Miracle-dz/UniFAR-FTUs huggingface dataset:
The relationship between diurnal variations in intraocular pressure measurements and central corneal thickness and corneal hysteresis.

PURPOSE To examine the relationship between office-hour changes in IOP, measured with the Goldmann applanation tonometer (GAT) and dynamic contour tonometer (DCT), and the corneal characteristics central corneal thickness (CCT) and corneal hysteresis (CH). METHODS Sixty-two eyes of 62 untreated normal subjects and patients with untreated glaucoma had IOP measurements performed with the GAT (mm Hg) and DCT (mm Hg) over an 8-hour period at 2-hour intervals beginning at 9 AM. CCT (micrometers) was measured using a noncontact optical low-coherence reflectometry (OLCR) pachymeter, and CH (mm Hg) was measured with an ocular response analyzer (ORA). The associations between IOP measurements and corneal characteristics for each patient over the measurement period were assessed by using multilevel modeling. RESULTS GAT and DCT IOP and CCT changed significantly during office hours (ANOVA; GAT: F = 19.9, P < 0.001; DCT: F = 4.6, P = 0.001; CCT: F = 16.4; P < 0.001). No significant changes were observed in CH (ANOVA; F = 1.8, P = 0.13). Multilevel modeling analysis of the interrelationships between CCT, CH, and age on IOP measurements revealed that both CCT and CH changes were significantly associated with GAT IOP changes (GAT IOP/CCT slope, 0.04 mm Hg/microm; 95% confidence intervals [CIs], 0.02-0.06; GAT IOP/CH slope, 0.20 mm Hg/mm Hg; 95% CI, 0.01-0.39). CCT, but not CH, changes were significantly associated with DCT IOP changes (DCT IOP/CCT slope, 0.03 mm Hg/microm; 95% CI, 0.00-0.05). However, although the association between CCT and GAT IOP was relatively uniform between subjects, association between CCT and DCT IOP showed greater intersubject variability. Age had no effect on the diurnal variation of IOP measured with either device. CONCLUSIONS Measured IOP and corneal characteristics covary during office hours. Changes in CCT and CH are associated with changes in GAT IOP and, less consistently, with DCT IOP. The data suggest that variations in corneal characteristics explain a small proportion of the change in IOP measurements made with the GAT during office hours.
Building a 2.4-GHZ radio transceiver using IEEE 802.15.4

IEEE CIRCUITS & DEVICES MAGAZINE ■ NOVEMBER/DECEMBER 2005 8755-3996/05/$20.00 ©2005 IEEE T he ZigBee Alliance has been developing a standard-based wireless network platform aimed at sensor and control applications with low-data rate and low-power consumption. IEEE 802.15. 4 [1], ratified in 2003, specifies the physical (PHY) layer and medium access control (MAC) layers, while the ZigBee Alliance defines upper layers such as network, security and application profile layers for an IEEE 802.15. 4-based system. IEEE 802.15. 4 assigns three frequency bands of operation: the 868-MHz, 915-MHz, and 2.4-GHz unlicensed industrial, scientific, and medical (ISM) bands. Among the three, the 2.4-GHz band is highly attractive, since this unlicensed band is commonly available throughout the world. Typical applications of this low data rate standard include
Candidate protein biodosimeters of human exposure to ionizing radiation

Purpose: To conduct a literature review of candidate protein biomarkers for individual radiation biodosimetry of exposure to ionizing radiation. Materials and methods: Reviewed ∼300 publications (1973 – April 2006) that reported protein effects in mammalian systems after either in vivo or in vitro radiation exposure. Results: We found 261 radiation-responsive proteins including 173 human proteins. Most of the studies used high doses of ionizing radiation (>4 Gy) and had no information on dose- or time-responses. The majority of the proteins showed increased amounts or changes in phosphorylation states within 24 h after exposure (range: 1.5- to 10-fold). Of the 47 proteins that are responsive at doses of 1 Gy and below, 6 showed phosphorylation changes at doses below 10 cGy. Proteins were assigned to 9 groups based on consistency of response across species, dose- and time-response information and known role in the radiation damage response. Conclusions: ATM (Ataxia telengiectasia mutated), H2AX (histone 2AX), CDKN1A (Cyclin-dependent kinase inhibitor 1A), and TP53 (tumor protein 53) are top candidate radiation protein biomarkers. Furthermore, we recommend a panel of protein biomarkers, each with different dose and time optima, to improve individual radiation biodosimetry for discriminating between low-, moderate-, and high-dose exposures. Our findings have applications for early triage and follow-up medical assessments.
Nicotine potentiates vascular endothelial growth factor expression in balloon-injured rabbit aortas

