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R M Klein

Publications and source records attributed to R M Klein.

At least 55 records · Page 3Linked to original sources
PubMed1999

Influence of previous visual stimulus or saccade on saccadic reaction times in monkey.

Influence of previous visual stimulus or saccade on saccadic reaction times in monkey. Saccadic reaction times (SRTs) to suddenly appearing targets are influenced by neural processes that occur before and after target presentation. The majority of previous studies have focused on how posttarget factors, such as target attributes or changes in task complexity, affect SRTs. Studies of pretarget factors have focused on how prior knowledge of the timing or location of the impending target, gathered through cueing or probabilistic information, affects SRTs. Our goal was to investigate additional pretarget factors to determine whether SRTs can also be influenced by the history of saccadic and visual activity even when these factors are spatially unpredictive as to the location of impending saccadic targets. Monkeys were trained on two paradigms. In the saccade-saccade paradigm, monkeys were required to follow a saccadic target that stepped from a central location, to an eccentric location, back to center, and finally to a second eccentric location. The stimulus-saccade paradigm was similar, except the central fixation target remained illuminated during presentation of the first eccentric stimulus; the monkey was required to maintain central fixation and to make a saccade to the second eccentric stimulus only on disappearance of the fixation point. In both paradigms, the first eccentric stimulus was presented at the same, opposite, or orthogonal location with respect to the final target location in a given trial. We measured SRTs to the final target under conditions in which all parameters were identical except for the location of the first eccentric stimulus. In the saccade-saccade paradigm, we found that the SRT to the final target was slowest when it was presented opposite to the initial saccadic target, whereas in the stimulus-saccade paradigm the SRT to the final target was slowest when it was presented at the same location as the initial stimulus. In both paradigms, these increases in SRTs were greatest during the shortest intervals between presentation of successive eccentric stimuli, yet these effects remained present for the longest intervals employed in this study. SRTs became faster as the direction and eccentricity of the two successive stimuli became increasingly misaligned from that which produced the maximal SRT slowing in each paradigm. The results of the stimulus-saccade paradigm are similar to the phenomenon of inhibition of return (IOR) in which human subjects are slower to respond to stimuli that are presented at previously cued locations. We interpret these findings in terms of overlapping representations of visuospatial and oculomotor activity in the same neural structures.

Animals↗
PubMed1999

Saccadic performance as a function of the presence and disappearance of auditory and visual fixation stimuli.

Relative to when a fixated stimulus remains visible, saccadic latencies are facilitated when a fixated stimulus is extinguished simultaneously with or prior to the appearance of an eccentric auditory, visual, or combined visual-auditory target. In a study of nine human subjects, we determined whether such facilitation (the "gap effect") occurs equivalently for the disappearance of fixated auditory stimuli and fixated visual stimuli. In the present study, a fixated auditory (noise) stimulus remained present (overlap) or else was extinguished simultaneously with (step) or 200 msec prior to (gap) the appearance of a visual, auditory (tone), or combined visual-auditory target 10 degrees to the left or right of fixation. The results demonstrated equivalent facilitatory effects due to the disappearance of fixated auditory and visual stimuli and are consistent with the presumed role of the superior colliculus in the gap effect.

Acoustic Stimulation↗
PubMed1998

Adenosine is worth trying in patients with paroxysmal supraventricular tachycardia on chronic theophylline medication.

Adenosine is widely used to terminate paroxysmal supraventricular tachycardia. However, it is usually considered of no value in patients on theophylline, for methylxanthines completely antagonize the A(1) -receptor mediated negative dromotropic adenosine effect. We report a case of a 69 year old man who had chronic obstructive lung disease and spontaneous pneumothorax. Supraventricular tachycardia with a heart rate of 200 bpm persisted even after a pleural drain was inserted and the lung became fully inflated. Although the patient was on theophylline medication with effective serum plasma levels, adenosine terminated the supraventricular tachycardia after three repeated doses of 3, 6 and 9 mg, respectively. This observation further nourishes previous hypotheses that chronic administration of an A1-receptor antagonist leads to up-regulation of the adenosine receptor number.

