gebhart/patrepeval huggingface dataset:
A natural variant of type I antifreeze protein with four ice‐binding repeats is a particularly potent antifreeze (1996)

A 4.3-kDa variant of Type I antifreeze protein (AFP9) was purified from winter flounder serum by size exclusion chromatography and reversed-phase HPLC. By the criteria of mass, amino acid composition, and N-terminal sequences of tryptic peptides, this variant is the posttranslationally modified product of the previously characterized AFP gene 21a. It has 52 amino acids and contains four 11-amino acid repeats, one more than the major serum AFP components. The larger protein is completely alpha-helical at 0 degree C, with a melting temperature of 18 degrees C. It is considerably more active as an antifreeze than the three-repeat winter flounder AFP and the four-repeat yellowtail flounder AFP, both on a molar and a mg/mL basis. Several structural features of the four-repeat winter flounder AFP, including its larger size, additional ice-binding residues, and differences in ice-binding motifs might contribute to its greater activity. Its abundance in flounder serum, together with its potency as an antifreeze, suggest that AFP9 makes a significant contribution to the overall freezing point depression of the host.
Temporal stability of photothermally fabricated micropatterns in supported phospholipid multilayers (2010)

The temporal stability of photothermally fabricated micropatterns in multilayered films of 1,2-dioleoyl-sn-glycero-3-phosphate on surface-oxidized silicon substrates is investigated. Multilayered films are fabricated via spin coating of diluted phospholipid solutions. A focused beam of an Ar+ laser at λ=514nm and a 1∕e2 spot diameter of 2.5μm is used to locally remove the coating and fabricate micropatterns. Subsequently, the temporal stability of such patterns at ambient conditions in air and in water is examined using optical microscopy. Generally, these patterns are stable on a time scale of several hours to days, both in air and in water, and hence provide sufficient time for most follow-on experiments. The spin-coated phospholipid films, though, are intrinsically unstable in water. In particular, some hours after immersion in water, dewetting of the film starts to set in. The implications of these results for potential applications are discussed.
Organization of the gene for human factor XI (1987)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTOrganization of the gene for human factor XIRei Asakai, Earl W. Davie, and Dominic W. ChungCite this: Biochemistry 1987, 26, 23, 7221–7228Publication Date (Print):November 1, 1987Publication History Published online1 May 2002Published inissue 1 November 1987https://pubs.acs.org/doi/10.1021/bi00397a004https://doi.org/10.1021/bi00397a004research-articleACS PublicationsRequest reuse permissionsArticle Views167Altmetric-Citations113LEARN 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
The sre gene (ORF469) encodes a site-specific recombinase responsible for integration of the R4 phage genome (1996)

The sre gene (ORF469) of the R4 phage encodes a protein similar to the resolvase-DNA invertase family proteins. Insertional gene disruption of sre prevented a lysogen from entering the lytic cycle, implying that Sre protein is a site-specific recombinase needed for excision of the R4 prophage genome (M. Matsuura, T. Noguchi, T. Aida, M. Asayama, H. Takahashi, and M. Shirai, J. Gen. Appl. Microbiol. 41:53-61, 1995). To determine whether this sre gene is also necessary for the integration reaction, we studied its function by integration plasmid analysis. When deletions, frameshifts, and site-directed mutations that caused an amino acid substitution of Ser-17 for Ala were introduced into the sre structural gene, transformation efficiency of Streptomyces parvulus 2297 with these plasmid DNAs was severely reduced. However, an adenine insertion just before the possible initiation codon of the sre gene did not significantly decrease the efficiency. These data suggest that the Sre protein is a site-specific recombinase responsible for integration of the R4 phage genome.
Solution Structure of a Hydrocarbon Stapled Peptide Inhibitor in Complex with Monomeric C-terminal Domain of HIV-1 Capsid (2008)

