bluuebunny/crossref_metadata_2025_split huggingface dataset:
Do flexible work policies improve parents’ health? A natural experiment based on the UK Millennium Cohort Study
Authors: Avendano Mauricio , Panico Lidia 
Published: December 2017

BackgroundThere is limited evidence of the impact of policies to promote work–family balance on family health. Exploiting the introduction of the UK Flexible Working Act (2003), we examined whether a policy that grants parentsthe right to requestflexible work influences their health and well-being.MethodsUsing the UK Millennium Cohort Study, we focus on 6424 mothers employed in 2001–2002, when the cohort child was 9 months old, until their child’s seventh birthday. We used a difference-in-differences (DiD) approach to compare changes in outcomes before and after the policy among mothers most likely to benefit and mothers unlikely to benefit from the policy.ResultsFlexible working increased in a small group of mothers (n=548) whose employer did not offer work flexibility before the reform (treatment group). By contrast, among mothers whose employer already offered flexible work before the reform (control group, n=5810), there was little change or a slight decline in flexible working. DiD estimates suggest that the policy was associated with an increase in flexible working (37.5 percentage points, 95% CI 32.9 to 41.6), but it had no impact on self-rated health (−1.6 percentage points, 95% CI −4.4 to 1.1), long-term illness (−1.87 percentage points, 95% CI −4.3 to 0.5) or life satisfaction scores (β=0.04, 95% CI −0.08 to 0.16).ConclusionThe Flexible Working Act increased flexible working only among a small group of mothers who had not yet the right to request work flexibility, but it had no impact on their health and well-being. Policies promoting work flexibility may require stronger incentives for both parents and employers.
Neuropsychological outcome after subtemporal versus transsylvian approach for selective amygdalohippocampectomy in patients with mesial temporal lobe epilepsy: a randomised prospective clinical trial
Authors: Vogt Viola Lara , Delev Daniel , Grote Alexander , Schramm Johannes , von Lehe Marec , Elger Christian Erich , Witt Juri-Alexander , Helmstaedter Christoph 
Published: December 2017

ObjectiveTo compare the effects of different surgical approaches for selective amygdalohippocampectomy in patients with pharmacoresistant mesial temporal lobe epilepsy with regard to the neuropsychological outcome and to replicate an earlier study employing a matched-pair design.Method47 patients were randomised to subtemporal versus transsylvian approaches. Memory, language, attentional and executive functions were assessed before and 1 year after surgery. Multivariate analyses of variance (MANOVAs) with presurgical and postsurgical assessments as within-subject variables and approach and side of surgery as between-subject factors were calculated. Additionally, the frequencies of individual performance changes based on reliable change indices were analysed.ResultsSeizure freedom International League Against Epilepsy (ILAE) 1a, was achieved in 62% of all patients without group difference. MANOVAs revealed no significant effects of approach on cognition. Tested separately for each parameter, verbal recognition memory declined irrespective of approach. Post hoc tests revealed that on group level, the subtemporal approach was associated with a worse outcome for verbal learning and delayed free recall as well as for semantic fluency. Accordingly, on individual level, more patients in the subtemporal group declined in verbal learning. Left side of surgery was associated with decline in naming regardless of approach.ConclusionThe main analysis did not confirm the effects of approach on memory outcome seen in our previous study. Post hoc testing, however, showed greater memory losses with the subtemporal approach. Previous findings were replicated for semantic fluency. The discrepant results are discussed on the background of the different study designs.
Mechanical determinants of myocardial oxygen consumption in conscious dogs
Authors: Elbeery Jospeh R. , Lucke John C. , Feneley Michael P. , Maier George W. , Owen Clarence H. , Lilly R. Eric , Savitt Michael A. , Hickey Mark St. J. , Gall Stanley A. , Davis James W. , VanTrigt Peter , Rankin J. Scott , Glower Donald D. 
Published: December 2017

