bluuebunny/crossref_metadata_2025_split huggingface dataset:
Schizophrenia and Schizoaffective Are Psychotic Mood Disorders
Authors: Aires Daniel J. , Hurwitz Nathaniel G. 
Published: February 2010

CME Educational Objectives

1.
Review the historical reasons for splitting functional psychotic illness into “schizophrenia,” and “schizoaffective disorder,” and “psychotic mood disorder.”

2.
Describe the modern data that link “schizophrenia,” and “schizoaffective disorder,” and “psychotic mood disorder” into a single illness with a spectrum of severity.

3.
Cite the potential to harm patients by splitting functional psychotic illness into “schizophrenia,” and “schizoaffective disorder,” and “psychotic mood disorder.”
Pediatric Education in Office Settings
Authors: Nagappan Suresh , Doyne Emanuel O. , Roberts Kenneth , DeWitt Thomas G. 
Published: February 2010

CME EDUCATIONAL OBJECTIVES

1.
Review the key aspects of office-based pediatric training at the medical student and resident levels.

2.
Define logistic issues encountered in office-based training of medical students and pediatric residents.

3.
Discuss the unique challenges posed by training medical students and house staff in the office setting.
Outcomes of Corneal Spherical Aberration-Guided Cataract Surgery Measured by the OPD-Scan
Authors: Solomon Jonathan D. 
Published: February 2010

Purpose:
To determine based on preoperative corneal spherical aberration, the practicality of targeting zero total ocular postoperative spherical aberration when selecting an aspheric intraocular lens (IOL).

Methods:
Consecutive cataract patients were selected to receive an aspheric IOL based on corneal spherical aberration. A target of zero postoperative total spherical aberration Z(4,0) was calculated. One of three IOLs was chosen, based on the corneal spherical aberration Z(4,0) measurement at the 6-mm optical zone. The IOL was selected based on the summation of the corneal spherical aberration and the aspheric value of the prolate optic. The intention was an absolute value of zero total spherical aberration. Statistical analysis of the postoperative total ocular wavefront profile was performed to assess the accuracy of aspheric IOL selection.

Results:
Forty eyes of 40 patients were available for postoperative assessment. The Tecnis Z9003 (Abbott Medical Optics) was implanted in 25 eyes with a preoperative corneal spherical aberration of +0.311±0.054 μm, the AcrySof IQ (Alcon Laboratories Inc) in 13 eyes (+0.188±0.034 μm), and the SofPort-Advanced Optic with Violet Shield (Bausch & Lomb) was implanted in 2 eyes (+0.0915 μm). Total postoperative ocular spherical aberration for the entire group measured +0.019±0.051 μm (Tecnis: +0.024±0.058 μm; AcrySof IQ: +0.010±0.035 μm; and SofPort AOV: +0.037 μm). Mean absolute predictive error, for the entire group, measured +0.025±0.020 μm.

Conclusions:
Skiascopy-derived total wavefront measurement of spherical aberration is a reproducible method of aspheric IOL selection and permits more precise control of total ocular spherical aberration.
Pentacam Characterization of Corneas with Fuchs Dystrophy Treated with Descemet Membrane Endothelial Keratoplasty
Authors: Kwon Robert O. , Price Marianne O. , Price Francis W. , Ambrósio Renato , Belin Michael W. 
Published: February 2010

Purpose:
To characterize central corneal thickness, curvature, and posterior surface elevation in eyes with Fuchs dystrophy that underwent Descemet membrane endothelial keratoplasty (DMEK) for endothelial decompensation and to compare these characteristics with those in normal eyes.

Methods:
Pre- and postoperative corneal tomography was prospectively evaluated using Pentacam (Oculus Optikgeräte GmbH) imaging on 29 eyes with Fuchs dystrophy treated with DMEK. Results were compared with data from a separate cohort of 198 normal eyes.

Results:

In the Fuchs cohort, the mean preoperative central corneal thickness was 656
μ
m (range: 574 to 731
μ
m). This significantly exceeded the mean thickness of 542
μ
m in the normal cohort (range: 439 to 611
μ
m,
P
<.0001) although the cohort thickness ranges overlapped. One month after DMEK, mean central corneal thickness decreased significantly to 539
μ
m (range: 465 to 669
μ
m,
P
<.0001) with no further significant decrease between 1 and 3 months after DMEK (mean difference = −4
μ
m,
P
=.39). In the Fuchs cohort, keratometry (average Sim K and delta K) did not change significantly after DMEK (
P
=.41 and
P
=.44, respectively); pre- and postoperative values were comparable to those in the normal cohort. The mean forward displacement of the posterior surface increased by 69
μ
m 1 month after DMEK (
P
<.0001) without further significant change between 1 and 3 months.

