated mice, it was shown that the response to the cholera somatic antigen was relatively independent of thymus cells, whereas the response to exotoxin required "helper" T-cells. The role of thymus and bone marrow cells in the intestinal tract in immune responses to the somatic and toxic antigens of cholera vibrios requires further investigation. Further studies should also provide additional information not only concerning the mechanism of the immune response to these antigens in terms of basic mechanisms of antibody formation, but also should provide valuable information in terms of anticholera immunity per se.

Animals↗
PubMed1975

Stimulation of cAMP levels and modulation of antibody formation in mice immunized with cholera toxin.

Injection of mice with 1.0 mu g of a purified exotoxin derived from Vitro cholerae together with a challenge injection of sheep erythrocytes (SRBC)P OR E. coli LPS markedly influenced the immune response to these antigens. Simultaneous injection of the toxin with antigen resulted in a delayed appearance of antibody-forming cells during the first few days after immunization, followed by a marked enhancement of the peak numbers of antibody-forming cells. In the case of the immune response to SRBC, both 19S and 7S plaque-forming cells (PFC) were enhanced on the peak day of response after simulataneous immunization of toxin-injected mice. The secondary immune response to SRBC was also similarly affected when cholera toxin was given along with a second injection of erythrocytes: i.e. a delay in appearance of the first antibody-forming cells followed by a marked enhancement of the peak 19S and 7S PFC response. Injection of cholera toxin 103 days prior to SRBC or LPS was immunosuppressive. The effect of cholera toxin on the level of splenic cyclic AMP appeared related to the effects on antibody formation.

Animals↗
PubMed1975

The disjunction property implies the numerical existence property.

Any recursively enumerable extension of intuitionistic arithmetic which obeys the disjunction property obeys the numerical existence property. Any recursively enumerable extension of intuitionistic arithmetic proves its own disjunction property if and only if it proves its own inconsistency.

Journal Article↗
PubMed1975

Lymphocyte surface receptors and leukemia virus-induced immunosuppression.

The number and distribution patterns of lymphocytes in the spleens and lymph nodes of Balb/c mice which express immunoglobulin surface receptors were studied in terms of the effects of a murine leukemia virus on the immune-response mechanism. Friend leukemia virus induces a prompt, marked depression of the immune response of mice to antigens such as sheep erythrocytes and E. coli LPS. A functioning T- and B-lymphocyte system is necessary for the response to the SRBC's whereas E. coli LPS, a T cell-independent antigen, stimulates B cells alone. Although the responses to both classes of antigen were markedly depressed in FLV-infected mice, the major defect appeared to be impairment of B-cell function, at least early in the course of infection. In order to examine in more detail the mechanism of interaction between FLV and lymphoid cells with Ig surface receptors, presumably B cells, immmunofluorescent analyses were performed with spleen, and lymph node cells from FLV-infected mice. Within a few days after infection there was a marked decrease in the percentage of spleen cells with Ig surface molecules, although the absolute number of these cells was either unchanged or increased due to marked splenomegaly caused by the virus. A marked decrease in the percentage of splenocytes with theta antigen, considered a marker for mature T cells, also was evident in infected mice. The number of spleen cells showing evidence of FLV infection (i.e., positive for FLV-associated antigens) increased rapidly during the first few days after infection, and within 2 to 2 1/2 weeks nearly all of the nucleated splenocytes were positive for the tumor antigen. In contrast to the results for spleen cells, there were increases rather than decreases in the percentages of Ig-positive and theta-positive cells in the lymph nodes after infection. The number of lymph-node cells that showed the presence of FLV antigen was much lower than in the spleen, and their appearance was also much slower as the leukemic process progressed. Despite these differences between spleen and lymph-node cells in terms of relative percentages of Ig- and theta-positive lymphocytes, relatively similar depressions were evident for the percentages of lymphoid cells that could redistribute their surface Ig receptors into polar caps when incubated with anti-Ig serum at 37 C. Marked impairment of the Ig-capping responses for both spleen and lymph-node cells paralleled the course of infection and development of immunosuppression. These observations indicate that murine leukemia virus infection can both alter the responsiveness of immunocompetent cells to T-dependent and independent antigens and depress the number and normal functional activity of these cells, as reflected by altered surface Ig receptors and antigens.

