The present study evaluated parent mealtime actions that mediate associations between children's fussy-eating and their weight and diet. Participants included 236 feeding-clinic children in three diagnostic groups: 50 with autism, 84 with other special needs, and 102 without special needs. Children's weight was measured as body mass index percentile (BMI%), with only 26.4% of the present sample found to be underweight (BMI% less than 10). Parents reported children's diet variety as the number of 139 common foods accepted, children's FUSSINESS with the Child Eating Behavior Questionnaire, and their own use of four actions from the Parent Mealtime Action Scale: POSITIVE PERSUASION, INSISTENCE ON EATING, SNACK MODELING, SPECIAL MEALS. Multiple regression found that only SPECIAL MEALS explained variance in children's BMI% and diet variety. For children without special needs, mediation analysis revealed that variance in children's BMI% explained by FUSSINESS was accounted for entirely by the parent's preparation of SPECIAL MEALS. For all diagnostic groups, mediation analyses revealed that variance in children's diet variety explained by FUSSINESS was accounted for by the parent's use of SPECIAL MEALS. We conclude that although the parent's use of SPECIAL MEALS may improve BMI% in fussy-eating clinic children, it may also perpetuate their limited diet variety.

We hypothesize that autism is associated with alterations in the plasma lipid profile and that some lipid fractions in autistic boys may be significantly different than those of healthy boys. A matched case control study was conducted with 29 autistic boys (mean age, 10.1 ± 1.3 years) recruited from a school for disabled children and 29 comparable healthy boys from a neighboring elementary school in South Korea. Fasting plasma total cholesterol (T-Chol), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), the LDL/HDL ratio, and 1-day food intakes were measured. Multiple regression analyses were performed to assess the association between autism and various lipid fractions. The mean TG level (102.4 ± 52.4 vs 70.6 ± 36.3; P = .01) was significantly higher, whereas the mean HDL-C level (48.8 ± 11.9 vs 60.5 ± 10.9 mg/dL; P = .003) was significantly lower in cases as compared to controls. There was no significant difference in T-Chol and LDL-C levels between cases and controls. The LDL/HDL ratio was significantly higher in cases as compared to controls. Multiple regression analyses indicated that autism was significantly associated with plasma TG (β = 31.7 ± 11.9; P = .01), HDL (β = −11.6 ± 2.1; P = .0003), and the LDL/HDL ratio (β = 0.40 ± 0.18; P = .04). There was a significant interaction between autism and TG level in relation to plasma HDL level (P = .02). Fifty-three percent of variation in the plasma HDL was explained by autism, plasma TG, LDL/HDL ratio, and the interaction between autism and plasma TG level. These results indicate the presence of dyslipidemia in boys with autism and suggest a possibility that dyslipidemia might be a marker of association between lipid metabolism and autism.

Animal species used in the preclinical studies for development of monoclonal antibody (mAb) drugs are surveyed in this review. Relevant animal species for preclinical studies of mAb candidates are those express desired epitope of mAb candidates. Cynomolgus monkeys cross-react with mAb drugs much higher than other animal species commonly used in preclinical studies such as absorption, distribution, metabolism and excretion (ADME), efficacy, and toxicity studies, for development of new drugs. Moreover, plasma exposure of the mAb drugs in humans is predicted well from the exposure in the monkeys, and the placental transfer of immunoglobulin G (IgG, all the mAb drugs contain IgG) from mother to fetus is similar between humans and the monkeys from a viewpoint of time course and plasma level of IgG transferred. These observed findings indicate that the monkeys are the most suitable animal species used in the ADME and toxicity studies for development of new mAb drugs.