Both nicotine and vascular endothelial growth factor (VEGF) have been proposed to play an important role in the development and progression of atherosclerosis. In vitro and ex vivo studies have demonstrated that nicotine significantly stimulates VEGF expression in several cell types. This study examined the effects and the mechanisms of nicotine on the expression of VEGF in a rabbit model of balloon-injured aortas. Forty-eight male New Zealand white rabbits were randomly divided into sham, control, nicotine, and nicotine plus hexamethonium (nicotine–hex) groups. Balloon catheter denuding injury iliac artery was performed in control, nicotine, and nicotine–hex animals fed with a high-cholesterol diet beginning 2 weeks before operation. Twenty-four hours after surgery, nicotine (0.05 μg/kg) or nicotine (0.05 μg/kg) and hexamethonium (6 mg/kg) was administered daily by intramuscular injection for 3 weeks in nicotine and nicotine–hex groups, respectively. Sham and control rabbits received an identical volume of phosphate-buffered saline injection, but without nicotine or hexamethonium. VEGF protein expression and intimal cell proliferation in balloon-injured aortas were determined by enzyme-link immunosorbent assay, immunohistochemistry, and Western blot analysis. Six rabbits died during the experiment. The remaining 42 rabbits were included in the study. VEGF protein expression in nicotine group was significantly higher than that in control group (P < 0.01). VEGF positive staining was seen in vascular endothelial cells, vascular smooth muscle cells, and infiltrative inflammatory cells. The number of the proliferative cells in intima was also significantly higher in nicotine group than in control group (P < 0.01). Hexamethonium, a nonselective antagonist of nicotinic acetylcholine receptors (nAChRs), significantly inhibited nicotine-induced VEGF protein expression (P < 0.01). The present study shows that intramuscular administration of nicotine markedly potentiates the expression of VEGF protein in balloon-injured rabbit aortas, which appears to be mediated through nAChRs.
The Influence Of Mobile Channel On Customer Behavior In Omni-Channel Banking Services

As mobile phones and tablets are in widespread use, the emergence of mobile channel is changing the way customers interact with financial institutions. In this research, we empirically examine how the use of mobile devices can improve customer informedness and affect customer behavior in financial transactions. We use a large-scale customer transaction data obtained from one of the largest commercial banks in the United States. Specifically, we investigate: (1) whether the use of mobile phones and tablets is associated with a higher level of customer informedness and demand for services; and (2) compared to customers that only transact through a PC, whether mobile phone and tablet users are less likely to incur overdraft and credit card penalty fees. This paper contributes new knowledge in omni-channel banking services by examining post-adoption customer behavioral changes using transaction-level observations. We also discuss insights for banks’ managers related to the design of new mobile channel, and strategic management of existing digital and physical channels.
Cathepsin E Is a Specific Marker of Dysplasia in APCMin/+ Mouse Intestine

Transcriptional profiling of APCMin/+ mouse intestinal epithelial tissue has revealed that cathepsin E (catE) manifests high relative expression in adenomas and carcinomas relative to normal epithelium. Real-time RT-PCR data presented previously confirm the presence of catE transcript in APCMin/+ adenomatous cells compared with samples derived from normal APCMin/+ and wild-type tissue. At the protein level, strong, highly specific immunohistochemical staining for catE is displayed in dysplastic lesions of APCMin/+ mice. Using Western immunoblot analyses, it was additionally established that the urine of tumor-bearing mice contains higher levels of the monomeric form of catE than their wild-type counterparts. These results authenticate the relationship between transcript abundance and protein levels in transformed tissue and suggest potential utility for catE as a marker for the inception and progression of intestinal cancers.
Epidemiology of lifetime fracture prevalence in England: a population study of adults aged 55 years and over.

