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Intrinsic Component (intrinsic + component)

Distribution by Scientific Domains

Medical Sciences	50%

Selected Abstracts

Immunotherapy of HIV-infected patients with Gc protein-derived macrophage activating factor (GcMAF)

JOURNAL OF MEDICAL VIROLOGY, Issue 1 2009
Nobuto Yamamoto
Abstract Serum Gc protein (known as vitamin D3 -binding protein) is the precursor for the principal macrophage activating factor (MAF). The MAF precursor activity of serum Gc protein of HIV-infected patients was lost or reduced because Gc protein is deglycosylated by ,- N -acetylgalactosaminidase (Nagalase) secreted from HIV-infected cells. Therefore, macrophages of HIV-infected patients having deglycosylated Gc protein cannot be activated, leading to immunosuppression. Since Nagalase is the intrinsic component of the envelope protein gp120, serum Nagalase activity is the sum of enzyme activities carried by both HIV virions and envelope proteins. These Nagalase carriers were already complexed with anti-HIV immunoglobulin G (IgG) but retained Nagalase activity that is required for infectivity. Stepwise treatment of purified Gc protein with immobilized ,-galactosidase and sialidase generated the most potent macrophage activating factor (termed GcMAF), which produces no side effects in humans. Macrophages activated by administration of 100 ng GcMAF develop a large amount of Fc-receptors as well as an enormous variation of receptors that recognize IgG-bound and unbound HIV virions. Since latently HIV-infected cells are unstable and constantly release HIV virions, the activated macrophages rapidly intercept the released HIV virions to prevent reinfection resulting in exhaustion of infected cells. After less than 18 weekly administrations of 100 ng GcMAF for nonanemic patients, they exhibited low serum Nagalase activities equivalent to healthy controls, indicating eradication of HIV-infection, which was also confirmed by no infectious center formation by provirus inducing agent-treated patient PBMCs. No recurrence occurred and their healthy CD,+,cell counts were maintained for 7 years. J. Med. Virol. 81:16,26, 2009. © 2008 Wiley-Liss, Inc. [source]

Assessment of the intrinsic urethral sphincter component function in postprostatectomy urinary incontinence

NEUROUROLOGY AND URODYNAMICS, Issue 3 2002
Christian Pfister
Abstract Postprostatectomy incontinence remains a disabling condition. Sphincter injury, detrusor instability, and decreased bladder compliance have been previously reported as major factors. The aim of this study was to evaluate the urethral sphincter intrinsic component, which may provide passive continence. A urodynamic evaluation was performed in 20 patients undergoing a radical retropubic prostatectomy in the preoperative period and 3 months after surgery. Patients with disabled urinary incontinence underwent a new urodynamic evaluation 6 months later. The urethral pressure profile was measured just before, then 10, 20, and 30 minutes after the injection of 0.5 mg/kg moxisylyte chlorhydrate, an alpha adrenergic blocker. Three different pressure components were defined in urethral sphincter capacity: baseline, adrenergic, and voluntary. A postoperative intrinsic urethral sphincter pressure component was found in 17 patients and its value was under 6 cm H2O in five cases of severe incontinence. No significant difference was observed for these patients on urethral profile components 6 months later. In contrast, in cases of significant intrinsic component value, no incontinence was observed in most patients. Passive continence after radical prostatectomy should be a matter of concern and may also explain paradoxical incontinence, despite high voluntary urethral pressure obtained after reeducation. A follow-up evaluation of the intrinsic sphincter component is suggested, by using an alpha receptor blockage test during urodynamic studies in the management of patients with postprostatectomy incontinence. Neurourol. Urodynam. 21:194,197, 2002. © 2002 Wiley-Liss, Inc. [source]

Pericranial muscular, respiratory, and heart rate components of the orienting response

PSYCHOPHYSIOLOGY, Issue 6 2002
J.J. Stekelenburg
We have earlier found that voluntary attention to weak auditory stimuli induces inhibition of respiration, heart rate, and electromyographic (EMG) activity of masticatory and lower facial muscles and that these responses lower the auditory threshold for low-frequency sounds. In the current study, we examined whether this inhibitory response pattern also occurs during involuntary orienting to novel, nonsignal sounds. Environmental sounds of low intensity were presented unexpectedly during the performance of a reading task. Orienting responses (ORs) were elicited as indicated by heart rate deceleration and skin conductance responses. Inhibitory respiratory and pericranial EMG responses appeared to be intrinsic components of the OR. Together with the autonomic responses, they habituated when a nonsignal auditory stimulus was repeatedly presented. Our results also suggest that eye and pinna movements occurred toward the sound source. The results of the current study are consistent with the hypothesis of Sokolov (1963) that the primary function of the OR is enhancement of sensory sensitivity. [source]

Chemotherapy and antiangiogenesis: drug-specific effects on microvessel sprouting

APMIS, Issue 11 2003
PER ALBERTSSON
Tumors are angiogenesis dependent. Some chemotherapeutics have been shown to be able to suppress angiogenesis and thus tumor growth in vivo at low, well-tolerated doses. Not much is known about the angiogenesis-modulating effects of chemotherapeutics in vivo, however. Microvessel sprouting is inherent to angiogenesis. Using the rat mesentery assay, we studied the effect of cyclophosphamide, doxorubicin and paclitaxel at a low, atoxic dose on the number of sprouts per unit tissue volume (No. SP) and their length (Le. SP) at the edge of the expanding network in VEGF165 -mediated angiogenesis. A single dose of each cytotoxic drug was administered i.v. 7 days before the animals were sacrificed. Cyclophosphamide significantly lengthened the shortest Le. SP and shortened the longest Le. SP, doxorubicin did not significantly affect Le. SP, whereas paclitaxel significantly shortened both the shortest and the longest Le. SP. No correlation was found between the present results and the distinctly drug-specific results of microvessel segment number and length analyzed within central parts of the same expanding network (1). To our knowledge, this is the first quantitative report on the effect of chemotherapy on angiogenesis sprouting in vivo. Collectively, the data suggest that cyclophosphamide, doxorubicin and paclitaxel at a non-toxic dose primarily target different intrinsic components of the angiogenic cascade, leading to distinctly drug-specific effects. [source]