Level-wise Subject adaptation to improve classification of motor and mental EEG tasks.

Classification of various cognitive and motor tasks using electroencephalogram (EEG) signals is necessary for building Brain Computer Interfaces (BCI) that are noninvasive. However, achieving high classification accuracy in a multi-subject multitask scenario is a challenge. A noticeable reduction in accuracy is observed when the subjects between train and test are mismatched. Drawing a similarity from speaker adaptation approaches in speech, we propose a method to perform subject-wise adaptation of EEG in order to improve the task classification performance. A Common Spatial Pattern (CSP) approach is employed for feature extraction. Gaussian Mixture Model (GMM) based subject-specific models are built for each of the tasks. Maximum a-posterior (MAP) adaptation is performed, and an absolute improvement of 1.22-7.26% is observed in the average accuracy.

Strange Case of Dr. Jekyll and Mr. Hyde-was Robert Louis Stevenson inspired by Horace Wells?

It has been suggested that Robert Louis Stevenson's masterpiece Strange Case of Dr. Jekyll and Mr. Hyde derived inspiration from the real-life tragedy of the final days of Connecticut dentist Horace Wells, innovator of the clinical use of the anesthetic properties of nitrous oxide. We examined Stevenson's letters, biographies, and other references in the literature, press, and online to determine whether any factual basis exists for Stevenson to be aware of Wells' life, and also if it played any role in creating the novel's plot. Stevenson was born in Scotland, several years after Wells had committed suicide in New York. Wells' life and death received widespread coverage in the northeastern United States, but there is no evidence that it was printed in newspapers or periodicals in England or Scotland. On the other hand, novelists of the period, psychologists, and the lay public were quite interested in the concept of split personalities and the dual nature of man, so these may have been natural substrates for the novel. There is evidence that Stevenson dreamt about episodes similar to those depicted in his novel. All claims to any relationship between Wells and the novel come from the United States, and none of them are backed by evidence. In the absence of evidence supporting a relationship between the behavior exhibited by Wells during his final days and any inspiration that Stevenson might have derived from it, we conclude that there is insufficient evidence to suggest any relationship between them.

Protective effect of Morus rubra L. leaf extract on diet-induced atherosclerosis in diabetic rats.

The antiatherosclerotic effect of aqueous leaves extract of Morus rubra was studied in streptozotocin-induced diabetic rats fed with atherosclerotic (Ath) diet [1.5 ml olive oil containing 8 mg (3, 20,000 IU) vitamin D2 and 40 mg cholesterol] for 5 consecutive days. A short-term toxicity assessment was also conducted in healthy rats to examine toxic effects of the extract. Oral administration of extract to diabetic rats (100, 200 and 400 mg/kg body weight per day for a period of 30 days) produced significant (p<0.001) fall in fasting blood glucose (FBG) in a dose-dependent manner. Treatment with the extract (400 mg/kg) showed significant (p<0.001) improvement in body weight and serum lipid profile i.e., total cholesterol, triglyceride, HDL-cholesterol, LDL-cholesterol and VLDL-cholesterol, when compared with diabetic control. Endothelial dysfunction parameters (sVCAM-1, Fibrinogen, total NO levels and oxidized LDL), apolipoprotein A and apolipoprotein B were significantly (p<0.001) reversed to near normal, following treatment with the extract. Thus, our study shows that aqueous leaf extract of Morus rubra (400 mg/kg) significantly improves the homeostasis of glucose and fat and possesses significant anti-atherosclerotic activity.

Cerebellar subacute syndrome due to corticosteroid-responsive encephalopathy associated with autoimmune thyroiditis (also called "Hashimoto's encephalopathy").

