gebhart/patrepeval huggingface dataset:
A multicentre evaluation of a new filtration protocol for leucocyte depletion of high‐haematocrit red blood cells collected by an automated blood collection system (2001)

Immediate, on-line, high-haematocrit filtration of red cells collected on Trima resulted in leucoreduced RBCs, which met the AABB and Council of Europe criteria.
Integration of Chloroplast Nucleic Acid Metabolism into the Phosphate Deprivation Response in Chlamydomonas reinhardtii (2007)

Cell survival depends on the cell's ability to acclimate to phosphorus (P) limitation. We studied the chloroplast ribonuclease polynucleotide phosphorylase (PNPase), which consumes and generates phosphate, by comparing wild-type Chlamydomonas reinhardtii cells with strains with reduced PNPase expression. In the wild type, chloroplast RNA (cpRNA) accumulates under P limitation, correlating with reduced PNPase expression. PNPase-deficient strains do not exhibit cpRNA variation under these conditions, suggesting that in the wild type PNPase limits cpRNA accumulation under P stress. PNPase levels appear to be mediated by the P response regulator PHOSPHORUS STARVATION RESPONSE1 (PSR1), because in psr1 mutant cells, cpRNA declines under P limitation and PNPase expression is not reduced. PNPase-deficient cells begin to lose viability after 24 h of P depletion, suggesting that PNPase is important for cellular acclimation. PNPase-deficient strains do not have enhanced sensitivity to other physiological or nutrient stresses, and their RNA and cell growth phenotypes are not observed under P stress with phosphite, a phosphate analog that blocks the stress signal. In contrast with RNA metabolism, chloroplast DNA (cpDNA) levels declined under P deprivation, suggesting that P mobilization occurs from DNA rather than RNA. This unusual phenomenon, which is phosphite- and PSR1-insensitive, may have evolved as a result of the polyploid nature of cpDNA and the requirement of P for cpRNA degradation by PNPase.
Regenerating Marrow Induces Systemic Increase in Osteo- and Chondrogenesis (1990)

Marrow ablation in long bones induces an increase in osteogenesis in distant skeletal sites. To test the role of marrow regeneration in this phenomenon, rat mandibular condyles were evaluated histomorphometrically during postablation healing of tibial marrow and after inhibition of healing. Ten days after removal of tibial marrow all bone formation parameters in the condylar subchondral bone were markedly elevated, indicating an enhanced osteoblastic activity. The thickness of the cartilaginous zone of calcification was also augmented. These changes were absent when postablation healing was inhibited in the tibia and after massive liver injury. Extensive periosteal injury induced only a slight increase in osteoblast activity. Except for a fall on day 7, the [methyl-3H]thymidine labeling index in the condylar cartilage and oral mucosa remained at control levels 3-18 days after ablation. These findings imply that stimulation of cell proliferation has only a secondary role in the skeletal response to marrow ablation. It is concluded that the systemic increase in osteogenesis occurs preferentially during marrow regeneration and is not a nonspecific skeletal reaction to tissue injury. Apparently, the systemic osteogenic response is mediated by circulating factors produced by the healing marrow; conceptually it is related to other instances where local repair in extraskeletal sites is accompanied by generalized alterations in respective tissues.
ERPs studies of cognitive processing during sleep (2008)

In the last few decades, several works on cognitive processing during sleep have emerged. The study of cognitive processing with event related potentials (ERPs) during sleep is a topic of great interest, since ERPs allow the study of stimulation with passive paradigms (without conscious response or behavioural response), opening multiple research possibilities during different sleep phases. We review ERPs modulated by cognitive processes during sleep: N1, Mismatch Negativity (MMN), P2, P3, N400-like, N300-N550, among others. The review shows that there are different cognitive discriminations during sleep related to the frequency, intensity, duration, saliency, novelty, proportion of appearance, meaning, and even sentential integration of stimuli. The fascinating results of cognitive processing during sleep imply serious challenges for cognitive models. The studies of ERPs, together with techniques of neuroimaging, have demonstrated the existence of cognitive processing during sleep. A fundamental question to be considered is if these cognitive phenomena are similar to processing that occurs during wakefulness. Based on this question we discussed the existence of possible mechanisms associated with sleep, as well as the specific cognitive and neurophysiologic differences of wakefulness and sleep. Much knowledge is still required to even understand the conjunction of dramatic changes in cerebral dynamics and the occurrence of cognitive processes. We propose some insights based on ERPs research for further construction of theoretical models for integrating both cognitive processing and specific brain sleep dynamics.
Effect of Sleeping Position on Upper Airway Patency in Obstructive Sleep Apnea Is Determined by the Pharyngeal Structure Causing Collapse (2017)

