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It is self‐evident that our chests expand and contract during breathing but, surprisingly, exactly how individual alveoli change shape over the respiratory cycle is still a matter of debate. Some argue that all the alveoli expand and contract rhythmically. Others claim that the lung volume change is due to groups of alveoli collapsing and reopening during ventilation. Although this question might seem to be an insignificant detail for healthy individuals, it might be a matter of life and death for patients with compromised lungs. Past analyses were based on static post‐mortem preparations primarily due to technological limitations, and therefore, by definition, incapable of providing dynamic information. In contrast, this study provides the first comprehensive dynamic data on how the shape of the alveoli changes, and, further, provides valuable insights into the optimal lung volume for efficient gas exchange. It is concluded that alveolar micro‐dynamics is nonlinear; and at medium lung volume, alveoli expand more than the ducts. [ABSTRACT FROM AUTHOR]

We sought to investigate the psychosocial characteristics of patients with uncontrolled hypertension and examine factors that influence blood pressure (BP) control. A total of 1011 patients with uncontrolled hypertension were enrolled in 13 tertiary hospitals. Uncontrolled hypertension was defined as systolic BP ≥140 mm Hg or diastolic BP ≥90 mm Hg despite on antihypertensive therapy. Socio-demographics, anthropometrics, behavioral risk factors, medication pattern, adherence, and measures of health-related quality of life (HRQoL; EuroQol 5D visual analog scale [EQ-5D VAS]) were assessed at baseline and during follow-up visits (3 and 6 months). Patients were divided into 2 groups based on BP control status at 6 months (controlled group [n = 532] vs uncontrolled group [n = 367]). There were no differences in clinical characteristics except the proportion of smokers and baseline BP between patients with controlled BP and uncontrolled BP. At 6 months, the adherence of antihypertensive medication did not differ between the groups but the proportion of combination therapy with ≥3 antihypertensives was significantly higher in patients with uncontrolled BP. EQ-5D VAS at follow-up was significantly lower in patients with uncontrolled BP despite similar baseline values. Multivariate logistic regression analysis revealed that EQ-5D VAS at follow-up significantly correlated with BP control. Patients with worse HRQoL had higher Charlson Comorbidity Index and higher proportion of taking ≥3 antihypertensives, but medication adherence was similar to those with better HRQoL. These findings suggest that along with pharmacologic intervention of hypertension, management of comorbid conditions or psychological support might be helpful for optimizing BP control in patients with uncontrolled hypertension. [ABSTRACT FROM AUTHOR]

Background: Studies have shown that the concomitant use of a vitamin K antagonist (VKA) and an antiplatelet (APL) drug increased the bleeding risk and was less effective at preventing ischemic events. This study aimed to investigate the control status of international normalized ratio (INR) and the discontinuation rate of a VKA in patients taking VKA plus an APL drug compared with those taking a VKA alone. Methods: Data were extracted from the KORean Atrial Fibrillation Investigation II registry, a multicenter noninterventional prospective observational study. Nonvalvular atrial fibrillation (NVAF) patients with CHADS2 scores ≥ 1 who newly started (within 3 months) a VKA were enrolled and followed up for 1 year. Results: A total of 866 NVAF patients (mean age, 67.7 years; 60.3% men) without a bleeding history were divided into the VKA+APL (n = 229) and VKA alone (n = 637) groups. During follow‐up, mean INR level was lower in the VKA+APL group than in the VKA alone group (1.7 ± 0.8 vs 1.9 ± 0.9, P = 0.0005). INR levels were poorly controlled in both groups (66.1% and 64.7%, respectively). Patients in the VKA+APL group more frequently discontinued VKA than patients in the VKA alone group (28.8% vs 24.2%, P = 0.045). Major causes of VKA discontinuation were uncontrolled INR level and patient dissatisfaction or concerns. Conclusions: The conditions of NVAF patients were inadequately controlled with VKA with or without an APL. These findings suggest that other antithrombotic treatment options are warranted in NVAF patients to achieve INR control. [ABSTRACT FROM AUTHOR]

