gebhart/patrepeval huggingface dataset:
Differential Expression of Voltage-Gated K + Channel Genes in Left Ventricular Remodeled Myocardium After Experimental Myocardial Infarction (1996)

Left ventricular (LV) remodeling after experimental myocardial infarction (MI) is associated with hypertrophy of noninfarcted myocardium and electrophysiological alterations. We have recently shown that post-MI hypertrophied LV myocytes have prolonged action potential duration (APD) and generate triggered activity from early afterdepolarizations. The prolonged APD was attributed to decreased density of the two outward K+ currents, I(to)-fast (I(to)-f) and I(to)-slow (I(to)-s), rather than changes in the density and/or kinetics of the L-type Ca2+ current. The changes in ionic current density may be related to alterations in the expression and levels of ion channel proteins. To test this hypothesis, rats underwent either left anterior descending coronary artery (LAD) ligation (post-MI group [n = 10]) or sham surgery (sham group [n = 10]). Three weeks later transcripts from the noninfarcted LV myocardium in the post-MI group (n = 6) and LV myocardium of the sham group (n = 6) were analyzed by RNase protection assay. Expressions of five K+ channel subunit mRNAs (Kv1.2, Kv1.4, Kv1.5, Kv2.1, and Kv4.2) reported in the rat ventricle were analyzed. Compared with the sham group, expressions of Kv1.4, Kv2.1 (putative I(to)-s), and Kv4.2 (putative I(to)-f) channel subunit mRNAs were significantly decreased by 60% (P < .03), 54% (P < .005), and 53% (P < .002), respectively, in the post-MI group. There was no significant change in the Kv1.2 and Kv1.5 mRNA levels. Western blotting demonstrated a similar decrease in the Kv2.1 and Kv4.2 immunoreactive protein levels (43% [P < .03] and 67% [P < .003], respectively [n = 4]) and no significant change in Kv1.5 immunoreactive protein level. Our results strongly correlate with the electrophysiological findings in this model and show that transcriptional regulation in the post-MI remodeled rat LV is distinct for each voltage-gated K+ channel subunit. These findings provide, at least in part, the molecular basis for the electrophysiological alterations observed in this model.
Selective serotonin reuptake inhibitor discontinuation syndrome: proposed diagnostic criteria. (2000)

Findings were used to construct diagnostic criteria for the SSRI discontinuation syndrome. These criteria are 2 or more of the following symptoms developing within 1 to 7 days of discontinuation or reduction in dosage of an SSRI after at least 1 month's use, when these symptoms cause clinically significant distress or impairment and are not due to a general medical condition or recurrence of a mental disorder: dizziness, light-headedness, vertigo or feeling faint; shock-like sensations or paresthesia; anxiety; diarrhea; fatigue; gait instability; headache; insomnia; irritability; nausea or emesis; tremor; and visual disturbances.
Intralesional interferon-alpha therapy in advanced malignant melanoma (1988)

Fifty-one evaluable patients with histologically proven metastatic melanoma and at least one skin metastasis were treated intralesionally with interferon-alpha (IFN-alpha). Twenty-six of the patients were given highly purified natural IFN-alpha 6 Mio. IU three times per week. Twenty-five patients were given 10 Mio. IU three times per week of a recombinant IFN-alpha 2b (rIFN-alpha 2b). All patients were examined for systemic and local responses to this treatment. The systemic responses consisted of nine objective remissions, each of which lasted from 2 to 18 or more months. There were 24 complete or partial local responses. Forty-two of the 51 patients had at least two skin metastases so that IFN-injected and noninjected tumor sites could be compared. The difference between systemic and local efficacy was highly significant statistically (P = 0.0004). The results show that IFN-alpha has clinically observable antitumor activity in malignant melanoma.
Redox Control of Cell Cycle Progression via Cdc25 Phosphatase (Mih1p) in S. cerevisiae (2006)