Improvement in pharyngeal patency with sleeping position is structure specific, with profound improvements seen in patients with epiglottic collapse, modest effects in those without tongue involvement and-unexpectedly-no effect in those with tongue-related obstruction. Our data refute the notion that the tongue falls back into the airway during sleep via gravitational influences.
Identification of Regions in Alleles of the Flax Rust Resistance Gene L That Determine Differences in Gene-for-Gene Specificity (1999)

Thirteen alleles (L, L1 to L11, and LH) from the flax L locus, which encode Toll/interleukin-1 receptor homology-nucleotide binding site-leucine-rich repeat (TIR-NBS-LRR) rust resistance proteins, were sequenced and compared to provide insight into their evolution and into the determinants of gene-for-gene resistance specificity. The predicted L6 and L11 proteins differ solely in the LRR region, whereas L6 and L7 differ solely in the TIR region. Thus, specificity differences between alleles can be determined by both the LRR and TIR regions. Functional analysis in transgenic plants of recombinant alleles constructed in vitro provided further information: L10-L2 and L6-L2 recombinants, encoding the LRR of L2, conferred L2 resistance specificity, and an L2-L10 recombinant, encoding the LRR of L10, conferred a novel specificity. The sequence comparisons also indicate that the evolution of L alleles has probably involved reassortment of variation, resulting from accumulated point mutations, by intragenic recombination. In addition, large deletion events have occurred in the LRR-encoding regions of L1 and L8, and duplication events have occurred in the LRR-encoding region of L2.
Targeted Degradation of c-Fos, But Not v-Fos, by a Phosphorylation-Dependent Signal on c-Jun (1992)

The proto-oncogene products c-Fos and c-Jun heterodimerize through their leucine zippers to form the AP-1 transcription factor. The transcriptional activity of the heterodimer is regulated by signal-dependent phosphorylation and dephosphorylation events. The stability of c-Fos was found to also be controlled by intracellular signal transduction. In transient expression and in vitro degradation experiments, the stability of c-Fos was decreased when the protein was dimerized with phosphorylated c-Jun. c-Jun protein isolated from phorbol ester-induced cells did not target c-Fos for degradation, which suggests that c-Fos is transiently stabilized after stimulation of cell growth. v-Fos protein, the retroviral counterpart of c-Fos, was not susceptible to degradation targeted by c-Jun.
Receptor-selective Variants of Human Vascular Endothelial Growth Factor (2000)

Vascular endothelial growth factor (VEGF) is a pleiotropic factor that exerts a multitude of biological effects through its interaction with two receptor tyrosine kinases, fms-like tyrosine kinase (Flt-1) or VEGF receptor 1 and kinase insert domain-containing receptor (KDR) or VEGF receptor 2. Whereas it is commonly accepted that KDR is responsible for the proliferative activities of VEGF, considerable controversy and uncertainty exist about the role of the individual receptors in eliciting many of the other effects. Based on a comprehensive mutational analysis of the receptor-binding site of VEGF, an Flt-1-selective variant was created containing four substitutions from the wild-type protein. This variant bound with wild-type affinity to Flt-1, was at least 470-fold reduced in binding to KDR, and had no activity in cell-based assays measuring autophosphorylation of KDR or proliferation of primary human vascular endothelial cells. Using a competitive phage display strategy, two KDR-selective variants were discovered with three and four changes from wild-type, respectively. Both variants had approximately wild-type affinity for KDR, were about 2000-fold reduced in binding to Flt-1, and showed activity comparable with the wild-type protein in KDR autophosphorylation and endothelial cell proliferation assays. These variants will serve as useful reagents in elucidating the roles of Flt-1 and KDR.
In vivo conversion of racemized β‐amyloid ([D‐Ser26]Aβ1–40) to truncated and toxic fragments ([D‐Ser26]Aβ25–35/40) and fragment presence in the brains of Alzheimer's patients (2002)

