Does B-type natriuretic peptide level predict outcome after arterial switch operation ?

Evaluation the predictive value of perioperative Plasma B-type natriuretic peptide level in arterial switch operation. Plasma B-type natriuretic peptide level was measured before and and 24 hours after surgery in 29 patients with arterial switch operation. We evaluated 29 patients (22 male,76,7 female 24) with mean age 67.93±84.09 days (range 6 days to 14months).The mean of BNP level before surgery was 7989.96±9691.94 and increased after surgery to 22391.35±11898.67 and difference between two groups was significant (P=0.003).In linear regression test the BNP did not correlate with sex(r=0.33, P=0.085) and age(r=0.14,P=0.45). Furthermore, BNP did not correlate with duration of mechanical ventilation (r=0.132,P=0.53), ICU stay (r=0.137,P=0.52) and with lactate level (r=0.41,P=0.054)after operation. During the study 4 patients(13.8) died and the mean of BNP 24h after operation among them was 35000.00±00.00.using chai-square and fisher exact test the correlation between BNP and death was significant(P=0.001). We implied that BNP level increased 24 hours after arterial switch operation, moreover we denoted it correlated well with the death rate and an increase in B-type natriuretic peptide 24 hours after surgery predicts poor postoperative outcome. However it did not correlate with duration of mechanical ventilation, ICU stay and lactate level in this patients

Association between self-efficacy and quality of life in women with breast cancer undergoing chemotherapy

Background: Self-efficacy is known as a factor which influences health behaviors, chronic diseases management and quality of life in patients with cancer. Objective: The aim of this study was to investigate the association of self-efficacy and quality of life in women with breast cancer undergoing chemotherapy. Methods: This cross sectional study was conducted in 100 women with breast cancer referred to Seyed Al-Shohada Hospital, Isfahan in 2015. The study subjects were selected by simple random sampling method. The measurement tools were the Sherer self-efficacy scale and the World Health Organization WHOQOL-BREF quality of life assessment. Data were analyzed using one-way ANOVA and Pearson’s correlation coefficient. Findings: Mean age was 48.25±11.93 years. The mean self-efficacy score and quality of life score were 55.78± 11 and 75.91±15.28, respectively and both of them were average. There was positive significant correlation between self-efficacy and quality of life. There was also significant association between self-efficacy and quality of life domains including physical health, mental health, social relationships and environment. Conclusion: With regards to the results, it seems that activities such as workshops for patients, presence of a psychologist in department of chemotherapy, and providing health facilities can be effective for increasing self-efficacy and quality of life in patients with cance

Linear Sequential Circuit Approximation of Grain and Trivium Stream Ciphers

Grain and Trivium are two hardware oriented synchronous stream ciphers proposed as the simplest candidates to the ECRYPT Stream Cipher Project, both dealing with 80-bit secret keys. In this paper we apply the linear sequential circuit approximation method to evaluate the strength of these stream ciphers against distinguishing attack. In this approximation method which was initially introduced by Golic in 1994, linear models are effectively determined for autonomous finite-state machines. We derive linear functions of consecutive key-stream bits which are held with correlation coefficient of about 2^-63.7 and 2^-126 for Grain and Trivium ciphers, respectively. Then using the concept of so-called generating function, we turn them into linear functions with correlation coefficient of 2^-29 for Grain and 2^-72 for Trivium. It shows that the Grain output sequence can be distinguished from a purely random sequence, using about 2^58 bits of the output sequence with the same time complexity. However, our attempt fails to find a successful distinguisher for Trivium

Nitration of Hsp90 induces cell death

Oxidative stress is a widely recognized cause of cell death associated with neurodegeneration, inflammation, and aging. Tyrosine nitration in these conditions has been reported extensively, but whether tyrosine nitration is a marker or plays a role in the cell-death processes was unknown. Here, we show that nitration of a single tyrosine residue on a small proportion of 90-kDa heat-shock protein (Hsp90), is sufficient to induce motor neuron death by the P2X7 receptor-dependent activation of the Fas pathway. Nitrotyrosine at position 33 or 56 stimulates a toxic gain of function that turns Hsp90 into a toxic protein. Using an antibody that recognizes the nitrated Hsp90, we found immunoreactivity in motor neurons of patients with amyotrophic lateral sclerosis, in an animal model of amyotrophic lateral sclerosis, and after experimental spinal cord injury. Our findings reveal that cell death can be triggered by nitration of a single protein and highlight nitrated Hsp90 as a potential target for the development of effective therapies for a large number of pathologies

CNS-targeted glucocorticoid reduces pathology in mouse model of amyotrophic lateral sclerosis

Hallmarks of CNS inflammation, including microglial and astrocyte activation, are prominent features in post-mortem tissue from amyotrophic lateral sclerosis (ALS) patients and in mice overexpressing mutant superoxide dismutase-1 (SOD1 G93A ). Administration of non-targeted glucocorticoids does not significantly alter disease progression, but this may reflect poor CNS delivery. Here, we sought to discover whether CNS-targeted, liposomal encapsulated glucocorticoid would inhibit the CNS inflammatory response and reduce motor neuron loss. SOD1 G93A mice were treated with saline, free methylprednisolone (MP, 10 mg/kg/week) or glutathione PEGylated liposomal MP (2B3-201, 10 mg/kg/week) and compared to saline treated wild-type animals. Animals were treated weekly with intravenous injections for 9 weeks from 60 days of age. Weights and motor performance were monitored during this period. At the end of the experimental period (116 days) mice were imaged using T 2-weighted MRI for brainstem pathology; brain and spinal cord tissue were then collected for histological analysis

