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Biomedical subjects

K Krug

Publications and source records attributed to K Krug.

At least 19 recordsLinked to original sources

In situ surface x-ray diffraction studies of homoepitaxial electrochemical growth on Au(100).

Direct in situ x-ray surface scattering studies of growth at a solid-liquid interface are demonstrated using the homoepitaxial electrodeposition on Au(100) as an example. With decreasing potential transitions from step-flow to layer-by-layer growth, manifested by layering oscillations in the x-ray intensity, then to multilayer growth, and finally back to layer-by-layer growth were observed. This complex growth behavior can be explained by the effect of anion coadsorbates and the potential-dependent Au surface reconstruction on the Au surface mobility.

Journal Article↗

Comparing perceptual signals of single V5/MT neurons in two binocular depth tasks.

Neurons in the extrastriate visual area V5/MT show perceptually relevant signals in binocular depth tasks, which can be measured as a choice probability (CP) for the neuron. The presence of a CP in a particular paradigm may be an indicator that the neuron is generally part of the substrate for the perception of binocular depth. We compared the responses of those single neurons that show CPs in one stereoscopic depth task with their responses in another stereo task. Each neuron was tested for the presence of 1) CPs during a task in which macaques responded to the sign of binocular depth in a structure-from-motion stimulus, to judge its direction of three-dimensional rotation and 2) a consistent response to the stereo disparity of binocularly anti-correlated stimuli. Previous work, confirmed here, shows that changing the disparity of these binocularly anti-correlated stimuli often fails to yield a coherent change in the depth percept. For each test alone, there are V5/MT neurons that carry signals that are congruent with the perceptual effects. However, on comparing tests, there is no fixed pool of neurons that can account for the binocular depth percept. Excitation of neurons with a measurable CP does not necessarily lead to a change in perception. The cortical circuitry must be able to make dynamic changes in the pools of neurons that underlie perceptual judgments according to the demands of the task.

Action Potentials↗

Perceptually bistable three-dimensional figures evoke high choice probabilities in cortical area MT.

The role of the primate middle temporal area (MT) in depth perception was examined by considering the trial-to-trial correlations between neuronal activity and reported depth sensations. A set of moving random dots portrayed a cylinder rotating about its principal axis. In this structure-from-motion stimulus, the direction of rotation is ambiguous and the resulting percept undergoes spontaneous fluctuations. The stimulus can be rendered unambiguous by the addition of binocular disparities. We trained monkeys to report the direction of rotation in a set of these stimuli, one of which had zero disparity. Many disparity-selective neurons in area MT are selective for the direction of rotation defined by disparity. Across repeated presentations of the ambiguous (zero-disparity) stimulus, there was a correlation between neuronal firing and the reported direction of rotation, as found by Bradley et al. (1998). Quantification of this effect using choice probabilities (Britten et al., 1996) allowed us to demonstrate that the correlation cannot be explained by eye movements, behavioral biases, or attention to spatial location. MT neurons therefore appear to be involved in the perceptual decision process. The mean choice probability (0.67) was substantially larger than that reported for MT neurons in a direction discrimination task (Britten et al., 1996). This implies that MT neurons make a different contribution to the two tasks. For the depth task, either the pool of neurons used is smaller or the correlation between neurons in the pool is larger.

Action Potentials↗

Responses of neurons in neonatal cortex and thalamus to patterned visual stimulation through the naturally closed lids.

In studies of the developing mammalian visual system, it has been axiomatic that visual experience begins with eye-opening. Any role for neuronal activity earlier in development has been attributed to the patterned spontaneous activity found in retina and lateral geniculate nucleus (LGN). Here we show that, as early as 2 wk before eye-opening, visual stimuli presented through the closed eyelids can drive neuronal activity in LGN and striate cortex of the ferret. At this age, spontaneous activity in cortex is much lower than in LGN, and the visual responses of many cortical, but not geniculate, neurons depend on the orientation of a moving grating. Furthermore the selectivity of cortical neurons to the orientation of gratings presented through the closed eyelids improves with age. Thus neuronal activity patterned by visual experience, rather than by spontaneous retinal activity, is present in visual cortex much earlier than previously thought. This could have important implications for the self-organization of visual cortex.

Action Potentials↗

The development of topography in the hamster geniculo-cortical projection.

