ソウザン ジ ノ センエン セイ ハイ コウケツアツショウ ニ タイ スル NO キュウニュウ リョウホウ ノ ユウコウ セイ ・ アンゼン セイ ノ ケントウ

新生児遷延性肺高血圧症(persistent pulmonary hypertension of the newborn:PPHN)は,出生早期に肺高血圧症を発症し高度の低酸素血症を来す疾患である.正期産児のPPHNに対しては,NO吸入療法(inhaled nitric oxide:iNO)が有効とされているが,早産児における有効性は確立していない.今回,我々は在胎30週未満の早産児に対するiNOの有効性および安全性について検討した.対象は,出生後3日以内にiNOを施行した在胎30週未満の早産児39例である.肺高血圧の原因疾患は肺炎・敗血症が多かった.基礎疾患によって有効率が異なったが,iNO開始1時間の時点で全体の64%の症例はPPHNが改善した.PPHN改善後は速やかにiNOを減量・離脱できた症例が多かった.無効症例は週数・出生体重がより小さい児で多かった.有害事象としてはメトヘモグロビン血症を2例認めた.iNOは早産児のPPHNに対して,短期間の加療で出生早期の循環動態を改善させる有用な治療法であると考えられた.Persistent pulmonary hypertension of the newborn (PPHN) is a disease in which newborns develop pulmonary hypertension soon after birth, causing severe hypoxemia. Inhaled nitric oxide (iNO) therapy is effective in treating PPHN in term infants;however, the efficacy of iNO in preterm infants has not been established. We investigated the efficacy and safety of iNO as a treatment for preterm infants born at <30 weeks\u27 gestation. The subjects were 39 preterm infants born at <30 weeks\u27 gestation who underwent iNO therapy within 3 days of birth. The subjects\u27 pulmonary hypertension was most commonly caused by pneumonia and sepsis. PPHN improved in 64 % of the subjects 1 hour after starting iNO. In many subjects, iNO was successfully reduced and withdrawn promptly after PPHN improved. Subjects in whom iNO was ineffective were commonly those born early and with lower birth weight. Mild methemoglobinemia was complicated in 2 subjects. In preterm infants with PPHN, iNO is a useful therapythat causes few adverse events and improves hemodynamics soon after birth within a short amount of time

LC-ESI/MS/MS analysis of neonicotinoids in urine of very low birth weight infants at birth

Objectives Neonicotinoid insecticides are widely used systemic pesticides with nicotinic acetylcholine receptor agonist activity that are a concern as environmental pollutants. Neonicotinoids in humans and the environment have been widely reported, but few studies have examined their presence in fetuses and newborns. The objective of this study is to determine exposure to neonicotinoids and metabolites in very low birth weight (VLBW) infants. Methods An analytical method for seven neonicotinoids and one neonicotinoid metabolite, N-desmethylacetamiprid (DMAP), in human urine using LC-ESI/MS/MS was developed. This method was used for analysis of 57 urine samples collected within 48 hours after birth from VLBW infants of gestational age 23–34 weeks (male/female = 36/21, small for gestational age (SGA)/appropriate gestational age (AGA) = 6/51) who were admitted to the neonatal intensive care unit of Dokkyo Hospital from January 2009 to December 2010. Sixty-five samples collected on postnatal day 14 (M/F = 37/22, SGA/AGA = 7/52) were also analyzed. Results DMAP, a metabolite of acetamiprid, was detected in 14 urine samples collected at birth (24.6%, median level 0.048 ppb) and in 7 samples collected on postnatal day 14 (11.9%, median level 0.09 ppb). The urinary DMAP detection rate and level were higher in SGA than in AGA infants (both p<0.05). There were no correlations between the DMAP level and infant physique indexes (length, height, and head circumference SD scores). Conclusion These results provide the first evidence worldwide of neonicotinoid exposure in newborn babies in the early phase after birth. The findings suggest a need to examine potential neurodevelopmental toxicity of neonicotinoids and metabolites in human fetuse

Occurrence and Source of Chlorinated Polycyclic Aromatic Hydrocarbons (Cl-PAHs) in Tidal Flats of the Ariake Bay, Japan