The human immunodeficiency virus type 1 (HIV-1) capsid protein plays a critical role in virus core particle assembly and is an important target for novel therapeutic strategies. In a previous study, we characterized the binding affinity of a hydrocarbon stapled helical peptide, NYAD-1, for the capsid protein (K(d) approximately 1 mum) and demonstrated its ability to penetrate the cell membrane (Zhang, H., Zhao, Q., Bhattacharya, S., Waheed, A. A., Tong, X., Hong, A., Heck, S., Goger, M., Cowburn, D., Freed, E. O., and Debnath, A. K. (2008) J. Mol. Biol. 378, 565-580). In cell-based assays, NYAD-1 colocalized with the Gag polyprotein during traffic to the plasma membrane and disrupted the formation of mature and immature virus particles in vitro systems. Here, we complement the cellular and biochemical data with structural characterization of the interactions between the capsid and a soluble peptide analogue, NYAD-13. Solution NMR methods were used to determine a high resolution structure of the complex between the inhibitor and a monomeric form of the C-terminal domain of the capsid protein (mCA-CTD). The intermolecular interactions are mediated by the packing of hydrophobic side chains at the buried interface and unperturbed by the presence of the olefinic chain on the solvent-exposed surface of the peptide. The results of the structural analysis provide valuable insight into the determinants for high affinity and selective inhibitors for HIV-1 particle assembly.
Synthesis of Potential Anticancer Agents. VII. Some 3-Chloropropionyl Amides1-3 (1962)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTSynthesis of Potential Anticancer Agents. VII. Some 3-Chloropropionyl Amides1-3Frank D. Popp, Ernest. Cullen, Robert B. Davis, and Warren. KirschCite this: J. Med. Chem. 1962, 5, 2, 398–403Publication Date (Print):March 1, 1962Publication History Published online1 May 2002Published inissue 1 March 1962https://doi.org/10.1021/jm01237a018RIGHTS & PERMISSIONSArticle Views86Altmetric-Citations4LEARN 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 (273 KB) Get e-Alerts
Expression of Respiratory Syncytial Virus-Induced Chemokine Gene Networks in Lower Airway Epithelial Cells Revealed by cDNA Microarrays (2001)

The Paramyxovirus respiratory syncytial virus (RSV) is the primary etiologic agent of serious epidemic lower respiratory tract disease in infants, immunosuppressed patients, and the elderly. Lower tract infection with RSV is characterized by a pronounced peribronchial mononuclear infiltrate, with eosinophilic and basophilic degranulation. Because RSV replication is restricted to airway epithelial cells, where RSV replication induces potent expression of chemokines, the epithelium is postulated to be a primary initiator of pulmonary inflammation in RSV infection. The spectrum of RSV-induced chemokines expressed by alveolar epithelial cells has not been fully investigated. In this report, we profile the kinetics and patterns of chemokine expression in RSV-infected lower airway epithelial cells (A549 and SAE). In A549 cells, membrane-based cDNA macroarrays and high-density oligonucleotide probe-based microarrays identified inducible expression of CC (I-309, Exodus-1, TARC, RANTES, MCP-1, MDC, and MIP-1 alpha and -1 beta), CXC (GRO-alpha, -beta, and -gamma, ENA-78, interleukin-8 [IL-8], and I-TAC), and CX(3)C (Fractalkine) chemokines. Chemokines not previously known to be expressed by RSV-infected cells were independently confirmed by multiprobe RNase protection assay, Northern blotting, and reverse transcription-PCR. High-density microarrays performed on SAE cells confirmed a similar pattern of RSV-inducible expression of CC chemokines (Exodus-1, RANTES, and MIP-1 alpha and -1 beta), CXC chemokines (I-TAC, GRO-alpha, -beta, and -gamma, and IL-8), and Fractalkine. In contrast, TARC, MCP-1, and MDC were not induced, suggesting the existence of distinct genetic responses for different types of airway-derived epithelial cells. Hierarchical clustering by agglomerative nesting and principal-component analyses were performed on A549-expressed chemokines; these analyses indicated that RSV-inducible chemokines are ordered into three related expression groups. These data profile the temporal changes in expression by RSV-infected lower airway epithelial cells of chemokines, chemotactic proteins which may be responsible for the complex cellular infiltrate in virus-induced respiratory inflammation.
Toward Understanding Insulin Fibrillation (1997)

Formation of insulin fibrils is a physical process by which partially unfolded insulin molecules interact with each other to form linear aggregates. Shielding of hydrophobic domains is the main driving force for this process, but formation of intermolecular beta-sheet may further stabilize the fibrillar structure. Conformational displacement of the B-chain C-terminal with exposure of nonpolar, aliphatic core residues, including A2, A3, B11, and B15, plays a crucial role in the fibrillation process. Recent crystal analyses and molecular modeling studies have suggested that when insulin fibrillates this exposed domain interacts with a hydrophobic surface domain formed by the aliphatic residues A13, B6, B14, B17, and B18, normally buried when three insulin dimers form a hexamer. In rabbit immunization experiments, insulin fibrils did not elicit an increased immune response with respect to formation of IgG insulin antibodies when compared with native insulin. In contrast, the IgE response increased with increasing content of insulin in fibrillar form. Strategies and practical approaches to prevent insulin from forming fibrils are reviewed. Stabilization of the insulin hexameric structure and blockage of hydrophobic interfaces by addition of surfactants are the most effective means of counteracting insulin fibrillation.
Local wound environment and epidermal healing. Mitotic response (1972)

