gebhart/patrepeval huggingface dataset:
A Nonlinear Finite Element Model of the Eye With Experimental Validation for the Prediction of Globe Rupture (2002)

Over 2.4 million eye injuries occur each year in the US, with over 30,000 patients left blind as a result of the trauma. The majority of these injuries occur in automobile crashes, military operations and sporting activities. This paper presents a nonlinear finite element model of the eye and the results of 22 experiments using human eyes to validate for globe rupture injury prediction. The model of the human eye consists of the cornea, sclera, lens, ciliary body, zonules, aqueous humor and vitreous body. Lagrangian membrane elements are used for the cornea and sclera, Lagrangian bricks for the lens, ciliary, and zonules, and Eulerian brick elements comprise the aqueous and vitreous. Nonlinear, isotropic material properties of the sclera and cornea were gathered from uniaxial tensile strip tests performed up to rupture. Dynamic modeling was performed using LS-Dyna. Experimental validation tests consisted of 22 tests using three scenarios: impacts from foam particles, BB's, and baseballs onto fresh eyes used within 24 hours postmortem. The energies of the projectiles were chosen so as to provide both globe rupture and no rupture tests. Displacements of the eye were recorded using high speed color video at 7100 frames per second. The matched simulations predicted rupture of the eye when rupture was seen in the BB and baseball tests, and closely predicted displacements of the eye for the foam tests. Globe rupture has previously been shown to occur at peak stresses of 9.4 MPa using the material properties included in the model. Because of dynamic effects and improvements in boundary conditions resulting from a more realistic modeling of the fluid in the anterior and posterior chambers, the stresses can be much higher than those previously predicted, with the globe remaining intact. The model is empirically verified to predict globe rupture for stresses in the corneoscleral shell exceeding 23 MPa, and local dynamic pressures exceeding 2.1 MPa. The model can be used as a predictive aid to reduce the burden of eye injury, and can serve as a validated model to predict globe rupture.
Alarm correlation and fault identification in communication networks (1994)

Presents an approach for modeling and solving the problem of fault identification and alarm correlation in large communication networks. A single fault in a large network may result in a large number of alarms, and it is often very difficult to isolate the true cause of the fault. This appears to be one of the most important difficulties in managing faults in today's networks. The problem may become worse in the case of multiple faults. The authors present a general methodology for solving the alarm correlation and fault identification problem. They propose a new alarm structure, propose a general model for representing the network, and give two algorithms which can solve the alarm correlation and fault identification problem in the presence of multiple faults. These algorithms differ in the degree of accuracy achieved in identifying the fault, and in the degree of complexity required for implementation.< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">&gt;</ETX>
Differing Lymphokine Profiles of Functional Subsets of Human CD4 and CD8 T Cell Clones (1991)

Functional subsets of human T cells were delineated by analyzing patterns of lymphokines produced by clones from individuals with leprosy and by T cell clones of known function. CD4 clones from individuals with strong cell-mediated immunity produced predominantly interferon-gamma, whereas those clones that enhanced antibody formation produced interleukin-4. CD8 cytotoxic T cells secreted interferon-gamma. Interleukin-4 was produced by CD8 T suppressor clones from immunologically unresponsive individuals with leprosy and was found to be necessary for suppression in vitro. Both the classic reciprocal relation between antibody formation and cell-mediated immunity and resistance or susceptibility to certain infections may be explained by T cell subsets differing in patterns of lymphokine production.
Xanthomonas axonopodis pv. glycines Soybean Cultivar Virulence Specificity Is Determined by avrBs3 Homolog avrXg1 (2009)

Three races of Xanthomonas axonopodis pv. glycines were identified on pustule disease resistant and susceptible soybean cultivars based on virulence phenotype. For race 3, an avrBs3 homolog, avrXg1 was identified that conferred resistance expressed as a hypersensitive response on resistant cultivar Williams 82. Mutations in two predicted functional domains of avrXg1 resulted in gained virulence on Williams 82 and an increase in bacterial population number on susceptible cultivars. Expression of avrXg1 in race 1, that is predicted to confer a nonspecific HR, led to virulence on susceptible cultivars Spencer and PI 520733. Expression of avrXg1 in race 2, that is predicted of carrying avrBs3-like genes, resulted in gained virulence and fitness of pathogen on both resistant and susceptible cultivars. The results demonstrate multifunctions for avrXg1 dependent on pathogen and plant genetic backgrounds.
Flow cytometric analysis of intracellular chemokines in chondrocytes in vivo: constitutive expression and enhancement in osteoarthritis and rheumatoid arthritis (1999)

