tbuckley/cabot-search huggingface dataset:
Real-time, Universal Screening for Acute HIV Infection in a Routine HIV Counseling and Testing Population
Authors: Christopher D. Pilcher, J. Todd McPherson, Peter A. Leone, Marlene Smurzynski, Judy Owen-O'Dowd, Amy L. Peace-Brewer, Juanita Harris, Charles B. Hicks, Joseph J. Eron, Susan A. Fiscus
Journal: JAMA (2002)

ContextAcute human immunodeficiency virus (HIV) infection cannot be diagnosed by routine antibody tests and is rarely diagnosed in clinical practice. However, HIV nucleic acid–based testing is widely used to screen for antibody-negative acute infection among low-risk blood donors.ObjectiveTo assess the feasibility of screening in high-volume laboratories for acute and long-term HIV infection in a routine HIV testing population, in which HIV infection prevalence is low, using specimen pooling and HIV RNA reverse transcriptase-polymerase chain reaction (RT-PCR) tests.Design and SettingClinical diagnostic performance evaluation at a state-funded public health virology and serology laboratory.ParticipantsA total of 8505 consecutive individuals presenting for routine HIV counseling and testing during a total of 20 business days to simulate a month of testing in August and December 2001 at 110 publicly funded testing sites in North Carolina.Main Outcome MeasuresPrevalence of acute and long-term HIV infection. Serum specimens negative by HIV enzyme immunoassay (EIA) were screened in pools by an ultrasensitive HIV RNA RT-PCR test. Results for individual HIV RNA–positive specimens were reclassified as true or false according to results of confirmatory testing.ResultsOf the 8505 individuals screened, 8194 had not previously tested HIV positive and had sufficient serum to complete the testing protocol. Of those, 39 had long-term HIV infection (prevalence, 47.6 per 10 000 at-risk persons [95% confidence interval, 33.8-65.0 per 10 000]). Of the 8155 at-risk individuals whose antibody tests were negative, 5 were HIV RNA positive. Four of those had true-positive acute infection (prevalence, 4.9 per 10 000 [95% confidence interval, 1.3-12.5 per 10 000]). All 4 were women; 2 developed symptoms consistent with an acute retroviral syndrome in the week after testing. Screening all specimens required 147 HIV RNA tests. Overall specificity of the strategy was 0.9999.ConclusionsThese findings suggest the widespread diagnosis of acute HIV infections in a routine testing population is not only possible but feasible using specimen pooling and nucleic acid testing. These additional procedures may increase diagnostic yield by approximately 10% compared with conventional HIV antibody testing.
Whole-Genome Sequencing
Authors: Boris Pasche
Journal: JAMA (2011)

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Adequacy of Well-Child Care and Immunization
Authors: Edgar K. Marcuse
Journal: JAMA (1995)

<h3>To the Editor.</h3> —We are concerned that the otherwise valuable study by Dr Mustin and colleagues<sup>1</sup>has been misinterpreted by the media and will be similarly misunderstood by others unaware of the limitations of secondary data analysis. Mustin et al<sup>1</sup>concluded that while most US infants have adequate well-child visits, many remain inadequately immunized. The authors defined adequate well-child visits as one prior to 3 months of age plus one between the ages of 3 and 6 months. They defined adequate immunization as receipt of three diphtheria and tetanus toxoids and pertussis (DTP) vaccines and two oral poliomyelitis vaccines (OPVs) by 6 months of age. Because three visits at least 4 weeks apart are required to administer these immunizations, by the authors' definitions many infants will be classified as having received adequate well-child visits, but will be inadequately immunized at 6 months of age. Furthermore, some of the
Quality-of-life outcomes from a randomized phase III trial of dose-dense weekly paclitaxel and carboplatin compared with conventional paclitaxel and carboplatin as a first-line treatment for stage II–IV ovarian cancer: Japanese Gynecologic Oncology Group Trial (JGOG3016)
Authors: K. Harano, F. Terauchi, N. Katsumata, F. Takahashi, M. Yasuda, S. Takakura, M. Takano, Y. Yamamoto, T. Sugiyama
Journal: Annals of Oncology (2013)
Activation of dendritic antigen-presenting cells expressing common heat shock protein receptor CD91 during induction of psoriasis.
Authors: O. Boyman, C. Conrad, C. Dudli, E. Kielhorn, B.J. Nickoloff, F.O. Nestle
Journal: British Journal of Dermatology (2005)

