Miracle-dz/UniFAR-FTUs huggingface dataset:
Different modulation of aromatase activity in frog testis in vitro by ACE and ANG II.

The aim of the present research was to study the role of angiotensin-converting enzyme (ACE) and ANG II in amphibian ( Rana esculenta) testicular steroidogenesis and prostaglandin production. Hormonal effects of ACE, ACE inhibitors, synthetic bullfrog ANG I, and [Val5]ANG II were determined in frog testis of prereproductive period. Production of 17β-estradiol, progesterone, androgens, and PGE2 and PGF2α was determined by incubating frog testes with ACE (2.5 mU/ml), captopril (0.1 mM), lisinopril (0.1 mM), [Val5]ANG II (1 μM), and synthetic bullfrog ANG I (1 μM). The analysis of the data showed an independent modulation of 17β-estradiol and androgen production by ACE and ANG II. The ACE pathway caused a decrease of 17β-estradiol production and an increase of androgen production in frog testes; on the other hand, the ANG II pathway increased 17β-estradiol production and decreased androgen production. The determination of testicular aromatase activity showed a positive regulation by ANG II and a negative regulation by ACE. As for prostaglandin production, only ANG II influenced PGF2α. These results suggest a new physiological role of ACE and ANG II in modulating steroidogenesis and prostaglandin production.
Fabrication and Anti-Oxidation Ability of SiC-SiO2 Coated Carbon Fibers Using Sol-Gel Method

The paper proposed a method to improve the anti-oxidation performance of carbon fibers (CF) at high temperature environment by coating silicon dioxide (SiO2) and silicon carbide (SiC). The modified sol-gel method had been used to ensure the proper interface between fibers and coating. We used polydimethylsiloxane and ethyl orthosilicate to make stable emulsion to uniformly disperse SiC nanoparticles. The modified SiO2/SiC coating had been coated on CF successfully. Compared with the untreated CF, the coated fibers started to be oxidized around 900 °C and the residual weight was 57% at 1400 °C. The oxidation mechanism had been discussed. The structure of SiC/SiO2 coated CF had been characterized by scanning electron microscope and X-ray diffraction analysis. Thermal gravimetric analysis was used to test the anti-oxidation ability of CF with different coatings.
Adrenergic induction of bimodal myocardial protection: signal transduction and cardiac gene reprogramming.

This study tested the hypothesis that in vivo norepinephrine (NE) treatment induces bimodal cardiac functional protection against ischemia and examined the roles of α1-adrenoceptors, protein kinase C (PKC), and cardiac gene expression in cardiac protection. Rats were treated with NE (25 μg/kg iv). Cardiac functional resistance to ischemia-reperfusion (25/40 min) injury was examined 30 min and 1, 4, and 24 h after NE treatment with the Langendorff technique, and effects of α1-adrenoceptor antagonism and PKC inhibition on the protection were determined. Northern analysis was performed to examine cardiac expression of mRNAs encoding α-actin and myosin heavy chain (MHC) isoforms. Immunofluorescent staining was performed to localize PKC-βI in the ventricular myocardium. NE treatment improved postischemic functional recovery at 30 min, 4 h, and 24 h but not at 1 h. Pretreatment with prazosin or chelerythrine abolished both the early adaptive response at 30 min and the delayed adaptive response at 24 h. NE treatment induced intranuclear translocation of PKC-βI in cardiac myocytes at 10 min and increased skeletal α-actin and β-MHC mRNAs in the myocardium at 4-24 h. These results demonstrate that in vivo NE treatment induces bimodal myocardial functional adaptation to ischemia in a rat model. α1-Adrenoceptors and PKC appear to be involved in signal transduction for inducing both the early and delayed adaptive responses. The delayed adaptive response is associated with the expression of cardiac genes encoding fetal contractile proteins, and PKC-βI may transduce the signal for reprogramming of cardiac gene expression.
TGF-b 3-null mutation does not abrogate fetal lung maturation in vivo by glucocorticoids

WEI SHI,1 NORA HEISTERKAMP,2 JOHN GROFFEN,2 JINGSONG ZHAO,3 DAVID WARBURTON,1,3 AND VESA KAARTINEN1 1Developmental Biology Program and 2Section of Molecular Carcinogenesis, Childrens Hospital Los Angeles and University of Southern California School of Medicine, Los Angeles 90027; and 3Center for Craniofacial Molecular Biology, University of Southern California School of Medicine and Dentistry, Los Angeles, California 90033
I4: Immersive, Interactive, Individualized Information

The next generation of information presentation requires a new paradigm of structure and narrative that changes according to a person’s preferences, interests and choices. A person will not only be immersed in interactive “stories” filled with multimedia elements and a wealth of customized background, but the information presentation will reform and change into different ‘experiences’ depending upon the viewer [1-4].
Attenuation of renal ischemia-reperfusion injury in inducible nitric oxide synthase knockout mice.