Precise point-to-point connectivity is the basis of ordered maps of the visual field. The immaturity of the newborn hamster's visual system has allowed us to examine emerging topography in the geniculo-cortical projection well before thalamic axons have reached their cortical target, layer IV. Using anterograde transneuronal labeling with wheat germ agglutinin conjugated to horseradish peroxidase (WGA-HRP), we visualized the ingrowth of the whole population of geniculate fibers in the neonatal hamster. Two days after birth (P2), the bulk of the fibers is in the deep cortical layers and the subplate. At the same age, injections of paired retrograde tracers (red and green fluorescent latex microspheres) into area 17 reveal an unordered projection from the dorsal lateral geniculate nucleus (dLGN) to cortex. Individual labeled cells are found throughout the dLGN, and quantitative analysis reveals no segregation of the red and the green populations. At P6, when the pattern of geniculate back label appears ordered and essentially adult-like, geniculate fibers have reached layer IV. The role of selective cell death in this process was investigated by making a tracer injection at P2 and allowing the animals to survive to P6 or P12, when the map is mature. The results show early labeled neurons that made inappropriate connections when the projection was scattered surviving through the period of geniculate cell death. We conclude that the geniculo-cortical map develops from an initially unordered projection to the subplate and the lower cortical layers. Selective cell death appears not to contribute significantly to this process.

Animals↗

Spatial-frequency tuning and geniculocortical projections in the visual cortex (areas 17 and 18) of the pigmented ferret.

We have examined the spatial-frequency selectivity of neurons in areas 17 and 18 of the adult pigmented ferret, by measuring how the amplitude of response depends on the spatial-frequency of moving sinusoidal gratings of optimal orientation and fixed contrast. Neurons in area 17 of the ferret respond optimally to low spatial frequencies [average 0.25 cycles per degree (c/deg)], much lower than the optima for cat area 17. The tuning curves are of the same form as those found in cat and monkey: unimodal with bandwidths in the range 0.8-3.5 octaves. Neurons in area 18 of the ferret respond optimally to even lower spatial frequencies (average 0.087 c/deg) than area 17 neurons, and the distributions of optimal spatial frequency for areas 17 and 18 hardly overlap. In both cortical areas, the bandwidth of the tuning curves is inversely correlated with optimal spatial frequency. This marked difference in tuning between the two cortical areas is probably attributable to differential geniculo-cortical projections. Small injections of fluorescent latex microspheres or horseradish peroxidase (HRP) were made into area 17 or area 18 in order to investigate the populations of geniculate neurons projecting to the two cortical areas. After injections into area 17, labelled neurons are found predominantly in the geniculate A layers, with a few neurons labelled in the C layers. Conversely, after an area 18 injection, similar numbers of labelled neurons are found in the C layers as in the A layers. Soma-size analysis of the neurons in the A-layers suggests the existence of two populations of relay neurons, which project differentially to areas 17 and 18. The different geniculate inputs and the different spatial-frequency tuning in areas 17 and 18 may imply that the two cortical areas process visual information more in parallel than in series.

Animals↗

Mitogenic, melanogenic, and cAMP responses of cultured neonatal human melanocytes to commonly used mitogens.

The following studies have been undertaken to compare and correlate the effects of 12-O-tetradecanoylphorbol acetate (TPA), basic fibroblast growth factor (bFGF), cholera toxin (CT), and isobutyl methylxanthine (IBMX) on neonatal human melanocyte (NHM) proliferation, tyrosinase activity, and cyclic adenosine monophosphate (cAMP) concentration. NHM proliferated at a maximal rate in medium containing 8 nM TPA, 200 ng/ml CT, and 10(-4) M IBMX. TPA alone did not result in optimal melanocyte proliferation, and, as previously shown, its mitogenic effect was greatly enhanced by the addition of CT and IBMX individually or concomitantly. Human recombinant (hr) bFGF could replace TPA in the NHM growth medium. Maximal proliferation was achieved using 3 ng/ml hrbFGF, 20 ng/ml CT, and 10(-4) M IBMX. The mitogenic effect of 1.2 ng/ml hrbFGF was potentiated in the concomitant but not individual presence of CT and IBMX. TPA alone in the absence of CT and IBMX caused a dose-dependent stimulation of tyrosinase activity. Maximal tyrosinase activity was obtained in the presence of 0.8 nM TPA, 20 ng/ml CT, and 10(-4) M IBMX. Unlike TPA, hrbFGF alone resulted in inhibition of tyrosinase activity. In the presence of hrbFGF, tyrosinase activity was potentiated by CT and IBMX, but not by CT alone. Neither TPA nor hrbFGF alone could increase intracellular cAMP levels. The effects of CT and IBMX on intracellular cAMP concentration were enhanced to a greater extent by TPA than by hrbFGF. Under our experimental conditions, in the presence of hrbFGF, CT but not IBMX resulted in a dose-dependent increase in cAMP concentration. Further studies on NHM will be aimed at determining the exact role of protein kinase C (PKC) in regulating proliferation and melanogenesis and the mechanism(s) activated by hrbFGF.

1-Methyl-3-isobutylxanthine↗

The long-term antihypertensive effects of prazosin and atenolol.