Pages H609–H620: Jospeh R. Elbeery, John C. Lucke, Michael P. Feneley, George W. Maier, Clarence H. Owen, R. Eric Lilly, Michael A. Savitt, Mark St. J. Hickey, Stanley A. Gall, Jr., James W. Davis, Peter VanTrigt, J. Scott Rankin, and Donald D. Glower. “Mechanical determinants of myocardial oxygen consumption in conscious dogs.” Page H618: Equations 12, 14, and 15 should read as follows. There should only be one SW term in Eq. 12 MVo2 = Hun + Hp + Hc + SW (12) Equations 14 and 15 should contain end-diastolic volume (EDV) instead of end-systolic volume (ESV) MVo2 = Hun + k · EDV · MEP + SW (14) = Hun + M(EDV · MEP + SW) (15)
Oxygen requirement of renal Na-K-ATPase-dependent sodium reabsorption
Authors: Sejersted Ole M. , Mathisen Ȗystein , Kiil Fredrik 
Published: December 2017

The oxygen requirement of the Na-K-ATPase-dependent sodium transport system was examined in anesthetized dogs infused with 15% mannitol-Ringer solutions at a rate of 35 ml/min. Because of renal vasodilatation and abolished autoregulation, filtered sodium (FNa) could be varied over a wide range by progressive aortic constriction. Sodium reabsorption.(RNa and renal oxygen consumption (RVo2) varied in proportion to FNa (r> 0.9). Ouabain, which inhibits Na-K-ATPases reduced RVo2 by 45 ± 6%. During subsequent aortic constriction, the ratio ΔRNa/ΔFNa averaged 0.45 (glomerulotubular balance) (r> 0.9), whereas RVo2 was not significantly altered. Comparisons of ΔRNa/ΔFNa before and after ouabain administration, indicate that about half of an increase in sodium delivery to the distal nephron is reabsorbed by the Na-K-ATPase-dependent sodium transport system and that ΔRNa/ΔRVo2 (Na/O2 ratio) of this system averages 14.5 ± 1.3. This Na/O2 ratio corresponds to 2.4 sodium ions transported per ATP dephosphorylated as found in other tissues. autoregulation; ATP; dog; glomerular filtration rate; mannitol; ouabain; renal blood flow; renal oxygen consumption Submitted on February 24, 1976
Possible modulation of rat renal prostaglandin production by oxygen
Authors: Zenser Terry V. , Levitt Monte J. , Davis Bernard B. 
Published: December 2017

The effect of oxygen on in vitro prostaglandin production by slices of rat renal inner medulla was evaluated. Oxygen increased prostaglandin production in a dose-response fashion. Double reciprocal plots of the relationship revealed a half-maximal stimulation of prostaglandin (PG) E2 production by 15.1% or 143 μM O2 and of PGF2α by 16.8% or 160 μM O2. An increased prostaglandin production at 95% O2 was measurable within 2 min of incubation and was maximal at approximately 15 min. Oxygen also increased inner medullary cyclic AMP content with a similar time course. Lowering oxygen did not alter the response of the inner medulla to increase cyclic AMP content when exposed to vasopressin. PGE2α increased cyclic AMP at 5% O2 but not at 95%, while PGF2α was ineffective at either oxygen concentration. In the presence of structurally dissimilar prostaglandin synthetase inhibitors, indomethacin and sodium meclofenamate, there was a reduction of basal cyclic AMP content as well as prostaglandin production. PGE2 increased cyclic AMP at 95% O2 in the presence of prostaglandin synthetase inhibitors while PGF2α remained inactive. This suggests that the oxygen-mediated increases in cyclic AMP content may be due to endogenously produced PGE2. The data are consistent with oxygen modulating inner medullary production of prostaglandins, and with endogenously produced prostaglandins exerting a hormone-like action in the inner medulla. cyclic AMP; vasopressin; renal medulla; renal countercurrent system Submitted on March 25, 1977
Mechanism of exaggerated diuresis in spontaneously hypertensive rats
Authors: DiBona Gerald F. , Rios Linda L. 
Published: December 2017

