If not detected and treated, gold Neonatal skin disease can lead to neurotoxic complications due to low indirect Bilirubin entering the brain causing death or lifelong brain damage. Bilirubin blood test is higher than normal. Simultaneously with jaundice, there are other abnormal symptoms such as: lethargy, lethargy, convulsions. The pathology is dark jaundice appearing early, not yellowing after 1 week for full-term infants and 2 weeks for preterm infants, the degree of yellowing of the whole body, palms, feet and even the conjunctiva of the eyes. Pathological Jaundice In some cases, jaundice is a manifestation of an underlying disease and in these cases the jaundice will appear as early as 24 hours after birth. When the baby is about 2 weeks old, the liver has developed more fully and is able to process Bilirubin, so jaundice will go away on its own without causing any dangerġ.2. Meanwhile, the baby's liver is not mature enough to remove all bilirubin from the blood, thus causing jaundice. This phenomenon is common in newborns because they have high levels of red blood cells, which are often broken down and replaced. The cause of physiological jaundice in newborns is the accumulation of Bilirubin, a yellow substance produced when red blood cells are broken down. In addition, the infant's urine is dark or yellow (infant urine is usually colorless) and the stool is pale. Bilirubin/blood rise rate is not more than 5mg% in 24 hours. Bilirubin/blood concentration is not more than 12mg% in term infants and not more than 14mg% in preterm infants. Mild degree of jaundice is only jaundice (yellowing of the face, neck, chest and abdomen above the navel) without other abnormal symptoms (anemia, hepatosplenomegaly, abortion, lethargy, duh.). Physiological Jaundice Physiological jaundice can be mild, in term infants, normal jaundice is considered physiological when jaundice appears after 24 hours of age, and usually disappears within 1 week in infants term and 2 weeks in preterm infants. The present review discusses the possibility of targeting cardioprotective signalling pathways and genes activated in the athlete's heart to treat or prevent heart failure.1.1. It is now clear that several signalling molecules play unique roles in the regulation of pathological and physiological cardiac hypertrophy. Physiological hypertrophy is characterized by normal organization of cardiac structure and normal or enhanced cardiac function, whereas pathological hypertrophy is commonly associated with upregulation of fetal genes, fibrosis, cardiac dysfunction and increased mortality. Physiological cardiac hypertrophy in response to exercise training differs in its structural and molecular profile to pathological hypertrophy associated with pressure or volume overload in disease. Cardiac hypertrophy that occurs in athletes (physiological hypertrophy) is a notable exception. Cardiac enlargement is a characteristic of most forms of heart failure. In general, cardiac hypertrophy (an increase in heart mass) is a poor prognostic sign.
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