gebhart/patrepeval huggingface dataset:
Cancer insurance policies in Japan and the United States. (1998)

Cancer care in the United States often results in financial hardship for patients and their families. Standard health insurance covers most medical costs, but nonmedical costs (such as lost wages, deductibles, copayments, and travel to and from caregivers) are paid out of pocket. Over the course of treatment, these costs can become substantial. Insurance companies have addressed the burden of these out-of-pocket costs by offering supplemental cancer insurance policies that, upon diagnosis of cancer, pay cash benefits for items that usually require out-of-pocket expenditures and are distinct from reimbursements made by traditional health insurance. Limitations associated with managed care have fostered increased consumer awareness and interest in the United States for cancer insurance and its ability to defray treatment expenditures that usually require out-of-pocket payments. Marketing campaigns are becoming more aggressive, and the number of cancer insurance policies sold has been steadily rising. While cancer insurance is only recently gaining popularity in the United States, it has been a successful product in Japan for over twenty years. In Japan, approximately one-quarter of the population own cancer insurance, and ten-year retention rates are estimated at 75%. As a result, individuals are afforded good access to nonmedical cancer services. Understanding the factors that led to the success of cancer insurance in Japan may assist policymakers in evaluating cancer insurance policies as they become more prevalent in the United States.
Exogenous BDNF Rescues Rat Spiral Ganglion Neurons In Vivo (2005)

The study has demonstrated the trophic advantage of exogenous BDNF in the mature rat cochlea and provides confidence that spiral ganglion neuron rescue after sensorineural hearing loss with exogenous BDNF may have clinical application.
Oligo(alpha-deoxynucleotide)s covalently linked to intercalating agents: differential binding to ribo- and deoxyribopolynucleotides and stability towards nuclease digestion. (1987)

An octathymidylate was synthesized with the alpha anomer of thymidine instead of the naturally occurring beta anomer. This oligonucleotide binds to complementary sequences containing beta-nucleosides. Binding to ribose-containing oligomers and polymers is much stronger than binding to deoxyribose-containing analogs. A derivative of acridine (9-amino-6-chloro-2-methoxyacridine) was covalently attached either to the 5' phosphate or to the 3' phosphate of the alpha-octathymidylate. A pentamethylene linker was used to bridge the phosphate group and the 9-amino group of the acridine derivative. In both cases the complexes with the complementary sequences were strongly stabilized due to the additional binding energy provided by intercalation of the acridine ring within the miniduplex structure formed by the oligonucleotide with its target sequence. The acridine-substituted alpha-oligothymidylates did not lose their discrimination between ribose and deoxyribose-containing complementary sequences. The alpha-oligothymidylates were much more resistant towards endonucleases than their beta analogs, independently of whether they were linked to the acridine derivative. Acridine substitution provided additional protection against the corresponding exonucleases. alpha-Oligodeoxynucleotides covalently linked or not to intercalating agents represent families of molecules that open possibilities to block mRNA translation or viral RNA expression in vitro and in vivo.
In vitro synthesis of infectious retroviral RNA (1988)

A plasmid was constructed in which a T7 RNA polymerase promoter was placed upstream of a recombinant amphotropic retrovirus genome containing a selectable neomycin resistance gene. To test the infectivity of the RNA produced by T7 RNA polymerase in vitro, the RNA was microinjected into the nuclei of psi 2 packaging cells. Infectious particles conferring G418 resistance were released.
Missing Value Imputation using Hybrid K-Means and Association Rules (2018)

Association rules is an important and well researched database mining function for discovering interesting relationship between variables in large database. The data mining architecture works on facts and figures which are used for any type of decision making. To perform any analysis and decision making, these facts must be complete so that the analyst can make a strategy for decision making. In fact the most important problem in knowledge discovery is the missing values of the attributes of the dataset. If such imperfections are there in database, it is cleaned during pre-processing and is prepared in order to be functional. Considering, the importance of handling missing instances in data mining and knowledge discovery, we proposed a hybrid algorithm for using a combination of association rules mining and k-nearest neighbour approach. We performed a detail experimental result on UCI datasets to check the effectiveness of our technique. For this, we have discretize the data using K-means technique and to generate rules in large volume of data using apriori association rule mining. The measurement metrics such as confidence, support, lift & coverage are then used to evaluate the discovered rules.
Metabolic Risk Factors Worsen Continuously across the Spectrum of Nondiabetic Glucose Tolerance: The Framingham Offspring Study (1998)

