Cow’s milk allergy is a common food allergy among infants. Symptoms of cow’s milk allergy are wide-ranging and depend on the mechanism involved. There are immunoglobulin E (IgE)-mediated, non–IgE-mediated, and mixed mechanisms of food allergy. Symptoms of IgE-mediated cow’s milk allergy may be mild or may progress to anaphylaxis, which can be life-threatening. Non–IgE-mediated allergy includes food protein–induced allergic proctocolitis (FPIAP), food protein–induced enterocolitis syndrome, food protein–induced enteropathy, and Heiner syndrome (pulmonary hemosiderosis). These diagnoses comprise about half of all cow’s milk allergies. The most common manifestation of cow’s milk allergy in infants is FPIAP. FPIAP is commonly seen in healthy, full-term infants who present with rectal bleeding and are otherwise well-appearing. This can occur in both formula-fed and exclusively breastfed infants. Food proteins secreted in maternal breast milk can contribute to the development of these symptoms. Maternal cow’s milk elimination diet is often successful in helping resolve symptoms. A period of reintroduction of cow’s milk resulting in re-emergence of symptoms in stable asymptomatic infants is an excellent diagnostic tool to confirm a cow’s milk allergy. Preterm infants are susceptible to food allergy, as demonstrated from several case reports of necrotizing enterocolitis–like illnesses that responded clinically to cow’s milk elimination. Further study is needed about food allergy in the preterm infant population.

No abstract

No abstract

Introduction: Mitochondria play a critical role in cardiac myocyte physiology and differentiation. Hypoxia decreases cardiac function. Changes in embryonic heart metabolism at the level of the electron transport chain (ETC) are regulated by a chaperone protein known as cyclophilin D (CypD). Inhibition of CypD with chemicals such as cyclosporin A (CsA) and N-methyl-4-isoleucine cyclosporin (NIM811) leads to more complex mitochondrial structure and effective oxidative phosphorylation. Hypothesis: Inhibition of CypD with CsA or NIM811 will rescue the detrimental effects of hypoxia on cardiac function and on ETC assembly and activity. Methods: Mice were exposed to continuous hypoxia (12% oxygen) immediately before birth (gestational age E19.5) to postnatal day 7 (P7). Hypoxic mice received no treatment (No Tx) or intraperitoneal injections 10mg/kg of vehicle (VEH), CsA, or NIM811 from P1 to P6. Litters of mice born into room air served as controls. On P7, mice were anesthetized and underwent echocardiography and/or hearts were harvested for mitochondrial isolation. Enzymatic activity of ETC complexes was quantified using spectrophotometry and normalized to total protein. To measure physical assembly of complex I & V of the ETC, high resolution clear native polyacrylamide gel electrophoresis (HCRN PAGE) followed by in-gel assays were utilized using appropriate protein loading controls. Results: Cardiac ejection fraction was decreased in hypoxic No Tx (P<0.0001) and VEH (P<0.0001), but was rescued by CsA or NIM811 when compared to room air controls (P>0.05). Heart weight to body weight ratio was increased in No Tx and VEH groups (P< 0.0001) and rescued in the CsA and NIM811 groups when compared to room air controls (P>0.05). Complex I enzymatic activity was rescued with treatment with CsA and NIM811. HCRN PAGE followed by in-gel ETC complex assay demonstrated assembly of complexes I and V into dimers and tetramer in the room air, CsA, and NIM811 groups that was not seen in the No Tx and VEH groups. Conclusion: Pharmacologic inhibition of CypD reversed the effects of hypoxia on cardiac function and ETC activity and assembly in the neonatal heart. Our studies may help develop therapies to treat neonatal cardiomyopathies and the effects of hypoxia on the neonatal heart.