Adenosine↗
PubMed1998

Selective chemokine mRNA expression following brain injury.

Injury in non-neuronal tissues stimulates chemokine expression leading to recruitment of inflammatory cells responsible for orchestration of repair processes. The signals involved in directing repair of damage to the brain are less well understood. We hypothesized that following brain injury, chemokines are expressed and regulate the rate and pattern of inflammatory cell accumulation. The two chemokine subfamilies are alpha(alpha)-chemokines, which primarily function as neutrophil chemoattractants, and the beta(beta)-chemokines, which function primarily as monocyte chemoattractants. We assessed alpha and beta chemokine mRNA expression patterns and leukocyte accumulation following a cerebral cortical lesion. Cortical lesions were produced with and without addition of endotoxin, Escherichia coli lipopolysaccharide (LPS), which stimulates cytokine expression. We studied the expression of the beta-chemokines: monocyte chemoattractant protein (gene product JE; MCP-1/JE), macrophage inflammatory protein-1 alpha and beta (MIP-1alpha and MIP-1beta), and the regulated upon activation normal T expressed and secreted chemokine (RANTES) as well as the alpha-chemokines: interferon-gamma-inducible protein (IP-10) and N51/KC (KC; a murine homologue of MIP-2). Changes in gene expression were analyzed by Northern analysis at different time points following injury. Leukocyte and macrophage densities were analyzed by immunohistochemistry at the same time intervals. All chemokines were elevated following cortical injury/endotoxin. MCP-1 and MIP-1alpha were elevated at 2 h and peaked 6 h, MIP-1beta peaked at 6 h, but declined more rapidly than MCP-1 or MIP-1alpha, and IP-10 peaked at 6 h and showed the most rapid decline. KC was elevated at 1 h, and peaked at 6 h following LPS. RANTES was elevated at 1 h and achieved a plateau level between 6 and 18 h, then declined. In contrast, sterile injuries produced in the absence of endotoxin only induced the mRNA of the beta-chemokine MCP-1, and its expression was delayed compared to the cortical injury/endotoxin group. The presence of chemokine message as early as 1 h indicates that expression of this class of molecules is an early response in the repair process following traumatic brain injury. Macrophage/microglia accumulation occurred more rapidly, activated microglia further from the lesion border, and more cells accumulated in cortical injury/endotoxin than in cortical lesions produced under sterile conditions. Thus, there was a positive correlation between beta-chemokine expression and the number of beta-chemokine responsive cells (i.e. microglia) accumulating in injury sites. This is the first comprehensive study using a panel of chemokine probes and specific marcophage/microglial markers to study in vivo activation of the brain following injury. Our data show that the brain is capable of expression of multiple chemokine genes upon appropriate stimulation (e.g. LPS-treatment). The gradient of microglial activation is consistent with physical damage stimulating release of chemokines that diffuse from the injury site. These data strongly suggest that chemokines are instrumental in the initiation of repair processes following brain injury.

Animals↗
PubMed1998

Characteristics of calcaneal bone infarction: an MR imaging investigation.

OBJECTIVE: Bone infarction (BI) of the calcaneus is an uncommon entity which has received little mention in the recent literature. In this paper, we review the MR images of six calcanei with BI, which demonstrate a pattern of presentation that may explain the etiology of BI at this unusual location. DESIGN: A retrospective review was performed of the transcribed reports of the foot or ankle MR examinations at our institution. MR images of examinations with any marrow signal abnormality were reviewed for presence of BI and its distribution. PATIENTS: Based on MRI criteria, four patients had calcaneal BI (none biopsy proven); they ranged in age from 37 to 51 years old. Two patients were diagnosed with systemic lupus erythematosus, one with fibrositis, and another with polymyositis. All were treated with corticosteroids. RESULTS: Six calcanei (in four patients) contained a region of calcaneal BI. In five of the six, the lesions were entirely or predominantly located in the posterior half of the calcaneus. CONCLUSION: Two theories are proposed which may explain why BI predominantly occurs in the posterior half of the calcaneus. First, the convergence of the recurrent intraosseous calcaneal vessels may occasionally produce the equivalent of a single dominant vessel that is more prone to vascular accidents. Secondly the region between the recurrent and the epiphyseal vessels may act as a watershed zone, increasing its susceptibility to ischemia.

