We quantify the oceanic sink for anthropogenic carbon dioxide (CO2) over the period 1994 to 2007 by using observations from the global repeat hydrography program and contrasting them to observations from the 1990s. Using a linear regression–based method, we find a global increase in the anthropogenic CO2inventory of 34 ± 4 petagrams of carbon (Pg C) between 1994 and 2007. This is equivalent to an average uptake rate of 2.6 ± 0.3 Pg C year−1and represents 31 ± 4% of the global anthropogenic CO2emissions over this period. Although this global ocean sink estimate is consistent with the expectation of the ocean uptake having increased in proportion to the rise in atmospheric CO2, substantial regional differences in storage rate are found, likely owing to climate variability–driven changes in ocean circulation.

Blood pressure varies in relation to factors such as physical activity, body position, ambient temperature, and autonomic nervous system activity. Therefore, we have developed a portable multibiomedical (PMB) recorder that monitors five parameters: indirect blood pressure, physical activity, body position, ambient temperature, and RR interval of the electrocardiogram. In the present study, we applied the PMB recorder over a 24-hour period to study the effect of insufficient sleep on blood pressure in subjects doing extensive overtime work. The parameters listed above were measured by the PMB recorder throughout a normal workday (mean period of sleep, 8 hours) and throughout a day with insufficient sleep (mean period of sleep, 3.6 hours) in 18 male technical workers aged 23 to 48 years old. Blood pressure (mean systolic/diastolic pressure +/- SD) significantly increased the day after a sleep-insufficient night (129 +/- 8/79 +/- 6 mm Hg) compared with the day after a normal night (123 +/- 8/76 +/- 7 mm Hg, P<.05). However, ambient temperature, mean number of steps per minute, and percentage of time spent in a standing position showed no significant difference between these days. Spectral analysis of RR intervals showed that the ratio of the low-frequency component on the RR power spectrum (0.05 to 0.15 Hz) to the high-frequency component (0.15 to 0.40 Hz) was higher on the sleep-insufficient day (2.17 +/- 0.37 versus 1.81 +/- 0.37), as was the urinary excretion of norepinephrine (P<.05). Heart rate was significantly higher on the sleep-insufficient day (81 +/- ll versus 76 +/- 8 beats per minute), after the data of two subjects with abnormal levels of physical activity were excluded (P<.Ol). These data suggest that lack of sleep may increase sympathetic nervous system activity on the following day, leading to increased blood pressure. The PMB recorder was useful for precisely evaluating the relationship between blood pressure and environmental factors.

Background The effects of pharmacological blood pressure lowering at normal or high-normal blood pressure ranges in people with or without pre-existing cardiovascular disease remains uncertain. We analysed individual participant data from randomised trials to investigate the effects of blood pressure lowering treatment on the risk of major cardiovascular events by baseline levels of systolic blood pressure. MethodsWe did a meta-analysis of individual participant-level data from 48 randomised trials of pharmacological blood pressure lowering medications versus placebo or other classes of blood pressure-lowering medications, or between more versus less intensive treatment regimens, which had at least 1000 persons-years of follow-up in each group. Trials exclusively done with participants with heart failure or short-term interventions in participants with acute myocardial infarction or other acute settings were excluded. Data from 51 studies published between 1972 and 2013 were obtained by the Blood Pressure Lowering Treatment Trialists' Collaboration (Oxford University, Oxford, UK). We pooled the data to investigate the stratified effects of blood pressure-lowering treatment in participants with and without prevalent cardiovascular disease (ie, any reports of stroke, myocardial infarction, or ischaemic heart disease before randomisation), overall and across seven systolic blood pressure categories (ranging from <120 to ≥170 mm Hg). The primary outcome was a major cardiovascular event (defined as a composite of fatal and non-fatal stroke, fatal or non-fatal myocardial infarction or ischaemic heart disease, or heart failure causing death or requiring admission to hospital), analysed as per intention to treat.Findings Data for 344 716 participants from 48 randomised clinical trials were available for this analysis. Pre-randomisation mean systolic/diastolic blood pressures were 146/84 mm Hg in participants with previous cardiovascular disease (n=157 728) and 157/89 mm Hg in participants without previous cardiovascular disease (n=186 988). There was substantial spread in participants' blood pressure at baseline, with 31 239 (19•8%) of participants with previous cardiovascular disease and 14 928 (8•0%) of individuals without previous cardiovascular disease having a systolic blood pressure of less than 130 mm Hg. The relative effects of blood pressure-lowering treatment were proportional to the intensity of systolic blood pressure reduction. After a median 4•15 years' follow-up (Q1-Q3 2•97-4•96), 42 324 participants (12•3%) had at least one major cardiovascular event. In participants without previous cardiovascular disease at baseline, the incidence rate for developing a major cardiovascular event per 1000 person-years was 31•9 (95% CI 31•3-32•5) in the comparator group and 25•9 (25•4-26•4) in the intervention group. In participants with previous cardiovascular disease at baseline, the corresponding rates were 39•7 (95% CI 39•0-40•5) and 36•0 (95% CI 35•3-36•7), in the comparator and intervention groups, respectively. Haz...

