Dietary modifications for infantile colic

Infantile colic can be defined as periods of inconsolable, unexplained, and incessant crying in a seemingly healthy infant that, quite understandably, leads to exhausted, frustrated, and concerned parents seeking to comfort their child (Landgren 2010). The prevalence of excessive crying varies according to the definition used although, most often, it peaks during the second month of life,with a prevalence of 1.5%to 11.9%(Reijneveld 2001).Traditionally, the definition of the condition was based on the rule of three (Wessel 1954): that is, unexplained episodes of paroxysmal crying for more than three hours per day, for three days per week, for at least three weeks. More recently a new definition has been proposed. It refers to a clinical condition of fussing and crying for at least one week in an otherwise healthy infant (Hyman 2006). Colic can be graded as mild, moderate, or severe, though there is no consensus for this classification. Colic can affect up to 10% to 30% of infants worldwide (Clifford 2002; Rosen 2007)

Chronic mild stress-induced alterations of clock gene expression in rat prefrontal cortex: modulatory effects of prolonged lurasidone treatment

Disruptions of biological rhythms are known to be associated with depressive disorders, suggesting that abnormalities in the molecular clock may contribute to the development of these disorders. These mechanisms have been extensively characterized in the suprachiasmatic nucleus, but little is know about the role exerted by individual clock genes in brain structures that are important for depressive disorders. Using the chronic mild stress model we found a significant reduction of BMAL1 and CLOCK protein levels in the nuclear compartment of the prefrontal cortex of CMS rats, which was paralleled by a down-regulation of the expression of several target genes, including Pers and Crys but also Reverb\u3b2 and Ppar\u3b1. Interestingly, chronic treatment with the multi receptor modulator lurasidone (3 mg/kg for 5 weeks) was able to normalize the molecular changes induced by CMS exposure in prefrontal cortex, but it was also able to regulate some of these genes within the hippocampus. We believe that changes in clock genes expression after CMS exposure may contribute to the disturbances associated with depressive disorders and that the ability of chronic lurasidone to normalize such alterations may be relevant for its therapeutic properties in ameliorating functions that are deteriorated in patients with major depression and other stress-related disorders

Analysis of Serum Th2 Cytokines in Infants with Non-IgE Mediated Food Allergy Compared to Healthy Infants

Background: The aim of this study is to assess the serum values of IL-4, IL-5, IL-10, and IL-13 in a group of infants with non-IgE mediated food allergies treated with a hydrolyzed formula and compare them with a group of healthy peers. Methods: A total of 53 infants aged 1 to 4 months, of which 34 with non-IgE mediated food allergies and 19 healthy infants were enrolled in this study. Infants were eligible if they had gastrointestinal symptoms of food allergy and needed to switch from their initial formula to hydrolyzed formulas with an improvement of symptoms. Controls were fed with either breastmilk or standard formula. Blood samples were taken within one week of a special diet for cases. Interleukinsin in peripheral blood was detected and analyzed using the real-time PCR MAMA method. Fecal calprotectin was evaluated using a quantitative assay. Results: Values of IL-4 and IL-13 were significantly higher in the non-IgE food allergy group compared to the control group (p < 0.05), while IL-5 and IL-10 were significantly lower than the control group (p < 0.05). Fecal calprotectin in the non-IgE food allergy group was significantly higher compared to the control group (p < 0.05). Conclusion: This study provides a theoretical basis that Th2 cytokine expression in infants with a non-IgE mediated food allergy is significantly different than in healthy infants; this finding supports the use of early dietetic treatment with hydrolyzed formulas

SERUM REFERENCE VALUES FOR LEPTIN IN HEALTHY INFANTS.

OBJECTIVE: Reports on leptin concentrations in pediatric populations lack reference values for infants in the first months of life. Our study was conducted on healthy full-term infants between 2002 and 2012 to determine serum leptin reference values in subjects less than 18 months old. METHODS: Routine outpatient blood tests for serum leptin were performed on 317 infants using a radioimmunoassay method. The median and 10th-90th percentiles were calculated to obtain reference values using quantile regression. Values established in this study were compared with another independent cohort of 110 infants. RESULTS: The median (IQR) serum leptin concentration in the infants was 2.37 (3.26) ng/ml (n = 317). The median leptin concentration was 2.81 (3.49) ng/ml (n = 202) in infants younger than 6 months of age, 1.44 (2.27) ng/ml (n = 59) in infants between 6-12 months of age and 1.77 (2.05) ng/ml (n = 56) in infants between 12-18 months of age. We obtained leptin reference values based on age by estimating the lower and upper percentiles. In the entire cohort, the median (IQR) leptin concentration was 2.22 (3.11) ng/ml in males (n = 168) and 2.60 (3.32) ng/ml in females (n = 149). According to the type of feeding median serum leptin concentration was higher in breast-fed infants (n = 188) than in formula-fed infants (n = 129) (2.63 (3.34) ng/ml vs. 2.12 (2.77) ng/ml; p<0.05). CONCLUSIONS: Our data revealed no gender difference in leptin concentration in early infancy. After 6 months of life, leptin concentrations decreased slightly. We used a large cohort to confirm that breast-fed infants had significantly higher serum leptin levels than formula-fed infants during the first 6 months of life, although this difference disappeared later in life. In this study, we defined the leptin reference range in healthy infants in the first 18 months of life according to the Clinical and Laboratory Standards Institute (CLSI)

