Miracle-dz/UniFAR-FTUs huggingface dataset:
A Putative Mg Chelatase Subunit from Arabidopsis thaliana cv C24 (Sequence and Transcript Analysis of the Gene, Import of the Protein into Chloroplasts, and in Situ Localization of the Transcript and Protein

We have isolated and sequenced a cDNA from Arabidopsis thaliana cv C24 that encodes a putative Mg chelatase subunit. The deduced amino acid sequence shows a very high level of identity to a gene previously characterized from Antirrhinum majus (olive) and also high similarity to bchH, a bacterial gene involved in the Mg chelatase reaction of bacteriochlorophyll biosynthesis. We suggest that this gene be called CHL H. Northern blot analyses were used to investigate the expression of CHL H, another putative Mg chelatase gene, ch-42, and ferrochelatase. The CHL H transcript was observed to undergo a dramatic diurnal variation, rising almost to its maximum level by the end of the dark period, then increasing slightly at the onset of the light and declining steadily to a minimum by the end of the light period; in contrast, transcripts for ch-42 and ferrochelatase remained constant. A model is proposed in which the CHL H protein plays a role in regulating the levels of chlorophyll during this cycle. In situ hybridization revealed that the transcripts are located over the surface of the chloroplasts, a feature in common with transcripts for the ch-42 gene. The CHL H protein was imported into the stromal compartment of the chloroplast and processed in an in vitro assay. Immunoblotting showed that the distribution of CHL H protein between the stroma and chloroplast membranes varies depending on the concentration of Mg2+. In situ immunofluorescence was used to establish that the CHL H and CH-42 proteins are localized within the chloroplast in vivo.
IN VITRO MINERALIZATION AND IMPLANT CALCIUM PHOSPHATE-HYDROXYAPATITE CRYSTALLINITY

Biological dissolution of implant calcium phosphate coatings release local concentrations of divalent ions, which may influence mineralization. The objective of this study was to determine the effects of calcium phosphate release from coated commercially pure titanium discs using a bone-like cell culture bioassay. Sandblasted discs were prepared with or without hydroxyapatite crystallinities (50, 75, and 90 percent). Samples of each coating were randomly assigned and either preincubated for 24 hours with media or not before the addition of cells (2200/mm2). Cultures were grown for 72 hours in culture medium containing 0.5 μCi/mL45Ca. After rinsing, the remaining calcium phosphate surface was dissolved and counted. Three independent trials were performed. Results indicated proliferation was not altered as a function of crystallinity (P > 0.05) among any of the groups. However, a significant (P < 0.01) inverse relationship was found for biologically mediated mineralization as a function of calcium phosphate crystallinity. Low crystalline surfaces (nominally 50 percent) had the highest level of mineralization, with 75 percent crystalline surfaces being intermediate and 90 percent crystalline samples having the lowest amount of relative mineral formation. Mineralization only occurred on sandblasted commercially pure titanium upon supplementation of the growth medium with an organophosphate (β-glycerophosphate), although this was less than on culture plastic. The results suggest calcium phosphate dissolution, as a function of implant coating crystallinity, can alter biological mineralization and may be one means in which enhanced mineral formation occurs around calcium phosphate-coated dental implants. (Implant Dent 1996;5:264–271)
Improving the harmonisation of the International Normalized Ratio (INR): time to think outside the box?

