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Biomedical subjects

R Hendrickson

Publications and source records attributed to R Hendrickson.

16 recordsLinked to original sources
PubMed2005

Limitations of Wada memory asymmetry as a predictor of outcomes after temporal lobectomy.

BACKGROUND: The intracarotid amobarbital (Wada) test can be used to evaluate hemispheric memory capacity before anterior temporal lobectomy (ATL). Most patients demonstrate better memory with injection ipsilateral to planned resection (expected asymmetry [EA]), but a substantial minority show better memory with contralateral injection (unexpected asymmetry [UA]). Both degree and direction of Wada memory asymmetry (WMA) have been associated with worse surgical outcome in small series. Reports also suggest that UA is associated with greater decline in verbal memory after left ATL (L-ATL). METHODS: The relationship between WMA and surgical outcome (at 3 months, 1 year, and last follow-up) was examined in a large group of ATL patients (108 L, 119 R) with both EA and UA. Also, memory in a subgroup (96 L, 108 R) was examined, comparing subscores of the Rey Auditory Verbal Learning Test obtained preoperatively, at 3 months, and at 1 year. RESULTS: Thirty-six percent of L-ATL and 8% of R-ATL patients had UA. UA was associated with worse surgical outcome at 1 year for R-ATL patients but was not associated with worse outcome for L-ATL patients. There was no correlation between WMA and persistent postoperative verbal memory change for patients with L- or R-ATL. CONCLUSIONS: Unexpected asymmetry is uncommon in patients with right anterior temporal lobectomy (R-ATL) and may be a risk marker of poor surgical outcome. This relationship may be obscured by language confounds in patients with L-ATL. The results suggest that Wada asymmetry (using mixed stimuli) does not predict postoperative verbal memory; it is unclear whether this finding is generalizable to centers using only nonverbal stimuli.

Adolescent↗
PubMed2005

Cognitive correlates of cortical cholinergic denervation in Parkinson's disease and parkinsonian dementia.

We recently reported findings that loss of cortical acetylcholinesterase (AChE) activity is greater in parkinsonian dementia than in Alzheimer's disease (AD). In this study we determined cognitive correlates of in vivo cortical AChE activity in patients with parkinsonian dementia (PDem, n = 11), Parkinson's disease without dementia (PD, n = 13), and in normal controls (NC, n = 14) using N-[(11)C]methyl-piperidin-4-yl propionate ([(11)C]PMP) AChE positron emission tomography (PET). Cortical AChE activity was significantly reduced in the PDem (-20.9%) and PD (-12.7 %) subjects (P < 0.001) when compared with the control subjects. Analysis of the cognitive data within the patient groups demonstrated that scores on the WAIS-III Digit Span, a test of working memory and attention, had most robust correlation with cortical AChE activity (R = 0.61, p < 0.005). There were also significant correlations between cortical AChE activity and other tests of attentional and executive functions, such as the Trail Making and Stroop Color Word tests. There was no significant correlation between cortical AChE activity and duration of motor disease (R = -0.01, ns) or severity of parkinsonian motor symptoms (R = 0.14, ns). We conclude that cortical cholinergic denervation in PD and parkinsonian dementia is associated with decreased performance on tests of attentional and executive functioning.

Acetylcholinesterase↗
PubMed2005

Degree of inhibition of cortical acetylcholinesterase activity and cognitive effects by donepezil treatment in Alzheimer's disease.

OBJECTIVES: To determine in vivo cortical acetylcholinesterase (AChE) activity and cognitive effects in subjects with mild Alzheimer's disease (AD, n = 14) prior to and after 12 weeks of donepezil therapy. METHODS: Cognitive and N-[(11)C]methyl-piperidin-4-yl propionate ([(11)C]PMP) AChE positron emission tomography (PET) assessments before and after donepezil therapy. RESULTS: Analysis of the PET data revealed mean (temporal, parietal, and frontal) cortical donepezil induced AChE inhibition of 19.1% (SD 9.4%) (t = -7.9; p<0.0001). Enzyme inhibition was most robust in the anterior cingulate cortex (24.2% (6.9%), t = -14.1; p<0.0001). Donepezil induced cortical inhibition of AChE activity correlated with changes in the Stroop Color Word interference scores (R(2) = 0.59, p<0.01), but not with primary memory test scores. Analysis of the Stroop test data indicated that subjects with AChE inhibition greater than the median value (>22.2%) had improved scores on the Stroop Color Word Test compared with subjects with less inhibition who had stable to worsening scores (t = -2.7; p<0.05). CONCLUSIONS: Donepezil induced inhibition of cortical AChE enzyme activity is modest in patients with mild AD. The degree of cortical enzyme inhibition correlates with changes in executive and attentional functions.

