Abstract. Objectives: To Highlight The Importance Of Cord

Researchers have studied the many possible causes of Sudden Infant Death Syndrome and four have been selected for this paper.

researchers stated that SIDS babies probably have a defect in the brain neurochemicals that usually operate the protective responses to changes in oxygen and carbon dioxide levels.(IntelliHealth 3)

One of the many changes that affect us every day is oxygen toxicity in premature

As I stated in the abstract, Sudden Infant Death Syndrome is the unexpected death of a healthy infant in its sleep usually under the age of one. It is also known as “crib death” because the death usually occurs in the crib. Sudden Infant Death Syndrome claims the lives of approximately 2,500 infants each year. The majority of SIDS deaths occur between 2 and 4 month year olds. The cause of SIDS is usually known and there are a number of causes. Causes of SIDS include: smoking or drinking during pregnancy, inadequate prenatal responsibility, prematurity, inexperienced mothers, smoking near or around the baby, enormous amounts of heating from blankets or pajamas, and placing a baby on its stomach (Floyd R. Livingston Jr., MD. Sudden Infant Death

Within the foetus, embryonic nerve cells grow exponentially, then migrate to their destinations and develop into a vast collection of distinctive neuronal cell categories unique to their specific function. In prearranged patterns, the cells later form networks with other brain cells. The metabolic process of alcohol instigates makes the cells vulnerable to cell damage by free radicals (harmful substances). Research has suggested that “free radical damage can kill sensitive populations of brain cells at critical times of development in the first trimester of pregnancy (Cartwright, M.M).” Additional experiments have suggested that the third trimester is a particularly susceptible stage for damage to brain cells linked to FASD. The metabolic breakdown of alcohol interferes with brain development through the alteration of the function or production of natural regulatory substances that assist in the promotion of the differentiation and orderly growth of

“Metabolomic profiling of brain from infants who died from Sudden Infant Death Syndrome reveals novel predictive biomarkers”

One of the most controversial behaviours parents can do is adjust the babies sleeping environment. There have been multiple arguments on this topic; however, research has shown that a babies sleeping environment can impact their sleeping safety tremendously. Some safety precautions all care givers can do is: placing the baby on their back to sleep, keeping the crib clean and clear of any toys or pillows, don’t overheat the baby with clothes or blankets instead try a sleeping sack, and lastly allow the baby to sleep in the caregivers room for the first six months or until the infant is capable of rolling over on their own. Another way to help prevent SIDS is by using a pacifier. Strangely enough, pacifiers can reduce the risk of SIDS due to the fact that they help prevent a baby from going into a deep sleep. Though, caregivers need to take precaution when doing this if an infant is breast feeding as they should not be introduced to pacifiers until they are nursing well. Consequently, one of the easiest ways to prevent SIDS is to not ignore sicknesses, especially respiratory related issues. In the first year of an infant’s life something as simple as a cough or old can impact them greatly. By taking an infant to a clinic, doctor, or even the emergency room as soon as any signs of sickness strike could save their life. Ultimately, there is no guaranteed that these precautions will work and unfortunately SIDS does happen. Despite that, there are multiple ways for caregivers to cope with this

The lack of solid markers to determine the long term outcome and prognosis in neonates with Hypoxic Ischaemic Encephalopathy makes parents counseling very challenging.

Sometimes a baby who seems healthy passes away during sleep. No parent wants to wake up and find their infant not breathing. Sudden Infant Death disorder (SIDS) is one of the leading causes for death among newborn children one month to one year of age. Taking the lives of around 2,500 Infants every year in the United States. An extra 3,500 babies pass on every year from different reasons for sudden and surprising newborn child demise (SUID, or, suffocation). Sudden infant death is a tragic event for any parent or caregiver, and is no one's fault. SIDS can happen even when everything done right.

SIDS, also known as crib death, continues to be the number 1 killer of children age one month to 1 year in the United States; however, most SIDS related deaths typically occur within the 1-4 month age range. The Mayo Clinic (2017), defines Sudden Infant Death Syndrome (SIDS) as the unexplained death, usually during sleep, of a seemingly healthy baby less than a year old. Although there is no definite etiology of SIDS, several risk factors have been identified.

