gebhart/patrepeval huggingface dataset:
Characterization of Late Blight Resistance Derived from Solanum pimpinellifolium L3708 against Multiple Isolates of the Pathogen Phytophthora infestans (2006)

Sixteen tomato [ Solanum lycopersicum L. (syn. Lycopersicon esculentum Mill.)] genotypes (inbred lines or hybrids) were tested against five Phytophthora infestans (Mont.) deBary isolates to characterize race specificity of late blight resistance transferred to tomato from Solanum pimpinellifolium L. [syn. Lycopersicon pimpinellifolium (L.) Mill.] accession L3708. The effects of plant genotype, isolate, genotype × isolate, and isolate × replication interactions were highly significant ( P = 0.001). Set of four sister lines fixed for late blight resistance (CU-R lines) exhibited full and equal resistance to the five pathogen isolates tested. In contrast, the heterozygous F 1 hybrids, created by crossing the resistant CU-R lines with a susceptible parent, were resistant to US-11; partially resistant to US-17, NC-1, and DR4B; and susceptible to US-7. Differential responses were also observed across pathogen isolates on a set of resistant sister lines (CLN-R lines), which also were bred from L3708. The CLN-R lines were resistant to the DR4B, NC-1, and US-11 isolates, but showed significant disease-affected areas and sporangium numbers following inoculation with either US-7 or US-17. Restriction fragment length polymorphism (RFLP) analysis confirms that both CU-R and CLN-R are homozygous for the Ph-3 gene derived from L3708. Since progeny tests also confirmed that the CLN-R lines are fixed for their level of resistance, these results suggest that late blight resistance in the CU-R lines is not controlled by Ph-3 alone, and that at least one additional gene conferring late blight resistance is missing from the CLN-R lines. Results of genetic tests of the (CU-R × CLN-R) F 1 and a (CU-R × CLN-R) F 2 population with the pathogen isolate US-17 strongly support a model in which resistance of the CU-R lines requires genes in addition to Ph-3 . The implications of this information in breeding for late blight resistance and using of the resulting resistant lines or hybrids are discussed.
Human parainfluenza type 3 virus hemagglutinin-neuraminidase glycoprotein: nucleotide sequence of mRNA and limited amino acid sequence of the purified protein (1986)

The nucleotide sequence of mRNA for the hemagglutinin-neuraminidase (HN) protein of human parainfluenza type 3 virus obtained from the corresponding cDNA clone had a single long open reading frame encoding a putative protein of 64,254 daltons consisting of 572 amino acids. The deduced protein sequence was confirmed by limited N-terminal amino acid microsequencing of CNBr cleavage fragments of native HN that was purified by immunoprecipitation. The HN protein is moderately hydrophobic and has four potential sites (Asn-X-Ser/Thr) of N-glycosylation in the C-terminal half of the molecule. It is devoid of both the N-terminal signal sequence and the C-terminal membrane anchorage domain characteristic of the hemagglutinin of influenza virus and the fusion (F0) protein of the paramyxoviruses. Instead, it has a single prominent hydrophobic region capable of membrane insertion beginning at 32 residues from the N terminus. This N-terminal membrane insertion is similar to that of influenza virus neuraminidase and the recently reported structures of HN proteins of Sendai virus and simian virus 5.
Random early detection gateways for congestion avoidance (1993)

The authors present random early detection (RED) gateways for congestion avoidance in packet-switched networks. The gateway detects incipient congestion by computing the average queue size. The gateway could notify connections of congestion either by dropping packets arriving at the gateway or by setting a bit in packet headers. When the average queue size exceeds a present threshold, the gateway drops or marks each arriving packet with a certain probability, where the exact probability is a function of the average queue size. RED gateways keep the average queue size low while allowing occasional bursts of packets in the queue. During congestion, the probability that the gateway notifies a particular connection to reduce its window is roughly proportional to that connection's share of the bandwidth through the gateway. RED gateways are designed to accompany a transport-layer congestion control protocol such as TCP. The RED gateway has no bias against bursty traffic and avoids the global synchronization of many connections decreasing their window at the same time. Simulations of a TCP/IP network are used to illustrate the performance of RED gateways.< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">&gt;</ETX>
Transient Receptor Potential Melastatin 7–like Current in Human Head and Neck Carcinoma Cells: Role in Cell Proliferation (2007)