Conclusions:
After DMEK, central corneal thickness in the Fuchs dystrophy cohort decreased significantly and the posterior corneal surface displaced forward, without significant change in anterior keratometric values or keratometric astigmatism. The preoperative central corneal thickness range in eyes with confluent central guttata overlapped the range in normal corneas.
Transepithelial Corneal Collagen Cross-Linking in Keratoconus
Authors: Leccisotti Antonio , Islam Tahmina 
Published: February 2010

Purpose:
To evaluate the clinical effects of transepithelial corneal cross-linking (CXL) on keratoconic eyes pre-treated with substances enhancing epithelial permeability.

Methods:
Prospective, consecutive, single-masked, paired-eye study on 51 patients. The eye with more severe keratoconus was treated; the fellow eye served as the control. Gentamicin, benzalkonium chloride, and ethylenediaminetetraacetic acid were instilled for 3 hours, then oxybuprocaine for 30 minutes. Riboflavin 0.1% in 20% dextran T500 and oxybuprocaine were instilled for 30 minutes. Finally, ultraviolet A irradiation to the central 7.5 mm of the cornea was applied for 30 minutes, while riboflavin was instilled every 5 minutes.

Results:

Mean corrected distance visual acuity improved by 0.036 logMAR after CXL and worsened by 0.039 logMAR in the control eyes (
P
<.05). Safety index was 1.05 after CXL and 0.96 in the control group. Mean spherical equivalent refraction decreased by 0.35 D (less myopic) after CXL and increased by 0.83 diopters (D) in the control eyes (
P
<.05). Mean apex curvature on tangential videokeratography increased by 0.51 D after CXL and by 1.61 D in the control eyes (
P
=.16). Mean average simulated keratometry decreased by 0.10 D after CXL and increased by 0.88 D in the control eyes (
P
<.05). Mean index of surface variance increased (worsened) by 0.9 after CXL and 5.3 in the control eyes (
P
<.05). Mean endothelial cell density was unchanged.

Conclusions:
A limited but favorable effect of transepithelial CXL was noted on keratoconic eyes, without complications. The effect appears to be less pronounced than described in the literature after CXL with de-epithelialization.
Conductive Keratoplasty to Treat Hyperopic Overcorrection After LASIK for Myopia
Authors: Chang John S.M. , Lau Silvania Y.F. 
Published: February 2010

Purpose:
To investigate the refractive outcomes and stability of conductive keratoplasty (CK) for retreatment of myopic LASIK overcorrection.

Methods:
Seven eyes (six patients) that were overcorrected after myopic LASIK by +1.00 to +2.75 diopters (D) manifest refraction spherical equivalent (MRSE) were retreated using CK. All eyes had insufficient stromal thickness for LASIK retreatment. LightTouch CK was performed at least 1 year after LASIK. Either 8 or 16 spots were applied at 7- and/or 8-mm zones on the cornea. Uncorrected distance visual acuity, manifest refraction, corrected distance visual acuity (CDVA), and postoperative complications were analyzed.

Results:
Mean MRSE after CK at last follow-up was +0.38±0.52 D (range: −0.38 to +1.13 D). The change in MRSE ranged from −0.63 to −2.38 D. Mean MRSE after CK changed from −0.60±2.07 D (range: −3.38 to +1.50 D) at 1 week to +0.45±0.69 D (range: −0.38 to +1.38 D) at 12 months. Two eyes experienced an initial overcorrection of −2.75 D and −3.38 D, respectively, at 1 week after CK. Cylinder ≤0.75 D was induced in four eyes, whereas one eye had a 0.75-D reduction in cylinder. All eyes had CDVA of logMAR 0.10 or better. Two eyes lost one line of CDVA and no eyes lost more than one line.

Conclusions:
LightTouch CK retreatment for over-corrected myopic LASIK can reduce the hyperopia but produces minimal change in cylinder, and may be appropriate for eyes with insufficient stromal tissue for repeated excimer laser surgery. Early regression occurs commonly.
Implantation of a Complete Corneal Ring in an Intrastromal Pocket for Keratoconus
Authors: Mahmood Haifa , Venkateswaran R.S. , Daxer Albert 
Published: February 2010

Purpose:
To evaluate the refractive and visual results of a new treatment for keratoconus using the corneal intrastromal implantation system (CISIS).

Methods:
Six eyes of four patients with keratoconus were treated with CISIS. Follow-up was 1, 3, and 6 months. After creating an intracorneal pocket of 9-mm diameter and 300-μm depth, a flexible full-ring implant was inserted via a 4-mm-wide corneal tunnel.