Aims: The long‐term safety and efficacy of gemigliptin was evaluated in the present extension study after a 12‐week study during a 40‐week follow‐up period. Methods: The main study was a randomized, placebo‐controlled, double‐blinded, phase IIIb study in which 50 mg of gemigliptin (N = 66) or placebo (N = 66) was administered to patients with type 2 diabetes mellitus (T2DM) and moderate or severe renal impairment over a 12‐week period. Patients with a glycated haemoglobin (HbA1c) level of 7% to 11% and an estimated glomerular filtration rate (eGFR) of 15 to 59 mL/min/1.73 m2 were enrolled in the main study. After 12 weeks, patients in the gemigliptin group continued to receive gemigliptin (N = 50), whereas patients in the placebo group were transitioned from placebo to linagliptin (N = 52). Each group received the indicated treatment over the subsequent 40‐week period. A total of 102 patients consented to participate in the extension study, and 79 patients ultimately completed the study. Results: The HbA1c levels of both groups were significantly reduced at week 52 compared with baseline. Specifically, the adjusted mean change ± standard error in HbA1c level in the gemigliptin and placebo/linagliptin groups was 1.00% ± 0.21% and 0.65% ± 0.22% lower at week 52 than at baseline (P < .001 and P = .003), respectively. No significant difference in the change in HbA1c level was found between the 2 groups (P = .148). Trends in fasting plasma glucose, fructosamine and glycated albumin levels in the 2 groups were similar to trends in HbA1c levels. The eGFR of both groups was also significantly lower at week 52 than at baseline, and no significant difference in change in eGFR was found between the 2 groups. In contrast, both drugs had little effect on urinary albumin excretion, although both drugs significantly reduced the urinary type IV collagen level. The overall rates of adverse events were similar between the 2 groups. Conclusions: Gemigliptin and linagliptin did not differ with respect to safety and efficacy in patients with T2DM and renal impairment. The 2 drugs had similar glucose‐lowering effects, and the changes in eGFR and albuminuria were also similar. Additionally, the risk of side effects, including hypoglycaemia, was similar between the 2 groups. [ABSTRACT FROM AUTHOR]

This study was conducted to evaluate effects of rhBMP-2 applied at different concentrations to sandblasted and acid etched (SLA) implants on osseointegration and bone regeneration in a bone defect of beagle dogs as pilot study using split-mouth design. Methods. For experimental groups, SLA implants were coated with different concentrations of rhBMP-2 (0.1, 0.5, and 1 mg/mL). After assessment of surface characteristics and rhBMP-2 releasing profile, the experimental groups and untreated control groups (n = 6 in each group, two animals in each group) were placed in split-mouth designed animal models with buccal open defect. At 8 weeks after implant placement, implant stability quotients (ISQ) values were recorded and vertical bone height (VBH, mm), bone-to-implant contact ratio (BIC, %), and bone volume (BV, %) in the upper 3 mm defect areas were measured. Results. The ISQ values were highest in the 1.0 group. Mean values of VBH (mm), BIC (%), and BV (%) were greater in the 0.5 mg/mL and 1.0 mg/mL groups than those in 0.1 and control groups in buccal defect areas. Conclusion. In the open defect area surrounding the SLA implant, coating with 0.5 and 1.0 mg/mL concentrations of rhBMP-2 was more effective, compared with untreated group, in promoting bone regeneration and osseointegration. [ABSTRACT FROM AUTHOR]

Blue phosphorescence organic light-emitting diodes (PHOLEDs) with interfacial mixed layer (IML) were fabricated to observe their electrical characteristics. The IML was composed of mCP as host material in the emissive layer (EML) and 3TPYMB as material for the electron transport layer (ETL) with the blue phosphorescent dopant FIrpic. PHOLEDs with IML were improved by 41% of current density and 35% of luminous efficiency compared to PHOLEDs without IML. The electron and energy transition mechanisms between EML and ETL in the presence of IML were confirmed through I-V-L characteristics and blue color coordinates. [ABSTRACT FROM AUTHOR]