Cdc25 phosphatases are key regulators of the eukaryotic cell cycle through their activation of the cyclin-dependent protein kinases (Cdk/Cyclins).1,2 Additionally the Cdc25 phosphatases, by their phosphorylation and subsequent degradation or sequestration, play an important role in integrating the signals of checkpoint control.3 Like other members of the protein tyrosine phosphatase family, Cdc25s are also directly and reversibly inhibited by oxidation.4,5 The initial oxidation product, the sulfenic acid of the active site cysteine, is rapidly and effectively trapped as an intramolecular disulfide by a so-called backdoor cysteine. This backdoor cysteine is conserved in all known Cdc25s as part of the Cdc25-homology domain A (CH2-A).6 Because the backdoor cysteine is located deep within the protein, the active site loop undergoes a major rearrangement during oxidation. The resulting intramolecular disulfide is buried and substrate binding and phosphatase activity is precluded.7 A new pocket next to the active site emerges to allow for ready access by thioredoxin, an efficient and physiologically relevant reductant for the Cdc25 phosphatases. In the yeast S. cerevisiae, the Cdc25 phosphatase homolog is Mih1p, which in the absence of one of two negative regulators (Hsl1p or Hsl7p) of the opposing kinase (Swe1p), is essential for normal growth due to Swe1p-mediated hyper-phosphorylation of the Cdk/Cyclins.8 This block in cell cycle progression is readily observable under the microscope as hyphal cell growth. Herein we use S. cerevisiae as a model organism to investigate the in vivo importance of Mih1p oxidation and the role of the backdoor cysteine (Cys270).
Incidence and characteristics of pain in a sample of medical-surgical inpatients (1987)

The purposes of this study were to determine the incidence and characteristics of pain in hospitalized patients and to explore the type and perceived effectiveness of pharmacologic and nonpharmacologic therapies. Three hundred and fifty-three randomly selected patients reported experiencing pain during this hospitalization; 58% of these patients experienced excruciating pain. Fewer than half of the patients with pain had a member of the health care team ask them about their pain or note the pain in the patient record. The methods perceived as most effective in decreasing pain were analgesics, sleep, immobilization and distraction. As in earlier studies, the dose of analgesic administered over a 24-h period was less than a quarter of the amount ordered. This study concluded that (1) pain in hospitalized patients is more prevalent than has previously been reported, (2) patients with pain continue to receive inadequate dosages of analgesics, and (3) the identification and treatment of patients with pain remains a significant health care problem.
Systematic High-Content Proteomic Analysis Reveals Substantial Immunologic Changes in Colorectal Cancer (2008)

The immune system is a significant determinant of epithelial tumorigenesis, but its role in colorectal cancer pathogenesis is not well understood. The function of the immune system depends upon the integrity of the protein network environment, and thus, we performed MELC immunofluorescence microscopy focusing on the lamina propria. By analyzing structurally intact tissues from colorectal cancer, ulcerative colitis, and healthy colonic mucosa, we used this unique and novel highly multiplexed robotic-imaging technology, which allows visualizing dozens of proteins simultaneously, and explored the toponome in colorectal cancer mucosa for the first time. We identified 1,930 motifs that distinguish control from colorectal cancer tissue. In colorectal cancer, the number of activated T cells is increased, explained by a lack of bax, caspase-3, and caspase-8. Whereas CD4(+)CD25(+) T cells are decreased and are, other than in ulcerative colitis, not activated, cytotoxic T cells are significantly increased in colorectal cancer. Furthermore, the number of activated human lymphocyte antigen (HLA)-DR(+) T-cells is increased in colorectal cancer, pointing to an altered antigen presentation. In colorectal cancer, CD3(+)CD29(+) expression and assembly of the LFA-1 and LFA-3 receptor are differentially changed, indicating a distinct regulation of T-cell adhesion in colorectal cancer. We also identified increased numbers of natural killer and CD44(+) cells in the colorectal cancer mucosa and nuclear factor-kappaB as regulator of apoptosis in these cell populations. High-content proteomic analysis showed that colorectal cancer induces a tremendous modification of protein expression profiles in the lamina propria. Thus, topological proteomic analysis may help to unravel the role of the adaptive immune system in colorectal cancer and aid the development of new antitumor immunotherapy approaches.
Factor XIII‐mediated cross‐linking of NH2‐terminal peptide of α2‐plasmin inhibitor to fibrin (1983)