Results:

No eyes showed loss of lines in uncorrected distance visual acuity (UDVA) or spectacle corrected distance visual acuity (CDVA) at any follow-up examination. Uncorrected and distance corrected visual acuity, keratometry, spherical and cylindrical refractive error as well as spherical equivalent refraction improved significantly (
P
<.05). Mean UDVA improved from 20/260 to 20/48 and mean CDVA improved from 20/41 to 20/27. A significant centralization and decrease of the corneal apex was found. No intra- or postoperative complications were observed.

Conclusions:
The corneal intrastromal implantation system using a complete ring implanted in a stromal pocket can achieve significant improvements in the visual function of patients with keratoconus. Uncorrected distance visual acuity improved by more than seven lines on average and CDVA improved by two lines.
Decision Assistant Wizard to Standardize Optimal Outcomes in Excimer Laser Refractive Corneal Surgery
Authors: Arbelaez Maria Clara , Ewering Tobias , Arba Mosquera Samuel 
Published: February 2010

Purpose:
To assess a decision tree analysis system to further optimize refractive surgery outcomes.

Methods:
A 5-step decision tree, the Decision Assistant Wizard, based on previous experience with the SCHWIND AMARIS laser, was applied for selecting a customized refractive surgery treatment mode (aspheric aberration neutral, corneal wavefront-guided, or ocular wavefront-guided) to eliminate or reduce total aberration.

Results:
Using the Decision Assistant Wizard, 6467 LASIK treatments were performed over a 30-month period; 5262 and 112 for myopic and hyperopic astigmatism, respectively, using aspheric aberration neutral (AF) profiles, 560 using corneal wavefront-guided profiles, and 533 using ocular wavefront-guided profiles. Twenty-two (0.3%) retreatments were performed overall; 18 (0.3%) and 0 (0%) after myopic and hyperopic astigmatism, respectively, using AF, 3 (0.5%) after corneal wavefront-guided profiles, and 1 (0.2%) after ocular wavefront-guided profiles.

Conclusions:
Decision assistant wizards may further optimize refractive surgical outcomes by providing the most appropriate ablation pattern based on an eye’s anamnesis, diagnosis, and visual demands. The general principles may be applied to other laser systems; however, specifics will depend on manufacturers’ specifications.
Post-Endoplasmic Reticulum Rescue of Unstable MHC Class I Requires Proprotein Convertase PC7
Authors: Leonhardt Ralf M. , Fiegl Dorothee , Rufer Elke , Karger Axel , Bettin Barbara , Knittler Michael R. 
Published: February 2010

Abstract
The function of the peptide-loading complex (PLC) is to facilitate loading of MHC class I (MHC I) molecules with antigenic peptides in the endoplasmic reticulum and to drive the selection of these ligands toward a set of high-affinity binders. When the PLC fails to perform properly, as frequently observed in virus-infected or tumor cells, structurally unstable MHC I peptide complexes are generated, which are prone to disintegrate instead of presenting Ags to cytotoxic T cells. In this study we show that a second quality control checkpoint dependent on the serine protease proprotein convertase 7 (PC7) can rescue unstable MHC I, whereas the related convertase furin is completely dispensable. Cells with a malfunctioning PLC and silenced for PC7 have substantially reduced MHC I surface levels caused by high instability and significantly delayed surface accumulation of these molecules. Instead of acquiring stability along the secretory route, MHC I appears to get largely routed to lysosomes for degradation in these cells. Moreover, mass spectrometry analysis provides evidence that lack of PLC quality control and/or loss of PC7 expression alters the MHC I-presented peptide profile. Finally, using exogenously applied peptide precursors, we show that liberation of MHC I epitopes may directly require PC7. We demonstrate for the first time an important function for PC7 in MHC I-mediated Ag presentation.
MyD88 Adaptor-Like D96N Is a Naturally Occurring Loss-of-Function Variant of TIRAP
Authors: George Julie , Kubarenko Andriy V. , Rautanen Anna , Mills Tara C. , Colak Elif , Kempf Tore , Hill Adrian V. S. , Nieters Alexandra , Weber Alexander N. R. 
Published: February 2010