Ion channels are involved in normal physiologic processes and in the pathology of various diseases. In this study, we investigated the presence and potential function of transient receptor potential melastatin 7 (TRPM7) channels in the growth and proliferation of FaDu and SCC25 cells, two common human head and neck squamous carcinoma cell lines, using a combination of patch-clamp recording, Western blotting, immunocytochemistry, small interfering RNA (siRNA), fluorescent Ca(2+) imaging, and cell counting techniques. Although voltage-gated K(+) currents were recorded in all cells, none of FaDu cells express voltage-gated Na(+) or Ca(2+) currents. Perfusion of cells with NMDA or acidic solution did not activate inward currents, indicating a lack of NMDA receptor and acid-sensing channels. Lowering extracellular Ca(2+), however, induced a large nondesensitizing current reminiscent of Ca(2+)-sensing cation current or TRPM7 current previously described in other cells. This Ca(2+)-sensing current can be inhibited by Gd(3+), 2-aminoethoxydiphenyl borate (2-APB), or intracellular Mg(2+), consistent with the TRPM7 current being activated. Immunocytochemistry, Western blot, and reverse transcription-PCR detected the expression of TRPM7 protein and mRNA in these cells. Transfection of FaDu cells with TRPM7 siRNA significantly reduced the expression of TRPM7 mRNA and protein as well as the amplitude of the Ca(2+)-sensing current. Furthermore, we found that Ca(2+) is critical for the growth and proliferation of FaDu cells. Blockade of TRPM7 channels by Gd(3+) and 2-APB or suppression of TRPM7 expression by siRNA inhibited the growth and proliferation of these cells. Similar to FaDu cells, SCC25 cells also express TRPM7-like channels. Suppressing the function of these channels inhibited the proliferation of SCC25 cells.
Novel approaches in the treatment of ankylosing spondylitis and other spondyloarthritides (2003)

The therapeutic options for patients suffering from severe forms of spondyloarthritis (SpA) have been rather limited in recent decades. There is now accumulating evidence that anti-TNF therapy is highly effective in SpA, especially in ankylosing spondylitis (AS) and psoriatic arthritis (PsA). Based on the data recently published on what is now several hundred AS and PsA patients, this treatment seems to be even more effective than the same therapy in rheumatoid arthritis (RA). The anti-TNF-α agents currently available, infliximab (Remicade®; Centocor), etanercept (Enbrel®; Amgen) and adalimumab (Humira™; Abbott), are approved for the treatment of RA in the US; infliximab and etanercept are approved in Europe. The situation in SpA is different to RA because there is an unmet medical need, especially in AS, since no therapies with disease-controlling antirheumatic drugs are available for severely affected patients, especially with spinal disease. Thus, TNF blockers might even be considered as first-line immunosuppressive agents in patients with active AS and PsA who are not sufficiently treated by non-steroidal anti-inflammatory drugs and sulfasalazine, if peripheral arthritis is present. For infliximab, a dosage of 5 mg/kg at intervals between 6 and 12 weeks was necessary to constantly suppress disease activity; this is also a major aim of long-term treatment. No dose-finding studies have yet been performed. The standard dose of etanercept is 25 mg s.c. twice-weekly. No studies on adalimumab (standard RA dose 20 – 40 mg s.c. every 2 weeks) have yet been conducted in SpA. The efficacy of etanercept was first demonstrated in PsA and etanercept is now approved for this indication. A double-blind study has also been performed in AS, with similarly clearcut efficacy. There is preliminary evidence that both agents do also work in other SpA such as undifferentiated SpA. Infliximab has recently been approved for short-term treatment of severe uncontrolled AS; the approval for etanercept is pending. Studies should be performed to document the long-term efficacy of this treatment. There is hope that ankylosis might be preventable but it remains to be shown whether patients benefit from long-term anti-TNF therapy and whether radiological progression and ankylosis can be stopped. Severe adverse events have remained rare. Complicated infections including tuberculosis have been reported. Tuberculosis can be mostly prevented if patients are checked for previous contact with tuberculosis. Currently, the benefits of anti-TNF therapy in AS seem to outweigh these shortcomings.
Optomechatronic System for Position Detection of a Mobile Mini-Robot (2005)

