Miracle-dz/UniFAR-FTUs huggingface dataset:
Expression of peroxisomal proliferator-activated receptors and retinoid X receptors in the kidney.

The discovery that 15-deoxy-Δ12,14-prostaglandin J2(15d-PGJ2) is a ligand for the γ-isoform of peroxisome proliferator-activated receptor (PPAR) suggests nuclear signaling by prostaglandins. Studies were undertaken to determine the nephron localization of PPAR isoforms and their heterodimer partners, retinoid X receptors (RXR), and to evaluate the function of this system in the kidney. PPARα mRNA, determined by RT-PCR, was found predominately in cortex and further localized to proximal convoluted tubule (PCT); PPARγ was abundant in renal inner medulla, localized to inner medullary collecting duct (IMCD) and renal medullary interstitial cells (RMIC); PPARβ, the ubiquitous form of PPAR, was abundant in all nephron segments examined. RXRα was localized to PCT and IMCD, whereas RXRβ was expressed in almost all nephron segments examined. mRNA expression of acyl-CoA synthase (ACS), a known PPAR target gene, was stimulated in renal cortex of rats fed with fenofibrate, but the expression was not significantly altered in either cortex or inner medulla of rats fed with troglitazone. In cultured RMIC cells, both troglitazone and 15d-PGJ2 significantly inhibited cell proliferation and dramatically altered cell shape by induction of cell process formation. We conclude that PPAR and RXR isoforms are expressed in a nephron segment-specific manner, suggesting distinct functions, with PPARα being involved in energy metabolism through regulating ACS in PCT and with PPARγ being involved in modulating RMIC growth and differentiation.
Effects of Different Dietary Interventions on Calcitriol, Parathyroid Hormone, Calcium, and Phosphorus: Results from the DASH Trial

The “Dietary Approaches to Stop Hypertension” (DASH) diet, rich in fiber and low-fat dairy, effectively lowers blood pressure. DASH’s effect on calcitriol and other markers of bone-mineral metabolism is unknown. This secondary analysis of the DASH trial aimed to determine the effect of dietary patterns on blood concentrations of calcitriol, parathyroid hormone (PTH), ionized calcium, and urinary excretion of calcium and phosphorus. Outcomes were available in 334 participants in the trial. After a 3-week run-in on the control diet, participants were randomized to control, fruits and vegetables (F&V), or DASH diets. Outcomes were assessed at the end of run-in, and during the last week of the intervention period. Mean age of participants was 45.7 ± 10.7 years, 46% female, and 57% African-American. Mean ± Standard Deviation(SD) baseline serum concentrations of calcitriol, PTH, and ionized calcium were 37.8 ± 9.2 pg/mL, 46.1 ± 18.5 pg/mL and 5.2 ± 0.23 mg/dL, respectively. Mean (±SD) urinary calcium and phosphorus excretions were 150.1 ± 77.8 and 708.0 ± 251.8 mg/24 h, respectively. Compared with control, DASH reduced calcitriol −3.32 pg/mL (p = 0.004). Otherwise, there was no significant effect on other biomarkers. DASH lowered serum calcitriol perhaps more among African-Americans. These results raise important questions about the interpretation and clinical significance of low calcitriol concentrations in the setting of recommended diets.
Programmed cell death induced by ischemia-reperfusion in rat intestinal mucosa.

Apoptosis after ischemia-reperfusion (I/R) was characterized in rat small intestine. Under halothane anesthesia, the superior mesenteric artery in the rat was occluded for 15 or 60 min, followed by reperfusion. Ratios of fragmented DNA to total DNA, electrophoresis, and immunohistochemical staining were examined after I/R. Some rats were pretreated with α-difluoromethylornithine (DFMO) to examine the relationship between intestinal apoptosis and ornithine decarboxylase (ODC) activity. The percentage of fragmented DNA significantly increased just after ischemia and peaked at 1 h after reperfusion in the jejunum and ileum. These increases were significantly higher in the 60-min ischemia group compared with the 15-min ischemia group. This increase decreased 6 h after reperfusion. The results were corroborated by histological evaluations of the intestine under the same conditions. DFMO completely abolished elevation of ODC activity 6 h after reperfusion but did not change the percentage of fragmented DNA. Apoptosis in rat small intestine was induced by ischemia of the gut, and this process was exacerbated by reperfusion. The changes in apoptosis were independent of ODC activity.
Lack of a relation between vitamin and mineral antioxidants and bone mineral density: results from the Women's Health Initiative.