The lag between beta-amyloid (A beta) deposition and neurodegeneration in Alzheimer's disease (AD) suggests that age-dependent factors are involved in the pathogenesis. Racemization of Ser and Asp in A beta is a typical age-dependent modification in AD. We have shown recently that A beta1-40 racemized at Ser(26) ([D-Ser(26)]A beta 1-40) is soluble and non-toxic to neuronal cells, but is easily converted by brain proteases to truncated toxic fragments, [D-Ser(26)]A beta 25-35/40. Furthermore, [D-Ser(26)]A beta1-40 in vivo, produced a drastic and synergistic neuronal loss by enhancing the excitotoxicity when co-injected into rat hippocampus with ibotenic acid, an excitatory amino acid, suggesting an in vivo conversion of non-toxic [D-Ser(26)]A beta1-40 to toxic fragments including [D-Ser(26)]A beta 25-35/40. In this study, we further investigated the mechanism behind the in vivo neuronal loss by [D-Ser(26)]A beta1-40 and ibotenic acid in rats, and also searched for the presence of [D-Ser(26)]A beta 25-35/40 antigens in AD brains. Quantitative analyses of the damaged area indicate clearly that non-toxic [D-Ser(26)]A beta 1-40 caused as much neurodegeneration as toxic [D-Ser(26)]A beta 25-35/40. MK-801, an NMDA receptor antagonist, completely inhibited the neurodegeneration. The immunohistochemical analyses using anti-[D-Ser(26)]A beta 25-35/40-specific antibodies demonstrated the presence of [D-Ser(26)]A beta 25-35/40 antigens in senile plaques and in degenerating hippocampal CA1 neurons in AD brains, but not in age-matched control brains. These results strengthen our hypothesis that soluble [D-Ser(26)]A beta1-40, possibly produced during aging, is released from plaques and converted by proteolysis to toxic [D-Ser(26)]A beta 25-35/40, which damage hippocampal CA1 neurons by enhancing excitotoxicity in AD. This may account for the lag between A beta deposition and neurodegeneration in AD.
Practical Synthetic Route to Functionalized Rhodamine Dyes (2003)

[reaction: see text] An efficient method for the synthesis of functionalized rhodamine derivatives has been developed. Multigram quantities of these water-soluble fluorophores can be prepared from inexpensive precursors and purified without the use of chromatography. A series of protein-reactive functional groups has been installed through subsequent reactions, providing materials for biomolecule modification. For multicolor applications, a solid-phase purification strategy has been developed to afford rhodamine derivatives possessing a wide range of spectral properties.
Detection of human immunodeficiency virus (HIV) by colorimetric assay for reverse transcriptase activity on magnetic beads (1993)

A colorimetric assay for detection of reverse transcriptase (RT) of the human immunodeficiency virus (HIV) was developed using oligodeoxythymidylic acid (oligo-dT)-linked magnetic beads and digoxigenin-deoxyuridine triphosphate (dig-dUTP). During the RT reaction, dig-dUTP was incorporated into oligo-dT which had been hybridized to polyadenylic acid [poly (A)]. At the detection step, an alkaline phosphatase-conjugated antibody to digoxigenin was added, followed by the addition of a colorimetric substrate for this enzyme. This method showed excellent correlation with the isotopic RT assay, which used tritiated thymidine triphosphate ([3H]dTTP), for detection of purified avian-myeloblastosis-virus RT (AMV-RT). This assay also demonstrated close correlation with the isotopic RT assay using human peripheral-blood lymphocytes infected in vitro with HIV. This colorimetric RT assay offers important advantages over the conventional radioactive RT assays with respect to its simplicity, safety and cost. The total assay time, including the RT reaction step, was less than 1 h, and therefore provides a reliable rapid assay for detection and quantification of HIV.
Orientation dependence of defect structure in EFG silcion ribbons (1976)

