Integrative executive function training in chronic stroke—A case example

Cognitive and functional impairments are common sequelae following stroke, often resulting in significant disabilities that persist years post‐stroke. While the degree of impairments varies with pathology and location of stroke, it is widely understood that executive dysfunction including disturbances of attention, complex information processing, inhibition, reasoning, and flexible thinking underlie a majority of the impairments. Existing rehabilitation approaches predominantly focus on mitigating targeted cognitive deficits (e.g., language disturbance, neglect of one side of the body, memory). Remediation approaches to address executive dysfunction in chronic stages of recovery post‐stroke are limited. The Strategic Memory Advanced Reasoning Training (SMART) that teaches strategies to improve higher order reasoning skills has proven to enhance executive functions, strengthen brain networks and improve participation in daily life activities in adults with traumatic brain injury. The current case example, part of an ongoing larger study, discusses post‐SMART performance of a 57‐year‐old female stroke survivor, who sustained a left middle cerebral artery infarct in July 2015. The participant showed gains in executive functions and participation in leisure pursuits following 10 SMART sessions. These preliminary findings prove feasibility of the training approach and offer promise of neuroplasticity during chronic stages of recovery.     

First description of blaNDM-1, blaOXA-48, blaOXA-181 producing Enterobacteriaceae strains in Romania

We report the first isolation and characterization of several Enterobacteriaceae strains harboring bla_NDM-1, bla_OXA-48 and/or bla_OXA-181 genes in a Romanian emergency teaching hospital. Between January 2010 and September 2012 nine carbapenemase-producing Enterobacteriaceae strains were identified. The bla_NDM-1 gene was present in two Enterobacter cloacae strains, an Escherichia coli and two Klebsiella pneumoniae strains. One of these K. pneumoniae strains also harbored the bla_OXA-181 gene. Three other K. pneumoniae strains and one Serratia marcescens carried bla_OXA-48.     

Humoral immune responses of Brucella-infected cattle, sheep, and goats to eight purified recombinant Brucella proteins in an indirect enzyme-linked immunosorbent assay.

Brucellosis research is currently focused on the identification of nonlipopolysaccharide (LPS) antigens which could potentially be useful for the specific serologic diagnosis of brucellosis as well as for vaccinal prophylaxis. On the basis of previous reports, we selected eight Brucella proteins (OMP36, OMP25, OMP19, OMP16, OMP10, p17, p15, and p39) as candidate antigens to be further evaluated. The genes encoding these proteins were cloned, sequenced, and overexpressed in Escherichia coli. The recombinant proteins were purified with a polyhistidine tag and metal chelate affinity chromatography and evaluated in an indirect enzyme-linked immunosorbent assay (iELISA). The specificity of the iELISA was determined with sera from healthy cattle, sheep, and goats and ranged from 95 to 99%, depending on the recombinant antigen and the species tested. Sera from experimentally infected, and from naturally infected, animals were used to evaluate the sensitivity of the iELISA. The antiprotein antibody response was often delayed when compared to the anti-smooth LPS (S-LPS) response and was limited to animals which developed an active brucellosis infection (experimentally infected pregnant animals and sheep and goats from areas where brucellosis is still endemic). Among the recombinant antigens, the three cytoplasmic proteins (p17, p15, and p39) gave the most useful results. More than 80% of the animals positive in S-LPS serology were also positive with one of these cytoplasmic proteins alone or a combination of two of them. None of the recombinant antigens detected experimentally infected nonpregnant cows and sheep or naturally infected cattle. This study is a first step towards the development of a multiprotein diagnostic reagent for brucellosis.     

