Miracle-dz/UniFAR-FTUs huggingface dataset:
Similar Prevalence of Renovascular Hypertension in Selected Blacks and Whites

Renovascular hypertension is a potentially curable form of high blood pressure that is thought to be extremely rare among blacks. We demonstrate, however, that in a clinically selected population, the prevalence of renovascular hypertension is similar in blacks and whites. We prospectively evaluated 167 hypertensive subjects who had one or more clinical features known to be associated with renovascular hypertension. All subjects had captopril-stimulated peripheral renin measurements and conventional renal arteriography. All significant renal artery stenoses (greater than 50% luminal narrowing) were treated with percutaneous transluminal angioplasty or surgery. Renovascular hypertension was diagnosed if there was a blood pressure response to interventional therapy, according to the criteria established by the Cooperative Study of Renovascular Hypertension. Of the total group evaluated, 24% (39 of 167) had renal artery stenosis and 14% (23 of 167) had renovascular hypertension. Renal artery stenosis or occlusion was found in 27% (26 of 97) of whites and 19% (13 of 67) of blacks (p=027). Renovascular hypertension was diagnosed in 18% (17 of 97) of whites and 9% (6 of 67) of blacks evaluated (p=0.25). Renovascular hypertension was associated with severe or refractory hypertension and with smoking, but there were no racial differences in these associations. Blacks with renovascular hypertension tended to have low captopril-stimulated peripheral renin activity. We conclude that blacks with clinical features suggestive of renovascular hypertension should be evaluated with angiography. Captopril-stimulated plasma renin may not be useful in detecting blacks with renovascular hypertension, but this and other potential screening tests require further evaluation.
Immunohistochemical and Ultrastructural Features of Neuroendocrine Differentiated Carcinomas of the Prostate: An Immunoelectron Microscopic Study

The purpose of this study was to further define the immunohistochemical and ultrastructural characteristics of neuroendocrine (NE) differentiated prostatic carcinomas. Seventy-seven specimens were obtained from prostatic carcinoma tumors during prostatectomy, transurethral resection of prostate or biopsy in 77 prostate cancer patients, and analyzed by immunohistochemical staining for chromogranin A (CgA). Nine of these tumors were also studied by elctron microscopy and 4 were examined by pre-embedding immunoelectron microscopy. CgA-stained cells were detected in 36 tumors (47%). Clinically advanced tumors or tumors with higher histological grades were associated with increased NE differentiation. Three of the tumors studied by electron microscopy contained cells showing unequivocal NE differentiation revealed by the presence of neurosecretory granules, while the poorly NE-differentiated malignant cells contained pleomorphic granules, which were lysosomal-like rather than NE-type granules. Immunoelectron microscopy demonstrated the presence of CgA immunoreactivity on the pleomorphic granules in the poorly differentiated malignant glands. This study suggests that NE-differentiated malignant cells in prostate cancer tissues may induce aggressive behavior in adjacent proliferating neoplastic cells via a paracrine mechanism.
Modest Reductions of Cardiac Calsequestrin Increase Sarcoplasmic Reticulum Ca2+ Leak Independent of Luminal Ca2+ and Trigger Ventricular Arrhythmias in Mice

Cardiac calsequestrin–null mice (Casq2−/−) display catecholaminergic ventricular tachycardia akin to humans with CASQ2 mutations. However, the specific contribution of Casq2 deficiency to the arrhythmia phenotype is difficult to assess because Casq2−/− mice also show significant reductions in the sarcoplasmic reticulum (SR) proteins junctin and triadin-1 and increased SR volume. Furthermore, it remains unknown whether Casq2 regulates SR Ca2+ release directly or indirectly by buffering SR luminal Ca2+. To address both questions, we examined heterozygous (Casq2+/−) mice, which have a 25% reduction in Casq2 but no significant decrease in other SR proteins. Casq2+/− mice (n=35) challenged with isoproterenol displayed 3-fold higher rates of ventricular ectopy than Casq2+/+ mice (n=31; P<0.05). Programmed stimulation induced significantly more ventricular tachycardia in Casq2+/− mice than in Casq2+/+ mice. Field-stimulated Ca2+ transients, cell shortening, L-type Ca2+ current, and SR volume were not significantly different in Casq2+/− and Casq2+/+ myocytes. However, in the presence of isoproterenol, SR Ca2+ leak was significantly increased in Casq2+/− myocytes (Casq2+/− 0.18±0.02 Fratio versus Casq2+/+ 0.11±0.01 Fratio, n=57, 60; P<0.01), resulting in a significantly higher rate of spontaneous SR Ca2+ releases and triggered beats. SR luminal Ca2+ measured using Mag-Fura-2 was not altered by Casq2 reduction. As a result, the relationship between SR Ca2+ leak and SR luminal Ca2+ was significantly different between Casq2+/− and Casq2+/+ myocytes (P<0.01). Thus, even modest reductions in Casq2 increase SR Ca2+ leak and cause ventricular tachycardia susceptibility under stress. The underlying mechanism is likely the direct regulation of SR Ca2+ release channels by Casq2 rather than altered luminal Ca2+.
Etiologic Pattern of Genital Ulcers in Lusaka, Zambia: Has Chancroid Been Eliminated?

