Miracle-dz/UniFAR-FTUs huggingface dataset:
Effects of vermicomposts and composts on plant growth in horticultural container media and soil

Summary Vermicomposts, which are produced by the fragmentation of organic wastes by earthworms, have a fine particulate structure and contain nutrients in forms that are readily available for plant uptake. In greenhouse trials, the growth of marigold and tomato seedlings, in a commercial horticultural potting medium (Metro-Mix 360), was enhanced significantly upon substitution of Metro-Mix 360 with 10% or 20% vermicomposted pig solids or vermicomposted food wastes, when all required nutrients were supplied. Same enhancement in marigold and tomato seedlings' growth occurred also upon substitution of Metro-Mix 360 with composted biosolids, but not with leaf compost. The shoot dry weights of raspberry plants, grown in a mineral soil mixed with vermicomposted pig wastes weighed more than those grown in unfertilized control soil, and were as great as those in soil receiving a complete fertilizer treatment. By comparison, raspberry shoot growth in soils amended with yard, leaf or bark composts, was poorer than that in the unfertilized control soil. Amending the soil with 4% chicken manure compost killed most of the raspberry plants. However, plant mortality was reduced and growth restored when the chicken manure compost was mixed with vermicomposted pig solids, but not with bark or yard composts. Plant growth in soils containing a mixture of chicken manure compost with 20% vermicomposted pig wastes was similar to that of plants grown in the unfertilized control. Our results showed that vermicomposts have the potential for improving plant growth when added to greenhouse container media or soil. However, there seem to be distinct differences between specific vermicomposts and composts in terms of their nutrient contents, the nature of their microbial communities, and their effects on plant growth.
A brief evaluation of tumor imaging in mice with 99mTc-glucarate including a comparison with 18F-FDG.

OBJECTIVE Recently 99mTc-glucarate, a radiolabeled glucose analogue, has been considered as a SPECT alternative to 18F-FDG and PET for non-invasive detection of certain tumors. Thus far there have been few studies on (99m) Tcglucarate for tumor imaging and fewer, if any, studies comparing (99m)Tc-glucarate with 18F-FDG. As a preliminary indication of the properties of (99m)Tc-glucarate as a possible substitute for 18F-FDG in animal studies, we have imaged mice bearing xenografts of four tumor types with (99m)Tc-glucarate and have compared in two mice with one of these tumor types the 99mTc and 18F biodistributions. METHODS Two mice bearing SUM190 breast cancer xenografts received 1 mCi of (99m)Tc-glucarate and were imaged on a NanoSPECT/CT small animal camera. One day later, the same animals received 1 mCi of 18F-FDG and were imaged on a MosaicHP PET small animal camera. In addition, 0.5-1 mCi of (99m)Tc-glucarate only was administered to mice bearing xenografts induced by BxPC3 pancreatic cancer cells, HEK-293 renal cell carcinomas cells or HCT-116 colorectal tumor cells. NanoSPECT/CT acquisitions were performed in these mice to evaluate tumor accumulations. RESULTS In the SUM190 xenografted mice, the average tumor accumulation was 1.4 % (ID%/cm3) for (99m)Tc-glucarate and 2.1 % (ID%/cm3) for 18F-FDG. While slightly higher than (99m)Tc-glucarate, the tumor accumulation of 18F-FDG was accompanied by higher bone marrow and muscle accumulations at levels that could interfere with the tumor image depending upon location. The whole body clearance of (99m)Tc-glucarate was faster than that of 18F-FDG. Tumor accumulation of (99m)Tc-glucarate varied among tumor types but the tumors were readily visible in all images. CONCLUSION In a direct comparison in the same two SUM190 tumored animals, SPECT images obtained with (99m)Tcglucarate compared favorably with PET images obtained with 18F-FDG. Tumor images with 99mTc-glucarate were also positive in three additional tumor mouse models. While further comparison studies are necessary, we conclude that (99m)Tcglucarate may be a more convenient and less expensive alternative to 18F-FDG for tumored mouse studies.
Corticotropin-Releasing Hormone Induces Vascular Endothelial Growth Factor Release from Human Mast Cells via the cAMP/Protein Kinase A/p38 Mitogen-Activated Protein Kinase Pathway