Metabolic risk factors for type 2 diabetes mellitus and for cardiovascular disease worsen continuously across the spectrum of glucose tolerance categories, beginning in the lowest quintiles of normal fasting glucose level.
Mechanism of Biological Control in a Fusarium-Suppressive Soil (2008)

Metz fine sandy loam soil from the Salinas Valley in California was suppressive to the <i>Fusarium</i> spp. which induce wilts of flax and carnation. Suppressiveness to <i>Fusarium oxysporum</i> f. sp. <i>dianthi</i> was transferred to conducive soil when the Metz fine sandy loam was added in small amounts to steamed greenhouse soil. Aerated steam treatment of the suppressive soil at 54 C for 30 min eliminated the suppressive effect. Lowering of pH values of the Metz fine sandy loam from 8.0 to 6.0 in unit increments eliminated the suppressive effect. Bacteria were isolated from mycelial mats of <i>F. oxysporum</i> f. sp. <i>lini</i> buried in the suppressive soil and conducive soils. Two isolates from suppressive soil introduced into conducive soil at 10<sup>5</sup> cells per gram of soil significantly reduced disease incidence of Fusarium wilt of flax. The more effective of these isolates inducing suppressiveness was a <i>Pseudomonas</i> sp. Viability of this organism was drastically reduced when soil was treated with aerated steam at 54 C. These results suggest that suppressiveness in the Metz fine sandy loam is biological in origin and that control of Fusarium wilt diseases may be accomplished through introduction of appropriate species of bacteria into conducive soil.
A Risk Score for Predicting Stroke or Death in Individuals With New-Onset Atrial Fibrillation in the Community (2003)

These risk scores can be used to estimate the absolute risk of an adverse event in individuals with AF, which may be helpful in counseling patients and making treatment decisions.
Isoform-specific interactions of apolipoprotein E with microtubule-associated protein tau: implications for Alzheimer disease. (1994)

The apolipoprotein E (apoE) type 4 allele (APOE4) is a susceptibility gene for late-onset familial and sporadic Alzheimer disease. ApoE is found in some neurofibrillary tangle-bearing neurons, one of the major pathologic hallmarks of the disease. Neurofibrillary tangles contain paired helical filaments formed from hyperphosphorylated microtubule-associated protein tau. In vitro, tau binds avidly to apoE3, but not to apoE4, forming a bimolecular complex. Tau phosphorylated with a brain extract does not bind either isoform. ApoE3 binds to the microtubule-binding repeat region of tau, which is also the region that is thought to cause self-assembly into the paired helical filament. Binding studies with fragments of ApoE demonstrate that the tau-binding region of apoE3 corresponds to its receptor-binding domain and is distinct from the region that binds lipoprotein particles or beta/A4 peptide. Isoform-specific interactions of apoE with tau may regulate intraneuronal tau metabolism in Alzheimer disease and alter the rate of formation of paired helical filaments and neurofibrillary tangles.
Giant Enhancement in UV Response of ZnO Nanobelts by Polymer Surface-Functionalization (2007)

High sensitivity photodetectors are of great significance in developing a new generation of optoelectronic devices in sensing, imaging, and other applications. In this Communication, highly sensitive UV detectors based on ZnO nanobelts (NBs) are achieved by polymer surface-functionalization. The UV-induced photoconductance in ZnO NBs increases by 5 orders of magnitude after functionalizing, using a polymer that exhibits large UV absorption. The huge increase in photoconductance is attributed to an electron−hole generation process as assisted by the energy states in the polymer. This study suggests that, by selecting polymers with different wavelengths of UV absorption, highly sensitive UV detectors with a large range of detection wavelengths can be fabricated using ZnO NBs.
Synaptic Targeting of Retrogradely Transported Trophic Factors in Motoneurons: Comparison of Glial Cell Line-Derived Neurotrophic Factor, Brain-Derived Neurotrophic Factor, and Cardiotrophin-1 with Tetanus Toxin (2005)

