A dataset consisting of a two-year long temperature and sound speed time series from acoustic tomography in Fram Strait.

Acoustic tomography systems provide an integrated, synoptic measurement of ocean temperature. By recording the time it takes for a sound signal to travel from a sound source to a receiver, the depth- and range-average sound speed along the geodesic path between the sound source and the receiver can be obtained through inversion. Sound speed and ocean temperature are empirically related; salinity plays a negligible role. The ACOBAR acoustic tomography experiment in central Fram Strait was carried out from September 2010 to September 2012. It consisted of 3 moorings with sound sources and receivers forming a triangle, and one mooring with only receivers in the middle. The steel-sphere flotation of the northernmost mooring imploded in the start of the experiment, so that mooring was not recovered. The three remaining moorings formed a smaller triangle that provided travel time measurements along three paths. Measurements were taken 8 times a day for two of the paths, 8 times every other day for the other paths. The distances covered by the acoustic measurements are 188 - 201 km. Complex data processing was used to determine peaks in the acoustic arrival coda and to correct them for mooring motion and clock drift; travel-time accuracy is O(10) ms. The travel time measurements were inverted to obtain range-depth average sound speed using a statistical approach. The sound speed obtained from each section was then converted to mean ocean temperature. The mean ocean temperature data are published as a set of 8 NetCDF files, compliant with Climate and Forecast (CF) [1] and OceanSITES metadata conventions [2]. Each file contains one year of measurements from one of the sections. The files contain the ocean temperature data, together with theoretical and statistical error estimates and metadata such as discovery metadata and adequate-use metadata. Each data point is provided with a statistical quality measure and a quality flag based on this measure.

Emerging investigator series: investigation of mercury emission sources using Hg isotopic compositions of atmospheric mercury at the Cape Hedo Atmosphere and Aerosol Monitoring Station (CHAAMS), Japan.

This study conducted mercury (Hg) isotopic analysis, which has been expected as a new indicator for understanding the behavior of atmospheric Hg. The dominant atmospheric Hg species, namely gaseous elemental mercury (GEM, Hg0), were collected at the Cape Hedo Atmosphere and Aerosol Monitoring Station (CHAAMS) in Okinawa, Japan, for evaluating possible source(s) and transformation process(es) of Hg. The Hg isotopic compositions of GEM samples showed that the mass-dependent fractionation (MDF) of δ202Hg and the mass-independent fractionation (MIF) of Δ199Hg ranged from -2.15‰ to 0.79‰ and from -0.32‰ to 0.00‰, respectively. The results were classified into two groups: (1) negative δ202Hg and near-zero Δ199Hg in summer and (2) near-zero δ202Hg and negative Δ199Hg in the other season. According to the NOAA Hybrid Single-Particle Lagrangian Integrated Trajectory (HYSPLIT) model, the dominant air masses traveled from East Asia during winter and South and East Asia during summer. However, the air masses also traveled from mainland Japan and rotated around Okinawa before reaching CHAAMS. In contrast, clear positive correlations between δ202Hg values and CO and PM2.5 concentrations were observed during summer. A small peak of Ox concentration was observed at three atmospheric monitoring stations, namely Nago, Naha, and Miyako Island during summer. Since Miyako Island is located ∼370 km southwest of CHAAMS, the main emission source of GEM transported to CHAAMS was not from mainland Okinawa but traveled from the southwest during summer.

Diversity of vacA and cagA genes of Helicobacter pylori in Japanese children.