Mast cells are involved in allergic reactions but also in innate immunity and inflammation. Corticotropin-releasing hormone (CRH), the key regulator of the hypothalamic-pituitary-adrenal axis, also has proinflammatory effects, apparently through mast cells. We showed recently that CRH selectively stimulates human leukemic mast cells and human umbilical cord blood-derived mast cells to release newly synthesized vascular endothelial growth factor (VEGF) without release of either preformed mediators or cytokines. This effect was mediated through the activation of CRH receptor-1 and adenylate cyclase with increased intracellular cAMP. However, the precise mechanism by which CRH induces VEGF secretion has not yet been defined. Here, we show that CRH-induced VEGF release was dose-dependently inhibited by the specific protein kinase A inhibitor N-[2-(4-bromocinnamylamino)ethyl]-5-isoquinoline (H89) or the p38 mitogen-activated protein kinase (MAPK) inhibitor 4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl)1H-imidazole (SB203580) but not by the specific inhibitor 2′-amino-3′-methoxyflavone (PD98059) of mitogen-activated protein kinase kinase, the upstream kinase of the extracellular signal-regulated protein kinase (ERK) or the c-Jun N-terminal kinase (JNK) inhibitor 1,9-pyrazoloanthrone anthra-(1,9-cd)pyrazol-6(2H)-one (SP600125). Furthermore, CRH significantly increased protein kinase A activity, which could be mimicked by the cell-permeable cAMP analog 8-bromo-cAMP, and was blocked by H89 or the adenylate cyclase inhibitor 9-(tetrahydro-2-furanyl)-9H-purine-6-amine (SQ22536). CRH also induced rapid phosphorylation of p38 MAPK, which was mimicked by 8-bromo-cAMP and was inhibited by H89 or SB203580. CRH did not stimulate ERK or JNK phosphorylation and did not increase intracellular calcium levels. These results indicate that CRH induces VEGF release in human mast cells via selective activation of the cAMP/protein kinase A/p38 MAPK signaling pathway, thereby providing further insight into the molecular mechanism of how CRH affects the release of a key proinflammatory mediator.
Pharmacokinetics and Safety of Intravenous Voriconazole in Children after Single- or Multiple-Dose Administration

ABSTRACT We conducted a multicenter study of the safety, tolerability, and plasma pharmacokinetics of the parenteral formulation of voriconazole in immunocompromised pediatric patients (2 to 11 years old). Single doses of 3 or 4 mg/kg of body weight were administered to six and five children, respectively. In the multiple-dose study, 28 patients received loading doses of 6 mg/kg every 12 h on day 1, followed by 3 mg/kg every 12 h on day 2 to day 4 and 4 mg/kg every 12 h on day 4 to day 8. Standard population pharmacokinetic approaches and generalized additive modeling were used to construct the structural pharmacokinetic and covariate models used in this analysis. In contrast to that in adult healthy volunteers, elimination of voriconazole was linear in children following doses of 3 and 4 mg/kg every 12 h. Body weight was more influential than age in accounting for the observed variability in voriconazole pharmacokinetics. Elimination capacity correlated with the CYP2C19 genotype. Exposures were similar at 4 mg/kg every 12 h in children (median area under the concentration-time curve (AUC), 14,227 ng · h/ml) and 3 mg/kg in adults (median AUC, 13,855 ng · h/ml). Visual disturbances occurred in 5 (12.8%) of the 39 patients and were the only drug-related adverse events that occurred more than once. No withdrawals from the study were related to voriconazole. We conclude that pediatric patients have a higher capacity for elimination of voriconazole per kilogram of body weight than do adult healthy volunteers and that dosages of 4 mg/kg may be required in children to achieve exposures consistent with those in adults following dosages of 3 mg/kg.
Comparison of simultaneously measured perfusion and BOLD signal increases during brain activation with T1‐based tissue identification

Perfusion and blood oxygenation level‐dependent (BOLD) signals were simultaneously measured during a finger‐tapping task at 3T using QUIPSS II with thin‐slice TI1 periodic saturation, a modified pulsed arterial spin labeling technique that provides quantitative measurement of perfusion. Perfusion and BOLD signal changes due to motor activation were obtained and correlated with the T1 values estimated from echo‐planar imaging (EPI)‐based T1 maps on a voxel‐by‐voxel basis. The peak perfusion signal occurs in voxels with a T1 of brain parenchyma while the peak BOLD signal occurs in voxels with a T1 characteristic of blood and cerebrospinal fluid. The locations of the peak signals of functional BOLD and perfusion only partially overlap on the order of 40%. Perfusion activation maps will likely represent the sites of neuronal activity better than do BOLD activation maps. Magn Reson Med 44:137–143, 2000. © 2000 Wiley‐Liss, Inc.
Characterization of Integrative and Conjugative Element ICEKp1-Associated Genomic Heterogeneity in a Klebsiella pneumoniae Strain Isolated from a Primary Liver Abscess