Glial cell line-derived neurotrophic factor (GDNF), brain-derived neurotrophic factor (BDNF), and cardiotrophin-1 (CT-1) are the most potent neurotrophic factors for motoneurons, but their fate after retrograde axonal transport is not known. Internalized trophic factors may be degraded, or they may be recycled and transferred to other neurons, similar to the known route of tetanus toxin. We tested whether neonatal rat hypoglossal motoneurons target retrogradely transported trophic factors to synaptic sites on their dendrites within the brainstem and subsequently transfer these trophins across the synaptic cleft to afferent synapses (transsynaptic transcytosis). Motoneurons retrogradely transport from the tongue radiolabeled GDNF, BDNF, and CT-1 as well as tetanus toxin. Quantitative autoradiographic electron microscopy showed that GDNF and BDNF were transported into motoneuron dendrites with labeling densities similar to those of tetanus toxin. Although tetanus toxin accumulated rapidly (within 8 h) at presynaptic sites, GDNF accumulated at synapses more slowly (within 15 h), and CT-1 never associated with synapses. Thus, some retrogradely transported neurotrophic factors are trafficked similarly but not identically to tetanus toxin. Both GDNF and BDNF accumulate at the external (limiting) membrane of multivesicular bodies within proximal dendrites. We conclude that tetanus toxin, GDNF, and BDNF are released from postsynaptic sites and are internalized by afferent presynaptic terminals, thus demonstrating transsynaptic transcytosis. CT-1, however, follows a strict degradation pathway after retrograde transport to the soma. Synaptic and transcytotic trafficking thus are restricted to particular neurotrophic factors such as GDNF and BDNF.
Transforming terpene-derived aldehydes into 1,2-epoxides via asymmetric α-chlorination: subsequent epoxide opening with carbon nucleophiles (2011)

Merging Jørgensen's and MacMillan's organocatalytic aldehyde chlorinations enables the synthesis of chiral vinylcyclopropanes and (-)-cis-aerangis lactone via terpene-derived 1,2-epoxides.
An elevated serum beta‐2‐microglobulin level is an adverse prognostic factor for overall survival in patients with early‐stage Hodgkin disease (2002)

The prognostic significance of a simple, widely available, and inexpensive blood test, beta-2M, has not been studied routinely in patients with Hodgkin disease and should be tested prospectively in large, cooperative group trials.
Localization of an essential ligand binding determinant of the human erythropoietin receptor to a domain N-terminal to the WSXWS motif: implications for soluble receptor function. (1995)

The interaction of erythropoietin (Epo) with the erythropoietin receptor (EpoR) supports erythropoiesis. The EpoR is a member of the well-recognized cytokine receptor superfamily characterized by four conserved cysteines and a WSXWS domain in the extracellular portion of the molecule. To localize ligand-binding determinants of the EpoR near the WSXWS domain, we tested the ligand-binding ability of the wild-type human EpoR extracellular domain (EREx), two truncated and three chimeric constructs with the interleukin-2 receptor beta subunit (IL2R beta). Constructs were expressed in E. coli as GST fusion proteins linked to a solid-phase support and assayed for binding to 125I Epo. As previously shown, Epo bound specifically to the expressed extracellular domain, EREx. Epo did not bind to truncated receptors lacking either the entire fifth exon or the WSXWS domain. Epo also did not bind to chimeric receptors that had the amino acids encoded by the fifth exon replaced by IL2R beta or that had the amino acids subsequent to asparagine residue 209 replaced by IL2R beta. Specific binding was demonstrated for a construct in which the WSXWS was replaced by that of IL2R beta. We conclude that the amino acids encoded by this 5' portion of exon 5 of the EpoR are necessary for ligand binding and that the WSXWS domain is necessary for Epo binding but is not involved in ligand-binding specificity. We also speculate that if the putative soluble form of the EpoR is expressed (predicted to lack exon 5), it does not bind Epo and therefore may serve a physiologic purpose other than ligand binding.
The Primary Structure of MEK, a Protein Kinase that Phosphorylates the ERK Gene Product (1992)