Abstract-Recently a point mutation of guanine to thymine at nucleotide position 1917 in the endothelial nitric oxide synthase (eNOS) gene has been reported to be associated with coronary artery spasm. In addition, a significant association of the 4a/b polymorphism in intron 4 of the eNOS gene with coronary artery disease has been reported. However, the implications of these polymorphisms with respect to acute myocardial infarction (AMI) remain to be established. We conducted a case-control study of 226 patients with AMI and 357 healthy gender-and age-matched control subjects. In the former group, coronary angiograms were evaluated according to angiographic criteria based on the number of diseased vessels (Ն75%) and the number of stenotic lesions (Ն50%). Homozygosity for the Glu-Asp298 polymorphism existed in 5 of 226 patients with AMI (2.2%) but not in any of the 357 control subjects (Pϭ.0085). However, when we evaluated the coronary angiograms of 226 case patients, there was no difference in the number of diseased vessels or the number of stenotic lesions between the patients with this homozygote and those without it. By contrast, there was no evidence of a significant increase in the risk of AMI or the severity of coronary atherosclerosis among individuals with the a/a genotype of the eNOS4a/b polymorphism. Our results imply that patients who are homozygous for the Glu-Asp298 polymorphism may be genetically predisposed to AMI; however, this mutation apparently is not related to the severity of coronary atherosclerosis. Further studies are needed to confirm our results and characterize the molecular mechanisms by which eNOS is involved in susceptibility to AMI. (Hypertension. 1998;32:521-526.)Key Words: endothelium-derived relaxing factor Ⅲ genes Ⅲ myocardial infarction Ⅲ atherosclerosis Ⅲ angiography S ince the identification of nitric oxide (NO) as an important endothelium-derived relaxing factor, there has been an explosion of new information on the physiological and pathophysiological roles of NO. NO is synthesized from the amino acid L-arginine by a family of enzymes, referred to as NO synthase (NOS). Three distinct isoforms of NOS have been identified to date.1 The inducible NOS is expressed in vessel walls and macrophages by certain cytokines and endotoxin lipopolysaccharides in pathological conditions. 2The constitutive neuronal NOS is expressed in the central and peripheral nervous systems as well as in macula densa of kidney. It plays important roles in physiological 3 and pathophysiological 4 conditions. The constitutive endothelial NO synthase (eNOS) is expressed in the endothelium, where it produces NO from L-arginine. NO diffuses from the endothelium to the vascular smooth muscle cells, where it increases the concentration of cGMP by stimulating soluble guanylate cyclase, leading to vascular relaxation.

Abstract. The Global Ocean Data Analysis Project (GLODAP) is a synthesis effort providing regular compilations of surface to bottom ocean biogeochemical data, with an emphasis on seawater inorganic carbon chemistry and related variables determined through chemical analysis of water samples. This update of GLODAPv2, v2.2019, adds data from 116 cruises to the previous version, extending its coverage in time from 2013 to 2017, while also adding some data from prior years. GLODAPv2.2019 includes measurements from more than 1.1 million water samples from the global oceans collected on 840 cruises. The data for the 12 GLODAP core variables (salinity, oxygen, nitrate, silicate, phosphate, dissolved inorganic carbon, total alkalinity, pH, CFC-11, CFC-12, CFC-113, and CCl4) have undergone extensive quality control, especially systematic evaluation of bias. The data are available in two formats: (i) as submitted by the data originator but updated to WOCE exchange format and (ii) as a merged data product with adjustments applied to minimize bias. These adjustments were derived by comparing the data from the 116 new cruises with the data from the 724 quality-controlled cruises of the GLODAPv2 data product. They correct for errors related to measurement, calibration, and data handling practices, taking into account any known or likely time trends or variations. The compiled and adjusted data product is believed to be consistent to better than 0.005 in salinity, 1 % in oxygen, 2 % in nitrate, 2 % in silicate, 2 % in phosphate, 4 µmol kg−1 in dissolved inorganic carbon, 4 µmol kg−1 in total alkalinity, 0.01–0.02 in pH, and 5 % in the halogenated transient tracers. The compilation also includes data for several other variables, such as isotopic tracers. These were not subjected to bias comparison or adjustments. The original data, their documentation and DOI codes are available in the Ocean Carbon Data System of NOAA NCEI (https://www.nodc.noaa.gov/ocads/oceans/GLODAPv2_2019/, last access: 17 September 2019). This site also provides access to the merged data product, which is provided as a single global file and as four regional ones – the Arctic, Atlantic, Indian, and Pacific oceans – under https://doi.org/10.25921/xnme-wr20 (Olsen et al., 2019). The product files also include significant ancillary and approximated data. These were obtained by interpolation of, or calculation from, measured data. This paper documents the GLODAPv2.2019 methods and provides a broad overview of the secondary quality control procedures and results.