Sustained growth of long lengths of silicon ribbons by the edge-defined film-fed growth (EFG) technique is shown to result in the attainment of an ’’equilibrium’’ defect structure and orientation by the crystals. The structure consists of parallel defect boundaries parallel to the edges of the ribbon with a ribbon orientation of {110} 〈211〉. The influence of seed orientation on the attainment of this structure has been examined.
Adaptive Optics Retinal Imaging: Emerging Clinical Applications (2010)

The human retina is a uniquely accessible tissue. Tools like scanning laser ophthalmoscopy and spectral domain-optical coherence tomography provide clinicians with remarkably clear pictures of the living retina. Although the anterior optics of the eye permit such non-invasive visualization of the retina and associated pathology, the same optics induce significant aberrations that obviate cellular-resolution imaging in most cases. Adaptive optics (AO) imaging systems use active optical elements to compensate for aberrations in the optical path between the object and the camera. When applied to the human eye, AO allows direct visualization of individual rod and cone photoreceptor cells, retinal pigment epithelium cells, and white blood cells. AO imaging has changed the way vision scientists and ophthalmologists see the retina, helping to clarify our understanding of retinal structure, function, and the etiology of various retinal pathologies. Here, we review some of the advances that were made possible with AO imaging of the human retina and discuss applications and future prospects for clinical imaging.
In Vivo Production of Artificial Nonribosomal Peptide Products in the Heterologous Host Escherichia coli (2004)

Nonribosomal peptide synthetases represent the enzymatic assembly lines for the biosynthesis of pharmacologically relevant natural peptides, e.g., cyclosporine, vancomycin, and penicillin. Due to their modular organization, in which every module accounts for the incorporation of a single amino acid, artificial assembly lines for the production of novel peptides can be constructed by biocombinatorial approaches. Once transferred into an appropriate host, these hybrid synthetases could facilitate the bioproduction of basically any peptide-based molecule. In the present study, we describe the fermentative production of the cyclic dipeptide D-Phe-Pro-diketopiperazine, as a prototype for the exploitation of the heterologous host Escherichia coli, and the use of artificial nonribosomal peptide synthetases. E. coli provides a tremendous potential for genetic engineering and was manipulated in our study by stable chromosomal integration of the 4'-phosphopantetheine transferase gene sfp to ensure heterologous production of fully active holoenzmyes. D-Phe-Pro-diketopiperazine is formed by the TycA/TycB1 system, whose components represent the first two modules for tyrocidine biosynthesis in Bacillus brevis. Coexpression of the corresponding genes in E. coli gave rise to the production of the expected diketopiperazine product, demonstrating the functional interaction of both modules in the heterologous environment. Furthermore, the cyclic dipeptide is stable and not toxic to E. coli and is secreted into the culture medium without the need for any additional factors. Parameters affecting the productivity were comprehensively investigated, including various genetic setups, as well as variation of medium composition and temperature. By these means, the overall productivity of the artificial system could be enhanced by over 400% to yield about 9 mg of D-Phe-Pro-diketopiperazine/liter. As a general tool, this approach could allow the sustainable bioproduction of peptides, e.g., those used as pharmaceuticals or fine chemicals.
The “Comparative Growth Assay”: Examining the Interplay of Anti-cancer Agents with Cells Carrying Single Gene Alterations (1999)

