Repeatability and Agreement of Central Vault for Implantable Collamer Lens Obtained by the Tomey OA-2000 Biometer and Spectralis OCT.

Objective: To assess repeatability and agreement of central vault for implantable collamer lens (ICL) measured by the Tomey OA-2000 biometry and Spectralis optical coherence tomography (OCT).

Methods: In this prospective study, the central vault was measured by the Tomey OA-2000 biometer and Spectralis OCT in 84 eyes (43 patients) after ICL implantation at six month follow-up. Three consecutive scans were obtained by one experienced technician using Tomey OA-2000 and the Spectralis OCT in the same day.

Posterior corneal elevation changes during 12 month of overnight orthokeratology.

Aims: the aim of this study to investigate the elevation changes in posterior corneal surface after 12 months of orthokeratology (ortho-k) treatment.

Methods: In this retrospective chart review, medical records of 37 Chinese children who wore ortho-k lenses over 12 months were reviewed. The data of only right eye were analyzed.

Crystalline lens thickness change is associated with axial length elongation and myopia progression in orthokeratology.

Aims: Considering individual variability in regards to the effects of orthokeratology (ortho-k) on myopia progression and controversies regarding the precise underlying mechanism, the aim of this study was to investigate several ocular measurements associated with axial length (AL) growth in children wearing ortho-k lenses.

Methods: In this retrospective chart review, medical records of 53 Chinese children who wore ortho-k lenses over the course of 12 months were reviewed. Baseline variables included age at initiation of ortho-k wear, refractive error (spherical equivalent, SE), central corneal thickness (CCT), and flat and steep keratometry of corneal principal meridians.

Estimating Lung Deposition of Fungal Spores Using Actual Airborne Spore Concentrations and Physiological Data.

Exposure to bioaerosols has been implicated in adverse respiratory symptoms, infectious diseases, and bioterrorism. Although these particles have been measured within residential and occupational settings in multiple studies, the deposition of bioaerosol particles within the human respiratory system has been only minimally explored. This paper uses real-world environmental measurement data of total fungal spores using Air-o-Cell cassettes in 16 different apartments and residents' physiological data in those apartments to predict respiratory deposition of the spores.

Presence and variability of culturable bioaerosols in three multi-family apartment buildings with different ventilation systems in the Northeastern US.

Bioaerosol concentrations in residential buildings located in the Northeastern US have not been widely studied. Here, in 2011-2015, we studied the presence and seasonal variability of culturable fungi and bacteria in three multi-family apartment buildings and correlated the bioaerosol concentrations with building ventilation system types and environmental parameters. A total of 409 indoor and 86 outdoor samples were taken.

Polycystin-1 Inhibits Cell Proliferation through Phosphatase PP2A/B56.

Autosomal dominant polycystic kidney disease (ADPKD) is associated with a number of cellular defects such as hyperproliferation, apoptosis, and dedifferentiation. Mutations in polycystin-1 (PC1) account for ∼85% of ADPKD. Here, we showed that wild-type (WT) or mutant PC1 composed of the last five transmembrane (TM) domains and the C-terminus (termed PC1-5TMC) inhibits cell proliferation and protein translation, as well as the downstream effectors of mTOR, consistent with previous reports.

Role of PKR in the Inhibition of Proliferation and Translation by Polycystin-1.

Autosomal dominant polycystic kidney disease (ADPKD) is mainly caused by mutations in the PKD1 (~85%) or PKD2 (~15%) gene which, respectively, encode polycystin-1 (PC1) and polycystin-2 (PC2). How PC1 regulates cell proliferation and apoptosis has been studied for decades but the underlying mechanisms remain controversial. Protein kinase RNA-activated (PKR) is activated by interferons or double-stranded RNAs, inhibits protein translation, and induces cell apoptosis.

Polycystin-1 inhibits eIF2α phosphorylation and cell apoptosis through a PKR-eIF2α pathway.

Autosomal dominant polycystic kidney disease (ADPKD) is caused by mutations in PKD1 or PKD2 which encodes polycystin-1 (PC1) and polycystin-2, respectively. PC1 was previously shown to slow cell proliferation and inhibit apoptosis but the underlying mechanisms remain elusive or controversial. Here we showed in cultured mammalian cells and Pkd1 knockout mouse kidney epithelial cells that PC1 and its truncation mutant comprising the last five transmembrane segments and the intracellular C-terminus (PC1-5TMC) down-regulate the phosphorylation of protein kinase R (PKR) and its substrate eukaryotic translation initiation factor 2 alpha (eIF2α).

