Miracle-dz/UniFAR-FTUs huggingface dataset:
Blood platelet monoamine oxidase activity, serotonin uptake and release rates in anorexia and bulimia patients and in healthy controls

Platelet monoamine oxidase (MAO) activity, serotonin uptake rate and serotonin efflux rate have all been suggested to be markers for central serotonergic mechanisms. Platelet MAO activity is associated with certain personality traits, with low activity linked to traits such as impulsiveness, sensation‐seeking and avoidance of monotony, all possible expressions of low central serotonergic activity. Low platelet serotonin uptake rate has been connected to unipolar depression and the rate of efflux, in the presence of the ATP uncoupler CCP, higher in bipolar depressives than in controls. Platelet MAO was found to be lower in 16 consecutive female inpatients fulfilling the DSM‐III criteria for bulimia nervosa than in 12 female controls. Rates of serotonin uptake and efflux in the presence of CCP were, on the other hand, similar to the controls. In the controls there were no correlations between platelet MAO activity and any of the other parameters estimated. Vmax for the platelet uptake of serotonin correlated positively with the Km for the uptake, but not with any other parameter. The uninfluenced rate of efflux of serotonin correlated positively with the efflux in the presence of the ATP uncoupler CCP.
Heparin inhibits autocrine stimulation but not fibroblast growth factor stimulation of cell proliferation of androgen‐responsive shionogi carcinoma 115

An androgen‐responsive cloned cell line (SC‐3) derived from Shionogi carcinoma 115 (SC115) has been shown to secrete fibroblast growth factor (FGF)‐like peptide in response to androgen, which binds to FGF receptor and promotes the proliferation of SC‐3 cells in an autocrine mechanism. Since the androgen‐induced autocrine factor has a property to bind heparin, we examined the effects of heparin on the growth of SC‐3 cells. Heparin was found to exhibit significant inhibition of testosterone‐induced growth in a concentration‐dependent manner: Approximately 50% inhibition was found at a concentration of 0.1 μg/ml. DNA synthesis of SC‐3 cells induced by testosterone was also inhibited strongly by heparin, and less strongly by heparan sulfate and dermatan sulfate. Proliferation of SC‐3 cells induced by acidic (a) or basic (b) FGF appeared not to be modulated by heparin. In contrast, heparin efficiently blocked DNA synthesis stimulated with androgen‐induced growth factor in the conditioned medium from testosterone‐treated cells. These results indicate that heparin inhibits autocrine loop in SC‐3 cells induced by androgen. Thus the autocrine growth factor possesses a different characteristic from aFGF and bFGF in that its bioactivities are negatively modulated by the glycosaminoglycan.
NKG2‐C is a receptor on human natural killer cells that recognizes structures on K562 target cells

NKG2‐C is a member of the recently discovered NKG2 family of genes and proteins, which are preferentially expressed on human natural killer (NK) cells. These potential NK cell receptors belong to a larger class of type II transmembrane proteins with a C‐type lectin domain. We show here that NKG2‐C is expressed as a 36‐kDa glycoprotein by translation in vitro, recombinant expression and immunoprecipitation from a human NK cell clone. Further, a recombinant soluble NKG2‐C‐receptor binds specifically to K562 cells, which are target cells for NK cell killing, and to RPMI 8866 cells, which are feeder cells for NK cells; several other hematopoietic cell lines tested do not show any binding. The binding structures on the surface of K562 cells disappear, concomitant with a loss in susceptibility to killing when the cells are induced to differentiate with phorbol ester and Ca2+ ionophore. Our data suggest the presence of specific target molecules for NKG2‐C on K562 cells, since overall glycosylation, Lewis X and Lewis Y structures, as well as the mucin‐like CD43 molecule, do not change following induction of the cells. We propose that NKG2‐C mediates a specific interaction of NK cells and their target cells with functional importance for NK cell killing.
The Role of the Built Environment: How Decentralized Nurse Stations Shape Communication, Patient Care Processes, and Patient Outcomes

ABSTRACT Increasingly, health communication scholars are attending to how hospital built environments shape communication, patient care processes, and patient outcomes. This multimethod study was conducted on two floors of a newly designed urban hospital. Nine focus groups interviews were conducted with 35 health care professionals from 10 provider groups. Seven of the groups were homogeneous by profession or level: nursing (three groups), nurse managers (two groups), and one group each of nurse care technicians (“techs”) and physicians. Two mixed groups were comprised of staff from pharmacy, occupational therapy, patient care facilitators, physical therapy, social work, and pastoral care. Systematic qualitative analysis was conducted using a conceptual framework based on systems theory and prior health care design and communication research. Additionally, quantitative modeling was employed to assess walking distances in two different hospital designs. Results indicate nurses walked significantly more in the new hospital environment. Qualitative analysis revealed three insights developed in relationship to system structures, processes, and outcomes. First, decentralized nurse stations changed system interdependencies by reducing nurse-to-nurse interactions and teamwork while heightening nurse interdependencies and teamwork with other health care occupations. Second, many nursing-related processes remained centralized while nurse stations were decentralized, creating systems-based problems for nursing care. Third, nursing communities of practices were adversely affected by the new design. Implications of this study suggest that nurse station design shapes communication, patient care processes, and patient outcomes. Further, it is important to understand how the built environment, often treated as invisible in communication research, is crucial to understanding communication within complex health care systems.
RNA polymerase II is aberrantly phosphorylated and localized to viral replication compartments following herpes simplex virus infection

