gebhart/patrepeval huggingface dataset:
Algebraic functions for recognition (1995)

In the general case, a trilinear relationship between three perspective views is shown to exist. The trilinearity result is shown to be of much practical use in visual recognition by alignment-yielding a direct reprojection method that cuts through the computations of camera transformation, scene structure and epipolar geometry. Moreover, the direct method is linear and sets a new lower theoretical bound on the minimal number of points that are required for a linear solution for the task of reprojection. The proof of the central result may be of further interest as it demonstrates certain regularities across homographics of the plane and introduces new view invariants. Experiments on simulated and real image data were conducted, including a comparative analysis with epipolar intersection and the linear combination methods, with results indicating a greater degree of robustness in practice and a higher level of performance in reprojection tasks.< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">&gt;</ETX>
Effects of local MCP-1 protein therapy on the development of the collateral circulation and atherosclerosis in Watanabe hyperlipidemic rabbits (2002)

MCP-1 accelerates arteriogenesis upon femoral artery ligation under hyperlipidemic conditions. Six months after treatment these pro-arteriogenic effects of MCP-1 can no longer be observed. The present data do not show an effect of local MCP-1 treatment on serum lipids or on atherosclerosis. It should be noted however that a high standard deviation was observed for the data on atherosclerotic surface area, necessitating additional experiments in a different model of atherosclerosis.
An acoustical zoom based on informed spatial filtering (2014)

In digital cameras, zooming allows for narrowing the apparent angle of view in a video or an image. When sounds compliment the visual information, a desirable function would be to provide an acoustical zoom which is aligned with the zoomed visual image. In this paper, an approach is presented to achieve such a zoom effect using a microphone array. Acoustical zooming is realized by a weighted sum of the extracted direct sound and diffuse sound, whereas the weights depend on the zooming factor. The proposed approach uses two recently proposed informed multi-channel filters for the extraction of the direct sound and diffuse sound. Simulation results indicate that the performance is good even in challenging double-talk scenarios.
Prolonged Insulin Independence After Islet Allotransplants in Recipients with Type 1 Diabetes (2008)

We sought to determine the long-term outcomes in type 1 diabetic recipients of intraportal alloislet transplants on a modified immunosuppressive protocol. Six recipients with hypoglycemia unawareness received one to two islet infusions. Induction therapy was with antithymocyte globulin (ATG) plus etanercept for tumor necrosis factor-alpha blockade. Recipients received cyclosporine and everolimus for maintenance immunosuppression for the first year posttransplant, with mycophenolic acid or mycophenolate mofetil subsequently substituted for everolimus. Recipients have been followed for 1173 +/- 270 days since their last infusion for islet graft function (insulin independence, hemoglobin A(1c) levels and C-peptide production) and for adverse events associated with the study protocol. Of the six recipients, five were insulin-independent at 1 year, and four continue to be insulin-independent at a mean of 3.4 +/- 0.4 years posttransplant. None of the six recipients experienced recurrence of severe hypoglycemia. Measured glomerular filtration rate decreased from 110.5 +/- 21.2 mL/min/1.73 m(2) pretransplant to 82.6 +/-19.1 mL/min/1.73 m(2) at 1 year posttransplant. In conclusion, islet transplants restored insulin independence for a mean of >3 years in four of six recipients treated with ATG and etanercept induction therapy and with cyclosporine and, initially, everolimus for maintenance. Our results suggest this immunosuppressive protocol may allow long-term graft survival.
Reversal of natural killing susceptibility in target cells expressing transfected class I HLA genes. (1989)

A number of studies have suggested that resistance of target cells to natural killing (NK) may be correlated with their level of expression of major histocompatibility complex (MHC) class I antigens. To examine this hypothesis directly, a NK-sensitive class I-deficient human B-cell line was transfected with MHC class I genes. The expression of transfected HLA, but not H-2, class I gene products resulted in loss of susceptibility to human NK-mediated conjugation and cytolysis. Furthermore, this protection did not extend to cytotoxicity mediated by interleukin 2-stimulated human NK effector cells.
Dissection of astrocyte-mediated cues in neuronal guidance and process extension (1999)