BACKGROUND Antioxidant defenses are one possible mechanism for decreasing oxidative damage and its potentially negative effects on age-related bone mass. OBJECTIVE This study cross-sectionally examined whether higher dietary intakes, total intakes, and serum concentrations of antioxidants may be associated with higher bone mineral density (BMD). DESIGN Total hip (and subregions), spine, and total-body BMDs were measured in 11,068 women aged 50-79 y enrolled in the Women's Health Initiative Observational Study and Clinical Trial at 3 clinics. Antioxidant intakes from diet (vitamin A, retinol, beta-carotene, vitamin C, vitamin E, and selenium) were estimated by using a self-reported food-frequency questionnaire. Antioxidants from supplements were estimated with an interviewer-administered questionnaire. A random subset (n = 379) had serum concentrations of retinol, carotenoids, and tocopherols measured. RESULTS After adjustment for important BMD-related covariates, increasing intakes of antioxidants were not independently associated with BMD. A significant interaction effect was observed between intake of total vitamin C (lower three-fourths compared with highest one-fourth) and use of hormone therapy (HT) (P < 0.01). The beneficial effect of current HT use on femoral neck BMD appeared to be greater in women with higher concentrations of total vitamin C. This interaction was also significant for total-body (P < 0.045), spine (P = 0.03), and total-hip BMDs (P = 0.029). CONCLUSIONS Our results do not support independent associations between dietary intake, total intake, or serum concentrations of antioxidants and BMD in women participating in the Women's Health Initiative. The extent to which HT use may interact with vitamin C intake and BMD warrants further exploration.
Characterization of receptors mediating AVP- and OT-induced glucagon release from the rat pancreas.

We characterized the receptors that mediate arginine vasopressin (AVP)- and oxytocin (OT)-induced glucagon release by use of a number of antagonists in the perfused rat pancreas and the fluorescence imaging of the receptors. AVP and OT (3 pM-3 nM) increased glucagon release in a concentration-dependent manner. The antagonist with potent V1b receptor-blocking activity, CL-4-84 (10 nM), abolished AVP (30 pM)-induced glucagon release but did not alter OT (30 pM)-induced glucagon release. d(CH2)5[Tyr(Me)2]AVP (10 nM), a V1a receptor antagonist, and L-366,948 (10 nM), a highly specific OT-receptor antagonist, failed to inhibit AVP-induced glucagon release. In contrast, L-366,948 (10 nM) abolished OT (30 pM)-induced glucagon release but did not change the effect of AVP. Fluorescent microscopy of rat pancreatic sections showed that fluorescence-labeled AVP and OT bound to their receptors in the islets of Langerhans and that the bindings were inhibited by 1 μM of Cl-4-84 and L-366,948, respectively. Because AVP and OT at physiological concentrations (3-30 pM) increased glucagon release, we conclude that AVP and OT increase glucagon release under the physiological condition through the activation of V1b and OT receptors, respectively.
Adenosine A2a-receptor activation enhances cardiomyocyte shortening via Ca2+-independent and -dependent mechanisms.

Adenosine A2a receptor (A2aR) stimulation enhances the shortening of ventricular myocytes. Whether the A2aR-mediated increase in myocyte contractility is associated with alterations in the amplitude of intracellular Ca2+ transients was investigated in isolated, contracting rat ventricular myocytes using the Ca2+-sensitive fluorescent dye fura 2-AM. In the presence of intact inhibitory G protein pathways, 10-4 M 2- p-(2-carboxyethyl)phenethyl-amino-5'- N-ethylcarboxamidoadenosine (CGS-21680), an A2aR agonist, insignificantly increased Ca2+transients by 8 ± 5%, whereas myocyte shortening increased by 54 ± 1%. In contrast, 2 × 10-7 M isoproterenol, a β-adrenergic receptor agonist, increased Ca2+ transients by 104 ± 15% and increased myocyte shortening by 61 ± 6%. When A2aR were stimulated in myocytes that had the antiadrenergic actions of adenosine (Ado) abolished by either treatment with pertussis toxin (PTx) or the presence of 8-cyclopentyl-1,3-dipropylxanthine (DPCPX), an adenosine A1-receptor antagonist, the maximum increases in Ca2+transients were similarly nominal (with PTx: 10-4 M CGS-21680, 14 ± 6% and 10-4 M Ado, 15 ± 4%; without PTx: 10-5 M Ado + 2 × 10-7 M DPCPX, 19 ± 1%). These results indicate that compared with β-adrenergic stimulation, which markedly increases myocyte Ca2+ transients and shortening, A2aR-mediated increases in myocyte shortening are accompanied by only modest increases in Ca2+ transients. These observations suggest that the A2aR-induced contractile effects are mediated predominantly by Ca2+-independent inotropic mechanisms.
Renal and hemodynamic effects of losartan in conscious dogs during controlled mechanical ventilation.

