gebhart/patrepeval huggingface dataset:
The effect of packaging after 1-MCP treatment on color changes and chlorophyll degradation of broccoli (Brassica oleracea var. italica cv. Monopoly) (2007)

Broccoli is a highly perishable floral vegetable whose postharvest quality is influenced by transport and storage environment, particularly ethylene. Endogenously produced ethylene promotes sepal yellowing and shortens storage life whereas packaging delays color changes and prolongs storage life because of reduced respiration and ethylene production. We tested the effectiveness of the ethylene action inhibitor 1methycyclopropene (1-MCP), as a complement to packaging to maintain postharvest quality of broccoli. ‘Monopoly’ broccoli (Brassica oleracea var. italica) heads were treated with 0.05 mg/l of MCP and packaged using three different packaging materials such as polyvinylchloride (PVC) films of 8.5 (P1) and 14 µm thickness (P2) and polyethylene (PE) bags (P3). After that broccoli heads were stored in a cold room set at 5°C temperature and 95-98% relative humidity (RH). Packaging especially in P1 bags after 1-MCP treatment delayed chlorophyll degradation and colour changes in broccoli. Hue angle of broccoli colour and chlorophyll loss were correlated. Also weight loss was reduced especially in P1 packaged broccoli.
Open Source System for Analyzing, Validating, and Storing Protein Identification Data (2004)

This paper describes an open-source system for analyzing, storing, and validating proteomics information derived from tandem mass spectrometry. It is based on a combination of data analysis servers, a user interface, and a relational database. The database was designed to store the minimum amount of information necessary to search and retrieve data obtained from the publicly available data analysis servers. Collectively, this system was referred to as the Global Proteome Machine (GPM). The components of the system have been made available as open source development projects. A publicly available system has been established, comprised of a group of data analysis servers and one main database server.
Increased expression of high mobility group protein I(Y) in high grade prostatic cancer determined by in situ hybridization. (1993)

In a previous study using the Dunning rat prostate cancer model, we found high mobility group protein I-(Y) [HMG-I(Y)] to be overexpressed in metastatic tumor lines when compared to nonmetastatic lines. Hence, overexpression of this 12-kDa non-histone chromosomal protein may be associated with tumor progression. Firstly, by Northern analysis we showed that HMG-I(Y) expression increases in high grade prostate tumors. These studies, however, required fresh material, and clinical follow-up was limited. To overcome this problem paraffin-embedded material must be made amenable for determination of HMG-I(Y) expression in retrospective studies. RNA in situ hybridization enables the evaluation of mRNA levels in such material. We studied tumors from 71 patients with prostate cancer. The microscopic analysis of each sample included: (a) hybridization on sections with sense HMG-I(Y) and (b) 28S rRNA probes (nonspecific signal); (c) hybridization with antisense 28S rRNA (RNA preservation); (d) hybridization with an antisense HMG-I(Y) probe [quantification of HMG-I(Y) mRNA in the expressing areas]. Data were quantified using an image analysis system. High expression of HMG-I(Y) was observed in regions with high Gleason grade (4 and 5); whereas in lesions of Gleason grade 3, both weak and no expression was observed. In areas of grade 1 and 2, as well as in normal glands, low or no expression was found. We conclude that HMG-I(Y) expression assessed by RNA in situ hybridization is related to tumor differentiation in prostate cancer. These findings indicate that HMG-I(Y) expression may be a marker in prostate cancer diagnosis, and the possible clinical implication of expression of this gene in malignancy is discussed in this report.
Levodopa-induced dyskinesias are improved by fluoxetine (1995)

We evaluated the severity of motor disability and dyskinesias in seven levodopa-responsive patients with Parkinson's disease after an acute challenge with the mixed dopamine agonist, apomorphine, before and after the administration of fluoxetine (20 mg twice per day) for 11 +/- 1 days. After fluoxetine treatment, there was a significant 47% improvement (p < 0.05) of apomorphine-induced dyskinesias without modification of parkinsonian motor disability. The dyskinesias were reduced predominantly in the lower limbs during the onset and disappearance of dystonic dyskinesias (onset- and end-of-dose dyskinesias) and in the upper limbs during choreic mid-dose dyskinesias. The results suggest that increased brain serotoninergic transmission with fluoxetine may reduce levodopa- or dopamine agonist-induced dyskinesias without aggravating parkinsonian motor disability.
Molecular Characterization of abLIM, a Novel Actin-binding and Double Zinc Finger Protein (1997)

