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Biomedical subjects

B Hartley

Publications and source records attributed to B Hartley.

At least 55 records · Page 3Linked to original sources
PubMed1987

Intraglomerular T cells and monocytes in nephritis: study with monoclonal antibodies.

Intraglomerular T cells, monocytes, total leucocytes and other mononuclear subsets were sought in renal biopsies from patients with glomerulonephritis, using monoclonal antibodies and immunoperoxidase techniques. Twenty-four biopsies with no significant glomerular proliferation on optical microscopy, thirty-two with only endocapillary hypercellularity, and twenty-one with extra capillary crescentic glomerular disease were studied. Few intra-glomerular leucocytes were seen in the non-proliferative group. In contrast, when compared with this group, biopsies with glomerular hypercellularity and particularly those with crescents showed increased numbers of intra-glomerular total leucocytes and monocytes/macrophages, as well as an excess of T lymphocytes and T cytotoxic/suppressor cells; T helper/inducer lymphocytes were significantly increased only in the crescentic group. Only small numbers of B lymphocytes and NK cells were found in all groups. The numbers of total glomerular T-cells and monocytes per glomerular cross section were highly correlated in the crescentic group. Only idiopathic IgA nephropathy failed to show a significant increase in the numbers of intra-glomerular leucocytes, in comparison with the non-proliferative group, Henoch-Schönlein purpura biopsies in contrast had an excess of both monocytes and T cell subsets. The finding of T lymphocytes as well as monocytes in glomeruli of proliferative nephritis suggests that cellular immune mechanisms may play a role in their pathogenesis, especially when crescents are present.

Antibodies, Monoclonal↗
PubMed1987

Respiratory depressant effects of GABA alpha- and beta-receptor agonists in the cat.

The aim of this study was to evaluate the cardiorespiratory effects of intravenously administered gamma-aminobutyric acid (GABA) alpha-(4,5,6,7-tetrahydroisoxazolo[5,4-c]pyridin-3-ol, THIP) and beta-(baclofen) receptor agonists and to locate the site of action of these drugs in the brain. THIP and baclofen were administered to alpha-chloralose-anesthetized cats while minute ventilation (VE), arterial blood pressure (AP), and heart rate were monitored. THIP, in doses of 0.5 to 2 mg/kg decreased VE, tidal volume (VT), and AP. No changes in respiratory rate (f) or inspiratory (TI) or expiratory (TE) duration were observed. Baclofen, in doses of 0.5 to 4 mg/kg, decreased VE, f, and AP. VT and TI increased and an "apneustic" breathing pattern was seen. THIP (9.5 micrograms), applied bilaterally to the glycine-sensitive area of the ventral medulla, reproduced the effects seen with intravenous administration. Application of 10 micrograms of bicuculline bilaterally to this area reversed the effects of intravenous THIP but not those of baclofen. Baclofen (5.6-56 micrograms), administered by the intracisternal route, produced the same respiratory effects seen with intravenous administration. We conclude that activation of GABA alpha- and beta-receptors produces cardiorespiratory depression. However, this is accomplished by different mechanisms and by actions exerted at different central nervous system sites.

Animals↗
PubMed1987

Abnormal podocyte CR-1 expression in glomerular diseases: association with glomerular cell proliferation and monocyte infiltration.

The expression of CR-1 complement receptors on glomerular epithelial cells, was studied in 77 renal biopsies from patients with (74) or without (3) glomerular diseases, employing an anti-CR-1 monoclonal antibody, and an indirect immunoperoxidase technique. Four patterns of CR-1 expression were recognised: normal (18); generally decreased (6); focal/segmental partial loss (44); and complete loss (9). Normal expression was detected in all three biopsies with non-glomerular diseases, and in glomerular diseases with normal glomeruli on light microscopy, but also in several glomerulonephritic biopsies (13), including diffuse proliferative lupus nephritis (1 of 7) and idiopathic membranous nephritis (5 of 14). However, the majority of biopsies from patients with glomerular diseases showed abnormal CR-1 expression (59 of 74), most evident in proliferative biopsies (43 of 49), with or without crescent formation (respectively, 18 of 20 and 25 of 29). Complete loss of CR-1 expression was almost restricted to crescentic biopsies (8 of 9). The abnormal CR-1 expression was unrelated to the presence of capillary immune deposits of Ig or C. More intraglomerular monocytes, assessed by monoclonal antibodies, were encountered in glomerulonephritic biopsies with partial CR-1 loss (median 6.2, P less than 0.05) or complete loss (median 14, P less than 0.03), than in biopsies with normal receptor expression (median 1.4). Thus, changes in glomerular CR-1 expression are frequently seen in many glomerular diseases and are associated with glomerular proliferative changes and monocyte infiltration, but not with the presence of capillary immune deposits.(ABSTRACT TRUNCATED AT 250 WORDS)

Antibodies, Monoclonal↗
PubMed1986

The Goodpasture antigen in Alport's syndrome: studies with a monoclonal antibody.

