Radiation Spectra from Advection-Dominated Accretion Flows in a Global Magnetic Field

We calculate the radiation spectra from advection-dominated accretion flows (ADAFs), taking into account the effects of a global magnetic field. Calculation is based on the analytic model for magnetized ADAFs proposed by Kaburaki, where a large-scale magnetic field controls the accretion process. Adjusting a few parameters, we find that our model can well reproduce the observed spectrum of Sagittarius A$^{*}$. The result is discussed in comparison with those of well-known ADAF models, where the turbulent viscosity controls the accretion process.Comment: Accepted for publication in Ap

Source identification of N2O produced during simulated wastewater treatment under different oxygen conditions using stable isotopic analysis

Nitrous oxide (N2O), a potent greenhouse gas which is important in climate change, is predicted to be the most dominant ozone depleting substance. It is mainly produced by oxidation of hydroxylamine (NH2OH) or reduction of nitrite (NO2-) during microbiological processes such as nitrification and denitrification. Wastewater treatment plant (WWTP) is one of the anthropogenic N2O sources because inorganic and organic nitrogen compounds are converted to nitrate (NO3-, in the case of standard system) or N2 (in the case of advanced system) by bacterial nitrification and denitrification in WWTP. We investigated the N2O production mechanisms during batch experiments that simulate wastewater treatment with activated sludge under various dissolved oxygen (DO) concentrations by stable isotope analysis. About 125mL of water was sampled from 30L incubation chamber for several times during the incubation, and concentration and isotopomer ratios of N2O and N-containing species were measured using gas chromatography/isotope ratio mass spectrometry (GC/IRMS). Ammonium (NH4+) consumption was accompanied by increment of nitrite (NO2-), and at the same time dissolved N2O concentration gradually increased to 4850 and 5650 nmol kg-1, respectively, during the four-hour incubation when DO concentrations were 0.2 and 0.5 mg L-1. Observed low SP values (0.2-8.9‰ at DO-0.2 mg L-1, -5.3-6.3‰ at DO-0.5 mg L-1, -1.0-8.3‰ at DO-0.8 mg L-1) in N2O and relationship of nitrogen isotope ratios between N2O and its potential substrates (NH4+, NO3-) suggested that N2O produced under the aerobic condition derived mainly from NO2- reduction by ammonia-oxidizing bacteria (nitrifier–denitrification).DOI: http://doi.dx.org/10.5564/mjc.v15i0.313Mongolian Journal of Chemistry  15 (41), 2014, p4-10

Calmodulin Binding to the 3614–3643 Region of RyR1 Is Not Essential for Excitation–Contraction Coupling in Skeletal Myotubes

Calmodulin is a ubiquitous Ca2+ binding protein that modulates the in vitro activity of the skeletal muscle ryanodine receptor (RyR1). Residues 3614–3643 of RyR1 comprise the CaM binding domain and mutations within this region result in a loss of both high-affinity Ca2+-bound calmodulin (CaCaM) and Ca2+-free CaM (apoCaM) binding (L3624D) or only CaCaM binding (W3620A). To investigate the functional role of CaM binding to this region of RyR1 in intact skeletal muscle, we compared the ability of RyR1, L3624D, and W3620A to restore excitation–contraction (EC) coupling after expression in RyR1-deficient (dyspedic) myotubes. W3620A-expressing cells responded normally to 10 mM caffeine and 500 μM 4-chloro-m-cresol (4-cmc). Interestingly, L3624D-expressing cells displayed a bimodal response to caffeine, with a large proportion of cells (∼44%) showing a greatly attenuated response to caffeine. However, high and low caffeine-responsive L3624D-expressing myotubes exhibited Ca2+ transients of similar magnitude after activation by 4-cmc (500 μM) and electrical stimulation. Expression of either L3624D or W3620A in dyspedic myotubes restored both L-type Ca2+ currents (retrograde coupling) and voltage-gated SR Ca2+ release (orthograde coupling) to a similar degree as that observed for wild-type RyR1, although L-current density was somewhat larger and activated at more hyperpolarized potentials in W3620A-expressing myotubes. The results indicate that CaM binding to the 3614–3643 region of RyR1 is not essential for voltage sensor activation of RyR1

H+ transport is an integral function of the mitochondrial ADP/ATP carrier.