Theoretical Investigations of the Chiral Transition of α-Amino Acid Confined in Various Sized Armchair Boron-Nitride Nanotubes.

We computationally study the chiral transition process of the α-Ala molecule under confined different sizes of armchair SWBNNTs to explore the confinement effect. We find that the influence of a confinement environment (in armchair SWBNNTs) on the α-Ala molecule would lead to different reaction pathways. Meanwhile, the preferred reaction pathway is also different in various sizes of armchair SWBNNTs, and their energy barriers for the rate-limiting step decrease rapidly with the decreasing of the diameters of the nanotubes.

Comparison of real-time instruments and gravimetric method when measuring particulate matter in a residential building.

Unlabelled: This study used several real-time and filter-based aerosol instruments to measure PM levels in a high-rise residential green building in the Northeastern US and compared performance of those instruments. PM 24-hr average concentrations were determined using a Personal Modular Impactor (PMI) with 2.5 µm cut (SKC Inc.

Comparison of particulate matter exposure estimates in young children from personal sampling equipment and a robotic sampler.

Accurate characterization of particulate matter (PM) exposure in young children is difficult, because personal samplers are often too heavy, bulky or impractical to be used. The Pretoddler Inhalable Particulate Environmental Robotic (PIPER) sampler was developed to help address this problem. In this study, we measured inhalable PM exposures in 2-year-olds via a lightweight personal sampler worn in a small backpack and evaluated the use of a robotic sampler with an identical sampling train for estimating PM exposure in this age group.

Airborne Particulate Matter in Two Multi-Family Green Buildings: Concentrations and Effect of Ventilation and Occupant Behavior.

There are limited data on air quality parameters, including airborne particulate matter (PM) in residential green buildings, which are increasing in prevalence. Exposure to PM is associated with cardiovascular and pulmonary diseases, and since Americans spend almost 90% of their time indoors, residential exposures may substantially contribute to overall airborne PM exposure. Our objectives were to: (1) measure various PM fractions longitudinally in apartments in multi-family green buildings with natural (Building E) and mechanical (Building L) ventilation; (2) compare indoor and outdoor PM mass concentrations and their ratios (I/O) in these buildings, taking into account the effects of occupant behavior; and (3) evaluate the effect of green building designs and operations on indoor PM.

Evaluation of particle resuspension in young children's breathing zone using stationary and robotic (PIPER) aerosol samplers.

Development of asthma in young children may be associated with high exposure to particulate matter (PM). However, typical stationary samplers may not represent the personal exposure of children ages 3 and younger since they may not detect particles resuspended from the floor as children play, thus reducing our ability to correlate exposure and disease etiology. To address this, an autonomous robot, the Pretoddler Inhalable Particulate Environmental Robotic (PIPER) sampler, was developed to simulate the movements of children as they play on the floor.

Filamin-a increases the stability and plasma membrane expression of polycystin-2.

Polycystin-2 (PC2), encoded by the PKD2 gene, is mutated in ~15% of autosomal dominant polycystic kidney disease. Filamins are actin-binding proteins implicated in scaffolding and membrane stabilization. Here we studied the effects of filamin on PC2 stability using filamin-deficient human melanoma M2, filamin-A (FLNA)-replete A7, HEK293 and IMCD cells together with FLNA siRNA/shRNA knockdown (KD).

Circulating levels of tumor necrosis factor-alpha receptor 2 are increased in heart failure with preserved ejection fraction relative to heart failure with reduced ejection fraction: evidence for a divergence in pathophysiology.

Background: Various pathways have been implicated in the pathogenesis of heart failure (HF) with preserved ejection fraction (HFPEF). Inflammation in response to comorbid conditions, such as hypertension and diabetes, may play a proportionally larger role in HFPEF as compared to HF with reduced ejection fraction (HFREF).

Methods And Results: This study investigated inflammation mediated by the tumor necrosis factor-alpha (TNFα) axis in community-based cohorts of HFPEF patients (n = 100), HFREF patients (n = 100) and healthy controls (n = 50).

Improved exposure characterization with robotic (PIPER) sampling and association with children's respiratory symptoms, asthma and eczema.

Particulate matter (PM) and its constituents are recognized risk factors for the development of respiratory symptoms and illness in children. Most measurements of exposure have relied upon stationary indoor monitors (SIMs), overlooking the role of resuspended PM. To improve exposure characterization to resuspended aerosol PM, a recently developed methodology has been employed.

Heterozygote loss of ACE2 is sufficient to increase the susceptibility to heart disease.