Renal ischemia-reperfusion (I/R) injury was investigated in inducible nitric oxide synthase (iNOS) knockout mice. After a 26-min bilateral renal pedicle clamp, serum creatinine concentrations (in mg/dl) in wild-type mice after a 24-h reperfusion were 0.25 ± 0.03 in sham-operated controls and 2.3 ± 0.38 in ischemic mice ( P < 0.01); after 48 h, concentrations (in mg/dl) were 0.25 ± 0.03 in controls and 2.0 ± 0.18 in ischemic mice ( P < 0.01). iNOS knockout mice demonstrated an attenuation of serum creatinine concentration after renal I/R injury. Serum creatinine concentrations (mg/dl) after a 24-h reperfusion were 2.3 ± 0.22 in wild-type ischemic and 1.21 ± 0.25 in iNOS knockout ischemic mice ( P < 0.05); after 48 h, concentrations were 2.0 ± 0.18 in wild-type ischemic and 0.96 ± 0.25 in iNOS knockout ischemic mice ( P< 0.01). Histological scoring of acute tubular necrosis in iNOS knockout mice was decreased compared with that in wild-type controls (0.88 ± 0.2 vs. 3.3 ± 0.3, P< 0.05). iNOS protein in the renal cortex of wild-type mice subjected to renal I/R injury was undetectable up to 48 h. However, a strong upregulation of heat shock protein 72 expression was observed in renal cortex of iNOS knockout mice under basal conditions. In conclusion, kidneys of iNOS knockout mice were protected against ischemic acute renal failure. This protective effect may be related to a compensatory upregulation of heat shock protein 72.
Global bathymetric patterns of standing stock and body size in the deep-sea benthos

We present the first global-scale analy- sis of standing stock (abundance and biomass) for 4 major size classes of deep-sea biota: bacteria, meta- zoan meiofauna, macrofauna and megafauna. The community standing stock decreases with depth; this is a universal phenomenon that involves a com- plex transition in the relative importance of the different size groups. Bacterial abundance and biomass show no decline with depth. All 3 animal size groups experience significant exponential de- creases in both abundance and biomass. The abun- dance of larger animals is significantly lower and decreases more rapidly than for smaller groups. The resulting drop in average body size with depth con- firms Thiel's size-structure hypothesis on very large spatial scales. In terms of their proportion of total community biomass, smaller size classes replace larger size classes. The upper continental slope is dominated by macrofaunal biomass, and the abyss by bacterial and meiofaunal biomass. The dramatic decrease in total community standing stock and the ascendancy of smaller organisms with depth has important implications for deep-sea biodiversity. The bathyal zone (200 to 4000 m) affords more eco- logical and evolutionary opportunity in the form of energy availability for larger organisms, and conse- quently supports higher macrofaunal and mega- faunal species diversity than the abyss (> 4000 m).
Subcutaneous glucose predicts plasma glucose independent of insulin: implications for continuous monitoring.

The present study investigated the relationship between blood and subcutaneous interstitial fluid (ISF) glucose by employing an amperometric glucose sensor specifically developed for 3-day continuous glucose monitoring. The apparent sensor sensitivity and ISF glucose equilibration delay were estimated on separate days during hyperglycemic clamps in four dogs in which insulin was either suppressed with somatostatin, allowed to change, or increased with an exogenous infusion. A 2-h sensor "settling-in" period was allowed before the clamps. During insulin deficiency, the sensor sensitivity and ISF glucose delay were 0.23 ± 0.03 nA per mg/dl and 4.4 ± 0.8 min. Sensitivity was not affected by increases in endogenous (0.30 ± 0.04 vs. 0.28 ± 0.04 nA per mg/dl) or exogenous insulin (0.18 ± 0.01 vs. 0.16 ± 0.01 nA per mg/dl) nor was the delay (3.3 ± 1.2 vs. 5.7 ± 1.1 and 9.2 ± 2.6 vs. 12.3 ± 1.7 min; P > 0.05 for all). Sensor glucose accurately predicted plasma glucose without correcting for delays <10 min ( r > 0.9 for all), whereas for longer delays a digital corrective filter was used ( r = 0.91 with filter). We conclude that the relationship between blood and ISF glucose is not affected by insulin and that delays in ISF glucose equilibration can be corrected with digital filters.
Endogenous nitric oxide inhibits chloride transport in the thick ascending limb.

