gebhart/patrepeval huggingface dataset:
Dissociation of estrogenic and cytotoxic properties of an estrogen receptor-binding platinum complex in human breast cancer cell lines. (1991)

The Pt complex [meso-1,2-bis(2,6-dichloro-4-hydroxyphenyl)-ethylenediamine]diaqua -Pt(II) sulfate (meso-6-PtSO4) was designed with the concept of combining the cytotoxic cisplatin with an estrogen receptor (ER)-binding ligand for targeting to ER+ mammary tumor cells. This Pt complex selectively inhibits growth of ER+ mammary tumors in rodents. To study the cellular mechanisms of action, cultures of two human mammary tumor cell lines, MCF-7 (ER+) and MDA-MB231 (ER-), were used and the effects of estradiol, tamoxifen, and cis-Pt compared with those of meso-6-PtSO4. The relative binding affinity of the meso-6-PtSO4 to the ER in MCF-7 cells was 0.35 compared to estradiol (relative binding affinity, 100). Nevertheless, the Pt complex was able to induce ER processing and increase the level of the progesterone receptor at concentrations of 1-10 nM. Growth of MCF-7 cells was inhibited at concentrations of meso-6-PtSO4 greater than 10 microM. MDA-MB231 cells were inhibited likewise by the Pt complex, indicating a lack of selectivity for the ER+ cells. The results show that meso-6-PtSO4 possesses both estrogen-like and cis-Pt-like properties. Since growth inhibition did not correlate with ER-mediated processes, these two properties are expressed independently at the cellular level. The selective growth inhibitory effect of meso-6-PtSO4 in vivo is suggested to involve endocrinological and/or immunological factors.
The Interleukin-1 Receptor-associated Kinase Is Degraded by Proteasomes following Its Phosphorylation (1997)

Following interleukin (IL)-1 stimulation, the majority of the cellular interleukin-1 receptor-associated kinase (IRAK) translocates to a discrete subset of the Type I IL-1 receptor (IL-1R1) in MRC-5 human lung fibroblasts. As the IRAK becomes multiphosphorylated, it is degraded by proteasomes at a rate comparable to that of the degradation of the phosphorylated IkappaBalpha protein. Proteasome inhibitors block the degradation of phosphorylated IRAK and correspondingly increase the amount of IL-1R1 that can be coimmunoprecipitated with IRAK. The nonspecific kinase inhibitor K-252b blocks IRAK phosphorylation and degradation, but does not inhibit IRAK association with the IL-1R1 indicating that translocation of IRAK to the IL-1R1 and its phosphorylation are independent events. The IL-1 specificity of these effects is indicated by the lack of IRAK phosphorylation and degradation by IL-1 in the presence of the IL-1 receptor antagonist or by the activation of MRC-5 cells by tumor necrosis factor alpha. Long term exposure of MRC-5 cells to IL-1 desensitizes the resynthesized IkappaBalpha to IL-1, but not to tumor necrosis factor alpha stimulation, but no additional effects on IRAK are seen.
Increased thrombogenesis and embolus formation in mice lacking glycoprotein V (2001)

The glycoprotein (GP) Ib-V-IX complex plays a critical role in initiating platelet adhesion to von Willebrand factor (vWF) at the site of vascular injury. The complex also forms a high-affinity binding site for thrombin. Using an intravital microscopy mouse model, it was previously established that vWF plays a critical role in mediating platelet adhesion and thrombus formation following mesenteric arteriolar injury induced by ferric chloride. Further characterization of this model showed that these thrombotic events were also thrombin dependent. Using this vWF- and thrombin-dependent model, this study shows that GP V gene deficiency significantly accelerates both platelet adhesion and thrombus formation in mice following arteriolar injury. The time required for vessel occlusion in GP V-deficient (GP V(-/-)) mice was significantly shorter than that in wild-type mice. Interestingly, large emboli were also produced in GP V(-/-) mice, but not in wild-type mice, causing frequent downstream occlusion. However, when the 2 genotypes were compared in the in vitro perfusion chamber where thrombin was inhibited by heparin, no significant differences were found in either initial single-platelet adhesion or thrombus volume. These results demonstrate that GP V(-/-) mice have accelerated thrombus growth in response to vascular injury and suggest that this is caused by enhanced thrombin-induced platelet activation rather than enhanced binding of GPIb-V-IX to vWF. Absence of GP V also compromises thrombus stability.
Generation of dopaminergic neurons and pigmented epithelia from primate ES cells by stromal cell-derived inducing activity (2002)