Neurites are believed to be guided by astrocyte boundaries during development. We have previously shown that in vitro astrocyte boundaries can be generated by combining two different astrocyte cell lines, one which is inhibitory to neurite outgrowth (Neu7) with one that is permissive (A7). The extracellular matrix molecules tenascin-C, chondroitin sulfate proteoglycans (CSPG) and keratan sulfate proteoglycans (KSPG) were implicated in boundary formation. We have now further addressed the roles of these molecules using additional astrocyte cell lines that differ in their potential to permit neurite extension and in their expression of extracellular matrix molecules. T34-2 and 27A1 cells are permissive to neurite extension. T34-2 cells express high amounts of tenascin-C, but very low levels of proteoglycans, while 27A1 cells express CSPG and KSPG, but very little tenascin-C. T34-2 cells formed boundaries to neurites, and these boundaries are greatly reduced in the presence of blocking antitenascin-C antiserum. The addition of the antiserum did not affect neurite extension. 27A1 cells also formed boundaries without affecting neurite extension. Chondroitinase ABC, but not keratanase, treatment reduced the boundary, suggesting that CSPG is a major boundary component. These results demonstrate that astrocyte tenascin-C and proteoglycans are distinct components of astrocyte boundaries. More importantly, these results suggest that growing neurites can be directed to their targets by astrocyte-derived guidance molecules independent of effects on process extension.
Programmed death 1 ligand signaling regulates the generation of adaptive Foxp3 + CD4 + regulatory T cells (2008)

Although mature dendritic cells (DCs) are potent initiators of adaptive immune response, immature steady-state DCs contribute to immune tolerance. In this study, we show that ex vivo splenic DCs are capable of inducing conversion of naïve CD4(+) T cells to adaptive Foxp3(+)CD4(+) regulatory T cells (aTreg) in the presence of TGF-beta. In particular, when compared with splenic CD8alpha(-) DCs, the CD8alpha(+) DC subset were superior in inducing higher frequencies of conversion. This was not attributable to the difference in basal level of costimulation, because deficiency of CD40 or CD80/86 signaling did not diminish the differential induction of Foxp3. Conversion was regulated by DC maturation status. Further insights into the molecular mechanisms of conversion were gained by analyzing the contribution of several costimulatory and coinhibitory receptors. Costimulatory signals through GITR suppressed conversion, whereas coinhibitory signaling via programmed death 1 ligand (PD-L1) but not PD-L2 was required for conversion. Ex vivo PD-L1(-/-) DCs failed to support Foxp3 induction in the presence of TGF-beta. In vivo blocking PD-L1 signaling abolished conversion in a tumor-induced aTreg conversion model. Collectively, this study highlights the cellular and molecular parameters that might be exploited to control the de novo generation of aTregs and peripheral tolerance.
Design and testing of biological scaffolds for delivering reparative cells to target sites in the lung (2009)

This study summarizes the development and testing of a scaffold to promote engraftment of cells in the distal lung. A fibrinogen-fibronectin-vitronectin hydrogel (FFVH) was developed and optimized with respect to its mechanical and biological properties for this application. In vitro, FFVH scaffolds promoted attachment, histiotypic growth and expression of basement membrane proteins by primary ovine lung mesenchymal cells derived from lung biopsies. In vivo testing was then performed to assess the ability of FFVHs to promote cell engraftment in the sheep lung. Treatment with autologous cells delivered using FFVH was clinically well tolerated. Cells labelled with a fluorescent dye (PKH-26) were detected at treatment sites after 1 month. Tissue mass (assessed by CT imaging) and lung perfusion (assessed by nuclear scintigraphy) were increased at emphysema test sites. Post-treatment histology demonstrated cell proliferation and increased elastin expression without scarring or collapse. No treatment-related pathology was observed at healthy control sites. FFVH scaffolds promote cell attachment, spreading and extracellular matrix expression in vitro and apparent engraftment in vivo, with evidence of trophic effects on the surrounding tissue. Scaffolds of this type may contribute to the development of cell-based therapies for patients with end-stage pulmonary diseases.
The essential mitotic peptidyl-prolyl isomerase Pin1 binds and regulates mitosis-specific phosphoproteins (1998)

