tbuckley/cabot-search huggingface dataset:
Lesson of the week: Fear of the dark in children: is stationary night blindness the cause?
Authors: S. S Sidiki
Journal: BMJ (2003)

Fear of the dark is a common complaint of pre-teenage children. 1 2 It should not be confused with night terrors or panics, in which a child becomes acutely agitated and terror-struck at night, appearing to be awake while in fact asleep and unable to be woken. 3 4 In contrast, fear of the dark can be experienced by the conscious child in dimly lit or dark conditions.When such fear is excessive it is often attributed to attention seeking behaviour or assumed to be an irrational fear that will abate with time.Most people can see a little in very dim lighting conditions after a short period of adaptation.However, a child with no visual problem obvious to the parents and who can see normally in well lit conditions can present as being unable to see at all in the dark even after a period for adaptation.In a child who cannot yet talk this may simply appear as fear of the dark.We describe two patients with congenital stationary night blindness, a diagnosis which may be missed without appropriate history taking from the parents, particularly if there is no family history of visual problems.
Abstract 12495: Fibrin-Thrombin Patch for Endothelial Cell Differentiation and Cardiac-Tissue Patch Manufacturing Using Human Induced-Pluripotent Stem Cells
Authors: Sophia Zhang, James Dutton, Liping Su, Jianyi Zhang, Lei Ye
Journal: Circulation (2014)

Aim: To explore the feasibility using fibrin-thrombin patch for endothelial cell differentiation and cardiac scaffold manufacturing using cardiac cells derived from human induced-pluripotent stem cells (hiPSCs). Method and Result: hiPSCs were dissociated into single cells and seeded into three-dimensional (3D) fibrin-thrombin patches and undergo a two-stage differentiation protocol. With this protocol, up to 45% of the differentiated hiPSCs assumed an EC phenotype, and after purification, greater than 95% of the cells displayed the EC phenotype (based on CD31 expression). The hiPSC-ECs continued to display EC characteristics for 4 weeks in vitro. Gene and protein expression levels of CD31, CD144 and von Willebrand factor-8 (vWF-8) were significantly up-regulated in differentiated hiPSC-ECs. hiPSC-ECs also have biological function to up-take Dil-conjugated acetylated LDL (Dil-ac-LDL) and form tubular structures on Matrigel. A human cardiac-tissue patch (hiCP) was developed by seeding the hiPSC-ECs with hiPSC-derived cardiomyocytes (hiPSC-CMs) and smooth muscle cells (hiPSC-SMCs) into a 3D fibrin scaffold. The hiCP began to contract 3 days after synthesis, 4 days earlier than patches that were created identically but without hiPSC-ECs, and continued to beat regularly (100-120 beats/min) for at least 4 weeks in vitro. Conclusion: These data demonstrate that this new 3D differentiation protocol can efficiently generate stable ECs from hiPSCs and, furthermore, that the differentiated hiPSC-ECs can be combined with hiPSC-CMs and -SMCs to construct an hiCP with improved contractile activity. Our observations also suggest that interactions between the cardiac endothelium and myocytes may contribute to the optimized beating of hiCPs.
Abstract 17596: Preliminary Results from EUglycemia for Renal Impairement Prevention After Contrast-medium Exposure (EURIPE) Randomized Study
Authors: Annunziata Nusca, Cosimo Marco Campanale, Claudio Proscia, Francesca Lassandro Pepe, Lucia Ammirati, Rocco Contuzzi, Germano Di Sciascio
Journal: Circulation (2014)

Introduction: Up-to-date, the gold standard for Contrast Induced-Acute Kidney Injury (CI-AKI) prevention is hydration with isotonic saline solution (ISS), whereas, the role of several protective agents, such as N-Acetyl-Cysteine (NAC) has been largely discussed, with conflicting results. Poor glycemic control has also been associated with increased incidence of CI-AKI. Hypothesis: Thus, we aimed to evaluate the efficacy of glucose-insulin-potassium (GIK) and NAC, in addition to ISS, for the prevention of renal contrast damage, assessed by serum Creatinine (sCr) and plasmatic Neutrophil Gelatinase-Associated Lipocalin (pNGAL) elevation, in patients undergoing percutaneous coronary intervention (PCI). Methods: To date, 102 diabetic and/or with chronic renal failure patients were randomized to 3 different protocols: ISS-GIK-NAC (group 1), ISS-GIK (group 2), ISS (group 3). ISS and GIK infusion started 12 hours before PCI and maintained up to 12 hours after the procedure. NAC was given before PCI (2400 mg). We...
Radiology of Bone Diseases.
Authors: George B. Greenfield
Journal: Annals of Internal Medicine (1981)

