Real characters in blocks

We consider real versions of Brauer's k(B) conjecture, Olsson's conjecture and Eaton's conjecture. We prove the real version of Eaton's conjecture for 2-blocks of groups with cyclic defect group and for the principal 2-blocks of groups with trivial real core. We also characterize G-classes, real and rational G-classes of the defect group of a block B

Impairment of neutrophil oxidative burst in children with sickle cell disease is associated with heme oxygenase-1.

Sickle cell disease is a risk factor for invasive bacterial infections, and splenic dysfunction is believed to be the main underlying cause. We have previously shown that the liberation of heme in acute hemolysis can induce heme oxygenase-1 during granulopoiesis, impairing the ability of developing neutrophils to mount a bactericidal oxidative burst, and increasing susceptibility to bacterial infection. We hypothesized that this may also occur with the chronic hemolysis of sickle cell disease, potentially contributing to susceptibility to infections. We found that neutrophil oxidative burst activity was significantly lower in treatment-naïve children with sickle cell disease compared to age-, gender- and ethnicity-matched controls, whilst degranulation was similar. The defect in neutrophil oxidative burst was quantitatively related to both systemic heme oxygenase-1 activity (assessed by carboxyhemoglobin concentration) and neutrophil mobilization. A distinct population of heme oxygenase-1-expressing cells was present in the bone marrow of children with sickle cell disease, but not in healthy children, with a surface marker profile consistent with neutrophil progenitors (CD49d(Hi) CD24(Lo) CD15(Int) CD16(Int) CD11b(+/-)). Incubation of promyelocytic HL-60 cells with the heme oxygenase-1 substrate and inducer, hemin, demonstrated that heme oxygenase-1 induction during neutrophilic differentiation could reduce oxidative burst capacity. These findings indicate that impairment of neutrophil oxidative burst activity in sickle cell disease is associated with hemolysis and heme oxygenase-1 expression. Neutrophil dysfunction might contribute to risk of infection in sickle cell disease, and measurement of neutrophil oxidative burst might be used to identify patients at greatest risk of infection, who might benefit from enhanced prophylaxis

Early-life experience reduces excitation to stress-responsive hypothalamic neurons and reprograms the expression of corticotropin-releasing hormone.

Increased sensory input from maternal care attenuates neuroendocrine and behavioral responses to stress long term and results in a lifelong phenotype of resilience to depression and improved cognitive function. Whereas the mechanisms of this clinically important effect remain unclear, the early, persistent suppression of the expression of the stress neurohormone corticotropin-releasing hormone (CRH) in hypothalamic neurons has been implicated as a key aspect of this experience-induced neuroplasticity. Here, we tested whether the innervation of hypothalamic CRH neurons of rat pups that received augmented maternal care was altered in a manner that might promote the suppression of CRH expression and studied the cellular mechanisms underlying this suppression. We found that the number of excitatory synapses and the frequency of miniature excitatory synaptic currents onto CRH neurons were reduced in "care-augmented" rats compared with controls, as were the levels of the glutamate vesicular transporter vGlut2. In contrast, analogous parameters of inhibitory synapses were unchanged. Levels of the transcriptional repressor neuron-restrictive silencer factor (NRSF), which negatively regulates Crh gene transcription, were markedly elevated in care-augmented rats, and chromatin immunoprecipitation demonstrated that this repressor was bound to a cognate element (neuron-restrictive silencing element) on the Crh gene. Whereas the reduced excitatory innervation of CRH-expressing neurons dissipated by adulthood, increased NRSF levels and repression of CRH expression persisted, suggesting that augmented early-life experience reprograms Crh gene expression via mechanisms involving transcriptional repression by NRSF

Mortality and cardiovascular diseases risk in patients with Barrett's oesophagus:a population-based nationwide cohort study

Background: Patients with Barrett's oesophagus may be at increased risk of mortality overall, and cardiovascular disease has been suggested as the main underlying cause of death. Aim: To examine cause-specific mortality and risk of cardiovascular events among patients with Barrett's oesophagus. Methods: Utilising existing Danish data sources (1997–2011), we identified all patients with histologically verified Barrett's oesophagus (n = 13 435) and 123 526 members of the general population matched by age, sex and individual comorbidities. We calculated cause-specific mortality rates and incidence rates of cardiovascular diseases. We then compared rates between patients with Barrett's oesophagus and the general population comparison cohort, using stratified Cox proportional hazard regression. Results: Patients with Barrett's oesophagus had a 71% increased risk of overall mortality. The cause-specific mortality rate per 1000 person-years for patients with Barrett's oesophagus was 8.5 for cardiovascular diseases, 14.7 for non-oesophageal cancers, and 5.4 for oesophageal cancer. Compared to the general population cohort, corresponding hazard ratios were 1.26 (95% confidence interval (CI): 1.15–1.38), 1.77 (95% CI: 1.65–1.90), and 19.4 (95% CI: 16.1–23.4), respectively. The incidence rates of cardiovascular diseases per 1000 person-years for Barrett's oesophagus patients and for persons from the general population cohort, respectively, varied from 0.4 and 0.2 for subarachnoid bleeding (hazard ratio 1.10, 95% CI: 0.87–1.39) to 8.1 and 5.9 for congestive heart failure (hazard ratio 1.33, 95% CI: 1.21–1.46). Conclusion: Prophylactic measures targeted at cardiovascular diseases and non-oesophageal cancers potentially could be more important than measures against oesophageal cancer, for improving prognosis among patients with Barrett's oesophagus

