gebhart/patrepeval huggingface dataset:
Effect of yeast culture (Saccharomyces cerevisiae) on adaptation of cows to postpartum diets and on lactational performance. (1999)

Multiparous (n = 26) and primiparous (n = 18) Holstein cows were fed prepartum and postpartum total mixed diets that were, or were not, supplemented with a yeast culture (YC) for approximately 23 d prepartum and 56 d postpartum. Multiparous cows supplemented with YC selected a prepartum diet higher in CP than did unsupplemented cows, although prepartum performance of cows of both parities, as assessed by DMI and measures of body status, was not influenced by YC. The extent of the prepartum DMI depression was not influenced by YC supplementation in cows of either parity. An intake behavior study with six multiparous cows suggested that cows supplemented with YC exhibited repeated diurnal feed intake patterns until approximately 7 d prepartum, vs 10 d prepartum for unsupplemented cows. Cows of both parities supplemented with YC had numerically higher DMI and production of milk and milk components, although only DMI for multiparous cows and milk production for primiparous cows approached statistical significance. Intake behavior results suggested that cows supplemented with YC achieved repeated diurnal feed intake patterns by approximately 14 d postpartum, vs 20 d postpartum for unsupplemented cows. Concentrations of ruminal metabolites and pH did not differ between treatments, although ruminal fluid collection occurred while diurnal feed intake patterns were repeated (regular). Overall, our results can be interpreted to support a trend toward a modest postpartum improvement in performance of primiparous and multiparous cows supplemented with this YC for 23 d prepartum and 56 d postpartum. However, primiparous cows seemed to achieve this modest overall improvement primarily through enhanced postpartum DMI, whereas in multiparous cows it was due almost equally to enhanced postpartum DMI and higher energy density of the diet.
Effect of decreased O2 affinity of hemoglobin on work performance during exercise in healthy humans. (1984)

A reduction in O2 affinity of hemoglobin should increase tissue oxygenation or maintain tissue oxygenation and at the same time spare cardiac work. Large, sustained reductions in O2 affinity of hemoglobin are induced best by primary (non-Bohr effect) stimulation of red blood cell 2,3-diphosphoglycerate (DPG) caused by a dual, cumulative effect on O2 affinity for hemoglobin, direct, from DPG itself, and indirect, from DPG-induced red blood cell acidosis. In an attempt to induce significant, sustained reductions in O2 affinity of hemoglobin by primary DPG stimulation, six normal humans were given a diphosphonate (etidronate disodium [Didronel] 20 mg/kg/day p.o.) followed by infusion of 10% fructose (0.5 L/hr for 3 hours) with added phosphate (0.28 mmol/kg/hr) and, subsequently, fructose-phosphate by itself. Participants underwent exercise testing (bicycle ergometer) and cardiopulmonary parameters were measured before and after administration of Didronel plus fructose-phosphate infusion, as well as before and after fructose-phosphate infusion alone. The sum of DPG and adenosine triphosphate as well as the P50 increased significantly after infusion of fructose-phosphate with and without prior administration of Didronel. DPG-ATP correlated closely with P50. When P50 was elevated, the cardiac index at high work load was lower than when P50 was normal (with comparable O2 consumption); changes in P50 correlated inversely with changes in cardiac index. Thus, with reduced O2 affinity of hemoglobin, participants could perform at comparable work loads and utilize the same amount of O2 with less cardiac work. Future studies should include adapting these findings to states of O2 deficit.
Beta cyclodextrin-insulin-encapsulated chitosan/alginate matrix: Oral delivery system (2000)

Cyclodextrins (CD) form inclusion complexes with many drug molecules. The complexed drugs have increased bioabsorption in in vivo system. We have attempted to complex insulin with β-Cyclodextrin (BCD) and encapsulate in the chitosan/calcium alginate matrix. For drug release studies insulin complexed with BCD for 20 min and that complexed with BCD for 150 min have been used for encapsulation in the chitosan/calcium alginate matrix. The two matrices seem to have different drug release profiles in simulated intestinal medium (pH 7.4) It appears that drug release from the 20-min BCD complexed system encapsulated in the chitosan/calcium alginate matrix begins only after an hour, where, being released from the 150-min BCD complexed system it begins in the first hour itself. Also, aggregation of the insulin molecules seems to be reduced by the complexation of the drug with BCD. Another noticeable fact is the change in the loading character, which is found to be inversely related to the concentration of BCD when it is above the stoichiometric equivalent of the drug. In an attempt to increase the payload of the drug in the matrix, the pH of the processing medium consisting of calcium chloride and chitosan is varied. It is found that the encapsulation efficiency increases as the pH is decreased from 6.0 to 4.0. Another way of increasing the loading is studied by decreasing the concentration gradient of insulin in the processing alginate solution and the crosslinking medium consisting of chitosan/calcium chloride. Preliminary animal studies on rabbits seem to be promising. © 2000 John Wiley & Sons, Inc. J Appl Polym Sci 75: 1089–1096, 2000
Uric acid and inflammatory markers (2006)