In 12 conscious dogs, we investigated whether the angiotensin II-receptor antagonist losartan increases renal sodium excretion and urine volume during controlled mechanical ventilation (CMV) with positive end-expiratory pressure. In four experimental protocols, the dogs were extracellular volume (ECV) expanded (electrolyte solution, 0.5 ml ⋅ kg-1 ⋅ min-1iv) or not and received losartan (100 μg ⋅ kg-1 ⋅ min-1iv) or not. They breathed spontaneously during the 1st and 4th hour and received CMV with positive end-expiratory pressure (mean airway pressure 20 cmH2O) during the 2nd and 3rd hours. In the expansion group, dogs with losartan excreted ∼18% more sodium (69 ± 7 vs. 38 ± 5 μmol ⋅ min-1 ⋅ kg-1) and 15% more urine during the 2 h of CMV because of a higher glomerular filtration rate (5.3 ± 0.3 vs. 4.5 ± 0.2 ml ⋅ min-1 ⋅ kg-1) and the tubular effects of losartan. In the group without expansion, sodium excretion (2.0 ± 0.6 vs. 2.6 ± 1.0 μmol ⋅ min-1 ⋅ kg-1) and glomerular filtration rate (3.8 ± 0.3 vs. 3.8 ± 0.4 ml ⋅ min-1 ⋅ kg-1) did not change, and urine volume decreased similarly in both groups during CMV. Plasma vasopressin and aldosterone increased in both groups, and plasma renin activity increased from 4.9 ± 0.7 to 7.8 ± 1.3 ng ANG I ⋅ ml-1 ⋅ h-1during CMV in nonexpanded dogs without losartan. Mean arterial pressure decreased by 10 mmHg in nonexpanded dogs with losartan. In conclusion, losartan increases sodium excretion and urine volume during CMV if the ECV is expanded. If the ECV is not expanded, a decrease in mean arterial blood pressure and/or an increase in aldosterone and vasopressin during CMV attenuates the renal effects of losartan.
Calcium waves in colonic myocytes produced by mechanical and receptor-mediated stimulation.

The mechanisms underlying intracellular Ca2+ waves induced by either mechanical or receptor-mediated stimulation of myocytes isolated from the longitudinal muscle layer of the rabbit distal colon were compared using fura 2 and fluorescence videomicroscopy. Light focal mechanical deformation of the plasma membrane or focal application of substance P resulted in localized intracellular Ca2+ concentration ([Ca2+]i) transients that propagated throughout the cell. In both cases, the Ca2+ response consisted of a transient peak response followed by a delayed-phase response. Substance P-mediated [Ca2+]iresponses involved generation of inositol 1,4,5-trisphosphate and release of Ca2+ from thapsigargin-sensitive stores, whereas mechanically induced responses were partially (29%) dependent on La3+-sensitive influx of extracellular Ca2+ and partially on release of intracellular Ca2+from thapsigargin-insensitive stores gated by ryanodine receptors. The delayed-phase response in both cases was dependent on extracellular Ca2+. However, although the response to substance P was sensitive to La3+, that after mechanical stimulation was not. In the later case, the underlying mechanism may involve capacitative Ca2+ entry channels that are activated after mechanical stimulation but not by substance P.
Radial EBUS versus CT-guided needle biopsy for evaluation of solitary pulmonary nodules