Background Genital ulcers are a public health problem in developing countries. The World Health Organization recommends the use of syndromic guidelines for sexually transmitted infection treatment in resource-constrained countries. Monitoring local etiologies provides information that may aid policy for sexually transmitted infection treatment. We investigated the etiology of genital ulcer disease among outpatients in Lusaka, Zambia. Methodology Swabs from genital ulcers of 200 patients were tested using polymerase chain reaction for Treponema pallidum, herpes simplex virus types 1 (HSV-1) and 2 (HSV-2), Haemophilus ducreyi, and Chlamydia trachomatis. Results The prevalence of the detected pathogens was as follows; HSV-2, 28%; T. pallidum, 11.5%; C. trachomatis, 3%; HSV-1, 0.5%; and H. ducreyi, 0%. Coinfection with HSV-2 and T. pallidum was 1.5%, and coinfection of HSV-2 and C. trachomatis was 1%. In 55% of the patients, no etiologic diagnosis could be established. Conclusions H. ducreyi was not detected, whereas HSV-2 and T. pallidum were the commonest pathogens. Nondetection of H. ducreyi requires further studies. If the present findings are validated, treatment guidelines would require to be revised in Zambia.
Phosphorylation Modulates Ameloblastin Self-assembly and Ca2+ Binding

Ameloblastin (AMBN), an important component of the self-assembled enamel extra cellular matrix, contains several in silico predicted phosphorylation sites. However, to what extent these sites actually are phosphorylated and the possible effects of such post-translational modifications are still largely unknown. Here we report on in vitro experiments aimed at investigating what sites in AMBN are phosphorylated by casein kinase 2 (CK2) and protein kinase A (PKA) and the impact such phosphorylation has on self-assembly and calcium binding. All predicted sites in AMBN can be phosphorylated by CK2 and/or PKA. The experiments show that phosphorylation, especially in the exon 5 derived part of the molecule, is inversely correlated with AMBN self-assembly. These results support earlier findings suggesting that AMBN self-assembly is mostly dependent on the exon 5 encoded region of the AMBN gene. Phosphorylation was significantly more efficient when the AMBN molecules were in solution and not present as supramolecular assemblies, suggesting that post-translational modification of AMBN must take place before the enamel matrix molecules self-assemble inside the ameloblast cell. Moreover, phosphorylation of exon 5, and the consequent reduction in self-assembly, seem to reduce the calcium binding capacity of AMBN suggesting that post-translational modification of AMBN also can be involved in control of free Ca2+ during enamel extra cellular matrix biomineralization. Finally, it is speculated that phosphorylation can provide a functional crossroad for AMBN either to be phosphorylated and act as monomeric signal molecule during early odontogenesis and bone formation, or escape phosphorylation to be subsequently secreted as supramolecular assemblies that partake in enamel matrix structure and mineralization.
Leptin-enhanced neointimal hyperplasia is reduced by mTOR and PI3K inhibitors