The corticosteroid-responsive encephalopathy associated with autoimmune thyroiditis (the so-called "Hashimoto's Encephalopathy") is a rare disorder with multiple symptomatology, breaking out with an acute or subacute onset and having a relapsing course, not correlated to thyroid hormone levels, with autoimmune pathogenesis, and usually associated with Hashimoto's thyroiditis. In this paper, we report on a case study regarding a 46 year-old woman showing a subacute course cerebellar syndrome, associated with Hashimoto's thyroiditis, diagnosed as "Hashimoto's encephalopathy". The possible pathogenesis and the major aspects of the differential diagnostic sector are discussed with particular reference to an ataxic syndrome caused by a progressive non-familial adult onset cerebellar degeneration (PNACD), associated with the thyroid disease itself.

Recombinant human insulin-like growth factor I has significant anabolic effects in adults with growth hormone receptor deficiency: studies on protein, glucose, and lipid metabolism.

The physiological effects of insulin-like growth factor I (IGF-I) on intermediate metabolism of substrates have been extensively studied in a variety of experimental situations in man, and its effects on linear growth of children with GH receptor mutations have proven beneficial. However, there is a paucity of data on the metabolic effects of IGF-I as replacement therapy in adults with GH receptor deficiency (Laron's syndrome). We designed these studies to investigate the in vivo effects of 8 weeks of therapy with recombinant human IGF-I (rhIGF-I) in a unique group of 10 adult subjects with profound IGF-I deficiency due to a mutation in the GH receptor gene (mean +/- SEM age, 29.2 +/- 2.0 yr; 4 males and 6 females). At baseline, patients had infusions of stable tracers, including L-[13C]leucine, [2H2]glucose, and d5-glycerol, as well as indirect calorimetry, assessment of body composition (dual energy x-ray absortiometry), and measurements of growth factor concentrations. Patients were then discharged to receive twice daily rhIGF-I (60 microg/kg, sc) for the next 8 weeks when the studies were repeated identically. Plasma IGF-I concentrations increased during rhIGF-I treatment from 9.3 +/- 1.5 microg/L to 153 +/- 23 (P = 0.0001). There was no change in weight during these studies, but a significant change in body composition was observed, with a decrease in percent fat mass (P = 0.003) and an increase in lean body mass (P = 0.001). These were accompanied by increased rates of protein turnover, decreased protein oxidation, and increased rates of whole body protein synthesis, as measured by leucine tracer methods (P < 0.01). These results are similar to those observed in GH-deficient subjects treated with GH. All measures of lipolytic activity and fat oxidation increased during treatment, with an 18% increase in the glycerol turnover rate (P = 0.04), an increase in free fatty acid and beta-hydroxybutyrate concentrations, and a significant increase in fat oxidation, as measured by indirect calorimetry (P = 0.04). There were significant decreases in insulin concentrations (P = 0.01) and a reciprocal increase in glucose production rates (P = 0.04) during rhIGF-I, yet plasma glucose concentrations remained constant, suggestive of a significant insulin-like action of this peptide. RhIGF-I was well tolerated by all patients. In conclusion, 8 weeks of treatment with rhIGF-I had significant positive effects on body composition and measures of intermediate metabolism independent of GH. These results suggest that, similar to GH treatment of adults with GH deficiency, rhIGF-I may be beneficial as long term replacement therapy for the adult patient with Laron's syndrome.

Insulin-like growth factor I and growth hormone (GH) treatment in GH-deficient humans: differential effects on protein, glucose, lipid, and calcium metabolism.

