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Biomedical subjects

A J Veerman

Publications and source records attributed to A J Veerman.

At least 145 records · Page 8Linked to original sources
PubMed1984

Differences in capping behavior between immunological phenotypes in childhood acute lymphoblastic leukemia. A study with ConA and an anti-HLA-ABC backbone.

Capping with concanavalin A (ConA) and monoclonal anti-HLA-ABC backbone was studied in childhood acute lymphoblastic leukemia (ALL). Capping with ConA and HLA gave quite different results, both in common ALL and T-ALL. With ConA most cases capped poorly, comparable to results described in chronic lymphatic leukemia and lymphoma, but in several cases capping was comparable to that of normal lymphocytes. In HLA capping T-ALL cells capped better than common ALL cells. HLA capping of T-ALL cells is comparable to that of normal lymphocytes. HLA capping results in handmirror cell formation giving support to the hypothesis that capping and motility are associated events.

Antibodies, Monoclonal↗
PubMed1984

Handmirror cells and central nervous system relapse in childhood acute lymphoblastic leukaemia.

In 53 children with acute lymphoblastic leukaemia (ALL), initial handmirror cell (HMC) count among lymphoblasts was studied in relation to the occurrence of a relapse in the central nervous system (CNS), taking into account the white blood cell count (WBC) and the immunological phenotype. The children were followed for a period limited by (1) the first CNS relapse, (2) death or (3) the closing day of this study. The median follow-up period was 30 months, range 2-106 months. HMC counts were available in bone marrow smears of 41 children and in cytospins of 35 children. Cytospins proved to give more reliable and consistent results than bone marrow smears. In the 35 'cytospin' children no CNS relapses occurred in the group of 16 children with non-T-non-B-ALL and HMC counts above 10%. However, in the group of 10 children with non-T-non-B-ALL and HMC counts below 10%, and in the group of 9 children with T-ALL (HMC less than or equal to 11%), 6 and 5, respectively, got a CNS relapse. The CNS relapse-free period was not significantly different between these last two groups, whereas both groups did differ significantly from the group mentioned first (p less than 0.01). This was not found in bone marrow smears of 41 children, presumably because of the inaccurate counting results. A low initial HMC count in cytospins is associated with an increased risk for the occurrence of a CNS relapse in children with ALL. This prognostic factor seems to be independent of other prognostic signs such as immunological phenotype and high WBC.

Adolescent↗
PubMed1983

Immunological phenotype related to acid alpha-naphthyl acetate esterase and acid phosphatase in childhood acute lymphoblastic leukaemia.

In 83 children with acute lymphoblastic leukaemia (ALL) the immunological phenotype of the lymphoblasts was determined using E rosetting, monoclonal anti-T cell sera, surface immunoglobulin staining and common ALL antiserum. The data were compared with acid alpha-naphthyl acetate esterase (ANAE) and acid phosphatase (AP) cytochemical data. The vast majority of T-ALL cells proved to be ANAE-negative (30/31) and AP-positive (29/31). Null-ALL was always AP-negative (12/12), the ANAE reaction was sometimes positive (4/12). In common ALL, findings ranged from negative to positive for both enzymes. Two cases of B-ALL were ANAE-negative and AP-negative. Enzyme cytochemical determinations gave thus preferential patterns, especially for T-ALL and null-ALL. In common ALL, considerable heterogeneity was found, which may be a reflection of differences in maturation between different cases of common ALL.

Acid Phosphatase↗
PubMed1983

Kartagener's syndrome: clinical symptoms and laboratory studies.

The purpose of this study was to develop a research program for the detection of congenital malfunction of cilia in the respiratory tract of selected patients with chronic respiratory infection. A clear difference was found between patients with Kartagener's syndrome and patients with respiratory tract infections of unknown etiology by studying patients employing this program, including examination of mucociliary clearance, ciliary motility and ciliary ultrastructure. The name "primary ciliary dyskinesia" is appropriate for emcompassing several ciliary abnormalities.

Adolescent↗
PubMed1983

[Disorders in mucociliary transport. Primary ciliary dyskinesia].