The NH2-terminal 12-residue peptide of alpha 2-plasmin inhibitor, Asn-Gln-Glu-Gln-Val-Ser-Pro-Leu-Thr-Gly-Leu-Lys-NH2 . AcOH, was found to be a good substrate for plasma transglutaminase (activated blood coagulation factor XIII) and rapidly incorporated into fibrin by the enzyme. A high concentration of the peptide inhibited the enzyme-mediated cross-linking of alpha 2-plasmin inhibitor to fibrin probably by competing with the inhibitor for the same site of fibrin alpha-chain.
Altered Profiles of Estradiol and Progesterone Associated with Prolonged Estrous Cycles and Persistent Vaginal Cornification in Aging C578L/6J Mice1 (1981)

Midday plasma concentrations of estradiol (E2) and progesterone (P) were measured in aging C57BL/6J mice showing either prolonged estrous cycles or persistent vaginal cornification (PVC). In younger mice (5.5-7.5 months), the modal cycle length was 4 days, and the profiles of these hormones during the cycle were similar to those previously reported. By 10-12.5 months, the modal cycle length had increased to 5 days. Although midday levels of P were unimpaired at this age, the profile of E2 was markedly altered. Proestrus (Day 1) and estrus (Day 2) levels of E2 were indistinguishable from those of younger mice, but basal values on Day 3 and the preovulatory rise beginning on Day 4 were reduced in older mice by 80% and 45%, respectively. As a result, attainment of preovulatory levels of E2 equivalent to those of younger mice was delayed by about 1 day, which corresponded to the average net increase in median cycle length at this age. In 14-month-old PVC mice, levels of E2 were comparable to the basal values of younger cycling mice and threefold greater than ovariectomized values. However, P levels were 50% lower than basal values in cycling mice and indistinguishable from values in ovariectomized mice. Consequently, the E2:P ratio was elevated nearly twofold in PVC mice. Because transient experimental suppression of the preovulatory rise of E2 lengthens estrous cycles in young rodents, we hypothesize that the delayed rise of E2 in older mice contributes to their prolonged cycles. In addition, the increased E2:P ratio in PVC mice creates a relatively unopposed estrogenic milieu which may accelerate the development of the pituitary tumors and hypothalamic dysfunction that characterize aged female mice.
Respect the implementation: Using NI myRIO in undergraduate control education (2016)

In this paper we present, due to it's low-cost, portability, and high-functionality, the National Instruments (NI) myRIO as an excellent platform for hands-on in systems and control education, from advanced to beginner courses. That said, implementing control algorithms by the beginner, especially, is not to be taken lightly on digital platforms like the myRIO. We show, using a simple electric circuit as a plant, how a student can get some catastrophic results when implementing even a simple proportional controller. These catastrophic results stem partially from discretization choice, determinism of the sampling rate, and sampling rate limitations. Throughout the paper we discuss how to enhance determinism and prevent catastrophic results by being aware of your hardware's limitations.
Clinical-pathological correlations of coronary disease progression and regression. (1992)

The initiation of atherosclerosis may result from blood flow oscillatory shear stress in certain vascular sites (bending points, bifurcations, etc.) producing chronic minimal injury resulting in functional alteration of the arterial endothelium type I injury; experimentally, this is potentiated by atherogenic risk factors such as hypercholesterolemia, hypertension, immunocomplexes, viral infections, and tobacco smoke. Such minimal injury leads to accumulation of lipid and monocytes (macrophages), and subsequently, toxic products released by the macrophages produce damage of the intimal surface with denuding endothelium type II injury or damage, which attracts platelets; all of these cells release growth factors, prompting migration and proliferation of smooth muscle cells and producing a "fibro-intimal lesion" or the outside of the capsule of a predominant "lipid lesion." The lipid lesions surrounded by a thin capsule tend to be small and rupture easily, causing type III injury or damage; that is, they are soft and weak, contain large numbers of macrophages, which may release collagenase and elastase to form abscesses, and by their location, are under the effect of flow shear forces. After plaque disruption there is thrombus formation; when thrombi are small, they can become organized and contribute to the growth of the atherosclerotic plaque; when thrombi are large and occlusive, they lead to the acute coronary syndromes. New data suggest that, at the time of plaque disruption, certain "thrombogenic" risk factors modulate the degree of thrombogenicity and, thereby, the growth of the plaque versus the various acute coronary syndromes. Aside from the need for better understanding of the basic biology of atherogenesis, emphasis on identifying and modifying the primary atherogenic and thrombogenic risk factors should continue for primary prevention. Also, new approaches should focus on the identification, stabilization, and regression of the small "lipid plaques" prone to rupture (these are not necessarily angiographically apparent), as well as on the use of better and safer antithrombotic agents for prevention of progression.
DNA stability in plant tissues: implications for the possible transfer of genes from genetically modified food (2000)