Phosphorylation of mitotic proteins on the Ser/Thr-Pro motifs has been shown to play an important role in regulating mitotic progression. Pin1 is a novel essential peptidyl-prolyl isomerase (PPIase) that inhibits entry into mitosis and is also required for proper progression through mitosis, but its substrate(s) and function(s) remain to be determined. Here we report that in both human cells and Xenopus extracts, Pin1 interacts directly with a subset of mitotic phosphoproteins on phosphorylated Ser/Thr-Pro motifs in a phosphorylation-dependent and mitosis-specific manner. Many of these Pin1-binding proteins are also recognized by the monoclonal antibody MPM-2, and they include the important mitotic regulators Cdc25, Myt1, Wee1, Plk1, and Cdc27. The importance of this Pin1 interaction was tested by constructing two Pin1 active site point mutants that fail to bind a phosphorylated Ser/Thr-Pro motif in mitotic phosphoproteins. Wild-type, but not mutant, Pin1 inhibits both mitotic division in Xenopus embryos and entry into mitosis in Xenopus extracts. We have examined the interaction between Pin1 and Cdc25 in detail. Pin1 not only binds the mitotic form of Cdc25 on the phosphorylation sites important for its activity in vitro and in vivo, but it also inhibits its activity, offering one explanation for the ability of Pin1 to inhibit mitotic entry. In a separate paper, we have shown that Pin1 is a phosphorylation-dependent PPIase that can recognize specifically the phosphorylated Ser/Thr-Pro bonds present in mitotic phosphoproteins. Thus, Pin1 likely acts as a general regulator of mitotic proteins that have been phosphorylated by Cdc2 and other mitotic kinases.
Inhibitors of sex hormones: development of experimental models. (1972)

Inhibitors of sex hormones and the development of experimental models are discussed. Compounds that inhibit the action of androgens and estrogens are defined, and the possible mechanisms of action presented are: 1) inhibition of hormone synthesis; 2) inhibition of uptake of hormone into target tissues; 3) inhibition of the retention of hormone in target tissues; 4) inhibition of the binding of hormone to nonenzyme macromolecules; and 5) inhibition of the metabolism of a hormone to a more active form. Effects of antiandrogen on skin such as hirsutism, sebum production, and acne are briefly covered. Methods of study included inhibition of in vitro metabolism of testosterone by human foreskin and the use of the hamster flank organ for the bioassay of antiandrogens.
Use of a Porcine Dermis Template to Enhance Widely Expanded Mesh Autologous Split-Thickness Skin Graft Growth (1997)

To answer the question whether a xenograft dermal substitute could enhance skin grafting, we used porcine dermis as a template for a widely expanded mesh autologous split-thickness skin (ASTS) graft in a rat model. Four groups of rats had received widely expanded meshed skin autografts to cover an excised back wound. Group 1 had a bed of autologous dermis, group 2 had porcine xenograft dermis, group 3 had widely expanded meshed autograft alone, and group 4 had no graft with the wound healing by contraction alone. Wounds were studied by clinical inspection for texture and contraction, and by histologic and immunofluorescent techniques. At 2 weeks, there was acceptable ASTS graft take, and most of the wound healed completely by 3 weeks. The integrity of this complex skin graft was maintained for 4 months but wound contraction gradually decreased overall wound size. Size was maintained better in the ASTS-autodermis and ASTS-xenodermis groups at postgraft 4, 5, and 6 weeks when compared with the ASTS graft, and there was no difference between the ASTS-autodermis and ASTS-xenodermis groups. Thus both allodermis and xenodermis provided a similar template to enhance widely expanded mesh skin growth and delay wound contraction. The pathologic studies indicate that the xenodermis collagen was replaced either by fibrosis or by biodegradation to rat collagen. The immunofluorescent study also reflected that anti-porcine antibody activity was hugely diminished in the ASTS-xenodermis graft wound after long-term follow-up. In conclusion, either autodermis or xenodermis enhances widely expanded mesh ASTS survival in a rat model, and could significantly maintain the original wound size better than ASTS graft without a template. In a long-term follow-up study, the porcine dermis was replaced either by fibrosis or biodegradation to rat dermis.
Investigation of the Lithiation and Delithiation Conversion Mechanisms of Bismuth Fluoride Nanocomposites (2006)