Acetylcholinesterase↗
PubMed1999

Phenotype dictates the growth response of vascular smooth muscle cells to pulse pressure in vitro.

The objective of this study was to determine the effect of phenotype on pulse pressure-induced signaling and growth of vascular smooth muscle cells in vitro. Using a perfused transcapillary culture system, cells were exposed to increases in pulsatile flow and hence pulse pressure and maintained for 72 h before cells were harvested. Cell proliferation was determined by cell number, DNA synthesis, and proliferating cell nuclear antigen expression. Mitogen-activated protein kinase (MAPK) levels were determined by immunoblot and kinase activity by phosphorylation of myelin basic protein. Cell phenotype was determined by immunoblot and immunocytofluorescence using antisera specific for the differentiation markers alpha-actin, myosin, calponin, osteopontin, and phospholamban. In cells that highly expressed these differentiation markers, there was a significant increase in cell growth in response to chronic increases in pulse pressure without a significant change in MAPK activity in these cells. In contrast, in cells that weakly expressed SMC differentiation markers, there was a significant decrease in cell growth concomitant with a significant decrease in MAPK signaling in these cells. We conclude that SMC phenotype dictates the growth response of SMC to mechanical force in vitro.

Actins↗
PubMed1998

Increased expression of endothelin receptors in the vasculature of portal hypertensive rats: role in splanchnic hemodynamics.

Portal hypertension (PHT) is characterized by increased portal pressure caused in part by a reduction in mesenteric vascular resistance. The aim of this study was to evaluate the role of endothelin (ET) and specific ET receptors in maintaining the vasculopathy of PHT. PHT was created in Sprague-Dawley rats by a partial portal vein ligation. Control animals were sham-operated. ET receptor expression was determined in the superior mesenteric artery of sham and PHT rats by in situ autoradiography, radioligand binding analysis, and reverse-transcription polymerase chain reactions (RT-PCR). The pressor response to ET-1 was determined in vitro using isolated vascular rings and in vivo by measuring mean arterial pressure, splanchnic blood flow, and portal venous pressure following treatment with ET and selective ET receptor antagonists. The pressor response to ET in vitro was significantly enhanced in PHT concomitant with increased ET-A and ET-B receptor expression. There was a significant increase in the peak pressor response to ET (10 microg/kg intravenously) in portal hypertensive rats without any significant change in plasma ET-1 levels. There was no significant difference in the peak splanchnic blood flow or portal venous pressure response following ET-A receptor blockade with JKC-301 infusion (200 microg/kg intravenously). In contrast, ET-B receptor blockade with IRL-1038 (200 microg/kg intravenously) preferentially decreased splanchnic blood flow and portal venous pressure in portal hypertensive rats. These data suggest that enhanced ET-B receptor expression in portal hypertensive vessels contributes to the maintenance of elevated portal pressure in these animals.

Animals↗
PubMed1998

Non-anticoagulant heparin increases endothelial nitric oxide synthase activity: role of inhibitory guanine nucleotide proteins.