A survey is given of the mucociliary transport in the airways. Disturbances in rheologic qualities (viscosity and elasticity) of the mucuslayer may adversely influence mucociliary transport. This plays a role in cystic fibrosis and chronic bronchitis of other etiology. Disturbances in ciliary action can be secondary to for instance viral infections, inhalated substances and drugs. Inborn errors in the architecture of the cilia may cause immotility or ineffective motility of cilia, resulting in frequent airway infections. The clinical characteristics, diagnostic possibilities and a proposal for therapeutic measures are discussed.

Adult↗
PubMed1982

Motility of leukemia cells prevents the recurrence of disease in the central nervous system.

Acute lymphoblastic leukemia in childhood is a curable disease. However, in some patients relapse occurs in the central nervous system (CNS). It is suggested that active motility of malignant lymphoblasts prevents CNS-relapse, because motile cells will be able to re-enter the bloodstream and so become subject to chemotherapy. Immotile lymphoblasts on the other hand, remain behind the blood brain barrier, escape chemotherapy and eventually give rise to CNS-relapse of leukemia.

Blood-Brain Barrier↗
PubMed1980

The immotile cilia syndrome: phase contrast light microscopy, scanning and transmission electron microscopy.

In the immotile cilia syndrome, transmission electron microscopy of the cilia shows abnormalities in the arrangement of the central pairs of tubules and in the dynein arms of the peripheral tubules, or in the radial spokes, We studied four nonrelated children, 9/12, 5, 6, and 6 years old, with situs inversus and a history of chronic sinusitis and bronchitis (Kartagener's syndrome) and four children in the same age group and with the same history, but without situs inversus. Under the phase contrast microscope no motile cilia were seen in the four patients with Kartagener's syndrome and in two of the four other children. Transmission electron microscopy showed aberrations in the cilia (absence of dyneim arms, random orientation of central tubules) in the patients with Kartagener's syndrome. Scanning electron microscopy revealed differences in morphology and arrangement of cilia between patients and controls. In the patients much more mucus was present on the mucosal surface. Furthermore, the cilia were in a state of disorder, with a multidirectional orientation instead of the parallel orientation seen in controls.

Child↗
PubMed1976

T- and B-areas in immune reactions. Volume changes in T and B cell compartments of the rat spleen following intravenous administration of a thymus-dependent (SRBC) and a thymus-independent (paratyphoid vaccin-endotoxin) antigen. A histometric study.

In the white pulp of rat spleens cell numbers were studied in the different compartments following intravenous administration of comparable doses of paratyphoid vaccine (PTV, thymus-independent) and sheep red blood cells (SRBC, thymus-dependent). In the periarteriolar lymphatic sheaths (PALS) both cell concentration and volume were measured. For the follicles and the marginal zone only volume was recorded in the first 5 days following antigen administration. Additionally, histologic observations were made. In the thymus-dependent area PTV caused oedema 12-24 hours after administration. Following SRBC administration an increase in lymphocyte numbers occurred until the second day, probably representing an influx of T cells from the recirculating pool. Both antigens gave rise to a plasmacellular reaction in the peripheral PALS (2nd-4th day). In the bone marrow-dependent areas a massive shift of medium-sized lymphocytes from the marginal zone to the follicles took place in the first 24 hours following PTV administration. These cells subsequently transformed into blasts. After SRBC (6 and 12 hours) only a few marginal zone lymphocytes seemed to migrate into the follicles. It is aruged that the endotoxin present in PTV is responsible for the fact that, following administration of the antigen, all marginal zone (B) cells responded. Endotoxin stimulation might provide a model for the fate of marginal zone cells stimulated by other agents, such as antigen (stimulating antigen binding B cells) or antigen-antibody complexes (stimulating Fc-receptor B cells).

Animals↗
PubMed1975

Lymphocyte capping and lymphocyte migration as associated events in the in vivo antigen trapping process. An electron-microscopic autoradiographic study in the spleen of mice.