In the preface to the second edition of this substantial work dealing with the radiology of diseases of bone, the author sets, for himself, four new tasks. It was his intention to update our understanding of bonedisease, to include further material related to bone dysplasias, to review the radiological literature of recent years relevant to bone radiology, and to add a chapter concerned with the radiological aspects of arthritis. In my opinion, he has succeeded in all of these endeavors. The sections dealing with metabolic bone disease and the additional reference material have been particularly well covered. There are more than eleven hundred references in the text, and they are remarkably up-to-date for any textbook. They include all of the important advances of the past five years, since the first edition was published. The chapter on the arthritides emphasizes, as was the author's plan, the radiological aspects of these diseases. Although relatively brief (pg. 126), all of the essential roentgenographic features are covered. This chapter adds an important facet to this book on bone disease. The purpose of the first edition are also followed. One of these, related to recent literature review, is certainly continued well into the second edition. Diseases continue to be grouped by their predominant roentgenographic features. Although, in general, this may be useful, it tends to group together some diseases that could not possibly be confused roentgenographically. The emphasis on the analytical approach to bone roentg~nology is particularly helpful to the student, but becomes, with experience, less important to the experienced bone roentgenologist. The illustrations are generally more than adequate in quality. With the possible exception of figures 4-44 to 4-46, I would agree with the diagnoses given; in that particular instance, we either have the first instance of bilateral Trevor's disease or are dealing with a case of vitamin A toxicity. Certainly, the vast number of illustrations cannot help but to appeal to the radiologist or student of the radiology of bone disease. In summary, I think the author has succeeded most admirably in accomplishing his objectives. This work is not only of value to the practicing radiologist, the student of bone radiology, the orthopedist, and now, the rheumatologist and internist, but also to the experienced bone radiologist. The cost is not excessive; the illustrative material is useful; the value great. I would not hesitate to recommend it to the library of any physician dealing with the radiology of bone disease. JEREMY J. KAY, M.D.
Elevated serum levels of interleukin 21 are associated with disease severity in patients with psoriasis
Authors: Z. He, L. Jin, Z.-F. Liu, L. Hu, E.-L. Dang, Z.-Z. Feng, Q.-J. Li, G. Wang
Journal: British Journal of Dermatology (2012)

Background Psoriasis is an immune disorder involving numerous cytokines. Recent studies have shown that interleukin (IL)‐21 plays an important role in a variety of inflammatory and autoimmune diseases. It is highly expressed in psoriatic plaques and promotes the proliferation of epidermis in mice. It seems that IL‐21 plays an important role in the pathogenesis of psoriasis. However, whether or not it is elevated in the peripheral blood of patients with psoriasis and is associated with disease severity is unclear. Therefore, our study focuses on serum IL‐21 levels and their correlation with disease severity. Objectives To detect serum IL‐21 levels in patients with psoriasis and investigate the correlation between these and the Psoriasis Area and Severity Index (PASI) scores. Methods Blood samples were collected from patients with plaque psoriasis and from healthy control subjects. Serum IL‐21 levels were measured by enzyme‐linked immunosorbent assay in 37 patients with psoriasis and 37 healthy controls. The PASI scores of patients with psoriasis and their correlation with serum IL‐21 levels were evaluated. Results Serum IL‐21 levels were higher in patients with psoriasis than in healthy controls (P <0·01). Serum IL‐21 levels were positively correlated with PASI scores in the patients with psoriasis (r =0·471, P < 0·01). Conclusions Serum IL‐21 levels in patients with psoriasis are elevated and positively correlate with PASI scores. These results indicate that IL‐21 may play an important role in the pathogenesis of psoriasis.
Abstract P354: Elevated Adiponectin And Tnf-alpha Levels Are Markers For Gluten And Lectin Sensitivity
Authors: Steven R Gundry
Journal: Circulation (2014)

