Quality of life and neuropsychological changes in mild head trauma - Late analysis and correlation with S100B protein and cranial CT scan performed at hospital admission

Introduction: mild head trauma (MHT) is defined as a transient neurological deficit after trauma with a history of impairment or loss of consciousness lasting less than 15 min and/or posttraumatic amnesia, and a Glasgow Coma Scale between 13 and 15 on hospital admission. We evaluated 50 MHT patients 18 months after the trauma, addressing signs and symptoms of post-concussion syndrome, quality of life and the presence of anxiety and depression. We correlate those findings with the S100B protein levels and cranial CT scan performed at hospital admission after the trauma. Method: patients were asked to fill out questionnaires to assess quality of life (SF36), anxiety and depression (HADS), and signs and symptoms of post-concussion syndrome. For the control group, we asked the patient`s household members, who had no history of head trauma of any type, to answer the same questionnaires for comparison. Results: total quality of life index for patients with MHT was 58.16 (+/-5), lower than the 73.47 (+/-4) presented by the control group. Twenty patients (55.2%) and four (11.1%) controls were depressed. Seventeen patients (47.2%) presented anxiety, whereas only eight (22.2%) controls were considered anxious. Victims of MHT complained more frequently of loss of balance, dry mouth, pain in the arms, loss of memory and dizziness than their respective controls (p < 0.05). We found no correlation between the presence of these signs and symptoms, quality of life, presence of anxiety and depression with S100B protein levels or with presence of injury in the cranial CT performed at hospital admission. Conclusion: MHT is associated with a higher incidence of post-concussion syndrome symptoms, lower quality of life and anxiety than their respective controls even 18 months after the trauma. (C) 2007 Elsevier Ltd. All rights reserved.

Effects of magnesium intake deficiency on bone metabolism and bone tissue around osseointegrated implants

Objectives: This study evaluated the effect of magnesium dietary deficiency on bone metabolism and bone tissue around implants with established osseointegration. Materials and methods: For this, 30 rats received an implant in the right tibial metaphysis. After 60 days for healing of the implants, the animals were divided into groups according to the diet received Control group (CTL) received a standard diet with adequate magnesium content, while test group (Mg) received the same diet except for a 90% reduction of magnesium. The animals were sacrificed after 90 days for evaluation of calcium, magnesium, osteocalcin and parathyroid hormone (PTH) serum levels and the deoxypyridinoline (DPD) level in the urine. The effect of magnesium deficiency on skeletal bone tissue was evaluated by densitometry of the lumbar vertebrae, while the effect of bone tissue around titanium implants was evaluated by radiographic measurement of cortical bone thickness and bone density. The effect on biomechanical characteristics was verified by implant removal torque testing. Results: Magnesium dietary deficiency resulted in a decrease of the magnesium serum level and an increase of PTH and DPD levels (P <= 0.05). The Mg group also presented a loss of systemic bone mass decreased cortical bone thickness and lower values of removal torque of the implants (P <= 0.01). Conclusions: The present study concluded that magnesium-deficient diet had a negative influence on bone metabolism as well as on the bone tissue around the implants.

Characterization of high density lipoprotein particles in familial apolipoprotein A-I deficiency

Our aim was to characterize HDL subspecies and fat-soluble vitamin levels in a kindred with familial apolipoprotein A-I (apoA-I) deficiency. Sequencing of the APOA1 gene revealed a nonsense mutation at codon 22, Q[22] X, with two documented homozygotes, eight heterozygotes, and two normal subjects in the kindred. Homozygotes presented markedly decreased HDL cholesterol levels, undetectable plasma apoA-1, tuboeruptive and planar xanthomas, mild corneal arcus and opacification, and severe premature coronary artery disease. In both homozygotes, analysis of HDL particles by two-dimensional gel electrophoresis revealed undetectable apoA-I, decreased amounts of small a-3 migrating apoA-II particles, and only modestly decreased normal amounts of slow a migrating apoA-IV- and apoE-containing HDL, while in the eight heterozygotes, there was loss of large alpha-1 HDL particles. There were no significant decreases in plasma fat-soluble vitamin levels noted in either homozygotes or heterozygotes compared with normal control subjects. Our data indicate that isolated apoA-I deficiency results in marked HDL deficiency with very low apoA-II alpha-3 HDL particles, modest reductions in the separate and distinct plasma apoA-IV and apoE HDL particles, tuboeruptive xanthomas, premature coronary atherosclerosis, and no evidence of fat malabsorption.