The efficacy and tolerability of the alpha-blocker prazosin was compared with that of atenolol, a beta-blocker, in the long-term treatment of uncomplicated, essential hypertension. Twelve patients were randomly assigned to prazosin treatment and 15 to treatment with atenolol. Drug therapy was titrated to reduce diastolic blood pressure by 10 mm Hg or to below 89 mm Hg, whichever was lower. If monotherapy with either study drug failed to do this, hydrochlorothiazide was added to the regimen. Once blood pressure control was established, patients received maintenance therapy at that dosage and were followed for up to 12 months. Blood pressure, side effects, and plasma lipid levels were monitored during this period. Seventy-five percent of patients receiving prazosin monotherapy attained blood pressure goals, compared with 60 percent of patients given atenolol monotherapy. With the addition of low-dose hydrochlorothiazide, those patients not having an adequate response to monotherapy attained blood pressure control. Blood pressure reductions were maintained without dosage adjustment throughout the maintenance period; patient acceptance was good, and there was no evidence of tolerance. Treatment with atenolol produced slight increases in plasma triglyceride levels and little change in total or low-density lipoprotein cholesterol. In contrast, patients treated with prazosin demonstrated no adverse effects with regard to lipid levels. Although a higher percentage of patients reached goal blood pressure with prazosin monotherapy than with atenolol, the response rates were comparable when hydrochlorothiazide was added to the regimens.

Atenolol↗

[Clinical aspects and prognosis of highly malignant non-Hodgkin's lymphomas].

Clinical data and courses of the disease of 56 patients with non-Hodgkin-lymphomas of high malignancy were demonstrated. The age-depending summit of the frequency was between the 51st and 60th year of age, the age median was about 48 years. The initial remission rate three months after the beginning of the therapy was 66%. Out of the responders in 44% relapsed, in which cases 70% of the relapses developed in the first year after the beginning of treatment. After twelve months the survival rate was 0.52 and after 48 months 0.32. Patients with initial remission, with localized stages I and II (Ann Arbor) as well as with primarily extranodal manifestation and with histology of centroblastoma had a clear prognostic advantage. Initial B-symptomas, an advanced stage of the disease and a histology of immunoblastoma and lymphoblastoma as well were negatively correlated to the prognosis.

Adolescent↗

[Adenosine deaminase activity in Hodgkin's disease (author's transl)].

The activity of adenosine deaminase (ADA) (EC3.5.4.4.) was determined in the blood plasma, erythrocytes, and lymphocytes of 23 patients with Hodgkin's disease and partly also in 99 control subjects. The enzyme activities were measured using adenosine as substrate and by analysis of ammonia. No correlation was found between the ADA activities in lymphocytes, erythrocytes, and blood plasma. The lymphocytes of the patients revealed lower ADA activities (U/g protein) than the lymphocytes of control subjects. The ADA activity is not reduced in plasma or erythrocytes. The lower activities of ADA in the lymphocytes of patients may be related to the impaired cell-mediated immunity of the Hodgkin's disease.

Adenosine Deaminase↗

[Megakaryocytic pseudomyelosis with severe thrombocytosis].

A 66-year-old female patient complained of loss of body weight and fatigue. The clinical examination revealed a thrombocytosis with a maximum count of 3.200 . 10(9) platelets and a leukocytosis with maximally 25 . 10(9) white cells in the peripheral blood. The bone marrow showed a large increase of megakaryocytes. Under the diagnosis of megakaryocytic myelosis a chemotherapy with 186 mg busulfan was performed. In the course of this treatment the clinical picture of a sepsis occurred which could not be controlled by antibiotics. The patient died four months after her admission to the clinic. The essential findings in autopsy were a caseous tuberculosis of the lymph nodes with haematogenic generalization which appeared as a septic tuberculosa gravissima ("typhobacillosis" Landouzy). The bone marrow was atrophic. Spleen liver and lymph nodes were without evidence for a myeloproliferative disorder. Thus, the initial diagnosis had to be changed to a megakaryocytic pseudomyelosis with massive thrombocytosis as a reaction to the tuberculous infection. The differential diagnosis of megakaryocytic myelosis, other disorders of the myeloproliferative syndrome, and the reactive thrombocytosis are discussed.

Aged↗

[Adenosine deaminase activity in leukemia patients].

The activities of adenosine deaminase (ADA) were measured in the blood plasma, erythrocytes, and lymphocytes of healthy reference persons and in patients affected with leukaemia. ADA is increased in patients with acute immature cell leukaemia, in patients with chronic lymphatic leukaemia it is comparatively low in lymphocytes. In chronic myeloic leukaemia ADA activities are different depending on the activity of the disease. ADA-activities in the blood plasma, erythrocytes, and lymphocytes do not correlate with each other. ADA-activities in leukaemias may be regarded as an indicator of increased purin metabolism rather a as parameter of disturbed cellular immunofunction.

Acute Disease↗