Objective This study is aimed to compare the diagnostic yield, complications and influencing factors between Radial endobroncheal ultrasonography guided bronchoscopy(R-EBUS) and CT-guided needle biopsy (CT-PNB), for evaluation of solitary pulmonary nodules(SPNs). Matrials and Methods 160 cases of consecutive patients with SPNs were enrolled and divided into R-EBUS and CT-PNB groups randomly. The diagnostic yield, complications and influencing factors between the two groups were evaluated. Results Sensitivity of R-EBUS for malignancy was 73.7% (42/57) and for benign, was 43.5% (10/23), overall diagnostic accuracy was 65% (52/80). In CT-PNB group, overall diagnostic accuracy was 85% (68/80), sensitivity for malignancy was 87.9% (51/58), and for benign was 81.0% (17/21), respectively. Both overall diagnostic yield and incidence of complications in CT-PNB group were higher than those in R-EBUS group (P = 0.006, P = 0.002). In R-EBUS group, the factors affecting diagnostic yield were size (P = 0.027), the distance between SPNs and pleura (P = 0.031) and the location of the probe to lesions (P = 0.009). In CT-PNB group, the distance from the lesions to pleura was correlated with the incidence of pneumothorax (P = 0.001) and pulmonary haemorrhage (P = 0.042). The location of SPNs were adjacent to great vessels was another influencing factor for pulmonary haemorrhage (P = 0.042). Conclusions Both R-EBUS and CT-PNB are valuable tools for diagnosis. SPNs located in medial 1/2 of lung field, or were adjacent to great vessels may be fit for R-EBUS. Those SPNs located in lateral 1/2 of lung field, near to pleura or with less vessels around may be more suitable for CT-PNB.
Neuro-Evolution for competitive co-evolution of biologically canonical predator and prey behaviors

This paper presents a simulation of predator (pursuer) and prey (evader) agents operating within a competitive co-evolution process. The aim of the study was to investigate the effects of different resource (food for the prey) distributions and amounts on the adaptation of predator (pursuit) and prey (evasion) behaviors. Predator and prey use Artificial Neural Network (ANN) controllers to simulate behavior, where behaviors are adapted by Neuro-Evolution. The research objectives were two-fold. First, to test the capability of NE for evolving predator and prey behaviors that are effective in environments other than that in which they were evolved. Second, to test the efficacy of NE as a behavioral modeling method for co-evolutionary predator-prey simulations. Results indicated that NE was effective at evolving predator and prey behaviors that also performed well in other environments. Also, NE was successful at deriving behaviors that maintained specific similarities with those reported upon in related predator-prey studies. A key goal of this research was to use a synthetic approach to elucidate behavioral evolution in nature.
Biphasic relaxation of the opossum lower esophageal sphincter: roles of NO ⋅, VIP, and CGRP.

Vasoactive intestinal polypeptide (VIP) and nitric oxide (NO ⋅) are thought to mediate lower esophageal sphincter (LES) relaxation. Transverse muscle strips from the opossum LES were used to test this hypothesis. Electrical field stimulation (EFS) produced a biphasic LES relaxation: a rapid component during the stimulus was more prominent at lower stimulus frequencies, and a sustained component was more prominent at higher frequencies. N ω-nitro-l-arginine and hemoglobin inhibited the rapid component but affected the sustained component less. Exogenous VIP decreased LES tone. A number of purported VIP antagonists blocked neither VIP-induced nor EFS-induced relaxation of the LES. The calcitonin gene-related peptide (CGRP) antagonist CGRP-(8-37) did not alter EFS-induced LES relaxation. EFS-induced relaxation of opossum LES muscle is biphasic, and the initial, rapid component of the relaxation is mediated primarily by NO ⋅. The mediator of the sustained component was not identified.
Comparison of posterior occlusion between patients with anterior open bite and scissor deep bite

Objective A minor alteration in the posterior occlusal height elicits a large transformation in the anterior vertical dimension. Thus, the present study was performed to determine whether a posterior cusp-to-cusp relation that increases the posterior vertical dimension contributes to an anterior open bite. Methods Study casts were examined from orthodontic patients aged 10 to 27 years, 21 with an open bite and 28 with a scissor deep bite. A logistic regression model was used to analyze the contribution of various factors to these two anterior occlusal patterns. The dental arch width and number of worn cusps were compared between the two groups. Results Patients with an open bite had a significantly higher incidence of a posterior buccal–lingual cusp-to-cusp relation, wider mandibular arch in the molar region, and larger numbers of worn maxillary buccal cusps and mandibular lingual cusps than patients with a scissor deep bite. Conclusions A posterior buccal–lingual cusp-to-cusp relation is associated with a larger anterior vertical dimension, such as that in patients with an open bite.
Aligned Carbon Nanotube Reinforcement of Advanced Composite Ply Interfaces

