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By clinical whole exome sequencing, we identified 12 individuals with ages 3 to 37 years, including three individuals from the same family, with a consistent phenotype of intellectual disability (ID), macrocephaly, and overgrowth of adenoid tissue. All 12 individuals harbored a rare heterozygous variant in ZBTB7A which encodes the transcription factor Zinc finger and BTB-domain containing protein 7A, known to play a role in lympho- and hematopoiesis. ID was generally mild. Fetal hemoglobin (HbF) fraction was elevated 2.2%–11.2% (reference value 6 months) in four of the five individuals for whom results were available. Ten of twelve individuals had undergone surgery at least once for lymphoid hypertrophy limited to the pharynx. In the most severely affected individual (individual 1), airway obstruction resulted in 17 surgical procedures before the age of 13 years. Sleep apnea was present in 8 of 10 individuals. In the nine unrelated individuals, ZBTB7A variants were novel and de novo. The six frameshift/nonsense and four missense variants were spread throughout the gene. This is the first report of a cohort of individuals with this novel syndromic neurodevelopmental disorder.

International audience; Nuclear receptor subfamily 2 group F member 1 (NR2F1) is an orphan receptor and transcriptional regulator that is involved in neurogenesis, visual processing and development, and cortical patterning. Alterations in NR2F1 cause Bosch-Boonstra-Schaaf optic atrophy syndrome (BBSOAS), a recently described autosomal dominant disorder characterized by intellectual and developmental disabilities and optic atrophy. This study describes the clinical and neurocognitive features of an individual with a de novo nonsense variant in NR2F1 (NM_005654.5:c.82C > T, p.Gln28*), identified by whole exome sequencing. The patient was diagnosed with autism spectrum disorder (ASD) and unlike most previously reported cases, he had no developmental delay, superior verbal abilities (verbal IQ = 141), and high educational attainment despite reduced non-verbal abilities (nonverbal IQ = 63). He had optic nerve hypoplasia with minimal visual impairment as well as mild dysmorphic features. Compared to both age-matched individuals with ASD and healthy controls, the patient showed reductions in manual motor speed, accuracy of saccadic eye movements, and rates of successful behavioral response inhibition. Although the majority of previously reported cases of BBSOAS have been associated with more global intellectual dysfunction, we report on a patient with selective disruption of nonverbal abilities and superior verbal abilities.

Chromosomal abnormalities, such as unbalanced translocations and copy number variants (CNVs), are found in autism spectrum disorders (ASDs) [Sanders et al. (2011) Neuron 70: 863-885]. Many chromosomal abnormalities, including sub microscopic genomic deletions and duplications, are missed by G-banded karyotyping or Fragile X screening alone and are picked up by chromosomal microarrays [Shen et al. (2010) Pediatrics 125: e727-735]. Translocations involving chromosomes 4 and 8 are possibly the second most frequent translocation in humans and are often undetected in routine cytogenetics [Giglio et al. (2002) Circulation 102: 432-437]. Deletions of 4p16 have been associated with Wolf-Hirschhorn syndrome while 4p16 duplications have been associated with an overgrowth syndrome and mild to moderate mental retardation [Partington et al. (1997) Journal of Medical Genetics 34: 719-728]. The 8p23.3 region contains the autism candidate gene DLGAP2, which can contribute to autism when disrupted [Marshall et al. (2008) The American Journal of Human Genetics 82: 477-488] . There has been a case report of a family with autism spectrum disorder (ASD), prominent obsessional behavior, and overgrowth in patients with der (8) t (4;8) p (16;23) [Partington et al. (1997)]. This is an independent report of a male patient with autism, obsessive compulsive disorder (OCD), attention-deficit hyperactivity disorder (ADHD), and an overgrowth syndrome, whose de novo unbalanced translocation der (8) t (4;8) p (16.1→ter; 23.1→ter) was initially missed by routine cytogenetics but detected with SNP microarray, allowing higher resolution of translocation breakpoints.