Unlabelled: Angiotensin-converting enzyme 2 (ACE2) metabolizes Ang II into Ang 1-7 thereby negatively regulating the renin-angiotensin system. However, heart disease in humans and in animal models is associated with only a partial loss of ACE2. ACE2 is an X-linked gene; and as such, we tested the clinical relevance of a partial loss of ACE2 by using female ACE2(+/+) (wildtype) and ACE2(+/-) (heterozygote) mice.

Angiotensin II induced proteolytic cleavage of myocardial ACE2 is mediated by TACE/ADAM-17: a positive feedback mechanism in the RAS.

Angiotensin converting enzyme (ACE) 2 is a key negative regulator of the renin-angiotensin system where it metabolizes angiotensin (Ang) II into Ang 1-7. We hypothesize that Ang II suppresses ACE2 by increasing TNF-α converting enzyme (TACE) activity and ACE2 cleavage. Ang II infusion (1.

Loss of Apelin exacerbates myocardial infarction adverse remodeling and ischemia-reperfusion injury: therapeutic potential of synthetic Apelin analogues.

Background: Coronary artery disease leading to myocardial ischemia is the most common cause of heart failure. Apelin (APLN), the endogenous peptide ligand of the APJ receptor, has emerged as a novel regulator of the cardiovascular system.

Methods And Results: Here we show a critical role of APLN in myocardial infarction (MI) and ischemia-reperfusion (IR) injury in patients and animal models.

TIMP2 and TIMP3 have divergent roles in early renal tubulointerstitial injury.

Tissue inhibitors of metalloproteinases (TIMPs) are endogenous inhibitors of matrix metalloproteinases (MMPs). While TIMP2 and TIMP3 inhibit MMPs, TIMP3 also inhibits activation of pro-MMP2, whereas TIMP2 promotes it. Here we assessed the differential role of TIMP2 and TIMP3 in renal injury using the unilateral ureteral obstruction model.

Loss of p47phox subunit enhances susceptibility to biomechanical stress and heart failure because of dysregulation of cortactin and actin filaments.

Rationale: The classic phagocyte nicotinamide adenine dinucleotide phosphate oxidase (gp91(phox) or Nox2) is expressed in the heart. Nox2 activation requires membrane translocation of the p47(phox) subunit and is linked to heart failure. We hypothesized that loss of p47(phox) subunit will result in decreased reactive oxygen species production and resistance to heart failure.

Loss of TIMP3 selectively exacerbates diabetic nephropathy.

Diabetic nephropathy is the most common cause of end-stage renal disease. Polymorphism in the tissue inhibitor of metalloproteinase-3 (TIMP3) gene, and the ECM-bound inhibitor of matrix metalloproteinases (MMPs), has been linked to diabetic nephropathy in humans. To elucidate the mechanism, we generated double mutant mice in which the TIMP3 gene was deleted in the genetic diabetic Akita mouse background.

Structural interaction and functional regulation of polycystin-2 by filamin.

Filamins are important actin cross-linking proteins implicated in scaffolding, membrane stabilization and signal transduction, through interaction with ion channels, receptors and signaling proteins. Here we report the physical and functional interaction between filamins and polycystin-2, a TRP-type cation channel mutated in 10-15% patients with autosomal dominant polycystic kidney disease. Yeast two-hybrid and GST pull-down experiments demonstrated that the C-termini of filamin isoforms A, B and C directly bind to both the intracellular N- and C-termini of polycystin-2.

Angiotensin-converting enzyme 2 antagonizes angiotensin II-induced pressor response and NADPH oxidase activation in Wistar-Kyoto rats and spontaneously hypertensive rats.

Angiotensin-converting enzyme 2 (ACE2), a monocarboxypeptidase capable of metabolizing angiotensin II (Ang II) into angiotensin-(1-7) [Ang-(1-7)], has emerged as a potential therapeutic target. We hypothesized that ACE2 is a negative regulator of Ang II-mediated pathological effects in vivo. In Wistar-Kyoto (WKY) rats, Ang II infusion (0.

Cardioprotective effects mediated by angiotensin II type 1 receptor blockade and enhancing angiotensin 1-7 in experimental heart failure in angiotensin-converting enzyme 2-null mice.

Loss of angiotensin (Ang)-converting enzyme 2 (ACE2) and inability to metabolize Ang II to Ang 1-7 perpetuate the actions of Ang II after biomechanical stress and exacerbate early adverse myocardial remodeling. Ang receptor blockers are known to antagonize the effect of Ang II by blocking Ang II type 1 receptor (AT(1)R) and also by upregulating the ACE2 expression. We directly compare the benefits of AT(1)R blockade versus enhancing Ang 1-7 action in pressure-overload-induced heart failure in ACE2 knockout mice.