Mitogen-activated protein (MAP) kinases, also known as extracellular signal-regulated kinases (ERKs), are thought to act at an integration point for multiple biochemical signals because they are activated by a wide variety of extracellular signals, rapidly phosphorylated on threonine and tyrosine, and highly conserved. A critical protein kinase lies upstream of MAP kinase and stimulates the enzymatic activity of MAP kinase. The structure of this protein kinase, denoted MEK1, for MAP kinase or ERK kinase, was elucidated from a complementary DNA sequence and shown to be a protein of 393 amino acids (43,500 daltons) that is related most closely in size and sequence to the product encoded by the Schizosaccharomyces pombe byr1 gene. The MEK gene was highly expressed in murine brain, and the product expressed in bacteria phosphorylated the ERK gene product.
Modelling prefrontal cortex deficits in schizophrenia: implications for treatment (2008)

Current treatments of schizophrenia are compromised by their inability to treat all symptoms of the disease and their side-effects. Whilst existing antipsychotic drugs are effective against positive symptoms, they have negligible efficacy against the prefrontal cortex (PFC)-associated cognitive deficits and negative symptoms. New models that reproduce core pathophysiological features of schizophrenia are more likely to have improved predictive validity in identifying new treatments. We have developed a NMDA receptor antagonist model that reproduces core PFC deficits of schizophrenia and discuss this in relation to pathophysiology and treatments. Subchronic and chronic intermittent PCP (2.6 mg/kg i.p.) was administered to rats. PFC activity was assessed by 2-deoxyglucose imaging, parvalbumin and Kv3.1 mRNA expression, and the attentional set-shifting test (ASST) of executive function. Affymetrix gene array technology was employed to examine gene expression profile patterns. PCP treatment reduced glucose utilization in the PFC (hypofrontality). This was accompanied by a reduction in markers of GABAergic interneurones (parvalbumin and Kv3.1 mRNA expression) and deficits in the extradimensional shift dimension of the ASST. Consistent with their clinical profile, the hypofrontality was not reversed by clozapine or haloperidol. Transcriptional analysis revealed patterns of change consistent with current neurobiological theories of schizophrenia. This model mirrors core neurobiological deficits of schizophrenia; hypofrontality, altered markers of GABAergic interneurone activity and deficits in executive function. As such it is likely to be a valuable translational model for understanding the neurobiological mechanisms underlying hypofrontality and for identifying and validating novel drug targets that may restore PFC deficits in schizophrenia.
Motor neuropathy in porphobilinogen deaminase–deficient mice imitates the peripheral neuropathy of human acute porphyria (1999)

Acute porphyrias are inherited disorders caused by partial deficiency of specific heme biosynthesis enzymes. Clinically, porphyrias are manifested by a neuropsychiatric syndrome that includes peripheral neuropathy. Although much is known about the porphyrias' enzyme defects and their biochemical consequences, the cause of the neurological manifestations remains unresolved. We have studied porphyric neuropathy in mice with a partial deficiency of porphobilinogen deaminase (PBGD). PBGD-deficient mice (PBGD-/-) imitate acute porphyria through massive induction of hepatic delta-aminolevulinic acid synthase by drugs such as phenobarbital. Here we show that PBGD-/- mice develop impairment of motor coordination and muscle weakness. Histologically femoral nerves of PBGD-/- mice exhibit a marked decrease in large-caliber (>8 microm) axons and ultrastructural changes consistent with primary motor axon degeneration, secondary Schwann cell reactions, and axonal regeneration. These findings resemble those found in studies of affected nerves of patients with acute porphyria and thus provide strong evidence that PBGD deficiency causes degeneration of motor axons without signs of primary demyelination, thereby resolving a long-standing controversy. Interestingly, the neuropathy in PBGD-/- mice developed chronically and progressively and in the presence of normal or only slightly (twofold) increased plasma and urinary levels of the putative neurotoxic heme precursor delta-aminolevulinic acid. These data suggest that heme deficiency and consequent dysfunction of hemeproteins can cause porphyric neuropathy.
O‐GlcNAc Modification Prevents Peptide‐Dependent Acceleration of α‐Synuclein Aggregation (2012)