Background Psoriasis is a common and chronic relapsing inflammatory skin disorder. Although a role for T cells in mediating the induction and maintenance of psoriatic lesions is well established, mechanisms responsible for activation of T cells by antigen-presenting cells (APCs) during disease relapse are poorly understood. Objectives (i) To determine whether expression of the common heat shock protein (HSP) receptor CD91 correlated with development of psoriasis in a mouse model of psoriasis, (ii) to characterize the lesional cells on which CD91 was expressed, and (iii) to investigate whether CD91+ cells in psoriasis showed signs of activation. Methods Two systems were used in order to study the above-mentioned objectives: (i) skin biopsies taken directly from patients with psoriasis (either psoriatic plaques or symptomless prepsoriatic skin) or from healthy donors, respectively, or (ii) (human) skin biopsies collected during development of psoriasis using a novel xenograft mouse model of psoriasis. The skin samples were then either processed for analysis by light microscopy, or labelled with fluorochrome-conjugated antibodies and analysed by confocal laser scanning microscopy. Results We observed a markedly increased number of CD91+ cells which paralleled development of new psoriatic lesions in the psoriasis mouse model and in established psoriatic plaques compared with symptomless prepsoriatic or healthy skin. Morphology as well as cell-specific markers showed that CD91 was predominantly expressed by dermal dendritic APCs characterized by activation of nuclear factor-κB signalling and the presence of tumour necrosis factor-α, an important proinflammatory cytokine in the immunopathogenesis of psoriasis. In addition, HSP70, a ligand for CD91, was increased in keratinocytes in close vicinity to CD91-bearing APCs in psoriatic lesions. Conclusions These findings indicate massive presence of CD91+ dendritic cells juxtaposed to lesional keratinocytes expressing HSP70, and suggest a novel pathophysiological pathway and therapeutic target for this chronic inflammatory skin disease.
Acetylcholinesterase Accelerates Assembly of Amyloid-β-Peptides into Alzheimer's Fibrils: Possible Role of the Peripheral Site of the Enzyme
Authors: Nibaldo C. Inestrosa, Alejandra Alvarez, Cristián A. Pérez, Ricardo D. Moreno, Matias Vicente, Claudia Linker, Olivia I. Casanueva, Claudio Soto, Jorge Garrido
Journal: Neuron (1996)

Acetylcholinesterase (AChE), an important component of cholinergic synapses, colocalizes with amyloid-β peptide (Aβ) deposits of Alzheimer's brain. We report here that bovine brain AChE, as well as the human and mouse recombinant enzyme, accelerates amyloid formation from wild-type Aβ and a mutant Aβ peptide, which alone produces few amyloid-like fibrils. The action of AChE was independent of the subunit array of the enzyme, was not affected by edrophonium, an active site inhibitor, but it was affected by propidium, a peripheral anionic binding site ligand. Butyrylcholinesterase, an enzyme that lacks the peripheral site, did not affect amyloid formation. Furthermore, AChE is a potent amyloid-promoting factor when compared with other Aβ-associated proteins. Thus, in addition to its role in cholinergic synapses, AChE may function by accelerating Aβ formation and could play a role during amyloid deposition in Alzheimer's brain.
Cardiac resynchronisation as a rescue therapy in patients with catecholamine‐dependent overt heart failure: Results from a short and mid‐term study
Authors: Paul Milliez, Olivier Thomas, Abdeddayem Haggui, Patrick Schurando, Pierre Squara, Alain Cohen‐Solal, Alexandre Mebazaa, Antoine Leenhardt
Journal: European Journal of Heart Failure (2008)
NG2 cells response to axonal alteration in the spinal cord white matter in mice with genetic disruption of neurofilament light subunit expression
Authors: Ya Jun Wu, Ya Fang Tang, Zhi Cheng Xiao, Zhen Min Bao, Bei Ping He
Journal: Molecular Neurodegeneration (2008)