The effects of air exposure and occlusion on the mitotic response to wounding were studied. Sites on the dorsal skin of six human volunteers were tape-stripped to remove the stratum corneum. This series of wounds was left either air-exposed, or covered by an occlusive film. The magnitude and duration of mitotic response were significantly greater in the air-exposed than occluded wounds. The wounded epidermis returned to the baseline levels of cell division at seven to ten days with occlusion and at 12 to 14 days with air exposure. The mitotic response to tape-stripping is mediated in a two fold manner: (1) mitosis induced by removal of the stratum corneum, and (2) a second, additive mitotic response to a loss of cells in the malpighian layer.
Phosphorylation Regulates c-Myc's Oncogenic Activity in the Mammary Gland (2011)

Expression of the c-Myc oncoprotein is affected by conserved threonine 58 (T58) and serine 62 (S62) phosphorylation sites that help to regulate c-Myc protein stability, and altered ratios of T58 and S62 phosphorylation have been observed in human cancer. Here, we report the development of 3 unique c-myc knock-in mice that conditionally express either c-Myc(WT) or the c-Myc(T58A) or c-Myc(S62A) phosphorylation mutant from the constitutively active ROSA26 locus in response to Cre recombinase to study the role of these phosphorylation sites in vivo. Using a mammary-specific Cre model, we found that expression of c-Myc(WT) resulted in increased mammary gland density, but normal morphology and no tumors at the level expressed from the ROSA promoter. In contrast, c-Myc(T58A) expression yielded enhanced mammary gland density, hyperplastic foci, cellular dysplasia, and mammary carcinoma, associated with increased genomic instability and suppressed apoptosis relative to c-Myc(WT). Alternatively, c-Myc(S62A) expression reduced mammary gland density relative to control glands, and this was associated with increased genomic instability and normal apoptotic function. Our results indicate that specific activities of c-Myc are differentially affected by T58 and S62 phosphorylation. This model provides a robust platform to interrogate the role that these phosphorylation sites play in c-Myc function during development and tumorigenesis.
SDR and MDR: completed genome sequences show these protein families to be large, of old origin, and of complex nature (1999)

Short-chain dehydrogenases/reductases (SDR) and medium-chain dehydrogenases/reductases (MDR) are protein families originally distinguished from characterisations of alcohol dehydrogenase of these two types. Screening of completed genome sequences now reveals that both these families are large, wide-spread and complex. In Escherichia coli alone, there are no fewer than 17 MDR forms, identified as open reading frames, considerably extending previously known MDR relationships in prokaryotes and including ethanol-active alcohol dehydrogenase. In entire databanks, 1056 SDR and 537 MDR forms are currently known, extending the multiplicity further. Complexity is also large, with several enzyme activity types, subgroups and evolutionary patterns. Repeated duplications can be traced for the alcohol dehydrogenases, with independent enzymogenesis of ethanol activity, showing a general importance of this enzyme activity.
Molecular bases of CRM+ factor X deficiency: a frequent mutation (Ser334Pro) in the catalytic domain and a substitution (Glul02Lys) in the second EGF‐like domain (1995)

The presence of gene lesions in coagulation factor X (FX, Stuart factor) was investigated in asymptomatic subjects with FX deficiency characterized by the presence of dysfunctional molecules in plasma, as demonstrated by the discrepancy between clotting activity and antigen level. A missense mutation (Ser334Pro) in the catalytic domain was found in three unrelated families in both the homozygous and the heterozygous conditions, and also in the compound heterozygous form with the substitution of Lys for 102 Glu. None of the mutations was detected in 40 unrelated subjects from the same geographic area. The Ser334Pro mutation affects a serine protease region characterized by extensive variation in the coagulation factors but conserved in mammalian factor X molecules. The Glu102Lys mutation affects a residue of the second EGF-like module also conserved in protein C. Both mutated residues are surface-exposed and found in protein regions suggested to be involved in macromolecular interactions which are impaired in the dysfunctional molecules.
Probabilistic calling context (2007)