Adult↗
PubMed1998

[Circulating adhesion molecules (cICAM-1, lcVCAM-1) in patients with suspected inflammatory heart muscle disease].

UNLABELLED: Some patients with non-ischemic heart failure show inflammatory changes in the myocardium which are thought to be of causal or pathogenetic relevance for the heart failure. The intercellular adhesion molecule-1 (ICAM-1) and the vascular adhesion molecule-1 (VCAM-1) are membrane proteins with receptor function from the immunoglobulin superfamily which mediate the vascular adhesion and transmigration of leucocytes into the tissue and undergo increased expression in chronic immunological-inflammatory processes. In addition to membrane-bound adhesion molecules, soluble forms can be detected in serum. In the present study we investigated the occurrence and the significance of circulating ICAM-1 and VCAM-1 in 71 patients with non-ischemic heart failure (47 M/24 F, mean age: 55 +/- 11 years). METHODS: Serum concentrations of cICAM-1 and cVCAM-1 were analyzed using ELISA-Kits. The severity of heart failure was assessed in accordance to the NYHA-classification and to hemodynamic parameters (mean pulmonary pressure, left ventricular ejection fraction). Inflammatory heart disease was assessed histologically and immunohistologically (T-lymphocytes > 7.0/mm2, increased expression of the histocompatibility antigens of class I and II) in right ventricular endomyocardial biopsies. 16 healthy, age-matched patients (8 M/8 F, mean age: 55 +/- 6 years, mean ejection fraction 76 +/- 3%) without signs of inflammation in the myocardium (mean T-lymphocytes < 3.5 cells/mm2, low expression of HLA-class I and II) served as controls. RESULTS: The mean serum concentrations of circulating ICAM-1 and VCAM-1 (cICAM-1, cVCAM-1) were higher in patients with non-ischemic heart failure (372 +/- 107 ng/ml and 949 +/- 439 ng/ml) than controls (264 +/- 37 and 710 +/- 164 ng/ml) (p < 0.05). The mean concentrations of both adhesion molecules varied as a function of the mean pulmonary pressure and the left ventricular ejection fracture (for cICAM-1: Pearson's r: 0.24 and -0.33, p < 0.05; for cVCAM-1: Pearson's r: 0.28 and -0.26, p < 0.05). In 38% (n = 16) of patients with elevated concentrations of cICAM-1 (> or = 337 ng/ml) and 41% (n = 7) of those with elevated serum levels of cVCAM-1 (> or = 1038 ng/ml), the myocardial biopsies showed increased lymphocytic infiltration between 7 and 22 T-lymphocytes/mm2 and an enhanced expression of the MHC antigens of class I/II as sign of an activated inflammatory process in the myocardium. All patients with more than 9.3 T-lymphocytes/mm2 in the myocardium (n = 7) had higher serum levels of cICAM-1 (447 +/- 146 ng/ml, p < 0.05 compared to controls) and of cVCAM-1 (1577 +/- 688 ng/ml, p < 0.001). Both adhesion molecules correlated significantly with the mean number of T-lymphocytes in the myocardium (Pearson's r: 0.31-0.37, p < 0.05). SUMMARY AND CONCLUSION: The present study shows that the elevated levels of cICAM-1 and cVCAM-1 are often found in the serum of patients with non-ischemic heart failure. These raised serum levels correlate with inflammatory infiltrates in the myocardial tissue and with the clinical and hemodynamic signs of heart failure, thus, confirming a connection between heart failure and inflammatory changes in the myocardium.

