A repeating fast radio burst source localized to a nearby spiral galaxy.

Fast radio bursts (FRBs) are brief, bright, extragalactic radio flashes1,2. Their physical origin remains unknown, but dozens of possible models have been postulated3. Some FRB sources exhibit repeat bursts4-7. Although over a hundred FRB sources have been discovered8, only four have been localized and associated with a host galaxy9-12, and just one of these four is known to emit repeating FRBs9. The properties of the host galaxies, and the local environments of FRBs, could provide important clues about their physical origins. The first known repeating FRB, however, was localized to a low-metallicity, irregular dwarf galaxy, and the apparently non-repeating sources were localized to higher-metallicity, massive elliptical or star-forming galaxies, suggesting that perhaps the repeating and apparently non-repeating sources could have distinct physical origins. Here we report the precise localization of a second repeating FRB source6, FRB 180916.J0158+65, to a star-forming region in a nearby (redshift 0.0337 ± 0.0002) massive spiral galaxy, whose properties and proximity distinguish it from all known hosts. The lack of both a comparably luminous persistent radio counterpart and a high Faraday rotation measure6 further distinguish the local environment of FRB 180916.J0158+65 from that of the single previously localized repeating FRB source, FRB 121102. This suggests that repeating FRBs may have a wide range of luminosities, and originate from diverse host galaxies and local environments.

Secular trends in established and novel cardiovascular risk factors in Welsh 12-13 year olds: a comparison between 2002 and 2007.

BACKGROUND: This study examines CVD risk factors trends in Welsh adolescents between 2002 and 2007. PARTICIPANTS AND METHODS: CVD risk factor data was examined from two cross-sectional studies. The first study (73 participants; aged 12.9 ± 0.3 years) was completed in 2002. The second study (90 participants; aged 12.9 ± 0.4 years) was conducted in 2007. Measurements included body mass index (BMI), waist circumference (WC), total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, triglyceride, fibrinogen (Fg) and high-sensitivity C-reactive protein (hs-CRP). RESULTS: In boys, mean BMI and WC were lower in 2007, although not significantly (p ≥ 0.05). In 2007, there were improvements in mean lipid, Fg and hs-CRP concentrations in both sexes (p < 0.05). In 2002, 42.8% of boys and 34.2% of girls were overweight or obese; in 2007, this was 23.7% and 28.9% for boys and girls, respectively. More adolescents in 2002 exceeded the recommended levels for lipids, Fg and hs-CRP. CONCLUSION: This is the only study to examine CVD risk factor trends in Welsh adolescents. Although overweight continues to be widespread in 12-13 year olds, this study did not identify significant mean changes in overweight and obesity between 2002 and 2007. Overall, the data presented a positive trend in lipid profile and inflammatory factors.

Endogenous angiotensin stimulation of vasopressin in the newborn lamb.

The effect of furosemide on plasma renin, vasopressin (AVP), and aldosterone concentrations was studied in 10 control and 6 nephrectomized lambs during the 1st 2 wk of life. In a separate study in 10 newborn lambs, 1-sarcosine-8-alanine-angiotensin II (saralasin acetate, 5 mug/kg per min) was infused alone for 40 min, after which furosemide 2 mg/kg i.v. was injected in association with continuing saralasin acetate infusion. Plasma renin activity increased from a mean (+/-SEM) of 21.3+/-3.4 ng/ml per h in the 10 control lambs to 39.4+/-8.2 ng/ml per h at 8 min (P < 0.001) and remained high through 120 min after furosemide. Plasma AVP and aldosterone concentrations increased from respective mean values of 2.1+/-0.4 muU/ml and 12.8+/-2.5 ng/dl to 9.8+/-2.0 muU/ml (P < 0.01) and 23.0+/-7.7 ng/dl (P < 0.05) at 35 min and 13.8+/-2.1 muU/ml and 23.0+/-4.4 ng/dl at 65 min after furosemide (each P < 0.01). There was an insignificant AVP response in the 10 lambs treated with angiotensin inhibitor: from a mean base line of 4.7+/-0.9 to 8.3+/-2.0 muU/ml at 35 min, and 7.4+/-2.0 muU/ml at 65 min after furosemide. There was no increase in AVP in the anephric lambs. The mean increment AVP response from base line in the newborn lambs without saralasin, Delta 10.8+/-2.0 muU/ml, was greater than in the lambs with saralasin, Delta4.0+/-1.9 (P < 0.05), and greater than in the anephric lambs, Delta3.3+/-2.1 muU/ml (P < 0.05). The mean blood pressure fell 6 mm Hg in the 10 control lambs (P < 0.05), 7 mm Hg in the anephric lambs (P < 0.05), and 16 mm Hg in the lambs treated with angiotensin inhibitor (P < 0.05) by 35 min after furosemide. However, the changes in plasma AVP were not related to the fall in blood pressure. These data support the view that the observed AVP response to furosemide in the newborn lamb was mediated through the renin-angiotensin system.

