tbuckley/cabot-search huggingface dataset:
Biocompatibility of hemodialysis membranes.
Authors: A K Cheung
Journal: Journal of the American Society of Nephrology (1990)

Exposure of blood to hemodialysis membranes results in numerous interactions between the blood elements and the membrane. Transformation and adsorption of plasma proteins (such as complement) and activation of blood cells (such as neutrophils and monocytes) have been studied most extensively by nephrologists in recent years. There is no consensus on the definition of biocompatibility for dialyzer membranes. An operational definition of biocompatibility is the lack of any perturbation of blood constituents. According to this "inert surface" definition, a membrane (for example, one that adsorbs beta 2-microglobulin) can be considered as bioincompatible and yet desirable. Because of the multitude of blood-membrane interactions that may occur during hemodialysis, multiple criteria for biocompatibility needs to be applied in the classification of membranes. A certain bioincompatible phenomenon can be further classified as beneficial or deleterious depending on its biological effects as well as its acute and chronic impacts on the dialysis patient.
A Family Study in Still's Disease
Authors: B. M. Ansell, E. G. L. Bywaters, J. S. Lawrence
Journal: Annals of the Rheumatic Diseases (1962)

Familial studies in inflammatory polyarthritis indicate strong hereditary factors, particularly in relationship to the serological tests (Lawrence and Ball, 1958).In a single kindred of some 3,000 persons reported briefly by Whittinghill, Hendricks, Taylor, and Thorp (1958), rheumatoid arthritis was distributed independently of spondylitis and Still's disease.The ten spondylitics had higher than random frequencies of other cases of spondylitis and of Still's disease among their first-degree relatives, suggesting a genetic origin for this dual susceptibility.The five cases of Still's disease had, as their close relatives, spondylitics rather than persons with other forms of juvenile or adult rheumatoid arthritis.Precise details of the criteria used for the diagnosis of Still's disease in this study are not available, and the evaluation of this relation- ship is complicated by the fact that a transient attack of polyarthritis precedes the onset of spondylitis in about 25 per cent. of patients, often some years before the spondylitic phase (Hollister and Engleman, 1958).Conflicting results have been obtained with sero- logical tests in Still's disease.We have found 45 per cent. of such patients to have a positive Rose-Waaler test on at least one occasion during a 4to 10-year follow-up, although only 13 per cent.were positive on the first test (Bywaters, Carter, and Scott, 1959a).McEwen, Ziff, Carmel, Ditata, and Tanner (1958), using the euglobulin fraction for the S.C.A.T., found 58 per cent.positive, but with their inhibition test 94 per cent.were positive.With a view to elucidating this problem further, a group of patients with Still's disease admitted to the Canadian Red Cross Hospital, Taplow, have been used as probands for a family study.
Phylogenetic-Signal Dissection of Nuclear Housekeeping Genes Supports the Paraphyly of Sponges and the Monophyly of Eumetazoa
Authors: E. A. Sperling, K. J. Peterson, D. Pisani
Journal: Molecular Biology and Evolution (2009)

The relationships at the base of the metazoan tree have been difficult to robustly resolve, and there are several different hypotheses regarding the interrelationships among sponges, cnidarians, ctenophores, placozoans, and bilaterians, with each hypothesis having different implications for the body plan of the last common ancestor of animals and the paleoecology of the late Precambrian. We have sequenced seven nuclear housekeeping genes from 17 new sponges, bringing the total to 29 species analyzed, including multiple representatives of the Demospongiae, Calcarea, Hexactinellida, and Homoscleromorpha, and analyzed a data set also including six nonmetazoan outgroups and 36 eumetazoans using a variety of phylogenetic methods and evolutionary models. We used leaf stability to identify rogue taxa and investigate their effect on the support of the nodes in our trees, and we identified clades most likely to represent phylogenetic artifacts through the comparison of trees derived using different methods (and models) and through site-stripping analyses. Further, we investigated compositional heterogeneity and tested whether amino acid composition bias affected our results. Finally, we used Bayes factors to compare our results against previously published phylogenies. All our maximum likelihood (ML) and Bayesian analyses find sponges to be paraphyletic, with all analyses finding three extant paraphyletic sponge lineages, Demospongiae plus Hexactinellida, Calcarea, and Homoscleromorpha. All but one of our ML and Bayesian analyses support the monophyly of Eumetazoa (here Cnidaria + Bilateria) and a sister group relationship between Placozoa (here Trichoplax adhaerens) and Eumetazoa. Bayes factors invariably provide decisive support in favor of poriferan paraphyly when compared against either a sister group relationship between Porifera and Cnidaria or with a monophyletic Porifera with respect to a monophyletic Eumetazoa. Although we were able to recover sponge monophyly using our data set, this was only possible under unrealistic evolutionary models, if poorly performing phylogenetic methods were used, or in situations where the potential for the generation of tree reconstruction artifacts was artificially exacerbated. Everything considered, our data set does not provide any support for a monophyletic Diploblastica (here Placozoa + Cnidaria + Porifera) and suggests that a monophyletic Porifera may be better seen as a phylogenetic artifact.
Pituitary function in patients with newly diagnosed untreated systemic lupus erythematosus
Authors: M D Koller
Journal: Annals of the Rheumatic Diseases (2004)