The fate of 125I labeled antigen-antibody complexes in the first two hours after intravenous injection was followed in the spleen of mice by light and electron microscopic autoradiography. It appeared that AAC were phagocytized by granulocytes and by macrophages in the marginal zone and were present over the surface of lymphocytes in that area. By rinsing the spleen before fixation it could be shown that AAC were indeed bound to the lymphocyte membrane and not merely present in the blood plasma between the cells. The label was present in a spotty fashion or over a so-called uropod. The majority of labeled uropods (13 out of 17) pointed away from the follicle. From this it was inferred that these lymphocytes moved to and most probably into, the follicles. Inside the follicles, at 1 hour post injectionem, most of the label was associated with interfaces between lymphocytes. At 2 hours post injectionem there was a preferential localization over interfaces between lymphocytes and dendritic reticulum cells. It is conceivable that antigen that is introduced into the circulation is ultimately presented to dendritic reticulum cells in a complexed form with antibody, probably with complement, and with the B-cell receptor, since receptor shedding is a normal event following capping.

Animals↗
PubMed1975

White pulp compartments in the spleen of rats and mice. A light and electron microscopic study of lymphoid and non-lymphoid celltypes in T- and B-areas.

The spleen of rats and mice was studied with the light and electron microscope. Special attention was paid to the delineation and composition of the white pulp compartments: periarteriolar lymphatic sheath (PALS), follicles and marginal zone. These three compartments each have their specific lymphoid and non-lymphoid cells. Reticulum cells and reticulin fibres, although occurring in all three compartments, from a characteristic pattern in each compartment. In the PALS two areas can be distinguished: a central area, largely devoid of reticulum cells, and a peripheral area where reticulum cells are arranged in cylindrical shells. The central PALS FORMS THE THYMUS DEPENDENT AREA OF THE SPLEEN, THE PERIPHERAL PALS contains both T- and B-lymphocytes. T-B-interactions requiring cell contact could take place in the latter area. Lymph vessels originate from the shells of reticulum cells around the smaller arterioles; these vessels follow the central arteriole to the hilus of the spleen. Circumstantial evidence suggests that the lymph vessels form a recirculation pathway for T-cells and possibly also for B-cells. In two areas of the splenic white pulp characteristic non-lymphoid cells are present. The central PALS contains interdigitating cells (IDC), which show a close contact with surrounding T-lymphocytes. The light zone of the follicle centre exhibits dendritic cells (DC). B-cells are found between the ramifications of the DC. It is conceivable that these cells play a role in the homing of T-cells and B-cells respectively. In addition they might create a microenvironment supporting differentiation and proliferation of T- and B-cells. The marginal zone does not contain a characteristic non-lymphoid cell type. However, in this compartment B-cells are directly exposed to the circulating blood. It is suggested that this factor constitutes one of the essentials of the microenvironment in the marginal zone.

Animals↗
PubMed1975

The postnatal development of the white pulp in the rat spleen and the onset of immunocompetence against a thymus-independent and a thymus-dependent antigen.

The spleen of the rat contains 5 well delineated compartments: a central and peripheral part of the periarteriolar lymphatic sheath (PALS), the marginal zone and the follicle with centre and corona. A study was made on the development of these compartments in correlation with the onset of immunocompetence of the spleen. The spleens of animals in the age range from 1-40 days were studied with the light and electron microscopes. Immunocompetence was assessed by measuring serum antibody levels 5 days after intravenous antigen administration. Comparable doses of paratyphoid vaccin (PTV) and sheep red blood cells (SRBC) were used: PTV as a thymus-independent, SRBC as a thymus-dependent antigen. At the first day of life few lymphocytes are present around small arterioles. The marginal zone is first present at 9 days of age. At 14 days of age the typical thymus-dependent area develops. Interdigitating cells, which seem to develop from monocytes, and lymphocytes are present in close apposition. Primary follicles were first seen on 20 days of age, follicle centres at 25 or 30 days of age. The appearance of "typical" dendritic cells coincided with the appearance of follicle centres. The first titre against PTV was seen after antigen administration at 9 days after birth, against SRBC after injection in 14 days old animals. As PTV is a thymus-independent antigen it needs only B-cells for a primary IgM response. The appearance of functional B-cells in sufficient numbers to give a measurable response therefore coincides with the appearance of the marginal zone. Although T-cells are present from birth, the response against SRBC is delayed until the thymus-dependent area has developed. Thus, in the first 2 weeks of life, T-cells are either immature, or they are not able to react, because their microenvironment is not yet adequate.

Animals↗