This study examined the effects of chemokine receptor polymorphisms on neurodevelopment and the onset of encephalopathy in children with perinatal HIV-1 infection. Infected children (N = 121) between the ages of I and 72 months were categorized into dichotomous groups (heterozygous or homozygous mutant vs. homozygous wild type) for each chemokine receptor 2 (CCR2) and chemokine receptor 5 (CCR5) allele. Neurodevelopmental measures included the Bayley Scales of Infant Development (BSID)for children ageor = 30 months and the McCarthy Scales of Children's Abilities (MSCA) for children aged30 months. A basic linear spline was used to model the mean value at each visit for the relevant test index, with determination of the slope between 4-12 months, 12-30 months, and 31-72 months of age. A mixed model analysis of variance was used to compare differences between slopes (AP) and intercepts (AX) according to the presence or absence of the specified CCR2 or CCR5 polymorphism. Survival analyses were used to compare the onset of encephalopathy by chemokine receptor allelic grouping. After adjusting for potential confounds, statistically significant differences emerged in CCR5-39353, 39356, and 39402. Although the protective effects appeared to be discrete and transient, children with mutant CCR5 genotypes exhibited better neurodevelopmental outcomes than children with the wild type alleles. Chemokine polymorphisms did not appear to impact the onset of encephalopathy. Although possibly a temporary effect, HIV-1 infected children with selected mutant chemokine receptor polymorphims CCR5-39353, 39356, and 39402 may exhibit better neurodevelopmental outcome than children with the wild type allele.

The predominance of the T14484C mutation in French Canadians with Leber hereditary optic neuropathy is due to a founder effect. By use of genealogical reconstructions of maternal lineages, a woman married in Quebec City in 1669 is identified as the shared female ancestor for 11 of 13 affected individuals, who were previously not known to be related. These individuals carry identical mitochondrial haplogroups. The current geographic distribution of French Canadian cases overlaps with that of the founder's female descendants in 1800. This is the first example of genealogical reconstruction to identify the introduction of a mitochondrial mutation by a woman in a founder population.

Background. Identifying HIV-1-infected children who are at greatest risk for disease-related morbidities is critical for optimal therapeutic as well as preventive care. Several factors have been implicated in HIV-1 disease onset and severity, including maternal and infant host characteristics, viral phenotype and timing of HIV-1 infection. Early HIV-1 culture positivity, i.e. intrauterine infection, has been associated with poor immunologic, virologic and clinical outcomes in children of HIV-infected women. However, a direct effect of timing of infection on neurodevelopmental outcome in infancy has not yet been identified. Methods. Serial neurodevelopmental assessments were performed with 114 infants vertically infected with HIV-1 in a multicenter natural history, longitudinal study. Median mental and motor scores were compared at three time points. Longitudinal regression analyses were used to evaluate the neurodevelopmental functioning of children with early positive cultures and those with late positive cultures. Results. Early infected infants scored significantly lower than late infected infants by 24 months of age and beyond on both mental (P = 0.05) and motor (P = 0.03) measures. Early HIV-1 infection was associated with a decline in estimated motor scores of 1 standard score point per month compared with 0.28 point in the late infected group (P < 0.02). Estimated mental scores of the early infected group declined 0.72 point/ month, whereas the average decline of the late infected group was 0.30 point/month (P < 0.13). Conclusion. Early HIV-1 infection increases a child's risk for poor neurodevelopmental functioning within the first 30 months of life.

