A criterion setting theory of discrimination learning that accounts for anisotropies and context effects

We can discriminate departures from the vertical or horizontal more accurately than from other orientations. This may reflect perceptual learning, but the mechanisms behind such learning are not well understood. Here we derive a theory of discrimination learning based on criterion setting theory (CST; Treisman and Williams, 1984), an extension of signal detection theory in which judgment of the current stimulus is partly determined by previous discriminations and context. The CST-based theory of discrimination learning (CST-DL) describes mechanisms which use information from previous acts of discrimination to improve current decision making. CST-DL distinguishes between types of decision criteria and provides an account of anisotropies and context effects affecting discrimination. Predictions from this model are tested in experiments on anisotropies in orientation and depth perception. The results obtained support CST-DL. They also support the conclusion that the account of the retention of sensory information in delayed discrimination provided by CST is superior to the traditional belief that information retention relies on a fixed memory trace or representation of the stimulus.     

Tumor Necrosis Factor-alpha in Gingival Crevicular Fluid as a Diagnostic Marker for Periodontal Diseases: A Systematic Review

Objectives

The aim of this systematic review was to evaluate human gingival crevicular fluid (GCF) tumor necrosis factor-alpha (TNF-α) as a potential biomarker for diagnosis of periodontal disease (International prospective register of systematic reviews [PROSPERO] number: CRD42015020199).

Original Article: Comparison of A23187 vs Ionomycin-induced Responses and Cytosolic Calcium Increases in Aequorin-loaded Human Platelets. Evidence for Ionophore-specific Differences in Intracellular Calcium Release

The dose-dependent induction of platelet aggregation, dense granule secretion and thromboxane formation by the divalent cation ionophores A23187 and ionomycin were compared in citrated platelet rich plasma (PRP), and measured simultaneously with the increases in cytosolic Ca(2+) levels in aequorin-loaded gel-filtered platelet (GFP). In citrated PRP, both ionophores induced similar extents of aggregation at comparable concentrations, whereas A23187 induced somewhat greater extents of secretion, and substantially greater extents of thromboxane B(2) (TxB(2)) formation, than ionomycin. When 5 mM EDTA or EGTA was added to PRP secretion and TxB(2) formation occurred only with A23187; ionomycin was inactive at all concentrations tested, up to 100 pM. In aequorin-loaded GFP containing 1 mM Ca(2+), 1 mM EGTA or 2 mM EDTA, ionomycin as well as A23187 induced these platelet responses, but the concentration dose-response curve for ionomycin was shifted to the right by approximately one order of magnitude relative to that for A23187. Simultaneous measurements of the cytosolic Ca(2+) ([Ca(2+)](1)) increases induced by the two ionophores showed that the increases produced by ionomycin were consistently 2040% less than those induced by A23187 at all ionophore concentrations tested. Analysis of the extents of secretion and TxB, formation obtained in EDTA- or EGTA-containing systems as a function of the [Ca(2+)](1) increases suggested that the data for both ionophores were described by the same [Ca(2+)](1) dose-response curve, indicating that the decreased extents of these responses seen with ionomycin vs A23187 were due primarily, if not solely, to the lower [Ca(2+)], increases produced by ionomycin. Since ionomycin is theoretically capable of transporting twice as much divalent cation as A23187, these findings in platelets, together with similar findings in certain other cell systems, provide evidence that factors associated with the intracellular environment may differentially affect the abilities of A23187 and ionomycin to induce cellular responses and, more specifically, to release intracellular Ca(2+) stores.     

Heterogeneous abnormalities of platelet dense granule ultrastructure in 20 patients with congenital storage pool deficiency

Studies on platelet dense granule structure were carried out in 20 patients with various types of congenital storage pool deficiency (SPD), including 15 with specific deficiencies of dense granules and dense granule substances (δ-SPD), and five with combined deficiencies of dense and α-granules (αδ-SPD). Dense granules were identified by their high affinity for uranyl ions (uranaffin reaction), by their ability to accumulate the fluorescent dye mepacrine, and by their inherent electron opacity on unfixed, unstained whole mount preparations. By all these methods, dense granules were markedly decreased in seven albino patients with the Hermansky-Pudlak syndrome (HPS) variant of δ-SPD. These findings suggest that the basic defect in these patients is a specific abnormality in organelle development which prevents the formation of an intact granule structure, a quantitative abnormality which may differ from that in animals with related pigment disorders. In contrast, eight non-albino patients with δ-SPD had, on average, only a slightly reduced number of uranaffin-positive and mepacrine-positive granules, but a shift in uranaffin-granule distribution towards those lacking a dense core (‘empty granules’), suggesting a more qualitative type of dense granule defect. These results are consistent with previous evidence suggesting a decreased uptake of ATP across the granule membrane in δ-SPD. In addition, on whole mounts, these patients’platelets contained substantial numbers of electron dense chains and clusters which contained P and Ca, but with a P/Ca ratio less than that of typical dense granules, and which were retained, along with a larger amount of ATP, after thrombin treatment of the platelets. The various findings in these patients raise the possibility that these structures may represent microvesicles, derived from the Golgi apparatus, which provide a transport mechanism for concentrating adenine nucleotides and calcium in dense granules and which is impaired in some patients with SPD. Additional defects may account for the more extensive granule abnormalities observed in αδ-SPD.     

Photodynamic therapy associated with full-mouth ultrasonic debridement in the treatment of severe chronic periodontitis: a randomized-controlled clinical trial

Background:

Photodynamic therapy (PDT) is a method of microbial reduction which can benefit periodontal treatment in areas of difficult access, such as deep pockets and furcations. The aim of this randomized controlled clinical trial was to evaluate the effects of PDT as an adjunct to full-mouth ultrasonic debridement in the treatment of severe chronic periodontitis.