Combined in situ X-ray diffraction, in situ X-ray absorption spectroscopy, and selected area electron diffraction analyses have confirmed the occurrence of a reversible conversion reaction in the nanocomposite upon cycling, which leads to the formation of and LiF during lithiation and the reformation of during delithiation. It has been shown that only the high-pressure tysonite phase of reforms during the oxidation sweep and that no bismuth fluoride compound with an oxidation state of the bismuth lower than 3 is formed as intermediate during the lithiation or delithiation reactions. Finally, it has been demonstrated that the different plateaus or pseudo plateaus observed on the lithiation and delithiation voltage profiles stem from polarization changes brought about by the dramatic structural changes occurring in the nanocomposite upon cycling. A model, based on the variation of the electronic and ionic transport mechanisms as a function of the state of completion of the conversion and reconversion reactions, is proposed to explain those polarization changes.
Increased Plasma and Platelet to Red Blood Cell Ratios Improves Outcome in 466 Massively Transfused Civilian Trauma Patients (2008)

Current transfusion practices and survival rates of MT patients vary widely among trauma centers. Conventional MT guidelines may underestimate the optimal plasma and platelet to RBC ratios. Survival in civilian MT patients is associated with increased plasma and platelet ratios. Massive transfusion practice guidelines should aim for a 1:1:1 ratio of plasma:platelets:RBCs.
Evaluation of Watermelon and Related Species for Resistance to Race 1W Powdery Mildew (2007)

Powdery mildew [ Podosphaera xanthii (Castagne) Braun &amp; Shishkoff (syn. Sphaerotheca fuliginea auct. p.p.)] is now a common disease on watermelon [ Citrullus lanatus (Thunb.) Matsum. &amp; Nakai] in the United States. In this study, the entire available U.S. Plant Introduction collection of Citrullus Schrad. ex Eckl. &amp; Zeyh. species was evaluated for resistance to P. xanthii race 1W. The collection consists of four Citrullus species and one Praecitrullus Pangalo species [ C. lanatus var. citroides (L.H. Bailey) Mansf., C. colocynthis (L.) Schrad., C. rehmii De Winter, and P. fistulosus (Stocks) Pangalo]. Wild-type accessions tended to be more resistant more often than the cultivated species, C. lanatus var. lanatus . None were immune, eight of the 1573 accessions exhibited high levels of resistance, and another 86 demonstrated intermediate resistance. Stem and leaf disease severity were weakly correlated ( r 2 = 0.64, P = 0.001). The majority of accessions having resistance were collected in Zimbabwe. Resistance was found in four species.
Different missense mutations at the tissue-nonspecific alkaline phosphatase gene locus in autosomal recessively inherited forms of mild and severe hypophosphatasia. (1992)

Hypophosphatasia is a heritable form of rickets/osteomalacia with extremely variable clinical expression. Severe forms are inherited in an autosomal recessive fashion; the mode of transmission of mild forms is uncertain. The biochemical hallmark of hypophosphatasia is deficient activity of the tissue-nonspecific isozyme of alkaline phosphatase (TNSALP). Previously, we demonstrated in one inbred infant that an identical missense mutation in both alleles of the gene encoding TNSALP caused lethal disease. We have now examined TNSALP cDNAs from four unrelated patients with the severe perinatal or infantile forms of hypophosphatasia. Each of the eight TNSALP alleles from these four individuals contains a different point mutation that causes an amino acid substitution. These base changes were not detected in at least 63 normal individuals and, thus, appear to be causes of hypophosphatasia in the four patients. (Two additional base substitutions, found in one allele from each of the four patients, are linked polymorphisms.) Twenty-three unrelated patients (of 50 screened), who reflect the entire clinical spectrum of hypophosphatasia, possess one of our of the above eight mutations. In two of these additional patients, mild forms of the disease are also inherited in an autosomal recessive fashion. Our findings indicate that hypophosphatasia can be caused by a number of different missense mutations and that the specific interactions of different TNSALP mutant alleles are probably important for determining clinical expression. Severe forms, perinatal and infantile disease, are largely the result of compound heterozygosity for different hypophosphatasia alleles. At least some cases of childhood and adult hypophosphatasia are inherited as autosomal recessive traits.
Unsupervised Learning by Convex and Conic Coding (1996)