Recombinant adenovirus vectors (AdV) hold promise as a means of delivering therapeutic genes to muscle in diseases such as Duchenne muscular dystrophy (DMD). However, we have previously shown that the use of AdV is hampered by the development of reduced force-generating capacity, which occurs within 1 week and is progressive up to at least 1 month after AdV delivery in immune-competent animals. Determinations of muscle force production provide a sensitive and clinically important measure of potential adverse effects of AdV-mediated gene transfer on muscle cell function. In the present study, we investigated the role of AdV-related gene expression and host T lymphocyte responses in the genesis of muscle dysfunction following AdV injection of muscle. We report that UV-irradiation of AdV particles, which reduced AdV transcriptional activity without impairing infectivity (as confirmed by in situ polymerase chain reaction), significantly reversed early (4 days post-injection) AdV-induced contractile impairment in immune-competent mice as well as in mice lacking effective CD8+ T cell activity. The superimposed additional reduction in force-generating capacity normally found between 4 and 30 days post-AdV delivery in immune-competent mice, along with the associated loss of transgene (beta-galactosidase) expression, was largely abrogated by the absence of an intact CD8+ T lymphocyte response. Furthermore, short-term administration of a neutralizing antibody against CD4+ T cells significantly prolonged transgene expression and showed a trend toward mitigation of AdV-induced reductions in force-generating capacity. Cellular infiltration and humoral immune responses against the vector and transgene product were also blunted to varying degrees in the setting of CD8+ or CD4+ T cell deficiency. We conclude that AdV-related gene expression has an early negative (probably toxic) effect on muscle cell function that is independent of CD8+ T cell-mediated immunity. In contrast, further progression of contractile impairment and the accompanying loss of transgene expression from AdV-injected muscle are largely dependent upon the activity of CD8+ T cells. These results have implications for the design of future generation vectors and the potential need for immunosuppressive therapy after AdV-mediated gene transfer to muscle.

Pigmentation development was studied in rainbow trout Oncorhynchus mykiss, chinook salmon O. tshawvytscha, and Atlantic salmon Salmo salar fed similar practical diets supplemented with 40, 70, or 100 mg astaxanthin/kg of diet. The initial mean body weights of the respective species were 158, 198, and 191 g. The rainbow trout were reared in freshwater at 6.0–11.3°C, the chinook salmon in seawater at 8.8–14.4°C, and the Atlantic salmon in seawater at 7.1–12.7°C. The response of flesh pigmentation to dietary pigment was most rapid in rainbow trout and slowest in Atlantic salmon. Chinook salmon showed the greatest variation in response to the different dietary concentrations of astaxanthin, followed by rainbow trout and Atlantic salmon. In both rainbow trout and Atlantic salmon, pigmentation was most intense in the distal section and decreased anteriorly. In chinook salmon, pigmentation was most intense in the midsection, followed by the anterior section and then the distal section. Postprandial plas...

Ataxin 2 binding protein 1 (A2BP1 aka FOX1, RBFOX1) is an RNA binding protein responsible for regulation of pre-mRNA splicing events in a number of critical developmental genes expressed in muscle, heart and neuronal cells [Shibata et al. (2000); Mamm Genome 12:595-601; Jin et al. (2003); EMBO J 22:905-912; Underwood et al. (2005); Mol Cell Biol 25:10005-10016]. Rare copy number abnormalities of A2BP1 have been previously associated with cognitive impairment, attention deficit disorder and autism [Martin et al. (2007); Am J Med Gen Part B 144B:869-876; Elia et al. (2010); Mol Psychiatry 15:637-646.]. Using a 1M Illumina SNP microarray, we identified a 1.3 kb deletion in A2BP1, which was subsequently validated by quantitative PCR. Here we present an in depth case study of an individual with autism and mild developmental hemiparesis in whom the deletion was detected. This study provides further support for the possible role of rare copy number variants in A2BP1 in the development of autism and associated motor asymmetries.