In this study, we hypothesize that natural photochemical reactions of polycyclic aromatic hydrocarbons (PAHs) in tidal flats are responsible for the occurrence of chlorinated polycyclic aromatic hydrocarbons (Cl-PAHs). This study aims to survey the impact of photochemical reactions using a combination of field surveys and lab-scale experiments. Concentrations and profiles of PAHs and Cl-PAHs in road dust and sediments collected from seven tunnels and two watersheds, respectively, were determined. In the lab-scale experiments, anthracene was irradiated with ultraviolet (UV) light under various salinity conditions. No detectable Cl-PAHs were found in the road dust. However, Cl-PAHs were detected in the sediments from 700 to 6.1 × 10³ pg g^–1 and specifically from downstream sites. 2-Monochloroanthracene (2-Cl-ANT) and 9,10-dichloroanthracene (9,10-di-Cl-ANT) were dominant in the sediments. In the Domen River watershed, the ∑Cl-PAHs and the salinity showed a significant positive correlation (<i>p</i> < 0.01) in the sediments, while such a correlation was not found for PAHs. 2-Cl-ANT, 9-monochloroanthracene, and 9,10-di-Cl-ANT were identified as transformation products in the UV irradiation experiments. Production of these Cl-PAHs was dependent on the solution salinity. These results support our hypothesis, and we conclude that photochemical reactions significantly contribute to the occurrence of Cl-PAHs in the studied tidal flats

LC-ESI/MS/MS analysis of neonicotinoids in urine of very low birth weight infants at birth.

OBJECTIVES:Neonicotinoid insecticides are widely used systemic pesticides with nicotinic acetylcholine receptor agonist activity that are a concern as environmental pollutants. Neonicotinoids in humans and the environment have been widely reported, but few studies have examined their presence in fetuses and newborns. The objective of this study is to determine exposure to neonicotinoids and metabolites in very low birth weight (VLBW) infants. METHODS:An analytical method for seven neonicotinoids and one neonicotinoid metabolite, N-desmethylacetamiprid (DMAP), in human urine using LC-ESI/MS/MS was developed. This method was used for analysis of 57 urine samples collected within 48 hours after birth from VLBW infants of gestational age 23-34 weeks (male/female = 36/21, small for gestational age (SGA)/appropriate gestational age (AGA) = 6/51) who were admitted to the neonatal intensive care unit of Dokkyo Hospital from January 2009 to December 2010. Sixty-five samples collected on postnatal day 14 (M/F = 37/22, SGA/AGA = 7/52) were also analyzed. RESULTS:DMAP, a metabolite of acetamiprid, was detected in 14 urine samples collected at birth (24.6%, median level 0.048 ppb) and in 7 samples collected on postnatal day 14 (11.9%, median level 0.09 ppb). The urinary DMAP detection rate and level were higher in SGA than in AGA infants (both p<0.05). There were no correlations between the DMAP level and infant physique indexes (length, height, and head circumference SD scores). CONCLUSION:These results provide the first evidence worldwide of neonicotinoid exposure in newborn babies in the early phase after birth. The findings suggest a need to examine potential neurodevelopmental toxicity of neonicotinoids and metabolites in human fetuses

Empagliflozin in Patients with Chronic Kidney Disease

Background The effects of empagliflozin in patients with chronic kidney disease who are at risk for disease progression are not well understood. The EMPA-KIDNEY trial was designed to assess the effects of treatment with empagliflozin in a broad range of such patients. Methods We enrolled patients with chronic kidney disease who had an estimated glomerular filtration rate (eGFR) of at least 20 but less than 45 ml per minute per 1.73 m(2) of body-surface area, or who had an eGFR of at least 45 but less than 90 ml per minute per 1.73 m(2) with a urinary albumin-to-creatinine ratio (with albumin measured in milligrams and creatinine measured in grams) of at least 200. Patients were randomly assigned to receive empagliflozin (10 mg once daily) or matching placebo. The primary outcome was a composite of progression of kidney disease (defined as end-stage kidney disease, a sustained decrease in eGFR to &lt; 10 ml per minute per 1.73 m(2), a sustained decrease in eGFR of &amp; GE;40% from baseline, or death from renal causes) or death from cardiovascular causes. Results A total of 6609 patients underwent randomization. During a median of 2.0 years of follow-up, progression of kidney disease or death from cardiovascular causes occurred in 432 of 3304 patients (13.1%) in the empagliflozin group and in 558 of 3305 patients (16.9%) in the placebo group (hazard ratio, 0.72; 95% confidence interval [CI], 0.64 to 0.82; P &lt; 0.001). Results were consistent among patients with or without diabetes and across subgroups defined according to eGFR ranges. The rate of hospitalization from any cause was lower in the empagliflozin group than in the placebo group (hazard ratio, 0.86; 95% CI, 0.78 to 0.95; P=0.003), but there were no significant between-group differences with respect to the composite outcome of hospitalization for heart failure or death from cardiovascular causes (which occurred in 4.0% in the empagliflozin group and 4.6% in the placebo group) or death from any cause (in 4.5% and 5.1%, respectively). The rates of serious adverse events were similar in the two groups. Conclusions Among a wide range of patients with chronic kidney disease who were at risk for disease progression, empagliflozin therapy led to a lower risk of progression of kidney disease or death from cardiovascular causes than placebo