Material and Methods:

Twenty-two patients with at least one pocket with a probing depth (PD) of ≥7 mm and one pocket with a PD of ≥5 mm and bleeding on probing (BOP) on each side of the mouth were included, characterizing a split mouth design. The control group underwent full-mouth ultrasonic debridement and the test group received the same treatment associated with PDT. The PDT was performed on only one side of the mouth and the initial step consisted of subgingival irrigation with 0.005% methylene blue dye. Two minutes after applying the photosensitizer, the low power laser - AsGaAl (Photon Lase III - PL7336, DMC, São Carlos -São Paulo, Brazil) was applied (660 nm, 100 mW, 9 J, 90 seconds per site, 320 J/cm², diameter tip 600 µm).The following clinical parameters were evaluated: plaque index, gingival index, BOP, gingival recession (GR), PD, and clinical attachment level (CAL). All parameters were collected before, 1, 3 and 6 months after treatment.

Results:

An improvement in BOP, PD and CAL was observed after treatment, in both groups, but without any difference between them. After 6 months, the PD decreased from 5.11±0.56 mm to 2.83±0.47 mm in the test group (p<0.05) and from 5.15±0.46 mm to 2.83±0.40 mm in the control group (p<0.05). The CAL changed, after 6 months, from 5.49±0.76 mm to 3.41±0.84 mm in the test group (p<0.05) and from 5.53±0.54 to 3.39±0.51 mm in the control group (p<0.05).

Conclusion:

Both approaches resulted in significant clinical improvements in the treatment of severe chronic periodontits, however, the PDT did not provide any additional benefit to those obtained with full-mouth ultrasonic debridement used alone.     

Roux-en-Y Gastric Bypass Improves the Nonalcoholic Steatohepatitis (NASH) of Morbid Obesity

Background: Hepatic steatosis and nonalcoholic steatohepatitis (NASH) have been increasingly implicated in the genesis of hepatic fibrosis and cirrhosis. However, no consensus exists about whether weight reduction may reverse this process. Methods: To assess the effect of Roux-en-Y gastric bypass (RYGBP) on the histological evolution of NASH diagnosed in 64 patients by routine liver biopsy ("first" biopsy) performed during surgery, we performed a "second" biopsy after 23.5 ± 8.4 months in 16 patients (14 female, 2 male). Results: From the first to the second biopsy, BMI decreased from 53.4 ± 8.8 kg/m² to 31.1 ± 4.7 kg/m², arterial hypertension decreased from 75% to 43.8%, and type 2 diabetes decreased from 43.8% to zero. On the first biopsy, nonalcoholic fatty liver disease (NAFLD) type 3 was observed in 12 patients (75%) and type 4 in 4 (25%). The second biopsy revealed complete regression of NAFLD in 15 patients (93.7%) and only 1 (6.3%) had NAFLD type 1 (mild steatosis without inflammation). Complete regression of necroinflammatory activity was observed in all patients. Among the 4 patients presenting fibrosis in the first biopsy, complete remission was observed in 1 and improvement in 1. Two continued to show the same degree of fibrosis without evidence of disease activity. No worsening of steatosis, necroinflammatory activity or fibrosis was observed in any of the patients, and none progressed to cirrhosis. Conclusion: RYGBP improves steatosis, necroinflammatory activity and hepatic fibrosis in patients with morbid obesity and NASH.     

Modulating motion-induced blindness with depth ordering and surface completion

Motion-induced blindness is a striking phenomenon in which salient static visual stimuli "disappear" for seconds at a time in the presence of specific moving patterns. Here we investigate whether the phenomenon is due to surface completion of the moving patterns. Stereo-depth information was added to the motion stimulus to create depth ordering between the static and moving components of the display. Depth ordering consistent with the perceptual occlusion of the static elements increased motion-induced blindness whereas placing the moving components behind the static elements decreased the static dot disappearance. In a second experiment we used an induced surface stimulus configuration to drive the motion-induced blindness phenomenon as further evidence of the importance of surface completion and interactions during visual processing.     

Inhibition of human platelet function in vitro and ex vivo by acetaminophen

The effects of acetaminophen (APAP) in vitro, or ex vivo following APAP ingestion, on human platelet aggregation, ¹⁴C-5HT secretion, and thromboxane B₂ (TxB₂) formation were assessed. APAP added in vitro to citrated platelet-rich plasma (PRP) inhibited aggregation, secretion, and TxB₂ formation induced by collagen, epinephrine, arachidonate, and the ionophore A23187, but had no effect on the responses induced by the endoperoxide analog U44069. Arachidonate-induced responses were inhibited by lower concentrations of APAP than were the responses to the other agonists. In PRP obtained 1 hour after ingestion of 650 mg or 1000 mg APAP, arachidonate-induced TxB₂ formation was inhibited by 40–99% in five subjects tested, whereas inhibition of collagen- or epinephrine-induced TxB₂ formation was less consistent. Aggregation and secretion responses were not altered by APAP ingestion m 4 of the 5 subjects, but were inhibited in the remaining subject, who had the highest plasma APAP levels. In contrast to aspirin and indomethacin, APAP-induced inhibition of collagen-stimulated TxB₂ formation could be partially overcome with increasing collagen concentrations. No such partial correction occurred with epinephrine, however. In washed platelet suspensions labeled with ³H-arachidonate, both APAP and aspirin inhibited the formation of labeled PGD₂ and PGE₂, as well as TxB₂. These results suggest that APAP acts in human platelets as a reversible inhibitor of cyclo-oxygenase, as found previously in other tissues, and that recent APAP ingestion can, on occasion, produce inhibition of platelet functional responses measured in vitro.