Context Studying sensorimotor and neurocognitive impairments in unaffected family members of individuals with autism may help identify familial pathophysiological mechanisms associated with the disorder. Objective To determine whether atypical sensorimotor or neurocognitive characteristics associated with autism are present in first-degree relatives of individuals with autism. Design Case-control comparison of neurobehavioral functions. Setting University medical center. Participants Fifty-seven first-degree relatives of individuals with autism and 40 age-, sex-, and IQ-matched healthy control participants (aged 8-54 years). Main Outcome Measures Oculomotor tests of sensorimotor responses (saccades and smooth pursuit); procedural learning and response inhibition; neuropsychological tests of motor, memory, and executive functions; and psychological measures of social behavior, communication skills, and obsessive-compulsive behaviors. Results On eye movement testing, family members demonstrated saccadic hypometria, reduced steady-state pursuit gain, and a higher rate of voluntary response inhibition errors relative to controls. They also showed lateralized deficits in procedural learning and open-loop pursuit gain (initial 100 milliseconds of pursuit) and increased variability in the accuracy of large-amplitude saccades that were confined to rightward movements. In neuropsychological studies, only executive functions were impaired relative to those of controls. Family members reported more communication abnormalities and obsessive-compulsive behaviors than controls. Deficits across oculomotor, neuropsychological, and psychological domains were relatively independent from one another. Conclusions Family members of individuals with autism demonstrate oculomotor abnormalities implicating pontocerebellar and frontostriatal circuits and left-lateralized alterations of frontotemporal circuitry and striatum. The left-lateralized alterations have not been identified in other neuropsychiatric disorders and are of interest given atypical brain lateralization and language development associated with the disorder. Similar oculomotor deficits have been reported in individuals with autism, suggesting that they may be familial and useful for studies of neurophysiological and genetic mechanisms in autism.

Experiments were conducted to determine whether poor intestinal absorption of astaxanthin or some other metabolic factor is primarily responsible for pigmentation failure in white chinook salmon and small juvenile fish of other salmonid species. None of the fish studied failed to absorb astaxanthin from a single oral dose of the pigment. Intensity of flesh pigmentation in coho ranging in weight from 30–400 g, and fed a diet supplemented with astaxanthin, was significantly correlated with body weight. There was no correlation, however, between flesh colour and plasma astaxanthin concentration or between body weight and plasma astaxanthin concentration. Dietary triiodothyronine reduced both flesh pigmentation and plasma astaxanthin. It is concluded that poor flesh pigmentation results from rapid metabolism of absorbed pigment to colourless derivatives rather than from failure of the fish to absorb pigment.

Diets supplemented with 5% of tallow or safflower oil were fed to White Leghorn pullets during the initial 14 wk of production. The diets contained .6% and 4.3% of linoleic acid, respectively. Egg weight was consistently greater with the diet high in linoleic acid. Yolk weights relative to egg weights were similar in each sample, as were the yolk concentrations of total, neutral, and polar lipids. The fatty-acid profiles for both the neutral and the polar fractions were also similar for the large and small eggs within treatment, but there were differences between treatments. The lipid concentrations in the liver at the conclusion of the experiment were greater in the birds fed the diet low in linoleic acid as a result of increases in the neutral lipids. As with the yolk fatty acids, the substitution of safflower oil for tallow in the diet decreased the concentrations of oleic acid and increased the concentrations of linoleic acid in both lipid fractions. The constancy of the proportions of protein, neutral lipid, and polar lipid in the yolk, despite the effect of dietary linoleic-acid concentration on yolk size, supports the hypothesis that linoleic acid, or longer-chain fatty acids of the linoleic-acid family, is required for the synthesis of the lipoproteins that can be transported to the ovary for uptake by the developing ova. Egg size cannot be maximized if the amount of linoleic acid available is not adequate to support the maximum rate of synthesis by the lipoproteins.