Heparin, which is widely used clinically, has recently been shown to have specific properties affecting the vascular endothelium. We hypothesized that heparin stimulates endothelial nitric oxide synthase (eNOS) activity by a mechanism independent of its anticoagulant properties and dependent on an inhibitory guanine nucleotide regulatory protein (Gi). We determined the effect of both heparin and N-acetyl heparin (Non-Hep), a heparin derivative without anticoagulant properties, on eNOS activity in cultured bovine aortic endothelial cells and on endothelium-dependent relaxation in isolated vascular rings. The eNOS activity was determined by measuring both citrulline and nitric oxide (NO) metabolite formation. Heparin and Non-Hep dose-dependently increased basal eNOS activity (ED50 1.0 microgram/ml or 0.15 U/ml), an effect that was significantly inhibited by pertussis toxin (100 ng/ml), a Gi-protein inhibitor. Agonist-stimulated (acetylcholine, 10 microM) eNOS activity was potentiated following pre-treatment with both heparin and Non-Hep and reversed by pertussis toxin. Heparin and Non-Hep induced a dose-dependent relaxation in preconstricted thoracic aortic rings, an effect that was significantly inhibited by pertussis toxin, endothelial inactivation (following treatment with sodium deoxycholate) and NG-nitro-L-arginine-methyl ester (L-NAME). We conclude that heparin and non-anticoagulant heparin induce endothelium-dependent relaxation following activation of eNOS by a mechanism involving a Gi-protein. Administration of heparin derivatives without anticoagulant properties may have therapeutic implications for the preservation of eNOS in conditions characterized by endothelial dysfunction.

Acetylcholine↗
PubMed1998

Evaluating the effects of treatment for medical disorders: has the value of neuropsychological assessment been fully realized?

Cognitive functioning can be affected by medical disorders and by the regimens used to treat them. To evaluate the cognitive risks and benefits of specific medical treatments, an increasing number of medical clinical trials have included a formal neuropsychological evaluation. This selective review has three goals: (a) to survey the range of assessment techniques used with different patient populations (e.g., those with diabetes, chronic obstructive pulmonary disease [COPD], hypertension, HIV, or cardiac disease) and treatment regimens (e.g., medical management, pharmacotherapy, surgery), (b) to demonstrate how cognitive outcome measures can contribute to an understanding of the value of certain treatments, and (c) to identify critical conceptual and methodological problems. The utility of this approach is incontrovertible-most large-scale medical trials have found either no adverse cognitive side effects or improved cognitive functioning following treatment. Nevertheless, before cognitive measures are routinely included in medical clinical trials, investigators will have to resolve problems that include the measurement of behavior change over time and the identification of clinically significant impairment.

Journal Article↗
PubMed1994

Cardiac rehabilitation in the Navy.

Cardiac rehabilitation has been effective in the management and recovery of the post-myocardial infarction population for almost 40 years. During that time, the fundamental components of rehabilitation have changed to reflect a growing complexity and number of cardiac patients. Great Lakes Naval Hospital has instituted a structured outpatient cardiac rehabilitation program. It is based on the needs of a large cardiac population with modifiable risk factors identified through quality improvement studies. Future implications and research in the area of cardiac rehabilitation include measurements of self-efficacy, long-term risk factor modification, cost effectiveness, gender-related differences, or morbidity and mortality.

Algorithms↗
PubMed1990

Behavior, affect, and cognition among psychogenic pain patients in group expressive psychotherapy.

In an exploratory study, the authors examined the cognitions, affect, and behaviors reported by eight female depressed chronic pain patients during experiential therapy sessions that focused on anger and depression. Subjects appeared to fit previously developed psychologic profiles of patients with chronic pain disorder: they presented as conscientious, compliant, passive, and rule-bound, viewing life and emotional expression as dangerous, avoiding conflict and risk, denying their own emotional needs. Their reports were compared with the self-reported affect behavior and cognitions of eight depressed female patients without chronic pain, under similar therapeutic conditions. Considerable differences in style and content were found. Implications of these findings for clinical practice are discussed.

Adult↗
PubMed1986

Hematologic abnormalities in simian acquired immune deficiency syndrome.

