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Biomedical subjects

J M Cruse

Publications and source records attributed to J M Cruse.

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

Constrictive structural elements in human cerebral arteries following aneurysmal subarachnoid haemorrhage.

Histoimmunological, histochemical, and histological studies were conducted on cerebral arteries from four living patients with a recent aneurysmal subarachnoid haemorrhage. There appeared to be a correlation between the severity of vasospasm and the magnitude of pathological findings. Large myofibroblast cells and type V collagen within the medial layer were abundant in arteries showing marked vasospasm, but were less conspicuous in those showing milder involvement. Intracranial arteries from patients who died from non-cerebral causes did not demonstrate these changes. In ruptured vessels, there was also a positive fluorescence for actin-myosin filaments in layers of the arterial wall other than the media. It is postulated that the intimal and adventitial actin-myosin, myofibroblasts and type V collagen may contribute to cerebral vasospasm by holding the damaged vessel in a contracted phase during the healing period.

Adult↗
PubMed1985

Auto-antibody to kidney tubular cells during retrograde chronic pyelonephritis in rats.

Retrograde pyelonephritis was induced in inbred Fischer rat kidneys with Proteus mirabilis (1 X 10(8) organisms/ml). Sera from pyelonephritic animals sacrificed at 4 and 6 weeks contained cytotoxic antibodies to cultured syngeneic 51Cr-labeled kidney tubular cells (p less than 0.02 and p less than 0.05, respectively) which could be absorbed with plasma membranes. Immune sera from 4- and 6-week pyelonephritic animals also displayed a granular fluorescent pattern along the surface of cultured kidney tubular cells. Quick-frozen syngeneic rat kidney sections stained positively with fluorescent antibody on the intraluminal side of kidney tubular cells. The results suggest that during chronic phases of pyelonephritis, auto-antibodies to kidney tubular cells are induced.

Animals↗
PubMed1985

Arterial wall changes in early human vasospasm.

Histological, histochemical, and histoimmunological studies were conducted on cerebral arteries from three living patients with a recent subarachnoid hemorrhage. There seemed to be a correlation between the severity of vasospasm and the magnitude of pathological alterations. Myofibroblasts and Type V collagen within the medial layer were abundant in vessels showing marked constriction, but were less conspicuous in those arteries showing milder involvement. Intracranial arteries from patients who died from noncerebral causes did not demonstrate these changes. Thus, myofibroblasts and Type V collagen may be related to cerebral vasospasm by holding the damaged vessel in a contracted phase for weeks during the healing period.

Adult↗
PubMed1984

Serial monitoring of T-cell subset ratios with monoclonal antibodies in steroid- and antithymocyte globulin-treated patients with renal allotransplants.

Sequential changes in T-cell subsets or their ratios were employed to predict severity of rejection crises and to identify those patients who might require future antirejection therapy. Forty-two percent of the transplant recipients had a pretransplant OKT4:8 ratio in the range of 1.3 +/- 0.5. By contrast, only 11% had a OKT4:8 ratio of 2.9 or greater. Examination of the entire study group demonstrated that the mean OKT4:8 ratios fell (P less than 0.01) in the first week following the transplant procedure. All patients had at least one episode of acute rejection. There was a marked increase (P less than 0.05) in the OKT4:8 ratio between the first week value and the value immediately preceding (within 3 days) the start of the rejection episode which was 2.64 +/- 0.27. The mean OKT4:8 ratio in the 15 patients leaving the hospital with a functioning transplant was 1.18 +/- 0.35. Three months post-transplant, the OKT4:8 ratio was 1.98 +/- 0.39 in the 12 patients with functioning allografts. This value was not different from those patients' initial pretransplant values. Clinically, the rejection episodes could be divided into two groups based on their response to intravenous methylprednisolone therapy. The first group (n = 9) had milder rejection crises which responded rapidly to administration of one course of methylprednisolone. The second group of patients (n = 9) were also treated initially with methylprednisolone, to which they did not respond, and subsequently received antithymocyte globulin in an attempt to control their ongoing rejection crises. Following the transplant procedure, the OKT4:8 ratio decreased in patients who were destined to have steroid-responsive rejection episodes (P less than 0.01). The OKT4:8 ratio however, failed to fall in those who required ATG for control of their transplant rejection episodes. The onset of rejection episodes was associated with an increase in OKT4:8 ratio in both groups. Following steroid administration, two patterns of OKT4:8 cell responses were observed. Those in whom renal function improved demonstrated a decline in OKT4:8 ratio from 2.4 +/- 0.4 to 1.4 +/- 0.4 (P less than 0.05). However, no change occurred in the OKT4:8 ratios with steroid therapy (2.6 to 2.4 +/- 0.33, P greater than 0.05) in individuals in whom the serum creatinine concentration failed to decline. The patients who failed to respond to steroid therapy were treated with antithymocyte globulin (ATG).(ABSTRACT TRUNCATED AT 400 WORDS)

Acute Disease↗
PubMed1983

Activation of macrophages by in vitro allostimulated T cells.

Murine peritoneal macrophages, parabiotically co-cultured with combinations of in vitro H-2 sensitized thymus-derived lymphocytes obtained from drug-pretreated mice, possessed an increased cytotoxicity against alloantibody-coated target cells. This heightened activity appeared to be accentuated by and dependent on T-cell synergy. After 5 days of in vitro allosensitization at 37 degrees C, cortisone-resistant thymocytes allosensitized in combination with cyclophosphamide-pretreated splenic T cells released molecules that produced strong antibody-dependent macrophage-mediated cytotoxicity (ADCC). This enhanced ADCC correlated with increased macrophage rosetting with IgG-sensitized erythrocytes. These heightened activities resulted from soluble mediators released by the activated T cells which diffused across a 0.22-microns Millipore filter and were not dependent on lymphocyte-macrophage contact. Evidence that these molecules originated from the highly enriched T-cell populations and were not synthesized de novo by macrophages was supported by results of pretreatment with protein and RNA synthesis inhibitors. Evidence that soluble Fc receptors released from the alloactivated T cells were responsible for the increased macrophage EA binding and ADCC was obtained in affinity chromatography experiments in which activity could be depleted by passage over a Sepharose-Fc-coupled column and recovered in the column eluate.

Antibody-Dependent Cell Cytotoxicity↗