Epilepsy is defined by the International League Against Epilepsy as a chronic neurological condition characterized by recurrent epileptic seizures. Most physicians who participate in the care of children are aware that epilepsy is one of the most common chronic disorders that affect children. Epilepsy is prevalent in every country, in every race and religion and in every socioeconomic status. There are of course founder effects for particular epilepsies in certain populations, but aside from these considerations the distribution of the epilepsies is remarkably similar across the planet. Epilepsy can begin at any age, although there are two more frequent ages of onset: in early childhood, reflecting hypoxic-ischemic encephalopathy, inborn errors of metabolism, genetic epilepsies and brain malformations, and in adolescence, reflecting for the most part age related genetic epilepsies. When a child with epilepsy presents for the first time to the clinic or to the emergency room, the presenting complaint is not usually of epilepsy but rather of staring spell, inattentiveness or loss of consciousness. It is the pediatric neurologist’s work to determine whether a particular child does in fact have epilepsy, or instead has convulsive syncope, breath-holding spells, myoclonus (either pathologic or of the benign nocturnal variety), chorea, dystonia, micro-sleeps, is inattentive or is enjoying the delights of day-dreaming. As with any disorder, taking a complete history is most important in determining what type of paroxysmal event occurred. Tests including electroencephalography andmagnetic resonance imaging are used to refine and confirm the clinical impression. Children with uncomplicated epilepsy are often returned to the care of their pediatricians, family physicians or pediatric nurse practitioners after diagnosis, although some continue to be cared for by a pediatric neurologist. When epilepsy is refractory, then referral to a pediatric epileptologist in an epilepsy center is warranted. When a child is diagnosed with epilepsy, his or her pediatric neurologist is careful to clearly explain the diagnosis and the principles of seizure management, the choices of anticonvulsant medications to be considered and their risks, benefits and side effects, seizure first aid, seizure precautions, lifestyle modifications and activities to avoid. Introductions to the clinic nurse and social worker are made. The primary health care provider receives an initial communication, and clinic contact information for questions or issues that arise between visits is provided to the family. All of these discussions and activities are extremely important, and yet there remains a large swath of a child’s life that is also affected by the diagnosis of epilepsy, either directly or indirectly. What of the child’s education, the after school activities, the effects on other medical conditions that a child may have, the general medical care of the child and the effects on the family as a whole? These issues are not usually highlighted in the education of a pediatric neurologist, and so this issue devoted to general health concerns for children with epilepsy has been prepared. I hope that you find the thoughtful discussions as interesting and as informative as I have. *Address for correspondence: Carol Macmillan, Department of Pediatrics, University of Chicago, 5841 South Maryland MC 3055, Chicago, IL 60637-1470, USA. Tel.: +1 773 702 6487; Fax: +1 773 702 4786; E-mail: cmacmill@peds.bsd.uchicago.edu. Journal of Pediatric Epilepsy 2 (2013) 145 DOI 10.3233/PEP-13055 IOS Press 145

The aim of this paper is to review the literature on eye-movement abnormalities associated with neurodevelopmental disorders. Eye-movement testing is a non-invasive quantitative approach for evaluating brain systems across the age spectrum. It thus provides a promising methodology for characterizing and documenting maturational abnormalities in brain systems associated with neurodevelopmental disorders.Recent oculomotor studies have made significant contributions to the understanding of neurodevelopmental disorders, most notably in autism, attention-deficit/hyperactivity disorder, and Tourette's syndrome. Notably different patterns of deficits have been found in these disorders and have helped to clarify their pathophysiology.Eye-movement studies have begun to serve as a useful approach for studying cognitive and neurophysiological aspects of neurodevelopmental disorders. They also have potential as a strategy for establishing quantitative endophenotypes for genetic research, and for monitoring beneficial and adverse effects of pharmacotherapies. Studies are needed that involve larger patient populations, longitudinal characterization of developmental failures, patients free from central nervous system-active medications, and that use functional imaging, as patients perform eye-movement tasks, for direct identification of clinically relevant abnormalities in brain systems.

Mutations in Sco2, a protein involved in copper trafficking to the terminal enzyme of the respiratory chain, cytochrome c oxidase, results in infantile hypertrophic cardioencephalomyopathy. We have recently shown that copper-histidine (Cu-his) supplementation of Sco2-deficient myoblasts rescues COX activity in vitro. Here, we report a patient with SCO 2 mutations and with resolution of severe hypertrophic cardiomyopathy. Weighing up the evidence, the most likely explanation for the improved cardiac function in this patient was the subcutaneous application of Cu-his.

