tbuckley/cabot-search huggingface dataset:
Increased Fructose Associates with Elevated Blood Pressure
Authors: Diana I. Jalal, Gerard Smits, Richard J. Johnson, Michel Chonchol
Journal: Journal of the American Society of Nephrology (2010)

The recent increase in fructose consumption in industrialized nations mirrors the rise in the prevalence of hypertension, but epidemiologic studies have inconsistently linked these observations. We investigated whether increased fructose intake from added sugars associates with an increased risk for higher BP levels in US adults without a history of hypertension. We conducted a cross-sectional analysis using the data collected from the National Health and Nutrition Examination Survey (NHANES 2003 to 2006) involving 4528 adults without a history of hypertension. Median fructose intake was 74 g/d, corresponding to 2.5 sugary soft drinks each day. After adjustment for demographics; comorbidities; physical activity; total kilocalorie intake; and dietary confounders such as total carbohydrate, alcohol, salt, and vitamin C intake, an increased fructose intake of ≥74 g/d independently and significantly associated with higher odds of elevated BP levels: It led to a 26, 30, and 77% higher risk for BP cutoffs of ≥135/85, ≥140/90, and ≥160/100 mmHg, respectively. These results suggest that high fructose intake, in the form of added sugar, independently associates with higher BP levels among US adults without a history of hypertension.
Puerperal Thromboembolic Disease in "High Risk" Cases
Authors: P. Jackson
Journal: BMJ (1973)

One hundred obstetric patients were studied for evidence of puerperal thromboembolic disease. Only one case of deep vein thrombosis was detected in patients thought to be in a "high risk" category because of age or operative intervention. Clinical findings were unreliable compared with measurements of (125)I-labelled fibrinogen uptake. Doppler ultrasound flow detection proved a simple screening technique but produced no abnormal findings in this series.
The influence of treatment modality and ethnicity on attitudes in type 2 diabetes.
Authors: J T Fitzgerald, L D Gruppen, R M Anderson, M M Funnell, S J Jacober, G Grunberger, L C Aman
Journal: Diabetes Care (2000)

OBJECTIVE: The study examines diabetes attitude differences by treatment modality (insulin vs. no insulin), race/ethnicity, and the interaction of these two variables for people with type 2 diabetes. RESEARCH DESIGN AND METHODS: Data were collected with the Diabetes Care Profile (DCP), an instrument that assesses psychosocial factors related to diabetes. Participants (n = 672) were recruited in the metropolitan Detroit, Michigan, area from 1993 to 1996. A total of 68% of these participants were African-Americans with type 2 diabetes, and 32% were Caucasians with type 2 diabetes. Analyses of covariance were performed to examine the effects of race/ethnicity, treatment, and their interaction for each DCP scale. RESULTS: The four patient categories (two ethnicities by two treatment modalities) differed by age, years with diabetes, education, and sex distribution. Treatment modality had a significant effect on 6 of the 16 DCP scales (Control, Social and Personal Factors, Positive Attitude, Negative Attitude, Self-Care Ability, and Exercise Barriers). Ethnicity was a significant effect for three scales (Control, Support, and Support Attitudes). The interaction of race/ethnicity and treatment modality was a significant effect for two related attitude scales (Positive Attitude and Negative Attitude). CONCLUSIONS: The results suggest that attitudes toward diabetes are similar for African-American and Caucasian patients with type 2 diabetes. The results also suggest that treatment modality has a greater effect on attitudes than either race/ethnicity or the interaction effect. However, Caucasian patients using insulin differed from the other patient groups by having the least positive and the most negative attitudes regarding diabetes.
Molecular Evolution and Patterns of Duplication in the SEP/AGL6-Like Lineage of the Zingiberales: A Proposed Mechanism for Floral Diversification
Authors: Roxana Yockteng, Ana M.R. Almeida, Kelsie Morioka, Elena R. Alvarez-Buylla, Chelsea D. Specht
Journal: Molecular Biology and Evolution (2013)