Maternal cocaine use during pregnancy: effect on the newborn infant.

The newborn infants of 56 mothers who used cocaine were prospectively studied in to determine the effects of cocaine. There were no differences with respect to maternal preeclampsia or cesarean section rate. Meconium-stained amniotic fluid was increased (10 of 56 cases [17.8%]) compared with the control group (3 of 56 cases [5.3%]) (X2 = 4.2, P less than .05). Fetal distress recorded with fetal monitoring and Apgar scores at 1 and 5 minutes were similar. The weight, length, and head circumference growth curves of the infants born to cocaine-using mothers were shifted below the 25th percentile. Microcephaly was present in 12 of 56 (21.4%) infants whose mothers used cocaine during pregnancy (X2 = 5.96, P less than .01), and 15 of 56 (26.7%) had intrauterine growth retardation (X2 = 9.53, P less than .01) compared with the control infants (2 of 5 [3.5%] and 3 of 56 [5.3%], respectively). There was no increase in teratogenicity. Neither narcotic withdrawal symptoms nor illness could distinguish the infants born of cocaine-using mothers from the control infants. In conclusion, cocaine use during pregnancy results in newborn infants with growth retardation and microcephaly.

Excretion of cyclic 3',5'-adenosine monophosphate in the early newborn period.

The relationship between cyclic 3',5'-adenosine monophosphate (cAMP) excretion and creatinine clearance, urinary phosphate excretion, and urinary osmolarity was studied under basal conditions in 29 babies of 28-40 weeks gestation, during the first few days of life. Urinary cAMP excretion was directly related to creatinine clearance, r = 0.89, P less than 0.001, and gestational age, r = 0.63, P less than 0.001. There was no relationship between urinary cAMP excretion and urinary phosphate excretion or urine osmolarity. These results indicate that urinary cAMP excretion is dependent on the rate of glomerular filtration and gestational age.

Fructose-1,6-diphosphatase and glucose-6-phosphatase in newborn rats with intrauterine growth retardation.

The activities of two gluconeogenic enzymes, glucose-6-phosphatase and fructose-1,6-diphosphatase were examined in the normal and intrauterine growth retarded (IUGR) rat during the first 5 days of life. The fructose-1,6-diphosphatase activity, 1.54 +/- 0.10 mumol/min/g liver (means +/- SEM) in control and 1.47 +/- 0.20 in the IUGR rats, increased in both groups on days 2--4 but remained significantly lower in the IUGR rats through day 4 (4.53 +/- 0.6 mumol/min/g liver in control and 3.09 +/- 0.22 mumul/min/g liver in the IUGR rats, P less than 0.01). The glucose-6-phosphatase activity increased similarly in both groups. The weight of the IUGR rats remained lower through the third postnatal day (6.47 +/- 0.42 compared to 8.64 +/- 0.27 g in control rats). Blood glucose concentrations at birth were 117 +/- 11 mg/dl in control rats and 73 +/- 11 mg/dl in the IUGR rats (P less than 0.01). Although the glucose concentrations increased in both groups on days 2--4, the IUGR rats maintained relatively lower levels (P less than 0.01). The results indicate that IUGR fetal rats do not have augmented gluconeogenesis in spite of hypoglycemia. In addition, effective gluconeogenesis in the neonatal period appears to be delayed.

