Long-term tooth survival and success following primary root canal treatment: a 5- to 37-year retrospective observation.

OBJECTIVES: The aims of the present longitudinal retrospective observational case series study were to investigate the survival and success rates of primary non-surgical endodontic therapy. MATERIALS AND METHODS: Patients with at least one endodontically treated tooth (ETT), with 5 years of follow-up and in compliance with the recall programme of at least 1 time per year in a private practice setting, were recruited. Kaplan-Meier survival analyses were performed considering (a) tooth extraction/survival and (b) endodontic success as the outcome variables. A regression analysis was performed to evaluate prognostic factors associated with tooth survival. RESULTS: Three hundred twelve patients and 598 teeth were included. The cumulative survival rates showed 97%, 81%, 76% and 68% after 10, 20, 30 and 37 years, respectively. The corresponding values for endodontic success were 93%, 85%, 81% and 81%, respectively. CONCLUSIONS: The study demonstrated high longevity in symptomless function as well as high success rates of ETT. The most significant prognostic factors associated with tooth extraction were the presence of deep (> 6 mm) periodontal pockets, the presence of pre-operative apical radiolucency and the lack of occlusal protection (no use of a night guard). CLINICAL RELEVANCE: The favourable long-term (> 30 years) prognosis of ETT must encourage clinicians to rely on primary root canal treatment when taking the decision regarding whether a tooth with pulpal and/or periapical diseases should be saved or be extracted and replaced with an implant.

Neighbors affect vocal behavior of tropical wrens: a multispeaker density-manipulation experiment.

For territorial animals, the behavior of conspecific neighbors sets the social context of communication. Despite numerous investigations of vocalizations related to territory defense and mate attraction, the effect of neighbor density on animal vocal behavior has received little attention, particularly in tropical animals and animals where both sexes produce complex acoustic signals. In this study, we used an innovative multispeaker playback experiment to manipulate the apparent density of neighbors in rufous-and-white wrens, Thryophilus rufalbus, living in Costa Rica's tropical dry forest. In this tropical songbird, both males and females defend year-round territories and sing complex, learned songs for territory defense. We recorded the singing behavior of 24 subjects (12 pairs), and then we used an array of 6 loudspeakers to simulate the presence of 6 new territorial neighbors (3 simulated pairs) outside each subject pair's breeding territory. The stimuli persisted for 3 consecutive days, with both male and female songs broadcast at a natural rate from dawn to dusk. We found that the mean male song rate increased by almost 50% in response to the simulated increase in local density. Females showed less frequent song-type switching rates following the simulated increase in local density, although it was a marginal increase. These findings reveal that male and female songbirds' vocal behavior varies with the local density of territorial neighbors. We conclude that birds are sensitive to acoustic signals of conspecific density arising from sounds beyond their territory boundaries, and that they use this public information to guide their vocal behavior.

Presence of a functional receptor for GLP-1 in osteoblastic cells, independent of the cAMP-linked GLP-1 receptor.

Glucagon-like peptide 1 (GLP-1) controls glucose metabolism in extrapancreatic tissues through receptors other than the pancreatic cAMP-linked GLP-1 receptor; also, GLP-1 induces an insulin- and PTH-independent bone anabolic action in insulin-resistant and type-2 diabetic rats. Here we searched for the presence and characteristics of GLP-1 receptors in osteoblastic MC3T3-E1 cells. [(125)I]-GLP-1 specific binding to MC3T3-E1 cells was time- and temperature-dependent, reaching maximal value at 30 min at 25 degrees C; in these conditions, [(125)I]-GLP-1 binding was dissociable, and displaced by GLP-1, partially by GLP-2, but not by exendin-4 (Ex-4), exendin-9 (Ex-9), glucagon or insulin; Scatchard analysis of the unlabeled GLP-1 data showed high and low affinity binding sites; cross-linking of GLP-1 binding revealed an estimated 70 kDa band, almost undetectable in the presence of 10(-6) M GLP-1. GLP-1, Ex-9, insulin or glucagon failed to modify cellular cAMP content, while GLP-2 and Ex-4 increased it. However, GLP-1 induced an immediate hydrolysis of glycosylphosphatidylinositols (GPIs) generating short-lived inositolphosphoglycans (IPGs), and an increase in phosphatidylinositol-3 kinase (PI3K) and mitogen activated protein kinase (MAPK) activities; Ex-4 also affected GPIs, but its action was delayed with respect to that of GLP-1. This incretin was found to decrease Runx2 but increased osteocalcin gene expression, without affecting that of osteoprotegerin or the canonical Wnt pathway activity in MC3T3-E1 cells which do not express the pancreatic GLP-1 receptor. Our data demonstrate for the first time that GLP-1 can directly and functionally interact with osteoblastic cells, possibly through a GPI/IPG-coupled receptor.