A positive and significant association between UA and several inflammatory markers was found in a large population-based sample of older persons and in a sub-sample of participants with normal UA. Accordingly, the prevalence of abnormally high levels of C-reactive protein and IL-6 increased significantly across UA quintiles.
Circadian Interleukin-6 Secretion and Quantity and Depth of Sleep (1999)

Patients with pathologically increased daytime sleepiness and fatigue have elevated levels of circulating interleukin-6 (IL-6). The latter is an inflammatory cytokine, which causes sickness manifestations, including somnolence and fatigue, and activation of the hypothalamic-pituitary-adrenal axis. In this study, we examined: 1) the relation between serial measurements of plasma IL-6 and quantity and depth of sleep, evaluated by polysomnography; and 2) the effects of sleep deprivation on the nyctohemeral pattern of IL-6 secretion. Eight healthy young male volunteers were sampled for 24 h twice, at the baseline state, after a normal night's sleep and after total overnight sleep deprivation. At the baseline state, IL-6 was secreted in a biphasic circadian pattern with two nadirs at 0800 and 2100 and two zeniths at 1900 and 0500 (P < 0.01). The baseline amount of sleep correlated negatively with the overall daytime secretion of the cytokine (P < 0.05). Also, depth of sleep at baseline correlated negatively with the postdeprivation increase of daytime secretion of IL-6 (P < 0.05). Sleep deprivation changed the temporal pattern of circadian IL-6 secretion but not the overall amount. Indeed, during the post-deprivation period, the mean daytime (0800-2200 h) levels of IL-6 were significantly higher (P < 0.05), whereas the nighttime (2200-0600 h) levels were lower than the predeprivation values. Thus, sleep-deprived subjects had daytime oversecretion and nighttime under-secretion of IL-6; the former might be responsible for their daylong somnolence and fatigue, the latter for the better quality (depth) of their sleep. These data suggest that a good night's sleep is associated with decreased daytime secretion of IL-6 and a good sense of well-being and that good sleep is associated with decreased exposure of tissues to the proinflammatory and potentially detrimental actions of IL-6. Sleep deprivation increases daytime IL-6 and causes somnolence and fatigue during the next day, whereas postdeprivation decreases nighttime IL-6 and is associated with deeper sleep.
Temperature-Insensitive Composite Micromechanical Resonators (2009)

Utilizing silicon and silicon dioxide's opposing temperature coefficients of Young's modulus, composite resonators with zero linear temperature coefficient of frequency are fabricated and characterized. The resulting resonators have a quadratic temperature coefficient of frequency of approximately -20 ppb/degC <sup xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">2</sup> and a tunable turnover temperature in the -55degC to 125degC range. Reduction of the temperature dependence of frequency is shown in flexural-mode resonators (700 kHz-1.3 MHz) and extensional-mode ring resonators (20 MHz). The linear temperature coefficient of Young's modulus of silicon dioxide is extracted from measurements to be +179 ppm/degC. The composite resonators are fabricated and packaged in a CMOS-compatible wafer-scale hermetic encapsulation process. The long-term stability of the resonators is monitored for longer than six months. Although most devices exhibit less than 2 ppm frequency drift, there is evidence of dielectric charging in the silicon dioxide.
A fiber Raman ring laser (1978)

A fiber Raman ring laser was synchronously pumped by a cavity-dumped argon laser. The Raman laser was tuned with either a piezoelectric intracavity interferometer or by varying the pump pulse rate.
Immunological Characterization and Therapeutic Activity of an Altered-Peptide Ligand, NBI-6024, Based on the Immunodominant Type 1 Diabetes Autoantigen Insulin B-Chain (9–23) Peptide (2002)