Molecules that couple the actin-based cytoskeleton to intracellular signaling pathways are central to the processes of cellular morphogenesis and differentiation. We have characterized a novel protein, the actin-binding LIM (abLIM) protein, which could mediate such interactions between actin filaments and cytoplasmic targets. abLIM protein consists of a COOH-terminal cytoskeletal domain that is fused to an NH2-terminal domain consisting of four double zinc finger motifs. The cytoskeletal domain is approximately 50% identical to erythrocyte dematin, an actin-bundling protein of the red cell membrane skeleton, while the zinc finger domains conform to the LIM motif consensus sequence. In vitro expression studies demonstrate that abLIM protein can bind to F-actin through the dematin-like domain. Transcripts corresponding to three distinct isoforms have a widespread tissue distribution. However, a polypeptide corresponding to the full-length isoform is found exclusively in the retina and is enriched in biochemical extracts of retinal rod inner segments. abLIM protein also undergoes extensive phosphorylation in light-adapted retinas in vivo, and its developmental expression in the retina coincides with the elaboration of photoreceptor inner and outer segments. Based on the composite primary structure of abLIM protein, actin-binding capacity, potential regulation via phosphorylation, and isoform expression pattern, we speculate that abLIM may play a general role in bridging the actin-based cytoskeleton with an array of potential LIM protein-binding partners. The developmental time course of abLIM expression in the retina suggests that the retina-specific isoform may have a specialized role in the development or elaboration of photoreceptor inner and outer segments.
Protein kinase inhibitors substantially improve the physical detection of T-cells with peptide-MHC tetramers (2008)

Flow cytometry with fluorochrome-conjugated peptide-major histocompatibility complex (pMHC) tetramers has transformed the study of antigen-specific T-cells by enabling their visualization, enumeration, phenotypic characterization and isolation from ex vivo samples. Here, we demonstrate that the reversible protein kinase inhibitor (PKI) dasatinib improves the staining intensity of human (CD8+ and CD4+) and murine T-cells without concomitant increases in background staining. Dasatinib enhances the capture of cognate pMHC tetramers from solution and produces higher intensity staining at lower pMHC concentrations. Furthermore, dasatinib reduces pMHC tetramer-induced cell death and substantially lowers the T-cell receptor (TCR)/pMHC interaction affinity threshold required for cell staining. Accordingly, dasatinib permits the identification of T-cells with very low affinity TCR/pMHC interactions, such as those that typically predominate in tumour-specific responses and autoimmune conditions that are not amenable to detection by current technology.
A microfluidic oligonucleotide synthesizer (2010)

De novo gene and genome synthesis enables the design of any sequence without the requirement of a pre-existing template as in traditional genetic engineering methods. The ability to mass produce synthetic genes holds great potential for biological research, but widespread availability of de novo DNA constructs is currently hampered by their high cost. In this work, we describe a microfluidic platform for parallel solid phase synthesis of oligonucleotides that can greatly reduce the cost of gene synthesis by reducing reagent consumption (by 100-fold) while maintaining a approximately 100 pmol synthesis scale so there is no need for amplification before assembly. Sixteen oligonucleotides were synthesized in parallel on this platform and then successfully used in a ligation-mediated assembly method to generate DNA constructs approximately 200 bp in length.
Cloning and expression of endostatin in escherichia coli (2000)

The total RNA was extracted from the fetal liver and the endostatin gene was amplifieated by RT-PCR. After identified by DNA sequencing, it was cloned into the expression vector pGEX-KG and then transformed into the host cells E. coli DH5alpha and BL21. Subsequently the recombinant GST-fusion protein was expressed and purified.
Immunopathogenesis of schistosomiasis (2004)