Nitric oxide (NO) inhibits transport in various nephron segments, and the thick ascending limb of the loop of Henle (TALH) expresses NO synthase (NOS). However, the effects of NO on TALH transport have not been extensively studied. We hypothesized that endogenously produced NO directly decreases NaCl transport by the TALH. We first determined the effect of exogenously added NO on net chloride flux ( J Cl). The NO donor spermine NONOate (SPM; 10 μM) decreased J Cl from 101.2 ± 9.6 to 65.0 ± 7.7 pmol ⋅ mm-1 ⋅ min-1, a reduction of 35.5 ± 6.4%, whereas controls did not decrease over time. To determine whether endogenous NO affects cortical TALH transport, we measured the effect of adding the NOS inhibitor N G-nitro-l-arginine methyl ester (l-NAME), the substratel-arginine (l-Arg), or its enantiomerd-arginine (d-Arg) on J Cl.l-NAME andd-Arg did not alter J Cl; in contrast, addition of 0.5 mM l-Arg decreased J Cl by 40.2 ± 10.4% from control. The inhibition of chloride flux by 0.5 mM l-Arg was abolished by pretreatment with l-NAME, indicating that cortical TALH NOS is active, but production of NO is substrate-limited in our preparation. Furthermore, cortical TALH chloride flux increased following removal of 0.5 mMl-Arg from the bath, indicating that the reductions in chloride flux observed in response tol-Arg are not the result of NO-mediated cytotoxicity. We conclude that 1) exogenous NO decreases cortical TALH J Cl; 2) cortical TALHs produce NO in the presence of l-Arg, which decreases J Cl; and 3) the response of cortical TALHs to l-Arg is reversible in vitro. These data suggest an important role for locally produced NO, which may act via an autocrine mechanism to directly affect TALH sodium chloride transport. Thus TALH NO synthesis and inhibition of chloride transport may contribute to the diuretic and natriuretic effects of NO observed in vivo.
Webcam-based Eye Gaze Tracking under Natural Head Movement

This manuscript investigates and proposes a visual gaze tracker that tackles the problem using only an ordinary web camera and no prior knowledge in any sense (scene set-up, camera intrinsic and/or extrinsic parameters). The tracker we propose is based on the observation that our desire to grant the freedom of natural head movement to the user requires 3D modeling of the scene set-up. Although, using a single low resolution web camera bounds us in dimensions (no depth can be recovered), we propose ways to cope with this drawback and model the scene in front of the user. We tackle this three-dimensional problem by realizing that it can be viewed as series of two-dimensional special cases. Then, we propose a procedure that treats each movement of the user's head as a special two-dimensional case, hence reducing the complexity of the problem back to two dimensions. Furthermore, the proposed tracker is calibration free and discards this tedious part of all previously mentioned trackers. Experimental results show that the proposed tracker achieves good results, given the restrictions on it. We can report that the tracker commits a mean error of (56.95, 70.82) pixels in x and y direction, respectively, when the user's head is as static as possible (no chin-rests are used). Furthermore, we can report that the proposed tracker commits a mean error of (87.18, 103.86) pixels in x and y direction, respectively, under natural head movement.
Population genetic structure, introgression, and hybridization in the genus Rhizophora along the Brazilian coast

Abstract Mangrove plants comprise plants with similar ecological features that have enabled them to adapt to life between the sea and the land. Within a geographic region, different mangrove species share not only similar adaptations but also similar genetic structure patterns. Along the eastern coast of South America, there is a subdivision between the populations north and south of the continent's northeastern extremity. Here, we aimed to test for this north‐south genetic structure in Rhizophora mangle, a dominant mangrove plant in the Western Hemisphere. Additionally, we aimed to study the relationships between R. mangle, R. racemosa, and R. × harrisonii and to test for evidence of hybridization and introgression. Our results confirmed the north‐south genetic structure pattern in R. mangle and revealed a less abrupt genetic break in the northern population than those observed in Avicennia species, another dominant and widespread mangrove genus in the Western Hemisphere. These results are consistent with the role of oceanic currents influencing sea‐dispersed plants and differences between Avicennia and Rhizophora propagules in longevity and establishment time. We also observed that introgression and hybridization are relevant biological processes in the northeastern coast of South America and that they are likely asymmetric toward R. mangle, suggesting that adaptation might be a process maintaining this hybrid zone.
Heterogeneous neurochemical responses to different stressors: a test of Selye's doctrine of nonspecificity.