BACKGROUND: Helicobacter pylori infection is generally acquired in childhood and persists as an asymptomatic infection for decades in most infected individuals. Only a minority develops a clinical outcome even in childhood, such as peptic ulcer. It has been reported that H. pylori infection with the type I strain, which expresses the VacA and CagA antigen, is associated with peptic ulcer. AIM: We examined the diversity of vacA and cagA genes in isolates obtained from Japanese paediatric patients with peptic ulcer or chronic gastritis to investigate the relationship between genetic diversity and clinical outcome. METHODS: The diversity of vacA and cagA genes was investigated by PCR and sequence analysis in 30 isolates obtained from Japanese paediatric patients with peptic ulcer (eight strains) or chronic gastritis (22 strains). RESULTS: All isolates from Japanese children were cagA-positive strains. Twenty-six strains (86.7%) had East Asian type CagA, and 4 (13.3%) had Western type CagA. The predominant vacA genotype was s1c/m1b (22/30, 73.3%). There was no significant association between the diversity of cagA and vacA genes and clinical outcome. All four children infected with Western CagA strain had a history of overseas travel or residence. CONCLUSION: The predominant genotype of H. pylori in Japanese children is East Asian CagA and vacA s1c/m1b genotype, regardless of clinical outcome. Japanese H. pylori strains are homogeneously of the East Asian type; however, Western strains can be introduced into Japan concomitant with host movement from foreign countries in childhood.

The effects of cure of Helicobacter pylori infection on the signal transduction of gastric epithelial cells.

BACKGROUND: The CagA protein of Helicobacter pylori is directly injected from the bacteria into cells via the bacterial type IV secretion system and undergoes tyrosine phosphorylation in the gastric epithelial cells. Translocated CagA forms a physical complex with the SRC homology 2 domain (SH2)-containing tyrosine phosphatase SHP-2, which plays an important role in mitogenic signal transduction in the host cells. AIM: We examined the effect of eradication therapy on the signal transduction pathway of gastric epithelial cells induced by the CagA protein of H. pylori. METHODS: Gastric biopsy samples were obtained from 20 H. pylori-positive atrophic gastritis patients before, and 3 months after, H. pylori infection eradication therapy, and subjected to immunoblot analysis to detect tyrosine phosphorylated CagA protein and CagA co-immunoprecipitated endogenous SHP-2. RESULTS: Tyrosine phosphorylated CagA protein and CagA co-immunoprecipitated endogenous SHP-2 were detected in the gastric mucosa from H. pylori-positive atrophic gastritis patients. All H. pylori strains from these patients were cagA-positive type I strains. After curing H. pylori infection, the tyrosine phosphorylated CagA protein and CagA co-immunoprecipitated endogenous SHP-2 disappeared from the gastric mucosa. CONCLUSION: The cure of infection reduces the stimulated signal transduction of gastric epithelial cells by the translocated CagA protein of H. pylori, and may confer a beneficial effect on the reduction of cancer risk.

Association of the HLA-DRB1 gene locus with gastric adenocarcinoma in Japan.

BACKGROUND AND AIM: Helicobacter pylori infection is associated with gastric adenocarcinoma, however, the odds ratio is relatively low. The aim of the present study was to investigate host genetic factors that increase the risk of gastric adenocarcinoma among H. pylori-infected individuals. METHODS: A total of 70 patients with early gastric adenocarcinoma and 121 unrelated healthy controls were examined for H. pylori infection and HLA-DRB1 genotyping. The frequencies of HLA-DRB1 alleles were compared among groups. RESULTS: The allele frequency of DRB1*04051 was significantly higher in patients with gastric adenocarcinoma (17.9%) than in controls (7.9%) (P(correct) = 0.045). The odds ratio of gastric adenocarcinoma associated with the presence of the HLA-DRB1*04051 allele compared with its absence was 2.55 (95% confidence limits, 1.35-4.83). This genetic risk was not associated with H. pylori infection. There was no significant difference in the HLA-DRB1 allele frequency between H. pylori-positive and H. pylori-negative controls. The frequency of genotypes that possessed the DRB1*04051 allele in gastric adenocarcinoma patients (34.3%) was significantly higher than that in H. pylori-negative controls (11.9%) (p = 0.0089) and H. pylori-positive controls (15.2%) (p = 0.0066). CONCLUSION: These findings suggest that immunogenetic factors for susceptibility to gastric adenocarcinoma are present in the host, the HLA-DRB1*04051 allele is a host genetic risk factor for gastric adenocarcinoma, and that this genetic risk is independent of H. pylori infection.