Adiponectin is a protein hormone secreted by adipose cells and is thought to be a precursor for the inflammatory cytokine TNF-alpha. Although low levels of Adiponectin are associated with visceral adiposity and high levels with weight loss, there is a strong association of elevated Adiponectin and TNF-alpha levels in thin women with dementia, osteopenia, and/or coronary artery disease. This paradox led us to consider that these biomarkers correlated to sensitivity to the plant defense proteins: gluten and other lectins. We studied serial Adiponectin and TNF-alpha levels every 3 months in 1,000 pts, M:F ratio 1:1 in response to a lectin and gluten elimination diet (The Matrix Diet). All samples were sent to a core lab (Singulex, Alameda, CA). The diet consisted of avoidance of grains, sprouted grains, pseudo-grains, beans and legumes, soy, peanuts, cashews, nightshades, melons and squashes, and non-Southern European cow milk products (Casein A1), and grain and/or bean fed animals. Eight hundred pts (80%) related some history of autoimmune disease (AID) personally or among family members, including Hashimotos thyroiditis, IBS, arthritis, RA, Lupus, Crohns, colitis, GERD, CAD, Type 1 DM. Adiponectin levels were elevated in all 800 pts with family hx or personal history of AID (16.6-83 ug/ml)(nl&lt;16.5). TNF-alpha levels were elevated in 760/800pts with AID hx (95%) (&gt;3.0 pg/mL). In contrast, Adiponectin was normal in 200 remaining pts without AID history (&lt;16.5 ug/ml), while TNF-alpha was normal in 100/200 (50%) of pts without AID. When the lectin and gluten free diet was instituted, all TNF-alpha levels became normal in all 1,000 pts (&lt;3.0 pg/mL), within 6 months and remained normal, if the diet was followed, for up to one year of study. However, despite normal TNF-alpha levels, Adiponectin levels remained elevated in 790/800 pts with AID hx. Late lack of adherence to the diet occurred in 56/1,000 pts (6%) (as determined by questionnaire) resulted in re-elevation of TNF-alpha in 56/56 pts (100%). We conclude that elevated Adiponectin is a marker for lectin and gluten sensitivity, while TNF-alpha can be used as a marker for gluten/lectin exposure in sensitive individuals. These findings probably explain the Adiponectin paradox. TNF-alpha levels appear to be useful as a marker of response to a lectin/gluten limited diet, and as a marker for degree of adherence to such a diet.
Comparative study of the usefulness of TST and three interferon-gamma release assasys (IGRAs) for the differential diagnosis of pulmonary tuberculosis
Authors: Yoshihiro Kobashi, Masaaki Abe, Keiji Mouri, Yasushi Obase, Naoyuki Miyashita, Mikio Oka
Journal: European Respiratory Journal (2011)

Objective:  We compared the usefulness of tuberculin skin test (TST) and three interferon-gamma release assays (IGRAs) (QuantiFERON-TB Gold (QFT-2G), QuantiFERON-TB Gold In-tube (QFT-3G), T-SPOT.TB) as the supportive method of diagnosing pulmonary tuberculosis (TB).   Methods:  The subjects were 70 patients who required the differentiation of pulmonary TB clinically. The final clinical diagnosis of pulmonary TB in 22 patients and non-pulmonary TB disease in 48 patients was established by clinical specimens.   Results:  In 22 patients with pulmonary TB, the positive response rate was 60% on TST, 80% on QFT-2G, 85% on QFT-3G and 95% on T-SPOT.TB. In 48 patients with non-pulmonary TB disease, the positive response rate was 47% on TST, 9% on QFT-2G, 9% on QFT-3G, 13% on T-SPOT.TB. Indeterminate results on three IGRAs were recognized in one patient each on QFT-2G and QFT-3G among patients with pulmonary TB in three patients on QFT-2G and two patients on QFT-3G among patients with non-pulmonary TB disease. However, there were no indeterminate results on T-SPOT.TB in either patient group. Patients with false-negative or indeterminate results on IGRAs had severe underlying diseases or were receiving immunosuppressive treatments.   Conclusions:  T-SPOT.TB provided the best positive response rate for patients with pulmonary TB among three IGRAs, although T-SPOT.TB may have problems in the specificity of diagnosing TB disease. Therefore, we think it is important to perform T-SPOT.TB in combination with QFT to elevate the sensitivity of the diagnosis of TB disease based on the findings in this study.
469. Improved Transfection with Mixtures of Cationic Lipids: Application to Human Umbilical Artery Endothelial Cells (HUAEC)
Authors: Li Wang, Robert C. MacDonald
Journal: Molecular Therapy (2004)