Abstract The prothrombin time (PT) assay is the most often requested coagulation test and used primarily for monitoring Vitamin K antagonist therapy, where results may be expressed as an International Normalised Ratio (INR). The INR is the patient's PT ‘mathematically adjusted’ or ‘standardised’ to take into account the specific test system used (i.e., comprising the test reagent/instrument combination). This standardisation or ‘adjustment’ is achieved by applying two ‘correction factors’, respectively defined by the ‘International Sensitivity Index’ (ISI) and the ‘mean normal prothrombin time’ (MNPT), according to the formula: INR=[patient PT/MNPT]ISI. While some manufacturers provide assigned ISI values for specific PT reagents and instrumentation, the vast number of possible reagent/instrument combinations usually precludes this in most situations. Even when an ISI is provided by the manufacturer, laboratories need to check or validate the assigned value. When a manufacturer does not provide an ISI, the laboratory needs to define its own (local ISI) value. The MNPT usually has to be locally defined, based on the population being tested. Current recommendations for defining ISI values include the classical, but prohibitively complex, World Health Organization (WHO) recommended procedure, and more recently the use of commercial reference-plasma calibration sets. The MNPT can also be defined using the WHO recommended procedure or with calibration sets. However, there is limited information to validate the performance of these in laboratory practice, and there are several unrecognised problems that limit the validity and utility of the ISI and MNPT values that are determined. Thus, it is perhaps time to start thinking outside the box, and to utilise additional methods for determining and/or validating ISI and MNPT values. This may include the use of regression analysis to assess ongoing peer-related performance in external quality assurance programmes, and to compare the behaviour of proposed replacement reagents with that of existing reagents. Such strategies have proven of considerable benefit to local laboratory practice, and should therefore enable other laboratories to optimise their practice in order to provide INRs that better reflect a patient's anticoagulant status, and thus assist in their clinical therapeutic management. Clin Chem Lab Med 2010;48:1079–90.
The as-grown-generation (AG) model: A reliable model for reliability prediction under real use conditions

Modeling the negative bias temperature instability (NBTI) can optimize circuit design. Several models have been proposed and all of them can fit test data well. These models are extracted typically by fitting short accelerated stress data. Their capability to predict NBTI aging outside the test range has not been fully demonstrated. This predictive capability for long term aging under low operation bias is what needed by circuit designers. In this work, we test the predictive capability of the well-known reaction-diffusion (RD) based framework for samples fabricated by a variety of processes. Results show that the RD model cannot make an acceptable generic prediction. The recently proposed As-grown-Generation (AG) model is then introduced. By dividing defects into two groups, as-grown and generated defects, and measuring the as-grown defects experimentally, we demonstrate that it can make reliable prediction for the same set of data where the RD model failed.
Testosterone manipulation protects motoneurons from dendritic atrophy after contralateral motoneuron depletion

Dendritic morphology is reactive to many kinds of injuries, including axotomy and deafferentation. In this study, we examined the response of motoneurons in the spinal nucleus of the bulbocavernosus (SNB), an androgen‐dependent population of motoneurons in the lumbar spinal cord of the rat, to partial motoneuron depletion. We depleted SNB motoneurons on one side only of the spinal cord by unilateral intramuscular injection of a retrogradely transported form of saporin, and examined the morphology of contralateral SNB motoneurons. Motoneuron morphology was assessed in normal control males, gonadally intact saporin‐treated males, and saporin‐treated males who had been castrated 6 weeks previously and given testosterone replacement beginning at the time of saporin injection. Untreated castrated males served as an additional control group. Four weeks after saporin treatment, SNB motoneurons contralateral to the saporin injection were retrogradely labeled with horseradish peroxidase conjugated to the cholera toxin B subunit and reconstructed in three dimensions. In gonadally intact males, unilateral motoneuron depletion caused regressive changes in contralateral SNB motoneurons: Soma size and dendritic length were both decreased. However, testosterone manipulation (i.e., castration followed by testosterone replacement) completely prevented the dendritic retraction. These data suggest a therapeutic role for testosterone in preventing, or accelerating recovery from, dendritic atrophy induced by motoneuron injury. J. Comp. Neurol. 469:96–106, 2004. © 2003 Wiley‐Liss, Inc.
The tissue pentraxin PTX3 limits C1q‐mediated complement activation and phagocytosis of apoptotic cells by dendritic cells

Pentraxins (PTX) and complement belong to the humoral arm of the innate immune system and have essential functions in immune defense to microbes and in scavenging cellular debris. The prototypic long PTX, PTX3, and the first component of the classical complement pathway, C1q, are innate opsonins involved in the disposal of dying cells by phagocytes. Whether the interaction between various innate opsonins impacts on their function is not fully understood. We show here that characterized Toll‐like receptor (TLR) ligands elicit the production of C1q and PTX3 by immature dendritic cells (DC). Moreover, these molecules bind to dying cells with similar kinetics, although they recognize different domains on the cell membranes. PTX3 binds in the fluid phase to C1q, decreasing C1q deposition and subsequent complement activation on apoptotic cells. C1q increases the phagocytosis of apoptotic cells by DC and the release of interleukin‐12 in the presence of TLR4 ligands and apoptotic cells; PTX3 inhibits both events. Moreover, PTX3 inhibited the cross‐presentation of the MELAN‐A/melanoma antigen‐reactive T cell 1 (MART‐1) tumor antigen expressed by dying cells, even in the presence of C1q. These results suggest that interaction of C1q and PTX3 influences the clearance of apoptotic cells by DC. The coordinated induction by primary, proinflammatory signals of C1q and PTX3 and their reciprocal regulation during inflammation influences the clearance of apoptotic cells by antigen‐presenting cells and possibly plays a role in immune homeostasis.
Subtype and regional regulation of prion biomarkers in sporadic Creutzfeldt–Jakob disease