Selye defined stress as the nonspecific response of the body to any demand. Stressors elicit both pituitary-adrenocortical and sympathoadrenomedullary responses. One can test Selye's concept by comparing magnitudes of responses at different stress intensities and assuming that the magnitudes vary with stress intensity, with the prediction that, at different stress intensities, ratios of increments neuroendocrine responses should be the same. We measured arterial plasma ACTH, norepinephrine, and epinephrine in conscious rats after hemorrhage, intravenous insulin, subctaneous formaldehyde solution, cold, or immobilization. Relative to ACTH increments, cold evoked large norepinephrine responses, insulin large epinephrine responses, and hemorrhage small norepinephrine and epinephrine responses, whereas immobilization elicited large increases in levels of all three compounds. The ACTH response to 25% hemorrhage exceeded five times that to 10%, and the epinephrine response to 25% hemorrhage was two times that to 10%. The ACTH response to 4% formaldehyde solution was two times that to 1%, and the epinephrine response to 4% formaldehyde solution exceeded four times that to 1%. These results are inconsistent with Selye's doctrine of nonspecificity and the existence of a unitary "stress syndrome," and they are more consistent with the concept that each stressor has its own central neurochemical and peripheral neuroendocrine "signature. "
Persistent anxiety and in-hospital complications after acute coronary syndrome

Objectives: To investigate the effects of pre-event persistent anxiety on in-hospital complications and length of stay (LOS) in patients who experienced acute coronary syndrome (ACS). Methods: This was a prospective study with patients seeking treatment for ACS events. Anxiety was measured 2 times before the event in 600 patients with pre-existing coronary heart disease (CHD). Patients were followed for 2 years or until they developed an ACS event. 120 patients developed ACS events (rate 20%). Complications and LOS were abstracted from medical records. Results: Persistently non-anxious patients have lower anxiety scores at 3 months follow-up than baseline (mean [standard deviation (SD)], 6.1 [0.24] vs. 3.9 [0.95], P <0.01). Patients with persistent anxiety had significantly higher complication rates than non-anxious patients (mean [SD], 0.71 [0.12] vs. 0.15 [0.11], P <0.05). In a multiple logistic regression, persistent anxiety was an independent predictor of complications. Patients who were persistently anxious were at 5 times higher risk for developing complications (odds ratio = 5.0, 95% confidence interval: 1.27–38.8, P < 0.05). Conclusion: Anxiety measured up to 2 years before an ACS event was predictive of in-hospital complications. Clinicians caring for patients with CHD need to be as equally aware of the importance of assessing and treating persistent anxiety as clinicians caring for patients hospitalized for an ACS.
Optical mapping of atrioventricular node reveals a conduction barrier between atrial and nodal cells.

The mechanisms responsible for atrioventricular (AV) delay remain unclear, in part due to the inability to map electrical activity by conventional microelectrode techniques. In this study, voltage-sensitive dyes and imaging techniques were refined to detect action potentials (APs) from the small cells comprising the AV node and to map activation from the "compact" node. Optical APs (124) were recorded from 5 × 5 mm (∼0.5-mm depth) AV zones of perfused rabbit hearts stained with a voltage-sensitive dye. Signals from the node exhibited a set of three spikes; the first and third ( peaks I and III) were coincident with atrial (A) and ventricular (V) electrograms, respectively. The second spike ( peak II) represented the firing of midnodal (N) and/or lower nodal (NH) cell APs as indicated by their small amplitude, propagation pattern, location determined from superimposition of activation maps and histological sections of the node region, dependence on depth of focus, and insensitivity to tetrodotoxin (TTX). AV delays consisted of τ1 (49.5 ± 6.59 ms, 300-ms cycle length), the interval between peaks I and II (perhaps AN to N cells), and τ2 (57.57 ± 5.15 ms), the interval between peaks II and III (N to V cells). The conductance time across the node was 10.33 ± 3.21 ms, indicating an apparent conduction velocity (ΘN) of 0.162 ± 0.02 m/s ( n = 9) that was insensitive to TTX. In contrast, τ1 correlated with changes in AV node delays (measured with surface electrodes) caused by changes in heart rate or perfusion with acetylcholine. The data provide the first maps of activation across the AV node and demonstrate that ΘN is faster than previously presumed. These findings are inconsistent with theories of decremental conduction and prove the existence of a conduction barrier between the atrium and the AV node that is an important determinant of AV node delay.
Effect of low zinc intake on absorption and excretion of zinc by infants studied with 70Zn as extrinsic tag.

