bluuebunny/crossref_metadata_2025_split huggingface dataset:
No uso de sonda orogástrica preoperatoria y régimen de alimentación postoperatorio en niños con estenosis hipertrófica de píloro
Authors: Editorial Comité , Anariba Raúl Virgilio , Quiroz Roberto Martínez , Rodríguez Gaspar 
Published: April 2012

Palabras claves: estenosis hipertrόfica de piloro; sonda orogástrica; regimen de dietaDOI: http://dx.doi.org/10.5377/rmpm.v13i3.627 Revista de los Postgrados de Medicina UNAH Vol. 13 N° 3 Agosto-Octubre 2010
Prevalencia de TDAH, Relación con Reprobación Escolar y Estado Nutricional en Población Escolar del Distrito Central
Authors: Editorial Comité , Duarte Zeni E , Reyes Eunice , Sosa Alfredo L , Risso Elena , Reyes Américo , Munguia Alejandra , Aguilar Mario 
Published: April 2012

Palabras Clave: TDAH; Reprobación Escolar; nutrición DOI: http://dx.doi.org/10.5377/rmpm.v13i3.631 Revista de los Postgrados de Medicina UNAH Vol. 13 N° 3 Agosto-Octubre 2010
Dietary fat types and 4‐year cognitive change in community‐dwelling older women
Authors: Okereke Olivia I. , Rosner Bernard A. , Kim Dae H. , Kang Jae H. , Cook Nancy R. , Manson JoAnn E. , Buring Julie E. , Willett Walter C. , Grodstein Francine 
Published: April 2012

AbstractObjective:A study was undertaken to relate dietary fat types to cognitive change in healthy community‐based elders.Methods:Among 6,183 older participants in the Women's Health Study, we related intake of major fatty acids (saturated [SFA], monounsaturated [MUFA], total polyunsaturated [PUFA], trans‐unsaturated) to late‐life cognitive trajectory. Serial cognitive testing, conducted over 4 years, began 5 years after dietary assessment. Primary outcomes were global cognition (averaging tests of general cognition, verbal memory, and semantic fluency) and verbal memory (averaging tests of recall). We used analyses of response profiles and logistic regression to estimate multivariate‐adjusted differences in cognitive trajectory and risk of worst cognitive change (worst 10%) by fat intake.Results:Higher SFA intake was associated with worse global cognitive (p for linear trend = 0.008) and verbal memory (p for linear trend = 0.01) trajectories. There was a higher risk of worst cognitive change, comparing highest versus lowest SFA quintiles; the multivariate‐adjusted odds ratio (OR) with 95% confidence interval (CI) was 1.64 (1.04–2.58) for global cognition and 1.65 (1.04–2.61) for verbal memory. By contrast, higher MUFA intake was related to better global cognitive (p for linear trend < 0.001) and verbal memory (p for linear trend = 0.009) trajectories, and lower OR (95% CI) of worst cognitive change in global cognition (0.52 [0.31–0.88]) and verbal memory (0.56 [0.34–0.94]). Total fat, PUFA, and trans‐fat intakes were not associated with cognitive trajectory.Interpretation:Higher SFA intake was associated with worse global cognitive and verbal memory trajectories, whereas higher MUFA intake was related to better trajectories. Thus, different consumption levels of the major specific fat types, rather than total fat intake itself, appeared to influence cognitive aging. ANN NEUROL 2012;
Accelerating progress in induced pluripotent stem cell research for neurological diseases
Authors: Ito Daisuke , Okano Hideyuki , Suzuki Norihiro 
Published: April 2012

AbstractIn 2006, Yamanaka's group pioneered a method for reprogramming somatic cells by introducing definite transcription factors, which enabled the generation of induced pluripotent stem cells (iPSCs) with pluripotency comparable to that of embryonic stem cells. These iPSCs are attracting considerable attention for their potential in rejection‐tolerance personalized replacement therapy. In recent years, patient‐derived iPSCs have been used to recapitulate the phenotypes of neurological diseases and broaden our understanding of the pathogenesis of many neurological diseases, including those of late onset. It is now expected that iPSCs will serve as an unlimited source of disease‐specific neural cells for use in disease modeling. This review outlines current progress in neurodegenerative disease research involving iPSCs and discusses the potential roles iPSCs may play in helping researchers elucidate the pathological processes of neurodegenerative diseases and in drug discovery and regenerative medicine. Ann Neurol 2012;72:167–174.
Concurrent acute brain infarcts in patients with monocular visual loss
Authors: Helenius Johanna , Arsava E. Murat , Goldstein Joshua N. , Cestari Dean M. , Buonanno Ferdinando S. , Rosen Bruce R. , Ay Hakan 
Published: April 2012