The mechanism of exaggerated diuresis and natriuresis was studied in spontaneously hypertensive rats (SHR) by renal clearance and micropuncture techniques. Control normotensive rats of the same age and sex [Wistar-Kyoto rats (WKY)] were also studied. During the hydropenic control and the volume-expansion experimental periods absolute and fractional water and sodium excretion were greater in SHR than in WKY. Although fractional and absolute water and sodium reabsorption were similar along the proximal convolution in SHR and WKY, fractional and absolute water reabsorption in Henle's loop was less in SHR than in WKY. Hydrostatic and colloid osmotic pressures in the cortical peritubular microvasculature were similar in WKY and SHR. Acute normalization of renal perfusion pressure by aortic constriction reversed the exaggerated diuresis and natriuresis in SHR by halving the filtered load of water and sodium; whole kidney and single nephron glomerular filtration rates and blood flows decreased by 50%. It is concluded that the exaggerated diuresis and natriuresis of the spontaneously hypertensive rat is caused by a decreased reabsorption in the loop of Henle. The mechanism of this decreased reabsorption in the loop of Henle cannot be explained by alterations in the measured physical forces in the renal cortical microvasculature. natriuresis; autoregulation; volume expansion Submitted on November 15, 1977 Accepted on June 7, 1978
Inhibition of toad urinary bladder sodium transport by carbamylcholine: possible role of cyclic GMP
Authors: Sahib M. K. , Schwartz J. H. , Handler J. S. 
Published: December 2017

Page F586: M. K. Sahib, J. H. Schwartz, and J. S. Handler. “Inhibition of toad urinary bladder sodium transport by carbamylcholine: possible role of cyclic GMP.” In Table 3 (page F589) the values 11.9 ± 0.6 for cAMP and 0.28 ± 0.02 for cGMP should be opposite 10 mU/ml AVP plus 100 μM carbamylcholine. Braces have been added to the table to define the paired experiments. The corrected table follows. (See PDF)
Branched-chain amino acids augment neither albuminuria nor albumin synthesis in nephrotic rats
Authors: Kaysen George A. , Al-Bander Hamoudi , Martin Victor I. , Jones Hardin , Hutchison Florence N. 
Published: December 2017

Both albuminuria (UalbV) and albumin synthesis (AlbSyn) are modulated by dietary protein in nephrotic rats, but the agent(s) linking diet to altered UalbV and AlbSyn is unknown. Others have reported that branched-chain amino acids (BCAA) cause neither increased renal blood flow nor glomerular filtration rate (GFR) normally induced by dietary protein nor increased blood glucagon thought to be necessary for protein-mediated effects on renal hemodynamics. The effect of BCAA on UalbV is unknown. Because BCAA increase AlbSyn in tissue culture and after a fast, it is possible that feeding BCAA may increase AlbSyn but not UalbV in nephrosis. Nephrotic rats were fed either 8.5% casein (LP); 21% casein (NP); 8.5% casein supplemented with valine, leucine, and isoleucine to the total amount provided by a 21% casein diet (2.37%) (LBC); or 8.5% casein plus 12.5% BCAA providing a diet isonitrogenous to 21% casein (HBC). UalbV and AlbSyn were significantly greater in NP compared with LP, LBC, or HBC and were the same in the latter three groups. Glucagon was infused into nephrotic rats fed 8.5% casein either subcutaneously or intraperitoneally in quantities sufficient to increase plasma levels to over 10 times control but had no effect on UalbV. The ability of dietary protein to increase AlbSyn or UalbV is not a result of total -amino nitrogen intake but is a result of the specific amino acid composition of the diet and must result entirely from the effect of one or more non-BCAA. Increased blood glucagon alone has no effect on UalbV. permselectivity; nephrotic syndrome; proteinuria; glucagon; corticosterone; Heymann nephritis Submitted on June 26, 1990 Accepted on October 3, 1990
Letters to the Editor
Authors: Coggan Andrew 
Published: December 2017