We fabricated white phosphorescent organic light-emitting diodes (PHOLEDs) with the primary color(Red, Green and Blue) in single emissive layer using NPB, TCTA and TAPC as hole transporting layer (HTL) having different triplet energy level to observe triplet exciton's behavior. White PHOLED with TAPC having higher triplet energy level shows 51cd/A of luminous efficiency, and CIEXY color coordinate of (0.35, 0.40) at 10V. [ABSTRACT FROM AUTHOR]

1. Effects of non-steroidal anti-inflammatory drugs on the local atrial natriuretic peptide (ANP) and nitric oxide (NO) systems in the kidney were investigated. 2. Male Sprague-Dawley rats were treated with indomethacin (5 mg/kg, every 12 h, i.p.) for 2 days. The expression of ANP and natriuretic peptide receptor-A (NPR-A) mRNA was determined in the kidney, as was that of endothelial NO synthase (NOS) proteins. Particulate and soluble guanylyl cyclase activities were determined separately. 3. Following treatment with indomethacin, urinary sodium excretion decreased significantly. Although the renal expression of ANP was not changed significantly, that of NPR-A decreased significantly. The expression of NOS increased significantly. Particulate guanylyl cyclase activity was decreased, whereas the activity of soluble guanylyl cyclase was increased. The catalytic activity of Na+/K+-ATPase was increased, with no significant changes in its expression. The expression of the type 3 Na/H exchanger and Na–K−2CL cotransporters increased significantly. 4. The indomethacin-induced decrease in urinary sodium excretion may be attributed, at least in part, to decreased activity of the local ANP/cGMP system. The increased activity of the NO/cGMP system may be a compensatory response to the diminished activity of the prostaglandin system. [ABSTRACT FROM AUTHOR]

Blue PHOLEDs with interfacial mixed layer (IML) were fabricated to observe their electrical characteristics. IML was composed of mCP as host material in EML and 3TPYMB as electron transport material with phosphorescent blue dopant of FIrpic. PHOLED with IML were improved 41% of current density and 35% of luminous efficiency comparing to PHOLED without IML. [ABSTRACT FROM AUTHOR]

Background Prehospital delay is an important contributor to poor outcomes in both acute ischemic stroke (AIS) and acute myocardial infarction (AMI). We aimed to compare the prehospital delay and related factors between AIS and AMI. Methods and Results We identified patients with AIS and AMI who were admitted to the 11 Korean Regional Cardiocerebrovascular Centers via the emergency room between July 2016 and December 2018. Delayed arrival was defined as a prehospital delay of >3 hours, and the generalized linear mixed-effects model was applied to explore the effects of potential predictors on delayed arrival. This study included 17 895 and 8322 patients with AIS and AMI, respectively. The median value of prehospital delay was 6.05 hours in AIS and 3.00 hours in AMI. The use of emergency medical services was the key determinant of delayed arrival in both groups. Previous history, 1-person household, weekday presentation, and interhospital transfer had higher odds of delayed arrival in both groups. Age and sex had no or minimal effects on delayed arrival in AIS; however, age and female sex were associated with higher odds of delayed arrival in AMI. More severe symptoms had lower odds of delayed arrival in AIS, whereas no significant effect was observed in AMI. Off-hour presentation had higher and prehospital awareness had lower odds of delayed arrival; however, the magnitude of their effects differed quantitatively between AIS and AMI. Conclusions The effects of some nonmodifiable and modifiable factors on prehospital delay differed between AIS and AMI. A differentiated strategy might be required to reduce prehospital delay.