We examined the effects of recombinant human (rh) insulin-like growth factor I (IGF-I) vs. rhGH in a variety of metabolic paths in a group of eight severely GH-deficient young adults using an array of contemporary tools. Protein, glucose, and calcium metabolism were studied using stable labeled tracer infusions of L-[1-13C]leucine, [6,6-2H2]glucose, and 42Ca and 44Ca; substrate oxidation rates were assessed using indirect calorimetry; muscle strength was determined by isokinetic and isometric dynamometry of the anterior quadriceps, as well as growth factors, hormones, glucose, and lipid concentrations in plasma before and after 8 weeks of rhIGF-I (60 microg/kg, sc, twice daily), followed by 4 weeks of washout, then 8 weeks ofrhGH (12.5 microg/kg-day, sc); the treatment order was randomized. In the doses administered, rhIGF-I and rhGH both increased fat-free mass and decreased the percent fat mass, with a more robust decrease in the percent fat mass after rhGH; both were associated with an increase in whole body protein synthesis rates and a decrease in protein oxidation. Neither hormone affected isokinetic or isometric measures of skeletal muscle strength. However, rhGH was more potent than rhIGF-I at increasing lipid oxidation rates and improving plasma lipid profiles. Both hormones increased hepatic glucose output, but rhGH treatment was also associated with decreased carbohydrate oxidation and increased glucose and insulin concentrations, indicating subtle insulin resistance. Neither hormone significantly affected bone calcium fluxes, supporting the concept that these hormones, by themselves, are not pivotal in bone calcium metabolism. In conclusion, rhIGF-I and rhGH share common effects on protein, muscle, and calcium metabolism, yet have divergent effects on lipid and carbohydrate metabolism in the GH-deficient state. These differences may allow for better selection of treatment modalities depending on the choice of desired effects in hypopituitarism.

Phenylbutyrate-induced glutamine depletion in humans: effect on leucine metabolism.

The present study was designed to determine whether sodium phenylbutyrate (phi B) acutely induces a decrease in plasma glutamine in healthy humans, and, if so, will decrease estimates of whole body protein synthesis. In a first group of three healthy subjects, graded doses (0, 0.18, and 0.36 g.kg-1.day-1) of phi B were administered for 24 h before study: postabsorptive plasma glutamine concentration declined in a dose-dependent manner, achieving an approximately 25% decline for a dose of 0.36 g phi B.kg-1.day-1. A second group of six healthy adults received 5-h infusions of L-[1-14C]leucine and L-[1-13C]glutamine in the postabsorptive state on two separate days: 1) under baseline conditions and 2) after 24 h of oral treatment with phi B (0.36 g.kg-1.day-1) in a randomized order. The 24-h phenylbutyrate treatment was associated with 1) an approximately 26% decline in plasma glutamine concentration from 514 +/- 24 to 380 +/- 15 microM (means +/- SE; P < 0.01 with paired t-test) with no change in glutamine appearance rate or de novo synthesis; 2) no change in leucine appearance rate (Ra), an index of protein breakdown (123 +/- 7 vs. 117 +/- 5 mumol.kg-1.h-1; not significant); 3) an approximately 22% rise in leucine oxidation (Ox) from 23 +/- 2 to 28 +/- 2 mumol.kg-1.h-1 (P < 0.01), resulting in an approximately 11% decline in nonoxidative leucine disposal (NOLD = Ra-Ox), an index of protein synthesis, from 100 +/- 6 to 89 +/- 5 mumol.kg-1.h-1 (P < 0.05). The data suggest that, in healthy adults, 1) large doses of oral phenylbutyrate can be used as a "glutamine trap" to create a model of glutamine depletion; 2) a moderate decline in plasma glutamine does not enhance rates of endogenous glutamine production; and 3) a short-term depletion of plasma glutamine decrease estimates of whole body protein synthesis.

Testosterone deficiency in young men: marked alterations in whole body protein kinetics, strength, and adiposity.