Chondroitin sulphate proteoglycan (NG2) expressing cells, morphologically characterized by multi-branched processes and small cell bodies, are the 4th commonest cell population of non-neuronal cell type in the central nervous system (CNS). They can interact with nodes of Ranvier, receive synaptic input, generate action potential and respond to some pathological stimuli, but the function of the cells is still unclear. We assumed the NG2 cells may play an active role in neuropathogenesis and aimed to determine if NG2 cells could sense and response to the alterations in the axonal contents caused by disruption of neurofilament light subunit (NFL) expression.In the early neuropathological development stage, our study showed that the diameter of axons of upper motor neurons of NFL-/- mice decreased significantly while the thickness of their myelin sheath increased remarkably. Although there was an obvious morphological distortion in axons with occasionally partial demyelination, no obvious changes in expression of myelin proteins was detected. Parallel to these changes in the axons and their myelination, the processes of NG2 cells were disconnected from the nodes of Ranvier and extended further, suggesting that these cells in the spinal cord white matter could sense the alteration in axonal contents caused by disruption of NFL expression before astrocytic and microglial activation.The structural configuration determined by the NFL gene may be important for maintenance of normal morphology of myelinated axons. The NG2 cells might serve as an early sensor for the delivery of information from impaired neurons to the local environment.
Energy intake in pregnant women carrying boys or girls: Difference is chance observation
Authors: S. Langley-Evans
Journal: BMJ (2003)

Editor—Tamimi et al report that women carrying male fetuses consume more energy and macronutrients than those carrying female fetuses.1 The marginal difference in energy intake is, however, likely to be less than the error inherent in the food frequency questionnaire used to obtain the data.

The paper does not consider important factors that affect both diet and fetal growth, such as ethnic origin. It is incorrectly said that the increased energy intake of the women carrying boys meets increased demand for growth. The total energy cost of pregnancy is 289-340 MJ, which is rarely met through increases in dietary energy2 and is instead achieved by adaptive reductions in energy expenditure.

Furthermore, our recent survey of the diets of 300 British women in early and late pregnancy, using five day food diaries,3 found that nutrient intakes were similar in women carrying boys and girls, with the exception of energy and saturated fat in the first trimester. Here, in contrast to Tamimi et al, we found that women carrying female fetuses consumed 5% more energy (P < 0.05) than women carrying male fetuses.

To follow the authors' hypothesis through would lead to the conclusion that with their faster growth rate and increased energy requirement, male fetuses are more vulnerable to growth retardation and effects of maternal undernutrition. There is no evidence that this is the case. The data presented in this paper look like the outcome of random chance and have no clinical significance.
Review: Proton-pump inhibitors are associated with increased risk for<i>Clostridium difficile</i>infection
Authors: Ronald L. Koretz
Journal: Annals of Internal Medicine (2012)

Source Citation Kwok CS, Arthur AK, Anibueze CI, et al. Risk of Clostridium difficile infection with acid suppressing drugs and antibiotics: meta-analysis. Am J Gastroenterol. 2012;107:1011-9. 22525304
Epidemiology and Molecular Mechanisms Tying Obesity, Diabetes, and the Metabolic Syndrome With Cancer
Authors: Emily J. Gallagher, Derek LeRoith
Journal: Diabetes Care (2013)

It is well recognized that the world is witnessing an epidemic of obesity and type 2 diabetes (T2D). Numerous studies have shown that both obesity and T2D are associated with an increased risk for developing many of the common epithelial cancers as well as an increased risk of cancer-related mortality. There are many factors that are commonly associated with obesity, T2D, and the metabolic syndrome; these include lifestyle factors such as diet and physical inactivity and biological factors such as abdominal obesity, increased inflammation, dyslipidemia, hyperglycemia, and altered hormone and adipokine levels. Human, animal, and in vitro cell studies have examined the potential contribution of many of these factors to the development and growth of multiple cancers. In this review, we will present the epidemiological evidence for this association and then discuss the multiple factors that may play a role in the increased cancer risk and mortality in individuals with obesity, T2D, and the metabolic syndrome.