Calling context enhances program understanding and dynamic analyses by providing a rich representation of program location. Compared to imperative programs, object-oriented programs use more interprocedural and less intraprocedural control flow, increasing the importance of context sensitivity for analysis. However, prior online methods for computing calling context, such as stack-walking or maintaining the current location in a calling context tree, are expensive in time and space. This paper introduces a new online approach called probabilistic calling context (PCC) that continuously maintains a probabilistically unique value representing the current calling context. For millions of unique contexts, a 32-bit PCC value has few conflicts. Computing the PCC value adds 3% average overhead to a Java virtual machine. PCC is well-suited to clients that detect new or anomalous behavior since PCC values from training and production runs can be compared easily to detect new context-sensitive behavior; clients that query the PCC value at every system call, Java utility call, and Java API call add 0-9% overhead on average. PCC adds space overhead proportional to the distinct contexts stored by the client (one word per context). Our results indicate PCC is efficient and accurate enough to use in deployed software for residual testing, bug detection, and intrusion detection.
IL-7 and IL-15 allow the generation of suicide gene–modified alloreactive self-renewing central memory human T lymphocytes (2008)

Long-term clinical remissions of leukemia, after allogeneic hematopoietic stem cell transplantation, depend on alloreactive memory T cells able to self-renew and differentiate into antileukemia effectors. This is counterbalanced by detrimental graft-versus-host disease (GVHD). Induction of a selective suicide in donor T cells is a current gene therapy approach to abrogate GVHD. Unfortunately, genetic modification reduces alloreactivity of lymphocytes. This associates with an effector memory (T(EM)) phenotype of gene-modified lymphocytes and may limit antileukemia effect. We hypothesized that alloreactivity of gene-modified lymphocytes segregates with the central memory (T(CM)) phenotype. To this, we generated suicide gene-modified T(CM) lymphocytes with a retroviral vector after CD28 costimulation and culture with IL-2, IL-7, or a combination of IL-7 and IL-15. In vitro, suicide gene-modified T(CM) cells self-renewed upon alloantigen stimulation and resisted activation-induced cell death. In a humanized mouse model, only suicide gene-modified T cells cultured with IL-7 and IL-15 persisted, differentiated in T(EM) cells, and were as potent as unmanipulated lymphocytes in causing GVHD. GVHD was halted through the activation of the suicide gene machinery. These results warrant the use of suicide gene-modified T(CM) cells cultured with IL-7 and IL-15 for the safe exploitation of the alloreactive response against cancer.
Analysis of single DNA molecules translocating through nanochannels fabricated in SiO2 (2008)

The electrokinetically-driven translocation of λ-phage DNA is measured in nanochannels with critical dimensions (width:depth=1:1) below 100 nm and as small as 20 nm. The channels are fabricated using focused ion beam milling of SiO2 substrates, accessed by microchannels fabricated using standard photolithography and wet etching protocols, and sealed by fusion bonding of a coverslip to the substrate.
Stent Fracture in the Coronary and Peripheral Arteries (2010)

Inherent risks of stenting include restenosis and thrombosis. Recently, stent fractures have been recognized as a complication that may result in thrombosis, perforation, restenosis, and migration of the stent resulting in morbidity and mortality. Stent fractures were originally seen in the superficial femoral arteries but have since then been reported in almost all vascular sites including the coronary, renal, carotid, iliac, and femoropopliteal arteries. Fractures are the result of the complex interplay between stent manufacturing, the stented segment, pulsatile and nonpulsatile biomechanical forces, and plaque morphology at a particular vascular site. The presentation of a patient with a fracture is highly variable, ranging from asymptomatic in nature, detected on routine screening without any sequelae, to sudden cardiac death related to a thrombosed coronary artery. Despite being recognized as an important complication, consensus on routine surveillance and diagnostic methods to detect fractures continues to be lacking. Fortunately, most cases are relatively benign and can be managed conservatively if detected. In the setting of recurrent symptoms, further intervention is usually sought. In review of the literature most cases are managed with placement of a stent over the fractured area, the stent-in-stent technique, but several other alternatives may be available. As the knowledge of the variables that make stents prone to fracture are identified, better technologies and techniques can be employed to minimize the risk of this complication. This article reviews the available literature on stent fractures and complications using data found on PubMed, MEDLINE, the Manufacturer and User Facility Device Experience (MAUDE) database, and the Cochrane databases.
Adaptive Classification on Brain-Computer Interfaces Using Reinforcement Signals (2012)

We introduce a probabilistic model that combines a classifier with an extra reinforcement signal (RS) encoding the probability of an erroneous feedback being delivered by the classifier. This representation computes the class probabilities given the task related features and the reinforcement signal. Using expectation maximization (EM) to estimate the parameter values under such a model shows that some existing adaptive classifiers are particular cases of such an EM algorithm. Further, we present a new algorithm for adaptive classification, which we call constrained means adaptive classifier, and show using EEG data and simulated RS that this classifier is able to significantly outperform state-of-the-art adaptive classifiers.