Creutzfeldt–Jakob disease (CJD) is a rapid progressive neurological disease leading to dementia and death. Prion biomarkers are altered in the cerebrospinal fluid (CSF) of CJD patients, but the pathogenic mechanisms underlying these alterations are still unknown. The present study examined prion biomarker levels in the brain and CSF of sporadic CJD (sCJD) cases and their correlation with neuropathological lesion profiles.
Design of the series fed microstrip patch planar array antenna by the parato genetic algorithm

Since the series fed microstrip patch array antenna has low feeding loss, it is especially effective for the millimeter wave application. In order to realize an array antenna with a high gain, low sidelobe level, and low VSWR, we have optimized the width and element spacing for each patch antenna by the parato genetic algorithm. As for such an evolution method as genetic algorithm, the calculation load is enormous. In this paper, to reduce the load, these parameters are optimized by a coarse mesh. After optimization, we check the performance by a fine mesh. By numerical simulation of a planar array, we confirmed the effectiveness of the proposed method.
High-LET Radiation-Induced Response of Microvessels in the Hippocampus

Abstract The hippocampus is critical for learning and memory, and injury to this structure is associated with cognitive deficits. The response of the hippocampal microvessels after a relatively low dose of high-LET radiation remains unclear. In this study, endothelial population changes in hippocampal microvessels exposed to 56Fe ions at doses of 0, 0.5, 2 and 4 Gy were quantified using unbiased stereological techniques. Twelve months after exposure, mice that received 0.5 Gy or 2 Gy of iron ions showed a 34% or 29% loss of endothelial cells, respectively, in the hippocampal cornu ammonis region 1 (CA1) compared to age-matched controls or mice that received 4 Gy (P < 0.05). We suggest that this “U-shaped” dose response indicates a repopulation from a sensitive subset of endothelial cells that occurred after 4 Gy that was stimulated by an initial rapid loss of endothelial cells. In contrast to the CA1, in the dentate gyrus (DG), there was no significant difference in microvessel cell and length density between irradiated groups and age-matched controls. Vascular topology differences between CA1 and DG may account for the variation in dose response. The correlation between radiation-induced alterations in the hippocampal microvessels and their functional consequences must be investigated in further studies.
Impact of contrast agent type (ionic versus nonionic) used for coronary angiography on angiographic, electrocardiographic, and clinical outcomes following thrombolytic administration in acute myocardial infarction

The goal of this study was to examine the relationship between contrast agent type (ionic vs. nonionic) and angiographic, electrocardiographic, and clinical outcomes after thrombolytic administration. Ionic or nonionic contrast agents were selected in a nonrandomized fashion for 90‐min angiography and percutaneous coronary intervention (PCI) following thrombolytic administration in the TIMI 14 trial [tissue plasminogen activator (tPA) or reteplase (rPA) vs. low‐dose lytic + abciximab]. There was no relationship between contrast agent type and overall patency, rate of TIMI grade 3 flow, or corrected TIMI frame counts (CTFCs) in open culprit arteries and in post‐PCI patency rates or post‐PCI CTFCs. In patients treated with ionic contrast, ejection fractions at 90 min were slightly but significantly lower (56.2 ± 16.5, n = 122, vs. 59.8 ± 14.4, n = 322; P = 0.02), chest pain duration was longer (2.8 ± 4.1 hr, n = 255, vs. 1.7 ± 3.6, n = 550; P = 0.0003), and complete ST segment resolution was less frequent (41.5% vs. 50.8%; P = 0.04). While there was no difference in epicardial blood flow, ionic contrast agent use was associated with poorer ST segment resolution, longer chest pain duration, and poorer ejection fractions, perhaps as a result of microvascular dysfunction. Cathet Cardiovasc Intervent 2001;53:6–11. © 2001 Wiley‐Liss, Inc.
Specific accessory sequences in Saccharomyces cerevisiae introns control assembly of pre‐mRNAs into spliceosomes.