ABSTRACT Genomic heterogeneity has been shown to be associated with Klebsiella pneumoniae strains causing pyogenic liver abscesses (PLA) and metastatic infections. In order to explore the mechanism responsible for genomic heterogeneity in K. pneumoniae, we compared the complete genomic sequences of strains NTUH-K2044 and MGH78578. An ∼76-kbp DNA fragment located adjacent to an asparagine (asn) tRNA gene was present in NTUH-K2044 but not in MGH78578. This fragment could be divided into three regions with different functions, and structurally it resembled a functional integrative and conjugative element (ICE), ICEEc1, in Escherichia coli. The 5′ region of this fragment contained genes similar to a high-pathogenicity island (HPI) of Yersinia pestis and Yersinia pseudotuberculosis. The middle region was similar to part of a large plasmid in K. pneumoniae, and the 3′ region contained genes responsible for DNA conjugative transfer. Therefore, this DNA fragment was designated ICEKp1. Precise excision and extrachromosomal circularization of ICEKp1 were detected in K. pneumoniae wild-type strain NTUH-K2044. ICEKp1 could integrate into the asn tRNA loci of the chromosome of another K. pneumoniae isolate. The prevalence of ICEKp1 was higher in PLA strains (38 of 42 strains) than in non-tissue-invasive strains (5 of 32 strains). Therefore, ICEKp1 may contribute to the transmission of the HPI and result in K. pneumoniae PLA infection-associated genomic heterogeneity.
Potassium channel modulation in rat portal vein by ATP depletion: a comparison with the effects of levcromakalim (BRL 38227)

1 The effects of levcromakalim and of adenosine 5′‐triphosphate (ATP) depletion on membrane potential and ionic currents were studied in freshly‐dispersed smooth muscle cells of rat portal vein by use of combined voltage‐ and current‐clamp techniques. 2 Levcromakalim (1 μm) induced a glibenclamide‐sensitive, non‐inactivating K‐current (IKCO) and simultaneously inhibited the slow, transient outward, delayed rectifier K‐current (ITO). Levcromakalim also hyperpolarized the portal vein cells by approximately 20 mV. 3 Reduction of intracellular ATP by removal of glucose and carboxylic acids from the recording pipette and of glucose from the bath fluid, induced a slowly‐developing, non‐inactivating and glibenclamide‐sensitive K‐current (Imet) within 60–300 s after breaking the membrane patch. Imet reached peak amplitude after 300–900 s, remained at a plateau for 200–800 s and then slowly ran down. At the peak of Imet, the cells were hyperpolarized by approximately 20 mV and their input conductance was increased by 42%. 4 At the time of maximum development of Imet, the delayed rectifier current, ITO, was reduced by 48%. 5 In the absence of glucose and carboxylic acids, addition of 1 μm free ATP to the recording pipette almost doubled the magnitude of Imet. At a holding potential of −10 mV, Imet was increased from 124 ± 11 pA to 228 ± 54 pA whereas the time‐course of development and run‐down of Imet was unaffected. 6 During the development and after the run‐down of Imet, levcromakalim (1–10 μm) failed to induce IKCO. 7 Stationary fluctuation analysis of the current noise associated with Imet revealed a unitary conductance of between 10–20 pS in a physiological potassium gradient. A second contaminating current with an underlying unitary conductance of approximately 150 pS remained after Imet had run down. 8 It is concluded that IKCO induced by levcromakalim and Imet are carried by the same population of relatively small conductance, glibenclamide‐sensitive K‐channels. The open state of these is increased by procedures designed to lower intracellular ATP concentrations. 9 The simultaneous inhibition of the delayed rectifier current (ITO) by both levcromakalim and during the development of Imet is highly significant. It suggests that levcromakalim could modify the interaction of ATP with sites linked to more than one type of K‐channel. This results in the opening of those channels which underlie IKCO (and which are normally inhibited by ATP binding) together with the modulation of phosphorylation‐dependent channels such as those which underlie ITO.
Joint Laxity in Children