A mouse monoclonal antibody (MCA-P1), which recognizes an antigenic determinant in human glomerular basement membrane against which autoantibodies are directed in Goodpasture's syndrome, was used in indirect immunofluorescence studies to investigate glomerular basement membrane structure in Alport's syndrome. We found reduced or absent binding of MCA-P1 to glomerular and distal tubular basement membranes in renal biopsy tissue from ten patients with Alport's syndrome. Antiglomerular basement membrane antibody eluted from the kidneys of a patient who had died from Goodpasture's syndrome was used to confirm these findings. In contrast, there was bright linear fluorescence of MCA-P1 on glomerular and tubular basement membranes of normal renal material and renal biopsy tissue obtained from patients with a variety of glomerulonephritides. These results suggest an abnormality or a variable quantity of the immunoreactive autoantigen in the glomerular basement membrane of patients with Alport's syndrome. Furthermore, MCA-P1 may be of value in the diagnostic interpretation of renal biopsies from patients with familial nephritis.

Anti-Glomerular Basement Membrane Disease↗
PubMed1985

Differentiation between allograft rejection and cyclosporin nephrotoxicity in renal-transplant recipients.

In a retrospective study of 60 renal-transplant patients immunosuppressed with cyclosporin no specific clinical features differentiated allograft dysfunction responsive to anti-rejection therapy from dysfunction responsive to reduction in cyclosporin dosage. Histologically, allograft dysfunction responsive to anti-rejection therapy was strongly associated with diffuse interstitial infiltration by mononuclear cells, oedema, and haemorrhage, vascular endothelial-cell proliferation, and infiltration of arterial walls by mononuclear cells. Arteriolar medial hypertrophy and hyalinosis were more commonly found in biopsy specimens from allografts with dysfunction responsive to reduction in cyclosporin dose than in those with dysfunction responsive to anti-rejection therapy and those with stable or improving function. Whole-blood cyclosporin concentrations were significantly lower in patients with dysfunction reversed by anti-rejection therapy than in those with dysfunction reversed by reduction in cyclosporin dose or in those with stable function. There was, however, considerable overlap between these groups, so that individual cyclosporin measurements were of little diagnostic value.

Adolescent↗
PubMed1985

Glomerular C3b receptor loss in renal allografts.

There is almost no data from the glomeruli of allografted kidneys with respect to changes in the CR-1 (C3b) receptor expressed on glomerular podocytes. We studied 22 renal graft biopsies from rejecting and stable allografts, using a panel of monoclonal antibodies. We found that the CR-1 expression was decreased in a focal and segmental fashion in some biopsies, particularly in rejecting kidneys. These changes correlated with the intensity of glomerular mononuclear cell infiltration, but in contrast no correlation was seen with peripheral capillary wall deposition of complement (C3). Thus, some active process is occurring in the glomeruli of rejecting grafts which affects the expression of the CR-1 receptor.

Graft Rejection↗
PubMed1985

Interstitial foam cells in the nephrotic syndrome belong to the monocyte/macrophage lineage.

Interstitial foam cells are occasionally seen in patients with the nephrotic syndrome. In a group of patients with the nephrotic syndrome we were able to demonstrate that these cells express markers characteristic of the monocyte/macrophage lineage. Their presence was related to the previous duration of proteinuria, but they had no apparent influence on the subsequent evolution of renal function. The mechanisms leading to their presence are unknown.

Adult↗
PubMed1985

A radiographic anthology of vertebral names.

There are many conditions of the spine to which various authors have applied descriptive names. This paper, an extensive review of the literature, provides the first complete source for such named vertebrae. Included are 88 names covering all categories of bone disease. A brief description of the radiographic appearance and its pathogenesis is provided for each, along with a consideration of the disease processes which may produce the appearance.

Humans↗
PubMed1984

Vasculitis affecting the kidney: presentation, histopathology and long-term outcome.

Fifty-three patients who by clinical and/or histological criteria were judged to have vasculitis affecting the kidney were reviewed. Patients with systemic lupus or Schönlein-Henoch purpura were excluded. Segmental necrotising glomerulitis was taken as a manifestation of vasculitis ('microscopic polyarteritis'). Those patients in whom vasculitis was confined to glomerular capillaries were compared with those who in addition had vascular lesions outside the glomeruli. The two groups were found to have identical clinical features. Clinical presentation was predominantly extrarenal, and exclusively renal in only two. Three patients were classified histologically as Wegener's granulomatosis, four had malignant tumours and two relapsing polychondritis. Hepatitis B surface antigen was absent in all of 37 patients tested. Renal disease presented with microscopic haematuria and minor proteinuria in the majority (32) but 16 patients presented with rapid deterioration of renal function, including seven with anuria. Histologically 42 patients showed segmental necrotising glomerulitis ('microscopic polyarteritis'), six diffuse proliferative glomerulonephritis,and in five only minor or ischaemic glomerular changes were present. Crescents were found in 41/42 of those with segmental necrotising glomerulitis, nd involved more than 50 per cent of glomeruli in 15 patients. Immunohistochemical studies were generally negative except the fibrin. Electron microscopy showed no evidence of immune deposits in necrotising glomerulitis, but these were present in 2/6 patients with diffuse proliferative glomerulonephritis. Overall prognosis was poor, 35 patients having died, 20 early in the course of the disease and 15 later. Oligoanuria and extensive crescent formation were adverse signs. Survivals were 54, 38 and 34 per cent at one, five and 10 years respectively. Of those who survived the initial illness, 12 were stable with apparently inactive disease, whilst 16 continued to show clinical signs of activity and required treatment. A variety of treatments was employed including oral and intravenous corticosteroids, immunosuppressive agents, anticoagulants; only one patient was treated by plasmapheresis. It is difficult to draw any firm conclusions as to the efficacy of treatment and survival rates remain unsatisfactory.

Acute Disease↗