We previously identified a stromal cell-derived inducing activity (SDIA), which induces differentiation of neural cells, including midbrain tyrosine hydroxylase-positive (TH(+)) dopaminergic neurons, from mouse embryonic stem cells. We report here that SDIA induces efficient neural differentiation also in primate embryonic stem cells. Induced neurons contain TH(+) neurons at a frequency of 35% and produce a significant amount of dopamine. Interestingly, differentiation of TH(+) neurons from undifferentiated embryonic cells occurs much faster in vitro (10 days) than it does in the embryo (approximately 5 weeks). In addition, 8% of the colonies contain large patches of Pax6(+)-pigmented epithelium of the retina. The SDIA method provides an unlimited source of primate cells for the study of pathogenesis, drug development, and transplantation in degenerative diseases such as Parkinson's disease and retinitis pigmentosa.
The biosynthesis of branched O-glycans. (1989)

The hypothesis put forward in this review is that the branching patterns at the core of Ser(Thr)-GalNAc oligosaccharides (O-glycans) determine the types of glycan that are synthesized and their functions. Biosynthetic pathways are presented for the four types of O-glycan core and for some of the more common glycans that are built on these cores. The four core types discussed are: (1) Gal beta 1-3GalNAc-alpha-Ser(Thr)-R, (2) Gal beta 1-3(GlcNAc beta 1-6)GalNAc-alpha-Ser(Thr)-R, (3) GlcNAc beta 1-3GalNAc-alpha-Ser(Thr)-R, and (4) GlcNAc beta 1-3(GlcNAc beta 1-6)GalNAc-alpha-Ser(Thr)-R. General rules concerning the control of synthesis of these molecules are derived.
Cell surface proteoglycan of mammary epithelial cells. Protease releases a heparan sulfate-rich ectodomain from a putative membrane-anchored domain. (1985)

Heparan sulfate-rich proteoglycan is present on the surface of NMuMG mouse mammary epithelial cells. All of this cell surface fraction is lipophilic, assessed by intercalation into lipid vesicles, and requires proteolytic cleavage to be released from the cell surface. No proteoglycan is competitively displaced by heparin. The cell surface lipophilic proteoglycan constitutes 52-55% of the total cellular proteoglycan while the remaining proteoglycan is apparently intracellular, comprising a nonlipophilic fraction (35%) and a small (10-13%) lipophilic fraction. Trypsin or chymotrypsin cleaves a labile site between the region of the cell surface proteoglycan bearing the glycosaminoglycan chains and the cell-associated portion of the core protein, producing a proteoglycan that is nonlipophilic, has an increased bouyant density, and is smaller than the parent molecule. We refer to this proteoglycan as the ectodomain of the cell surface proteoglycan. The correlation between its cell surface location and lipophilic properties suggests that a hydrophobic domain of its core protein may anchor this proteoglycan in the plasma membrane. In vivo, the proteoglycan may be cleaved from this putative anchor, generating nonlipophilic proteoglycan present as a matrix component, or it may remain a membrane component, anchoring the cell directly to the extracellular matrix.
Effects of enteric-coated methylnaltrexone in preventing opioid-induced delay in oral-cecal transit time (2000)

Our results suggest that there is a prevailing direct and local luminal effect of enteric-coated methylnaltrexone and that the enteric-coated formulation exerts its gut pharmacologic actions more efficiently than the uncoated formulation.
Facilitation of dimethylbenz[a]anthracene-induced rat mammary tumorigenesis by restraint stress: role of β-endorphin, prolactin and naltrexone (1991)