Joint laxity was measured clinically in 2,360 normal Chinese children aged 3–13 years with equal sex distribution using the Carter Wilkinson five tests and scoring system. Results showed minimal differences due to gender. The degree of joint laxity diminished with age. The knee extension and ankle extension tests were more sensitive than other tests. Chinese children were far more lax throughout the age range, with 100% “laxity” at age 3, 67% laxity at age 6, and 28% laxity at age 12, in contrast to 50, 5, and 1% laxity in the same age group respectively, in large series of Caucasian children.
Distributed Detection in a Wireless Sensor Network Using Hybrid MAC

In this paper, distributed detection is investigated in a wireless sensor network (WSN) using the hybrid multiple-access channel (MAC) which is a composite of orthogonal and nonorthogonal MACs. Specifically, a simple ideal sensing (IS) fusion rule is proposed, and the corresponding detection error probability upper bound and approximate system outage probability are analytically derived. Performance results show that the IS fusion rule provides nearly minimum detection error probability under high sensor observation signal-to-noise power ratios, and offers a diversity gain in system outage probability which is equal to the number of orthogonal channels. Moreover, the hybrid MAC WSN with IS fusion rule is shown to provide more performance choices than orthogonal and nonorthogonal MAC WSNs with IS fusion rule in terms of detection error probability and system outage probability.
Anatomy correlations: introducing clinical skills to improve performance in anatomy.

BACKGROUND AND OBJECTIVES Gross anatomy is one of the preclinical cornerstones of medical education, but many practitioners feel that medical students' knowledge of anatomy is inadequate. To help students understand the clinical relevance of anatomy studies, Ohio State University faculty developed a course called "Anatomy Correlations. " This course introduces students to basic physical examination techniques correlated to gross anatomy dissections and allows them to practice techniques learned. METHODS Anatomy grades prior to the introduction of the course were compared with anatomy grades after the introduction of the course to see if the course improved knowledge of gross anatomy. Analysis controlled for initial differences in academic aptitude. RESULTS Students taking the course in its new form scored higher in anatomy than did students taking anatomy before the course was offered. CONCLUSION Introducing physical examination skills that correlate with anatomy studies can lead to improvement in anatomy scores.
Measles virus, immune control, and persistence.

Measles remains one of the most important causes of child morbidity and mortality worldwide with the greatest burden in the youngest children. Most acute measles deaths are owing to secondary infections that result from a poorly understood measles-induced suppression of immune responses. Young children are also vulnerable to late development of subacute sclerosing panencephalitis, a progressive, uniformly fatal neurologic disease caused by persistent measles virus (MeV) infection. During acute infection, the rash marks the appearance of the adaptive immune response and CD8(+) T cell-mediated clearance of infectious virus. However, after clearance of infectious virus, MeV RNA persists and can be detected in blood, respiratory secretions, urine, and lymphoid tissue for many weeks to months. This prolonged period of virus clearance may help to explain measles immunosuppression and the development of lifelong immunity to re-infection, as well as occasional infection of the nervous system. Once MeV infects neurons, the virus can spread trans-synaptically and the envelope proteins needed to form infectious virus are unnecessary, accumulate mutations, and can establish persistent infection. Identification of the immune mechanisms required for the clearance of MeV RNA from multiple sites will enlighten our understanding of the development of disease owing to persistent infection.
Saccharomyces cerevisiae Mob1p Is Required for Cytokinesis and Mitotic Exit