In experiments involving deletion and rearrangement of intron sequences two small regions of the intron in the yeast CYH2 ribosomal protein gene were found to play important roles in splicing of the pre‐mRNA. One element lies downstream of the 5′ splice site, and the other is upstream of the branchpoint sequence UACUAAC. Deletion of the element upstream of the branchpoint prevents spliceosome formation and blocks splicing in vivo and in vitro. Deletion of the element downstream of the 5′ splice site does not on its own block splicing but rescues spliceosome formation and splicing of pre‐mRNA lacking the element upstream of the branchpoint. These elements correspond to two regions of sequence complementarity which are a conserved feature of the introns in yeast pre‐mRNAs. Mixing and matching of the elements from the ACT1 and CYH2 gene introns showed that these elements can cooperate in an intron‐specific fashion to control spliceosome assembly.
THE METHOD OF DISTANCE MEASUREMENT AND TORSO LENGTH INFLUENCES THE RELATIONSHIP OF PULSE WAVE VELOCITY TO CARDIOVASCULAR MORTALITY: PP.31.235

Objective: The method of estimating the distance traveled by the pulse wave, used in the calculation of pulse wave velocity (PWV), is not standardized. Our objective was to assess whether different methods of distance measurement influenced the association of PWV to cardiovascular mortality in hemodialysis patients. Design and Methods: 98 chronic hemodialysis patients had their PWV measured using three methods for distance estimation; PWV1: sternal notch–femoral site minus sternal notch–carotid site, PWV2: carotid–femoral site, PWV3: carotid–femoral site minus sternal notch–carotid site. Carotid–femoral distance was used to approximate torso length. Patients were followed for a median of 30 (range 1–51) months and the association of PWV and cardiovascular mortality was assessed using survival analysis before and after stratification for torso length. Results: The three methods resulted in significantly different PWV values (11.2 (3.3), 14.8 (4.2), 12.6 (3.7) m/s, respectively). During follow up 50 patients died (mortality rate 20.3/100 patient years), 32 of cardiovascular causes. In log-rank tests only PWV1 tertiles but not those of PWV2 or PWV3 were significantly related to outcome (p-values 0.017, 0.257, 0.138, respectively). In adjusted Cox proportional hazards regression only PWV1 was related to cardiovascular mortality (HR for 1m/s higher PWV 1.18[1.03–1.35], 1.10[0.99–1.21], 1,13[1.00–1.27], for the three PWVs respectively). In stratified analysis, however, among patients with below median torso length all three PWV values were related to outcome, while in patients with above median torso length neither PWV methods resulted in significant relationship to outcome. Conclusion: PWV calculated using the sternal notch–femoral distance minus sternal notch–carotid distance provides the strongest relationship to cardiovascular mortality. Longer torso weakens the predictive value of PWV, possibly due to more tortuosity of the aorta hence more error introduced when using surface tape measurements.
Pulmonary arterial hypertension in paediatric and adult patients with congenital heart disease

Pulmonary arterial hypertension (PAH) commonly arises in patients with congenital heart disease (CHD). Greater numbers of patients with PAH associated with CHD (PAH-CHD) are now surviving into adulthood, many with increasingly complex cardiac defects. Patients with cardiac defects which result in left-to-right shunting are at risk of developing PAH, owing to the increased shear stress and circumferential stretch induced by increased pulmonary blood flow, which leads to endothelial dysfunction and progressive vascular remodelling and, thus, increased pulmonary vascular resistance. Although PAH-CHD shares similar lung histology with idiopathic PAH, differences do exist between these aetiologies. Management of PAH-CHD can involve surgical correction of the cardiac defect and/or treatment of the PAH, depending on the underlying cardiac defect and status of disease progression. Transplantation surgery can be curative but is not without limitations. The timing of intervention in patients with PAH-CHD is important, but the optimums are sometimes difficult to define, with limited robust data to inform management decisions. Uncontrolled studies suggest that prostacyclin analogues and phosphodiesterase type-5 inhibitors may have benefits in advanced pulmonary vascular disease. In the only randomised controlled trial dedicated to end-stage PAH-CHD, bosentan significantly reduced pulmonary vascular resistance and significantly increased 6-minute walk distance without compromising peripheral oxygen saturation, in patients with Eisenmenger syndrome. These data suggest that targeted therapies are beneficial in the PAH-CHD population, and warrant further research.
Horizontal Cu/SiO2/Si/SiO2/Cu plasmonic waveguide components integrated in silicon photonic circuits