In schistosomiasis mansoni, the chronic egg-induced granulomatous response in the liver and intestines may eventually cause extensive tissue scarring and development of portal hypertension. Indeed, much of the morbidity and mortality associated with this disease is directly attributable to the deposition of connective tissue elements in affected tissues. Elucidating the mechanisms that regulate the severity of schistosomiasis has been a major research objective over the past several years. Research conducted with DNA microarrays as well as investigations with a variety of gene knock-out mice have been particularly helpful in achieving this goal. A notable accomplishment in the past few years was the identification of interleukin-13 (IL-13) and the IL-13 receptor complex as central regulators of disease progression in schistosomiasis. Liver fibrogenesis is severely decreased in infected IL-13-deficient mice as well as in wildtype animals treated with IL-13 antagonists. In contrast, IL-13 effector function increases dramatically in IL-13 receptor alpha2 (IL-13Ralpha2)-deficient mice. These mice develop severe hepatic fibrosis, fail to downregulate granuloma formation in the chronic phase of S. mansoni infection, and succumb to the disease at an accelerated rate; thus, identifying the 'decoy' IL-13 receptor as a critical life sustaining 'off' switch for tissue damaging egg-induced inflammation.
Combinations of Cytochrome P450 Gene Polymorphisms Enhancing the Risk for Sporadic Colorectal Cancer Related to Red Meat Consumption (2007)

Susceptibility to sporadic colorectal cancers (CRC) is generally thought to be the sum of complex interactions between environmental and genetic factors, all of which contribute independently, producing only a modest effect on the whole phenomenon. However, to date, most research has concealed the notion of interaction and merely focused on dissociate analyses of risk factors to highlight associations with CRC. By contrast, we have chosen a combinative approach here to explore the joint effects of several factors at a time. Through an association study based on 1,023 cases and 1,121 controls, we examined the influence on CRC risk of environmental factors coanalyzed with combinations of six single nucleotide polymorphisms located in cytochrome P450 genes (c.-163A>C and c.1548T>C in CYP1A2, g.-1293G>C and g.-1053C>T in CYP2E1, c.1294C>G in CYP1B1, and c.430C>T in CYP2C9). Whereas separate analyses of the SNPs showed no effect on CRC risk, three allelic variant combinations were found to be associated with a significant increase in CRC risk in interaction with an excessive red meat consumption, thereby exacerbating the intrinsic procarcinogenic effect of this dietary factor. One of these three predisposing combinations was also shown to interact positively with obesity. Provided that they are validated, our results suggest the need to develop robust combinative methods to improve genetic investigations into the susceptibility to CRC.
Osmometric study of the subunit dissociation of hemoglobin Porto Alegre [beta 9(A6)Ser----Cys] dissulfide polymer. (1987)

The hemoglobin Porto Alegre (HbPA) disulfide polymer dodecamer and the HbPA, HbA disulfide polymer octamer subunit dissociation by NaCl was studied by measuring the osmotic pressure of CO-hemoglobin solutions at pH = 6.9 and 20 degrees C. The dissociation equilibrium constants were evaluated from the osmotic pressure data. The subunit dissociation of the two types of disulfide polymers follows a reaction of the type A3 in equilibrium 3A. The HbPA disulfide polymer dodecamer appears to be more susceptible to NaCl induced dissociation than is normal HbA and less resistant to dissociation on protein dilution. The HbPA, HbA disulfide polymer octamer appears to be much more susceptible to dissociation on protein dilution than is the HbPA disulfide polymer dodecamer and normal HbA. The standard free energy of dissociation of the HbPA disulfide polymer at 2 M NaCl is delta GOD(25 degrees C) = 12 kcal/mole. The type of dissociation reaction (A3 in equilibrium with 3A) support the conclusion that the HbPA disulfide polymer has a quaternary molecular structure of a closed ring of three tetramers.
Computer-aided molecular design of highly potent HIV-1 RT inhibitors: 3D QSAR and molecular docking studies of efavirenz derivatives (2006)

Ligand- and structure-based design approaches have been applied to an extended series of 74 efavirenz compounds effectively inhibiting wild type (WT) and mutant type (K103N) HIV-1 reverse transcriptase (RT). For ligand-based approach, three dimensional quantitative structure-activity relationship (3D-QSAR) methods, comparative molecular field analysis (CoMFA) and comparative similarity indices analysis (CoMSIA), were performed. The starting geometry of efavirenz was obtained from X-ray crystallographic data. The efavirenz derivatives were constructed and fully optimized by ab-initio molecular orbital method at HF/3-21G level. Reliable QSAR models for high predictive abilities were developed. Regarding WT and K103N inhibitions, CoMFA models with r2/cv = 0.651 and 0.678 and CoMSIA models with r2/cv = 0.662 and 0.743 were derived, respectively. The interpretation obtained from the models highlights different structural requirements for inhibition of WT and K103N HIV-1 RT. To elucidate potential binding modes of efavirenz derivatives in the binding pocket of WT and K103N HIV-1 RT, structure-based approach based on computational docking studies of selected efavirenz compounds were performed by using GOLD and FlexX programs. The results derived from docking analysis give additional information and further probe the inhibitor-enzyme interactions. The correlation of the results obtained from 3D QSAR and docking models validate each other and lead to better understanding of the structural requirements for the activity. Therefore, these integrated results are informative to provide key features and a helpful guideline for novel compound design active against HIV-1 RT.
Pd–carbene catalyzed carbonylation reactions of aryl iodides (2011)