This paper presents an optomechatronic system which can detect, by triangulation, the position of a light point source, fastened onto a robot part. The sensing system consists of two positioning modules for optical transducers, which automatically follow the direction of the light point source. The system control is accomplished by means of data acquisition boards and LabVIEW programming.
ATP13A2 missense mutations in juvenile parkinsonism and young onset Parkinson disease (2007)

We confirm that ATP13A2 homozygous mutations are associated with human parkinsonism, and expand the associated genotypic and clinical spectrum, by describing a homozygous missense mutation in this gene in a patient with a phenotype milder than that initially associated with ATP13A2 mutations (Kufor-Rakeb syndrome). Our data also suggest that ATP13A2 single heterozygous mutations might be etiologically relevant for patients with YOPD and further studies of this gene in Parkinson disease are warranted.
DXplain. An evolving diagnostic decision-support system (1987)

DXplain is an evolving computer-based diagnostic decision-support system designed for use by the physician who has no computer expertise. DXplain accepts a list of clinical manifestations and then proposes diagnostic hypotheses. The program explains and justifies its interpretations and provides access to a knowledge base concerning the differential diagnosis of the signs and symptoms. DXplain was developed with the support and cooperation of the American Medical Association. The system is distributed to the medical community through AMA/NET--a nationwide computer communications network sponsored by the American Medical Association--and through the Massachusetts General Hospital Continuing Education Network. A key element in the distribution of DXplain is the planned collaboration with its physician-users whose comments, criticisms, and suggestions will play an important role in modifying and enhancing the knowledge base.
Apoptotic signaling through CD95 (Fas/Apo-1) activates an acidic sphingomyelinase. (1994)

Intracellular pathways leading from membrane receptor engagement to apoptotic cell death are still poorly characterized. We investigated the intracellular signaling generated after cross-linking of CD95 (Fas/Apo-1 antigen), a broadly expressed cell surface receptor whose engagement results in triggering of cellular apoptotic programs. DX2, a new functional anti-CD95 monoclonal antibody was produced by immunizing mice with human CD95-transfected L cells. Crosslinking of CD95 with DX2 resulted in the activation of a sphingomyelinase (SMase) in promyelocytic U937 cells, as well as in other human tumor cell lines and in CD95-transfected murine cells, as demonstrated by induction of in vivo sphingomyelin (SM) hydrolysis and generation of ceramide. Direct in vitro measurement of enzymatic activity within CD95-stimulated U937 cell extracts, using labeled SM vesicles as substrates, showed strong SMase activity, which required pH 5.0 for optimal substrate hydrolysis. Finally, all CD95-sensitive cell lines tested could be induced to undergo apoptosis after exposure to cell-permeant C2-ceramide. These data indicate that CD95 cross-linking induces SM breakdown and ceramide production through an acidic SMase, thus providing the first information regarding early signal generation from CD95, and may be relevant in defining the biochemical nature of intracellular messengers leading to apoptotic cell death.
N-Arylsulfonyl Hydrazones as Inhibitors of IMP-1 Metallo-β-Lactamase (2002)

Members of a family of N-arylsulfonyl hydrazones have been identified as novel inhibitors of IMP-1, a metallo-beta-lactamase of increasing prevalence. Structure-activity relationship studies have indicated a requirement for bulky aromatic substituents on each side of the sulfonyl hydrazone backbone for these compounds to serve as efficient inhibitors of IMP-1. Molecular modeling has provided insight into the structural basis for the anti-metallo-beta-lactamase activity exhibited by this class of compounds.
Amelioration of Ischemic Acute Renal Injury by Neutrophil Gelatinase-Associated Lipocalin (2004)

Acute renal failure secondary to ischemic injury remains a common problem, with limited and unsatisfactory therapeutic options. Neutrophil gelatinase-associated lipocalin (NGAL) was recently shown to be one of the maximally induced genes early in the postischemic kidney. In this study, the role of NGAL in ischemic renal injury was explored. Intravenous administration of purified recombinant NGAL in mice resulted in a rapid uptake of the protein predominantly by proximal tubule cells. In an established murine model of renal ischemia-reperfusion injury, intravenous NGAL administered before, during, or after ischemia resulted in marked amelioration of the morphologic and functional consequences, as evidenced by a significant decrease in the histopathologic damage to tubules and in serum creatinine measurements. NGAL-treated animals also displayed a reduction in the number of apoptotic tubule cells and an increase in proliferating proximal tubule cells after ischemic injury. The results indicate that NGAL may represent a novel therapeutic intervention in ischemic acute renal failure, based at least in part on its ability to tilt the balance of tubule cell fate toward survival.
Is Phentolamine Stable in Solution with Papaverine (1988)