During lytic infection, herpes simplex virus subverts the host cell RNA polymerase II transcription machinery to efficiently express its own genome while repressing the expression of most cellular genes. The mechanism by which RNA polymerase II is directed to the viral delayed-early and late genes is still unresolved. We report here that RNA polymerase II is preferentially localized to viral replication compartments early after infection with herpes simplex virus type 1. Concurrent with recruitment of RNA polymerase II into viral compartments is a rapid and aberrant phosphorylation of the large subunit carboxy-terminal domain (CTD). Aberrant phosphorylation of the CTD requires early viral gene expression but is not dependent on viral DNA replication or on the formation of viral replication compartments. Localization of RNA polymerase II and modifications to the CTD may be instrumental in favoring transcription of viral genes and repressing specific transcription of cellular genes.
Physicians, Patients, and the Electronic Health Record: An Ethnographic Analysis

PURPOSE Little is known about the effects of the electronic health record (EHR) on physician-patient encounters. The objectives of this study were to identify the factors that influence the manner by which physicians use the EHR with patients. METHODS This ethnographic study included 4 qualitative components: 80 hours of participant observation in 4 primary care offices in the Pacific Northwest; individual interviews with 52 patients, 12 office staff members, 23 physicians, and 1 nurse-practitioner; videotaped reviews of 29 clinical encounters; and 5 focus-group interviews with physicians and computer advocates. The main outcome measures were factors that influence how physicians use the EHR. Researchers qualitatively derived these factors through serial reviews of data. RESULTS This study identified 14 factors that influence how EHRs are used and perceived in medical practice today. These factors were categorized into 4 thematic domains: (1) spatial—effect of the physical presence and location of EHRs on interactions between physicians and patients; (2) relational—perceptions of physicians and patients about the EHR and how those perceptions affected its use; (3) educational—issues of developing physicians’ proficiency with and improving patients’ understandings about EHR use; and (4) structural—institutional and technological forces that influence how physicians perceived their use of EHR. CONCLUSIONS This study found that the introduction of EHRs into practice influences multiple cognitive and social dimensions of the clinical encounter. It brings into focus important questions that through further inquiry can determine how to make best use of the EHR to enhance therapeutic relationships.
[18F]Fluorodeoxyglucose Uptake in Neonatal Acute Lung Injury Measured by Positron Emission Tomography1

The objective of this study was to evaluate positron emission tomography(PET) of [18F]fluorodexoyglucose (18FDG) uptake as a measure of neonatal acute lung injury. Inasmuch as intrapulmonary sequestration of neutrophils is a hallmark of acute lung injury, quantification of neutrophil activity using 18FDG may offer a novel, in vivo technique to examine the progression and resolution of this disease. Ten newborn piglets were studied; six received bronchoalveolar lavage followed by 4 h of high pressure ventilation to create acute lung injury. Four healthy piglets served as controls. 18FDG (0.8 mCi/kg; 29.6 MBq) was given i.v. and PET (ECAT 953/31, Siemens) was performed for 90 min. During PET, all animals were sedated, paralyzed, and ventilated to maintain normal blood gases. The time course of radioactivity in lung regions and in plasma was used to calculate the rate constant for the metabolic trapping of 18FDG in tissue according to the method of C. S. Patlak. Median 18FDG influx constants were significantly higher in injured piglets (0.0187 min-1) than in control piglets (0.0052 min-1) (p < 0.01). Moreover, consistent with the 18FDG uptake data, injured piglets had moderate to severe injury on lung histology whereas control piglets had only slight and focal histologic changes. We conclude that PET of 18FDG uptake is an accurate, readily repeatable in vivo measure of neonatal acute lung injury.
Adequacy of the iodine supply in The Netherlands.