Effect of Weight Loss on Aerobic Capacity in Patients with Severe Obesity Before and After Bariatric Surgery

Severe obesity has been associated with adverse effects on physical capacity. In a prospective study, the aerobic capacity of severely obese patients was measured in order to observe the physiological response to weight loss from bariatric surgery. Sixty-five consecutive patients (40.4 +/- 8.4 years old; 93.8% female; body mass index = 49.4 +/- 5.4 kg/m(2)) were evaluated before bariatric surgery and then 6 and 12 months after surgery. Aerobic capacity was assessed with a scientific treadmill to measure maximal oxygen consumption (VO(2max)), heart rate, blood pressure, time on the treadmill, and distance walked (modified Bruce test). For the three observational periods, VO(2max) was 25.4 +/- 9.3, 29.8 +/- 8.1, and 36.7 +/- 8.3 ml/kg/min; time on the treadmill was 5.4 +/- 1.4, 6.4 +/- 1.6, and 8.8 +/- 1.0 min; and distance walked was 401.8 +/- 139.1, 513.4 +/- 159.9, and 690.5 +/- 76.2 m. For these variables, significant results (p = 0.0000) were observed for the two postoperative periods in relation to the preoperative period. Severely obese individuals increased their aerobic capacity after successful bariatric surgery. The data also suggests that a positive and progressive relationship between weight loss and improvement in fitness as a moderate loss of weight 6 months after surgery already showed some benefit and an additional reduction in weight was associated with a better performance in the aerobic capacity tests at the 12-month follow-up.

Long-term nutritional assessment of patients with severe short bowel syndrome managed with home enteral nutrition and oral intake

Background: Parenteral nutrition (PN) is used to control the nutritional state after severe intestinal resections. Whenever possible, enteral nutrition (EN) is used to promote intestinal rehabilitation and reduce PN dependency. Our aim is to verify whether EN + oral intake (01) in severe short bowel syndrome (SBS) surgical adult patients can maintain adequate nutritional status in the long term. Methods: This longitudinal retrospective study included 10 patients followed for 7 post-operative years. Body mass index (BMI), percentage of involuntary loss of usual body weight (UWL), free fat mass (FFM), and fat mass (FM) composition assessed by bioelectric impedance, and laboratory tests were evaluated at 6, 12, 24, 36, 48, 60, 72, and 84 months after surgery. Energy and protein offered in HPN and at long term by HEN+ oral intake (01), was evaluated at the same periods. The statistical model of generalized estimating equations with p <0,05 was used. Results: With long term EN + 01 there was a progressive increase in the UWL, a decrease in BMI, FFM, and FM (p < 0,05). PN weaning was possible in eight patients. Infection due to central venous catheter (CVC) contamination was the most common complication (1.2 episodes CVC/patient/year). There was an increase in energy and protein intake supply provided by HEN+OI (p <0.05). All patients survived for at least 2 years, seven for 5 years and six for 7 years of follow-up. Conclusions: In the long term SBS surgical adult patients fed with HEN+OI couldn`t maintain adequate nutritional status with loss of FM and FFM. (Nutr Hosp. 2011;26:834-842) DOI:10.3305/nh.2011.26.4.5153

Improvement of Insulin Resistance and Reduction of Cardiovascular Risk Among Obese Patients with Type 2 Diabetes with the Duodenojejunal Bypass Liner

This study aims to evaluate the effectiveness of the duodenojejunal bypass liner (DJBL) in the improvement of insulin resistance and reduction of cardiovascular risk among morbidly obese patients with type 2 diabetes mellitus, using the triglyceride/high-density lipoprotein (HDL) cholesterol ratio, percentage of weight loss, and glycemic control. We used the TG/HDL ratio with a cutoff value of 3.5 to identify patients with insulin resistance. The value of the initial ratio was compared with the ratio obtained 6 months after implantation to evaluate whether an improvement in insulin resistance occurred. We also evaluated the improvement of glycated hemoglobin levels and the weight loss resulted from the use of the device and correlated that with the improvement of the TG/HDL ratio. All patients implanted with the device presented a statistically significant reduction of the HbA1c levels, with most patients (70.3%) obtaining diabetes control with HbA1c levels lower than 7% at the end of the study. All patients also presented a significant weight reduction, with an average loss of 12.6% of their initial weight. We observed an important improvement in insulin resistance and metabolic syndrome, with a significant reduction of the TG/HDL ratio from 5.75 to 4.36 (p < 0.001) and 42.6% of the patients presenting a TG/HDL ratio lower than 3.5 at the end of the study. The DJBL, when used for a period of 6 months, is effective in the control of diabetes, weight loss, improvement of insulin resistance, and decrease of cardiovascular risk among morbidly obese patients with type 2 diabetes mellitus.