The renal response to acute asphyxia in spontaneously breathing newborn lambs.

The effects of acute asphyxia on neonatal renal function were examined in spontaneously breathing newborn lambs. 25 min of asphyxia were induced by addition of a respiratory dead space to reduce PaO2 to 41 +/- 3 mm Hg, pH to 7.03 +/- 0.05 and increase PaCO2 to 68 +/- 5 mm Hg (mean +/- S.E.M.). Glomerular filtration rates did not change significantly during or after asphyxia. Immediately following asphyxia significant (P less than 0.05) increases over the baseline were found in urinary flow rates, fractional sodium excretion, absolute sodium excretion and osmolar clearances. These changes were in part secondary to significant (P less than 0.05) increases in plasma glucose concentrations associated with increases (P less than 0.05) in circulating arterial catecholamine concentrations. The percentage of tubular reabsorption of glucose decreased significantly (P less than 0.05) and urinary glucose excretion increased significantly. Renal blood flow was unchanged. Therefore, asphyxia induced significant hyperglycemia which contributed to the concomitant natriuresis and osmotic diuresis in these newborn lambs.

Cryorenin in the newborn human and lamb.

Renin and big renin (cryorenin) were measured in the plasma of 78 babies at birth, and studied in six newborn lambs 2-3 weeks of age in response to angiotensin II (0.25 microgram/kg per min) infusion. There were (mean +/- S.E.M.) 15.9 +/- 2.0 ng/ml per h of renin and 11.1 +/- 2.3 of cryorenin, measured as plasma renin activity (PRA) in newborn cord blood. Cryorenin and renin decreased in parallel in the newborn lamb from 19 +/- 2.3 ng/ml per h and 28.6 +/- 2.7 to 6.5 +/- 1.8 (P less than 0.001) and 15.9 +/- 1.8 (P less than 0.01), respectively after 30 min of the angiotensin II infusion. Mean aortic blood pressure increased 30 mm Hg. These data suggest that cryorenin levels are high in the newborn lamb and human, and that both cryorenin and renin are under angiotensin II control in the newborn lamb.

Decreased vascular and increased adrenal and renal sensitivity to angiotensin II in the newborn lamb.

The effects of two doses of angiotensin II (0.025 micrograms/kg per min and 0.25 micrograms/kg per min) on plasma renin activity (PRA), aldosterone concentration, creatinine clearance, and sodium and potassium excretion were studied in two groups of 2- to 3-week-old lambs. The 0.025 micrograms/kg per min dose of angiotensin II also was studied in six adult ewes. In response to the angiotensin II infusions, PRA decreased in the newborns from baselines of 24.5 +/- 2.3 ng/ml per hr (mean +/- SE) and 22.9 +/- 3.5 to 13.6 +/- 0.8 and 13.0 +/- 2.2 at 30 minutes (P < 0.01), respectively, and returned to baseline at 60 minutes; PRA decreased from 1.7 +/- 0.1 to 0.95 +/- 0.3 ng/ml per hr at 30 minutes (P < 0.01) in the ewe and returned to baseline at 60 minutes. Plasma aldosterone increased in the newborns from baselines of 17.4 +/- 5.0 ng/dl and 14.7 +/0 3.9 to 33.1 +/- 6.9 and 32.5 +/- 6.3, respectively, at 15 minutes (P < 0.01) and returned to baseline at 60 minutes. Plasma aldosterone increased from 4.3 +/- 0.7 to 9.2 +/- 2.0 ng/dl in the ewe, and returned to baseline at 60 minutes. The change in the PRA and aldosterone responses from baseline to peak for the low and high angiotensin dose was similar in the newborn lambs and greater than in the ewe (P < 0.01). There was no change in the creatinine clearance, plasma sodium, or hematocrit. Urine sodium excretion increased from 0.16 +/- 0.04 total mEq/30 min to 0.87 +/- 0.27 (P < 0.05) in the newborns during the 0.25 micrograms/kg per min angiotensin II infusion. We conclude that, under basal conditions, the newborn lamb has high PRA and aldosterone levels with decreased pressor and increased aldosterone and renin release responsiveness to angiotensin II compared to the adult.