Chemokines play a key role in modulating leukocyte functions at sites of inflammation. To assess chondrocyte contribution to the chemotactic environment of inflamed joints the intracellular content of CC and CXC chemokines was investigated. IL-8, GROalpha, MCP-1, RANTES, MIP-1alpha and MIP-1beta expression was evaluated by flow cytometric analysis and RT-PCR in chondrocytes isolated from cartilage specimens obtained from patients with osteoarthritis and rheumatoid arthritis and multiorgan donors as normal controls. All the chemokines except RANTES were found in normal chondrocytes, with different degrees of staining intensity. In osteoarthritis and rheumatoid arthritis patients, an enhancement of IL-8, GROalpha, MIP-1alpha and MIP-1beta was observed.
In vitro generated extracellular matrix and fluid shear stress synergistically enhance 3D osteoblastic differentiation (2006)

This study instituted a unique approach to bone tissue engineering by combining effects of mechanical stimulation in the form of fluid shear stresses and the presence of bone-like extracellular matrix (ECM) on osteodifferentiation. Rat marrow stromal cells (MSCs) harvested from bone marrow were cultured on titanium (Ti) fiber mesh discs for 12 days in a flow perfusion system to generate constructs containing bone-like ECM. To observe osteodifferentiation and bone-like matrix deposition, these decellularized constructs and plain Ti fiber meshes were seeded with MSCs (Ti/ECM and Ti, respectively) and cultured in the presence of fluid shear stresses either with or without the osteogenic culture supplement dexamethasone. The calcium content, alkaline phosphatase activity, and osteopontin secretion were monitored as indicators of MSC differentiation. Ti/ECM constructs demonstrated a 75-fold increase in calcium content compared with their Ti counterparts after 16 days of culture. After 16 days, the presence of dexamethasone enhanced the effects of fluid shear stress and the bone-like ECM by increasing mineralization 50-fold for Ti/ECM constructs; even in the absence of dexamethasone, the Ti/ECM constructs exhibited approximately a 40-fold increase in mineralization compared with their Ti counterparts. Additionally, denatured Ti/ECM* constructs demonstrated a 60-fold decrease in calcium content compared with Ti/ECM constructs after 4 days of culture. These results indicate that the inherent osteoinductive potential of bone-like ECM along with fluid shear stresses synergistically enhance the osteodifferentiation of MSCs with profound implications on bone-tissue-engineering applications.
Dual Loss of ER Export and Endocytic Signals with Altered Melanosome Morphology in thesilverMutation of Pmel17 (2006)

Pmel17 is a pigment cell-specific integral membrane protein that participates in the formation of the intralumenal fibrils upon which melanins are deposited in melanosomes. The Pmel17 cytoplasmic domain is truncated by the mouse silver mutation, which is associated with coat hypopigmentation in certain strain backgrounds. Here, we show that the truncation interferes with at least two steps in Pmel17 intracellular transport, resulting in defects in melanosome biogenesis. Human Pmel17 engineered with the truncation found in the mouse silver mutant (hPmel17si) is inefficiently exported from the endoplasmic reticulum (ER). Localization and metabolic pulse-chase analyses with site-directed mutants and chimeric proteins show that this effect is due to the loss of a conserved C-terminal valine that serves as an ER exit signal. hPmel17si that exits the ER accumulates abnormally at the plasma membrane due to the loss of a di-leucine-based endocytic signal. The combined effects of reduced ER export and endocytosis significantly deplete Pmel17 within endocytic compartments and delay proteolytic maturation required for premelanosome-like fibrillogenesis. The ER export delay and cell surface retention are also observed for endogenous Pmel17si in melanocytes from silver mice, within which Pmel17 accumulation in premelanosomes is dramatically reduced. Mature melanosomes in these cells are larger, rounder, more highly pigmented, and less striated than in control melanocytes. These data reveal a dual sorting defect in a natural mutant of Pmel17 and support a requirement of endocytic trafficking in Pmel17 fibril formation.
Influence of IFN- α and IFN- γ on Lymphangiogenesis (2006)