The nonobese diabetic (NOD) mouse is a good model for human type 1 diabetes, which is characterized by autoreactive T-cell-mediated destruction of insulin-producing islet beta-cells of the pancreas. The 9-23 amino acid region of the insulin B-chain [B((9-23))] is an immunodominant T-cell target antigen in the NOD mouse that plays a critical role in the disease process. By testing a series of B((9-23)) peptide analogs with single or double alanine substitutions, we identified a set of altered peptide ligands (APLs) capable of inhibiting B((9-23))-induced proliferative responses of NOD pathogenic T-cell clones. These APLs were unable to induce proliferation of these clones. However, vaccinations with the APLs induced strong cellular responses, as measured by in vitro lymphocyte proliferation and Th2 cytokine production (i.e., interleukin [IL]-4 and IL-10, but not gamma-interferon [IFN-gamma]). These responses were cross-reactive with the native antigen, B((9-23)), suggesting that the APL-induced Th2 responses may provide protection by controlling endogenous B((9-23))-specific Th1 (i.e., IFN-gamma-producing) pathogenic responses. One of these APLs that contained alanine substitutions at residues 16 and 19 (16Y-->A, 19C-->A; NBI-6024) was further characterized for its therapeutic activity because it consistently induced T-cell responses (e.g., T-cell lines and clones) that were of the Th2 type and that were cross-reactive with B((9-23)). Subcutaneous injections of NBI-6024 to NOD mice administered either before or after the onset of disease substantially delayed the onset and reduced the incidence of diabetes. This study is the first to report therapeutic activity of an APL derived from an islet beta-cell-specific antigen in type 1 diabetes.
Mechanisms of Cell Death in Oxidative Stress (2006)

Reactive oxygen or nitrogen species (ROS/RNS) generated endogenously or in response to environmental stress have long been implicated in tissue injury in the context of a variety of disease states. ROS/RNS can cause cell death by nonphysiological (necrotic) or regulated pathways (apoptotic). The mechanisms by which ROS/RNS cause or regulate apoptosis typically include receptor activation, caspase activation, Bcl-2 family proteins, and mitochondrial dysfunction. Various protein kinase activities, including mitogen-activated protein kinases, protein kinases-B/C, inhibitor-of-I-kappaB kinases, and their corresponding phosphatases modulate the apoptotic program depending on cellular context. Recently, lipid-derived mediators have emerged as potential intermediates in the apoptosis pathway triggered by oxidants. Cell death mechanisms have been studied across a broad spectrum of models of oxidative stress, including H2O2, nitric oxide and derivatives, endotoxin-induced inflammation, photodynamic therapy, ultraviolet-A and ionizing radiations, and cigarette smoke. Additionally ROS generated in the lung and other organs as the result of high oxygen therapy or ischemia/reperfusion can stimulate cell death pathways associated with tissue damage. Cells have evolved numerous survival pathways to counter proapoptotic stimuli, which include activation of stress-related protein responses. Among these, the heme oxygenase-1/carbon monoxide system has emerged as a major intracellular antiapoptotic mechanism.
The Use of Magnesium-Containing Phosphate Binders in Patients with End-Stage Renal Disease on Maintenance Hemodialysis (1982)

We investigated the safety and efficacy of magnesium hydroxide as a phosphate binder in patients with end-stage renal disease on maintenance hemodialysis, 9 volunteers participated in a four-phase study during which each ingested (1) no phosphate binders, (2) magnesium hydroxide (Mg(OH)2) alone, (3) Mg(OH)2 and aluminum hydroxide (A1(OH)3) together and (4) A1(OH)3 alone. Serum magnesium (SMg) concentrations were maintained at less than 4.5 mEq/1 (2.3 mmol/l) in all subjects while they were ingesting 0.75-3 g Mg(OH)2/day and no magnesium toxicity was noted. In individuals taking a constant daily dose, SMg remained stable over 8-12 weeks. Serum phosphorus (SP) decreased from 9.0 mg/dl (2.9 mmol/l)d during the control period to 8.1 mg/dl (2.6 mmol/l) during the Mg(OH)2 period (p less than 0.05) and increased from 6.1 mg/dl (2.0 mmol/l) during the Mg(OH)2 and A1(OH)3 period to 7.0 mg/dl (2.3 mmol/l) during the Al(OH)3 period (p less than 0.05) indicating that Mg(OH)2 could significantly lower SP. However, SP was best controlled (6.1 mg/dl; 2.0 mmol/l) when Al(OH)3 and Mg(OH)2 were used together and all participants preferred the combination therapy to either of the agents alone. These results indicate that Mg(OH)2 is a potentially useful adjunct to A1(OH)3 for managing hyperphosphatemia in patients on maintenance hemodialysis. In this short-term study Mg(OH)3 for managing hyperphosphatemia in patients on maintenance hemodialysis. In this short-term study Mg(OH)2 was well tolerated and with appropriate monitoring did not cause uncontrolled hypermagnesemia. Further studies are clearly required to determine whether long-term therapy with Mg-containing agents is safe in dialysis patients.
Species-specific signals for the splicing of a short Drosophila intron in vitro. (1993)