BACKGROUND fractures remain a substantial public health problem but epidemiological studies using survey data are sparse. This study explores the association between lifetime fracture prevalence and socio-demographic factors, health behaviours and health conditions. METHODS fracture prevalence was calculated using a combined dataset of annual, nationally representative health surveys in England (2002-07) containing 24,725 adults aged 55 years and over. Odds of reporting any fracture was estimated separately for each gender using logistic regression. RESULTS fracture prevalence was higher in men than women (49 and 40%, respectively). In men, factors having a significant independent association with fracture included being a former regular smoker [odds ratios, OR: 1.18 (1.06-1.31)], having a limiting long-standing illness [OR: 1.47 (1.31-1.66)] and consuming >8 units of alcohol on the heaviest drinking day in the past week [OR: 1.65 (1.37-1.98)]. In women, significant factors included being separated/divorced [OR: 1.30 (1.10-1.55)], having a 12-item General Health Questionnaire (GHQ-12) score of 4+ [OR: 1.59 (1.27-2.00)], consuming >6 units of alcohol in the past week [OR: 2.07 (1.28-3.35)] and being obese [OR: 1.25 (1.03-1.51)]. CONCLUSION a range of socio-demographic, health behaviour and health conditions, known to increase the risk of chronic disease and premature death, are also associated with fracture occurrence, probably involving the aetiological pathways of poor bone health and fall-related trauma.
Cdc 7 p-Dbf 4 p becomes famous in the cell cycle

During reproduction, cellular components and organelles need to be replicated and maintained. However, chromosome number needs to be exactly duplicated. Any heritable changes in chromosome number can result in disastrous consequences for the organism. Therefore, elaborate mechanisms to replicate and segregate chromosomes during the cell division cycle have evolved. It has become apparent in the past decade that these mechanisms include reversible protein phosphorylation catalyzed by several protein kinases and phosphatases (see review by Nurse, 2000). Most famous of all these kinases are the cyclin-dependent kinases (CDKs) – see reviews by Morgan, 1995; Roberts, 1999; Sherr and Roberts, 1999). CDKs regulate both the G1-S phase and the G 2-M transitions of the cell cycle and probably phosphorylate several different substrates to this end. However, the lesser-known Cdc7p kinase, which like CDKs requires a regulatory subunit (Dbf4p) for activity, has very few protein substrates. Cdc7p-Dbf4p regulates a specific step during the initiation of DNA replication in all eukaryotes studied, including human cells (see recent reviews by Johnston et al., 1999; Masai et al., 1999). Barinaga (1994) reported the emergence of the Cdc7p-Dbf4 complex as an important player in the cell cycle. Here I summarize recent exciting developments that show that this prediction was warranted and elevate the importance of Cdc7p to a level comparable to that of CDKs. CELLULAR PHYSIOLOGY
Study of the mechanisms of the modifying actions of hexamethonium on the cardiovascular response to norepinephrine.

In the pentobarbital-anestimetized dog, the administration of hexamethonium increased the systemic blood pressure response to norepinephrine (NE) given in a rapid single i.v. injection. The homeostatic reflex vasodilatioum induced by the pressor agent was demonmstmated in the autoperfused hind leg of the dog and its block by hexamethonium is one countribunting factor to this poteintiation. With the perfused leg of the dog and bloodbathed organs as bioassay teclnnques, it was shown that hexametimonium treatment results in a delay in the iniactivationm of circulatiumg NE: this is a second contributing factor to the potentiation. Large doses (10 mg/kg) of hexametimonmiunm. in addition to blocking the homeostatic reflexes and delayinig the inactivation of circunlatinsg NE. also resulted in increased perfunsioun pressure responses to i.a. NE, suggesting that third conmtributing factor to the potentiation is some peripheral action of the hexamethonium.
Innervation of the Lumbar Intervertebral Disc by Nerve Growth Factor-Dependent Neurons Related to Inflammatory Pain