### Obesity and cancer

The World Health Organization classifies weight in adults based on BMI, and many studies examine the link between obesity and cancer using BMI as a measure of obesity. The Cancer Prevention Study II (CPS II) examined the risk of cancer mortality in obese men and women in the U.S. They reported that obesity is associated with a significant increase in mortality from multiple cancers, including esophageal, colorectal, liver, gallbladder, pancreatic, breast, endometrial, cervical, ovarian, renal, brain, kidney, and prostate cancer; non-Hodgkin lymphoma; and multiple myeloma (1). A subsequent meta-analysis of 221 datasets revealed an increased incidence of many similar tumors associated with increased BMI, as well as thyroid cancer in both men and women and malignant melanoma in men (2). It has been estimated that overall overweight and obesity cause ~20% of all cancer cases (3). The highest association is between obesity and endometrial …
Explaining and Predicting Preeclampsia
Authors: Marshall D. Lindheimer, Jason G. Umans
Journal: New England Journal of Medicine (2006)

Preeclampsia, either alone or superimposed on another disorder, is a major cause of maternal and fetal death and the leading cause of premature delivery worldwide.1 Underappreciated is the strain that preeclampsia places on the health care resources of all nations. This disease increases the need for neonatal intensive care; in addition, early birth may lead to health problems later in life. Considerable evidence suggests that premature delivery increases the incidence of remote cardiovascular and metabolic health problems, which themselves create enormous economic health burdens.2,3 Thus, the ability to predict or prevent preeclampsia or the development of therapy that safely . . .
Unchain my heart: the scientific foundations of cardiac repair
Authors: Stefanie Dimmeler, Andreas M. Zeiher, Michael D. Schneider
Journal: Journal of Clinical Investigation (2005)

In humans, the biological limitations to cardiac regenerative growth create both a clinical imperative — to offset cell death in acute ischemic injury and chronic heart failure — and a clinical opportunity; that is, for using cells, genes, and proteins to rescue cardiac muscle cell number or in other ways promote more efficacious cardiac repair. Recent experimental studies and early-phase clinical trials lend credence to the visionary goal of enhancing cardiac repair as an achievable therapeutic target.
Prevention of Spinal Cord Injury in Hyperextension of the Fetal Head
Authors: Bo Hellström
Journal: JAMA (1968)

Cervical cord injuries occurred in two infants where the intrauterine position had been abnormal with maximal hyperextension of the fetal head. The importance of diagnosing such fetal positions is emphasized. Cesarean section can prevent injury to the fetus. The injuries of the cervical cord can give rise to a picture which, from a roentgenological point of view, resembles that of an intramedullary tumor.
Different molecular behavior of CD40 mutants causing hyper-IgM syndrome
Authors: Gaetana Lanzi, Simona Ferrari, Mauno Vihinen, Stefano Caraffi, Necil Kutukculer, Luisa Schiaffonati, Alessandro Plebani, Luigi Daniele Notarangelo, Anna Maria Fra, Silvia Giliani
Journal: Blood (2010)
Failed Atrial Septal Defect Repair Versus Pulmonary Hypertension With Right Ventricular Failure
Authors: Andrei Iagaru, Heidi Wassef, Robert Henderson
Journal: Clinical Nuclear Medicine (2005)

We present images obtained during a ventilation/perfusion (V/Q) lung scintigraphy requested for evaluation of shortness of breath. The patient is a 27-year-old woman who presented initially in May 2004 for evaluation of chest pain. Physical examination at that time revealed a murmur, which was found on echocardiogram to be secondary to an atrial septal defect (ASD). This was repaired in July 2004 using a transcatheter approach. In October 2004, the patient was readmitted for recurrence of symptoms. A V/Q scan was ordered as part of the evaluation. The ventilation study was normal. The perfusion study showed slow blood pool clearance, which allowed visualization of the cardiac blood pool, massive enlargement of the pulmonary artery, and a pericardial effusion. The scan was interpreted as right ventricular failure. Absence of radiotracer on the brain images excluded the possibility of failed ASD repair. A subsequent lateral chest x-ray demonstrated the ASD-closing device in place.
Endemic pemphigus foliaceus (fogo selvagem) in Native Americans from Brazil
Authors: Horacio Friedman, Iphis Campbell, Rosicler Rocha-Alvarez, Iris Ferrari, Carlos E.A Coimbra, Jose R Moraes, Nancy M Flowers, Peter Stastny, Marcelo Fernandez-Viña, Monica Olague-Alcala, Luis A Diaz
Journal: Journal of the American Academy of Dermatology (1995)
THE FATE OF INTRAVENOUSLY ADMINISTERED CALCIUM. EFFECT ON URINARY CALCIUM AND PHOSPHORUS, FECAL CALCIUM AND CALCIUM-PHOSPHORUS BALANCE 1
Authors: Curtis H. Baylor, Helen E. Van Alstine, E. Henry Keutmann, Samuel H. Bassett
Journal: Journal of Clinical Investigation (1950)