To determine whether hormonal dysfunction involving the hypothalamic-pituitary-adrenal (HPA) axis, prolactin (PRL) secretion, and sex hormone status contribute to development of systemic lupus erythematosus (SLE).11 patients with SLE and 9 healthy controls were tested for their total anterior pituitary gland reserve by simultaneous injection of corticotropin-, growth hormone- (GH), thyrotropin-, and gonadotropin-releasing hormone (GnRH). Serum concentrations of adrenocorticotropin (ACTH), cortisol, GH, thyroid stimulating hormone (TSH), PRL, luteinising hormone (LH), and follicle stimulating hormone (FSH) were measured at baseline and after injection. Baseline values of oestradiol, testosterone, and thyroxine were determined.Basal and stimulated serum concentrations of ACTH, cortisol, GH, and PRL were similar in both groups. In contrast, despite similar basal thyroxine levels the TSH response to TRH was significantly higher in patients than in controls. LH and FSH levels in premenopausal female patients of both groups were identical. In contrast, two of the three male patients were hypogonadal without compensatory increases of basal LH and FSH levels, but they retained excessive stimulatory capacity in response to GnRH.No significant alteration of the HPA axis was found in patients with SLE, which is inadequate in view of the continuing inflammation. GH and PRL secretion were normal. The pituitary-thyroid and pituitary-gonadal axes were affected in patients with newly diagnosed, untreated SLE.
Determinants of epithelial differentiation during early nephrogenesis.
Authors: B M Brenner
Journal: Journal of the American Society of Nephrology (1990)

Organogenesis from undifferentiated progenitor cells and initiation of a society's new journal are developmental processes which share common elements. Both initially require a potent inducing stimulus followed in relatively rapid sequence by the appearance of organ-specific differentiation markers. These events are prerequisites to subsequent proliferation and maturation. Insofar as many postnatal forms of renal disease (e.g., hereditary glomerulopathies, infantile and adult forms of polycystic kidney disease, congenital dysplasias) owe their origins ultimately to disordered nephrogenesis, it is my belief that research in this area of nephrology should expand. It is further hoped that JASN will adopt this particular differentiation marker and serve as a forum for reporting the much-needed new knowledge to be gained. To "induce" the Journal's activity in this area I have summarized current knowledge and suggest directions in need of further investigation.
Noninvasive Urinary Metabolomic Profiling Identifies Diagnostic and Prognostic Markers in Lung Cancer
Authors: Ewy A. Mathé, Andrew D. Patterson, Majda Haznadar, Soumen K. Manna, Kristopher W. Krausz, Elise D. Bowman, Peter G. Shields, Jeffrey R. Idle, Philip B. Smith, Katsuhiro Anami, Dickran G. Kazandjian, Emmanuel Hatzakis, Frank J. Gonzalez, Curtis C. Harris
Journal: Cancer Research (2014)