The following is the abstract of the article discussed in the subsequent letter: Friedlander, Anne L., Gretchen A. Casazza, Michael A. Horning, Melvin J. Huie, and George A. Brooks. Training-induced alterations of glucose flux in men. J. Appl. Physiol. 82(4): 1360–1369, 1997.—We examined the hypothesis that glucose flux was directly related to relative exercise intensity both before and after a 10-wk cycle ergometer training program in 19 healthy male subjects. Two pretraining trials [45 and 65% of peak O2 consumption (V˙o 2 peak)] and two post- training trials (same absolute and relative intensities as 65% pretraining) were performed for 90 min of rest and 1 h of cycling exercise. After training, subjects increasedV˙o 2 peak by 9.4 ± 1.4%. Pretraining, the intensity effect on glucose kinetics was evident with rates of appearance (Ra; 5.84 ± 0.23 vs. 4.73 ± 0.19 mg ⋅ kg−1 ⋅ min−1), disappearance (Rd; 5.78 ± 0.19 vs. 4.73 ± 0.19 mg ⋅ kg−1 ⋅ min−1), oxidation (Rox; 5.36 ± 0.15 vs. 3.41 ± 0.23 mg ⋅ kg−1 ⋅ min−1), and metabolic clearance (7.03 ± 0.56 vs. 5.20 ± 0.28 ml ⋅ kg−1 ⋅ min−1) of glucose being significantly greater ( P ≤ 0.05) in the 65% than the 45%V˙o 2 peak trial. When Rd was expressed as a percentage of total energy expended per minute (Rd E), there was no difference between the 45 and 65% intensities. Training did reduce Ra(4.63 ± 0.25), Rd(4.65 ± 0.24), Rox(3.77 ± 0.43), and Rd E(15.30 ± 0.40 to 12.85 ± 0.81) when subjects were tested at the same absolute workload ( P ≤ 0.05). However, when they were tested at the same relative workload, Ra, Rd, and Rd E were not different, although Roxwas lower posttraining (5.36 ± 0.15 vs. 4.41 ± 0.42, P ≤ 0.05). These results show 1) glucose use is directly related to exercise intensity; 2) training decreases glucose flux for a given power output; 3) when expressed as relative exercise intensity, training does not affect the magnitude of blood glucose use during exercise; 4) training alters the pathways of glucose disposal.
Letters to the Editor
Authors: Heller Hartmut , Hoffmann Georg , Schuster Klaus-Dieter , Schobersberger Wolfgang 
Published: December 2017

The following is the abstract of the article discussed in the subsequent letter: Steudel, Wolfgang, Hans-Joachim Krämer, Daniela Degner, Simone Rosseau, Hartwig Schütte, Dieter Walmrath, and Werner Seeger. Endotoxin priming of thromboxane-related vasoconstrictor responses in perfused rabbit lungs. J. Appl. Physiol. 83(1): 18–24, 1997.—In prior studies of perfused lungs, endotoxin priming markedly enhanced thromboxane (Tx) generation and Tx-mediated vasoconstriction in response to secondarily applied bacterial exotoxins. The present study addressed this aspect in more detail by employing precursor and intermediates of prostanoid synthesis and performing functional testing of vasoreactivity and measurement of product formation. Rabbit lungs were buffer perfused in the absence or presence of 10 ng/ml endotoxin. Repetitive intravascular bolus applications of free arachidonic acid provoked constant pulmonary arterial pressor responses and constant release reactions of TxA2 and prostaglandin (PG) I2 in nonprimed lungs. Within 60–90 min of endotoxin recirculation, which provoked progressive liberation of tumor necrosis factor-α but did not effect any hemodynamic changes by itself, both pressor responses and prostanoid release markedly increased, and both events were fully blocked by cyclooxygenase (Cyclo) inhibition with acetylsalicylic acid (ASA). The unstable intermediate PGG2 provoked moderate pressor responses, again enhanced by preceding endotoxin priming and fully suppressed by ASA. Vasoconstriction also occurred in response to the direct Cyclo product PGH2, again amplified after endotoxin pretreatment, together with markedly enhanced liberation of TxA2 and PGI2. In the presence of ASA, the priming-related increase in pressor responses and the prostanoid formation were blocked, but baseline vasoconstrictor responses corresponding to those in nonprimed lungs were maintained. Pressor responses to the stable Tx analog U-46619 were not significantly increased by endotoxin pretreatment, but some generation of TxA2 and PGI2 was also noted under these conditions. We conclude that endotoxin priming exerts profound effects on the lung vascular prostanoid metabolism, increasing the readiness to react with Tx-mediated vasoconstrictor responses to various stimuli, suggesting that enhanced Cyclo activity is an important underlying event.
Opium Addiction and Ischemic Stroke in Isfahan, Iran: A Case-Control Study
Authors: Ebrahimi Homa , Haghjoo Javanmard Shaghayegh , Asgary Sedigheh , Dehghani Leila , Amiri Masoud , Saadatnia Mohammad 
Published: December 2017