Intermittency layers associated to turbulent interfaces

In this study we focus on the transport across an interface which separates two regions with homogeneous and isotropic turbulence in absence of a mean shear. The turbulent transport resulting presents an internal structure. Indeed, in the case of turbulent self-diffusion, both experiments and simulations show that the fluid velocity field is marked by a high intermittency front located aside the interface, which is the source of turbulent bursts penetrating the low turbulence region. The presence of an inner structure inside a layer of turbulence self-transport highlights the different nature of the turbulent transport with respect to the Gaussian diffusion. By including other effects, for instance a passive scalar transport or a mass transport in presence of a density stratification, the phenomenology is much enriched. For instance, our preliminary numerical experiments on the passive scalar transport reveals the presence of two intermittency fronts, one on each side of the interface. As can be seen if the figure below, the intermittency level in the fronts is high. This is true both for the scalar and the scalr derivative statistics. A gradual decay in time is observed while they propagate toward the lateral isotropic regions of the flow. In the presence of a kinetic energy gradient across the interface, the locations and intensity of the intermittency fronts are no more symmetric to respect to the interface. The front on the high energy side of the mixing region penetrates deeper and exhibits stronger intermittency. Analogous features are observed also in two dimensions

A point mutation in the hair cell nicotinic cholinergic receptor prolongs cochlear inhibition and enhances noise protection

The transduction of sound in the auditory periphery, the cochlea, is inhibited by efferent cholinergic neurons projecting from the brainstem and synapsing directly on mechanosensory hair cells. One fundamental question in auditory neuroscience is what role(s) this feedback plays in our ability to hear. In the present study, we have engineered a genetically modified mouse model in which the magnitude and duration of efferent cholinergic effects are increased, and we assess the consequences of this manipulation on cochlear function. We generated the Chrna9L9′T of knockin mice with a threonine for leucine change (L9′T) at position 9′ of the second transmembrane domain of the α9 nicotinic cholinergic subunit, rendering α9-containing receptors that were hypersensitive to acetylcholine and had slower desensitization kinetics. The Chrna9L9′T allele produced a 3-fold prolongation of efferent synaptic currents in vitro. In vivo, Chrna9L9′T mice had baseline elevation of cochlear thresholds and efferent-mediated inhibition of cochlear responses was dramatically enhanced and lengthened: both effects were reversed by strychnine blockade of the α9α10 hair cell nicotinic receptor. Importantly, relative to their wild-type littermates, Chrna9L9′T/L9′T mice showed less permanent hearing loss following exposure to intense noise. Thus, a point mutation designed to alter α9α10 receptor gating has provided an animal model in which not only is efferent inhibition more powerful, but also one in which sound-induced hearing loss can be restrained, indicating the ability of efferent feedback to ameliorate sound trauma.Fil: Taranda, Julian. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; Argentina. Tufts University School of Medicine; Estados UnidosFil: Maison, Stéphane F.. Massachusetts Eye and Ear Infirmary; Estados UnidosFil: Ballestero, Jimena Andrea. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; ArgentinaFil: Katz, Eleonora. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; ArgentinaFil: Savino, Jessica. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; ArgentinaFil: Vetter, Douglas E.. Tufts University School of Medicine; Estados UnidosFil: Boulter, Jim. University of California at Los Angeles; Estados UnidosFil: Liberman, M. Charles. Massachusetts Eye and Ear Infirmary; Estados UnidosFil: Fuchs, Paul A.. The Johns Hopkins University School of Medicine; Estados UnidosFil: Elgoyhen, Ana Belen. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Farmacología; Argentin

Energy and water vapor transport across a simplified cloud-clear energy air interface

We consider a simplified physics of the could interface where condensation, evaporation and radiation are neglected and momentum, thermal energy and water vapor transport is represented in terms of the Boussinesq model coupled to a passive scalar transport equation for the vapor. The interface is modeled as a layer separating two isotropic turbulent regions with different kinetic energy and vapor concentration. In particular, we focus on the small scale part of the inertial range of the atmospheric boundary layer as well as on the dissipative range of scales which are important to the micro-physics of warm clouds. We have numerically investigated stably stratified interfaces by locally perturbing at an initial instant the standard temperature lapse rate at the cloud interface and then observing the temporal evolution of the system. When the buoyancy term becomes of the same order of the inertial one, we observe a spatial redistribution of the kinetic energy which produce a concomitant pit of kinetic energy within the mixing layer. In this situation, the mixing layer contains two interfacial regions with opposite kinetic energy gradient, which in turn produces two intermittent sublayers in the velocity fluctuations field. This changes the structure of the field with respect to the corresponding non-stratified shearless mixing: the communication between the two turbulent region is weak, and the growth of the mixing layer stops. These results are discussed with respect to Large Eddy Simulations data for the Planetary Boundary Layers