Although the intracorporeal injection of mixtures of phentolamine and papaverine is used commonly in the diagnosis and treatment of erectile dysfunction, pharmacological data relating to the stability of such drug mixtures are lacking. The stability of phentolamine mesylate in aqueous solution and in solution with papaverine (0.83 mg. per cc phentolamine and 25 mg. per cc papaverine) was ascertained by high performance liquid chromatography and gas chromatography with mass spectrometry. No degradation of phentolamine occurred during 40 days whether the drug or drug combination was refrigerated or stored at room temperature. Phentolamine is stable for at least 40 days when mixed with papaverine.
An achievable rate of large block-fading MIMO systems with no CSI via successive decoding (2010)

A Rayleigh block-fading multiple-input multiple-output (MIMO) channel with channel state information (CSI) available neither to the transmitter nor to the receiver is considered. A lower bound on the capacity is formulated based on a successive decoding (SD) scheme. An analytical expression of the lower bound is derived in the large-system limit, by using the replica method. Furthermore, the achievable rate of the linear minimum mean-squared error (LMMSE) receiver with SD is also evaluated in the large-system limit. The lower bound is superior to the lower bound derived by Hassibi and Hochwald for all signal-to-noise ratios (SNRs).
Benign Prostatic Hyperplasia In A Transgenic Mouse: A New Hormonally Sensitive Investigatory Model (1993)

Recent advances in molecular biology have enabled incorporation of proto-oncogenes into the mouse germline. In this study we use a transgenic mouse line that overexpresses the fibroblastic growth factor (FGF) family member, int-2, under the control of mouse mammary tumor virus (MMTV) regulatory elements. One of the tissues targeted by MMTV is the mouse prostate. Expression of the MMTV-int-2 transgene in male transgenic mouse carriers results in a dramatic enlargement of the prostate gland which on histologic examination closely resembles the epithelial/glandular BPH observed in human and canine models. Pre- and postpubertal transgenic (NR) and wild-type (WT) FVB/N male mice were evaluated for the effects of hormonal manipulation by orchiectomy and orchiectomy followed by androgen replacement. Orchiectomy results in a significant decrease in size of the prostate in both NR and WT mice (p < 0.05), regardless of sexual maturity. Exogenous hormonal replacement with testosterone or dihydrotestosterone following orchiectomy results in significant regrowth of the prostate in both NR and WT mice. Flutamide, a potent nonsteroidal anti-androgen, resulted in a 55% reduction in size of the NR prostate (p < 0.002) and a similar 44% reduction in size of the WT prostate. Similarly, treatment of both NR and WT mice with leuprolide, a GnRH agonist, resulted in a significant decrease in prostate size (p < 0.05). Treatment of both NR and WT mice with finasteride (MK-906), a 5-alpha reductase inhibitor, failed to produce any significant regression in prostatic tissue. Based upon these data, we conclude that this transgenic mouse model, expressing int-2, produces an epithelial BPH histologically similar to other animal models. This transgenic model is hormonally sensitive and appears to represent a unique model for the investigation of BPH and growth factor induced epithelial cell hyperplasia.
An Inflammatory Pathomechanism for Parkinsons Disease? (2006)

Parkinson's disease (PD) is a slowly progressive neurodegenerative disorder characterized by the loss of dopaminergic neurons in the Substantia Nigra pars compacta (SNpc), striatal dopamine deficiency and appearance of Lewy bodies. Inflammatory and immune, or even autoimmune, stigmata, have been described in post-mortem brains of PD patients. Although disputed in humans, a reactive astrocytosis and a lymphocytic infiltration in the SNpc have been observed in animal models of PD, which need further examination. This review summarizes the current knowledge on brain inflammation in humans with PD, and how inflammation and/or (auto)immune reactions within the SNpc could be linked to other pathophysiological mechanisms that have been hypothesized for the etiology of PD, such as oxidative stress, exposure to neurotoxins, and post-infectious or post-traumatic injuries. In particular, we discuss how microglial cells could be activated during the course of PD, and present a new hypothesis that PD-linked protein (alpha-synuclein, in particular) aggregates could be implicated in their activation, to induce a chronic and sustained inflammation involved in the progression, at least, of the disease. The current status of anti-inflammatory agents, either already tried in PD clinical trials or putatively usefull as adjuvant therapies for PD, is also discussed.
3-D object reconstruction using spatially extended voxels and multi-hypothesis voxel coloring (2002)