Sweet relief: the Parkinson's disease- associated protein α-synuclein is post-translationally modified by N-acetylglucosamine (O-GlcNAc), but the biochemical consequences are unknown. Here we show that an O-GlcNAc-modified peptide does not participate in α-synuclein aggregation, thus suggesting that O-GlcNAc might directly inhibit aggregation in cells.
Molecular structure of a DNA decamer containing an anticancer nucleoside arabinosylcytosine: conformational perturbation by arabinosylcytosine in B-DNA (1991)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTMolecular structure of a DNA decamer containing an anticancer nucleoside arabinosylcytosine: conformational perturbation by arabinosylcytosine in B-DNAYi Gui Gao, Gijs A. Van der Marel, Jacques H. Van Boom, and Andrew H. J. WangCite this: Biochemistry 1991, 30, 41, 9922–9931Publication Date (Print):October 1, 1991Publication History Published online1 May 2002Published inissue 1 October 1991https://pubs.acs.org/doi/10.1021/bi00105a016https://doi.org/10.1021/bi00105a016research-articleACS PublicationsRequest reuse permissionsArticle Views87Altmetric-Citations34LEARN 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-Alertsclose Get e-Alerts
Gastric Adenocarcinoma (2005)

Predictive models generate important information allowing a logical evolution in the surgical and pathologic understanding and therapy for gastric cancer. However, a greater understanding of the molecular changes associated with gastric cancer is needed to guide surgical and medical therapy.
Pseudopeptide Inhibitors of Ras Farnesyl-Protein Transferase (1994)

Inhibitors of Ras farnesyl-protein transferase are described. These are reduced pseudopeptides related to the C-terminal tetrapeptide of the Ras protein that signals farnesylation. Deletion of the carbonyl groups between the first two residues of the tetrapeptides either preserves or improves activity, depending on the peptide sequence. The most potent in vitro enzyme inhibitor described (IC50 = 5 nM) is Cys [psi CH2NH]Ile[psi CH2NH]Phe-Met (3). To obtain compounds able to suppress Ras farnesylation in cell culture, further structural modification to include a homoserine lactone prodrug was required. Compound 18 (Cys[psi CH2NH]Ile[psi CH2NH]Ile-homoserine lactone) reduced the extent of Ras farnesylation by 50% in NIH3T3 fibroblasts in culture at a concentration of 50 microM. Structure-activity studies also led to 12 (Cys[psi CH2NH]Val-Ile-Leu), a potent and selective inhibitor of a related enzyme, the type-I geranylgeranyl protein transferase.
Evidence that Tristetraprolin Binds to AU-Rich Elements and Promotes the Deadenylation and Destabilization of Tumor Necrosis Factor Alpha mRNA (1999)

Mice deficient in tristetraprolin (TTP), the prototype of a family of CCCH zinc finger proteins, develop an inflammatory syndrome mediated by excess tumor necrosis factor alpha (TNF-alpha). Macrophages derived from these mice oversecrete TNF-alpha, by a mechanism that involves stabilization of TNF-alpha mRNA, and TTP can bind directly to the AU-rich element (ARE) in TNF-alpha mRNA (E. Carballo, W. S. Lai, and P. J. Blackshear, Science 281:1001-1005, 1998). We show here that TTP binding to the TNF-alpha ARE is dependent upon the integrity of both zinc fingers, since mutation of a single cysteine residue in either zinc finger to arginine severely attenuated the binding of TTP to the TNF-alpha ARE. In intact cells, TTP at low expression levels promoted a decrease in size of the TNF-alpha mRNA as well as a decrease in its amount; at higher expression levels, the shift to a smaller TNF-alpha mRNA size persisted, while the accumulation of this smaller species increased. RNase H experiments indicated that the shift to a smaller size was due to TTP-promoted deadenylation of TNF-alpha mRNA. This CCCH protein is likely to be important in the deadenylation and degradation of TNF-alpha mRNA and perhaps other ARE-containing mRNAs, both in normal physiology and in certain pathological conditions.