The clinical relevance of cytokeratin phenotyping in needle biopsy of liver metastasis

Although cytokeratin (CK) phenotyping of metastatic tumors is now routine in many laboratories, the clinical relevance of the procedure has seldom been addressed. We carried out a prospective clinical study of 134 consecutive cases of metastatic adenocarcinoma of the liver diagnosed by needle biopsies stained routinely for CK20 and CK7. The most probable localization of the primary tumor, deduced from this staining pattern, was stated in the original pathology report. The present study compared this assignment with the information available at the time of interpretation of the liver biopsy, to the results of the subsequent clinical investigation, and to the officially reported cause of death as outcome. As expected, the primary tumors were localized in the colon or in the rectum in 85% (34/40) of the CK20+/CK7- metastases. The definite diagnosis remained metastatic colorectal carcinoma in 83% (15/18) of the cases with diagnosed colorectal cancer before the liver biopsy. In the cases without a known primary tumor when the liver biopsy was interpreted, primary colorectal localization was accurately predicted in 86% (19/22) of the patients. Compared to the outcome, 77% (36/47) of the CK20+/CK7+ metastases had the expected pancreaticobiliary primary localization in 83% (30/36) without any primary tumor being known at the time of interpretation of the liver biopsy. In contrast, the majority of CK20- metastatic carcinomas had an unexpected primary localization, 50% (16/32) in the CK20-/CK7+ and 60% (9/15) in the CK20-/CK7- subgroup. In addition, the origin of the liver metastasis remained unknown in 37% (12/32) of CK20-/CK7+ cases. Thus, the CK20+/CK7- phenotype indicates a colorectal origin of the liver metastasis with considerable accuracy and independently of the available clinical information. The same is true for CK20+/CK7+ metastases, which indicate primary tumor localization in the pancreas or in the biliary tree. The results in the CK20- subgroups of the liver metastases are disappointing and cannot substantially help the clinical investigation.     

Outbreak of septicaemic cases caused by Acinetobacter ursingii in a neonatal intensive care unit

Neonatal infections may be caused by various microorganisms, but as far as we are aware, Acinetobacter ursingii has not yet been reported in connection with nosocomial infections of premature infants. During 2 months, 3 premature babies were treated with nosocomial infection caused by A. ursingii at the same ward, and on the basis of molecular typing results the same strain was responsible for all of these cases. Traditional biochemical methods and automatic identification systems failed to identify this bacterium on the species level, and only 16S rDNA sequencing gave acceptable species identifications. The isolated strains proved to be susceptible to all of the tested antimicrobials, including ampicillin/sulbactam, doxycyclin, netilmicin, ciprofloxacin, piperacillin/tazobactam, ceftazidime, imipenem, meropenem, trimethoprim/sulfametoxazole, gentamicin, tobramycin, amikacin, and levofloxacin according to the CLSI standard. In spite of the environmental screening, the source of the infection could not be clarified. One of 3 neonates died, the others recovered and were discharged home after several months of hospitalization.     

Monitoring the Chemical Heterogeneity and the Crystallization Behavior of PP‐g‐PS Graft Copolymers Using SEC‐FTIR and CRYSTAF

Graft copolymers of propene with styrene were analyzed with regard to their chemical heterogeneity using both SEC coupled to FT‐IR spectroscopy and CRYSTAF. The SEC‐FTIR indicates chemical homogeneity of the copolymer samples. The decrease in crystallization temperature in CRYSTAF does not correlate with the concentration of PS in the samples but it correlates decisively with the branching frequency. The length of the PS branches does not influence the crystallization temperature in CRYSTAF, although the longest branches in the individual samples were 44 times longer than the shortest ones.

     

Expression of nectin-1 in normal and herpes simplex virus type 1-infected murine brain.