Genetic and biochemical characterization of glutamyl endopeptidase of Staphylococcus warneri M.

A Staphylococcus warneri strain M, newly isolated from processed seafood (smoked Watasenia scintillans), produced an extracellular protease. The protease, designated to as m-PROM (the mature form of PROM), selectively cleaved the carbonyl side of glutamic acid residues in beta-casein. Sequence of N-terminal 27 amino acids of m-PROM, RANVILPNNDRHQINDTTLGHYAPVTF, was found to be similar to those of other glutamyl endopeptidases, V8 protease (Staphylococcus aureus strain V8) and SPase (S. aureus ATCC 12600). To determine the complete primary structure and precursor of PROM, its gene (proM) was cloned and sequenced. The gene proM was found to encode for a protein of 316 amino acids. The amino acid residues from 64 to 90 completely coincided with the N-terminal 27 amino acids of the m-PROM, suggesting that the N-terminal 63 amino acids region of p-PROM (the precursor form of PROM) might be processed posttranslationally. Moreover, the whole amino acid sequence deduced from the primary structure of proM shows significant similarity to those of other glutamyl endopeptidases, V8 protease and SPase. These results suggested that PROM belongs to the glutamyl endopeptidase class. PROM, however, differs from V8 and SPase proteases in the processing site and the C-terminal region.

Maternal epidermal growth factor deficiency causes fetal hypoglycemia and intrauterine growth retardation in mice: possible involvement of placental glucose transporter GLUT3 expression.

We investigated the physiological role of epidermal growth factor (EGF) in fetal growth in mice in which midgestational sialoadenectomy induced maternal EGF deficiency. Sialoadenectomy decreased the fetal weight significantly, indicating that maternal EGF deficiency caused intrauterine growth retardation. The weight of the fetal liver in the sialoadenectomized mice was reduced in proportion to the decrease in body weight (82.7+/-10.2 vs. 70.9+/-10.9 mg), whereas the brain weight was not reduced. Sialoadenectomy significantly decreased the glucose concentration in fetal plasma (86.0+/-13.0 vs. 63.0+/-11.8 mg/dl) without affecting the maternal plasma level of glucose. Transplacental transfer of 3H-2-deoxyglucose was significantly decreased by sialoadenectomy (5.17+/-1.25 vs. 2.94+/-1.02%), but transfer of 14C-aminoisobutyric acid was not affected. Northern blot analysis and in situ hybridization of glucose transporter isoform GLUT1 and GLUT3 messenger RNAs (mRNAs) in placenta revealed that sialoadenectomy significantly reduced the expression of GLUT3 mRNA without affecting GLUT1 mRNA levels. Administration of anti-EGF antiserum enhanced the effects of EGF deficiency, which were almost completely corrected by EGF supplementation. These results indicate that EGF plays an important role in fetal growth by regulating the transplacental supply of glucose via GLUT3 expression in the placenta.

Presence of ERK2 in rat retinal cells.

PURPOSE: Extracellular signal-regulated kinase 2 (ERK2) participates in the phosphorylation cascade that is activated in the an early intracellular response to various hormones and growth factors. We examined the expression and distribution of the ERK2 protein and mRNA in the rat retina before and after light exposure. METHODS: Rats were held on a 12 hr light/dark cycle and their retinas were removed and examined either just before or 2 or 30 min after light exposure. The tissue was processed for Western blotting to evaluate the presence of the protein for ERK2, and for in situ hybridization to evaluate the mRNA of ERK2. RESULTS: The Western blotting method showed a strong specific staining of a 42 kDa protein band in the retinal samples. This band corresponded to the expected size of p42 MAP kinase (ERK2). In situ hybridization histochemistry showed an intense localization of ERK2 mRNA in the outer nuclear layer (ONL), the inner nuclear layer (INL), and the ganglion cell layer (GCL) of the retina. The intensity and distribution of these signals did not differ among the animals, regardless of exposure to light. CONCLUSIONS: While ERK2 may be involved in the signal transduction system activated in retinal cells by light exposure, its precise role remains to be defined.