*† ‡ § ** , This work presents the fabrication and characterization of three hybrid multiscale advanced composite materials. Long (>20 micron), aligned carbon nanotubes (CNTs) are placed at the interface of existing advanced composite plies and used as a reinforcement and to enhance electrical properties of the laminate. Three fabrication routes utilizing aligned CNTs at ply interfaces are presented: transplantation of CNT forests between prepreg carbon/epoxy plies, transfer of aligned CNTs and layup between woven carbon fiber plies that are subsequently infused to form a laminate, and in situ growth of aligned CNTs on the interior (and surface) of alumina fiber woven cloth prior to hand layup. Aerospace-grade thermoset epoxies, without modification, are noted to wet and penetrate the unfunctionalized aligned CNT forests, which is consistent with initial studies on solely CNT-polymer interactions. In all the fabrication routes, aligned CNTs are observed at the interface after laminate fabrication. Both mechanical (interlaminar) and multifunctional (electrical) property modifications are noted for the laminates containing CNTs. Significant interlaminar property enhancement has been observed and the mechanisms of this reinforcement are investigated via optical and scanning electron microscopy. Further improvements in the fabrication routes are discussed, and further testing of additional laminate-level property enhancements are suggested. Nomenclature
Multi-layer skin simulation with adaptive constraints

We present an approach for physics based simulation of the wrinkling of multi-layer skin with heterogeneous material properties. Each layer of skin is simulated with an adaptive mesh, with the different layers coupled via constraints that only permit wrinkle deformation at wavelengths that match the physical properties of the multi-layer model. We use texture maps to define varying elasticity and thickness of the skin layers, and design our constraints as continuous functions, which we discretize at run time to match the changing adaptive mesh topology. In our examples, we use blend shapes to drive the bottom layer, and we present a variety of examples of simulations that demonstrate small wrinkles on top of larger wrinkles, which is a typical pattern seen on human skin. Finally, we show that our physics-based wrinkles can be used in the automatic creation of wrinkle maps, allowing the visual details of our high resolution simulations to be produced at real time speeds.
Mechanism of proximal tubule bicarbonate absorption in NHE3 null mice.

NHE3 is the predominant isoform responsible for apical membrane Na+/H+exchange in the proximal tubule. Deletion of NHE3 by gene targeting results in an NHE3-/-mouse with greatly reduced proximal tubule[Formula: see text] absorption compared with NHE3+/+ animals (P. J. Schultheis, L. L. Clarke, P. Meneton, M. L. Miller, M. Soleimani, L. R. Gawenis, T. M. Riddle, J. J. Duffy, T. Doetschman, T. Wang, G. Giebisch, P. S. Aronson, J. N. Lorenz, and G. E. Shull. Nature Genet. 19: 282-285, 1998). The purpose of the present study was to evaluate the role of other acidification mechanisms in mediating the remaining component of proximal tubule [Formula: see text] reabsorption in NHE3-/- mice. Proximal tubule transport was studied by in situ microperfusion. Net rates of[Formula: see text] ( J HCO3) and fluid absorption ( J v) were reduced by 54 and 63%, respectively, in NHE3 null mice compared with controls. Addition of 100 μM ethylisopropylamiloride (EIPA) to the luminal perfusate caused significant inhibition of J HCO3 and J v in NHE3+/+ mice but failed to inhibit J HCO3 or J v in NHE3-/- mice, indicating lack of activity of NHE2 or other EIPA-sensitive NHE isoforms in the null mice. Addition of 1 μM bafilomycin caused a similar absolute decrement in J HCO3 in wild-type and NHE3 null mice, indicating equivalent rates of[Formula: see text] absorption mediated by H+-ATPase. Addition of 10 μM Sch-28080 did not reduce J HCO3 in either wild-type or NHE3 null mice, indicating lack of detectable H+-K+-ATPase activity in the proximal tubule. We conclude that, in the absence of NHE3, neither NHE2 nor any other EIPA-sensitive NHE isoform contributes to mediating [Formula: see text] reabsorption in the proximal tubule. A significant component of[Formula: see text] reabsorption in the proximal tubule is mediated by bafilomycin-sensitive H+-ATPase, but its activity is not significantly upregulated in NHE3 null mice.