Adult↗
PubMed1998

Evidence of endothelial dysfunction of epicardial coronary arteries in patients with immunohistochemically proven myocarditis.

BACKGROUND: Recent reports indicate that myocarditis can be associated with acute myocardial ischemia and even myocardial infarction in patients with normal arteriograms. We therefore tested the hypothesis that patients with biopsy-proven myocarditis have endothelial dysfunction despite angiographically smooth epicardial coronary arteries. METHODS AND RESULTS: Graded concentrations of the endothelium-dependent vasodilator acetylcholine (10(-6) to 10(-4) mol/L) and for comparison, the non-endothelium-dependent vasodilator nitroglycerin (0.3 mg intracoronary), were infused into the left coronary arteries of 18 patients (mean age 47+/-9 years, 8 women and 10 men) with biopsy-proven myocarditis but without angiographically demonstrable coronary artery disease. Vascular responses were analyzed by quantitative coronary angiography. Three patients had an intact vasodilator response to acetylcholine concentrations of up to 10(-4) mol/L in all segments of the left coronary artery, with a mean dilatation of +9.9%+/-2%. In contrast, paradoxical constriction by acetylcholine occurred in 9 patients, who showed a mean change in coronary artery diameter of - 11%+/-3%. Six patients had no significant change in any segments in response to acetylcholine (-2.5%+/-4%). There was a significant inverse correlation between the number of T-lymphocytes in the myocardium and the response of the epicardial coronary arteries to acetylcholine (Pearson correlation coefficient -0.49, P=.03). CONCLUSIONS: It can be assumed that the process of myocarditis is associated with impairment of endothelium-dependent vasodilation in response to acetylcholine in most patients. Vasoconstriction in the presence of acetylcholine in myocarditis is likely to reflect an abnormality of endothelial function. Endothelial dysfunction of coronary arteries may explain the occurrence of myocardial ischemia in patients with myocarditis.

Acetylcholine↗
PubMed1998

The effects of nicotine on spatial and non-spatial expectancies in a covert orienting task.

The present study examined how nicotine influences shifts of visuo spatial attention in casual smokers at each of three delays after smoking one cigarette: immediately, 1 h and 24 h. Informative peripheral cues were used to exogenously orient attention to the location where an increase or decrease in the size of a peripheral object was most likely to occur. One size change was more likely to occur than the other and the task was choice (expansion/contraction) reaction time. The performance decrement obtained when the target appeared at an uncued location was smallest in sessions run immediately after smoking (when nicotine levels were highest), suggesting that nicotine may increase the ease with which attention can be disengaged from a cued location. This finding confirms previous research which suggests a specific role for the basal forebrain cholinergic system in visual orienting. In contrast, nicotine was not found to affect non-spatial expectancies based on stimulus-response (expansion/contraction) probability. These findings, together with recent converging evidence, strongly support the proposition that different attentional operations are mediated by different neural subsystems.

Adult↗
PubMed1998

Splitting versus sharing focal attention: comment on Castiello and Umiltà (1992).

A popular metaphor for visual attention is that of a spotlight that enhances perceptual processing within its beam. Many studies on the orienting of visual attention have addressed whether the beam is a unified structure or whether it can be split between noncontiguous locations in space. Although most of the evidence favors the unified model, U. Castiello and C. Umiltà (1992) claimed recently to have results that could most easily be accounted for by a model of visual attention in which resources can be allocated flexibly to independent locations in space. It is argued that Castiello and Umiltà used only indirect empirical evidence to support their position and that their results are not inconsistent with the unified model. Two studies are reported in which important aspects of Castiello and Umiltà's experiments were maintained and a probe procedure was implemented to assess directly if attention was split between 2 spatial locations or if a unified focus of attention was expanded to incorporate the 2 locations. The results clearly supported the latter position.