Effect of exendin-4 treatment upon glucose uptake parameters in rat liver and muscle, in normal and type 2 diabetic state.

Exendin-4, like GLP-1, is insulinotropic, antidiabetic and glucoregulatory among other properties, which are thought to be exerted through the pancreatic GLP-1 receptor; exendin-4 is also an agonist of the GLP-1 stimulatory action upon liver and muscle glucose metabolism, where GLP-1 receptor is distinct from that in the pancreas. We investigated the action of prolonged treatment with exendin-4 upon glucose transport parameters in skeletal muscle and liver of normal rats and streptozotocin-induced type 2 diabetic rats (T2D). Muscle of T2D showed lower than normal glucose transport; exendin-4 did not modify the value in normal but normalized that in the T2D; unlike previously detected with GLP-1, no apparent modification was observed in GLUT-4 expression in either group after exendin-4, except for an increased GLUT-4 protein in normal rats. Yet, exendin-4 significantly stimulated liver GLUT-2-mRNA and -protein in T2D and normal rats, the effect upon GLUT-2-protein in T2D being higher than that in normal animals; this was accompanied by a normalizing action of exendin-4 upon the lower than normal liver glycogen in T2D rats. These data suggest that the liver may represent at least one of the major target organs for exendin-4 to exert its plasma lowering effect in diabetic state.

Characteristics of GLP-1 and exendins action upon glucose transport and metabolism in type 2 diabetic rat skeletal muscle.

Exendin-4, a peptide 53% structurally homologous with glucagon-like peptide 1 (GLP-1), is insulinotropic and has an antidiabetic effect even more prolonged than that of GLP-1. Exendin-9 is an antagonist of GLP-1 receptor and action in several cell systems, but shows GLP-1- and exendin-4-agonistic characteristics in human muscle cells and tissue. The action of GLP-1 upon glucose transport and metabolism in muscle is mediated by specific receptors. In this study we investigated the effect of both exendin-4 and -9, relative to that of GLP-1, upon glucose transport and metabolism in the skeletal muscle from a streptozotocin-induced type 2 diabetic rat model, compared to normal. In normal rats, exendin-4, like GLP-1 and insulin, enhanced glucose uptake. This effect, which is mediated to a certain extent by some kinases (PI3K/ PKB, p70s6k and MAPKs), may be caused by the peptide acting, at least in part, through the muscle GLP-1 receptors. Exendin-9 also stimulated the same kinases, except for PKB, but failed to modify basal glucose uptake. Type 2 diabetic rats showed lower than normal basal muscle glucose transport and oxidation value, and higher glycogen synthase alpha activity and pyruvate release; however, no modification of glucose uptake by GLP-1 or exendin-4 was detected, at variance with insulin, and basal activity of PI3K/PKB was lower than normal, while that of p70s6k and MAPKs was higher. GLP-1 failed to affect the activity of any of the kinases, while exendin-4 increased the activity of PI3K, p70s6k and MAPKs, but not PKB, suggesting that this enzyme plays a major role in exendin-4 effect upon glucose transport in muscle.

The action of GLP-1 and exendins upon glucose transport in normal human adipocytes, and on kinase activity as compared to morbidly obese patients.