Despite the use of the sirolimus (rapamycin) drug-eluting coronary stent, diabetics are at increased risk of developing in-stent restenosis for unclear reasons. Hyperleptinemia, which often coexists with diabetes and metabolic syndrome, is an independent risk factor for progression of coronary artery disease. It has not been determined whether elevated circulating leptin decreases the efficacy of the sirolimus drug-eluting stent in inhibiting neointimal hyperplasia, the process underlying restenosis after stenting. Here we show that leptin activates the mammalian target of rapamycin (mTOR) signaling pathway in primary murine vascular smooth muscle cells (VSMC) and stimulates VSMC proliferation in a PI3K-dependent fashion. Exogenous leptin, administered at levels comparable to those found in obese humans, promotes neointimal VSMC hyperplasia in a murine femoral artery wire injury model. Leptin significantly increases the dose of the mTOR inhibitor sirolimus that is required for effective inhibition of neointimal formation. Combination therapy with LY294002, a PI3K inhibitor, and sirolimus effectively inhibits leptin-enhanced neointimal hyperplasia. These data show that, in the setting of hyperleptinemia, higher doses of an mTOR inhibitor, or combination therapy with mTOR and PI3K inhibitors, inhibits neointimal hyperplasia after arterial injury. These studies may explain the higher rates of restenosis observed in diabetics treated with a sirolimus-eluting coronary stent and suggest a potential novel therapeutic approach for inhibiting in-stent restenosis in such patients.
Reducing infections through nanotechnology and nanoparticles

The expansion of bacterial antibiotic resistance is a growing problem today. When medical devices are inserted into the body, it becomes especially difficult for the body to clear robustly adherent antibiotic-resistant biofilm infections. In addition, concerns about the spread of bacterial genetic tolerance to antibiotics, such as that found in multiple drug-resistant Staphylococcus aureus (MRSA), have significantly increased of late. As a growing direction in biomaterial design, nanomaterials (materials with at least one dimension less than 100 nm) may potentially prevent bacterial functions that lead to infections. As a first step in this direction, various nanoparticles have been explored for improving bacteria and biofilm penetration, generating reactive oxygen species, and killing bacteria, potentially providing a novel method for fighting infections that is nondrug related. This review article will first examine in detail the mechanisms and applications of some of these nanoparticles, then follow with some recent material designs utilizing nanotechnology that are centered on fighting medical device infections.
Effect of Acetyl Choline on the Secretion of Glucagon and Insulin from the Isolated, Perfused Canine Pancreas

During perfusions with glucose concentrations of 25 and 150 mg. /100 ml. , the effect of infusions of acetyl choline on glucagon and insulin release was investigated in five perfusion experiments. Acetyl choline at concentrations of 10 to 100 μM. stimulated release of glucagon both at the low glucose strength as well as at the high concentration, which in itself inhibits basal glucagon release. Glucagon was released in a monophasic pattern, resembling the release pattern found after catecholamines and contrasting with the biphasic pattern obtained after stimulation with gastrointestinal hormones and amino acids, as previously reported from our laboratory. Acetyl choline always stimulated release of insulin in a biphasic pattern, at the high glucose concentration, while no consistent effect was obtained at the low glucose concentration. At the termination of the acetyl choline infusions, a rebound increase in insulin was observed during perfusion with both low and high glucose concentrations. Infusion of atropine at a concentration of 25 μM. completely abolished the stimulatory effect of acetyl choline on both glucagon and insulin release. The results suggest that the parasympathetic nervous system may play a direct role in the control mechanism of the release of the pancreatic hormones during food ingestion.
Targeting the vascular endothelial growth factor in hematologic malignancies

There exists increasing evidence that apart from solid tumors, angiogenic growth factors also play important roles in the development and/or maintenance of hematolymphoid malignancies. Thus, in these cancers, angiogenesis and bone marrow microvessel density often correlate with prognosis and disease burden. Several reports speculated on the role of angiogenesis and the resulting possible therapeutic options in hematologic malignancies. The most prominent angiogenic factor, vascular endothelial growth factor (VEGF), is expressed in a number of established leukemic cell lines as well as in freshly isolated human leukemias and lymphomas, and several human leukemias express VEGF receptor 1 and/or VEGF receptor 2. VEGF/VEGF‐receptor interactions are also involved in proliferation, migration, and survival of leukemic cells by autocrine and paracrine mechanisms. As a consequence, a possible drugable effect by inhibiting VEGF signaling in different hematologic malignancies has been discussed. This review focuses on angiogenesis‐independent effects of VEGF on survival and proliferation of leukemic or lymphoma cells and on possible therapeutic approaches using anti‐VEGF/VEGF‐receptor therapies to inhibit proliferation or induce apoptosis of malignant cells in hematologic diseases.
Two Cases of Melasma with Unusual Histopathologic Findings