AbstractObjective:Embolism from a proximal source to the retinal circulation could be a sign of embolism from the same source to the hemispheric circulation. We sought to determine the frequency of acute brain infarcts on diffusion‐weighted imaging (DWI) in patients with monocular visual loss of presumed ischemic origin (MVL).Methods:We retrospectively studied 129 consecutive patients with MVL secondary to retinal ischemia. All patients underwent DWI, comprehensive ophthalmologic and neurologic examination, and diagnostic evaluations for the underlying etiology. Statistical analyses explored univariate and multivariate predictors of DWI evidence of acute brain infarcts.Results:DWI revealed concurrent acute brain infarct(s) in 31 of the 129 patients (24%). The probability of positive DWI was higher in embolic versus nonembolic MVL (28 vs 8%, p = 0.04), in MVL characterized by permanent visual loss versus transient symptoms (33 vs 18%, p = 0.04), and in MVL associated with concurrent hemispheric symptoms versus isolated MVL (53 vs 20%, p < 0.01). Patients with positive DWI were more likely to harbor a major underlying etiology as compared to those with normal DWI (odds ratio, 3.7; 95% confidence interval, 1.5–9.4).Interpretation:This study demonstrates that MVL does not always represent an isolated disease of the retina; approximately 1 of every 4 patients with MVL demonstrates acute brain infarcts on DWI. Because patients with concurrent brain infarcts are more likely to exhibit a cardiac or vascular source of embolism, imaging evidence of brain injury in patients with MVL may be a useful marker to guide the timing and extent of diagnostic examinations. ANN NEUROL 2012;72:286–293.
Adult polyglucosan body disease: Natural History and Key Magnetic Resonance Imaging Findings
Authors: Mochel Fanny , Schiffmann Raphael , Steenweg Marjan E. , Akman Hasan O. , Wallace Mary , Sedel Frédéric , Laforêt Pascal , Levy Richard , Powers J. Michael , Demeret Sophie , Maisonobe Thierry , Froissart Roseline , Da Nobrega Bruno Barcelos , Fogel Brent L. , Natowicz Marvin R. , Lubetzki Catherine , Durr Alexandra , Brice Alexis , Rosenmann Hanna , Barash Varda , Kakhlon Or , Gomori J. Moshe , van der Knaap Marjo S. , Lossos Alexander 
Published: April 2012

AbstractObjective:Adult polyglucosan body disease (APBD) is an autosomal recessive leukodystrophy characterized by neurogenic bladder, progressive spastic gait, and peripheral neuropathy. Polyglucosan bodies accumulate in the central and peripheral nervous systems and are often associated with glycogen branching enzyme (GBE) deficiency. To improve clinical diagnosis and enable future evaluation of therapeutic strategies, we conducted a multinational study of the natural history and imaging features of APBD.Methods:We gathered clinical, biochemical, and molecular findings in 50 APBD patients with GBE deficiency from Israel, the United States, France, and the Netherlands. Brain and spine magnetic resonance images were reviewed in 44 patients.Results:The most common clinical findings were neurogenic bladder (100%), spastic paraplegia with vibration loss (90%), and axonal neuropathy (90%). The median age was 51 years for the onset of neurogenic bladder symptoms, 63 years for wheelchair dependence, and 70 years for death. As the disease progressed, mild cognitive decline may have affected up to half of the patients. Neuroimaging showed hyperintense white matter abnormalities on T2 and fluid attenuated inversion recovery sequences predominantly in the periventricular regions, the posterior limb of the internal capsule, the external capsule, and the pyramidal tracts and medial lemniscus of the pons and medulla. Atrophy of the medulla and spine was universal. p.Y329S was the most common GBE1 mutation, present as a single heterozygous (28%) or homozygous (48%) mutation.Interpretation:APBD with GBE deficiency, with occasional exceptions, is a clinically homogenous disorder that should be suspected in patients with adult onset leukodystrophy or spastic paraplegia with early onset of urinary symptoms and spinal atrophy. ANN NEUROL 2012;72:433–441.
Chondroitin sulfate proteoglycans in demyelinated lesions impair remyelination
Authors: Lau Lorraine W. , Keough Michael B. , Haylock‐Jacobs Sarah , Cua Rowena , Döring Axinia , Sloka Scott , Stirling David P. , Rivest Serge , Yong V. Wee 
Published: April 2012