Abstract
Signals elicited by TLRs following the detection of microbes are integrated and diversified by a group of four cytoplasmic adaptor molecules featuring an evolutionarily conserved Toll/IL-1R signaling domain. Single nucleotide polymorphisms (SNPs) in TLRs and their adaptor molecules have been shown to influence susceptibility to a range of infectious and other diseases. The adaptor MyD88 adaptor-like (Mal)/Toll/IL-1R–containing adaptor protein is involved in TLR2 and 4 signal transduction by recruiting another adaptor molecule, MyD88, to the plasma membrane. In this study, we used naturally occurring variants of Mal as tools to study the molecular biology of Mal in more detail in cellular model systems and to thereby identify functionally interesting variants whose corresponding nonsynonymous SNPs might be of further epidemiological interest. Of seven reported variants for Mal, we found Mal D96N associated with reduced NF-κB signaling and cytokine production after overexpression in HEK293 and Huh-7 cells. The D96N mutation prevented Mal from recruiting its signaling partner MyD88 to the plasma membrane and altered posttranslational modification of Mal. These findings led us to investigate the frequency of heterozygosity for the corresponding SNP rs8177400 in a Caucasian case-control study on the etiology of lymphoma, a disease in which TLRs have been implicated. Although rs8177400 did not modify lymphoma risk in general, its frequency of heterozygosity was accurately determined to 0.97%. Our data add rs8177400 (D96N) to the list of functionally important variants of Mal and warrant further research into its immunological, epidemiological, and diagnostic relevance.
CC Chemokine Ligand 3 Overcomes the Bacteriocidal and Phagocytic Defect of Macrophages and Hastens Recovery from Experimental Otitis Media in TNF−/− Mice
Authors: Leichtle Anke , Hernandez Michelle , Ebmeyer Joerg , Yamasaki Kenshi , Lai Yuping , Radek Katherine , Choung Yun-Hoon , Euteneuer Sara , Pak Kwang , Gallo Richard , Wasserman Stephen I. , Ryan Allen F. 
Published: February 2010

Abstract
Innate immune mechanisms are crucial in defense against bacterial illnesses in humans, as evidenced by abnormal antibacterial responses due to defects in TLR signaling, seen in children with MyD88 or IL-1R–associated kinase 4 deficiency. Otitis media (OM) is the most common disease of childhood, and the role of innate immune molecules in this disorder remains unclear. In a murine model of OM, we show that, in the absence of TNF, a key effector of innate immunity, this disease is prolonged after middle ear infection with nontypeable Haemophilus influenzae (NTHi). In the absence of TNF, mice fail to upregulate both TLRs and downstream genes and proteins, such as CCL3, resulting in defects in both inflammatory cell recruitment and macrophage function. Peritoneal macrophages of mice lacking TNF have a diminished ability to phagocytose and kill NTHi, and this defect is partially corrected in vitro by exogenous rTNF. Addition of rCCL3 alone or in combination with rTNF restores phagocytosis and killing by TNF-deficient macrophages to that of unstimulated wild-type macrophages. In vivo administration of rCCL3 to animals deficient in TNF fully restores the ability to control OM due to NTHi, whereas a CCL3-blocking Ab impaired the ability of wild-type mice to recover from OM. Thus, CCL3 is a potent downstream effector of TNF-mediated inflammation in vitro and in vivo. Manipulation of CCL3 and/or TNF may prove to be effective therapeutic approaches in OM or other conditions associated with defective TNF generation.
The Association of MHC Class I Proteins with the 2B4 Receptor Inhibits Self-Killing of Human NK Cells
Authors: Betser-Cohen Gili , Mizrahi Saar , Elboim Moran , Alsheich-Bartok Osnat , Mandelboim Ofer 
Published: February 2010

Abstract
The killing activity of NK cells is carried out by several activating NK receptors, which includes NKp46, NKp44, NKp30, NKp80, NKG2D, and 2B4. The ligands of these receptors are either self-derived, pathogen-derived, stress-induced ligands or tumor ligands. Importantly, none of these killer ligands are expressed on NK cells and thus self-killing of NK cells is prevented. A notable exception with this regard, is the ligand of the 2B4 receptor. This unusual receptor can exert both activating and inhibiting signals; however, in human NK cells, it serves mainly as an activating receptor. The ligand of 2B4 is CD48 and in contrast to the ligands of all the other NK activating receptors, CD48 is also present on NK cells. Thus, NK cells might be at risk for self-killing that is mediated via the 2B4-CD48 interaction. In this study, we identify a novel mechanism that prevents this self-killing as we show that the association of the MHC class I proteins with the 2B4 receptor, both present on NK cells, results in the attenuation of the 2B4-mediated self-killing of NK cells.
The Anti-Inflammatory Actions of Platelet Endothelial Cell Adhesion Molecule-1 Do Not Involve Regulation of Endothelial Cell NF-κB
Authors: Privratsky Jamie R. , Tourdot Benjamin E. , Newman Debra K. , Newman Peter J. 
Published: February 2010