A role of GLP-1 (glucagon-like peptide-1) in the recovery of the metabolic conditions of morbidly obese patients after bariatric surgery has been proposed. Exendin 4 (Ex-4) and exendin 9 (Ex-9) both have GLP-1-like effects upon glucose metabolism in human myocytes. We investigated in normal human adipocytes the effect of GLP-1, Ex-4 and Ex-9, compared with insulin upon the activity of PI3K, PKB, MAPKs and p70s6 kinases, and the participation of these enzymes in their action upon 2-deoxy-D-glucose transport by using potential inhibitors. The study was extended to morbidly obese patients. In normal subjects, GLP-1, Ex-4 and insulin, but not Ex-9, increased glucose uptake. In addition, GLP-1 and Ex-4 stimulated PI3K and MAPKs, similar to insulin, but not PKB. Ex-9 only enhanced PI3K, while none affected p70s6k. Inhibition of both PI3K and MAPKs blocked the stimulatory action of GLP-1, Ex-4 and insulin upon glucose transport. In obese patients, basal PI3K, PKB and MAPK activity was, as a rule, lower than that in normal subjects, while cells maintained their normal incremental response to GLP-1, Ex-4 or insulin; Ex-9 induced a clear stimulation of p42 MAPK. In summary, in normal human adipocytes, GLP-1 and Ex-4 have a protein kinase-dependent increasing effect upon glucose transport, which is impaired in obese patients. The participation of GLP-1 in the normalization of the metabolic conditions of the obese may occur through its effects on lipid metabolism or through effects upon glucose transport and/or metabolism in the liver and muscle, which in human obesity remain to be investigated.

Speech rhythm alterations in Spanish-speaking individuals with Alzheimer's disease.

Rhythm is the speech property related to the temporal organization of sounds. Considerable evidence is now available for suggesting that dementia of Alzheimer's type is associated with impairments in speech rhythm. The aim of this study is to assess the use of an automatic computerized system for measuring speech rhythm characteristics in an oral reading task performed by 45 patients with Alzheimer's disease (AD) compared with those same characteristics among 82 healthy older adults without a diagnosis of dementia, and matched by age, sex and cultural background. Ranges of rhythmic-metric and clinical measurements were applied. The results show rhythmic differences between the groups, with higher variability of syllabic intervals in AD patients. Signal processing algorithms applied to oral reading recordings prove to be capable of differentiating between AD patients and older adults without dementia with an accuracy of 87% (specificity 81.7%, sensitivity 82.2%), based on the standard deviation of the duration of syllabic intervals. Experimental results show that the syllabic variability measurements extracted from the speech signal can be used to distinguish between older adults without a diagnosis of dementia and those with AD, and may be useful as a tool for the objective study and quantification of speech deficits in AD.

Effect of GLP-1 on D-glucose transport, lipolysis and lipogenesis in adipocytes of obese subjects.

GLP-1 has anorectic properties and regulates fuel homeostasis through both its insulinotropic and insulinotrophic actions and effects in extrapancreatic tissue. This study is aimed at characterizing the response to GLP-1 of adipocytes from obese patients, in terms of D-glucose transport and lipid metabolism, in comparison with data from normal subjects. Adipocytes were obtained by enzymatic digestion from the abdominal fat tissue of 25 morbidly obese patients and 8 normal subjects undergoing bariatric or inguinal hernia surgery, respectively. Basal GLUT4 expression, D-glucose transport, glycerol release and lipogenesis were measured in cells treated, when required, with 10(-12)-10(-9) M GLP-1, insulin, glucagon and the GLP-1 structurally related peptides, exendin-4 and exendin-9. In obese patients, versus normal subjects, a trend towards lower values was found in GLUT4 protein or mRNA, although the differences were not statistically significant; insulin-stimulated glucose uptake was higher and cells did not respond to GLP-1, while both exendins (10(-10) and 10(-9) M) exerted an inhibitory action; basal lipolysis was higher and so was the effect of GLP-1 and glucagon, whereas insulin abolished the lipolytic action of all peptides; both basal lipogenesis and the response to insulin were higher while GLP-1 and exendin-4 were ineffective. These results document the analogies and dissimilarities between the response to GLP-1, exendin-4 and exendin-9, as well as to insulin and glucagon, relative to glucose transport and lipid metabolism of fat tissue from obese patients versus normal subjects, the reduced lipogenic effect and enhanced lipolytic action of GLP-1 being, perhaps, adequate for its therapeutic use in obesity.

Effects of glucagon-like peptide-1 and exendins on kinase activity, glucose transport and lipid metabolism in adipocytes from normal and type-2 diabetic rats.