<b><i>Background:</i></b> The effect of opium addiction (OA) on cerebrovascular disease is controversial. The aim of this study was to clarify this relationship in Iranian patients with ischemic stroke. <b><i>Methods:</i></b> In a case-control study, 672 patients with ischemic stroke and 293 controls without a previous history of cerebrovascular or cardiovascular diseases were compared. OA as well as other risk factors such as diabetes mellitus (DM), hypertension (HTN), hyperlipidemia, tobacco smoking (TS) were compared between the 2 groups. <b><i>Results:</i></b> OA percentage, TS, TS amount (pack/year), HTN and DM history were significantly higher in the case group compared to controls (<i>p</i> &#x3c; 0.05). After regression analysis between risk factors, a significant difference remained between 2 groups with regards to HTN (OR 4.21, 95% CI 3.05–5.81, <i>p</i> &#x3c; 0.001), TS (OR 2.33, 95% CI 1.51–3.59, <i>p</i> &#x3c; 0.001), and OA (OR 2.36, 95% CI 1.16–4.85, <i>p</i> = 0.018). <b><i>Conclusion:</i></b> Our study showed OA is a risk factor for stroke. However, a follow-up study with a larger cohort is required to confirm the results.
Reduction of Arterial Stiffness After Kidney Transplantation: A Systematic Review and Meta‐Analysis
Authors: Sidibé Aboubacar , Fortier Catherine , Desjardins Marie‐Pier , Zomahoun Hervé Tchala Vignon , Boutin Amélie , Mac‐Way Fabrice , De Serres Sacha , Agharazii Mohsen 
Published: December 2017

Background

End‐stage kidney disease is associated with increased arterial stiffness. Although correction of uremia by kidney transplantation (
KT
x) could improve arterial stiffness, results from clinical studies are unclear partly due to small sample sizes.

Method and Results

We conducted a systematic review and meta‐analysis of before‐after design studies performed in adult
KT
x patients with available measures of arterial stiffness parameters (pulse wave velocity [
PWV
], central pulse pressure [PP], and augmentation index) before and at any time post‐
KT
x. Mean difference of post‐ and pre‐
KT
x values of different outcomes were estimated using a random effect model with 95% confidence interval. To deal with repetition of measurement within a study, only 1 period of measurement was considered per study by analysis. Twelve studies were included in meta‐analysis, where a significant decrease of overall
PWV
by 1.20 m/s (95%
CI
0.67‐1.73, I
2
=72%), central
PWV
by 1.20 m/s (95%
CI
0.16‐2.25, I
2
=83%), peripheral
PWV
by 1.17 m/s (95%
CI
0.17‐2.17, I
2
=79%), and brachial‐ankle
PWV
by 1.21 m/s (95%
CI
0.66‐1.75, I
2
=0%) was observed. Central
PP
(reported in 4 studies) decreased by 4.75 mm Hg (95%
CI
0.78–10.28, I
2
=50%). Augmentation index (reported in 7 studies) decreased by 10.5% (95%
CI
6.9‐14.1, I
2
=64%). A meta‐regression analysis showed that the timing of assessment post‐
KT
x was the major source of the residual variance.

