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329 results on '"Haisch, C."'

83. Differential effects of intravenous anaesthetic agents on cell-mediated immunity in the Rhesus monkey.

Author

Thomas, Judith, Carver, Melinda, Haisch, C., Thomas, F., Welch, J., and Carchman, R.

Subjects
CELLULAR immunity, PRIMATES, ANTICONVULSANTS, KETAMINE, IMMUNITY, KILLER cells, CELL death
Abstract

Considerable evidence has accumulated to implicate general anaesthetic agents as a cause of post-surgical immune depression. In the present study we evaluated the immunosuppressive effects of three in vivo administered anaesthetic agents on cellular immune function in sub-human primules which did not undergo surgery. Normal rhesus monkeys received a minimal anaesthetic dose of ketamine HCl, meperidine HCl, or sodium pentobarbital. Peripheral blood mononuclear cells were assayed for mitogen-induced lymphocyte proliferative responses and cell-mediated cytotoxicity (CC), including antibody-dependent CC, spontaneous CC and alloimmune CC. In vivo administration of the three agents caused significant reduction in lymphocyte functional capabilities. Within 30 min after administration of ketamine HCl or sodium pentobarbital, cytotoxic effector function was significantly depressed, with variable recovery occurring at 48 hr; cytolytic effector function was not impaired after meperidine HCl or in untreated controls. Kelamine HCl selectively suppressed effector function; mitogen-induced lymphocyte proliferative responses were not suppressed. Monkeys given meperidine HCl showed stable effector function and depressed lymphocyte proliferative function. Effects from sodium pentobarbital were non-selective, with reduced cytotoxic and proliferative lymphocyte functions. In summary, this study shows that intravenous anaesthetic agents are immunosuppressive in primates and exhibit disparate effects on afferent and efferent expressions of cellular immunity. [ABSTRACT FROM AUTHOR]

Published
1982

85. Hypothermia - a Limiting Factor in Using Warm Ischemically Damaged Kidneys

Author

Brasile, L., Stubenitsky, B.M., Booster, M.H., Arenada, D., Haisch, C., and Kootstra, G.

Abstract

A study was performed to determine the limiting factors to expanding the donor pool with warm ischemically (WI) damaged kidneys. Canine kidneys were damaged by 30 min of WI, and then either cold stored (CS) in ViaSpan (4 °C) for 18 h, or warm perfused with exsanguineous metabolic support (EMS) technology (32 °C) for 18 h, or subjected to combinations of both techniques. The kidneys were autotransplanted with contralateral nephrectomy. In kidneys with WI and CS alone, the mean peak serum creatinine value was 6.3 mg/dL and took 14 days to normalize. In contrast, kidneys where renal metabolism was resuscitated ex vivo during 18 h of warm perfusion demonstrated mild elevations in the serum chemistries (2.6 mg/dL). The damage in kidneys CS for 18 h was ameliorated with 3 h of subsequent warm perfusion and eliminated by 18 h of warm perfusion. In contrast, reversing the order with CS following WI and 18 h of warm perfusion resulted in a time-dependent increase in damage. These results identify hypothermia as a major limiting factor to expanding indications for kidney donation. While hypothermia represents the foundation of preservation in the heart-beating donor, its use in WI damaged organs appears to represent a limiting factor.

Published
2001
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88. Influence of Semicrystalline Homopolymer Addition on the Morphology of Semicrystalline Diblock Copolymers

Author

Rangarajan, P., Haisch, C. F., Register, R. A., Adamson, D. H., and Fetters, L. J.

Abstract

We have studied blends of polyethylene “homopolymer” (hydrogenated polybutadiene) with diblock copolymers of polyethylene-poly(ethylene-alt-propylene), E/EP, varying both homopolymer loading and the block copolymer and homopolymer molecular weights. The pure block copolymers form homogeneous melts which are miscible with the homopolymer. The two components readily cocrystallize, even at homopolymer loadings as high as 75 wt % and even for a homopolymer which has nearly three times the molecular weight of the E block in the diblock. Small-angle X-ray scattering (SAXS) shows a single domain structure up to at least 50 wt % homopolymer addition, a result confirmed by transmission electron microscopy (TEM). Surprisingly, the Bragg spacing observed by SAXS, which reflects the sum of E and EP lamellar thicknesses, decreases continuously and substantially as homopolymer is added. The strong chain stretching in the EP block is progressively relaxed as E homopolymer is added; the reduction in Bragg spacing is only weakly opposed by the enthalpic resistance to formation of additional internal interface between E and EP domains, due to the small interaction parameter between the two blocks.

Published
1997

89. Clinical and experimental aspects of viral myocarditis

Author

Leslie, K, Blay, R, Haisch, C, Lodge, A, Weller, A, and Huber, S

Abstract

Picornaviruses are frequently implicated as the etiological agents of acute myocarditis. This association is based historically on serological evidence of rising antibody titers to specific pathogens and more recently on identification of viral genomic material in endocardial biopsy specimens through in situ hybridization. Only rarely is infectious virus isolated from either the patient or the heart during periods of maximum myocardial inflammation and injury. Thus, despite a probable viral etiology, much interest centers on the role of the immune system in cardiac damage and the likelihood that the infection triggers an autoimmune response to heart-specific antigens. Heart-reactive antibodies and T cells are found in most myocarditis patients, and immunosuppressive therapy has proven beneficial in many, though not all, cases. Furthermore, murine models of coxsackievirus group B type 3-induced myocarditis also demonstrate that virus infection initiates autoimmunity and that these autoimmune effectors are predominately responsible for tissue injury. How virus-host interactions overcome presumed self-tolerance to heart antigens is discussed, and evidence supporting various theories of virus-initiated autoimmunity and disease pathogenesis are delineated.

Published
1989
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98. 672P New insights into Pompe disease using Raman-microscopy.

Author

Hintze, S., Krois, E., Wieland, K., Meinke, P., Haisch, C., and Schoser, B.

Subjects
*GLYCOGEN storage disease, *GLYCOGEN storage disease type II, *MUSCLE weakness, *MUSCULAR atrophy, *GLYCOGEN
Abstract

Morbus Pompe is an autosomal recessive glycogen storage disease caused by missing or reduced activity of the lysosomal enzyme α-1,4-Glucosidase (GAA). The resulting inability to break down glycogen within the lysosomes leads to a pathological accumulation of glycogen in lysosomes, followed by lysosomal rupture and cellular damage. Successively, this leads to progressive muscle weakness and atrophy throughout the body and affects various body tissues. Since the existing glycogen measurements can only be performed in bulk or are unspecific, e.g. the histological PAS staining, we investigated using Raman-microcopy for single-cell glycogen measurement in primary myoblast from late-onset Pompe patients and controls. Raman-microscopy detected glycogen enrichment in Pompe myoblasts. For that Raman-microscopy could be used to show the efficiency of existing or future therapeutic approaches on a single cell level. [ABSTRACT FROM AUTHOR]

Published
2024
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