Abstract
PECAM-1 is a cell adhesion and signaling receptor that is expressed on many hematopoietic cells and at endothelial cell–cell junctions. Accumulating evidence from a number of in vitro and in vivo model systems suggests that PECAM-1 suppresses cytokine production and vascular permeability induced by a wide range of inflammatory stimuli. In several of these models of inflammatory disease, endothelial, and not leukocyte or platelet, PECAM-1 conferred protection against inflammatory insult. However, the mechanism by which endothelial PECAM-1 functions as an anti-inflammatory protein is poorly understood. It was recently suggested that PECAM-1 exerts its anti-inflammatory effects in endothelial cells by inhibiting the activity of NF-κB, a proinflammatory transcription factor. To confirm and extend these observations, we examined the effect of engaging, cross-linking, or expressing PECAM-1 on NF-κB activation in a variety of human cells. PECAM-1 had no effect on the phosphorylation of the NF-κB inhibitory protein, IκBα; on the nuclear translocation of NF-κB; on the suppression of cytokine-induced transcriptional activation of an NF-κB luciferase reporter plasmid; or on the cytokine-stimulated upregulation of ICAM-1, an NF-κB target gene, in endothelial cells. Taken together, these studies strongly suggest that the anti-inflammatory actions of PECAM-1 in endothelial cells are not likely to involve its regulation of NF-κB.
A Distinct Subset of Proinflammatory Neutrophils Isolated from Patients with Systemic Lupus Erythematosus Induces Vascular Damage and Synthesizes Type I IFNs
Authors: Denny Michael F. , Yalavarthi Srilakshmi , Zhao Wenpu , Thacker Seth G. , Anderson Marc , Sandy Ashley R. , McCune W. Joseph , Kaplan Mariana J. 
Published: February 2010

Abstract
Neutrophil-specific genes are abundant in PBMC microarrays from lupus patients because of the presence of low-density granulocytes (LDGs) in mononuclear cell fractions. The functionality and pathogenicity of these LDGs have not been characterized. We developed a technique to purify LDGs from lupus PBMCs and assessed their phenotype, function, and potential role in disease pathogenesis. LDGs, their autologous lupus neutrophils, and healthy control neutrophils were compared with regard to their microbicidal and phagocytic capacities, generation of reactive oxygen species, activation status, inflammatory cytokine profile, and type I IFN expression and signatures. The capacity of LDGs to kill endothelial cells and their antiangiogenic potential were also assessed. LDGs display an activated phenotype, secrete increased levels of type I IFNs, TNF-α, and IFN-γ, but show impaired phagocytic potential. LDGs induce significant endothelial cell cytotoxicity and synthesize sufficient levels of type I IFNs to disrupt the capacity of endothelial progenitor cells to differentiate into mature endothelial cells. LDG depletion restores the functional capacity of endothelial progenitor cells. We conclude that lupus LDGs are proinflammatory and display pathogenic features, including the capacity to synthesize type I IFNs. They may play an important dual role in premature cardiovascular disease development in systemic lupus erythematosus by simultaneously mediating enhanced vascular damage and inhibiting vascular repair.
IFN-γ Receptor Signaling Regulates Memory CD8+ T Cell Differentiation
Authors: Sercan Özen , Stoycheva Diana , Hämmerling Günter J. , Arnold Bernd , Schüler Thomas 
Published: February 2010

Abstract
IFN-γ regulates multiple processes in the immune system. Although its antimicrobial effector functions are well described, less is known about the mechanisms by which IFN-γ regulates CD8+ T cell homeostasis. With the help of adoptive T cell transfers, we show in this study that IFN-γR signaling in CD8+ T cells is dispensable for expansion, contraction, and memory differentiation in response to peptide vaccination. In contrast, host IFN-γR signaling counterregulates CD8+ T cell responses and the generation of effector memory T cell processes, which are partially regulated by CD11b+ cells. Similar to vaccination-induced proliferation, host IFN-γR signaling limits the expansion of naive CD8+ T cells and their differentiation into effector memory-like T cells in lymphopenic mice. In contrast to peptide vaccination, IFN-γR signaling in CD8+ T cells contributes to memory fate decision in response to lymphopenia, an effect that is fully reversed by high-affinity TCR ligands. In conclusion, we show that host IFN-γR signaling controls the magnitude of CD8+ T cell responses and subsequent memory differentiation under lymphopenic and nonlymphopenic conditions. In contrast, IFN-γR signaling in CD8+ T cells does not affect cell numbers under either condition, but it directs memory fate decision in response to weak TCR ligands.