OBJECTIVE To assess the adequacy of the iodine supply in the Netherlands and to study possible ways of increasing the iodine intake. DESIGN, SETTINGS AND SUBJECTS: Goitre and nutrition surveillance studies (intake and urinary excretion of iodine) among population groups (age: 12-85 y, n=57-1704) in the Netherlands in the period 1981-1993. Simulation studies, based on the Dutch Nutrition Food Consumption Surveys (n=6000), calculating iodine intake among population groups after fictively iodizing different food groups. RESULTS Mean intake of iodine, measured with different food consumption methods in the period 1984-1993, met the recommended amount of 150-300 microg per day in males, but not in females. Median urinary iodine excretion levels were in the range for mild Iodine Deficiency Disorders in both sexes. According to dietary methods reflecting habitual intake and urinary iodine excretion per kg body weight or per mmol creatinin the prevalence of low iodine supply among adults is between 4 and 20% for women and between 5 and 15% for men. Iodization of different products would increase mean iodine intakes by up to 45% and would give a reduction of roughly 65% in the prevalence of low iodine intakes. CONCLUSION The present goitre prophylaxis in the Netherlands is not optimally effective. The iodine supply is below cut-off points in 4-20% of the adult population. It is possible to decrease the prevalence of low iodine intakes without a clear risk of exceeding the maximum acceptable daily iodine intake by increasing the iodine content of baker's salt and/or by adding iodine to other foods.
Tumour necrosis factor‐α drives Alport glomerulosclerosis in mice by promoting podocyte apoptosis

Chronic renal failure involves the progressive loss of renal parenchymal cells. For example, Alport syndrome develops from mutated type IV collagen that fosters the digestion of glomerular basement membranes and podocyte loss, followed by progressive glomerulosclerosis, ie Alport nephropathy. Here we show that autosomal recessive Alport nephropathy in collagen 4a3‐deficient mice is associated with increased intrarenal expression of the pro‐apoptotic cytokine tumour necrosis factor‐alpha (TNF‐α) in glomerular cells including podocytes as well as in infiltrating leukocytes. We therefore hypothesized that TNF‐α contributes to Alport glomerulosclerosis by inducing podocyte apoptosis. To address this issue, we treated 4‐week‐old collagen 4a3‐deficient mice with either vehicle or the TNF‐α antagonist etanercept for a period of 5 weeks. Etanercept treatment prolonged mean survival from 68 to 81 days as compared to vehicle‐treated mice. The beneficial effect of etanercept on survival was associated with a significant improvement of the glomerulosclerosis score, proteinuria, and the glomerular filtration rate at 9 weeks of age. Etanercept treatment specifically reduced the numbers of apoptotic podocytes, increased total podocyte counts, and increased the renal mRNA expression of nephrin and podocin without affecting markers of renal inflammation. TNF‐α‐induced podocyte loss is a previously unrecognized pathological mechanism of Alport glomerulosclerosis, and TNF‐α blockade might be a therapeutic option to delay the progression of Alport nephropathy and potentially of other forms of glomerulosclerosis. Copyright © 2011 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
The use of a rigid disc to protect exposed structures in wounds treated with negative pressure wound therapy: Effects on wound bed pressure and microvascular blood flow

There are increasing reports of deaths and serious complications associated with the use of negative pressure wound therapy (NPWT). Bleeding may occur in patients when NPWT is applied to a wound with exposed blood vessels or vascular grafts, possibly due to mechanical deformation and hypoperfusion of the vessel walls. Recent evidence suggests that using a rigid barrier disc to protect underlying tissue can prevent this mechanical deformation. The aim of this study was to examine the effect of rigid discs on the tissue exposed to negative pressure with regard to tissue pressure and microvascular blood flow. Peripheral wounds were created on the backs of eight pigs. The pressure and microvascular blood flow in the wound bed were measured when NPWT was applied. The wound was filled with foam, and rigid discs of different designs were inserted between the wound bed and the foam. The discs were created with or without channels (to accommodate exposed sensitive structures such as blood vessels and nerves), perforations, or a porous dressing that covered the underside of the discs (to facilitate pressure transduction and fluid evacuation). When comparing the results for pressure transduction to the wound bed, no significant differences were found using different discs covered with dressing, whereas pressure transduction was lower with bare discs. Microvascular blood flow in the wound bed decreased by 49 ± 7% when NPWT was applied to control wounds. The reduction in blood flow was less in the presence of a protective disc (e.g., −6 ± 5% for a dressing‐covered, perforated disc, p = 0.006). In conclusion, NPWT causes hypoperfusion of superficial tissue in the wound bed. The insertion of a rigid barrier counteracts this effect. The placement of a rigid disc over exposed blood vessels or nerves may protect these structures from rupture and damage.
Purified E255L Mutant SERCA1a and Purified PfATP6 Are Sensitive to SERCA-type Inhibitors but Insensitive to Artemisinins*