AbstractObjective:Failure of remyelination is a critical impediment to recovery in multiple sclerosis (MS). Chondroitin sulfate proteoglycans (CSPGs) have been reported to accumulate in MS lesions, and we thus examined the functional roles of CSPGs on oligodendrocyte precursor cells (OPCs), oligodendrocytes, and remyelination.Methods:We evaluated the expression of CSPGs in lysolecithin‐injected mouse spinal cord, an animal model of demyelination and spontaneous remyelination. The functional impact of CSPGs on OPCs and remyelination was investigated using cultured adult murine and human OPCs and by treating demyelinated mice with xyloside to reduce the CSPG deposition that occurred following injury.Results:Early and robust upregulation of CSPGs following lysolecithin‐induced demyelination was cleared during remyelination. In culture, CSPGs anchored onto the substratum reduced the adhesion of mouse and human OPCs and their subsequent morphological differentiation into process‐bearing oligodendrocytes. Soluble CSPGs added to already adherent OPCs reduced the development of processes, whereas the acquisition of mature myelin proteins was unimpeded. Stripe assays of alternating CSPG and control substrata confirmed the nonpermissive nature of CSPGs for OPC adhesion and morphological differentiation. Enzymatic degradation of CSPGs with chondroitinase ABC was sufficient to overcome CSPG‐dependent inhibition of human oligodendrocytes. Finally, in vivo xyloside treatment to reduce CSPG synthesis in lysolecithin‐demyelinated mice increased numbers of OPCs and oligodendrocytes in lesions, and culminated in improved remyelination.Interpretation:These results identify CSPGs as a nonpermissive substrate for OPCs and oligodendrocytes, and as a prominent impediment to remyelination. The data suggest the requirement for the neutralization of CSPGs for repair after demyelination. ANN NEUROL 2012;72:419–432.
Neonatal exposure to antiepileptic drugs disrupts striatal synaptic development
Authors: Forcelli Patrick A. , Janssen Megan J. , Vicini Stefano , Gale Karen 
Published: April 2012

AbstractObjective:Drug exposure during critical periods of brain development may adversely affect nervous system function, posing a challenge for treating infants. This is of particular concern for treating neonatal seizures, as early life exposure to drugs such as phenobarbital is associated with adverse neurological outcomes in patients and induction of neuronal apoptosis in animal models. The functional significance of the preclinical neurotoxicity has been questioned due to the absence of evidence for functional impairment associated with drug‐induced developmental apoptosis.Methods:We used patch‐clamp recordings to examine functional synaptic maturation in striatal medium spiny neurons from neonatal rats exposed to antiepileptic drugs with proapoptotic action (phenobarbital, phenytoin, lamotrigine) and without proapoptotic action (levetiracetam). Phenobarbital‐exposed rats were also assessed for reversal learning at weaning.Results:Recordings from control animals revealed increased inhibitory and excitatory synaptic connectivity between postnatal day (P)10 and P18. This maturation was absent in rats exposed at P7 to a single dose of phenobarbital, phenytoin, or lamotrigine. Additionally, phenobarbital exposure impaired striatal‐mediated behavior on P25. Neuroprotective pretreatment with melatonin, which prevents drug‐induced neurodevelopmental apoptosis, prevented the drug‐induced disruption in maturation. Levetiracetam was found not to disrupt synaptic development.Interpretation:Our results provide the first evidence that exposure to antiepileptic drugs during a sensitive postnatal period impairs physiological maturation of synapses in neurons that survive the initial drug insult. These findings suggest a mechanism by which early life exposure to antiepileptic drugs can impact cognitive and behavioral outcomes, underscoring the need to identify therapies that control seizures without compromising synaptic maturation. ANN NEUROL 2012;72:363–372
Thalamic Connections of Auditory Cortex in Marmoset Monkeys: Lateral Belt and Parabelt Regions
Authors: de la Mothe Lisa A. , Blumell Suzanne , Kajikawa Yoshinao , Hackett Troy A. 
Published: April 2012