Histologic Study of Perifascial Areolar Tissue Implanted in Rabbit Vocal Folds: An Experimental Study

Objectives: Perifascial areolar tissue (PAT) consists of loose areolar tissue with viscoelastic properties that are similar to those found in tissues in the superficial layer of the vocal fold. The aim of this study was to quantify the inflammatory process and the collagen content of the graft, as well as that of the host tissue, after placement of a strip of PAT into the rabbit vocal fold. Methods: Surgeries were performed on 30 rabbits. The grafts were implanted in pockets that were surgically created in the right vocal fold. The left vocal fold (control group) was subjected only to surgical manipulation. The animals were divided into 3 groups for evaluations at 15 days, 3 months, and 6 months, and their larynx tissues were subsequently reviewed by histology. Results: The grafts were characterized by disorganized and thick collagen bundles and were identified in all study groups. The collagen density stayed constant over time. There was an acute inflammatory response induced by the graft at 15 clays that did not exist in the specimens taken at 3 and 6 months. Deposition of collagen fibers in the lamina propria was observed starting at 15 days after the operation and was more intense in the experimental vocal fold than in the control vocal fold. Conclusions: Our findings indicated that PAT has a low tendency for promoting an inflammatory response. However, there was a loss of the original architecture of the graft tissue and a greater deposition of collagen in the implanted vocal folds than in the control group.

The outer wall of small airways is a major site of remodeling in fatal asthma

Background: Structural and inflammatory changes in asthma involve both the large and small airways, with involvement of the distal lung being related to disease severity. We have previously shown that changes in the extracellular matrix (ECM) composition of the distal lung are associated with loss of alveolar attachments in patients with fatal asthma. However, major ECM elements, such as collagen I and fibronectin and their regulators, have not been addressed at the distal level. Objective: We sought to evaluate ECM remodeling in the distal lungs of asthmatic patients. Methods: Using immunohistochemistry and image analysis, we determined the content of collagen I and III, fibronectin, and matrix metalloproteinases; (MMPs) 1, 2, and 9 and tissue inhibitors of metalloproteinase (MMPs) 1 and 2 in the large and small airways and lung parenchyma of 24 patients with fatal asthma and compared the results with those of 11 nonasthmatic control subjects. Protein content was defined as the area of positive staining divided by basement membrane or septum length. Results: We observed increased collagen I and decreased collagen III content in the small airways of asthmatic patients compared with that seen in control subjects. Greater fibronectin and MMP-1, MMP-2, and MMP-9 content was observed at the outer area of the small airways in asthmatic patients. NIMP content was also increased in the peribronchiolar parenchyma in asthmatic patients. In contrast, TIMP expression was only increased in the large airways of asthmatic patients compared with that seen in control subjects. Conclusions: The outer area of the small airways is a major site of ECM remodeling in fatal asthma, potentially contributing to functional changes and the loss of airway-parenchyma interdependence observed in patients with fatal asthma. (J Allergy Clin Immunol 2009;123:1090-7.)

Mutations in NOTCH2 cause Hajdu-Cheney syndrome, a disorder of severe and progressive bone loss

We used an exome-sequencing strategy and identified an allelic series of NOTCH2 mutations in Hajdu-Cheney syndrome, an autosomal dominant multisystem disorder characterized by severe and progressive bone loss. The Hajdu-Cheney syndrome mutations are predicted to lead to the premature truncation of NOTCH2 with either disruption or loss of the C-terminal proline-glutamate-serine-threonine-rich proteolytic recognition sequence, the absence of which has previously been shown to increase Notch signaling.

Nonsense Mutations in FGF8 Gene Causing Different Degrees of Human Gonadotropin-Releasing Deficiency