We have developed a "comparative growth assay" that complements current assays of drug effects based on cytotoxicity. A co-culture of two cell lines, one of which is fluorescently labeled, is exposed to a cytotoxic agent and the proportion of fluorescent cells is compared with that of a baseline unexposed co-culture. For demonstration purposes, two HCT116 cell lines (an hMLH1 homozygous and an hMLH1 heterozygous mutant), altered by insertion of vector alone or the same vector carrying an insert for the expression of enhanced green fluorescent protein (EGFP), were exposed to numerous "anti-cancer" agents. The assay was further validated in a system of two cell lines differing only in the expression of the breast cancer resistance protein (BRCP). The assay allowed the estimation of the duration of action of a particular agent. Assessment of the agent's differential activity over a given time in culture could be expressed as a selection rate, which we chose to describe on an "average selection per day" basis. We conclude that this assay: 1) provides insight into the differential dynamic effects of chemotherapeutic agents or radiation; and 2) allows, through the use of matched cell lines, the investigation of critical physiologic features that govern cell sensitivity.
Increase in PDX-1 Levels Suppresses Insulin Gene Expression in RIN 1046-38 Cells (1999)

RIN1046–38 cells (RIN-38) exhibit a passage-dependent reduction in both basal and glucose-regulated insulin secretion, accompanied by decreased insulin content. In an attempt to explain the mechanism of the gradual decrease in insulin production in cultured cells, we analyzed the insulin promoter activity and the levels of an important trans-activator of the insulin gene, PDX-1, as a function of aging in culture. We demonstrate that the decrease in insulin content and secretion is reflected in decreased promoter activity and is associated with a decrease in E47 and BETA2 nuclear factors, but with a paradoxical 3-fold increase in PDX-1 protein levels. To dissect the effect of increased PDX-1 from the decrease in the additional transcription factors on insulin promoter activity, we overexpressed PDX-1 protein in low passage RIN-38 cells by recombinant adenovirus technology. PDX-1 overexpression did not reduce E47 and BETA2 levels, but was sufficient to suppress rat insulin promoter activity in a dose-dependent manner. The fact that PDX-1 levels participate in trans-activation of insulin promoter activity was demonstrated in HIT-T15 cells. Treating HIT-T15 cells with 1–2 multiplicity of infection of AdCMV-PDX-1 increased rat insulin promoter activity, whereas higher doses repressed insulin promoter activity in these cells as in RIN-38 cells. Our data demonstrate that PDX-1 regulates transcription of the insulin gene in a dose-dependent manner. Depending on its nuclear dosage and the levels of additional cooperating transcription factors, PDX-1 may act as an activator or a repressor of insulin gene expression, such that low as well as high doses may be deleterious to insulin production.
In vitro and in vivo antibacterial activity of KW1070, a new aminoglycoside antibiotic (1980)

KW1070, a new aminoglycoside antibiotic with the novel aminocyclitol, fortamine, has a broad spectrum of activity in vitro and in vivo against gram-positive and gram-negative bacteria. The minimum inhibitory concentrations of KW1070 are similar to those of kanamycin against aminoglycoside-susceptible strains, slightly less than those of gentamicin or 3',4'-dideoxykanamycin B. Minimal bactericidal concentrations were found to be near minimal inhibitory concentrations. KW1070 was active in vitro against many aminoglycoside-resistant bacterial strains that possess aminoglycoside-inactivating enzymes, particularly AAC(6'), AAC(2'), AAD(2''), and APH(3'). The activities of KW1070 in mice infected with Staphylococcus aureus, Escherichia coli, Proteus sp., and Serratia marcescens compared favorably with the activities of amikacin and kanamycin; KW1070 was also singificantly active in mice infected with resistant strains bearing the aminoglycoside-inactivating enzymes listed above.
Infiltrative potentiality of brain tumors in organ culture (1975)

The invasive potential of 15 brain tumors (seven meningiomas, and eight astrocytomas) as studied in cultures with Gelfoam used as a substrate. A three-stage system is introduced to classify in vitro invasiveness according to the depth of Gelfoam infiltration after 2 weeks' culture. This system proved to be simple and accurate. Meningiomas revealed greater activity in culture as compared to astrocytomas and infiltrated deeper into the Gelfoam. Dura mater explants were placed next to the culture of the tumors to study their interaction. Dura mater acted as a relatively strong barrier against tumor cell invasion in culture. In the majority of the explants, tumor cells revealed either contact arrest or spread underneath the dura and rarely spread over it. Tumor cells were seen infiltrating the dural explants in three cases, all of which were meningiomas.