AbstractThe primate auditory cortex is comprised of a core region of three primary areas, surrounded by a belt region of secondary areas and a parabelt region lateral to the belt. The main sources of thalamocortical inputs to the auditory cortex are the medial geniculate complex (MGC), medial pulvinar (PM), and several adjoining nuclei in the posterior thalamus. The distribution of inputs varies topographically by cortical area and thalamic nucleus, but in a manner that has not been fully characterized in primates. In this study, the thalamocortical connections of the lateral belt and parabelt were determined by placing retrograde tracer injections into various areas of these regions in the marmoset monkey. Both regions received projections from the medial (MGm) and posterodorsal (MGpd) divisions of the medial geniculate complex (MGC); however, labeled cells in the anterodorsal (MGad) division were present only from injections into the caudal belt. Thalamic inputs to the lateral belt appeared to come mainly from the MGC, whereas the parabelt also received a strong projection from the PM, consistent with its position as a later stage of auditory cortical processing. The results of this study also indicate that the organization of the marmoset auditory cortex is similar to other primates. Anat Rec, 2012. © 2012 Wiley Periodicals, Inc.
Abnormal Development at Early Postimplantation Stage in Mouse Embryos After Preimplantation Genetic Diagnosis
Authors: Yang Yang , Zeng Yan , Lv Zhuo , Wan Ru , Tong Man , Zhu Hui , Wang Liu , Zhou Zuomin , Zhou Qi , Sha Jiahao 
Published: April 2012

AbstractPreimplantation genetic diagnosis (PGD) is an established procedure for the genetic analysis of embryos. To assess the effect of the procedure on early embryonic development, we generated a murine experimental system, including mice implanted with biopsied in vitro cultured embryos, control mice implanted with in vitro cultured embryos without biopsy, and mice with naturally conceived embryos. Embryos at the 7.5‐dpc stage were isolated from all three groups and the embryo implantation rate, the survival rate of implanted embryos, and the developmental stage of surviving embryos were carefully assessed and compared among all three groups. We found the implantation rate was similar between biopsied and control group embryos (67.92% vs. 66.67%). However, the survival rate of implanted embryos in the biopsied group (49.31%) was significantly lower than that of the control (60.91%) and normal groups (96.24%) at 7.5 dpc. In addition, the survival rate of control group embryos was significant lower than that of normal group embryos. Classification of the precise developmental stages of randomly selected live implanted embryos at 7.5 dpc revealed no differences among the three groups. Our results indicate that blastomere biopsy does not adversely affect embryo implantation. The PGD procedure, in particular blastomere biopsy, increases the rate of embryo death at 4.5–7.5 dpc, but does not affect the development of surviving 7.5 dpc embryos. Anat Rec, 2012. © 2012 Wiley Periodicals, Inc.
Production of angiotensin‐I‐converting enzyme inhibitory peptides from β‐lactoglobulin‐ and casein‐derived peptides: An integrative approach
Authors: Welderufael Fisseha T. , Gibson Trevor , Jauregi Paula 
Published: April 2012

AbstractAngiotensin I‐converting enzyme (ACE) inhibition is one of the mechanisms by which reduction in blood pressure is exerted. Whey proteins are a rich source of ACE inhibitory peptides and have shown a blood pressure reduction effect i.e. antihypertensive activity. The aim of this work was to develop a simplified process using a combination of adsorption and microfiltration steps for the production of hydrolysates from whey with high ACE inhibitory activity and potency; the latter was measured as the IC50, which is the peptide concentration required to reduce ACE activity by half. This process integrates the selective separation of β‐lactoglobulin‐ and casein‐derived peptides (CDP) from rennet whey and their hydrolysis, which results in partially pure, less complex hydrolysates with high bioactive potency. Hydrolysis was carried out with protease N “Amano” in a thermostatically controlled membrane reactor operated in a batch mode. By applying the integrative approach it was possible to produce from the same feedstock two different hydrolysates that exhibited high ACE inhibition. One hydrolysate was mainly composed of casein‐derived peptides with IC50 = 285 μg/mL. In this hydrolysate we identified the well‐known potent ACE‐inhibitor and antihypertensive tripeptide Ile‐Pro‐Pro (IPP) and another novel octapeptide Gln‐Asp‐Lys‐Thr‐Glu‐Ile‐Pro‐Thr (QDKTEIPT). The second hydrolysate was mainly composed of β‐lactoglobulin derived peptides with IC50 =128 μg/mL. This hydrolysate contained a tetrapeptide (Ile‐Ile‐Ala‐Glu) IIAE as one of the two major peptides. A further advantage to this process is that enzyme activity was substantially increased as enzyme product inhibition was reduced. © 2012 American Institute of Chemical Engineers Biotechnol. Prog., 2012
Identifying bottlenecks in transient and stable production of recombinant monoclonal‐antibody sequence variants in chinese hamster ovary cells
Authors: Mason Megan , Sweeney Bernadette , Cain Katharine , Stephens Paul , Sharfstein Susan T. 
Published: April 2012