A series of carbene complexes [PdBr(2)((i)Pr(2)-bimy)L] (C2-C13) with different types of co-ligands (L) have been tested for their catalytic activities in the carbonylative annulation of 2-iodophenol with phenylacetylene in DMF to afford the respective flavone 2a. Complex C12 with an N-phenylimidazole co-ligand showed the best activity and also afforded high yields when the substrate scope was extended to other aryl or pyridyl acetylenes. In addition, catalyst C12 was also efficient in the carbonylative annulation of 2-iodoaniline with acid chlorides giving the desirable 2-substituted 4H-3,1-benzoxazin-4-ones (4) in good yields. Additionally, this Pd-NHC complex also proved to be a very efficient catalyst for the hydroxycarbonylation of iodobenzene derivatives at low catalyst loading and under low CO pressure. These results demonstrate the versatility and efficiency of this phosphine-free Pd(II)-NHC complex in different types of carbonylations of aryl iodides under mild conditions.
The Escherichia coli AlkB protein protects human cells against alkylation-induced toxicity (1994)

Escherichia coli can ameliorate the toxic effects of alkylating agents either by preventing DNA alkylation or by repairing DNA alkylation damage. The alkylation-sensitive phenotype of E. coli alkB mutants marks the alkB pathway as an extremely effective defense mechanism against the cytotoxic effects of the SN2, but not the SN1, alkylating agents. Although it is clear that AlkB helps cells to better handle alkylated DNA, no DNA alkylation repair function could be assigned to the purified AlkB protein, suggesting that AlkB either acts as part of a complex or acts to regulate the expression of other genes whose products are directly responsible for alkylation resistance. However, here we present evidence that the provision of alkylation resistance is an intrinsic function of the AlkB protein per se. We expressed the E. coli AlkB protein in two human cell lines and found that it confers the same characteristic alkylation-resistant phenotype in this foreign environment as it does in E. coli. AlkB expression rendered human cells extremely resistant to cell killing by the SN2 but not the SN1 alkylating agents but did not affect the ability of dimethyl sulfate (an SN2 agent) to alkylate the genome. We infer that SN2 agents produce a class of DNA damage that is not efficiently produced by SN1 agents and that AlkB somehow prevents this damage from killing the cell.
Genomic Evolution of Breast Cancer Metastasis and Relapse (2017)

Patterns of genomic evolution between primary and metastatic breast cancer have not been studied in large numbers, despite patients with metastatic breast cancer having dismal survival. We sequenced whole genomes or a panel of 365 genes on 299 samples from 170 patients with locally relapsed or metastatic breast cancer. Several lines of analysis indicate that clones seeding metastasis or relapse disseminate late from primary tumors, but continue to acquire mutations, mostly accessing the same mutational processes active in the primary tumor. Most distant metastases acquired driver mutations not seen in the primary tumor, drawing from a wider repertoire of cancer genes than early drivers. These include a number of clinically actionable alterations and mutations inactivating SWI-SNF and JAK2-STAT3 pathways.
A robotic architecture for action selection and behavioral organization inspired by human cognition (2012)