Objective: To report three unrelated infants with a distinctive phenotype of Leigh-like syndrome, neurogenic muscular atrophy, and hypertrophic obstructive cardiomyopathy. The patients all had a homozygous missense mutation in SCO2. Background: SCO2 encodes a mitochondrial inner membrane protein, thought to function as a copper transporter to cytochrome c oxidase (COX), the terminal enzyme of the respiratory chain. Mutations in SCO2 have been described in patients with severe COX deficiency and early onset fatal infantile hypertrophic cardioencephalomyopathy. All patients so far reported are compound heterozygotes for a missense mutation (E140K) near the predicted CxxxC metal binding motif; however, recent functional studies of the homologous mutation in yeast failed to demonstrate an effect on respiration. Methods: Here we present clinical, biochemical, morphologic, functional, MRI, and MRS data in two infants, and a short report in an additional patient, all carrying a homozygous G1541A transition (E140K). Results: The disease onset and symptoms differed significantly from those in compound heterozygotes. MRI and muscle morphology demonstrated an age-dependent progression of disease with predominant involvement of white matter, late appearance of basal ganglia lesions, and neurogenic muscular atrophy in addition to the relatively late onset of hypertrophic cardiomyopathy. The copper uptake of cultured fibroblasts was significantly increased. Conclusions: The clinical spectrum of SCO2 deficiency includes the delayed development of hypertrophic obstructive cardiomyopathy and severe neurogenic muscular atrophy. There is increased copper uptake in patients’ fibroblasts indicating that the G1541A mutation effects cellular copper metabolism.

The discovery of new cytogenetic and molecular genetic techniques and principles has been explosive in recent years. A secure diagnosis based on molecular evidence has become possible for many syndromes previously only clinically defined, which has helped enormously in predicting children's developmental progress, in allowing knowledgeable surveillance for potential associated health problems, in genetic counseling, and in prenatal diagnosis. This article reviews several of the most significant recently described cytogenetic and molecular genetic principles and techniques in relation to the child who presents with developmental delay.

Design Nonexperimental-Descriptive. Sample The inclusion criteria were trauma patients, ages 15 and older, who were hospitalized for > 2 days, and who did not have preexisting skin breakdown. A total of 148 consecutive trauma patients admitted to the study institution meeting the inclusion criteria were prospectively enrolled. Methods Patients were assessed every 3 days for skin breakdown. Information on the patient's bed type, therapies, medical devices, and nutrition was collected. The Braden Scale for predicting pressure ulcer risk was completed at each assessment. Findings Of the 148 patients enrolled, 30 developed at least one area of skin breakdown for a prevalence of 20.3% in patients hospitalized more than 2 days. The most common cause of breakdown was positional pressure (47.4%). Cervical collars were the second leading cause at 23.7%, followed by tracheostomy/endotracheal tubes at 10.5%. The mobility subscale of the Braden Pressure Ulcer Risk Assessment tool was significantly predictive of skin breakdown (p Implications for nursing research Skin breakdown is a significant problem in trauma patients who are hospitalized for more than 2 days. Aggressive protocols on positioning, cervical collar use, and airway adjuncts, as well as additional active nursing interventions for immobile patients, may be ways to decrease the skin breakdown prevalence in this population.