Attention↗
PubMed1998

A submaximal all-extremity exercise test to predict maximal oxygen consumption.

PURPOSE: Submaximal aerobic exercise testing is utilized with a variety of populations to assess fitness level and predict maximal oxygen uptake (VO2peak) when a maximal test is not possible or preferable. Many submaximal tests have been developed on traditional exercise equipment, such as the treadmill and the cycle ergometer, but are not available for newer equipment such as an all-extremity ergometer. The purpose of this study was to develop and validate a submaximal exercise test using the Pro II Power Trainer, an all-extremity ergometer, in women ages 30-60 without disability and with varying fitness levels. A secondary purpose was to compare VO2peak values achieved during the all-extremity maximal test and the treadmill test. METHODS AND RESULTS: A linear regression equation was developed to predict VO2peak from submaximal data using heart rates and power output at the sixth and ninth minutes of the submaximal test. The linear regression derived for the submaximal all-extremity test was VO2peak L.min-1 = -0.01 (age in years) - 0.0029 (HR 1) - 0.0099 (HR2) - 0.0029 (PO1) + 0.0151(PO2) + 3.010. Predicted residual sum of squares of the linear equation revealed an R2 value of 0.722 and standard error of estimate of 0.216 L.min-1. Treadmill VO2 speak values correlated strongly with all-extremity VO2 speak values (r = 0.918) and were not significantly different (P, 0.05). CONCLUSION: A similar submaximal test needs to be developed for field estimates of VO2peak for subpopulations of individuals with physical disabilities such as rheumatoid arthritis, head or spinal cord injury, cerebral vascular accident, multiple sclerosis, amputation, and cerebral palsy.

Adult↗
PubMed1998

Disinhibition of return: unnecessary and unlikely.

Recently, from data obtained with a temporal order judgment (TOJ) task, Gibson and Egeth (1994) concluded that inhibition of return (IOR; a response time effect that reveals slower responding to targets at previously cued versus uncued locations) reflects impaired perceptual processing. By replotting their data, we demonstrate that the perception of temporal order is influenced only by the facilitatory effect of a cue at short stimulus onset asynchronies (SOAs) and is unaffected by IOR at long SOAs. The target paper proposed that, when extra stimuli are presented at task-relevant locations (i.e., in the TOJ task), IOR is prevented by a hypothetical process that is known as disinhibition of return (DOR). We argue that the assumptions that IOR affects perceptual processing and that DOR exists are unnecessary, as a more parsimonious response-based interpretation of IOR is consistent with their data. Further, we summarize recent results and present new data that demonstrate that DOR is unlikely.

Humans↗
PubMed1998

[Results and complications of fiber bronchoscopy in HIV positive patients].

Fibreoptic bronchoscopy is an established diagnostic procedure for HIV-associated pulmonary infections. We retrospectively evaluated the diagnostic effectivity and safety of fibreoptic bronchoscopy with bronchoalveolar lavage (BAL) and transbronchial biopsy (TBB) in 153 patients with late-stage HIV infection and clinical signs of pulmonary infection or abnormal chest radiograph. Bronchoscopy leads to diagnosis in 82.4% and changed therapy in 54%. 45 patients (30%) were found to have pneumocystis carinii pneumonia (PCP), the most common bronchoscopic finding, followed by bacterial lung disease (29.3%). BAL had a sensitivity of 78% for PCP. Diagnostic yield of BAL for PCP was higher in patients without previous treatment (positive results in 82%) with regard to PCP independend of the prior treatment. Serious complication occurred in 22 cases (pneumothorax: 6 (3.9%), bleeding: 12 (7.8%), hypoxaemia: 4 (2.6%)). High serum levels of lactate dehydrogenase (LDH) correlated with pulmonary complications like pneumothorax. Age, sex and kind of pulmonary infection did not influence complication rates. 6 (3.9%) episodes of spontaneous pneumothorax occurred in the further course, 3 of them concurrently with PCP or prior history of PCP. We conclude that fibreoptic bronchoscopy is of great value for diagnosing pulmonary infection in HIV-seropositive patients. TBB provides incremental diagnostic information not available from BAL, especially in patients pretreated with cotrimoxazol or pentamidin. For that reason we believe that TBB should be performed in these patients.