In order to investigate the involvement of opioid peptides and prolactin in stress-facilitated mammary cancer, we studied the effect of chronic restraint stress on dimethylbenz[a]-anthracene (DMBA)-induced mammary tumorigenesis and the effect of an opiate antagonist, naltrexone, on this process. Female Fischer-344 rats (n = 160) were administered 15 mg DMBA/ml of sesame oil/rat by intragastric intubation. Eighty rats were subjected to daily 30 min restraint stress in a plastic cylinder, and 80 rats served as control not subjected to the stressor. Half of the rats from each group received naltrexone (1 mg/kg, i.p. daily). Five rats from each group (restraint stress +/- naltrexone and control +/- naltrexone) were killed every 2-3 weeks. Rats subjected to restraint stress developed a greater number of tumors earlier. Naltrexone decreased the tumor incidence in the stressed animals from 32 to 12% (P less than 0.001) and in unstressed rats from 27 to 15% (P less than 0.001) at the end of 18 weeks. Stressed rats showed a decrease of 48% (P less than 0.001) in the level of hypothalamic beta-endorphin. Plasma prolactin increased from 4-13 ng/ml in the control rats to 109-396 ng/ml (P less than 0.001) in the stressed rats throughout the 18 week period. The beneficial effect of naltrexone was associated with 42% (P less than 0.01) increase in T cell proliferation, but greater than 90% (P less than 0.001) decrease in plasma prolactin level was observed in naltrexone-treated rats compared to the untreated animals. Rats subjected to restraint stress showed a 15% (P less than 0.001) decrease in weight gain at the end of the experiment (18 weeks). Neither restraint stress nor naltrexone administration affected the caloric intake of rats during this period. Thus, we believe that restraint stress facilitates DMBA-induced mammary tumors by releasing beta-endorphin and prolactin, and naltrexone shows a beneficial effect by opposing the effect of beta-endorphin on prolactin release in the stressed animals.
Antibiotics and antiviral compounds : chemical synthesis and modification (1993)

New methodology applied to antibiotic synthesis macrolide antibiotics beta-lactames, quinolones and cyclopentanoid antibiotics peptides and glycopeptides enediyne antibiotics carbohydrates in antibiotic synthesis antiviral agents.
Host-vector system for integration of recombinant DNA into chromosomes of transformable and nontransformable streptococci (1988)

We describe a genetic system in which transformation of Streptococcus pneumoniae and Streptococcus sanguis was used to insert recombinant DNA into the conjugative chromosomal element omega (cat tetM) 6001 (omega 6001). The element containing the recombinant DNA was then transferred by conjugation to the chromosome of transformable and nontransformable streptococci. When Escherichia coli plasmid pDP36 was used as donor in transformation, it was capable of inserting 5.9 kilobases of heterologous DNA into the chromosome of competent streptococcal strains carrying omega 6001; the transformants were scored for erythromycin resistance. Genetic analysis showed that in a fraction of the erythromycin-resistant transformants the integration via flanking homology of the heterologous DNA caused inactivation of the tetM gene of omega 6001. By analyzing the stability of the resistance markers, we found that stable integration of heterologous DNA was achieved only in the erythromycin-resistant, tetracycline-sensitive transformants. It was possible to detect conjugal transfer of the heterologous sequences from stable transformants to strains of S. pneumoniae, S. sanguis, Streptococcus pyogenes, and Streptococcus faecalis. The omega 6001-pDP36 host-vector system opens new possibilities for gene transfer in streptococci. By this method cloned streptococcal DNA (possibly mutagenized in vitro) can be returned to the original host, greatly facilitating complementation tests and fine physiological studies.
Modular parallel-plate THz components for cost-efficient biosensing systems (2005)