Several kinases have been implicated in the metabolic response of human and rat myocytes to glucagon-like peptide-1 (GLP-1), exendin-4 (Ex-4) and exendin-9 (Ex-9). We have investigated, in isolated rat adipocytes, the changes caused by GLP-1, Ex-4 and Ex-9 compared with those provoked by insulin or glucagon, upon the activity of phosphatidylinositol-3-kinase (PI3K), protein kinase B (PKB), p42/44 MAP kinases (MAPKs) and p70s6 kinase (p70s6k), and the participation of these kinases and protein kinase C (PKC) in their action upon 2-deoxy-d-glucose uptake, lipolysis and lipogenesis. The study was conducted in normal rats, and extended to a streptozotocin-induced type-2 diabetic model (STZ-rats). The participation of distinct kinases was estimated by using potential kinase inhibitors, including wortmannin, PD98059, rapamycin, H-7 and RO31-8220. In normal rat adipocytes, GLP-1 and both exendins share with insulin an increasing action upon the activity of all kinases studied (except PKB), PI3K, p44 and p42 MAPKs and possibly PKC, all being required for their stimulating effect upon glucose uptake. Ex-4 and Ex-9, like GLP-1 and insulin, have lipogenic action, while only Ex-4 shares with GLP-1 its lipolytic effect which is antagonized by Ex-9. MAP kinases and PKC seem to have an essential role in the GLP-1 and Ex-4 lipolytic action, as does PI3K in that of Ex-4. An increase in PI3K and MAPKs activity for the lipogenic effect of Ex-4, Ex-9 and GLP-1 are required, and in the case of Ex-4 and Ex-9, a stimulation of p70s6k activity is also needed. In cells from STZ-rats the magnitude of the above parameters was, in general, comparable to that in normal animals, with some exceptions: basal PI3K activity and lipogenesis were higher, GLP-1, Ex-4 and Ex-9 failed to modify basal lipogenesis but increased PKB activity, insulin failed to affect the activity of MAPKs and the insulin-induced glucose uptake was impaired. The impaired insulin effects upon some of the variables in the STZ-rat, distinct from those of GLP-1 and exendins, adds knowledge to the mechanism of the beneficial action of GLP-1 and Ex-4 in diabetic states.

Changes in glucagon-like peptide-1 (GLP-1) secretion after biliopancreatic diversion or vertical banded gastroplasty in obese subjects.

BACKGROUND: Bariatric operations promote weight loss and improve glucose homeostasis. Glucagon-like peptide-1 (GLP-1) is considered as a possible mediator of the antidiabetic effects of such operations. METHODS: The present study aimed to gain information on the time course for changes in glucose tolerance, as well as insulin, glucagon and GLP-1 secretion, during an oral glucose tolerance test (OGTT), in 31 obese patients examined 1, 3 and 6 months after Larrad's biliopancreatic diversion (BPD) or 6 months after vertical banded gastroplasty (VBG). RESULTS: A time-related progressive decrease in body weight coincided with lowering of plasma triglycerides, decrease of basal plasma glucose and its incremental area during OGTT, and reduction of basal plasma insulin together with an increase of its incremental area. The time-related decrease of plasma glucagon during OGTT was comparable before and after surgery. Both the basal plasma GLP-1 concentration and its incremental area during the OGTT increased strikingly after surgery, a steady-state situation being reached 3 months after surgery. The most striking differences between the somewhat older and less glucose-tolerant subjects of VBG compared to BPD after surgery, consisted in a decrease in cholesterol and LDL only observed in BPD and a much more pronounced increase in basal and incremental plasma GLP-1 in BPD. GLP-1, like glucagon, increased lipolysis, but failed to duplicate the lipogenetic action of insulin in isolated adipocytes obtained at the time of surgery. CONCLUSION: These findings support the postulated role of GLP-1, secreted by the hindgut, as a key mediator of the antidiabetic effects of bariatric operations.

Effect of GLP-1 on glucose transport and its cell signalling in human myocytes.