We report experimental realization of various Cu/SiO2/Si/SiO2/Cu plasmonic waveguide based building blocks, including low loss (~0.28 dB/Lim) waveguides, low loss (~0.52 dB/turn) bends, power splitters, and Mach-Zehnder interferometers with ER of ~18.7 dB. This is a significant step toward plasmonic nanocircuits on the Si platform.
Inactivation of EF-hands Makes GCAP-2 (p24) a Constitutive Activator of Photoreceptor Guanylyl Cyclase by Preventing a Ca2+-induced “Activator-to-Inhibitor” Transition*

Guanylyl cyclase activator proteins GCAP-1 and GCAP-2 (Dizhoor et al., 1995, Gorczyca et al., 1995) are members of a recently identified subclass of EF-hand type Ca2+-binding proteins that respond to Ca2+ differently than any other known members of the EF-hand superfamily. GCAPs acquire an activating conformation only in their Ca2+-free form. Free Ca2+ concentrations corresponding to levels in dark-adapted vertebrate photoreceptors inhibit the ability of GCAPs to activate photoreceptor guanylyl cyclases (RetGCs). We studied the effects of mutations that block binding of Ca2+ to the EF-hands of GCAP-2. Unlike other EF-hand proteins, which fail to activate their target when their EF-hands are inactivated by mutations, GCAP-2 with any single EF-hand inactivated remains active and is 3-6 times less sensitive to the inhibitory effect of Ca2+. Inactivation of any two or all three EF-hands produces active forms of GCAP-2 that are insensitive to inhibition by physiological intracellular concentrations of Ca2+. Unexpectedly we also found that activation of RetGCs by a Ca2+-insensitive mutant is inhibited by Ca2+-loaded wild type GCAP-2. We propose the following. 1) GCAP-2 can exist in two extreme functional forms: an apo form that activates RetGCs and a Ca2+-loaded form that blocks activation of RetGCs. 2) All three EF-hands of GCAP-2 contribute to the inhibitory effect of Ca2+. 3) Inactivation of two or three EF-hands is sufficient to shift the “activator-inhibitor” transition outside the physiological range of intracellular free Ca2+.
The effects of age on lens transport.

PURPOSE Age-related nuclear cataracts involve denaturation and aggregation of intracellular proteins. We have documented age-dependent changes in membrane transport in the mouse lens to see what might initiate changes in the intracellular milieu. METHODS Microelectrode-based intracellular impedance studies of intact lenses were used to determine gap junction coupling conductance, fiber and surface cell membrane conductances, effective extracellular resistivity, and intracellular voltage. Fiber cell connexin expression was detected by Western blotting. Intracellular hydrostatic pressure was measured with a microelectrode/manometer system. Concentrations of intracellular sodium and calcium were measured by intracellular injection of sodium-binding benzofuran isophthalate and Fura2, respectively. RESULTS In adult lenses, as age increased: fiber cell gap junction coupling conductance declined significantly, correlating with decreases in Cx46 and Cx50 labeling in Western blots; fiber and surface cell membrane conductances did not change systematically; effective extracellular resistivity increased monotonically; center to surface gradients for intracellular pressure, sodium, calcium, and voltage all increased, but in an interdependent manner that moderated changes. In newborn pup lenses, there were changes that did not simply fit with the above paradigm. CONCLUSIONS In newborn pup lenses, the observed changes may relate to growth factors that are not related to age-dependent changes seen in adult lenses. The major change in adult lenses was an age-dependent decrease in gap junction coupling, probably due to oxidative damage leading to degradation of connexin proteins. These changes clearly lead to compromise of intracellular homeostasis and may be a causal factor in age-related nuclear cataracts.