Hematologic abnormalities were defined in 31 rhesus monkeys (Macaca mulatta) with simian acquired immune deficiency syndrome (SAIDS). Animals manifested anemia (hypochromic/microcytic), severe neutropenia and progressive lymphopenia, monocytosis and occasional thrombocytopenia. Bone marrow studies showed erythroid hyperplasia with a marked left shift and adequate megakaryocytes. Two animals showed profound hypoplasia of all hematopoietic elements. Most animals were iron deficient, but the course of the anemia suggested additional factors. There was no evidence of immune hemolysis. The pathogenesis of these abnormalities is not clear and will require further study. This reproducible disease will allow studies to elucidate the mechanisms of viral-induced hematologic abnormalities.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Comparison of arginase activity in red blood cells of lower mammals, primates, and man: evolution to high activity in primates.

Arginase activity in red blood cells (RBC) of various mammalian species including man was determined. In nonprimate species, the activity generally fell below the level of detectability of the assay: less than 1.0 mumol urea/g hemoglobin per hr. Activities in higher nonhuman primates were equal to or of the same order of magnitude as those in man (approximately 950 mumol/g hemoglobin per hr). RBC arginase deficiency with normal liver arginase activity has been shown to segregate as an autosomal codominant trait in Macaca fascicularis established and bred in captivity. This study confirms the presence of this polymorphism in wild populations trapped in several geographic areas and demonstrates the absence of immunologically cross-reactive material in the RBC of RBC arginase-deficient animals. These data when taken together suggest that the expression of arginase in RBC is the result of a regulatory alteration, has evolved under positive selective pressure, and is not an example of the vestigial persistence of an arcane function. The expression of arginase in the RBC results in a marked drop in the arginine content of these cells.

Animals↗
PubMed1980

Properties of arginase from liver of Macaca fascicularis; comparison of normals with red blood cell arginase deficient monkeys.

Deficiency of arginase (E.C. 3.5.3.1), the fifth enzyme of the urea cycle, was found in the red blood cells (RBCs) of Macaca fascicularis monkeys (less than 0.2 micromol arginine cleaved/g Hb/min; normal equals 49.2). Liver biopsies were obtained from two of these monkeys and from one monkey with normal levels of RBC arginase activity. Arginase from both groups of animals required Mn2+ for maximal enzyme activity and demonstrated a pH optimum of 10.2 in vitro. The activity of arginase in the livers of all three monkeys was 1.1 millimol arginine cleaved per g protein per min. The apparent Km for arginine of arginase in the livers of the RBC-deficient monkeys was 7.4 and 5.9 mM and in the normal monkey was 6.9 mM. Similar patterns of heat denaturation was seen at 69 C without Mn2+ present and 79 C in the presence of 20mM Mn2+. No difference in mobility on either RBC-deficient or normal monkeys was found. In addition, liver arginase from all three monkeys reacted similarly with anti-human liver arginase antibody. Liver arginases in RBC-deficient and normal monkeys were identical by ten criteria. These studies do not distinguish among several hypotheses for the genetic determination of arginase in different organs of this species and of man.

Amino Acid Metabolism, Inborn Errors↗
PubMedDate not supplied

The role of cryosurgery in external ocular and periocular disease.

This preliminary report suggests that cryosurgery has a definite place in the management of certain external periocular and ocular problems. Cryosurgery for basal or squamous cell carcinoma of the lid is easily performed, gives excellent cosmetic results, and has a low recurrence rate. It is not recommended for lesions involving the fornices, or sclerotic and morphea-type basal cell carcinomas. Tumor recurrences following radiation, surgery, or cryosurgery can still be retreated with cryosurgery. To date, there is no evidence that cryosurgery at temperatures above -40 C causes damage to the lacrimal outflow system. Cryosurgery is of value in the management of trichiasis, reactive lymphoid hyperplasia, spider hemangioma, molluscum contagiosum, and conjunctival dysplasia. Cryotherapy for management of intraepithelial epithelioma and squamous cell carcinoma of the conjunctiva and cornea is still under investigation. Cryosurgery will, in our opinion, become the treatment of choice for basal and squamous cell carcinomas of the eyelids. The 96% cure rate with one treatment for these lesions reported here is artificially high since the follow-up period is too short. However, retreatment with cryosurgery is a simple ten-minute outpatient procedure which is certainly not the case with recurrences after other forms of therapy.

Basal Cell Carcinoma↗