Correlation of suppressed linoleic acid metabolism with the hypocholesterolemic action of eritadenine in rats.

The dose-dependent effects of dietary eritadenine on the metabolism of linoleic acid and on the plasma cholesterol concentration were investigated to clarify the mechanism of the hypocholesterolemic action of eritadenine in rats. Rats were fed control or eritadenine-supplemented (2 to 20 mg/kg) diets for 14 d. Eritadenine supplementation significantly decreased both the plasma cholesterol concentration and the 20:4n-6/18:2n-6 ratio of liver microsomal and plasma phosphatidylcholine (PC) in a dose-dependent manner. Eritadenine was also found to decrease the activity of delta 6 desaturase in liver microsomes; there was significant correlation between the delta 6-desaturase activity and the 20:4n-6/18:2n-6 ratio in the PC of liver microsomes (r = 0.989, P < 0.001) or plasma (r = 0.986, P < 0.001). Certain plasma PC molecular species, as represented by 16:0-18.2, were increased by eritadenine in a dose-dependent manner, and certain plasma PC molecular species, as represented by 18:0-20:4, were conversely decreased by eritadenine. There was a significant correlation between the plasma total cholesterol concentration and the proportion of the sum of plasma PC molecular species which contain 18:1 or 18:2 in the sn-2 position. These results support the idea that the suppression of linoleic acid metabolism by eritadenine might be associated with the hypocholesterolemic action of eritadenine.

Coronary vasoconstrictive effects of neuropeptide Y and their modulation by the ATP-sensitive potassium channel in anesthetized dogs.

OBJECTIVES: This study examined the coronary vasoconstrictive action of endogenous neuropeptide Y (NPY) during sympathetic nerve stimulation and its modulation by the adenosine triphosphate (ATP)-sensitive potassium (KATP) channel in vivo. BACKGROUND: Exogenous NPY was characterized by its potent vasoconstrictive effect. However, endogenous NPY has failed to show any vasoconstrictive activity in vivo. METHODS: We studied 70 anesthetized dogs with vagotomy under beta-adrenergic blockade. Ansae subclaviae stimulation and intracoronary administration of the neurotransmitters (NPY and norepinephrine) were done with or without alpha-adrenergic blockade, NPY antagonist BIBP3226 or KATP channel acting agents. We measured coronary vascular resistance (CVR) and the neurotransmitter levels in systemic arteries and the great cardiac vein, and the amount of overflow (venoarterial difference times myocardial blood flow). RESULTS: During nerve stimulation, NPY levels correlated significantly with CVR at the highest r value (r = 0.850, p < 0.0001) obtained for the venous level under alpha-blockade, but norepinephrine showed no correlation. Treatment with BIBP3226 abolished the correlation between NPY level and CVR under alpha-blockade. Without alpha-blockade, norepinephrine levels correlated significantly with CVR; however, NPY showed no correlation. The amount of NPY overflow during the stimulation was nearly 1,000-fold lower than norepinephrine overflow. Exogenous NPY had a 100-fold more potent coronary vasoconstrictive action than that of norepinephrine. The KATP channel antagonist glibenclamide enhanced vasoconstriction of NPY, and the agonist pinacidil suppressed it with a predominant effect in the subepicardial region. CONCLUSIONS: During sympathetic nerve stimulation, the vasoconstrictive actions of NPY are masked by norepinephrine under intact alpha-adrenoceptor conditions, manifest during alpha-blockade and modulated by KATP channel activity.