Abstract Lung cancer remains the most common cause of cancer deaths worldwide, yet there is currently a lack of diagnostic noninvasive biomarkers that could guide treatment decisions. Small molecules (&amp;lt;1,500 Da) were measured in urine collected from 469 patients with lung cancer and 536 population controls using unbiased liquid chromatography/mass spectrometry. Clinical putative diagnostic and prognostic biomarkers were validated by quantitation and normalized to creatinine levels at two different time points and further confirmed in an independent sample set, which comprises 80 cases and 78 population controls, with similar demographic and clinical characteristics when compared with the training set. Creatine riboside (IUPAC name: 2-{2-[(2R,3R,4S,5R)-3,4-dihydroxy-5-(hydroxymethyl)-oxolan-2-yl]-1-methylcarbamimidamido}acetic acid), a novel molecule identified in this study, and N-acetylneuraminic acid (NANA) were each significantly (P &amp;lt; 0.00001) elevated in non–small cell lung cancer and associated with worse prognosis [HR = 1.81 (P = 0.0002), and 1.54 (P = 0.025), respectively]. Creatine riboside was the strongest classifier of lung cancer status in all and stage I-II cases, important for early detection, and also associated with worse prognosis in stage I-II lung cancer (HR = 1.71, P = 0.048). All measurements were highly reproducible with intraclass correlation coefficients ranging from 0.82 to 0.99. Both metabolites were significantly (P &amp;lt; 0.03) enriched in tumor tissue compared with adjacent nontumor tissue (N = 48), thus revealing their direct association with tumor metabolism. Creatine riboside and NANA may be robust urinary clinical metabolomic markers that are elevated in tumor tissue and associated with early lung cancer diagnosis and worse prognosis. Cancer Res; 74(12); 3259–70. ©2014 AACR.
Mutagen Sensitivity as aPredictor of Tumor Recurrence in Patients With Cancer of the Upper Aerodigestive Tract
Authors: Margaret R. Spitz, Hong Jiang, Scott M. Lippman, J. Jack Lee, T. C. Hsu, Zoltan Trizna, Stimson P. Schantz, Steven Benner, Fadlo Khuri, Waun K. Hong
Journal: JNCI Journal of the National Cancer Institute (1998)
The Role of Androgens in Male Gender Role Behavior
Authors: Jean D. Wilson
Journal: Endocrine Reviews (1999)

I. Introduction II. Sexual Behavior of Animals III. Control of Libido and Potentia in Humans IV. Gender Identity/Role Behavior in the Human A. Normal and abnormal sexual development B. Behavior studies in subjects with abnormal sexual development V. Gender Role Behavior in Individuals with Male Pseudohermaphroditism A. 17β-Hydroxysteroid dehydrogenase 3 deficiency B. Steroid 5α-reductase 2 deficiency C. Features common to 17β-hydroxysteroid dehydrogenase 3 and steroid 5α-reductase 2 deficiencies D. Androgen receptor mutations VI. Discussion VII. Conclusions
Acute Insulin Response and β-Cell Compensation in Normal Subjects Treated With Olanzapine or Risperidone for 2 Weeks
Authors: Thomas A. Hardy, Adam L. Meyers, Jun Yu, Sudha S. Shankar, Helmut O. Steinberg, Niels K. Porksen
Journal: Diabetes Care (2006)

A recent report by Ader et al. (1) suggested that olanzapine, an atypical antipsychotic, impaired β-cell compensation for insulin resistance in dogs. Such a mechanism could contribute to the important, but poorly understood, increase in diabetes risk among antipsychotic users. We previously reported that olanzapine and risperidone did not impair insulin secretory response based on a prospective study (2) of normal subjects using steady-state measurements during a hyperglycemic clamp. Here, we report additional data from this study focusing on the acute insulin response (AIR), allowing a comparison with the results of Ader et al. (1) by calculating a disposition index (DI) as a measure of β-cell compensation (3). Our hypothesis was that olanzapine treatment did not significantly change the DI derived from indexes of AIR and insulin sensitivity.

A detailed description of this study has been reported previously (2). Briefly, lean (mean BMI ∼24 kg/m2) healthy volunteers were randomized to treatment with placebo ( n = 18), olanzapine (10 mg/day; n = 17), or risperidone (4 mg/day; n = 13). Subjects were treated with half-maximal doses for 4 days before dose escalation. Subjects underwent hyperglycemic clamps (4) before randomization and after 15–17 days of treatment. Hyperglycemia was initiated with an intravenous priming dose of 20% (wt/vol) glucose estimated to produce a target level of glycemia (11.1 mmol/l). Half of the priming dose was …
Ovarian Carcinomas: CCN Genes Are Aberrantly Expressed and CCN1 Promotes Proliferation of these Cells
Authors: Sigal Gery, Dong Xie, Dong Yin, Hani Gabra, Carl Miller, Heming Wang, Diane Scott, William S. Yi, Miriam L. Popoviciu, Johathan W. Said, H. Phillip Koeffler
Journal: Clinical Cancer Research (2005)