Glucagon-like peptide-1 (GLP-1) controls glucose metabolism in extrapancreatic tissues participating in glucose homeostasis, through receptors not associated to cAMP. In rat hepatocytes, activation of PI3K/PKB, PKC and PP-1 mediates the GLP-1-induced stimulation of glycogen synthase. We have investigated the effect of GLP-1 in normal human myocytes, and that of its structurally related peptides exendin-4 (Ex-4) and its truncated form 9-39 (Ex-9) upon glucose uptake, and the participation of cellular enzymes proposed to mediate insulin actions. GLP-1 and both exendins activated, like insulin, PI3K/PKB and p42/44 MAPK enzymes, but p70s6k was activated only by GLP-1 and insulin. GLP-1, Ex-4 and Ex-9, like insulin, stimulated glucose uptake; wortmannin blocked the action of GLP-1, insulin and Ex-9, and reduced that of Ex-4; PD98059 abolished the effect of all peptides/hormones, while rapamycin blocked that of insulin and partially prevented that of GLP-1. H-7 abolished the action of GLP-1, insulin and Ex-4, while Ro 31-8220 prevented only the Ex-4 and Ex-9 effect. In conclusion, GLP-1, like insulin, stimulates glucose uptake, and this involves activation of PI3K/PKB, p44/42 MAPKs, partially p70s6k, and possibly PKC; Ex-4 and Ex-9 both have GLP-1-like effect upon glucose transport, in which both share with GLP-1 an activation of PI3K/PKB--partially in the case of Ex-4--and p44/42 MAPKs but not p70s6k.

GLP-1 signalling and effects on glucose metabolism in myocytes from type 2 diabetic patients.

Changes in the activity of glycogen synthase a and related kinases (phosphatidylinositol-3-kinase, protein kinase B, p44/42 MAP kinases and p70s6 kinase) evoked by GLP-1 in human myocytes from normal subjects were recently implied in the effect of this hormone upon D-glucose transport and glycogen synthesis in the same cells. The major aims of the present study were i) to investigate the possible extension of this knowledge to myocytes obtained from type 2 diabetic patients, ii) to compare in these patients the response to GLP-1, insulin or the structurally related GLP-1 peptides, exendin (1-39)amide and exendin(9-39)amide, and iii) to explore possible differences in the responsiveness to these agents between normal and diabetic subjects. Apart from the much higher basal PI3K activity and impaired response to insulin of p44/42 MAP kinases in the diabetic patients, the changes in enzyme activity caused by either hormone or peptide, although not identical, were essentially comparable. Nevertheless, significant differences in glucose transport and metabolism parameters were observed in the diabetic patients vs. normal subjects: in the diabetic patients, basal 2-deoxy-glucose uptake and glycogen synthase a activity were lower, accompanied by a similar increasing effect of GLP-1 or insulin; yet, the basal value for glycogen synthesis was higher, coinciding with a lesser relative increment in response to GLP-1 or insulin.

Can the Acoustic Analysis of Expressive Prosody Discriminate Schizophrenia?

Emotional states, attitudes and intentions are often conveyed by modulations in the tone of voice. Impaired recognition of emotions from a tone of voice (receptive prosody) has been described as characteristic symptoms of schizophrenia. However, the ability to express non-verbal information in speech (expressive prosody) has been understudied. This paper describes a useful technique for quantifying the degree of expressive prosody deficits in schizophrenia, using a semi-automatic method, and evaluates this method's ability to discriminate between patient and control groups. Forty-five medicated patients with a diagnosis of schizophrenia were matched with thirty-five healthy comparison subjects. Production of expressive prosodic speech was analyzed using variation in fundamental frequency (F0) measures on an emotionally neutral reading task. Results revealed that patients with schizophrenia exhibited significantly more pauses (p < .001), were slower (p < .001), and showed less pitch variability in speech (p < .05) and fewer variations in syllable timing (p < .001) than control subjects. These features have been associated with «flat¼ speech prosody. Signal processing algorithms applied to speech were shown to be capable of discriminating between patients and controls with an accuracy of 93.8%. These speech parameters may have a diagnostic and prognosis value and therefore could be used as a dependent measure in clinical trials.

Normalizing action of exendin-4 and GLP-1 in the glucose metabolism of extrapancreatic tissues in insulin-resistant and type 2 diabetic states.