Malignant cancers commonly spread by local invasion followed by metastasis through venous or lymphatic passages or both to distant sites. Angiogenesis and its relation to tumor growth and metastasis have been extensively researched. To date, however, the role played by lymphangiogenesis and metastasis of cancer has been overlooked. Inhibition of lymphangiogenesis, compared with inhibition of angiogenesis, may provide new insight to the mechanisms of metastasis of cancers. The current study was designed to examine the effect of two commonly used inhibitors of angiogenesis, interferon-alpha (IFN-alpha ) and IFN-gamma, on the growth and proliferation of lymphatic endothelial (LE) cells isolated from pig thoracic duct under in vitro condition. The LE cells were isolated and marked using specific markers, such as VEGFR-3 and LYVE-1, before experimental studies. The results showed that treatment of LE cells derived from the thoracic duct with these two inhibitors caused a decrease in the rate of cell proliferation in a dose-dependent manner, as assessed by MTT assays (tetrazolium salt colorimetric assay). Cell migration rate was assessed by the speed at which the cell migrated out from the scrape-wound margin; the speed of migration of LE cells was significantly inhibited in a dose-dependent fashion compared with controls. Treatment with both IFN-alpha and IFN-gamma caused an increase in apoptosis of LE cells, as assessed by Hoechst staining and caspase-3 staining. Our results showed that both IFN-alpha and IFN-gamma were able to inhibit LE cell growth in a dose-dependent manner and that the inhibition may be through induction of apoptosis of endothelial cells.
A Novel High-Cell-Density Protein Expression System Based on Ralstonia eutropha (2002)

We describe the development of a novel protein expression system based on the industrial fermentation organism Ralstonia eutropha (formerly known as Alcaligenes eutrophus) NCIMB 40124. This new system overcomes some of the shortcomings of traditional Escherichia coli-based protein expression systems, particularly the propensity of such systems to form inclusion bodies during high-level expression. Using a proteomics approach, we identified promoters that can be induced by simple process parameters or medium compositions in high-density cell culture or shake flasks, respectively. By combining newly developed molecular biological tools with a high-cell-density fermentation process, we were able to produce high levels (>1 g/liter) of soluble, active organophosphohydrolase, a model enzyme prone to inclusion body formation in E. coli.
Muscle-specific PPARγ-deficient mice develop increased adiposity and insulin resistance but respond to thiazolidinediones (2003)

Activation of peroxisome proliferator-activated receptor (PPAR) by thiazolidinediones (TZDs) improves insulin resistance by increasing insulin-stimulated glucose disposal in skeletal muscle.It remains debatable whether the effect of TZDs on muscle is direct or indirect via adipose tissue.We therefore generated mice with muscle-specific PPAR knockout (MuPPARKO) using Cre/loxP recombination.Interestingly, MuPPARKO mice developed excess adiposity despite reduced dietary intake.Although insulin-stimulated glucose uptake in muscle was not impaired, MuPPARKO mice had whole-body insulin resistance with a 36% reduction (P < 0.05) in the glucose infusion rate required to maintain euglycemia during hyperinsulinemic clamp, primarily due to dramatic impairment in hepatic insulin action.When placed on a high-fat diet, MuPPARKO mice developed hyperinsulinemia and impaired glucose homeostasis identical to controls.Simultaneous treatment with TZD ameliorated these high fat-induced defects in MuPPARKO mice to a degree identical to controls.There was also altered expression of several lipid metabolism genes in the muscle of MuPPARKO mice.Thus, muscle PPAR is not required for the antidiabetic effects of TZDs, but has a hitherto unsuspected role for maintenance of normal adiposity, whole-body insulin sensitivity, and hepatic insulin action.The tissue crosstalk mediating these effects is perhaps due to altered lipid metabolism in muscle.
The future of bladder control-intravesical drug delivery, a pinch of pepper, and gene therapy. (2002)