C3 Peptide Promotes Axonal Regeneration and Functional Motor Recovery after Peripheral Nerve Injury

Peripheral nerve injuries are frequently seen in trauma patients and due to delayed nerve repair, lifelong disabilities often follow this type of injury. Innovative therapies are needed to facilitate and expedite peripheral nerve regeneration. The purpose of this study was to determine the effects of a 1-time topical application of a 26-amino-acid fragment (C3156-181), derived from the Clostridium botulinum C3-exoenzyme, on peripheral nerve regeneration in 2 models of nerve injury and repair in adult rats. After sciatic nerve crush, different dosages of C3156-181 dissolved in buffer or reference solutions (nerve growth factor or C3bot-wild-type protein) or vehicle-only were injected through an epineurial opening into the lesion sites. After 10-mm nerve autotransplantation, either 8.0 nmol/kg C3156-181 or vehicle were injected into the proximal and distal suture sites. For a period of 3 to 10 postoperative weeks, C3156-181-treated animals showed a faster motor recovery than control animals. After crush injury, axonal outgrowth and elongation were activated and consequently resulted in faster motor recovery. The nerve autotransplantation model further elucidated that C3156-181 treatment accounts for better axonal elongation into motor targets and reduced axonal sprouting, which are followed by enhanced axonal maturation and better axonal functionality. The effects of C3156-181 are likely caused by a nonenzymatic down-regulation of active RhoA. Our results indicate the potential of C3156-181 as a therapeutic agent for the topical treatment of peripheral nerve repair sites

A Randomized, Double Blind, Placebo-Controlled Trial of Pioglitazone in Combination with Riluzole in Amyotrophic Lateral Sclerosis

BACKGROUND: Pioglitazone, an oral anti-diabetic that stimulates the PPAR-gamma transcription factor, increased survival of mice with amyotrophic lateral sclerosis (ALS). METHODS/PRINCIPAL FINDINGS: We performed a phase II, double blind, multicentre, placebo controlled trial of pioglitazone in ALS patients under riluzole. 219 patients were randomly assigned to receive 45 mg/day of pioglitazone or placebo (one: one allocation ratio). The primary endpoint was survival. Secondary endpoints included incidence of non-invasive ventilation and tracheotomy, and slopes of ALS-FRS, slow vital capacity, and quality of life as assessed using EUROQoL EQ-5D. The study was conducted under a two-stage group sequential test, allowing to stop for futility or superiority after interim analysis. Shortly after interim analysis, 30 patients under pioglitazone and 24 patients under placebo had died. The trial was stopped for futility; the hazard ratio for primary endpoint was 1.21 (95% CI: 0.71-2.07, p = 0.48). Secondary endpoints were not modified by pioglitazone treatment. Pioglitazone was well tolerated. CONCLUSION/SIGNIFICANCE: Pioglitazone has no beneficial effects on the survival of ALS patients as add-on therapy to riluzole. TRIAL REGISTRATION: Clinicaltrials.gov NCT00690118

TNF-dependent regulation and activation of innate immune cells are essential for host protection against cerebral tuberculosis

BACKGROUND: Tuberculosis (TB) affects one third of the global population, and TB of the central nervous system (CNS-TB) is the most severe form of tuberculosis which often associates with high mortality. The pro-inflammatory cytokine tumour necrosis factor (TNF) plays a critical role in the initial and long-term host immune protection against Mycobacterium tuberculosis (M. tuberculosis) which involves the activation of innate immune cells and structure maintenance of granulomas. However, the contribution of TNF, in particular neuron-derived TNF, in the control of cerebral M. tuberculosis infection and its protective immune responses in the CNS were not clear. METHODS: We generated neuron-specific TNF-deficient (NsTNF / ) mice and compared outcomes of disease against TNF f/f control and global TNF / mice. Mycobacterial burden in brains, lungs and spleens were compared, and cerebral pathology and cellular contributions analysed by microscopy and flow cytometry after M. tuberculosis infection. Activation of innate immune cells was measured by flow cytometry and cell function assessed by cytokine and chemokine quantification using enzyme-linked immunosorbent assay (ELISA). RESULTS: Intracerebral M. tuberculosis infection of TNF / mice rendered animals highly susceptible, accompanied by uncontrolled bacilli replication and eventual mortality. In contrast, NsTNF / mice were resistant to infection and presented with a phenotype similar to that in TNF f/f control mice. Impaired immunity in TNF / mice was associated with altered cytokine and chemokine synthesis in the brain and characterised by a reduced number of activated innate immune cells. Brain pathology reflected enhanced inflammation dominated by neutrophil influx. CONCLUSION: Our data show that neuron-derived TNF has a limited role in immune responses, but overall TNF production is necessary for protective immunity against CNS-TB