To investigate specific effects of androgens on whole body metabolism, we studied six healthy lean men (mean +/- SEM age, 23.2 +/- 0.5 yr) before and after gonadal steroid suppression with a GnRH analog (Lupron), given twice, 3 weeks apart. Primed infusions of [13C]leucine, indirect calorimetry, isokinetic dynamometry, growth factor measurements, and percutaneous muscle biopsies were performed at baseline (D1) and after 10 weeks of treatment (D2); each subject served as his own control. Testosterone concentrations were markedly suppressed after 10 weeks of treatment (D1, 535 +/- 141 ng/dL; D2, 31 +/- 9). Leucine's rate of appearance (index of proteolysis) was markedly suppressed after 10 weeks of hypogonadism (-13%; P = 0.01) as well as the nonoxidative leucine disposal, an index of whole body protein synthesis (-13%; P = 0.01) without any changes in plasma amino acid concentrations. All subjects studied after 10 weeks showed a decrease in fat-free mass, as measured by skinfold calipers and dual emission x-ray absortiometry scans (D1, 56.5 +/- 2.9 kg; D2, 54.4 +/- 2.5; P = 0.005), and an increase in percent fat mass (D1, 19.2 +/- 2.5%; D2, 22.2 +/- 2.5; P = 0.001). Rates of lipid oxidation decreased (-31%; P = 0.05) after treatment, with parallel changes in resting energy expenditure (-9%; P = 0.05). Mean and peak GH concentrations (measured every 10 min for 6 h) and GH production rates did not decrease after testosterone deficiency, with an actual increase in basal secretion (P < 0.02). Plasma insulin-like growth factor I (IGF-I) concentrations did not change significantly after 10 weeks of treatment (D1, 227 +/- 44 micrograms/L; D2, 291 +/- 60; P = 0.08). Isokinetic dynamometry of leg extensors at 60 degrees and 180 degrees/s was also decreased after 10 weeks of hypogonadism. Total ribonucleic acid (RNA) was isolated from muscle biopsy samples, and ribonuclease protection assays were performed using human complementary DNA clones for IGF-I, IGF-binding protein-4, myosin, and actin. Ten weeks after Lupron treatment, messenger RNA (mRNA) concentrations of IGF-I decreased significantly, whereas there was a trend toward higher IGF-binding protein-4 concentrations, with no change in myosin or actin mRNA concentrations. In conclusion, testosterone deficiency in young men is associated with a marked decrease in measures of whole body protein anabolism, decreased strength, decreased fat oxidation, and increased adiposity. These effects of testosterone deficiency are independent of changes in peripheral GH production and IGF-I concentrations, even though im IGF-I mRNA concentrations decrease. These data suggest a direct effect of androgens on whole body lipid and protein metabolism.

Ovarian hyperandrogenism is associated with insulin resistance to both peripheral carbohydrate and whole-body protein metabolism in postpubertal young females: a metabolic study.

The role of endogenous androgens in enhancing the body's protein anabolic capacity has been controversial. To examine this question we chose to study whole-body protein and glucose kinetics in a group of 21 young, postpubertal females (16.3 +/- 0.6 yr), 8 of whom had clinical and laboratory evidence of ovarian hyperandrogenism (OH) (BMI = 37.8 +/- 1.3 kg/m2). We used L-[1-13C]leucine and [6,6,2H2]glucose tracer infusions before and after suppression of their endogenous androgens with estrogen/progesterone supplementation in the form of Triphasil for 4 weeks. Their baseline data were also compared with those of similar aged girls, 7 obese (OB) (BMI = 36.4 +/- 1.5) and 6 lean (LN) (BMI = 20.9 +/- 0.7) who were normally menstruating and had no evidence of androgen excess. Despite comparable glucose concentrations, both OH and OB groups had significant hyperinsulinemia (OH > OB), both basally and after iv glucose stimulation, as compared to LN controls (basal insulin: OH, 252 +/- 52 pmol/L; OB, 145 +/- 41; LN, 60 +/- 9, P = 0.009 OH vs. LN; peak insulin: OH, 2052 +/- 417; OB, 1109 +/- 127, LN, 480 +/- 120, P = 0.0009 OH vs. LN). The rate of appearance (Ra) of glucose, a measure of glucose production, was greater in the LN controls than in the OH or OB groups (OH, 2.0 +/- 0.1 mg/kg.fat free mass.min; OB, 1.9 +/- 0.1; LN, 3.3 +/- 0.1, P < 0.004 vs. LN). Calculated total rates of whole-body protein breakdown (leucine Ra), oxidation, and protein synthesis (nonoxidative leucine disposal) were substantially higher in the OH and OB groups as compared with LN controls (P < 0.04 vs. LN); however, when data are expressed on a per kilogram of fat free mass basis, the OH group had higher rates of proteolysis than the OB and LN, with indistinguishable rates between the latter two groups. None of the above-mentioned parameters changed after 1 month of administration of Triphasil, despite marked improvement in circulating testosterone and free testosterone concentrations after treatment (testosterone, -50%, P = 0.003; free testosterone, -70%, P = 0.02). We conclude that obesity in young postpubertal females is associated with insulin resistance for both peripheral carbohydrate and protein metabolism, and that patients with the OH syndrome have even greater insulin resistance as compared with simple obesity, regardless of treatment for the androgen excess. Carefully designed studies targeting interventions to improve both the hyperandrogenic and hyperinsulinemic state may prove useful even in the early juvenile stages of this disease.