The incidence of urinary incontinence and overactive bladder problems will continue to grow as the population ages. Future treatments are likely to include an implantable drug delivery system, gene therapy, and the intravesical use of the vallinoids capsaicin and resiniferatoxin (RTX). An understanding of the urothelium is essential for effective design of these therapies. Intravesical anticholinergic drug treatment is currently not widely used, but intravesical pumps are under development to provide less cumbersome treatment methods and will provide nonsurgical options for patients who cannot tolerate oral anticholinergic agents. Research on the use of capsaicin as an intravesicular drug has had limited success, but trials have confirmed the efficacy of intravesical capsaicin for detrusor hyperreflexia. RTX is as effective as capsaicin but without side effects, such as pain and inflammatory neuropeptide release. RTX treatment may eliminate the need for surgical and other drug treatments of lower urinary tract dysfunction in patients with spinal cord injuries. Gene therapy will change the practice of urology by addressing the deficiencies that cause symptoms rather than attacking the symptoms themselves.
CD4 counting technologies for HIV therapy monitoring in resource-poor settings – state-of-the-art and emerging microtechnologies (2013)

Modern advancements in pharmaceuticals have provided individuals who have been infected with the human immunodeficiency virus (HIV) with the possibility of significantly extending their survival rates. When administered sufficiently soon after infection, antiretroviral therapy (ART) allows medical practitioners to control onset of the symptoms of the associated acquired immune deficiency syndrome (AIDS). Active monitoring of the immune system in both HIV patients and individuals who are regarded as "at-risk" is critical in the decision making process for when to start a patient on ART. A reliable and common method for such monitoring is to observe any decline in the number of CD4 expressing T-helper cells in the blood of a patient. However, the technology, expertise, infrastructure and costs to carry out such a diagnostic cannot be handled by medical services in resource-poor regions where HIV is endemic. Addressing this shortfall, commercialized point-of-care (POC) CD4 cell count systems are now available in such regions. A number of newer devices will also soon be on the market, some the result of recent maturing of charity-funded initiatives. Many of the current and imminent devices are enabled by microfluidic solutions, and this review will critically survey and analyze these POC technologies for CD4 counting, both on-market and near-to-market deployment. Additionally, promising technologies under development that may usher in a new generation of devices will be presented.
Isolation of human glucose-6-pbosphate debydrogenase (G6PD) cDNA clones: primary structure of the protein and unusual 5' non-coding region (1986)

Glucose-6-phosphate dehydrogenase (G6PD) is an ubiquitous enzyme which by determining the NADPH level has a crucial role in NADPH-mediated reductive processes in all cells (1). The structural gene for G6PD, Gd, is X-linked in mammals and on the basis of its expression in many tissues, it can be regarded as a typical "housekeeping" gene (2). Over 300 variants of the protein are known, many of which have deficient enzyme activity. Nearly 100 of these variants are polymorphic in various populations (3). The mammalian enzyme is a homodimer or a homotetramer with a subunit molecular weight of approximately 56000 daltons (4). Here we report the isolation of cDNA clones from HeLa cells, SV40-transformed human fibroblasts, human placenta and human teratocarcinoma cell lines. These clones have enabled us to sequence the entire coding region of Gd. Thus, the entire amino acid sequence of human G6PD is provided for the first time. This work is the first step for structural analysis of G6PD variants and for an understanding of the biological features of this enzyme at the molecular level.
Neuroprotective effect of exogenous vascular endothelial growth factor on rat spinal cord neurons in vitro hypoxia (2005)