Cationic lipids have been widely used for the delivery of plasmid and antisense DNA into eukaryotic cells; however, inefficiency of transfection is a major problem confronting their use in gene therapy. To date, the primary approach to improving the transfection properties of cationic lipids has been the synthesis of new kinds of cationic amphipaths or the inclusion of non-cationic helper lipids. Here it is reported that an alternative approach can be unusually effective, namely, the combination of two cationic lipid derivatives with differing amounts of hydrophobicity. EDLPC (1, 2-dilauroyl-sn-glycero-3-ethylphosphocholine), when combined with EDOPC (1, 2-dioleoyl-sn-glycero-3-ethylphosphocholine), dramatically enhances (up to 30-fold or more) the transfection of human umbilical artery endothelial cells (HUAEC) even though, individually, EDOPC or EDLPC are quite weak transfection reagents for these cells. Similarly, the combinations of EDOPC/di-C14 dimethylammonium, di-C18 dimethylammonium/di-C14 dimethylammonium, EDOPC/DC-cholesterol and EDOPC/DMTAP transfected DNA into HUAEC ~10–100 times more efficiently than either compound separately. A possible explanation of this synergy is that the incorporation of the shorter chain molecule increases the propensity for fusion of the lipoplex lipid with cellular membranes, so that the positive charge becomes neutralized and release of DNA is facilitated. To test this hypothesis, membrane fusion was measured using a FRET assay based on reduction of energy transfer between NBD-PE and Rh-PE in cationic lipids of the lipoplexes upon fusion with egg PC liposomes containing 20% DOPG. The extent of fusion of mixed-lipid lipoplexes was significantly greater than that of pure EDOPC. Also, by fluorescence microscopy of labeled lipid and oligonucleotides, it was seen that EDOPC lipoplexes remained undissociated in the cytoplasm whereas in the case of mixed-lipid lipoplexes, the oligonucleotide accumulated in the nucleus (especially at 2 h) while the lipid remained in the cytoplasm. These results also suggest that inclusion of the medium-chain lipid accelerates mixing of the lipoplex and cellular lipids and release of DNA. Until now, phosphatidylethanolamine and cholesterol have been used as the helper lipids to improve the transfection properties of cationic lipids. These data reveal that a second cationic lipid can dramatically improve the nucleic acid delivery properties of lipoplexes.
Abstract 17073: Accumulation of P62 by Dysregulation of Autophagy Induces Rip1-dependent Necroptosis in Cardiomyocytes: a Novel Interplay Between Autophagy and Necroptosis
Authors: Makoto Ogasawara, Toshiyuki Yano, Takayuki Miki, Masaya Tanno, Atsushi Kuno, Hidemichi Kouzu, Hiromichi Murase, Toshiyuki Tobisawa, Shingo Muratsubaki, Keitaro Nishizawa, Masashi Mizuno, Satoko Ishikawa, Tetsuji Miura
Journal: Circulation (2014)

Background: Necroptosis, a recently recognized form of cell death, has been implicated in various pathological conditions including myocardial infarction. Activation of receptor-interacting protein kinase (RIP) 1, leading to RIP1-RIP3 complex formation, is a trigger event of necroptosis, but the mechanism for RIP1 activation has not been characterized fully. Objective: We examined the relationship between RIP1-dependent necroptosis and autophagy in cardiomyocytes. Methods: In H9c2 cardiomyoblasts, the necroptotic pathway was activated using TNF-α (TNF, 50 ng/ml) alone or co-incubation of TNF-α with 20 μM z-VAD-fmk, a pan-caspase inhibitor (TNF/zVAD). As an index of necrosis, the amount of LDH released into the culture medium 24 h after serum withdrawal was expressed as a percentage of total LDH. Necrostatin-1 (Nec-1, 20 μM) and cyclosporine A (CsA, 1 μM) were used for inhibiting RIP1-dependent necroptosis and mitochondrial permeability transition pore opening, respectively. Results: Treatment with TNF ind...
Isolate-dependent use of claudins for cell entry by hepatitis C virus
Authors: Sibylle Haid, Christina Grethe, Michael T. Dill, Markus Heim, Lars Kaderali, Thomas Pietschmann
Journal: Hepatology (2013)