Study Design. We used anatomic tracers and immunoreactivity in rats to define dorsal root ganglion neuron populations innervating the lumbar discs in physiologic and inflammatory states. Objectives. To investigate the percentages of calcitonin gene-related peptide-immunoreactive (CGRP-ir) and isolectin B4 (IB4)-binding neurons innervating lumbar discs. Summary of Background Data. Small neurons are classified into two types. One contains CGRP and expresses the nerve growth factor receptor. The other binds IB4 and expresses the glial cell line-derived neurotrophic factor receptor. Methods. A neurotracer, Fluoro-Gold, was applied to the L5–L6 disc in rats. Five days later, 50-μL saline (control group: n = 8) or Complete Freund’s adjuvant (inflammatory group: n = 8) was applied to the disc. Seven days after the second operation, T13–L5 dorsal root ganglions were processed for double staining of CGRP and IB4. Results. Of the Fluoro-Gold-labeled neurons, 50.1 ± 4.6% (mean ± SEM) were positive for CGRP and 0.7 ± 0.6% positive for IB4 in the control group, while 65.6 ± 4.7% were positive for CGRP and 1.0 ± 1.0% positive for IB4 in the inflammatory group. The percentage of CGRP-ir neurons was significantly higher than that of IB4-binding neurons in both groups (P < 0.001, each). The percentage of CGRP-ir neurons in the inflammatory group was significantly higher than in the control group (P < 0.05). Conclusions. We found that most small neurons innervating the disc were CGRP-ir. Furthermore, disc inflammation caused an increase in CGRP-ir neurons but not IB4-binding neurons, suggesting that CGRP-ir, nerve growth factor-dependent neurons are more responsible for discogenic pain.
A coactivator trap identifies NONO (p54nrb) as a component of the cAMP-signaling pathway

Signal transduction pathways often use a transcriptional component to mediate adaptive cellular responses. Coactivator proteins function prominently in these pathways as the conduit to the basic transcriptional machinery. Here we present a high-throughput cell-based screening strategy, termed the “coactivator trap,” to study the functional interactions of coactivators with transcription factors. We applied this strategy to the cAMP signaling pathway, which utilizes two families of coactivators, the cAMP response element binding protein (CREB) binding protein (CBP)/p300 family and the recently identified transducers of regulated CREB activity family (TORCs1–3). In addition to identifying numerous known interactions of these coactivators, this analysis identified NONO (p54nrb) as a TORC-interacting protein. RNA interference experiments demonstrate that NONO is necessary for cAMP-dependent activation of CREB target genes in vivo. Furthermore, TORC2 and NONO complex on cAMP-responsive promoters, and NONO acts as a bridge between the CREB/TORC complex and RNA polymerase II. These data demonstrate the utility of the coactivator trap by identification of a component of cAMP-mediated transcription.
Genome Analysis B 73-Mo 17 Near-Isogenic Lines Demonstrate Dispersed Structural Variation in Maize 1 [ W ] [ OA ]

Recombinant inbred lines developed from the maize (Zea mays ssp. mays) inbreds B73 and Mo17 have been widely used to discover quantitative trait loci controlling a wide variety of phenotypic traits and as a resource to produce high-resolution genetic maps. These two parents were used to produce a set of near-isogenic lines (NILs) with small regions of introgression into both backgrounds. A novel array-based genotyping platform was used to score genotypes of over 7,000 loci in 100 NILs with B73 as the recurrent parent and 50 NILs with Mo17 as the recurrent parent. This population contains introgressions that cover the majority of the maize genome. The set of NILs displayed an excess of residual heterozygosity relative to the amount expected based on their pedigrees, and this excess residual heterozygosity is enriched in the low-recombination regions near the centromeres. The genotyping platform provided the ability to survey copy number variants that exist in more copies in Mo17 than in B73. The majority of these Mo17-specific duplications are located in unlinked positions throughout the genome. The utility of this population for the discovery and validation of quantitative trait loci was assessed through analysis of plant height variation.
Dopamine in the lobster Homarus gammarus: II. Dopamine‐immunoreactive neurons and development of the nervous system

Dopamine‐immunoreactive neurons were revealed in lobster embryos, larvae, and postlarvae, and staining patterns were compared to neuronal labeling in the juvenile lobster nervous system (Cournil et al. [1994] J. Comp. Neurol. 344:455–469). Dopamine immunoreactivity is first detected by midembryonic life in 35–40 neuroi somata located anteriorly in brain and subesophageal ganglion. When the lobsters assume a benthic life during the first postlarval stage, an average of 58 cell bodies are labeled. The acquisition of dopamine in lobster neurons is a protracted event spanning embryonic, larval, and postlarval life and finally reaching the full complement of roughly 100 neurons in juvenile stages.
Exercise Increases Ca2+–Calmodulin‐Dependent Protein Kinase II Activity in Human Skeletal Muscle