In the title compound, [PdBr(2)(C(10)H(8)N(2))]·CH(2)Cl(2), the Pd(2+) ion is four-coordinated in a slightly distorted square-planar environment by two N atoms of the chelating 2,2'-bipyridine ligand and two bromide ions. The compound displays intra-molecular C-H⋯Br hydrogen bonds and pairs of complex mol-ecules are assembled by inter-molecular C-H⋯Br hydrogen bonds. These pairs are connected by additional C-H⋯Br hydrogen bonds, forming a layer structure extending parallel to (011). Inter-molecular π-π inter-actions between the pyridine rings of the ligand are also present, the shortest centroid-centroid distance being 4.090 (9) Å.

The asymmetric unit of the title compound, [Pd(C(6)H(4)NO(2))(4)]·2H(2)O, consists of a quarter of a neutral Pd(IV) complex and half of a solvent water mol-ecule. In the complex, the Pd(IV) ion is located on a fourfold inversion axis and eight-coordinated in a distorted dodeca-hedral environment by four N and four O atoms from four symmetry-related pyridine-2-carboxyl-ate (pic) anionic ligands. In the crystal, the water mol-ecule is involved in O-H⋯O hydrogen bonding, and weak inter-molecular C-H⋯O hydrogen bonds occur. There are also inter-molecular π-π inter-actions between adjacent pyridine rings, with a centroid-centroid distance of 3.715 (3) Å.

In the dication of the title salt, C(6)H(16)N(2) (2+)·2C(6)H(4)NO(2) (-), the two ammonium groups are in the equatorial positions of the chair-shaped cyclo-hexyl ring. In the crystal, the cations and anions are linked by N-H⋯O and N-H⋯N hydrogen bonds, forming a layer network parallel to the ac plane. Weak π-π inter-actions between adjacent pyridine rings with a centroid-centroid distance of 3.589 (2) Å are also present.

The asymmetric unit of the title compound, C(10)H(26)N(4) (2+)·2C(6)H(4)NO(2) (-)·2H(2)O, consists of half of a doubly protonated 1,4,8,11-tetra-azacyclo-tetra-decane (cyclam) dication, a pyridine-2-carboxyl-ate anion and a solvent water mol-ecule. The complete dication is generated by a crystallographic centre and adopts an endodentate conformation which may be influenced by intra-molecular N-H⋯N hydrogen bonding. The carboxyl-ate group of the anion appears to be delocalized on the basis of the C-O bond lengths [1.257 (2) and 1.250 (2) Å]. In the crystal structure, the components are linked by inter-molecular N-H⋯O, N-H⋯N and O-H⋯O hydrogen bonds.

In the title compound, C(12)H(12)N(2) (2+)·2ClO(4) (-), the dihedral angle between the two outer pyridine rings of the dication is 44.8 (1)°. In the crystal, weak intermolecular C-H⋯O hydrogen bonds occur.

The asymmetric unit of the title compound, C(4)H(14)N(2) (2+)·2C(6)H(4)NO(2) (-)·H(2)O, consists of half of a doubly protonated tetra-methyl-enediammonium dication, a pyridine-2-carboxyl-ate anion and half of a solvent water mol-ecule; the dication is located on a centre of inversion and a twofold rotation axis passes through the O atom of the water mol-ecule. The carboxyl-ate group of the anion appears to be delocalized on the basis of the C-O bond lengths. In the crystal structure, the components are linked by inter-molecular N-H⋯O, N-H⋯N and O-H⋯O hydrogen bonds.

In the title compound, C(10)H(26)N(4) (2+)·2Cl(-)·0.5H(2)O, the cyclam (1,4,8,11-tetra-azacyclo-tetra-decane) dication adopts an endodentate conformation which my be inflenced by intra-molecular N-H⋯N hydrogen bonding. In the crystal structure, the components are linked by N-H⋯Cl and O-H⋯Cl hydrogen bonds into chains along [100]. The water molecule is disordered over two sites in a 50:50 ratio.