The effects of branchpoint sequence, the pyrimidine stretch, and intron size on the splicing efficiency of the Drosophila white gene second intron were examined in nuclear extracts from Drosophila and human cells. This 74-nucleotide intron is typical of many Drosophila introns in that it lacks a significant pyrimidine stretch and is below the minimum size required for splicing in human nuclear extracts. Alteration of sequences of adjacent to the 3' splice site to create a pyrimidine stretch was necessary for splicing in human, but not Drosophila, extracts. Increasing the size of this intron with insertions between the 5' splice site and the branchpoint greatly reduced the efficiency of splicing of introns longer than 79 nucleotides in Drosophila extracts but had an opposite effect in human extracts, in which introns longer than 78 nucleotides were spliced with much greater efficiency. The white-apricot copia insertion is immediately adjacent to the branchpoint normally used in the splicing of this intron, and a copia long terminal repeat insertion prevents splicing in Drosophila, but not human, extracts. However, a consensus branchpoint does not restore the splicing of introns containing the copia long terminal repeat, and alteration of the wild-type branchpoint sequence alone does not eliminate splicing. These results demonstrate species specificity of splicing signals, particularly pyrimidine stretch and size requirements, and raise the possibility that variant mechanisms not found in mammals may operate in the splicing of small introns in Drosophila and possibly other species.
Insertional Torque and Pull-out Strengths of Conical and Cylindrical Pedicle Screws in Cadaveric Bone (1996)

A conical screw profile increases insertion torque, although insertional torque is not a reliable predictor of pull-out strength in cadaveric bone. Screw profile (with similar dimensions) has little effect on straight axial pull-out strengths in cadaveric bone.
A Platform with Six Degrees of Freedom (1966)

Abstract This paper describes a mechanism which has six degrees of freedom, controlled in any combination by six motors, each having a ground abutment. It is considered that by its particular arrangement, this mechanism may form an elegant design for simulating flight conditions in the training of pilots. Unlike most simulators, it has no fixed axes relative to the ground, and therefore within the limits of amplitude of the design it can truly simulate the conditions of banking by carrying the simulation of control surfaces into the axes of the new attitude. Variations in control arrangements are described and their respective design merits considered. Other possible uses for this mechanism are mentioned including automation of production.
Leptosins isolated from marine fungus Leptoshaeria species inhibit DNA topoisomerases I and/or II and induce apoptosis by inactivation of Akt/protein kinase B (2005)

DNA topoisomerases (topo) I and II are molecular targets of several potent anticancer agents. Thus, inhibitors of these enzymes are potential candidates or model compounds for anticancer drugs. Leptosins (Leps) F and C, indole derivatives, were isolated from a marine fungus, Leptoshaeria sp. as cytotoxic substances. In vitro cytotoxic effects of Lep were measured using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide-based viability assay. Lep F inhibited the activity of topos I and II, whereas Lep C inhibited topo I in vitro. Interestingly both of the compounds were found to be catalytic inhibitors of topo I, as evidenced by the lack of stabilization of reaction intermediate cleavable complex (CC), as camptothecin (CPT) does stabilize. Furthermore, Lep C inhibited the CC stabilization induced by CPT in vitro. In vivo band depletion analysis demonstrated that Lep C likewise appeared not to stabilize CC, and inhibited CC formation by CPT, indicating that Lep C is also a catalytic inhibitor of topo I in vivo. Cell cycle analysis of Lep C-treated cells showed that Lep C appeared to inhibit the progress of cells from G(1) to S phase. Lep C induced apoptosis in RPMI8402 cells, as revealed by the accumulation of cells in sub-G(1) phase, activation of caspase-3 and the nucleosomal degradation of chromosomal DNA. Furthermore, Leps F and C inhibited the Akt pathway, as demonstrated by dose-dependent and time-dependent dephosphorylation of Akt (Ser473). Our study shows that Leps are a group of anticancer chemotherapeutic agents with single or dual catalytic inhibitory activities against topos I and II.
Investigation of allogeneic mesenchyrnal stem cell‐based alveolar bone formation: preliminary findings (2003)