Abstract Purpose: The connective tissue growth factor/cysteine-rich 61/nephroblastoma overexpressed (CCN) family consists of six matricellular proteins that are involved in various cellular functions, such as proliferation, development, and angiogenesis. The purpose of this study was to explore the possibility that CCN genes are involved in ovarian cancers. Experimental Design: We quantified CCN expression in a series of 59 ovarian cancers using quantitative real-time reverse transcription-PCR. CCN1 protein levels were further determined by immunohistochemistry and Western blot analysis. Overexpression and inhibition of CCN1 expression by small interfering RNA were used to examine its role in ovarian cancer cell proliferation in vitro and in vivo. Results: We found dysregulation of levels of the various CCN mRNAs in ovarian cancers compared with their expression in normal whole ovaries. Expression of CCN1 protein was detected in normal ovarian epithelial cells and ovarian tumors as well as in ovarian cancer cell lines. Furthermore, estrogen increased CCN1 mRNA and protein levels in ovarian cancer cells. Ectopic expression of CCN1 enhanced the growth of ovarian cancer cells in liquid culture, whereas inhibition of its expression decreased proliferation and increased apoptosis in these cells. The observed changes in cell growth were accompanied with activation of Akt and extracellular signal-regulated kinase (ERK) signaling pathways. Stable expression of CCN1 in SKOV3 cells significantly increased tumorigenicity in nude mice. Finally, overexpression of CCN1 conferred resistant to carboplatin-induced apoptosis in SKOV3 cells. Conclusions: This is the first study to show abnormalities in CCN expression in ovarian carcinomas. Furthermore, our results suggest that CCN1 may play a role in ovarian carcinogenesis by stimulating survival and antiapoptotic signaling pathways.
Improvements in productivity at paid work and within the household, and increased participation in daily activities after 24 weeks of certolizumab pegol treatment of patients with psoriatic arthritis: results of a phase 3 double-blind randomised placebo-controlled study
Authors: A Kavanaugh, D Gladman, D van der Heijde, O Purcaru, P Mease
Journal: Annals of the Rheumatic Diseases (2014)

To evaluate the effect of certolizumab pegol (CZP) on productivity outside and within the home, and on participation in family, social and leisure activities in adult patients with psoriatic arthritis (PsA).
A Simple and Fast Method for the Simultaneous Detection of Nine Fibroblast Growth Factor Receptor 3 Mutations in Bladder Cancer and Voided Urine
Authors: Johanna M.M. van Oers, Irene Lurkin, Antonius J.A. van Exsel, Yvette Nijsen, Bas W.G. van Rhijn, Madelon N.M. van der Aa, Ellen C. Zwarthoff
Journal: Clinical Cancer Research (2005)

Abstract Purpose: Mutations in the fibroblast growth factor receptor 3 (FGFR3) occur in 50% of primary bladder tumors. An FGFR3 mutation is associated with good prognosis, illustrated by significantly lower percentage of patients with progression and disease-specific mortality. FGFR3 mutations are especially prevalent in low grade/stage tumors, with pTa tumors harboring mutations in 85% of the cases. These tumors recur in 70% of patients. Efficient FGFR3 mutation detection for prognostic purposes and for detection of recurrences in urine is an important clinical issue. In this paper, we describe a simple assay for the simultaneous detection of nine different FGFR3 mutations. Experimental Design: The assay consists of one multiplex PCR, followed by extension of primers for each mutation with a labeled dideoxynucleotide. The extended primers are separated by capillary electrophoresis, and the identity of the incorporated nucleotide indicates the presence or absence of a mutation. Results: The assay was found to be more sensitive than single-strand conformation polymorphism analysis. Mutations could still be detected with an input of only 1 ng of genomic DNA and in a 20-fold excess of wild-type DNA. Moreover, in urine samples from patients with a mutant tumor, the sensitivity of mutation detection was 62%. Conclusions: We have developed a fast, easy to use assay for the simultaneous detection of FGFR3 mutations, which can be of assistance in clinical decision-making and as an alternative for the follow-up of patients by invasive cystoscopy for the detection of recurrences in urine.
Galectin-3 regulates hepatic progenitor cell expansion during liver injury
Authors: Wei-Chen Hsieh, Alison C Mackinnon, Wei-Yu Lu, Jonathan Jung, Luke Boulter, Neil C Henderson, Kenneth J Simpson, Baukje Schotanus, Davina Wojtacha, Tom G Bird, Claire N Medine, David C Hay, Tariq Sethi, John P Iredale, Stuart J Forbes
Journal: Gut (2014)