The effect of low dietary intake of zinc was studied in six normal infants with the use of 70Zn as an extrinsic tag. Of the two study formulas, one provided a zinc intake similar to that of customary infant formulas ("high" intake), whereas the other provided a "low" zinc intake. Two zinc absorption studies were performed with each formula (sequence: high-low-low-high). Extrinsically labeled formula was fed for 24 h and excreta were collected for 72 h. Zinc isotope ratios were determined by inductively coupled plasma mass spectrometry (ICP/MS). When zinc intake was high, net zinc absorption was 9.1 +/- 8.7% (mean +/- SD) of intake and net zinc retention was 74 +/- 91 micrograms/(kg.d). True zinc (70Zn) absorption was 16.8 +/- 5.8% of intake and fecal excretion of endogenous zinc was 78 +/- 56 micrograms/(kg.d). When zinc intake was low, net absorption of zinc increased significantly (P less than 0.001) to 26.0 +/- 13.0% of intake, but net retention was not significantly different at 42 +/- 33 micrograms/(kg.d). True absorption of zinc also increased significantly (P less than 0.001) to 41.1 +/- 7.8% of intake, whereas fecal endogenous zinc decreased (P less than 0.05) to 34 +/- 16 micrograms/(kg.d) during low zinc intake. Thus, infants maintain zinc balance in the face of low zinc intake through increased efficiency of absorption and decreased excretion of endogenous zinc.
Ischemic preconditioning depends on interaction between mitochondrial KATP channels and actin cytoskeleton.

Both mitochondrial ATP-sensitive K+(KATP) channels and the actin cytoskeleton have been proposed to be end-effectors in ischemic preconditioning (PC). For evaluation of the participation of these proposed end effectors, rabbits underwent 30 min of regional ischemia and 3 h of reperfusion. PC by 5-min ischemia + 10-min reperfusion reduced infarct size by 60%. Diazoxide, a mitochondrial KATP-channel opener, administered before ischemia was protective. Protection was lost when diazoxide was given after onset of ischemia. Anisomycin, a p38/JNK activator, reduced infarct size, but protection from both diazoxide and anisomycin was abolished by 5-hydroxydecanoate (5-HD), an inhibitor of mitochondrial KATP channels. Isolated adult rabbit cardiomyocytes were subjected to simulated ischemia by centrifuging the cells into an oxygen-free pellet for 3 h. PC was induced by prior pelleting for 10 min followed by resuspension for 15 min. Osmotic fragility was assessed by adding cells to hypotonic (85 mosmol) Trypan blue. PC delayed the progressive increase in fragility seen in non-PC cells. Incubation with diazoxide or pinacidil was as protective as PC. Anisomycin reduced osmotic fragility, and this was reversed by 5-HD. Interestingly, protection by PC, diazoxide, and pinacidil could be abolished by disruption of the cytoskeleton by cytochalasin D. These data support a role for both mitochondrial KATP channels and cytoskeletal actin in protection by PC.
Screening Indication Associated With Lower Likelihood of Minor Adverse Events in Patients Undergoing Outpatient Colonoscopy

We sought to determine, among outpatients at one university hospital endoscopy center, rates of self-reported minor adverse events (MAEs) at 2, 14, and 30 days postcolonoscopy and to identify predictors of MAEs at Day 2 postcolonoscopy. A single-center longitudinal cohort study with follow-ups at Days 2, 14, and 30 postcolonoscopy was conducted in Montreal, Canada. Baseline self-report data included patient age, gender, gastrointestinal discomforts and other discomforts in the preceding month, and comorbidity. Intracolonoscopy procedures and the method of insufflation were obtained from endoscopy reports. Minor adverse event data were obtained by either phone or Internet survey. Multivariate logistic regression was used to identify predictors of MAEs at Day 2. Of 705 individuals approached, 420 (mean age = 58.7 years; SD = 8.4, 45.7% female) were eligible and consented to study participation, and 378 (90%) participated in at least one follow-up. At Days 2, 14, and 30, 86 (25.1%), 46 (13.7%), and 13 (3.1%) patients, respectively, experienced at least one MAE. At the Day 30 follow-up, 2 (0.53%) patients reported having experienced a serious adverse event. The multivariable analysis results showed that screening compared with nonscreening colonoscopy was protective for MAEs at 2 days (OR = 0.5, 95% CI [0.3, 0.9]). We found that 25% of patients experienced at least one MAE at 2 days postcolonoscopy, and screening compared with nonscreening colonoscopy patients were half as likely to experience these early MAEs. Nurses may use these findings to educate and reassure patients about colonoscopy risks. Large, longitudinal multicenter studies are needed to corroborate our findings.