Hepatitis C Virus (HCV) entry involves at least four cellular factors, including CD81, the scavenger receptor class B type I (SCARB-1), occludin (OCLN), and claudin-1 (CLDN1). In addition, CLDN6 and CLDN9 have been shown to substitute for CLDN1 as HCV entry factors in human nonliver cells. We examined the role of different CLDN proteins during HCV entry by using cell lines expressing either predominantly CLDN1 (Huh-7.5) or CLDN6 (HuH6). Huh-7.5 cells were susceptible to all tested HCV isolates, whereas HuH6 cells were only permissive to some viral strains. Silencing of CLDN6 in HuH6 cells revealed that these cells are infected in a CLDN6-dependent fashion, and ectopic expression of CLDN1 or CLDN6 in 293T cells lacking endogenous CLDN expression confirmed that only some HCV strains efficiently use CLDN6 for infection. CLDN1-specific neutralizing antibodies (Abs) fully abrogated infection of Huh-7.5 cells by isolates that use CLDN1 only, whereas viruses with broad CLDN tropism were only partially inhibited by these Abs. Importantly, infection by these latter strains in the presence of anti-CLDN1 Ab was further reduced by silencing CLDN6, suggesting that viruses with broad CLDN usage escape CLDN1-specific Abs by utilization of CLDN6. Messenger RNA (mRNA) levels of HCV entry factors in liver biopsies of HCV patients infected with different genotype and with variable degree of liver fibrosis were determined. Uniformly high levels of CD81, SCARB-1, OCLN, and CLDN1 mRNA were detected. In contrast, abundance of CLDN6 mRNA was highly variable between patients.These findings highlight differential CLDN usage by HCV isolates, which may evolve based on variable expression of CLDN proteins in human liver cells. Broad CLDN tropism may facilitate viral escape from CLDN1-specific therapeutic strategies.
Abstract P4-05-17: Mammaglobin is a potent regulator of breast cancer processes leading to disease progression
Authors: Roxann Guerrette, Nadia Picot, Gilles Robichaud
Journal: Cancer Research (2015)

Abstract Metastasis is the major cause of death in women suffering from breast cancer. To provide a better understand breast cancer progression, we have studied the role of mammaglobine-1 (MGB1) gene in breast cancer pathogenesis. MGB1 has been extensively studied as a diagnostic biomarker due to its abundant expression in mammary cancer cells. Yet, MGB1's role in disease progression is still unknown. Our experimental results demonstrate for the first time that MGB1 in a pivotal regulator on breast cancer malignancy. More precisely, loss of MGB1 expression correlates with a decrease in proliferation, spheroid formation, migration, and invasion capacities of breast cancer cells. Concomitantly, we also observe that MGB1 expression activates pro-malignant signaling cascades such as MAPKs, focal adhesion kinase (FAK) and NFkB pathways. Moreover, MGB1 promote epithelial to mesenchymal (EMT) features which coincide with our findings. Our study provides the first evidence for MGB1 as regulator of breast cancer malignancy and disease progression. Citation Format: Roxann Guerrette, Nadia Picot, Gilles Robichaud. Mammaglobin is a potent regulator of breast cancer processes leading to disease progression [abstract]. In: Proceedings of the Thirty-Seventh Annual CTRC-AACR San Antonio Breast Cancer Symposium: 2014 Dec 9-13; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2015;75(9 Suppl):Abstract nr P4-05-17.
Devices for In-Stent Restenosis
Authors: Jane E. Henney
Journal: JAMA (2001)

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Abstract 19631: Incidence and Correlates of Symptomatic Heart Failure After Pulmonary Vein Isolation
Authors: Henry D Huang, Jonathan W Waks, Fernando Contreras, Mark E Josephson
Journal: Circulation (2014)

Introduction: The incidence and correlates of new-onset symptomatic heart failure (HF) after pulmonary vein isolation (PVI) for atrial fibrillation (AF) are unclear. Methods: We prospectively enrolled consecutive AF pts presenting for radiofrequency PVI between November 2013-June 2014. Pts with recent HF hospitalization or symptomatic HF on the day of PVI were excluded. Post-discharge symptoms were assessed via telephone follow-up in all pts and clinic visits when appropriate. Primary outcome was development of new symptomatic HF requiring treatment with new/increased diuretic dosing. Secondary outcomes were prolonged index hospitalization and readmission for HF ≤ 30d. Univariate and multivariable logistic regression were used to assess relationships between pt and procedural characteristics and post-PVI HF. Results: Among 113 pts (median age 62.1 yrs, 89.0% male, 22.7% non-paroxsymal AF, median LVEF 55%), 30 pts (26.5%) developed new symptomatic HF. Symptoms occurred within 2 days in 80% of pts. 7 pts (6...