In this work, a new THz-device configuration for biosensing applications is demonstrated. A modular approach in a parallel-plate configuration using separate components for signal generation, biosensing transducer and signal detection is demonstrated. The low-cost disposable biosensing transducer is based on metallized periodic groove structures as high-Q photonic band gap resonators. Photoconductively activated slot launchers are used as signal generators and detectors of THz parallel-plate waves. In comparison to the former planar strip line approaches, this modular concept provides a cost-efficient solution given the exchangeability, disposability or reusability of components. This parallel-plate waveguide approach allows coupling modular components with a high positioning tolerance and broadband matching with minimal losses. Significantly, higher Q-factors for the resonant sensing components are achieved with this new approach.
Forecasting the demand for construction skills in Hong Kong (2006)

Efficient manpower planning has been recognized as a critical aspect for the development of an economy. In 2001, the Works Bureau of the Hong Kong SAR Government (predecessor of Environment, Transport and Works Bureau) commissioned an HKPolyU consultancy team to develop a computer-based model to estimate the demand for different categories of construction personnel. This article presents the concept and features of the manpower demand-forecasting model developed for the construction industry of Hong Kong. The forecasting model is formulated on the basis of the labour multiplier approach by deriving the relationship between the number of workers required and the project expenditure in the given project duration. Multipliers for 61 project types were derived for 38 labour trades using completed project data. The labour demand by occupation for each project can then be estimated by multiplying the corresponding multipliers and the estimated project expenditure. Several unique features of the model have been developed, including ‘normalization’ and ‘contract cost adjustment factor’. Normalizing the labour multipliers can facilitate the prediction of occupational labour requirements at different stages of a construction project. The adjustment factor is introduced to eliminate the discrepancy between the original estimates and final contract values so as to enhance the estimation accuracy. The model can also be used to predict the number of jobs created for a given level of investment. The government can apply this model to check and compare which project types will generate most jobs before committing public money. This model could be easily adopted and adapted by foreign construction authorities while planning manpower.
Iron in sickle cell disease: A review why less is better (2003)

Sickle cell anemia (SCA) is an inherited disorder of hemoglobin synthesis that is characterized by life-long severe hemolytic anemia, attacks of pain crisis, and chronic organ system damage. A third of the hemolysis in SCA is intravascular and the resulting urinary losses of iron may lead to iron deficiency. There is no evidence of iron overload in SCA and iron deficiency may be more common than suspected, especially in men. Absence of bone marrow iron remains a gold standard for the diagnosis of iron deficiency in these patients. Although low serum ferritin is highly specific for the diagnosis of iron deficiency, its sensitivity is quite low in SCA because of non-specific elevation due to increased red cell turnover. The kinetics of sickling is strongly concentration dependent such that small decreases in the mean corpuscular deoxyhemoglobin-S concentration (MCHC-S) cause a substantial delay in sickle hemoglobin polymerization. Prolongation of the "delay time of gelation" in excess of the capillary transit time may allow the erythrocyte to traverse the capillary bed to escape to the arterial side before there is rheologic impairment of the erythrocyte from polymerization of sickle hemoglobin. Overt iron deficiency lowers the MCHC-S and thereby decreases the sickling tendency and the severity of hemolysis. The clinical improvement in SCA following the induction of iron deficient erythropoiesis by repeated phlebotomies or by erythrocytapheresis has been reported. Prospective controlled studies are needed to evaluate further, the therapeutic strategy of inducing controlled iron-deficient erythropoiesis in selected patients with SCA.
AD lesions and infarcts in demented and non‐demented Japanese‐American men (2004)