Background Vascular endothelial growth factor (VEGF) is well known as a hypoxia-induced protein. That it markedly increased expression of VEGF and improvement of rat motor function after spinal cord injury suggested that VEGF could play a neuroprotective role in ischaemic tolerance. This study investigated whether vascular endothelial growth factor has direct neuroprotective effects on rat spinal cord neurons. Methods We employed primary cultures of embryonic rat spinal cord neurons, then administrated different concentrations of VEGF164 in the culture medium before hypoxia when the number of neurons was counted and the cell viability was detected by MTT. The neuronal apoptosis and expression of VEGF and its receptor genes were evaluated by terminal deoxynucleotidyl transferase mediated dUTP nick-end labelling (TUNEL) and immunohistochemistry. The VEGFR2/FLK-1 inhibitor, SU1498, was used to confirm whether the neuroprotective effect of VEGF was mediated through VEGFR2/Flk-1 receptors. Result In hypoxic conditions,the number and viability of neurons decreased progressively, while the number of TUNEL-positive cells increased along with the prolongation of hypoxic exposure. When the concentration of VEGF in cell culture medium reached 25 ng/ml, the cell viability increased 11% and neuronal apoptosis reduced to half, this effect was dose dependent and led to an approximately 25% increase in cell viability and about threefold decrease in TUNEL-positive cells at a maximally effective concentration of 100 ng/ml. In normal conditions, VEGF/Flk-1 but not VEGF/Flt-1 gene expressed at a low level: after hypoxia, the expression of VEGF/Flk-1, but not VEGF/Flt-1 was significantly increased. The protective effect of VEGF was blocked by the VEGFR2/Flk-1 receptor tyrosine kinase inhibitor, SU1498. Conclusions VEGF has direct neuroprotective effects on rat spinal cord neurons, which may be mediated in vitro through VEGFR2/Flk-1 receptors.
Implementing Remote procedure calls (1983)

Remote procedure calls ( RPC ) are a useful paradigm for providing communication across a network between programs written in a high level language. This paper describes a package, written as part of the Cedar project, providing a remote procedure call facility. The paper describes the options that face a designer of such a package, and the decisions we made. We describe the overall structure of our RPC mechanism, our facilities for binding RPC clients, the transport level communication protocol, and some performance measurements. We include descriptions of some optimisations we used to achieve high performance and to minimize the load on server machines that have many clients. Our primary aim in building an RPC package was to make the building of distributed systems easier. Previous protocols were sufficiently hard to use that only members of a select group of communication experts were willing to undertake the construction of distributed systems. We hoped to overcome this by providing a communication paradigm as close as possible to the familiar facilities of our high level languages. To achieve this aim, we concentrated on making remote calls efficient, and on making the semantics of remote calls as close as possible to those of local calls.
Androgen-Dependent Nitric Oxide Release in Rat Penis Correlates with Levels of Constitutive Nitric Oxide Synthase Isoenzymes1 (1999)

Androgens are known to influence penile erection and nitric oxide synthase (NOS) activity in cavernosal tissue homogenates. The present study was an assessment of the effects of castration and androgen replacement on the in vivo release of nitric oxide (NO), and of the simultaneously recorded intracavernosal pressure (ICP) changes elicited by electrostimulation of the cavernosal nerves (SCN) in the anesthetized rat. The extracellular levels of NO in the corpora were monitored electrochemically using porphyrin microsensors. The content of NOS isoenzymes in corporal homogenates was determined by immunoblotting. The responses of castrated rats with or without testosterone (T) implants were compared to those of intact animals. Castration virtually abolished both the NO and the ICP responses to SCN. There was a concomitant significant decrease in the content of both the neuronal (nNOS) and the endothelial (eNOS) isoenzymes in the cavernosal tissue. All these effects of castration were prevented by T replacement. The NO response to SCN was positively correlated with the levels of nNOS and eNOS, especially when the values of the two isoforms were added (r = 0.71, P < 0.001). These data suggest that the facilitatory action of androgens on penile erection involves the up-regulation of both constitutive NOS isoenzymes in the corpora cavernosa.
Solid-state NMR studies of Klebsiella pneumoniae grown under nitrogen-fixing conditions. (1987)

The carbon and nitrogen metabolism of Klebsiella pneumoniae M5a1 has been characterized using 13C and 15N labeling with detection by cross-polarization magic-angle spinning solid-state NMR. Cells grown on ammonium typically require some 20 h to derepress fully for nitrogenase when transferred to medium devoid of any source of fixed nitrogen. We have established that during this period some cellular proteins are catabolized with the liberated nitrogen being used for the synthesis of purines needed for formation of ribosomal RNA. The 20-h derepression period can be shortened to 6 h by the introduction of fixed nitrogen in certain specific forms. Serine is the most successful agent we have examined for shortening the derepression period and glycine among the least successful. We attribute this difference to the advantage of serine over glycine in providing both specific and nonspecific carbon and nitrogen sources for complete purine synthesis. These determinations were made by tracing the metabolism of 13C- and 15N-labeled chemical bonds from the 2 amino acids during derepression.