This study was designed to evaluate mesenchymal stem cell (MSC)-based alveolar bone regeneration in a canine alveolar saddle defect model. MSCs were loaded onto hydroxyapatite/tricalcium phosphate (HA/TCP) matrices. Scanning electron microscopic (SEM) evaluation demonstrated greater than 75% MSC coverage of the HA/TCP porous surface prior to placement regardless of MSC donor. Matrices, 6 mm x 6 mm x 20 mm, with and without cells, were implanted for 4 and 9 weeks, then removed for histological evaluation of bone formation. Cell-free control matrices were compared with MSC-loaded matrices post implantation. Histomorphometrical analysis showed that equivalent amounts of new bone were formed within the pores of the matrices loaded with autologous MSCs or MSCs from an unrelated donor. Bone formation in the cell-free HA/TCP matrices was less extensive. There was no histologic evidence of an immunological response to autologous MSCs. Surprisingly, allogeneic MSC implantation also failed to provoke an immune response. Analysis of circulating antibody levels against MSCs supported the hypothesis that neither autologous nor allogeneic MSCs induced a systemic response by the host. Analysis of dye-labelled MSCs in histological sections confirmed that the MSCs persisted in the implants throughout the course of the experiment. At 9 weeks, labelled cells were present within the lacunae of newly formed bone. We conclude that autologous and allogeneic MSCs have the capacity to regenerate bone within craniofacial defects.
The novel endocannabinoid receptor GPR55 is activated by atypical cannabinoids but does not mediate their vasodilator effects (2007)

These results demonstrate that while GPR55 is activated by atypical cannabinoids, it does not appear to mediate the vasodilator effects of these agents.
Carboxyl-terminal Vesicular Stomatitis Virus G Protein-tagged Intestinal Na+-dependent Glucose Cotransporter (SGLT1) (1996)

The Na+-dependent glucose transporter (SGLT1) mediates absorption of luminal glucose by the intestine. However, available intestinal cell lines that recapitulate a monolayer phenotype only express SGLT1 at low levels. Thus, to facilitate studies of the biology of SGLT1 function in epithelial monolayers, we engineered an epitope-tagged construct containing the YTDIEMNRLGK sequence (from the vesicular stomatitis virus G protein). The tag was placed at the carboxyl terminus since this is the least conserved portion of SGLT1. Transiently transfected COS-1 cells demonstrated surface expression of the immunoreactive protein and enhanced Na+-dependent glucose uptake that was phloridzin-sensitive (a specific competitive inhibitor of SGLT1). However, subsequent detailed analyses of epitope-tagged SGLT1 using stably transfected clones derived from the Caco-2 human intestinal epithelial cell line revealed substantial effects of the epitope on critical functions of SGLT1. When compared with native SGLT1 transfectants, the apparent Km for sugar transport was increased 23-fold (313 microM to 7.37 mM for native versus epitope-tagged SGLT1). In contrast, the apparent KNa for epitope-tagged SGLT1 was similar to that for native SGLT1. Permeabilization studies indicated that the C-terminal epitope tag was intracellular and thus could not directly disrupt extracellular ligand-binding sites. Immunolocalization and functional assays designed to detect polarized surface expression indicated that epitope tagging resulted in loss of apical targeting and enrichment of basolateral expression. Functional isolation of the small apical pool of epitope-tagged SGLT1 (by selective inhibition of basolateral epitope-tagged SGLT1) revealed that, despite the documented kinetic alterations in sugar transport, epitope-tagged SGLT1 could promote absorptive Na+ currents. These data show that 1) the C terminus of SGLT1 is intracellular; 2) disruption of protein structure by addition of a C-terminal tag leads to selective modifications of SGLT1 function; 3) the kinetics of sugar transport can be altered independently of influences on the Na+-binding site of SGLT1; and 4) the weak basolateral targeting sequence present within the epitope tag is dominant over endogenous SGLT1 apical targeting information and can direct polytopic membrane protein localization. The data also caution that subtle effects of foreign sequences must be considered when epitope tagging polytopic membrane proteins.