Neocortical neuritic plaques and neurofibrillary tangles are hallmark neuropathological lesions of dementia. Concomitant cerebrovascular lesions increase dementia severity in patients meeting neuropathological criteria for Alzheimer's disease and contribute to cognitive impairment in persons with mild entorhinal Alzheimer lesions. This study investigates whether individuals with sparse neocortical neuritic plaques experience increased odds of crossing the threshold to clinical dementia when they have coexistent cerebrovascular lesions. Dementia examinations were given to 3,734 men during the 1991-1993 Honolulu-Asia Aging Study examination and to 2,603 men during the 1994-1996 examination. Lesion quantification was done without clinical data. Among 333 autopsied men, 120 had dementia, 115 had marginal results, and 98 had normal cognition. In men with neurofibrillary tangles, dementia frequency increased with increasing neuritic plaque density, and increased further in the presence of cerebrovascular lesions. The association was strongest in men with sparse neuritic plaques (1-3/mm(2)) where dementia frequency more than doubled with coexistent cerebrovascular lesions (45 vs 20%). Among all dementia cases, 24% were linked to cerebrovascular lesions. Findings suggest cerebrovascular lesions are associated with a marked excess of dementia in cases with low neuritic plaque frequency. Prevention of cerebrovascular lesions may be critically important in preserving late-life cognitive function.
Nitroglycerin. The explosive drug (1971)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTNitroglycerin. The explosive drugLinda Culp Holmes and Frederick J. DiCarlo Cite this: J. Chem. Educ. 1971, 48, 9, 573Publication Date (Print):September 1, 1971Publication History Received3 August 2009Published online1 September 1971Published inissue 1 September 1971https://doi.org/10.1021/ed048p573RIGHTS & PERMISSIONSArticle Views599Altmetric-Citations7LEARN 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 InReddit PDF (3 MB) Get e-Alerts Get e-Alerts
Clinical Features of a Stargardt-Like Dominant Progressive Macular Dystrophy With Genetic Linkage to Chromosome 6q (1994)

This autosomal dominant macular dystrophy is clinically similar to Stargardt's disease, with the exception of its pattern of inheritance. The clearly progressive nature of the disease distinguishes it from North Carolina macular dystrophy, whose causative gene is also located on the long arm of chromosome 6. Identification of the gene involved in this disease may provide clues to the pathogenesis of age-related macular degeneration.
Kinetics of Polymer Melt Intercalation (1995)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTKinetics of Polymer Melt IntercalationRichard A. Vaia, Klaus D. Jandt, Edward J. Kramer, and Emmanuel P. GiannelisCite this: Macromolecules 1995, 28, 24, 8080–8085Publication Date (Print):November 1, 1995Publication History Published online1 May 2002Published inissue 1 November 1995https://pubs.acs.org/doi/10.1021/ma00128a016https://doi.org/10.1021/ma00128a016research-articleACS PublicationsRequest reuse permissionsArticle Views1460Altmetric-Citations614LEARN 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
Multiwavelength erbium-doped power limiting amplifier in all-optical self-healing ring network (1996)

A multiwavelength self-healing interoffice all-optical protection ring network requires optical amplifiers with a large dynamic range. We demonstrate that an erbium-doped multiwavelength optical power limiting amplifier (OLA) fulfils the dynamic range requirement. A single three-WDM-channel OLA serving the ring size of 150 km at channel rates of 2.488 Gb/s is presented.
Cloning and Characterization of Helicobacter pyloriSuccinyl CoA:Acetoacetate CoA-transferase, a Novel Prokaryotic Member of the CoA-transferase Family (1997)

Sequencing of a fragment of Helicobacter pylori genome led to the identification of two open reading frames showing striking homology with Coenzyme A (CoA) transferases, enzymes catalyzing the reversible transfer of CoA from one carboxylic acid to another. The genes were present in all H. pylori strains tested by polymerase chain reaction or slot blotting but not in Campylobacter jejuni. Genes for the putative A and B subunits of H. pylori CoA-transferase were introduced into the bacterial expression vector pKK223-3 and expressed in Escherichia coli JM105 cells. Amino acid sequence comparisons, combined with measurements of enzyme activities using different CoA donors and acceptors, identified the H. pylori CoA-transferase as a succinyl CoA:acetoacetate CoA-transferase. This activity was consistently observed in different H. pylori strains. Antibodies raised against either recombinant A or B subunits recognized two distinct subunits of Mr approximately 26,000 and 24, 000 that are both necessary for H. pylori CoA-transferase function. The lack of alpha-ketoglutarate dehydrogenase and of succinyl CoA synthetase activities indicates that the generation of succinyl CoA is not mediated by the tricarboxylic acid cycle in H. pylori. We postulate the existence of an alternative pathway where the CoA-transferase is essential for energy metabolism.