The mitochondrial ADP/ATP carrier (AAC) is a major transport protein of the inner mitochondrial membrane. It exchanges mitochondrial ATP for cytosolic ADP and controls cellular production of ATP. In addition, it has been proposed that AAC mediates mitochondrial uncoupling, but it has proven difficult to demonstrate this function or to elucidate its mechanisms. Here we record AAC currents directly from inner mitochondrial membranes from various mouse tissues and identify two distinct transport modes: ADP/ATP exchange and H+ transport. The AAC-mediated H+ current requires free fatty acids and resembles the H+ leak via the thermogenic uncoupling protein 1 found in brown fat. The ADP/ATP exchange via AAC negatively regulates the H+ leak, but does not completely inhibit it. This suggests that the H+ leak and mitochondrial uncoupling could be dynamically controlled by cellular ATP demand and the rate of ADP/ATP exchange. By mediating two distinct transport modes, ADP/ATP exchange and H+ leak, AAC connects coupled (ATP production) and uncoupled (thermogenesis) energy conversion in mitochondria

Spin Seebeck Effect in Layered Ferromagnetic Insulators CrSiTe₃ and CrGeTe₃

We have studied the longitudinal spin Seebeck effect (LSSE) in the layered ferromagnetic insulators CrSiTe₃ and CrGeTe₃ covered by Pt films in the measurement configuration where spin current traverses the ferromagnetic Cr layers. The LSSE response is clearly observed in the ferromagnetic phase and—in contrast to a standard LSSE magnet Y₃Fe₅O₁₂—persists above the critical temper- atures in both CrSiTe₃/Pt and CrGeTe₃/Pt samples. With the help of a numerical calculation, we attribute the LSSE signals observed in the paramagnetic regime to exchange-dominated interlayer transport of in-plane paramagnetic moments reinforced by short-range ferromagnetic correlations and strong Zeeman effects

Inhibition of DUSP6 sensitizes ovarian cancer cells to chemotherapeutic agents via regulation of ERK signaling response genes

Dual specificity phosphatase 6 (DUSP6) is a protein phosphatase that deactivates extracellular-signal-regulated kinase (ERK). Since the ovarian cancer biomarker human epididymis protein 4 (HE4) interacts with the ERK pathway, we sought to determine the relationship between DUSP6 and HE4 and elucidate DUSP6’s role in epithelial ovarian cancer (EOC). Viability assays revealed a significant decrease in cell viability with pharmacological inhibition of DUSP6 using (E/Z)-BCI hydrochloride in ovarian cancer cells treated with carboplatin or paclitaxel, compared to treatment with either agent alone. Quantitative PCR was used to evaluate levels of ERK pathway response genes to BCI in combination with recombinant HE4 (rHE4), carboplatin, and paclitaxel. Expression of EGR1, a promoter of apoptosis, was higher in cells co-treated with BCI and paclitaxel or carboplatin than in cells treated with chemotherapeutic agents alone, while expression of the proto-oncogene c-JUN was decreased with co-treatment. The effect of BCI on the expression of these two genes opposed that of rHE4. Pathway focused quantitative PCR also revealed suppression of ERBB3 in cells co-treated with BCI plus carboplatin or paclitaxel. Finally, expression levels of DUSP6 in EOC tissue were evaluated by immunohistochemistry, revealing significantly increased levels of DUSP6 in serous EOC tissue compared to adjacent normal tissue. A positive correlation between HE4 and DUSP6 levels was determined by Spearman Rank correlation. In conclusion, DUSP6 inhibition sensitizes ovarian cancer cells to chemotherapeutic agents and alters gene expression of ERK response genes, suggesting that DUSP6 could plausibly function as a novel therapeutic target to reduce chemoresistance in EOC

General anesthesia for electroconvulsive therapy with Brugada electrocardiograph pattern