Context: FGFR1 mutations cause isolated hypogonadotropic hypogonadism (IHH) with or without olfactory abnormalities, Kallmann syndrome, and normosmic IHH respectively. Recently, missense mutations in FGF8, a key ligand for fibroblast growth factor receptor (FGFR) 1 in the ontogenesis of GnRH, were identified in IHH patients, thus establishing FGF8 as a novel locus for human GnRH deficiency. Objective: Our objective was to analyze the clinical, hormonal, and molecular findings of two familial IHH patients due to FGF8 gene mutations. Methods and Patients: The entire coding region of the FGF8 gene was amplified and sequenced in two well-phenotyped IHH probands and their relatives. Results: Two unique heterozygous nonsense mutations in FGF8(p.R127X and p.R129X) were identified in two unrelated IHH probands, which were absent in 150 control individuals. These two mutations, mapped to the core domain of FGF8, impact all four human FGF8 isoforms, and lead to the deletion of a large portion of the protein, generating nonfunctional FGF8 ligands. The p.R127X mutation was identified in an 18-yr-old Kallmann syndrome female. Her four affected siblings with normosmic IHH or delayed puberty also carried the p.R127X mutation. Additional developmental anomalies, including cleft lip and palate and neurosensorial deafness, were also present in this family. The p.R129X mutation was identified in a 30-yr-old man with familial normosmic IHH and severe GnRH deficiency. Conclusions: We identified the first nonsense mutations in the FGF8 gene in familial IHH with variable degrees of GnRH deficiency and olfactory phenotypes, confirming that loss-of-function mutations in FGF8 cause human GnRH deficiency. (J Clin Endocrinol Metab 95: 3491-3496, 2010)

Effects of exercise on leukocyte death: prevention by hydrolyzed whey protein enriched with glutamine dipeptide

Lymphocyte and neutrophil death induced by exercise and the role of hydrolyzed whey protein enriched with glutamine dipeptide (Gln) supplementation was investigated. Nine triathletes performed two exhaustive exercise trials with a 1-week interval in a randomized, double blind, crossover protocol. Thirty minutes before treadmill exhaustive exercise at variable speeds in an inclination of 1% the subjects ingested 50 g of maltodextrin (placebo) or 50 g of maltodextrin plus 4 tablets of 700 mg of hydrolyzed whey protein enriched with 175 mg of glutamine dipeptide dissolved in 250 mL water. Cell viability, DNA fragmentation, mitochondrial transmembrane potential and production of reactive oxygen species (ROS) were determined in lymphocytes and neutrophils. Exhaustive exercise decreased viable lymphocytes but had no effect on neutrophils. A 2.2-fold increase in the proportion of lymphocytes and neutrophils with depolarized mitochondria was observed after exhaustive exercise. Supplementation of maltodextrin plus Gln (MGln) prevented the loss of lymphocyte membrane integrity and the mitochondrial membrane depolarization induced by exercise. Exercise caused an increase in ROS production by neutrophils, whereas supplementation of MGln had no additional effect. MGln supplementation partially prevented lymphocyte apoptosis induced by exhaustive exercise possibly by a protective effect on mitochondrial function.

Role of Ulnar Nerve Sonography in Leprosy Neuropathy With Electrophysiologic Correlation

Objective. The purpose of this study was to evaluate the diagnostic usefulness of ulnar nerve sonography in leprosy neuropathy with electrophysiologic correlation. Methods. Twenty-one consecutive patients with leprosy (12 men and 9 women; mean age +/- SD, 47.7 +/- 17.2 years) and 20 control participants (14 men and 6 women; mean age, 46.5 +/- 16.2 years) were evaluated with sonography. Leprosy diagnosis was established on the basis of clinical, bacteriologic, and histopathologic criteria. The reference standard for ulnar neuropathy in this study was clinical symptoms in patients with proven leprosy The sonographic cross-sectional areas (CSAs) of the ulnar nerve in 3 different regions were obtained. Statistical analyses included Student t tests and receiver operating characteristic curve analysis. Results. The CSAs of the ulnar nerve were significantly larger in the leprosy group than the control group for all regions (P < .01). Sonographic abnormalities in leprosy nerves included focal thickening (90.5%), hypoechoic areas (81%), loss of the fascicular pattern (33.3%), and focal hyperechoic areas (4.7%). Receiver operating characteristic curve analysis showed that a maximum CSA cutoff value of 9.8 mm(2) was the best discriminator (sensitivity, 0.91; specificity, 0.90). Three patients with normal electrophysiologic findings had abnormal sonographic findings. Two patients had normal sonographic findings, of which 1 had abnormal electrophysiologic findings, and the other refused electrophysiologic testing. Conclusions. Sonography and electrophysiology were complementary for identifying ulnar nerve neuropathy in patients with leprosy, with clinical symptoms as the reference standard. This reinforces the role of sonography in the investigation of leprosy ulnar neuropathy.