We reported two cases of clinically typical melasma presenting with unusual histopathologic findings. In one case, the epidermal melanocytes were markedly increased in number and protruded into the dermis, and in the other case, increased epidermal pigmentation as well as dermal melanocytosis were found. We suggested that the various treatment modalities of melasma should be applied depend on its histopathologic finding.
Oral pancreatic enzyme substitution therapy in chronic pancreatitis: is clinical response an appropriate marker for evaluation of therapeutic efficacy?

CONTEXT Malnutrition secondary to pancreatic exocrine insufficiency plays a prognostic role in chronic pancreatitis. Enzyme substitution therapy is generally prescribed to avoid diarrhea and weight loss, although it is unknown whether this is associated with normal absorption of nutrients and a normal nutritional status. OBJECTIVE We aimed to evaluate whether an adequate clinical response to enzyme therapy can be used to predict a normal nutritional status in patients with chronic pancreatitis. PATIENTS Thirty-one consecutive patients (25 males, 6 females; mean age 52 years,) with severe chronic pancreatitis and steatorrhea were enrolled in the study. INTERVENTION Enzyme substitution therapy was indicated in cases with severe steatorrhea (more than 15 g/day), diarrhea and/or weight loss. Therapy was optimized in individual patients to obtain complete symptom relief. MAIN OUTCOME MEASURE A nutritional evaluation including body mass index and serum levels of retinol-binding protein, prealbumin and transferrin was carried out. RESULTS Ten out of ten patients with asymptomatic steatorrhea, who did not fulfill the criteria for enzyme substitution therapy, and 11 out of 21 patients (52.4%) with symptomatic or more severe steatorrhea, who were under enzyme substitution therapy, showed a deficient nutritional status. CONCLUSIONS An appropriate clinical response to enzyme substitution therapy does not allow the prediction of a normal nutritional status in patients with chronic pancreatitis.
Agent communication languages: the current landscape

Despite the substantial number of multiagent systems that use an agent communication language, the dust has not yet settled over the ACL landscape. Although semantic specification issues have monopolized the debate, other important pragmatic issues must be resolved quickly if ACLs are to support the development of robust agent systems. We introduce some concepts useful in discussing agent communication languages and then compare and evaluate the two major ACLs.
Notch2 negatively regulates myofibroblastic differentiation of myoblasts

Myofibroblasts are one of the key cellular components involved in fibrosis of skeletal muscle as well as in other tissues. Transforming growth factor‐β1 (TGF‐β1) stimulates differentiation of mesenchymal cells into myofibroblasts, but little is known about the regulatory mechanisms of myofibroblastic differentiation. Since Notch2 was shown to be downregulated in TGF‐β1‐induced non‐muscle fibrogenic tissue, we investigated whether Notch2 also has a distinctive role in myofibroblastic differentiation of myogenic cells induced by TGF‐β1. TGF‐β1 treatment of C2C12 myoblasts led to expression of myofibroblastic marker α‐smooth muscle actin (α‐SMA) and collagen I with concomitant downregulation of Notch2 expression. Overexpression of active Notch2 inhibited TGF‐β1‐induced expression of α‐SMA and collagen I. Interestingly, transient knockdown of Notch2 by siRNA in C2C12 myoblasts and primary cultured muscle‐derived progenitor cells resulted in differentiation into myofibroblastic cells expressing α‐SMA and collagen I without TGF‐β1 treatment. Furthermore, we found Notch3 was counter‐regulated by Notch2 in C2C12 cells. These findings suggest that Notch2 is inhibiting differentiation of myoblasts into myofibroblasts with downregulation of Notch3 expression. J. Cell. Physiol. 210: 358–369, 2007. © 2006 Wiley‐Liss, Inc.
Detection and diagnosis of faulty quantum circuits