Exendin-4 (Ex-4) mimics glucagon-like peptide-1 (GLP-1 or GCG as listed in the HUGO database), being anti-diabetic and anorectic, in stimulating glucose and lipid metabolism in extrapancreatic tissues. We studied the characteristics of Ex-4 and GLP-1 action, during prolonged treatment, on GLUTs expression (mRNA and protein), glycogen content (GC), glucose transport (GT), glycogen synthase a (GSa), and kinase (PI3K and MAPKs) activity, in liver, muscle, and fat of insulin-resistant (IR, by fructose) and type 2 diabetic (T2D, streptozotocin at birth) rats compared with normal rats. In both IR and T2D, the three tissues studied presented alterations in all measured parameters. In liver, GLP-1 and also Ex-4 normalized the lower than normal Glut2 (Slc2a2) expression and showed a trend to normalize the reduced GC in IR, and GLP-1, like Ex-4, also in T2D, effects mediated by PI3K and MAPKs. In skeletal muscle, neither GLP-1 nor Ex-4 modified Glut4 (Slc2a4) expression in either experimental model but showed normalization of reduced GT and GSa, in parallel with the normalization of reduced PI3K activity in T2D and MAPKs in both models. In adipose tissue, the altered GLUT4 expression in IR and T2D, along with reduced GT in IR and increased GT in T2D, and with hyperactivated PI3K in both, became normal after GLP-1 and Ex-4 treatment; yet, MAPKs, that were also higher, became normal only after Ex-4 treatment. The data shows that Ex-4, as well as GLP-1, exerts a normalizing effect on IR and T2D states through a distinct post-receptor mechanism, the liver being the main target for Ex-4 and GLP-1 to control glucose homeostasis.

Characteristic of GLP-1 effects on glucose metabolism in human skeletal muscle from obese patients.

Direct effects of GLP-1, kinase-mediated, on glucose and lipid metabolism in rat and human extrapancreatic tissues, are amply documented and also changes in type-2 diabetic (T2D) patients. Here, we explored the characteristics of the GLP-1 action and those of its analogs Ex-4 and Ex-9, on muscle glucose transport (GT) and metabolism in human morbid obesity (OB), as compared with normal and T2D subjects. In primary cultured myocytes from OB, GT and glycogen synthase a (GSa) activity values were lower than normal, and comparable to those reported in T2D patients; GT was increased by either GLP-1 or Ex-9 in a more efficient manner than in normal or T2D, up to normal levels; the Ex-4 increasing effect on GSa activity was two times that in normal cells, while Ex-9 failed to modify the enzyme activity. In OB, the control value of all kinases analyzed - PI3K, PKB, MAPKs, and p70s6K - although lower than that in normal or T2D subjects, the cells maintained their response capability to GLP-1, Ex-4, Ex-9 and insulin, with some exceptions. GLP-1 and exendins showed a direct normalizing action in the altered glucose uptake and metabolism in the muscle of obese subjects, which in the case of GLP-1 could account, at least in part, for the reported restoration of the metabolic conditions of these patients after restrictive surgery.

Effects of an olive oil-enriched diet on plasma GLP-1 concentration and intestinal content, plasma insulin concentration, and glucose tolerance in normal rats.

The present study aims mainly at measuring, in normal rats, the GLP-1 response to oral intake of an olive oil-enriched diet (OO), and at assessing the long-term effects of such a diet on the GLP-1 content of the intestinal tract, as well as the plasma D-glucose, insulin, and GLP-1 pattern during an oral glucose tolerance test. In meal-trained rats, the mean increment in plasma GLP-1 concentration at min 10 and 20 was 1.39 +/- 0.23 ng/mL higher (p < 0.001) in the rats given access to the OO diet rather than control diet. Relative to the initial value (d 0), the gain in body weight at d 50 was also higher in the animals fed the OO rather than control diet. At d 50, the GLP-1 content of the jejunum, ileum, colon, and cecum were not significantly different in the two groups of rats. At d 19 and 36, the increment in both plasma insulin concentration and paired ratio between plasma insulin and D-glucose concentrations were again higher, during an oral glucose tolerance test conducted in overnight fasted animals, in the rats otherwise fed the OO, as distinct from control, diet. The intake of an olive oil-enriched diet thus increases, in normal rats, GLP-1 release, this coinciding during long-term exposure to the OO diet with higher body weight gain, increased secretory response of insulin-producing cells to oral glucose administration, and, after 36 d, improved glucose tolerance.

Can the acoustic analysis of expressive prosody discriminate schizophrenia?