The diversity of floral forms in the plant order Zingiberales has evolved through alterations in floral organ morphology. One striking alteration is the shift from fertile, filamentous stamens to sterile, laminar (petaloid) organs in the stamen whorls, attributed to specific pollination syndromes. Here, we examine the role of the SEPALLATA (SEP) genes, known to be important in regulatory networks underlying floral development and organ identity, in the evolution of development of the diverse floral organs phenotypes in the Zingiberales. Phylogenetic analyses show that the SEP-like genes have undergone several duplication events giving rise to multiple copies. Selection tests on the SEP-like genes indicate that the two copies of SEP3 have mostly evolved under balancing selection, probably due to strong functional restrictions as a result of their critical role in floral organ specification. In contrast, the two LOFSEP copies have undergone differential positive selection, indicating neofunctionalization. Reverse transcriptase-polymerase chain reaction, gene expression from RNA-seq data, and in situ hybridization analyses show that the recovered genes have differential expression patterns across the various whorls and organ types found in the Zingiberales. Our data also suggest that AGL6, sister to the SEP-like genes, may play an important role in stamen morphology in the Zingiberales. Thus, the SEP-like genes are likely to be involved in some of the unique morphogenetic patterns of floral organ development found among this diverse order of tropical monocots. This work contributes to a growing body of knowledge focused on understanding the role of gene duplications and the evolution of entire gene networks in the evolution of flower development.
Feed-Forward Reciprocal Activation of PAFR and STAT3 Regulates Epithelial–Mesenchymal Transition in Non–Small Cell Lung Cancer
Authors: Jie Chen, Tian Lan, Weimin Zhang, Lijia Dong, Nan Kang, Shumin Zhang, Ming Fu, Bing Liu, Kangtai Liu, Qimin Zhan
Journal: Cancer Research (2015)

Abstract Platelet-activating factor receptor (PAFR), a G-protein–coupled receptor, has been implicated in tumorigenesis, but its contributions to metastatic progression have not been investigated. Here, we show that PAFR is overexpressed in non–small cell lung cancer (NSCLC) as well as in breast, colorectal, and gastric carcinomas. Expression of PAFR correlates closely with clinical stages, survival time, and distant metastasis. In human NSCLC cells, activation of the PAF/PAFR signaling axis accentuated malignant character, including by stimulating epithelial–mesenchymal transition (EMT). In contrast, silencing PAFR in aggressive NSCLC cells inhibited these effects. Mechanistic investigations showed that PAFR stimulated EMT by activating STAT3 via upregulation of G-protein–dependent SRC or JAK2 kinase activity. Notably, STAT3 transcriptionally elevated PAFR expression. Thus, activation of PAFR in NSCLC cells initiated a forward feedback loop responsible for mediating the aggressive malignant character of NSCLC cells in vitro and in vivo. Reinforcing this reciprocal activation loop, PAF/PAFR signaling also upregulated IL6 expression and thereby STAT3 activation. Overall, our results elucidated an important role for PAFR dysregulation in the pathogenicity of NSCLC and unraveled a forward feedback loop between PAFR and STAT3 that acts to drive the malignant progression of NSCLC. Cancer Res; 75(19); 4198–210. ©2015 AACR.
Interleukin-22 Induces Interleukin-18 Expression from Epithelial Cells during Intestinal Infection
Authors: Melba Muñoz, Celine Eidenschenk, Naruhisa Ota, Kit Wong, Uwe Lohmann, Anja A. Kühl, Xiaoting Wang, Paolo Manzanillo, Yun Li, Sascha Rutz, Yan Zheng, Lauri Diehl, Nobuhiko Kayagaki, Menno van Lookeren-Campagne, Oliver Liesenfeld, Markus Heimesaat, Wenjun Ouyang
Journal: Immunity (2015)
Gut Bacteria Products Prevent AKI Induced by Ischemia-Reperfusion
Authors: Vinicius Andrade-Oliveira, Mariane T. Amano, Matheus Correa-Costa, Angela Castoldi, Raphael J.F. Felizardo, Danilo C. de Almeida, Enio J. Bassi, Pedro M. Moraes-Vieira, Meire I. Hiyane, Andrea C.D. Rodas, Jean P.S. Peron, Cristhiane F. Aguiar, Marlene A. Reis, Willian R. Ribeiro, Claudete J. Valduga, Rui Curi, Marco Aurelio Ramirez Vinolo, Caroline M. Ferreira, Niels Olsen Saraiva Câmara
Journal: Journal of the American Society of Nephrology (2015)