Amniotic fluid concentrations of renin and aldosterone during development in the fetal sheep.

Simultaneous plasma renin activity and aldosterone levels were measured in the chronically catheterized fetal lamb and pregnant ewe between 100 days gestation and term (140 to 150 days). Amniotic fluid renin levels were not statistically different after the addition of sheep renin substrate [0.76 +/- 0.18 ng/ml/hr (mean and S.E.) under 120 days and 1.33 +/- 0.29 after 125 days]. Amniotic fluid renin levels were unmeasurable without the addition of renin substrate. Basal plasma renin activity levels increased from 4.27 +/- 0.66 ng/ml/hr (P less than 0.01) (mean and S.E.) between 95 to 120 days of gestation in the fetal lamb to 10.14 +/- 1.46 between 125 to 150 days; these levels were greater than the amniotic fluid levels (P less than 0.001). Basal plasma renin activity levels in the pregnant ewe increased from 2.61 +/- 0.40 ng/ml/hr under 120 days of gestation to 7.13 +/- 1.41 (P less than 0.01) after 125 days; these levels were greater than the simultaneous amniotic fluid levels (P less than 0.001). The basal amniotic fluid, fetal, and maternal aldosterone levels of 5.0 +/- 0.53, and 5.83 +/- 0.76 ng/dl (mean and S.E.) increased to 8.97 +/- 0.86, 6.67 +/- 1.21, and 12.28 +/- 2.87 ng/dl, respectively, (P less than 0.05). Neither the fetal nor the maternal levels were statistically different from the amniotic fluid aldosterone levels during development. These data suggest that active renin and renin substrate pass poorly into the amniotic fluid; however, aldosterone from both the fetus and mother pass easily and contribute to the level of this steroid in amniotic fluid.

Renal handling of calcium in the early newborn period.

Urinary calcium excretion was studied in two matched groups of 28 clinically-well preterm and fullterm infants between 24 and 48 hours of life. In the developmental period from 28 to 40 weeks gestation, urinary calcium excretion was positively correlated to the gestational age (r = 0.583, P less than 0.01), serum calcium levels (r = 0.512, P less than 0.01), the rate of glomerular filtration (r = 0.715, P less than 0.001), and urinary cyclic AMP excretion (r = 0.717, P less than 0.001). Urinary calcium excretion was independent of sodium and calcium intake, and urinary sodium and phosphate excretion. The mean fractional total calcium excretion and fractional ionized calcium excretion in babies less than or equal to 32 weeks was less than 1.0%, compared to greater than 2.5% for sodium. Serum calcium levels were positively correlated with gestational age (r = 0.803, P less than 0.001), and serum phosphate levels (r = 0.85, P less than 0.001). Whole blood ionized calcium levels were positively correlated to gestational age (r = 0.625, P less than 0.001), and serum total calcium levels (r = 0.440, P less than 0.05). The newborn kidney in babies less than or equal to 32 weeks gestation, did not have impaired conservation of calcium as for sodium; and neither sodium nor calcium intake appeared to affect urinary calcium excretion in the well newborn infant. Probably neither excess excretion of calcium nor serum phosphate levels contribute to early neonatal hypocalcemia.

Effects of exogenous inactive renin on blood pressure and adrenal secretion of aldosterone and cortisol in the canine puppy.

To determine whether plasma inactive renin, M.W. 56,000, has an effect on blood pressure, renal function, and adrenal hormones in the newborn, one microgram of purified human plasma inactive renin was infused in ten canine puppies. After 30 minutes, mean aortic blood pressure increased 9 mm Hg (p less than .02), and plasma renin activity (PRA) increased from 22 to 64 mg/ml/hr (p less than .001). Plasma cortisol increased from 3 to 9 microgram/dl after 60 minutes (p less than .05). There was an increase in sodium and potassium excretion (p less than .05), without a change in glomerular filtration rate. This data suggests that human exogenous plasma inactive renin. M.W. 56,000 may have a physiological function in the canine puppy.