Conclusions

This meta‐analysis suggests a reduction of the overall arterial stiffness in patients with end‐stage kidney disease after
KT
x.
Atrial Fibrillation Promotion in a Rat Model of Rheumatoid Arthritis
Authors: Dai Hui , Wang Xiaoyu , Yin Shuangli , Zhang Yun , Han Yu , Yang Ning , Xu Jicheng , Sun Li , Yuan Yue , Sheng Li , Gong Yongtai , Li Yue 
Published: December 2017

Background

The prevalence of atrial fibrillation (
AF
) is significantly higher in rheumatoid arthritis (
RA
) patients, but the underlying mechanisms remain poorly understood. The goal of this study was to assess the effects of
RA
on
AF
susceptibility and atrial arrhythmogenic remodeling in a rat model of
RA
.

Methods and Results

Collagen‐induced arthritis was induced in rats by immunization with type
II
collagen in Freund's incomplete adjuvant. Among the rats that developed arthritis,
AF
susceptibility and atrial remodeling were examined 8 weeks after the primary immunization.
AF
inducibility and duration were substantially increased in collagen‐induced arthritis rats, and
AF
duration was significantly and positively correlated with the serum
IL
‐6 and
TNF
‐α levels. Rats with collagen‐induced arthritis showed prolonged atrial conduction time with no changes in the atrial effective refractory period. Atrial conduction delay was accompanied by significantly increased atrial fibrosis. In addition, atrial structural and autonomic remodeling, including left atrial dilation, apoptosis and autophagy of atrial myocytes, and atrial heterogeneous sympathetic hyperinnervation, was observed. Interestingly, we found that collagen‐induced arthritis had no significant effects on connexins, Nav1.5, and the main ion channels' protein expressions in atria.

Conclusions

We demonstrated that
RA
increased
AF
susceptibility by inducing
AF
‐promoting atrial remodeling. This study may provide insights into mechanisms underlying
RA
‐induced
AF
and validate a model that is suitable for further mechanistic and therapeutic exploration.
Growth and nutritional status, and their association with lung function: a study from the international Primary Ciliary Dyskinesia Cohort
Authors: Goutaki Myrofora , Halbeisen Florian S. , Spycher Ben D. , Maurer Elisabeth , Belle Fabiën , Amirav Israel , Behan Laura , Boon Mieke , Carr Siobhan , Casaulta Carmen , Clement Annick , Crowley Suzanne , Dell Sharon , Ferkol Thomas , Haarman Eric G. , Karadag Bulent , Knowles Michael , Koerner-Rettberg Cordula , Leigh Margaret W. , Loebinger Michael R. , Mazurek Henryk , Morgan Lucy , Nielsen Kim G. , Phillipsen Maria , Sagel Scott D. , Santamaria Francesca , Schwerk Nicolaus , Yiallouros Panayiotis , Lucas Jane S. , Kuehni Claudia E. 
Published: December 2017

Chronic respiratory disease can affect growth and nutrition, which can influence lung function. We investigated height, body mass index (BMI), and lung function in patients with primary ciliary dyskinesia (PCD).In this study, based on the international PCD (iPCD) Cohort, we calculated z-scores for height and BMI using World Health Organization (WHO) and national growth references, and assessed associations with age, sex, country, diagnostic certainty, age at diagnosis, organ laterality and lung function in multilevel regression models that accounted for repeated measurements.We analysed 6402 measurements from 1609 iPCD Cohort patients. Height was reduced compared to WHO (z-score −0.12, 95% CI −0.17 to −0.06) and national references (z-score −0.27, 95% CI −0.33 to −0.21) in male and female patients in all age groups, with variation between countries. Height and BMI were higher in patients diagnosed earlier in life (p=0.026 and p<0.001, respectively) and closely associated with forced expiratory volume in 1 s and forced vital capacity z-scores (p<0.001).Our study indicates that both growth and nutrition are affected adversely in PCD patients from early life and are both strongly associated with lung function. If supported by longitudinal studies, these findings suggest that early diagnosis with multidisciplinary management and nutritional advice could improve growth and delay disease progression and lung function impairment in PCD.