Short-chain fatty acids (SCFAs) are fermentation end products produced by the intestinal microbiota and have anti-inflammatory and histone deacetylase–inhibiting properties. Recently, a dual relationship between the intestine and kidneys has been unraveled. Therefore, we evaluated the role of SCFA in an AKI model in which the inflammatory process has a detrimental role. We observed that therapy with the three main SCFAs (acetate, propionate, and butyrate) improved renal dysfunction caused by injury. This protection was associated with low levels of local and systemic inflammation, oxidative cellular stress, cell infiltration/activation, and apoptosis. However, it was also associated with an increase in autophagy. Moreover, SCFAs inhibited histone deacetylase activity and modulated the expression levels of enzymes involved in chromatin modification. In vitro analyses showed that SCFAs modulated the inflammatory process, decreasing the maturation of dendritic cells and inhibiting the capacity of these cells to induce CD4 + and CD8 + T cell proliferation. Furthermore, SCFAs ameliorated the effects of hypoxia in kidney epithelial cells by improving mitochondrial biogenesis. Notably, mice treated with acetate-producing bacteria also had better outcomes after AKI. Thus, we demonstrate that SCFAs improve organ function and viability after an injury through modulation of the inflammatory process, most likely via epigenetic modification.
ENLARGEMENT OF THE THYROID GLAND IN MALARIA
Authors: J. B. Hume
Journal: BMJ (1919)

TRIBRTSN 66I28. Ypui see here the metacarpal bone of a child.Here is the iower epiphysis of the radius.That child had sarcoma of its testicle removed and deveTopeci a growth in the bone.1919-ACUTE N-PHRITI8.M-.D c&TJounzas Hospital with malaria.Bilateral enlargement, some discom- fort in throat, but no dysphagia or dyspnioea.Pulse 1207130.Spleen not enlarged.Progress as in Case V.CASE VII.Cpl. J., aged 24.Two previousg attacks.Benign tertian parasites.Constriction in throat and dyspnoea noticed after second attack.Had slight bilateral enlargement of thyroid, accompanied by marked tachycardia-120 and slight tremor.
Development of autologous human dermal-epidermal composites based on sterilized human allodermis for clinical use
Authors: K.H. Chakrabarty, R.A. Dawson, P. Harris, C. Layton, M. Babu, L. Gould, J. Phillips, I. Leigh, C. Green, E. Freedlander, S. Mac Neil
Journal: British Journal of Dermatology (1999)

The aim of this study was to identify a sterilization technique for the preparation of human allodermis which could be used as a dermal component in wound healing and as the dermal base for production of dermal–epidermal composites for one‐stage grafting in patients. We report that it is possible to produce dermal–epidermal composites which perform well in vitro and in vivo using a standard ethylene oxide sterilization methodology. Prevention of ethylene oxide‐induced damage to the dermis was achieved using gentle dehydration of the skin prior to ethylene oxide sterilization. The issue of whether viable fibroblasts are required for composite production was examined in comparative studies using glycerol vs. ethylene oxide sterilized dermis. Where good collagen IV retention was achieved following preparation of acellular de‐epidermized dermis there was no advantage to having fibroblasts present in vitro or in vivo; however, where collagen IV retention was poor or where keratinocytes were initially expanded in culture then there was a significant advantage to introducing fibroblasts to the composites during their preparative 10‐day period in vitro. The requirement for fibroblasts became less evident when composites were grafted on to nude mice. In conclusion, we report a protocol for the successful sterilization of human allodermis to achieve an acellular dermis with good retention of collagen IV. This acellular dermis would be appropriate for clinical use as a dermal replacement material. It can also be used for the production of dermal–epidermal composites using autologous keratinocytes (with or without fibroblasts).
Early Childhood Infections and the Risk of Islet Autoimmunity
Authors: Janet K. Snell-Bergeon, Jennifer Smith, Fran Dong, Anna E. Barón, Kathy Barriga, Jill M. Norris, Marian Rewers
Journal: Diabetes Care (2012)

Type 1 diabetes is a common chronic childhood disease, and the incidence is increasing globally. Childhood infections are considered a potential environmental trigger of type 1 diabetes. Alternatively, improved hygiene and reduced childhood infections could explain the increase in type 1 diabetes in developed countries. The association of reported illnesses during infancy and later development of islet autoimmunity (IA) were examined in the Diabetes Autoimmunity Study in the Young.Complete illness interviews through 9 months of age were collected for 1,729 children-1,174 without a family history of type 1 diabetes and 555 with a first-degree relative with type 1 diabetes. Persistent IA was defined as positive antibodies to insulin, glutamic acid decarboxylase, or tyrosine phosphatase on at least two consecutive study visits.There were 109 children with persistent IA among the 1,729 children with illness records. A greater number of gastrointestinal illnesses were associated with an increased risk of IA, but only among children who were exposed to gluten-containing grains (wheat or barley) either <4 months of age (hazard ratio 1.37 [95% CI 1.22-1.55]; P < 0.0001) or ≥7 months of age (1.12 [1.05-1.19]; P = 0.0005) compared with 4-6 months of age (P for interaction = 0.02). There were no associations of upper respiratory symptoms, respiratory illnesses, or fevers with IA.Specific pathogens such as enteroviruses or rotavirus may increase the risk of IA in the presence of existing inflammation induced by diet.
Substance P induces a cardiovascular defense reaction in the rat: pharmacological characterization.
Authors: T Unger, S Carolus, G Demmert, D Ganten, R E Lang, C Maser-Gluth, H Steinberg, R Veelken
Journal: Circulation Research (1988)