Brugada syndrome is characterized by an electrocardiograph pattern of right bundle-branch block and has an increased risk for cardiac arrest due to malignant arrhythmia. We describe the successful anesthetic management for electroconvulsive therapy in a patient with Brugada electrocardiograph pattern. Patients with Brugada ECG pattern are not recommended to use neostigmine which augments ST elevation. Sugammadex was administered as a neuromuscular reversal agent in this case. Sugammadex provides rapid reversal of profound rocuronium-induced neuromuscular blockade under propofol anesthesia

Carcinoma Arising from Brunner's Gland in the Duodenum after 17 Years of Observation – A Case Report and Literature Review

A 60-year-old man presented with melena and hematemesis in 1984. Esophagogastroduodenoscopy (EGD) detected a small protruding lesion in the duodenal bulb, which was diagnosed as Brunner's adenoma. No significant change was detected in subsequent annual EGD and biopsies for 10 years, after which the patient was not observed for 7 years. The patient presented with melena again in 2001. The lesion had changed shape to become a 10 mm sessile tumor with a central depression, and following a biopsy was diagnosed as an adenocarcinoma. The patient underwent partial resection of the duodenum. Histopathological assessment showed acidophilic cells with swollen nuclei, and clear cells forming a tubular or papillary tubule in the mucosal lamina propria and submucosal layer. The tumor cells stained positive for lysozyme, indicating that they arose from Brunner's gland. The patient showed no sign of recurrence and was disease-free for more than 34 months after surgery. The patient died of pneumonia. This is an extremely rare case of primary duodenal carcinoma arising from Brunner's gland in a patient observed for 17 years

A frameshift mutation in NOD2 associated with susceptibility to Crohn's disease

Crohn's disease is a chronic inflammatory disorder of the gastrointestinal tract, which is thought to result from the effect of environmental factors in a genetically predisposed host. A gene location in the pericentromeric region of chromosome 16, IBD1, that contributes to susceptibility to Crohn's disease has been established through multiple linkage studies(1-6), but the specific gene(s) has not been identified. NOD2, a gene that encodes a protein with homology to plant disease resistance gene products is located in the peak region of linkage on chromosome 16 (ref. 7). Here we show, by using the transmission disequilibium test and case-control analysis, that a frameshift mutation caused by a cytosine insertion, 3020insC, which is expected to encode a truncated NOD2 protein, is associated with Crohn's disease. Wild-type NOD2 activates nuclear factor NF-kappaB, making it responsive to bacterial lipopolysaccharides; however, this induction was deficient in mutant NOD2. These results implicate NOD2 in susceptibility to Crohn's disease, and suggest a link between an innate immune response to bacterial components and development of disease.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/62856/1/411603a0.pd

Inhibition of Casein Kinase 2 Modulates XBP1-GRP78 Arm of Unfolded Protein Responses in Cultured Glial Cells

Stress signals cause abnormal proteins to accumulate in the endoplasmic reticulum (ER). Such stress is known as ER stress, which has been suggested to be involved in neurodegenerative diseases, diabetes, obesity and cancer. ER stress activates the unfolded protein response (UPR) to reduce levels of abnormal proteins by inducing the production of chaperon proteins such as GRP78, and to attenuate translation through the phosphorylation of eIF2α. However, excessive stress leads to apoptosis by generating transcription factors such as CHOP. Casein kinase 2 (CK2) is a serine/threonine kinase involved in regulating neoplasia, cell survival and viral infections. In the present study, we investigated a possible linkage between CK2 and ER stress using mouse primary cultured glial cells. 4,5,6,7-tetrabromobenzotriazole (TBB), a CK2-specific inhibitor, attenuated ER stress-induced XBP-1 splicing and subsequent induction of GRP78 expression, but was ineffective against ER stress-induced eIF2α phosphorylation and CHOP expression. Similar results were obtained when endogenous CK2 expression was knocked-down by siRNA. Immunohistochemical analysis suggested that CK2 was present at the ER. These results indicate CK2 to be linked with UPR and to resist ER stress by activating the XBP-1-GRP78 arm of UPR