AbstractThe increasing demand for antibody‐based therapeutics has emphasized the need for technologies to improve recombinant antibody titers from mammalian cell lines. Moreover, as antibody therapeutics address an increasing spectrum of indications, interest has increased in antibody engineering to improve affinity and biological activity. However, the cellular mechanisms that dictate expression and the relationships between antibody sequence and expression level remain poorly understood. Fundamental understanding of how mammalian cells handle high levels of transgene expression and of the relationship between sequence and expression are vital to the development of new antibodies and for increasing recombinant antibody titers. In this work, we analyzed a pair of mutants that vary by a single amino acid at Kabat position 49 (heavy‐chain framework), resulting in differential transient and stable titers with no apparent loss of antigen affinity. Through analysis of mRNA, gene copy number, intracellular antibody content, and secreted antibody, we found that while translational/post‐translational mechanisms are limiting in transient systems, it appears that the amount of available transgenic mRNA becomes the limiting event on stable integration of the recombinant genes. We also show that amino acid substitution at residue 49 results in production of a non‐secreted HC variant and postulate that stable antibody expression is maintained at a level which prevents toxic accumulation of this HC‐related protein. This study highlights the need for proper sequence engineering strategies when developing therapeutic antibodies and alludes to the early analysis of transient expression systems to identify the potential for aberrant stable expression behavior. © 2012 American Institute of Chemical Engineers Biotechnol. Prog., 2012
Characteristic distributions of fatty acids in different lipids from Jack beans (Canavalia gladiata DC.)
Authors: Yoshida Hiromi , Yoshida Naoko , Tomiyama‐Sakamoto Yuka , Mizushina Yoshiyuki 
Published: April 2012

AbstractExtracted lipids obtained from Jack beans (white and red) were fractionated by TLC into nine subfractions. The major components were TAGs (TAG: 43.8–45.7 wt%) and phospholipids (PL: 46.7–47.0 wt%), while other components were also present in minor proportions (0.3–2.7 wt%). The principal fatty acids (FA) are generally palmitic (18.8–28.8%), stearic (0.7–6.8%), oleic (42.0–51.8%), linoleic (16.2–22.8%), and α‐linolenic (3.0–8.2%) acids, the distribution of which differs according to these lipid classes. There were no significant differences (p>0.05) in the positional distribution of FA in the TAG; unsaturated FA (97.5%) were predominantly concentrated in the sn‐2 position while saturated FA (33.3%) primarily occupied the sn‐1 position or sn‐3 position. However, significant differences (p<0.05) in FA distribution existed when the individual PL were compared between the white and red beans. Based on the FA composition of these lipids, it seems that the two cultivars of Jack beans are very similar to each other with a few exceptions. The results could be useful to both producers and consumers for our daily diet to improve value of the Japanese diet.Practical applications: The lipid composition suggests that these beans could be a good source of nutraceuticals with providing heath benefits. The white and red beans may be well incorporated into our daily Japanese diets to improve nutritional value. The data obtained in this study provide valuable information for manufacturing functional drinks such as Jack bean tea in Japan.
Study of the porous structure of white chocolate by confocal Raman microscopy
Authors: Dahlenborg Hanna , Millqvist‐Fureby Anna , Brandner Birgit D. , Bergenstahl Bjorn 
Published: April 2012

AbstractConfocal Raman microscopy has been shown to be a useful technique for investigation of white chocolate surfaces. The appearance of protrusions and pores, and the distribution of fat, sucrose, and milk powder at and below the surface of white chocolate pralines were investigated using confocal Raman microscopy. Raman horizontal and depth scans showed that the protrusions and pores continue at least 10 µm into the chocolate shell and that some protrusions and channels mainly consist of fat, while some consisted of a fat layer, leaving a hollow space underneath. Further, the pores and their continuing channels consisted of nothing but air. These findings indicate that the protrusions might be connected to channels where we suggest a pressure driven convective flow of liquid fat from within the chocolate matrix that, depending on temperature, moves up to the surface or goes back into the matrix, leaving an empty pore with a shell of fat at the surface, which in some cases collapse and leaves a hollow pore and channel. Therefore, these findings support that the protrusions could be connected to oil migration in chocolate and, thus, further to fat bloom development.Practical applications: Confocal Raman microscopy can be used to investigate the local distribution of different components in white chocolate. This technique offers the possibility to acquire the local distribution of different components within the sample, with a resolution down to the optical diffraction limit. Further, the analysis can be performed at ambient conditions, without requiring any special sample preparation or marker molecules. The results obtained by using this technique suggest that specific surface imperfections on chocolate could be part of a network of pore structures at and beneath the chocolate surface, which could be related to oil migration and thus, to fat bloom formation.