As I stated in the abstract, Sudden Infant Death Syndrome is the unexpected death of a healthy infant in its sleep usually under the age of one. It is also known as “crib death” because the death usually occurs in the crib. Sudden Infant Death Syndrome claims the lives of approximately 2,500 infants each year. The majority of SIDS deaths occur between 2 and 4 month year olds. The cause of SIDS is unknown in infants under one, but for infants over the age of one, there is a cause. A few of the causes of SIDS include: smoking or drinking during pregnancy, inadequate prenatal responsibility, prematurity, inexperienced mothers, smoking near or around the baby, enormous amounts of heating from blankets or pajamas, and placing a baby on its stomach (Floyd R. Livingston Jr., MD. Sudden Infant Death Syndrome. KidsHealth. 2014. Web).

A cohort of mice underwent a second mTBI after 24 hours. Mice from both WT and Tg groups were assessed 2 days, 9 weeks, and 16 weeks after mTBI treatment. Primarily, H&E stain was employed along with Gomori’s iron stain to localize site and severity of mTBI injury. The degree of A deposition in the somatosensory cortex (SSC), the perihippocampal cortex (PHC), and the hippocampus (HP) of both hemispheres was determined by 4G8 immunostaining. In addition, GFAP staining was used to quantify the population of astrocytes at the site of the injury. Furthermore, Sandwich ELISA was utilized in mice groups 16 weeks after injury to measure A40 and A42 peptide levels in various brain regions, including the cerebral cortex, the hippocampus, and the cerebellum. Such tissues were also analyzed for isoprostane levels that are produced by lipid peroxidation. Isoprostanes were also detected in urine samples at various survival periods. Moreover, mice underwent Morison water maze (MWM) and composite neuroscore (NS) tests at 16 weeks’ post-injury to examine cognitive and motor functions respectively. Uryu and collegues found a significant increase in iron deposits and reactive astrocytes in the repetitive mTBI postmortem sections of Tg mice, when compared to other groups at 16 weeks after the injury. This was not the case in WT mice. Similarly, there was a significant increase in the A burden within select brain regions (i.e. SSC, PHC, HP) of single and

Herpes simplex virus encephalitis(HSVE) can occur at second or third trimester of pregnancy and I also learn from this paper that this infection can also occur in postpartum period without common symptoms like fever and headache. The physiological immunosuppression during pregnancy and weak natural-killer cell cytotoxicity in late pregnancy are indicated as the factors for herpes simplex virus type 1 infections in postpartum period. The studies show that as the time between the onset of the symptoms and the treatment is prolonged, the morbidity and mortality rates increase. The symptoms of HSVE are fever, headache, focal edema, necrosis, aphasia, stupor, motor weakness, generalized seizure, coma, and hemorrhage in temporal and frontal lobes. This case paper review focuses on the basic functions and roles of herpes simplex virus gene products and reviews the current knowledge of medical applications of genetically engineered HSV mutants using different strategies and also allowed the development of potential therapeutic agents and vectors for human

Hypoxic Ischemic Encephalopathy is a serious brain injury that results from an inadequate flow of oxygenated blood to an infant’s brain. It is most common in full-term infants.

Neonatal hypoxia-ischemia (HI) is a major cause of mortality and morbidity in infants and children. The most important consequences of neonatal HI is epilepsy. Epilepsy is a common neurodegenerative disorder characterized by recurrent of unprovoked seizures due to hyperexcitability and hypersynchrony of neuronal activity. Recent studies uncovered important molecular and cellular aspects of HI brain injury that may provide therapeutic target for intervening in the epileptogenesis in the developing brain. In our experiment approaches, we administrate RAGE antagonist to protect brain tissue from the effect of HI induced and inhibit apoptotic pathway and downstream products, including IL-6. Most importantly, the specific interaction between S100B