The asymmetric unit of the title compound, [MnBr(2)(C(6)H(4)NO(2))(H(2)O)(2)](n), contains one monomeric unit of the neutral linear coordination polymer. The Mn(3+) ions are bridged by anionic pyridine-2-carboxyl-ate (pic) ligands, thereby forming a chain-like structure along the c axis, and are six-coordinated in a distorted octa-hedral environment by two O atoms of the two different carboxyl-ate groups, two O atoms of two water mol-ecules and two Br atoms. The complex displays inter-molecular O-H⋯Br, O-H⋯N, O-H⋯O, C-H⋯O and C-H⋯Br hydrogen bonding. There may also be inter-molecular π-π inter-actions between adjacent pyridine rings, with a centroid-centroid distance of 3.993 (8) Å.

In the title complex, [PdBr(2)(C(7)H(8))], the Pd(II) ion lies in a distorted square-planar environment defined by the two Br atoms and the mid-points of the two π-coordinated double bonds of bicyclo-[2.2.1]hepta-2,5-diene. The complex is disposed about a crystallographic mirror plane parallel to the ac plane passing through the Pd, Br atoms and the centre of the diene ligand.

The title compound, C(6)H(18)N(2) (2+)·2C(6)H(4)NO(2) (-), consists of a doubly protonated hexa-methyl-enediammonium dication and two pyridine-2-carboxyl-ate anions. These ions inter-act by means of inter-molecular N-H⋯O and N-H⋯N hydrogen bonds to form a two-dimensional array. The carboxyl-ate groups of the anions appear to be delocalized on the basis of the C-O bond lengths.

The asymmetric unit of the title compound, [PtCl(2)(C(6)H(4)NO(2))(2)]·CH(3)CN, contains a neutral Pt(IV) complex and an acetonitrile solvent mol-ecule. In the complex, the Pt(4+) atom is six-coordinated in a distorted octa-hedral environment by two N atoms and two O atoms from two pyridine-carboxyl-ate (pic) ligands and two Cl atoms. The Cl atoms are cis with respect to each other. The compound displays inter- and intra-molecular C-H⋯O and C-H⋯Cl hydrogen bonding.

In the title compound, [PdCl(2)(C(10)H(8)N(2))]·CH(2)Cl(2), the Pd(2+) ion is four-coordinated in a slightly distorted square-planar environment by two N atoms of the 2,2'-bipyridine (bipy) ligand and two chloride ions. The compound displays intra-molecular C-H⋯Cl hydrogen bonds and pairs of complex mol-ecules are connected by inter-molecular C-H⋯Cl hydrogen bonds. Inter-molecular π-π inter-actions are present between the pyridine rings of the ligand, the shortest centroid-centroid distance being 4.096 (3) Å. As a result of the electronic nature of the chelate ring, it is possible to create π-π inter-actions to its symmetry-related counterpart [3.720 (2) Å] and also with a pyridine ring [3.570 (3) Å] of the bipy unit. The present structure is a redetermination of a previous structure [Vicente et al. (1997 ▶). Private communication (refcode PYCXMN02). CCDC, Cambridge, England]. In the new structure refinement all H atoms were located in a difference Fourier synthesis. Their coordinates were refined freely, together with isotropic displacement parameters.

The asymmetric unit of the title compound, {(C(6)H(18)N(2))(0.5)[MnBr(2)(C(6)H(4)NO(2))(H(2)O)]}(n), contains the repeat unit of the complex anion and one-half of a hexane-1,6-diammonium cation that is located on a twofold rotation axis. In the anionic polymer, the Mn(2+) ions are bridged by the pyridine-carboxyl-ate (pic) anion ligand, forming a chain structure along the c axis. The Mn(2+) ion is six-coordinated in a distorted octa-hedral environment by one N atom of the pyridine ring, two O atoms of the two carboxyl-ate groups, one O atom of the water mol-ecule and two Br atoms. The compound displays inter-molecular N-H⋯O, N-H⋯Br, O-H⋯Br and O-H⋯O hydrogen bonding. There may also be inter-molecular π-π inter-actions between adjacent pyridine rings, with a centroid-centroid distance of 3.992 (4) Å.