The potential for transfer of antibiotic resistance genes from genetically modified (GM) plant material to microbes through genetic recombination in the human or animal gut is a consideration that has engendered caution in the use of GM foods. This study was aimed at defining the optimal physical and chemical conditions necessary to ensure sufficient fragmentation of DNA in plant tissues to a size where it would be unlikely to be stably transferred to bacterial gut microflora. The ribulose 1,5-bisphosphate carboxylase/oxygenase small subunit (Rubisco SS) genes are of similar size (approximately 1.4 kb) to transgenes present in GM plants. DNA analysis and PCR amplification of Rubisco SS genes showed that fresh maize and maize silage contained high molecular weight DNA and intact Rubisco SS genes. Relatively high temperatures and pressurised steam were necessary to degrade fully genomic DNA and Rubisco SS genes in maize and wheat grains, the source of most animal feedstuffs. Furthermore, chemical expulsion and extrusion of oilseeds resulted in residues with completely degraded genomic DNA. These results imply that stringent conditions are needed in the processing of GM plant tissues for feedstuffs to eliminate the possibility of transmission of transgenes.
A molecule containing the OWOWO unit. Synthesis, structure and spectroscopy of hexaneopentylditungsten trioxide (1984)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTA molecule containing the OWOWO unit. Synthesis, structure and spectroscopy of hexaneopentylditungsten trioxideIrene Feinstein-Jaffe, Dan Gibson, Stephen J. Lippard, Richard R. Schrock, and Alan SpoolCite this: J. Am. Chem. Soc. 1984, 106, 21, 6305–6310Publication Date (Print):October 1, 1984Publication History Published online1 May 2002Published inissue 1 October 1984https://pubs.acs.org/doi/10.1021/ja00333a032https://doi.org/10.1021/ja00333a032research-articleACS PublicationsRequest reuse permissionsArticle Views215Altmetric-Citations63LEARN ABOUT THESE METRICSArticle Views are the COUNTER-compliant sum of full text article downloads since November 2008 (both PDF and HTML) across all institutions and individuals. These metrics are regularly updated to reflect usage leading up to the last few days.Citations are the number of other articles citing this article, calculated by Crossref and updated daily. Find more information about Crossref citation counts.The Altmetric Attention Score is a quantitative measure of the attention that a research article has received online. Clicking on the donut icon will load a page at altmetric.com with additional details about the score and the social media presence for the given article. Find more information on the Altmetric Attention Score and how the score is calculated. Share Add toView InAdd Full Text with ReferenceAdd Description ExportRISCitationCitation and abstractCitation and referencesMore Options Share onFacebookTwitterWechatLinked InRedditEmail Other access optionsGet e-AlertscloseSupporting Info (1)»Supporting Information Supporting Information Get e-Alerts
Current Reversal in Asymmetric Pumping (1995)

Particles in an asymmetric structure can be transported over macroscopic distances without any large-scale force requirement provided energy is dissipated. We show here that the transport direction is determined both by time characteristics and potential shape.
Antigen-specific vaccines for cancer treatment (2014)