There is evidence in rodents that Ca2+‐calmodulin‐dependent protein kinase II (CaMKII) activity is higher in contracting skeletal muscle, and this kinase may regulate skeletal muscle function and metabolism during exercise. To investigate the effect of exercise on CaMKII in human skeletal muscle, healthy men (n= 8) performed cycle ergometer exercise for 40 min at 76 ± 1 % peak pulmonary O2 uptake (V̇O2peak), with skeletal muscle samples taken at rest and after 5 and 40 min of exercise. CaMKII expression and activities were examined by immunoblotting and in vitro kinase assays, respectively. There were no differences in maximal (+ Ca2+, CaM) CaMKII activity during exercise compared with rest. Autonomous (‐ Ca2+, CaM) CaMKII activity was 9 ± 1 % of maximal at rest, remained unchanged at 5 min, and increased to 17 ± 1 % (P < 0.01) at 40 min. CaMKII autophosphorylation at Thr287 was 50‐70 % higher during exercise, with no differences in CaMKII expression. The effect of maximal aerobic exercise on CaMKII was also examined (n= 9), with 0.7‐ to 1.5‐fold increases in autonomous CaMKII activity, but no change in maximal CaMKII activity. CaMKIV was not detected in human skeletal muscle. In summary, exercise increases the activity of CaMKII in skeletal muscle, suggesting that it may have a role in regulating skeletal muscle function and metabolism during exercise in humans.
An open-label, non-randomized study of the pharmacokinetics of the nutritional supplement nicotinamide riboside (NR) and its effects on blood NAD+ levels in healthy volunteers

Objectives The co-primary objectives of this study were to determine the human pharmacokinetics (PK) of oral NR and the effect of NR on whole blood nicotinamide adenine dinucleotide (NAD+) levels. Background Though mitochondrial dysfunction plays a critical role in the development and progression of heart failure, no mitochondria-targeted therapies have been translated into clinical practice. Recent murine studies have reported associations between imbalances in the NADH/NAD+ ratio with mitochondrial dysfunction in multiple tissues, including myocardium. Moreover, an NAD+ precursor, nicotinamide mononucleotide, improved cardiac function, while another NAD+ precursor, nicotinamide riboside (NR), improved mitochondrial function in muscle, liver and brown adipose. Thus, PK studies of NR in humans is critical for future clinical trials. Methods In this non-randomized, open-label PK study of 8 healthy volunteers, 250 mg NR was orally administered on Days 1 and 2, then uptitrated to peak dose of 1000 mg twice daily on Days 7 and 8. On the morning of Day 9, subjects completed a 24-hour PK study after receiving 1000 mg NR at t = 0. Whole-blood levels of NR, clinical blood chemistry, and NAD+ levels were analyzed. Results Oral NR was well tolerated with no adverse events. Significant increases comparing baseline to mean concentrations at steady state (Cave,ss) were observed for both NR (p = 0.03) and NAD+ (p = 0.001); the latter increased by 100%. Absolute changes from baseline to Day 9 in NR and NAD+ levels correlated highly (R2 = 0.72, p = 0.008). Conclusions Because NR increases circulating NAD+ in humans, NR may have potential as a therapy in patients with mitochondrial dysfunction due to genetic and/or acquired diseases.
Perspectives of a Systems Biology of the Brain: The Big Data Conundrum Understanding Psychiatric Diseases

Abstract Psychiatric diseases provoke human tragedies. Asocial behaviour, mood imbalance, uncontrolled affect, and cognitive malfunction are the price for the biological and social complexity of neurobiology. To understand the etiology and to influence the onset and progress of mental diseases remains of upmost importance, but despite the much improved care for the patients, more then 100 years of research have not succeeded to understand the basic disease mechanisms and enabling rationale treatment. With the advent of the genome based technologies, much hope has been created to join the various dimension of -omics data to uncover the secrets of mental illness. Big Data as generated by -omics do not come with explanations. In this essay, I will discuss the inherent, not well understood methodological foundations and problems that seriously obstacle in striving for a quick success and may render lucky strikes impossible.