The asymmetric unit of the title compound, [PtCl(3.66)I(0.34)(C(12)H(8)N(2))]·0.5(Cl(0.13)I(1.87)), contains a neutral Pt(IV) complex and one half of a halogen molecule. The Pt(IV) ion is six-coordinated in a distorted octa-hedral environment by two N atoms of the 1,10-phenanthroline ligand and Cl or I atoms. The refinement of the structure and the EDX analysis indicate that the compound is a solid solution in which there is some substitution of Cl for I and vice versa. The chemical formula of the pure state of the compound would have been [PtCl(4)(C(12)H(8)N(2))]·0.5I(2). In the analysed crystal, two Cl atoms are partially (ca 25% and 9%) replaced by I atoms, and the I(2) mol-ecule has a minor component modelled as ICl. As a result of the disorder, the different trans effects of the N and Cl/I atoms are not distinct. The complex displays inter-molecular π-π inter-actions between the six-membered rings, with a centroid-centroid distance of 3.771 (4) Å. There are also weak intra-molecular C-H⋯Cl hydrogen bonds.

The asymmetric unit of the title compound, [Mn(2)Cl(4)(C(30)H(36)N(6))], contains one-half of the formula unit; a centre of inversion is located at the mid-point of the mol-ecule. The two Mn(2+) ions are bridged by the dual tri-dentate N,N,N',N'-tetra-kis(2-pyridylmeth-yl)hexane-1,6-diamine ligand to form a dinuclear complex. Each Mn atom is five-coordinated in an approximately square-pyramidal geometry by three N atoms from the ligand and two Cl atoms. Inter-molecular π-π inter-actions between adjacent pyridine rings with a centroid-centroid distance of 3.576 (2) Å are reported.

In the title complex, [PtCl(4)(C(12)H(8)N(2))]·H(2)O, the Pt(4+) ion is six-coordinated in a distorted octa-hedral environment by two N atoms of a 1,10-phenanthroline ligand and by four Cl atoms. As a result of the different trans effects of the N and Cl atoms, the Pt-Cl bonds trans to the N atom are slightly shorter than those trans to the Cl atom. The compound displays inter-molecular π-π inter-actions between the six-membered rings, with a centroid-centroid distance of 3.834 Å. There are also weak intra-molecular C-H⋯Cl hydrogen bonds. According to the IR spectrum, solvent water was present in the crystal, but owing to the high thermal motion of the uncoordinated O atom, the H atoms could not be detected.

The asymmetric unit of the title compound, [PtCl(4)(C(12)H(8)N(2))]·0.5CH(3)CN, contains two crystallographically independent Pt(IV) complexes with very similar geometry and one solvent mol-ecule. In the complexes, each Pt(IV) ion is six-coordinated in a distorted octa-hedral environment by two N atoms of the 1,10-phenanthroline ligand and four Cl atoms. Because of the different trans effects of the N and Cl atoms, the Pt-Cl bonds trans to the N atom are slightly shorter than those trans to the Cl atom. The compound displays numerous inter-molecular π-π inter-actions between six-membered rings, with a shortest centroid-to-centroid distance of 3.654 Å. There are also weak intra- and inter-molecular C-H⋯Cl hydrogen bonds.

In the title complex, [PtCl(2)(C(10)H(8)N(2))(2)]Cl(2)·H(2)O, the Pt(4+) ion is six-coordinated in a distorted octa-hedral environment by four N atoms from the two 2,2'-bipyridine ligands and two Cl atoms. As a result of the different trans influences of the N and Cl atoms, the Pt-N bonds trans to the Cl atom are slightly longer than those trans to the N atom. The compound displays inter-molecular hydrogen bonding between the water mol-ecule and the Cl anions. There are inter-molecular π-π inter-actions between adjacent pyridine rings, with a centroid-centroid distance of 3.962 Å.