Vaccines targeting pathogens are generally effective and protective because based on foreign non-self antigens which are extremely potent in eliciting an immune response. On the contrary, efficacy of therapeutic cancer vaccines is still disappointing. One of the major reasons for such poor outcome, among others, is the difficulty of identifying tumor-specific target antigens which should be unique to the tumors or, at least, overexpressed on the tumors as compared to normal cells. Indeed, this is the only option to overcome the peripheral immune tolerance and elicit a non toxic immune response. New and more potent strategies are now available to identify specific tumor-associated antigens for development of cancer vaccine approaches aiming at eliciting targeted anti-tumor cellular responses. In the last years this aspect has been addressed and many therapeutic vaccination strategies based on either whole tumor cells or specific antigens have been and are being currently evaluated in clinical trials. This review summarizes the current state of cancer vaccines, mainly focusing on antigen-specific approaches.
Oxidative stress in HIV demented patients and protection ex vivo with novel antioxidants (2003)

Increased oxidative stress is present in brain and CSF of HIV-infected patients. There is also an accumulation of toxic substances in the CSF that are capable of inducing oxidative stress. The authors have identified several novel compounds that are capable of blocking the CSF-induced toxicity, the therapeutic potential of which is worthy of further exploration.
Impact of Visual Cues on Directional Benefit and Preference: Part I—Laboratory Tests (2009)

These results suggest that AO laboratory testing overestimates the DIR benefit and preference for DIR processing that hearing aid users may have in most face-to-face conversations in typical SNR, real-world environments. Additionally, because the DIR benefit measured in the AV condition cannot be predicted by the benefit score obtained from traditional AO laboratory testing, the effect of visual cues should be considered in establishing a valid laboratory/clinical environment and protocol for DIR microphone hearing aid testing. In light of these findings, consultations should be provided for hearing aid users with superior lipreading skills to help them adjust their expectations regarding the possibly small perceivable benefit gained from DIR microphone hearing aids.
Asymptotic Spectral Efficiency of the Uplink in Spatially Distributed Wireless Networks with Multi-Antenna Base Stations (2013)

The spectral efficiency of a representative uplink of a given length, in interference-limited, spatially-distributed wireless networks with hexagonal cells, simple power control, and multiantenna linear Minimum-Mean-Square-Error receivers is found to approach an asymptote as the numbers of base-station antennas N and wireless nodes go to infinity. An approximation for the area-averaged spectral efficiency of a representative link (averaged over the spatial base-station and mobile distributions), for Poisson distributed base stations, is also provided. For large N, in the interference-limited regime, the area-averaged spectral efficiency is primarily a function of the ratio of the product of N and the ratio of base-station to wireless-node densities, indicating that it is possible to scale such networks by linearly increasing the product of the number of base-station antennas and the relative density of base stations to wireless nodes, with wireless-node density. The results are useful for designers of wireless systems with high inter-cell interference because it provides simple expressions for spectral efficiency as a function of tangible system parameters like base-station and wireless-node densities, and number of antennas. These results were derived combining infinite random matrix theory and stochastic geometry.
Will Mobile Computing's Future Be Location, Location, Location? (2009)

As mobile computing has been more widely adopted in recent years, proponents have said location-based services could have a bright future. However, LBS has failed to take off in the marketplace yet.
Antisense DNAs as multisite genomic modulators identified by DNA microarray (2001)

Antisense oligodeoxynucleotides can selectively block disease-causing genes, and cancer genes have been chosen as potential targets for antisense drugs to treat cancer. However, nonspecific side effects have clouded the true antisense mechanism of action and hampered clinical development of antisense therapeutics. Using DNA microarrays, we have conducted a systematic characterization of gene expression in cells exposed to antisense, either exogenously or endogenously. Here, we show that in a sequence-specific manner, antisense targeted to protein kinase A RIalpha alters expression of the clusters of coordinately expressed genes at a specific stage of cell growth, differentiation, and activation. The genes that define the proliferation-transformation signature are down-regulated, whereas those that define the differentiation-reverse transformation signature are up-regulated in antisense-treated cancer cells and tumors, but not in host livers. In this differentiation signature, the genes showing the highest induction include genes for the G proteins Rap1 and Cdc42. The expression signature induced by the exogenously supplied antisense oligodeoxynucleotide overlaps strikingly with that induced by endogenous antisense gene overexpression. Defining antisense DNAs on the basis of their effects on global gene expression can lead to identification of clinically relevant antisense therapeutics and can identify which molecular and cellular events might be important in complex biological processes, such as cell growth and differentiation.