Values for Ca, P, and N were determined by the analysis of sample diets.Protein = Diet N X 6.25.Fat and carbohydrate have been estimated from tables.
Bipolar (Spectrum) Disorder and Mood Stabilization: Standing at the Crossroads?
Authors: Jürgen De Fruyt, Koen Demyttenaere
Journal: Psychotherapy and Psychosomatics (2007)

Diagnosis and treatment of bipolar disorder has long been a neglected discipline. Recent years have shown an upsurge in bipolar research. When compared to major depressive disorder, bipolar research still remains limited and more expert based than evidence based. In bipolar diagnosis the focus is shifting from classic mania to bipolar depression and hypomania. There is a search for bipolar signatures in symptoms and course of major depressive episodes. The criteria for hypomania are softened, leading to a bipolar prevalence that now equals that of major depressive disorder. Anti-epileptics and atypical antipsychotics have joined lithium in the treatment of bipolar disorder. Fortunately, mood stabilization has become the core issue in bipolar disorder treatment. In contrast with recent trends in the diagnosis of bipolar disorder, treatment research remains more focused on classic mania than depression or hypomania. This leaves the clinician with the difficult task of diagnosing ‘new bipolar patients’ for whom no definite evidence-based treatment is available. An important efficacy-effectiveness gap further compromises the translation of the evidence base on bipolar disorder treatment into clinical practice. The recent upsurge of research on bipolar disorder is to be applauded, but further research is needed: for bipolar disorder in general, and for bipolar depression and the long-term treatment specifically. Given the complexity of the disorder and the many clinical uncertainties, effectiveness studies should be installed.
Abnormal atrial natriuretic peptide and renal responses to saline infusion in nonmodulating essential hypertensive patients.
Authors: C Ferri, C Bellini, S Coassin, R Baldoncini, R L Luparini, A Perrone, A Santucci
Journal: Circulation (1994)

BACKGROUND Nonmodulation seems to represent an inheritable trait characterized by abnormal angiotensin-mediated control of aldosterone release and renal blood supply and salt-sensitive hypertension. Recently, we demonstrated that atrial natriuretic peptide (ANP) response to angiotensin II also is altered in nonmodulators. Moreover, an abnormal ANP response to acute volume expansion has been shown by others in hypertensive patients displaying some features of nonmodulators. These data induced us to hypothesize that nonmodulators. These data induced us to hypothesize that nonmodulation could be characterized by an abnormal ANP response to saline load. METHODS AND RESULTS Forty-three essential hypertensive men were subdivided into low-renin patients (n = 12), nonmodulators (n = 15), and modulators (n = 16) according to their renin profile and ability to modulate aldosterone and p-aminohippurate clearance responses to a graded angiotensin II infusion (1.0 ng.kg-1.min-1 and 3.0 ng.kg-1.min-1 for 30 minutes each) on both a low- (10 mmol Na+ per day) and a high- (210 mmol Na+ per day) Na+ intake. The intravenous saline load (0.25 mL.kg-1.min-1 for 2 hours) performed on a low-Na+ diet increased plasma ANP levels in low-renin (from 14.30 +/- 4.68 to 23.30 +/- 7.52 fmol/mL at 120 minutes, P &lt; .05) and modulating patients (from 10.95 +/- 3.55 to 18.21 +/- 5.42 fmol/mL at 120 minutes, P &lt; .05), whereas it did not change the hormone levels in nonmodulators (from 10.77 +/- 3.25 to 13.83 +/- 5.70 fmol/mL at 120 minutes, P = NS). When patients switched from a low- to a high-NaCl diet, plasma ANP levels increased significantly in all groups. However, when the saline load was repeated on a high-NaCl intake, ANP levels increased in both low-renin and modulating patients (P &lt; .05), whereas it failed to increase in nonmodulators. CONCLUSIONS Nonmodulating hypertensive patients showed a reduced ANP response to saline infusion in the presence of a normal increase of plasma ANP with dietary NaCl load. The impaired ANP response to saline infusion could be due to a different distribution of volume load and contribute to determining the reduced ability to excrete sodium that is commonly described in nonmodulators.