Emotional states, attitudes and intentions are often conveyed by modulations in the tone of voice. Impaired recognition of emotions from a tone of voice (receptive prosody) has been described as characteristic symptoms of schizophrenia. However, the ability to express non-verbal information in speech (expressive prosody) has been understudied. This paper describes a useful technique for quantifying the degree of expressive prosody deficits in schizophrenia, using a semi-automatic method, and evaluates this method’s ability to discriminate between patient and control groups. Forty-five medicated patients with a diagnosis of schizophrenia were matched with thirty-five healthy comparison subjects. Production of expressive prosodic speech was analyzed using variation in fundamental frequency (F0) measures on an emotionally neutral reading task. Results revealed that patients with schizophrenia exhibited significantly more pauses (p < .001), were slower (p < .001), and showed less pitch variability in speech (p < .05) and fewer variations in syllable timing (p < .001) than control subjects. These features have been associated with «flat» speech prosody. Signal processing algorithms applied to speech were shown to be capable of discriminating between patients and controls with an accuracy of 93.8%. These speech parameters may have a diagnostic and prognosis value and therefore could be used as a dependent measure in clinical trials (AU)

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Plasma D-glucose, D-fructose and insulin responses after oral administration of D-glucose, D-fructose and sucrose to normal rats.

OBJECTIVE: To assess whether oral D-fructose modifies the plasma D-glucose and insulin responses to oral D-glucose administration in normal rats. DESIGN: Oral D-glucose (1.7, 3.5, 6.9 or 13.9 micromol/g body weight), D-fructose (6.9 micromol/g), both D-glucose and D-fructose (1.7 or 3.5 micromol/g of each hexose) or sucrose (3.7 micromol/g) were administered intragastrically to overnight fasted rats and the plasma concentration of D-glucose, D-fructose and insulin measured over the ensuing 120 minutes. Control experiments were conducted after oral administration of H(2)O or saline. RESULTS: The administration of D-fructose, given as the free hexose or as sucrose, instead of augmenting the plasma D-glucose concentration evoked by the concomitant administration of D-glucose, tended both to improve the insulin response of the pancreatic B-cell and to minimize hyperglycemia, when compared to the results of experiments including the administration of equimolar amounts of D-glucose alone. For instance, the area under the plasma D-glucose curve was comparable in the rats receiving both D-glucose and D-fructose (3.5 micromol/g of each hexose) and the rats receiving only D-glucose (3.5 micromol/g), averaging respectively 836 +/- 32 and 850 +/- 34 mM . min each. Likewise, the paired ratio between the areas under the plasma insulin and D-glucose curves, when corrected for the threshold concentration for the insulinotropic action of the hexose (2.05 +/- 0.10 mM), averaged 44.3 +/- 3.0 nmol/mol in the 16 rats receiving D-fructose alone, sucrose alone or both D-glucose and D-fructose, as compared to 37.7 +/- 2.9 nmol/mol in the 22 rats receiving increasing amounts of D-glucose alone. CONCLUSIONS: The intake of D-fructose, as the free hexose or as sucrose, favours D-glucose homeostasis. This is likely to be attributable to the reciprocal effects of the aldose and ketose upon their respective phosphorylation by glucokinase in both hepatocytes and insulin-producing pancreatic islet cells.

Glucagon-like peptide 1 content of intestinal tract in adult rats injected with streptozotocin either during neonatal period or 7 d before sacrifice.

Glucagon-like peptide 1 (GLP-1) content of the intestinal tract was recently found to be lower in diabetesprone BioBreeding (BBdp) rats than in the corresponding control animals (BBc rats), a finding compatible with the idea that an inflammatory intestinal state precedes insulitis in these diabetes-prone animals. This study aimed at measuring GLP-1 content of the intestinal tract both in another animal model of type 1 diabetes and in an animal model of type 2 diabetes. GLP-1 content of the jejunum, ileum, colon, and cecum was measured in male and female adult control rats and animals injected with streptozotocin (STZ) either during the neonatal period or 7 d before sacrifice. GLP-1 content of the intestinal tract was higher in type 1 diabetic rats than in control animals. Such was not the case in the type 2 diabetic rats. The findings recorded in the rats injected with STZ either during the neonatal period or later in life indicate that hyperglycemia and/or insulin deficiency do not cause a decrease in GLP-1 content of the intestinal tract. On the contrary, such a content may increase when the glucose intolerance and hypoinsulinemia are sufficiently pronounced, as was the case in the type 1 diabetic rats. These findings are thus compatible with the view that the decreased GLP-1 content of the intestinal tract in BBdp rats may result from intestinal inflammation.