Can early hyperglycemia affect the morbidity/mortality of very low birth weight premature infants?

BACKGROUND: The study aimed to examine the effect of early hyperglycemia on the morbidity/mortality of very low birth weight premature infants. METHODS: This retrospective study included all premature infants with gestational age ≤32 gestational weeks, hospitalized at the Department of Intensive Neonatal Care, Clinical Center Kragujevac, during the period 2017-2019. Hyperglycemia was defined as glycemia of ≥12 mmol/l in one measurement, or > 10 mmol/l in two measurements, at repeated intervals of 2-4 hours. Glycemia was determined from capillary blood, using a gas analyzer of Gem Premier 3000, during the first 7 days of life. Continuous intravenous insulin infusion was administered after ineffective glucose restriction at glycemic values of > 14 mmol/l. RESULTS: Patients with normoglycemia (41/72 (56.94%)) and hyperglycemia (31/72 (43.06%)) did not differ in gender, gestational age, mode of delivery and antenatal administration of steroids, while birth weight had a tendency to be lower in the hyperglycemic group (p=0.052). Hyperglycemia was significantly associated with a low APGAR score at the fifth minute (p=0.048), necrotizing enterocolitis (p=0.011), and shorter duration of mechanical ventilation (p=0.006). Hyperglycemia was associated with significantly more frequent fatal outcomes (35.5%) when compared with the normoglycemic group (4.9%). Accordingly, these patients required inotropic (r=0.036) and insulin therapy (r < 0.001) more often. Retinopathy of prematurity, bronchopulmonary dysplasia and sepsis did not correlate with hyperglycemia in our study. Intraventricular hemorrhage of the first degree was more often associated with normoglycemia in premature infants on prolonged mechanical ventilation while more severe intracranial hemorrhage was more common in the hyperglycemic group but did not result in statistical significance due to the small number of patients. CONCLUSIONS: Monitoring glucose levels in the blood of very low birth weight premature infants is clinically important because abnormalities in glucose homeostasis can have serious short-term and long-term consequences.

Maternal Deprivation in Rats Decreases the Expression of Interneuron Markers in the Neocortex and Hippocampus.

Early life stress has profound effects on the development of the central nervous system. We exposed 9-day-old rat pups to a 24 h maternal deprivation (MD) and sacrificed them as young adults (60-day-old), with the aim to study the effects of early stress on forebrain circuitry. We estimated numbers of various immunohistochemically defined interneuron subpopulations in several neocortical regions and in the hippocampus. MD rats showed reduced numbers of parvalbumin-expressing interneurons in the CA1 region of the hippocampus and in the prefrontal cortex, compared with controls. Numbers of reelin-expressing and calretinin-expressing interneurons were also reduced in the CA1 and CA3 hippocampal areas, but unaltered in the neocortex of MD rats. The number of calbinin-expressing interneurons in the neocortex was similar in the MD rats compared with controls. We analyzed cell death in 15-day-old rats after MD and found no difference compared to control rats. Thus, our results more likely reflect the downregulation of markers than the actual loss of interneurons. To investigate synaptic activity in the hippocampus we immunostained for glutamatergic and inhibitory vesicular transporters. The number of inhibitory synapses was decreased in the CA1 and CA3 regions of the hippocampus in MD rats, with the normal number of excitatory synapses. Our results indicate complex, cell type-specific, and region-specific alterations in the inhibitory circuitry induced by maternal deprivation. Such alterations may underlie symptoms of MD at the behavioral level and possibly contribute to mechanisms by which early life stress causes neuropsychiatric disorders, such as schizophrenia.

Pharmacology of repair after peripheral nerve injury.

Peripheral nerve injuries are common and present with a broad spectrum of symptoms, some of which may be the cause of life-long disabilities. The peripheral nerves show a far greater capacity for regeneration than those in the central nervous system, and the process of nerve regeneration resembles developmental processes to a certain degree. The regeneration of peripheral nerves does not always lead to a full functional recovery. That is why surgical methods are still the most reliable therapeutic options after injuries of peripheral nerves. However, there is an array of potential pharmacological options that could enhance the repair processes after surgery. This review gives a summary of the recent literature relevant to different classes of pharmacologically active substances that are used either as supplements or off-label as potential enhancers of peripheral nerve repair. Antioxidants, vitamins, calcium channel blockers, immunosuppressive drugs, growth factors, and neuroactive glycans are among the most researched in this field. More research is necessary to understand their mechanisms of action at the cellular and molecular level, and randomized clinical trials in order to establish their efficacy and safety, as well as possible synergistic or adverse interactions among them.