[Chronic idiopathic hypertransaminasemia]. / Ipertransaminasemia cronica idiopatica.

The elevation of aminotransferase serum levels is frequently encountered in pediatric practice. We have retrospectively evaluated the clinical patterns of 108 patients with chronic, so called "idiopathic", alterations of aminotransferases, by sending a questionnaire to 11 Italian Pediatric Centers. The average period of follow-up was 22 months. Patients, whose ages ranged through all pediatric ages, were mostly asymptomatic and with a rather insignificant physical examination. The average rise of aminotransferases value was generally limited within 2 times the upper normal level and the highest value, during the period of follow-up, never exceeded 5 times the upper normal level. Other liver function tests did not result generally altered significant. Just 25,9% of the patients normalized aminotransferases serum level during the follow-up period. All maintained good physical status with no clinical signs of liver disease. A muscular cause of hyper-transaminasemia was excluded in all the cases. Possible infective causes (HBV and HCV) autoimmune hepatitis, Wilson disease, alfa1 antitripsine deficiency and hyperammoniemia were excluded. Ultrasound investigation did not seem to be a sensitive investigation, resulting negative in 54/82. Histologic liver examination was more informative. This evaluation, performed in 46/108 patients, showed infarct metabolic alterations (steatosis, nucleus glucogenic degeneration, cytoplasmatic clarification) in 65% of cases and inflammatory findings in only 13% of cases. In conclusion, our results suggest the opportunity to enclose liver histologic study in the diagnostic approach of children with hepatic idiopathic chronic hypertransaminasemia. This approach may address the clinician, in a more aimed way, towards further investigations.

Family Medical Leave Act: ready or not!

Many employers already have policies in place that grant job leaves for a variety of reasons. It is no longer optional for employers to grant job leaves; appropriate leave is now the law.

[Liver transplant in childhood: our experience]. / Il trapianto epatico in età pediatrica: la nostra esperienza.

From december 1984 to december of 1991, 12 children underwent on orthotopic liver transplantation (OLT): 6 had extrahepatic biliary atresia (EHBA), 2 had Byler disease, 2 hepatocellular carcinoma (HCC), 1 Alagille Syndrome and 1 had a hyperacute Wilson disease. The children, transplanted for the most part a broad, return for observation 3 months after OLT. A patient with hyperacute Wilson's Disease had 2 emergency OLTs and died of sepsis (due to Aspergillus); another with EHBA, operated for hepatoportoenterostomy, without result, died after OLT because of a ruptured aortic aneurysm. The other 10 are living with a variable follow-up between 8 months and 7 years. The post-operatory complications were present in 4 cases: in the same patient (15 months old) a hepatic artery thrombosis and then a portal vein thrombosis were observed; 3 patients had to have their biliary-digestive anastomosis redone. 7 of 10 patients had acute rejection. During the first month after OLT infection episodes were mostly due to bacteria (G-), Candida and Pneumocystis carinii (blood and intraabdominal sepsis). In the second period (1-3 months) there were viral infections, in particular CMV. An emergency transplanted patient, incompletely vaccinated, developed HBV infection. During long term follow-up (after the 3rd months from OLT) the children usually have mild infections of the respiratory and urinary tracts. After 1 year, they have a mean annual growth velocity that is between the 50th and 90th percentile. They showed a good rehabilitation. Their hospitalizations rate was reduced if compared with the period before OLT. Health, motor function and general behavior improved significantly.(ABSTRACT TRUNCATED AT 250 WORDS)