THE INFLUENCE OF VIBRISSAL SOMATOSENSORY PROCESSING IN RAT SUPERIOR COLLICULUS ON PREY CAPTURE

The lateral part of intermediate layer of superior colliculus (SCI) is a critical substrate for successful predation by rats. Hunting-evoked expression of the activity marker Fos is concentrated in SCI while prey capture in rats with NMDA lesions in SCI is impaired. Particularly affected are rapid orienting and stereotyped sequences of actions associated with predation of fast moving prey. Such deficits are consistent with the view that the deep layers of SC are important for sensory guidance of movement. Although much of the relevant evidence involves visual control of movement, less is known about movement guidance by somatosensory input from vibrissae. Indeed, our impression is that prey contact with whiskers is a likely stimulus to trigger predation. Moreover, SCI receives whisker and orofacial somatosensory information directly from trigeminal complex, and indirectly from zona incerta, parvicelular reticular formation and somatosensory barrel cortex. To better understand sensory guidance of predation by vibrissal information we investigated prey capture by rats after whisker removal and the role of superior colliculus (SC) by comparing Fos expression after hunting with and without whiskers. Rats were allowed to hunt cockroaches, after which their whiskers were removed. Two days later they were allowed to hunt cockroaches again. Without whiskers the rats were less able to retain the cockroaches after capture and less able to pursue them in the event of the cockroach escaping. The predatory behaviour of rats with re-grown whiskers returned to normal. In parallel, Fos expression in SCI induced by predation was significantly reduced in whiskerless animals. We conclude that whiskers contribute to the efficiency of rat prey capture and that the loss of vibrissal input to SCI, as reflected by reduced Fos expression, could play a critical role in predatory deficits of whiskerless rats. (C) 2011 IBRO. Published by Elsevier Ltd. All rights reserved.

Differentially expressed genes in eutopic and ectopic endometrium of women with endometriosis

Objective: To elucidate the potential mechanisms involved in the physiopathology of endometriosis. We analyzed the differential gene expression profiles of eutopic and ectopic tissues from women with endometriosis. Design: Prospective laboratory study. Setting: University hospital. Patient(s): Seventeen patients in whom endometriosis was diagnosed and 11 healthy fertile women. Intervention(s): Endometrial biopsy specimens from the endometrium of healthy women without endometriosis and from the eutopic and ectopic endometrium tissues of patients with endometriosis were obtained in the early proliferative phase of the menstrual cycle. Main Outcome Measure(s): Six paired samples of eutopic and ectopic tissue were analyzed by subtractive hybridization. To evaluate the expression of genes found by rapid subtraction hybridization methods, we measured CTGF, SPARC, MYC, MMP and IGFBP1 genes by real-time polymerase chain reaction in all samples. Result(s): This study identified 291 deregulated genes in the endometriotic lesions. Significant expression differences were obtained for SPARC, MYC, and IGFBP1 in the peritoneal lesions and for MMP3 in the ovarian endometriomas. Additionally, significant differences were obtained for SPARC and IGFBP1 between the peritoneal and ovarian lesions. No significant differences were found for the studied genes between the control and the eutopic endometrium. Conclusion(s): This study identified 291 genes with differential expression in endometriotic lesions. The deregulation of the SPARC, MYC, MMP3, and IGFBP1 genes may be responsible for the loss of cellular homeostasis in endometriotic lesions. (Fertil Steril(R) 2010;93:1750-73. (C) 2010 by American Society for Reproductive Medicine.)

Glycodelin expression in the endometrium of healthy women and in the eutopic and ectopic endometrium of women with endometriosis

Objective: To analyze the expression of the glycodelin gene to better understand the molecular environment of endometriotic lesions and to elucidate the potential mechanisms that underlie the complex physiopathology of endometriosis. Design: Prospective laboratory study. Setting: University hospital. Patient(s): Eleven healthy fertile women and 17 patients with endometriosis in the early proliferative phase of the menstrual cycle. Intervention(s): Endometrial biopsy specimens were obtained from the endometrium of healthy women without endometriosis (controls) and from eutopic and ectopic endometrium tissues (pelvic and ovarian endometriotic implants) of endometriosis patients. Main Outcome Measure(s): The glycodelin relative expression level by real-time polymerase chain reaction (PCR) analysis. Result(s): The glycodelin down-regulation found in the endometriotic lesions was 332.26 and 123.17-fold lower, respectively, when compared with the eutopic tissue and the control endometrium. Conclusion(s): Glycodelin may be one of the molecules that contributes to the loss of cellular homeostasis in endometriotic lesions. (Fertil Steril (R) 2009;91:1676-80. (C)2009 by American Society for Reproductive Medicine.)