Following chronic liver injury or when hepatocyte proliferation is impaired, ductular reactions containing hepatic progenitor cells (HPCs) appear in the periportal regions and can regenerate the liver parenchyma. HPCs exist in a niche composed of myofibroblasts, macrophages and laminin matrix. Galectin-3 (Gal-3) is a β-galactoside-binding lectin that binds to laminin and is expressed in injured liver in mice and humans.We examined the role of Gal-3 in HPC activation. HPC activation was studied following dietary induced hepatocellular (choline-deficient ethionine-supplemented diet) and biliary (3,5-diethoxycarbonyl-1,4-dihydrocollidine supplemented diet) injury in wild type and Gal-3(-/-) mice.HPC proliferation was significantly reduced in Gal-3(-/-) mice. Gal-3(-/-) mice failed to form a HPC niche, with reduced laminin formation. HPCs isolated from wild type mice secrete Gal-3 which enhanced adhesion and proliferation of HPCs on laminin in an undifferentiated form. These effects were attenuated in Gal3(-/-) HPCs and in wild type HPCs treated with the Gal-3 inhibitor lactose. Gal-3(-/-) HPCs in vitro showed increased hepatocyte function and prematurely upregulated both biliary and hepatocyte differentiation markers and regulated cell cycle genes leading to arrest in G0/G1.We conclude that Gal-3 is required for the undifferentiated expansion of HPCs in their niche in injured liver.
Risk factors and basic mechanisms of chronic thromboembolic pulmonary hypertension: a current understanding
Authors: Irene M. Lang, Raffaele Pesavento, Diana Bonderman, Jason X-J. Yuan
Journal: European Respiratory Journal (2012)

All available evidence today indicates that chronic thromboembolic pulmonary hypertension (CTEPH) is primarily caused by venous thromboembolism, as opposed to primary pulmonary vascular in situ thrombosis. Both the initial magnitude of clot and pulmonary embolism (PE) recurrence may contribute to the development of CTEPH. Only few specific thrombophilic factors, such as phospholipid antibodies, lupus anticoagulant and elevated factor VIII, are statistically associated with CTEPH. A mechanistic view of CTEPH as a disease caused by obliteration of central pulmonary arteries by pulmonary emboli is too simplistic. Based on available data one may speculate that PE may be followed by a pulmonary vascular remodelling process modified by infection, immune phenomena, inflammation, circulating and vascular-resident progenitor cells, thyroid hormone replacement or malignancy. Both plasmatic factors (hypercoagulation, “sticky” red blood cells, high platelet counts and uncleavable fibrinogens) and a misguided vascular remodelling process contribute to major vessel and small vessel obliteration. Endothelial dysfunction and endothelial–mesenchymal transition may be important, but their precise roles remain obscure. There exists no animal model for CTEPH; therefore, experimentation in the future must include human tissues and clinical data in parallel.
Cardiovascular Disease in Children with Chronic Kidney Disease
Authors: Mark M. Mitsnefes
Journal: Journal of the American Society of Nephrology (2012)

More than a decade ago, cardiovascular disease (CVD) was recognized as a major cause of death in children with advanced CKD. This observation has sparked the publication of multiple studies assessing cardiovascular risk, mechanisms of disease, and early markers of CVD in this population. Similar to adults, children with CKD have an extremely high prevalence of traditional and uremia-related CVD risk factors. Early markers of cardiomyopathy, such as left ventricular hypertrophy and dysfunction, and early markers of atherosclerosis, such as increased carotid artery intima-media thickness, carotid arterial wall stiffness, and coronary artery calcification, are frequently present in these children, especially those on maintenance dialysis. As a population without preexisting symptomatic cardiac disease, children with CKD potentially receive significant benefit from aggressive attempts to prevent and treat CVD. Early CKD, before needing dialysis, is the optimal time to both identify modifiable risk factors and intervene in an effort to avert future CVD. Slowing the progression of CKD, avoiding long-term dialysis and, if possible, conducting preemptive transplantation may represent the best strategies to decrease the risk of premature cardiac disease and death in children with CKD.
Surgical management of pneumothorax in cystic fibrosis.
Authors: D J Seddon, M E Hodson
Journal: Thorax (1988)

Twenty seven adults with cystic fibrosis who had had either a surgical pleurodesis or pleurectomy for the management of pneumothorax were studied. There were no significant differences in postoperative respiratory function, incidence of recurrent pneumothorax, or incidence of major postoperative complications between the two groups.