ABSTRACT The Saccharomyces cerevisiae mitotic exit network (MEN) is a conserved set of genes that mediate the transition from mitosis to G1 by regulating mitotic cyclin degradation and the inactivation of cyclin-dependent kinase (CDK). Here, we demonstrate that, in addition to mitotic exit, S. cerevisiae MEN gene MOB1 is required for cytokinesis and cell separation. The cytokinesis defect was evident in mob1mutants under conditions in which there was no mitotic-exit defect. Observation of live cells showed that yeast myosin II, Myo1p, was present in the contractile ring at the bud neck but that the ring failed to contract and disassemble. The cytokinesis defect persisted for several mitotic cycles, resulting in chains of cells with correctly segregated nuclei but with uncontracted actomyosin rings. The cytokinesis proteins Cdc3p (a septin), actin, and Iqg1p/ Cyk1p (an IQGAP-like protein) appeared to correctly localize inmob1 mutants, suggesting that MOB1functions subsequent to actomyosin ring assembly. We also examined the subcellular distribution of Mob1p during the cell cycle and found that Mob1p first localized to the spindle pole bodies during mid-anaphase and then localized to a ring at the bud neck just before and during cytokinesis. Localization of Mob1p to the bud neck requiredCDC3, MEN genes CDC5,CDC14, CDC15, and DBF2, and spindle pole body gene NUD1 but was independent ofMYO1. The localization of Mob1p to both spindle poles was abolished in cdc15 and nud1 mutants and was perturbed in cdc5 and cdc14mutants. These results suggest that the MEN functions during the mitosis-to-G1 transition to control cyclin-CDK inactivation and cytokinesis.
In Vitro‐ and In Vivo‐Induced Transgene Expression in Human Embryonic Stem Cells and Derivatives

The use of human embryonic stem cells (hESCs) as a research and therapeutic tool will be facilitated by conditional gene expression. Here, we report drug‐induced transgene expression, both in vitro and in vivo, from a tet‐on hESC line with >95% purity. Using green fluorescent protein as an indicator, we demonstrated that the tet‐on system allowed a tight control of the gene expression in both undifferentiated hESCs and differentiated cells of the three germ layers. More importantly, after the cells were transplanted into animals, the gene expression remained to be regulated by an orally administered drug. These results provide a technical basis for regulation of gene expression in hESCs and derivatives in vitro and in vivo.
The Picker Patient Experience Questionnaire: development and validation using data from in-patient surveys in five countries.

OBJECTIVE The purpose of this study was to develop and test a core set of questions to measure patients' experiences of in-patient care. Questions were selected from the bank of items developed for use in in-patient surveys undertaken by the Picker Institute for the purposes of assessing the quality of care. DESIGN The data reported here come from surveys of patients who had attended acute care hospitals in five countries: the United Kingdom, Germany, Sweden, Switzerland, and the USA. Questionnaires were mailed to patients' homes within 1 month of discharge, either to all patients, or to a random sample, discharged during a specified period. SAMPLE A total of 62 925 questionnaires were returned, with response rates of 65% (UK), 74% (Germany), 63% (Sweden), 52% (Switzerland), and 46% (USA). RESULTS Fifteen items were selected from the bank of questions included in the Picker in-patient questionnaires. These items have a high degree of face validity and when summed to an index they show a high degree of construct validity and internal reliability consistency. DISCUSSION Fifteen items derived from the longer form Picker in-patient survey have been found to provide a meaningful picture of patient experiences of health care, and constitute the 15-item Picker Patient Experience Questionnaire. These questions comprise a core set that should be measured in all in-patient facility surveys. The Picker Patient Experience Questionnaire represents a step forward in the measurement of patient experience as it provides a core set of questions around which further optional modules may be added. Scores are easy to interpret and actionable. CONCLUSION This small set of questions could be incorporated into in-patient surveys in different settings, enabling the comparison of hospital performance and the establishment of national or international benchmarks.
Current Collapse and High-Electric-Field Reliability of Unpassivated GaN/AlGaN/GaN HEMTs

Long-term ON-state and OFF-state high-electric-field stress results are presented for unpassivated GaN/AlGaN/GaN high-electron-mobility transistors on SiC substrates. Because of the thin GaN cap layer, devices show minimal current-collapse effects prior to high-electric-field stress, despite the fact that they are not passivated. This comes at the price of a relatively high gate-leakage current. Under the assumption that donor-like electron traps are present within the GaN cap, two-dimensional numerical device simulations provide an explanation for the influence of the GaN cap layer on current collapse and for the correlation between the latter and the gate-leakage current. Both ON-state and OFF-state stresses produce simultaneous current-collapse increase and gate-leakage-current decrease, which can be interpreted to be the result of gate-drain surface degradation and reduced gate electron injection. This study shows that although the thin GaN cap layer is effective in suppressing surface-related dispersion effects in virgin devices, it does not, per se, protect the device from high-electric-field degradation, and it should, to this aim, be adopted in conjunction with other technological solutions like surface passivation, prepassivation surface treatments, and/or field-plate gate