Unsupervised learning algorithms based on convex and conic encoders are proposed. The encoders find the closest convex or conic combination of basis vectors to the input. The learning algorithms produce basis vectors that minimize the reconstruction error of the encoders. The convex algorithm develops locally linear models of the input, while the conic algorithm discovers features. Both algorithms are used to model handwritten digits and compared with vector quantization and principal component analysis. The neural network implementations involve feedback connections that project a reconstruction back to the input layer. 1 Introduction Vector quantization (VQ) and principal component analysis (PCA) are two widely used unsupervised learning algorithms, based on two fundamentally different ways of encoding data. In VQ, the input is encoded as the index of the closest prototype stored in memory. In PCA, the input is encoded as the coefficients of a linear superposition of a set of basis ...
HIV-1 Protease Inhibitors (1997)

<h3>Objective.</h3> —The clinical care of people infected with human immunodeficiency virus (HIV) has been substantially affected by the introduction of HIV-specific protease inhibitors (Pis). The 4 Pls available are saquinavir mesylate, ritonavir, indinavir sulfate, and nelfinavir mesylate. Comparison studies have not been reported; therefore, an assessment of the available data to aid clinicians and patients in choosing appropriate treatment will be presented. <h3>Data Sources.</h3> —A systematic review of peer-reviewed publications, abstracts from national and international conferences, and product registration information through September 1996. <h3>Study Selection and Data Extraction.</h3> —Criteria used to select studies include their relevance to Pls, having been published in the English language, and pertinence for clinicians. Data quality and validity included the venue of the publication and relevance to clinical care. <h3>Data Synthesis.</h3> —Oral adminstration of ritonavir, indinavir, or nelfinavir generates sustainable drug serum levels to effectively inhibit the protease enzyme; however, saquinavir may not generate sustained levels necessary to inhibit the protease enzyme. Patients treated with ritonavir, indinavir, or nelfinavir experience similar reductions in viral load and increases in CD4<sup>+</sup>lymphocytes; smaller effects occur among those treated with saquinavir. Two randomized placebo-controlled studies conducted among patients with severe immune system suppression and substantial zidovudine treatment experience demonstrated reduced HIV disease progression and reduced mortality with PI treatment. Genotypic resistance to Pls occurs; the clinical relevance of resistance is unclear. The costs of these agents including required monitoring impose new and substantial costs. <h3>Conclusions.</h3> —The Pls have emerged as critical drugs for people with HIV infection. Optimal use involves combination with reverse transcriptase inhibitors. Resistance develops to each agent, and cross-resistance is likely. These agents must be used at full doses with attention to ensuring patient compliance. The expense of these agents may be offset by forestalling disease progression and death and returning people to productive life. Selecting the initial PI must be individualized, and factors to consider include proven activity, possible toxicities, dosing regimens, drug interactions, and costs.
Overcoming Translational Barriers in Acute Kidney Injury (2018)

AKI is a complex clinical condition associated with high mortality, morbidity, and health care costs. Despite improvements in methodology and design of clinical trials, and advances in understanding the underlying pathophysiology of rodent AKI, no pharmacologic agent exists for the prevention or treatment of AKI in humans. To address the barriers that affect successful clinical translation of drug targets identified and validated in preclinical animal models of AKI in this patient population, the National Institute of Diabetes and Digestive and Kidney Diseases convened the "AKI Outcomes: Overcoming Barriers in AKI" workshop on February 10-12, 2015. The workshop used a reverse translational medicine approach to identify steps necessary to achieve clinical success. During the workshop, breakout groups were charged first to design feasible, phase 2, proof-of-concept clinical trials for delayed transplant graft function, prevention of AKI (primary prevention), and treatment of AKI (secondary prevention and recovery). Breakout groups then were responsible for identification of preclinical animal models that would replicate the pathophysiology of the phase 2 proof-of-concept patient population, including primary and secondary end points. Breakout groups identified considerable gaps in knowledge regarding human AKI, our understanding of the pathophysiology of AKI in preclinical animal models, and the fidelity of cellular and molecular targets that have been evaluated preclinically to provide information regarding human AKI of various etiologies. The workshop concluded with attendees defining a new path forward to a better understanding of the etiology, pathology, and pathophysiology of human AKI.