Nectin-1 is an adherens junction protein that serves as an entry receptor for neurotropic herpes simplex virus (HSV). The expression of nectin-1 in the central nervous system (CNS) has not been well defined. Furthermore, it is not known whether HSV infection has an effect on nectin-1 expression in the brain. To better understand nectin-1 expression in normal and HSV-infected brain, the authors used immunohistochemistry to characterize the expression of nectin-1 in brain tissue of uninfected adult mice and mice infected with HSV-1. In the CNS of untreated and mock-infected mice, virtually all neurons, ependymal cells, choroid plexus epithelial cells, meningothelial cells, and vascular endothelial cells expressed nectin-1. Many oligodendrocytes, astrocytes, and vascular smooth muscle cells also demonstrated nectin-1 expression, but a minority of these cells did not stain for nectin-1. Brain tissue derived from mice euthanized 5 to 8 days after intracerebral inoculation of HSV-1 showed inflammation and widespread expression of HSV-1 proteins in neurons. In HSV-1-infected brains, many inflammatory cells showed nectin-1 expression and neuronal nectin-1 staining showed a wider variation in signal strength than that detected in uninfected tissues. Many neurons showing nuclear fragmentation consistent with the morphologic appearance of apoptosis showed little or no evidence of nectin-1 expression, whereas occasional neurons stained more intensely positive for nectin-1 than those in uninfected brain tissue. These findings confirm and extend previous observations of nectin-1 expression in the nervous system and suggest that HSV-1 infection leads to changes in nectin-1 expression in the CNS, which may contribute to HSV-induced pathology and dissemination.     

Upper airway distensibility and collapsibility in patients with obstructive sleep apnea

The present study was performed to evaluate the distensibility and collapsibility characteristics of regional segments of the UA in patients with OSA and in normal subjects in response to changes in airway pressure. Seventeen male patients with moderately severe OSA and 13 normal subjects underwent CT of the UA in the supine position while awake. Axial views were obtained from the level of the hard palate to the hypopharynx under conditions of -5, 0, and +10 cm H2O of CAP. The results indicated that the Amin occurred within 20 mm of the hard palate in the retropalatal region of the UA in 16 (94 percent) of the 17 patients and in 12 (92 percent) of the 13 normal subjects. Continuous negative airway pressure of -5 cm H2O failed to significantly decrease either Amin or Amean in either the patients or normal subjects, suggesting good UA load compensation during wakefulness. Continuous positive airway pressure of 10 cm H2O significantly increased Amin and Amean to a similar extent in both groups. The Amin was significantly smaller by 40 percent, 33 percent, and 37 percent in the patients with OSA, compared to the normal subjects, at -5, 0, and +10 cm H2O of CAP, respectively. In contrast, Amean did not differ between the groups. The CT scan criterion of Amin less than or greater than 1.0 cm2 during tidal ventilation of atmospheric pressure correctly categorized patients with OSA and normal subjects with an accuracy of 70 percent. While the behavior of the UA in response to nasal CPAP and CNAP failed to increase the accuracy of CT scan criteria to a level sufficient for clinical use in the diagnosis of OSA, the results clearly indicate that structural changes in the UA contribute to the development of OSA.     

Effects of exercise cessation on lipids and lipoproteins in distance runners and power athletes

Summary The purpose of this study was to determine the effects of short-term exercise cessation on lipid and lipoprotein profile and insulin sensitivity in highly trained runners (n=12; mean age 19.9 years) and power athletes (n=12; mean age 24.4 years). Following 14 days of exercise cessation, running time to exhaustion and maximal oxygen uptake decreased by 9.2% and 4.8% (P < 0.05) in the runners, while in the power athletes one repetition maximum squat and bench press did not change (P>0.05). No changes occurred in body composition. Data from a 2-h oral glucose tolerance test revealed an impairment of the glycemic state in all athletes (P<0.05). In contrast, exercise cessation did not significantly (P>0.05) alter plasma levels of cholesterol, triglycerides, and low density (LDL) and high density lipoprotein (HDL). No changes were observed in HDL₂, HDL_2b, and HDL₃ subfractions, LDL diameter, and qualitative LDL pattern (P>0.05). These data thus suggest that despite a decrease in insulin sensitivity, short-term exercise cessation, independent of exercise mode, was insufficient to alter plasma lipid and lipoprotein profiles in well-trained athletes.