The antimalarial drugs artemisinins have been described as inhibiting Ca2+-ATPase activity of PfATP6 (Plasmodium falciparum ATP6) after expression in Xenopus oocytes. Mutation of an amino acid residue in mammalian SERCA1 (Glu255) to the equivalent one predicted in PfATP6 (Leu) was reported to induce sensitivity to artemisinin in the oocyte system. However, in the present experiments, we found that artemisinin did not inhibit mammalian SERCA1a E255L either when expressed in COS cells or after purification of the mutant expressed in Saccharomyces cerevisiae. Moreover, we found that PfATP6 after expression and purification from S. cerevisiae was insensitive to artemisinin and significantly less sensitive to thapsigargin and 2,5-di(tert-butyl)-1,4-benzohydroquinone than rabbit SERCA1 but retained higher sensitivity to cyclopiazonic acid, another type of SERCA1 inhibitor. Although mammalian SERCA and purified PfATP6 appear to have different pharmacological profiles, their insensitivity to artemisinins suggests that the mechanism of action of this class of drugs on the calcium metabolism in the intact cell is complex and cannot be ascribed to direct inhibition of PfATP6. Furthermore, the successful purification of PfATP6 affords the opportunity to develop new antimalarials by screening for inhibitors against PfATP6.
Eriocalyxin B Inhibits Nuclear Factor-κB Activation by Interfering with the Binding of Both p65 and p50 to the Response Element in a Noncompetitive Manner

Nuclear factor-κB (NF-κB) has been recognized to play a critical role in cell survival and inflammatory processes. It has become a target for intense drug development for the treatment of cancer, inflammatory, and autoimmune diseases. Here, we describe a potent NF-κB inhibitor, eriocalyxin B (Eri-B), an ent-kauranoid isolated from Isodon eriocalyx, an anti-inflammatory remedy. The presence of two α,β-unsaturated ketones give this compound the uniqueness among the ent-kauranoids tested. Eri-B inhibited the NF-κB transcriptional activity but not that of cAMP response element-binding protein. It suppressed the transcription of NF-κB downstream gene products including cyclooxygenase-2 and inducible nitric-oxide synthase induced by tumor necrosis factor-α or lipopolysaccharide in macrophages and hepatocarcinoma cells. Chromatin immunoprecipitation assay indicated that Eri-B selectively blocked the binding between NF-κB and the response elements in vivo without affecting the nuclear translocation of the transcription factor. Down-regulation of the endogenous p65 protein sensitized the cells toward the action of the compound. Furthermore, in vitro binding assays suggested that Eri-B reversibly interfered with the binding of p65 and p50 subunits to the DNA in a noncompetitive manner. In summary, this study reveals the novel action of a potent NF-κB inhibitor that could be potentially used for the treatment of a variety of NF-κB-associated diseases. Modification of the structure of this class of compounds becomes the key to the control of the behavior of the compound against different cellular signaling pathways.
Overexpression of human X-box binding protein 1 (XBP-1) in colorectal adenomas and adenocarcinomas.

BACKGROUND Human X-box binding protein 1 (XBP-1) is a transcription factor essential for hepatocyte growth, as well as for plasma cell differentiation. Recently, overexpression of XBP-1 has been reported in breast cancer including non-invasive carcinomas, and was suggested to play an important role in breast carcinogenesis. To investigate the involvement of XBP-1 in colorectal tumorigenecity, the expression of XBP-1 was examined in four colon cancer cell lines, six colorectal polyps and five colorectal carcinomas. MATERIALS AND METHODS The study population consisted of eleven patients who had undergone resection for colorectal cancer or adenoma from 2000 to 2002. Four colon cancer cell lines, DLD1, SW480, HCT15 and WiDr, were also analyzed for expression of XBP-1. Reverse transcription-polymerase chain reaction was performed using eleven primary colon tumors. XBP-1 expression was then investigated using an immunohistochemical method for archived paraffin-embedded sections. RESULTS The XBP-1 gene was overexpressed in four cases out of five primary colorectal carcinomas and in four cases out of six colorectal adenomas. Also all four cancer cell lines expressed XBP-1 mRNA. Immunohistochemical staining demonstrated that XBP-1 protein was strongly stained in the cytoplasms of cancer cells, whereas it was unreactive in the normal colon epithelial cells and stromal cells. CONCLUSION These data indicate that increased expression of XBP-1 gene may play some role in human colon carcinogenesis through impairment of cell differentiation regulation.
The Measurement of Autonomic Arousal: Some Basic Issues Illustrated by the Covariation of Heart Rate and Skin Conductance

&NA; Empirical evidence is presented to demonstrate that there is no true relationship between such physiological measures as heart rate and skin conductance, but that (depending on circumstances) heart rate and skin conductance covary directly, inversely, or not at all. It is contended that a solution to the general measurement of arousal will not be found by transforming single measures, by innovations in data reduction, or by combining measures. Instead, the solution lies in learning more about the unique properties of different physiological systems by establishing how they vary as a function of the parameters of stimulus input‐‐such as intensity, rate of stimulation, and time since stimulus onset.