Robotic agents that interact with humans and perform complex, everyday tasks in natural environments will require a system to autonomously organize their behavior. Current systems for robotic behavioral organization typically abstract from the low-level sensory-motor embodiment of the robot, leading to a gap between the level at which a sequence of actions is planned and the levels of perception and motor control. This gap is a major bottleneck for the autonomy of systems in complex, dynamic environments. To address this issue, we present a neural-dynamic framework for behavioral organization, in which the action selection mechanism is tightly coupled to the agent's sensory-motor systems. The elementary behaviors (EBs) of the robot are dynamically organized into sequences based on task-specific behavioral constraints and online perceptual information. We demonstrate the viability of our approach by implementing a neural-dynamic architecture on the humanoid robot NAO. The system is capable of producing sequences of EBs that are directed at objects (e.g., grasping and pointing). The sequences are flexible in that the robot autonomously adapts the individual EBs and their sequential order in response to changes in the sensed environment. The architecture can accommodate different tasks and can be articulated for different robotic platforms. Its neural-dynamic substrate is particularly well-suited for learning and adaptation.
Enhanced chemosensitivity to CPT-11 with proteasome inhibitor PS-341: implications for systemic nuclear factor-kappaB inhibition. (2001)

Inducible activation of nuclear factor-kappaB (NF-kappaB) inhibits the apoptotic response to chemotherapy and irradiation. Activation of NF-kappaB via phosphorylation of an inhibitor protein IkappaB leads to degradation of IkappaB through the ubiquitin-proteasome pathway. We hypothesized that inactivation of proteasome function will inhibit inducible NF-kappaB activation, thereby increasing levels of apoptosis in response to chemotherapy and enhancing antitumor effects. To assess the effects of proteasome inhibition on chemotherapy response, human colorectal cancer cells were pretreated with the dipeptide boronic acid analogue PS-341 (1 microM) prior to exposure to SN-38, the active metabolite of the topoisomerase I inhibitor, CPT-11. Inducible activation of NF-kappaB and growth response were evaluated in vitro and in vivo. Effects on p53, p21, p27 and apoptosis were determined. Pretreatment with PS-341 inhibited activation of NF-kappaB induced by SN-38 and resulted in a significantly higher level of growth inhibition (64-75%) compared with treatment with PS-341 alone (20-30%) or SN-38 alone (24-47%; P < 0.002). Combination therapy resulted in a 94% decrease in tumor size compared with the control group and significantly improved tumoricidal response to treatment compared with all treatment groups (P = 0.02). The level of apoptosis was 80-90% in the treatment group that received combination treatment compared with treatment with single agent alone (10%). Proteasome inhibition blocks chemotherapy-induced NF-kappaB activation, leading to a dramatic augmentation of chemosensitivity and enhanced apoptosis. Combining proteasome inhibition with chemotherapy has significant potential to overcome the high incidence of chemotherapy resistance. Clinical studies are currently in development to evaluate the role of proteasome inhibition as an important adjuvant to systemic chemotherapy.
In vivo Cerebral Protein Synthesis Rates with Leucyl-Transfer RNA Used as a Precursor Pool: Determination of Biochemical Parameters to Structure Tracer Kinetic Models for Positron Emission Tomography (1989)

Leucine oxidation and incorporation into proteins were examined in the in vivo rat brain to determine rates and compartmentation of these processes for the purpose of structuring mathematical compartmental models for the noninvasive estimation of in vivo human cerebral protein synthesis rates (CPSR) using positron emission tomography (PET). Leucine specific activity (SA) in arterial plasma and intracellular free amino acids, leucyl-tRNA, alpha-ketoisocaproic acid (KIC), and protein were determined in whole brain of the adult rat during the first 35 min after intravenous bolus injection of L-[1-14C]leucine. Incorporation of leucine into proteins accounted for 90% of total brain radioactivity at 35 min. The lack of [14C]KIC buildup indicates that leucine oxidation in brain is transaminase limited. Characteristic specific activities were maximal between 0 to 2 min after bolus injection with subsequent decline following the pattern: plasma leucine greater than or equal to leucyl-tRNA approximately KIC greater than intracellular leucine. The time integral of leucine SA in plasma was about four times that of tissue leucine and twice those of leucyl-tRNA and KIC, indicating the existence of free leucine, leucyl-tRNA, and KIC tissue compartments, communicating directly with plasma, and separate secondary free leucine, leucyl-tRNA, and KIC tissue compartments originating in unlabeled leucine from proteolysis. Therefore, a relatively simple model configuration based on the key assumptions that (a) protein incorporation and catabolism proceed from a precursor pool communicating with the plasma space, and (b) leucine catabolism is transaminase limited is justified for the in vivo assessment of CPSR from exogenous leucine sources using PET in humans.