Distribution and disappearance of exogenous [125I] big renin in the newborn puppy.

The distribution and metabolism of infused exogenous [125I] inactive plasma big renin, molecular weight 56,000 was studied in five newborn puppies. The animals were sacrificed and the organs removed and studied by chromatography, along with periodic blood samples taken during the 120-min study, for evidence of conversion of high-molecular-weight renin to low-molecular-weight renin. The decay curve suggested an initial rapid distribution (alpha) phase of 10 +/- 1.5 min followed by a slower elimination (beta) phase of 40 +/- 4.6 min [125I]-Big renin was taken up by the red blood cell and released slowly. The liver, kidneys, and lungs had the highest % of [125I]-big renin at the termination of the study. There was no chromatographic evidence of a change in molecular weight of the [125I]-big renin. These data show that big renin has a two-compartment disappearance curve and that there is no evidence of conversion of high-molecular-weight renin to low-molecular-weight renin systemically or in the tissues of the newborn canine puppy.

Using the proposed NCCLS protocol for evaluation of automated instruments.

We compared four instruments (Sequential Multiple Analyzer Computer (SMAC), AutoAnalyzer II (AAII), StatLyte, and PVA-4) for the determination of Na, K, Cl and CO2 using a protocol (PSEP-1) of the National Committee for Clinical Laboratory Standards (NCCLS) for evaluation of precision and accuracy of automated instruments. The protocol was applied concurrently to all four instruments. NCCLS has revised this protocol into three separate protocols by which the manufacturer can make performance claims. Protocols specifically aimed at the user are now under development. Although PSEP-1 is no longer in use, many parts of it have been incorporated into PSEP-2, PSEP-3 and PSEP-4. This article will describe the adaptation of the protocol to evaluate four automated instruments in our laboratory.

Plasma renin activity after birth and in the early newborn period.

Plasma renin activity (PRA) was studied during delivery in umbilical cord venous blood and serially in the first 48 hours of life. PRA after cesarean section without labor, 15.2 +/- 2.3 ng/ml/hr (mean and SEM), was less than after cesarean section with labor, 44.1 +/- 8.9 (P less than .02), and vaginal delivery, 34.7 +/- 4.3 (P less than .05). PRA decreased during the first 30 minutes after vaginal delivery from 34.7 +/- 4.3 ng/ml/hr to 19.3 +/- 3.5 (P less than .01); PRA subsequently increased by four hours of life to 38.6 +/- 6.7 mg/ml/hr (P less than .05) and remained elevated throughout the 48-hour study period. These data show that PRA is stimulated during labor, decreases postnatally, and is again restimulated in the early newborn period.

Ontogeny of the renin-angiotensin-aldosterone system in the fetal and newborn lamb.

Thirteen chronic fetal lamb preparations between 95 and 142 days of gestation (term 145--150 days), and 10 newborn lambs were studied before and after the acute (1--2 min) infusion of furosemide (2 mg/kg). The baseline to peak plasma renin activity (PRA) response to furosemide increased from delta 3.0 +/- 1.3 ng/ml/hr (M and SEM) and 95--106 days of gestation to delta 18.4 +/- 4.0 (P less than 0.01) at 123--142 days and delta 33.6 +/- 6.5 (P less than 0.001) in the newborn. Baseline plasma aldosterone concentrations were similar in the fetus and pregnant ewe; aldosterone levels were higher in the newborn lamb than in the nonpregnant ewe. The newborn plasma aldosterone response to furosemide via the endogenous renin-angiotensin was delta 17.1 +/- 4.2 ng/dl (P less than 0.01); the fetal lamb plasma aldosterone level did not increase. The results indicate that the renin-angiotensin system cannot be stimulated by furosemide under 106 days of gestation; the response after 110 days increases with gestational age. Aldosterone concentrations in the fetal lamb are probably maintained primarily by the pregnant ewe and do not increase in response to endogenous renin stimulation as in the newborn.