AIDS-Related Opportunistic Infections↗
PubMed1998

Comparison of tamoxifen effects on the actions of triiodothyronine or growth hormone in the ovariectomized-hypothyroid rat.

Recent studies have suggested that a subset of estrogen responses arise via modulation of triiodothyronine (T3) actions, and depend on T3 for expression: other estrogen responses are not T3-dependent. Moreover, tamoxifen acts as a full estrogen agonist in T3-dependent responses but behaves as an antiestrogen in T3-independent responses. T3 directly induces a variety of metabolic enzymes and proteins, and also induces rat growth hormone (GH). Thus, some T3-dependent tamoxifen effects might reflect modulation of GH rather than T3 actions. To address this issue, tamoxifen effects on somatotropic and metabolic actions of T3 and GH were compared in ovariectomized rats with methimazole-induced hypothyroidism. Rats were given T3 (10 micrograms/kg/day) or ovine GH (2 mg/kg/day) with or without tamoxifen (0.5 mg/kg/day) for 30 days. GH was poorly effective in producing a sustained increase in somatic growth in hypothyroid rats compared to T3; nonetheless, GH effects to increase body weight, tibia length and serum insulin-like growth factor I while decreasing fat mass and evoking small increases in body temperature were not inhibited by tamoxifen. Tamoxifen also did not inhibit GH trends to increase tibia bone mineral density. T3 increased body temperature, insulin-like growth factor I levels and all measures of somatic growth and, unlike GH, increased food intake and tended to decrease tibia bone mineral density. Tamoxifen inhibited the somatotropic actions of T3 (including increases in insulin-like growth factor I levels), and produced significant increases in tibia bone mineral density only in T3-treated rats. Tamoxifen had no effect on T3 actions to increase food intake or body temperature. T3 alone increased fat mass and exhibited a tendency to decrease serum triglycerides: tamoxifen had no effect on these parameters in the absence of T3. However, coadministration of tamoxifen with T3 produced a marked decrease in fat mass and increased serum triglycerides. GH had no effect on serum triglycerides in either the presence or absence of tamoxifen. Serum glucose levels appeared normal in all groups. The data indicate that multiple tamoxifen effects on growth and metabolism may reflect modulation of T3 rather than GH actions.

Animals↗
PubMed1997

Early generation of glia in the intermediate zone of the developing cerebral cortex.

Radial glia are present at the earliest stage of cerebral cortical development, and later they transform into astrocytes. Other glial cells including astrocytes and oligodendrocytes are thought to appear only after neuron generation is complete and the cortical layers are formed. Little is known of when and where microglia enter the central nervous system and proliferate. We addressed the question of the origin of these three glial cell types in the developing ferret cerebral cortex. We assessed the temporal pattern of glial cell division by administering [3H]thymidine to label cells in S phase, and by using survival periods of 1-2 h to label dividing cells in situ. Labeled cells were identified in the developing intermediate zone of the ferret cerebral wall. These cells were present at E28, and reached a maximum number at P1. Double labeling experiments identified these cells as astrocytes, oligodendrocytes or microglia. None of the dividing cells expressed neuronal markers. These data show that all three types of glia are generated in the developing subcortical white matter, and that glial progenitors are present in the intermediate zone as soon as it becomes a recognizable structure. These data also show that the period of glial generation overlaps extensively with the period of neuron generation, since neuron generation is not complete until the end of the second postnatal week in the ferret.

Animals↗