In this study in conscious rats, we tested the hypothesis that substance P, a central pressor peptide and a potential transmitter substance of pain pathways, could be involved in the cardiovascular defense reaction that is typically associated with unpleasant sensory stimuli. The hemodynamic responses to centrally administered substance P were pharmacologically characterized. The increases in blood pressure and heart rate after intracerebroventricular injections of substance P were accompanied by mesenteric and renal vasoconstriction and hind limb vasodilation (pulsed-Doppler flow probes). The pressor and vasoconstrictor responses were attenuated by peripheral alpha 1-adrenoceptor blockade with prazosin but were not influenced by blockade of vascular vasopressin receptors with d(CH2)5Tyr(Me) arginine vasopressin (AVP). Cardiac beta 1-adrenoceptor blockade with metoprolol abolished the tachycardic and reduced the pressor responses. Substance P-induced hind limb vasodilation was not sensitive to intravenous atropine but was largely prevented by peripheral beta 2-adrenoceptor blockade with ICI 118,551. Thus, the substance P-induced pressor effects are mediated by alpha 1-adrenergic sympathetic vasoconstriction and beta 1-adrenergic cardiac stimulation, whereas the hind limb vasodilation is mainly due to beta 2-adrenergic stimulation. Substance P dose-dependently (0.01-10 micrograms i.c.v.) released oxytocin but not vasopressin or adrenocorticotropic hormone (ACTH) from the pituitary gland. High doses reduced basal ACTH levels. Together with the hemodynamic responses, a behavioral arousal reaction was observed, which included increased locomotion, grooming, scratching, and skin biting. Our results demonstrate that a neuropeptide can induce classic cardiovascular defense reaction.(ABSTRACT TRUNCATED AT 250 WORDS)
STUDIES IN THE RELATION OF THE HEMOLYTIC STREPTOCOCCUS TO RHEUMATIC FEVER
Authors: T. N. Harris
Journal: The Journal of Experimental Medicine (1948)

Complement-fixing antibodies to the cytoplasmic particles (CP) and to the S fraction of streptococcal nucleoproteins are present in normal human sera, the range of concentrations varying among the age groups. The titer of these antibodies rises between the first half-week and the 3rd week of scarlet fever, in more than 80 per cent of the cases. The titers then remain elevated for at least 4 months. In children, 91 per cent of the normal sera examined showed anti-CP titers up to 32; 87 per cent of sera in active rheumatic disease had titers above this level. Corresponding data with S fell in the same range of percentage distribution. Anti-CP and anti-S titers remained elevated long after the rheumatic process had reached quiescence. No correlation of serologic titer with the degree of clinical activity was found in the case of either antibody.
TAMOXIFEN AND THE UTERUS AND ENDOMETRIUM
Authors: Patrick Neven, Xavier De Muylder, Yves Van Belle, Guido Vanderick, Edgard De Muylder, HelenJ. Stewart, GillianM. Knight, Antonio Cano, Pilar Matallin, Vicente Legua, Miguel Tortajada, Fernando Bonilla-Musoles
Journal: The Lancet (1989)
Calcium Deficiency Reduces Circulating Levels of FGF23
Authors: María E. Rodriguez-Ortiz, Ignacio Lopez, Juan R. Muñoz-Castañeda, Julio M. Martinez-Moreno, Alan Peralta Ramírez, Carmen Pineda, Antonio Canalejo, Philippe Jaeger, Escolastico Aguilera-Tejero, Mariano Rodriguez, Arnold Felsenfeld, Yolanda Almaden
Journal: Journal of the American Society of Nephrology (2012)