Animals↗
PubMed1975

Use of erythrocytes sensitized with purified enterotoxin from Vibrio cholerae for the assay of antibody and antibody-forming cells.

A method was developed for the sensitization of ovine erythrocytes with a purified enterotoxin from Vibrio cholerae. Sensitized cells were used for the titration of serum antibody by passive hemagglutination and in a hemolytic plaque assay for both IgM and IgG antibody-secreting cells. Inhibition experiments with various antigens of V. cholerae indicated that the toxin, whether unheated or heat-inactivated, significantly reduced the expected antitoxic plaque-forming cell response, whereas a lipopolysaccharide-rich extract from homologous vibiros was not inhibitory.

Animals↗
PubMed1975

Reversal of leukemia virus-induced immunosuppression in vitro by peritoneal macrophages.

When spleen cells from mice infected with Rowson-Parr virus (RPV) were cultivated with sheep red blood cells (SRBC), antibody plaque responses were markedly lower than those in similarly cultivated spleen cells from normal mice. Addition of as few as 10(3) spleen cells from RPV-infected mice to cultures of normal aplenocytes markedly depressed the expected immune response. Although RPV-infected mice showed maximum immunodpression in vivo only during the first week after infection, their spleen cells, obtained later in the course of infection, depressed the immunologic responsiveness of normal splenocytes in vitro. Increased doses of SRBC or addition of bacterial lipopolysaccharide to cultures of spleen cells from immunodepressed, RPV-infected mice stimulated antibody formation, and near-normal numbers of antibody-producing cells were evident. Peritoneal exudate (PE) cells, but not thymus, bone marrow, or unfractioned spleen cells, restored immunocompetence to cultures of spleen cells from RPV-infected mice but did not affect the suppressive properties of the infected cells on normal splenocytes. The function of PE cell macrophages in restoring immunocompetence to infected spleen cells in cultures seemed related to a possible antigen-focusing activity of the cells; antibody-producing cell precursors in infected cultures seemed to be preferentially affected by the presence of normal PE cells.

Animals↗
PubMed1975

Elevated cyclic AMP levels in mouse lymphoid tissue after stimulation by cholera enterotoxin in vitro (38468)

Addition of CT to suspensions of thymus, lymph node, spleen, or bone marrow cells in vitro resulted in a marked accumulation of cAMP with peak levels occurring 4-5 hr after incubation of cells with CT. Thymus cells showed the largest increase in cAMP, approximately 40-fold at 10 ng/ml CT. Bone marrow cells accumulated the least cAMP (1.5x), while intermediate levels were observed for spleen and lymph node cells (10-12x). Antiserum to CT prevented stimulation of increased cAMP levels. Repopulation studies using X-irradiated mice also showed that thymus-derived spleen cells accumulated more cAMP/10-7 cells than spleen cells from recipients given spleen or marrow cells. Spleen cells from athymic (nu/nu) mice also responded much less than did spleen cells from normal mice. Thymocytes appeared to bind CT to a greater degree than bone marrow cells. Spleen and lymph node cell suspensions also contained CT-binding cells and the number of CT-binding cells in these peripheral lymphoid tissues appeared approximately equal to the summation of the numbers observed in thymocyte and bone marrow cell suspensions. Stimulation of cAMP in lymphoid cells, especially thymocytes, by CT provides a pharmacological tool to investigate the mechanism and role of this nucleotide in the early events of antibody formation.

Animals↗
PubMed1975

Immunosuppression in vitro induced by leukemia virus-infected splenocytes (38544).

Immunization of dispersed spleen cells from normal mice in vitro with SRBC was suppressed by simultaneous incubation of the spleen cell cultures with splenocytes from mice previously infected with FLV. Cell-free virus preparations alone did not suppress the antibody response. In contrast, relatively small numbers of splenocytes from infected mice, even when present at a ratio of 1-500 normal spleen cells, significantly suppressed the in vitro immune response to SRBC. Viable leukemic splenocytes were necessary for immunosuppression although the leukemic cells did not have to be in direct contact with the normal spleen cells. Specific anti-FLV serum, when added to the leukemic splenocytes or to normal spleen cells separated from infected cells by cell-impermeable membranes, prevented immunodepression.

Animals↗