We describe a voxel-based 3-D reconstruction technique from multiple calibrated camera views that makes explicit use of the finite size footprint of a voxel when projected into the image plane. We derive a class of computationally efficient axis-aligned volume traversal orders that ensure that a processed voxel cannot occlude previously processed voxels. For each view, one out of 79 different cases of volume traversal is identified depending on the relative position between camera and voxel volume. Views belonging to the same visibility class can be processed simultaneously. Our voxel coloring strategy is based on a color hypothesis test that ensures the consistency of the projected reconstruction with the original images. A surface voxel list is constantly updated during reconstruction ensuring that only a minimum number of voxels has to be processed. Experimental results that compare the reconstruction quality for voxels with and without spatial extent underscore the conclusion that it is worthwhile taking into account the exact footprint of the projected voxels.
IL-15Rα Is a Negative Regulator of TCR-Activated Proliferation in CD4+ T Cells (2004)

Although IL-15 is known to be a T cell growth factor, the function in T cells of IL-15Ralpha, its high affinity receptor, remains unclear. We found that murine IL-15Ralpha(-/-) CD4(+) T cells hyperproliferated in response to TCR stimulation, in vitro and in vivo, and displayed a lower TCR activation threshold than wild-type CD4(+) T cells. TCR-induced activation of Zap70 and of the phospholipase C-gamma1-NFATp, Ras-ERK-c-Fos, and Rac-JNK-c-Jun pathways was all augmented in IL-15Ralpha(-/-) CD4(+) T cells. This in turn led to earlier IL-2Ralpha induction and higher IL-2 production, which most likely contribute to the hyperproliferation of IL-15Ralpha(-/-) CD4(+) T cells. Exogenous IL-15 reduced levels of TCR-activated signals, transcription factors, IL-2, and IL-2Ralpha, and division in wild-type CD4(+) T cells. These results reveal IL-15Ralpha to be a negative regulator for CD4(+) T cell activation and demonstrate a novel layer of regulation of TCR signaling by a cytokine system.
Novel mutations in the CLN6 gene causing a variant late infantile neuronal ceroid lipofuscinosis (2003)

The neuronal ceroid lipofuscinoses (NCLs) are a heterogeneous group of autosomal recessive neurodegenerative diseases comprising Batten and other related diseases plus numerous variants. They are characterized by progressive neuronal cell death. The CLN6 gene was recently identified, mutations in which cause one of the variant late infantile forms of NCL (vLINCL). We describe four novel mutations in the CLN6 gene. This brings the total number of CLN6 mutations known to 11 in 38 families. This suggests that the CLN6 gene may be highly mutable. An American patient of Irish/French/Native American origin was heterozygous for a 4-bp insertion (c.267_268insAACG) in exon 3. The other allele had a point mutation (c.898T>C) in exon 7 resulting in a W300R amino acid change. Two Trinidadian siblings of Indian origin were homozygous for a mutation at the 5' donor splice site of exon 4 (IVS4+1G>T), affecting the first base of the invariant GT at the beginning of intron 4. The fourth novel mutation, a double deletion of 4 bp and 1 bp in exon 7 (c.829_832delGTCG;c.837delG), was identified in a Portuguese patient heterozygous for the I154del Portuguese CLN6 mutation. Four of the 11 mutations identified are in exon 4. Three Portuguese patients with clinical profiles similar to CLN6 patients without defects in CLN6 or other known NCL genes are described. We conclude the following: 1) the CLN6 gene may be a highly mutable gene; 2) exon 4 must code for a segment of the protein crucial for function; 3) vLINCL disease in Portugal is genetically heterogeneous; 4) the I154del accounts for 81.25% of affected CLN6 Portuguese alleles; and 5) three vLINCL Portuguese patients may have defects in a new NCL gene.