We studied multiple different postmortem tissue samples from a woman and two of her daughters with the MELAS (mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes) tRNA(Leu(UUR)) mutation at nucleotide 3243 in mitochondrial DNA (mtDNA). All tissues examined were heteroplasmic for the mutation. The mean proportion of mutant mtDNAs in the mother's tissues (0.30 +/- 0.10) was significantly lower than that of each of her daughters' (0.76 +/- 0.11, p < 0.03, and 0.72 +/- 0.13, p < 0.001); there was no difference in the fraction of mutant mtDNAs between the daughters (p < 0.71). This difference in the mean proportion of mtDNA mutants between family members correlates with their clinical profiles; the mother had the latest onset of disease and lived longest, while the two daughters had a strikingly similar clinical course. In individual patients, the mean proportion of mutant mtDNAs was not different in tissues deriving from ectodermal, mesodermal, and endodermal germ layers. Variance in the mutant:wild-type mtDNA ratio was normally distributed about the mean, both when all tissues were considered together and when different regions of the CNS were considered separately. Thus, the proportion of mtDNAs carrying the tRNA(Leu(3243)) mutation was not uniform in members of this pedigree and did not undergo rapid mitotic segregation along germ-layer divisions. These findings are consistent with the hypothesis that the overall proportion of mtDNAs carrying this mutation is primarily determined by segregation during oogenesis or early embryologic development and that random replicative (mitotic) segregation, subsequent to the establishment of primary germ layers, is responsible for the variation between tissues.

The caeca and small intestine of chickens consistently contain trimethylamine (TMA). The caecal contents in the birds studied ranged from 4 to 55 μg TMA/g and contained the higher concentrations when the diet contained rapeseed meal or supplementary choline. The amounts of TMA in the small intestine were lower (1 to 21 μg/g) and were less influenced by dietary composition. Supplementary choline in the diet of laying birds induced the production of tainted eggs by some birds. The yolks of tainted eggs contained concentrations of TMA which were consistent for each bird. TMA was also present in the follicular yolks of all sizes in the ovaries of birds which laid tainted eggs. It is postulated that, in birds laying tainted eggs, failure of the liver to oxidize TMA is responsible for deposition of TMA in egg yolk.

Female broiler-type chickens were fed diets containing different concentrations of protein and fat in two experiments. The first experiment was for 4 weeks. The mean weights of the abdominal fat pads were inversely related to dietary concentrations of protein between 20 and 35%. Adipocyte size and cellularity of the fat pads were lower with 30 than 20% protein. Fat deposition in the abdominal pad was increased in 3-week-old chicks by isocaloric substitution of oil for starch in the diets. At 4 weeks of age the effect of oil was not significant with 30 or 20% dietary protein (no measurements were made in chicks fed 35 or 25% protein). In Experiment 2, the development of the abdominal fat pad in birds fed 18 to 33% protein was monitored for 22 weeks. By 7 weeks the distribution of adipocyte size was bimodal. The initial adipocyte population showed comparatively little increase in numbers after 12 weeks, but cell size continued to increase. The numbers of adippcytes in the second population of adipocytes was still increasing rapidly at 22 weeks, although the size of the cells in this population remained small. At 22 weeks the small cells constituted 62% of the total adipocyte population but contained only 2.4% of the lipid in the fat pad. Adipocyte cell size was significantly affected by dietary protein and energy until 9 weeks of age, but the effects subsequently declined.

One thousand broiler-type pullets were reared with feed restriction from 5 weeks of age to attain a target average body weight of 1.64 kg at 18 weeks of age. Thereafter feed was supplied at the rate of 130 g per bird per day until 47 weeks at which time half the population was fed ad libitum. An additional treatment was imposed at 86 weeks when 12 birds were gradually but severely restricted in feed intake until, by 97 weeks, they were receiving only 40 g feed per day. Birds restricted in feed intake until 47 weeks and then fed ad libitum increased consumption sharply and in proportion to body weight for approximately 2 weeks. Thereafter, intake declined to about 20% in excess of the restricted level for the next 16 weeks. Body weight increased with the increased feed intake. Average adipocyte diameter increased with the age of the birds even when feed was restricted. There was no increase in the number of adipocytes present in the retroperitoneal fat pad after 27 weeks of age. The size distribution of adipocytes was consistently bimodal except following severe feed restriction when the weight of the fat pad regressed and the secondary peak of small adipocytes disappeared.