Membrane fluidity matters: Hyperthermia from the aspects of lipids and membranes

Hyperthermia is a promising treatment modality for cancer in combination both with radio- and chemotherapy. In spite of its great therapeutic potential, the underlying molecular mechanisms still remain to be clarified. Due to lipid imbalances and 'membrane defects' most of the tumour cells possess elevated membrane fluidity. However, further increasing membrane fluidity to sensitise to chemo-or radiotherapy could have some other effects. In fact, hyperfluidisation of cell membrane induced by membrane fluidiser initiates a stress response as the heat shock protein response, which may modulate positively or negatively apoptotic cell death. Overviewing some recent findings based on a technology allowing direct imaging of lipid rafts in live cells and lipidomics, novel aspects of the intimate relationship between the 'membrane stress' of tumour cells and the cellular heat shock response will be highlighted. Our findings lend support to both the importance of membrane remodelling and the release of lipid signals initiating stress protein response, which can operate in tandem to control the extent of the ultimate cellular thermosensitivity. Overall, we suggest that the fluidity variable of membranes should be used as an independent factor for predicting the efficacy of combinational cancer therapies

A DRIFT Spectroscopic Study of Potassium Acetate Intercalated Mechanochemically Activated Kaolinite

Kaolinite has been mechanochemically activated by dry grinding for periods of time up to 10 h. The kaolinite was then intercalated with potassium acetate and the changes in the structure followed by DRIFT spectroscopy. Intercalation of the kaolinite with potassium acetate is difficult and only the layers, which remain hydrogen bonded, are intercalated. The mechanochemical activation of the kaolinite may be followed by the loss of intensity of the hydroxyl-stretching vibrations. The intensity of the 3695 and 3619 cm−1 bands reach a minimum after 10 h of grinding. The observation of a band at 3602 cm−1 is indicative of the intercalation of the kaolinite with potassium acetate. The degree of intercalation decreases with mechanochemical treatment. The effect of exposure of the intercalated mechanochemically activated kaolinite to moist air results in de-intercalation. The effect of the mechanochemical treatment is loss of layer stacking, which prevents the intercalation of the kaolinite

Deintercalation of Hydrazine-intercalated Kaolinite in Dry and Moist Air

The deintercalation of a low defect kaolinite intercalated with hydrazine has been followed by X-ray diffraction, diffuse reflectance infrared spectroscopy (DRIFT) and Raman microscopy over an extended period of time. X-ray diffraction showed the kaolinite was totally intercalated and that more than 120 hours were required for the hydrazine intercalate to be decomposed. The Raman spectra of the hydrazine intercalate showed only a single band at 3620 cm-1 attributed to the inner hydroxyl group. Upon deintercalation additional Raman bands were observed at 3626 and 3613 cm-1. These bands decreased in intensity with further deintercalation. As deintercalation occurs the bands assigned to the inner surface hydroxyl groups at 3695, 3682, 3670 and 3650 cm-1 appeared and increased in intensity. DRIFT spectra showed two bands at 3620 and 3626 cm-1 for the fully intercalated kaolinite only. Upon deintercalation an additional band assigned to intercalated water was observed at 3599 cm-1 and increased in intensity at the expense of the 3626 cm-1 band. Further, the bands attributed to the inner surface hydroxyl groups increased in intensity with deintercalation. Both the Raman and DRIFT spectra showed complexity in the NH stretching region with two sets of NH symmetric and asymmetric stretching bands observed. Deintercalation was easily followed by the loss of intensity of these bands. Significant changes were also observed in the hydroxyl deformation and water bending modes as a result of deintercalation. A new model of hydrazine intercalation of kaolinite based on the insertion of a hydrazine-water unit is proposed. The hydrated end of the hydrazine molecule hydrogen bonds with the inner surface hydroxyl groups resulting in the formation of the new band at 3626 cm-1 in the DRIFT spectra