A new approach to detecting and diagnosing faults in quantum circuits is introduced. In order to account for the probabilistic nature of quantum circuits, collections of test experiments, called binary tomographic tests (BTTs), are generated. A BTT can identify a fault with respect to some user-defined confidence threshold τ. We present an algorithm to generate BTTs that either detect, or ensure the absence of, all modeled faults in a given circuit. We also present an adaptive diagnostic method to locate quantum faults. While classical circuits, even probabilistic ones, only handle ordinary probabilities, quantum circuits deal with quantum states, which have phase as an extra probabilistic parameter. The tomographic testing methods introduced previously for probabilistic circuits are unable to detect differences in phase, and therefore leave many quantum faults undetected. In contrast, we develop a design-for-test method which is specifically intended to detect faults that only affect the phase of a quantum state. We give experimental results for benchmark and random circuits which show high coverage of quantum faults by BTTs, and good resolution in the case of the adaptive diagnosis method.
An estimation-theoretic framework for image-flow computation

A novel framework for computing image flow from time-varying imagery is described. This framework offers the following principal advantages. First, it allows estimation of certain types of discontinuous flow fields without any prior knowledge about the location of discontinuities. The flow fields thus recovered are not blurred at motion boundaries. Second, covariance matrices (or alternatively, confidence measures) are associated with the estimate of image flow at each stage of computation. The estimation-theoretic nature of the framework and its ability to provide covariance matrices make it very useful in the context of applications such as incremental estimation of scene-depth using techniques based on Kalman filtering. The framework is used to recover image flow from two image sequences. To illustrate an application, the image-flow estimates and their covariance matrices thus obtained are also used to recover scene depth. <<ETX>>
European Conference on Information Systems ( ECIS ) Summer 10-6-2011 IT QUALITY AND EGOVERNMENT NET BENEFITS : A CITIZEN PERSPECTIVE

The ultimate question about the success of eGovernment depends on how citizens perceive its value. Understanding success in Information Systems (IS) is however a complex challenge made more difficult when set in the public sector environment. While private sector studies may focus on profitability efficiency, quality and reliability, public sector evaluation must combine these concerns with accountability, citizen trust and the creation of public value. This research adopts the Public Value approach to provide the first empirical assessment of eGovernment success from a citizen perspective. It is also the first study to identify the important IT Quality dimensions that have a positive impact on success. This paper identifies the specific constructs within Information, System and Service Quality that predict citizen value perceptions. This level of granularity provides an important contribution in advancing a deeper understanding of the dynamics of eGovernment success. The novel environment of Web 2.0 in eGovernment is also explored, resulting in new findings that define what citizens’ value in this mode of interaction. This research therefore contributes to the body of knowledge by increasing our understanding of what citizens’ value in eGovernment services and what aspects of IT Quality influence eGovernment success.
Estimation of field‐scale soil hydraulic and dielectric parameters through joint inversion of GPR and hydrological data

A method is described for the joint use of time‐lapse ground‐penetrating radar (GPR) travel times and hydrological data to estimate field‐scale soil hydraulic parameters. We build upon previous work to take advantage of a wide range of cross‐borehole GPR data acquisition configurations and to accommodate uncertainty in the petrophysical function, which relates soil porosity and water saturation to the effective dielectric constant. We first test the inversion methodology using synthetic examples of water injection in the vadose zone. Realistic errors in the petrophysical function result in substantial errors in soil hydraulic parameter estimates, but such errors are minimized through simultaneous estimation of petrophysical parameters. In some cases the use of a simplified GPR simulator causes systematic errors in calculated travel times; simultaneous estimation of a single correction parameter sufficiently reduces the impact of these errors. We also apply the method to the U.S. Department of Energy (DOE) Hanford site in Washington, where time‐lapse GPR and neutron probe (NP) data sets were collected during an infiltration experiment. We find that inclusion of GPR data in the inversion procedure allows for improved predictions of water content, compared to predictions made using NP data alone. These examples demonstrate that the complimentary information contained in geophysical and hydrological data can be successfully extracted in a joint inversion approach. Moreover, since the generation of tomograms is not required, the amount of GPR data required for analyses is relatively low, and difficulties inherent to tomography methods are alleviated. Finally, the approach provides a means to capture the properties and system state of heterogeneous soil, both of which are crucial for assessing and predicting subsurface flow and contaminant transport.