Virginiamycin at a dietary concentration of 22 ppm stimulated growth rate and improved efficiency of feed conversion in broilers fed different diets. The dietary variations were practical ones which would alter the milieu of the intestinal bacteria. They involved the use of wheat vs. corn as principal dietary cereal, different levels of fat, and different levels of protein. All the diets supported similar performance and there were no significant interactions in response between diet and antibiotic. Body weights at 53 days of age averaged 5% heavier in the virginiamycin-fed birds and the average rate of improvement in feed conversion efficiency was 5.4%. At 26 days respective values for the above were 10.3% and 9.5%. The energy metabolized from the diets was increased by 7.2% when the diets contained virginiamycin.

White Leghorn chicks were fed diets containing either soybean meal or rapeseed meal as the source of supplementary protein. The diets were modified by the addition of corn oil, corn oil plus erucic acid, cornstarch, or herring meal. Excreta from the chicks were analyzed for ether-soluble lipid and for the amounts of fatty acids present in soaps. The birds fed the different soybean meal-containing diets in three experiments excreted, on the average, 30.2% of lipid in the form of soap fatty acid. Those fed the equivalent diets containing rapeseed meal excreted 16.6% of lipid in the form of soap fatty acid. Differences in the proportions of fatty acids excreted as soaps are attributed primarily to differences in concentration of ionic calcium in the intestinal lumen.

No significant differences in plasma corticosterone concentrations were noted among chicks fed diets containing 16 to 25% protein or diets containing 2,800, 3,200, or 3,600 kcal metabolizable energy per kg to 6 wk of age. The ingredients used in diet formulation did, however, affect plasma corticosterone. Higher plasma corticosterone was associated with 2,800-kcal diets containing high concentrations of cornstarch and no cereal grains compared with 2,800-kcal diets containing low concentrations of cornstarch and cereal grains. In a second experiment, chicks were fed diets containing different concentrations of lysine and methionine from hatching to 4 wk of age. Half the chicks on each dietary treatment were conditioned to handling by daily gentling. Plasma corticosterone concentrations were reduced in the conditioned chicks. Plasma corticosterone increased during a period of up to 15 min after catching when the chicks were kept in a box prior to drawing blood samples. Excess dietary lysine significantly reduced plasma corticosterone in the gentled chicks but not in the control chicks.

Selection of the test fish for uniformity of body weight allowed bioassays for protein quality to be conducted within a 3-week period with small numbers of fish. Slope-ratios from the linear responses of body weight gain to graded levels of protein intake gave practical comparisons of the quality of protein sources. The use of different dietary concentrations of protein sources under test may indicate responses to factors other than those associated with protein per se. The slope-ratio technique lends itself to simultaneous estimations of the relative efficiency of protein energy utilization, which are important in evaluation of plant protein concentrates.

Three rapeseed meals were analyzed and found to contain 4650, 5060, and 5720 mg choline per kilogram, respectively. Three broiler diets formulated with 20% of the respective rapeseed meals, and each containing in excess of 1500 mg choline per kilogram, did not promote as rapid growth as did a control soybean meal diet containing 1000 mg choline per kilogram. Incidence of perosis was higher with the rapeseed meal diets than with the soybean meal diets. Addition of choline to the soybean meal diet affected neither growth nor incidence of perosis in the birds fed this diet. Supplementary choline increased growth and decreased incidence of perosis in the birds fed the rapeseed meal diets. In a second experiment to study availability of choline from rapeseed meal, chicks were fed a diet containing 28% rapeseed meal and 2310 mg choline per kilogram or a soybean meal diet supplemented with choline to provide a total of 2110 mg choline per kilogram. The freeze-dried contents of the lower intestine contained 4.92 mg choline per gram from the rapeseed meal-fed chicks and 2.45 mg/g from the soybean meal-fed chicks. The results of the third experiment showed that unabsorbed choline in the intestine was associated with an increase in bacterial production of trimethylamine. The caecal contents of chicks fed 28% of dietary rapeseed meal contained significantly more trimethylamine than those of chicks fed a control soybean meal diet although both diets contained 2310 mg choline per kilogram.