Fibroblast growth factor (FGF) 23 inhibits calcitriol production, which could exacerbate calcium deficiency or hypocalcemia unless calcium itself modulates FGF23 in this setting. In Wistar rats with normal renal function fed a diet low in both calcium and vitamin D, the resulting hypocalcemia was associated with low FGF23 despite high parathyroid hormone (PTH) and high calcitriol levels. FGF23 correlated positively with calcium and negatively with PTH. Addition of high dietary phosphorus to this diet increased FGF23 except in rats with hypocalcemia despite high PTH levels. In parathyroidectomized rats, an increase in dietary calcium for 10 days increased serum calcium, with an associated increase in FGF23, decrease in calcitriol, and no change in phosphorus. Also in parathyroidectomized rats, FGF23 increased significantly 6 hours after administration of calcium gluconate. Taken together, these results suggest that hypocalcemia reduces the circulating concentrations of FGF23. This decrease in FGF23 could be a response to avoid a subsequent reduction in calcitriol, which could exacerbate hypocalcemia.
STUDIES UPON MINUTE HEMOLYTIC STREPTOCOCCI
Authors: Perrin H. Long, Eleanor A. Bliss
Journal: The Journal of Experimental Medicine (1934)

The cultural and biochemical characteristics of a group of minute hitherto undescribed beta hemolytic streptococci from human sources have been recorded and upon the basis of these cultural reactions it is suggested that these organisms may represent new species of the genus streptococcus.
Two peaks of interleukin 1 expression in human leukocytes cultured with tobacco glycoprotein.
Authors: T Francus, G Manzo, M Canki, L C Thompson, P Szabo
Journal: The Journal of Experimental Medicine (1989)

We have previously shown that tobacco glycoprotein (TGP), a polyphenol-rich glycoprotein isolated from tobacco or from cigarette smoke, affects the immune system. In this study we show that TGP induces human PBL and adherent cells to produce IL-1 alpha and IL-1 beta. Two peaks of IL-1 activity were observed; one at 18-24 h, the second at 4-6 d after initiation of culture. A similar pattern was observed for the steady state level of IL-1 mRNA. These data suggest that the production of IL-1 by cells stimulated with TGP might be a factor in cardiovascular disease associated with cigarette smoking.
PWE-111 Lipopolysaccharide induces small intestinal epithelial cell apoptosis and shedding which is regulated by NFκB signalling
Authors: J M Williams, C A Duckworth, B J Campbell, D M Pritchard
Journal: Gut (2012)

<h3>Introduction</h3> The gut barrier is formed by a single cell thick, simple columnar epithelium consisting of intestinal epithelial cells (IECs) held together by tight junctions. In the small intestine, IECs are generated in the crypt, migrate up the crypt-villus axis and are shed at the villus tip. When IECs detach from the villus during the process of shedding, discontinuities occur in the epithelium. IEC shedding increases in response to pro-inflammatory cytokines, resulting in larger discontinuities and increased intestinal permeability. Understanding the mechanisms which regulate IEC shedding may allow development of therapeutic strategies which ameliorate its detrimental effects on gut barrier function in intestinal disease states. <h3>Aims</h3> To investigate whether IEC apoptosis and shedding are increased during induction of endotoxic shock, and the genetic regulation of this process. <h3>Methods</h3> Lipopolysaccharide (LPS) from <i>Escherichia coli</i> O111:B4, was administered to adult female C57BL/6 mice at 10 mg/kg by intraperitoneal injection (n=6 per group). Animals were euthanased 1–6 h after LPS administration. The duodenum, jejunum and ileum were fixed in formalin. Histopathological examination of H&amp;E stained sections, quantification of villus length, and immunolabelling of IECs for active caspase 3 was performed. Dose response experiments were performed using 0.125 to 20 mg/kg LPS, sacrificing mice (n=4 per group) at 1.5 h. Transgenic mice (NFκB1−/−, NFκB2−/− and cREL−/−) were administered 10 mg/kg or 0.125 mg/kg LPS and euthanased at 1.5 h (n=6). Statistical comparisons were made by t-test with Bonferroni correction. <h3>Results</h3> In C57BL/6 mice, 10 mg/kg LPS caused a 20–50-fold increase in IEC apoptosis and shedding, with consequent villus atrophy, which was greatest in the duodenum and jejunum at 1.5 h, and in the ileum at 2 h. IEC apoptosis and shedding had subsided by 6 h after LPS administration. LPS at 0.125 mg/kg caused an attenuated response in C57BL/6 mice in terms of villus injury and amounts of apoptosis and shedding at 1.5 h, whereas at this dose NFκB1−/− mice were severely affected, while NFκB2−/− mice were minimally affected. <h3>Conclusion</h3> These findings suggest that endotoxic shock causes dynamic and hyperacute selective injury to the murine small intestine, prior to obvious pathological alterations in other organ systems. The induced apoptosis and cell shedding occurs within a well defined time period, and varies in intensity and time course in different intestinal segments. The differing sensitivity to LPS in transgenic mice implicates NFκB signalling in the pathogenesis of this type of intestinal injury. <h3>Competing interests</h3> None declared.