- Neonatal and fetal brain pathology
- Neonatal Respiratory Health Research
- Neuroscience of respiration and sleep
- Anesthesia and Neurotoxicity Research
- Traumatic Brain Injury and Neurovascular Disturbances
- Fetal and Pediatric Neurological Disorders
- Cardiac Arrest and Resuscitation
- Neuroscience and Neuropharmacology Research
- Immune Response and Inflammation
- Mitochondrial Function and Pathology
- Birth, Development, and Health
- Advanced Neuroimaging Techniques and Applications
- Infant Development and Preterm Care
- Neurogenesis and neuroplasticity mechanisms
- Neuroendocrine regulation and behavior
- Congenital Diaphragmatic Hernia Studies
- Neuroinflammation and Neurodegeneration Mechanisms
- Thermal Regulation in Medicine
- Hyperglycemia and glycemic control in critically ill and hospitalized patients
- Neonatal Health and Biochemistry
- Infant Nutrition and Health
- Dialysis and Renal Disease Management
- Cell death mechanisms and regulation
- Intensive Care Unit Cognitive Disorders
- Pediatric health and respiratory diseases
Johns Hopkins Medicine
2016-2025
Johns Hopkins University
2016-2025
Karolinska Institutet
2024
Nationwide Children's Hospital
2024
Centre Hospitalier Universitaire Sainte-Justine
2024
Université de Montréal
2024
University Hospital of Bern
2023
Johns Hopkins Hospital
2010-2022
RELX Group (United States)
2022
Academic Pediatric Association
2022
Perinatal hypoxic-ischemic encephalopathy (HIE) is a significant cause of mortality and morbidity in infants young children. Therapeutic opportunities are very limited for neonatal pediatric HIE. Specific neural systems populations cells selectively vulnerable HIE; however, the mechanisms degeneration unresolved. These involve oxidative stress, excitotoxicity, inflammation, activation several different cell death pathways. Decades ago structural mechanistic basis cellular HIE was thought to...
We performed a cross-sectional study to determine the epidemiology of Cryptosporidium in human immunodeficiency virus (HIV)—infected persons at 3 diagnostic levels: microscopy, genotypes Cryptosporidium, and subtype families C. hominis parvum. The enrolled 2490 HIV-infected Lima, Peru, 230 were microscopy positive for infection. Specimens from 193 participants available genotyping. They had (141 persons), parvum (22 meleagridis (17 canis (6 felis suis (1 person) Although results showed that...
Necrostatin-1 inhibits receptor-interacting protein (RIP)-1 kinase and programmed necrosis is neuroprotective in adult rodent models. Owing to the prominence of continuum cell death neonatal hypoxia-ischemia (HI), we tested whether necrostatin was developing brain. Postnatal day (P)7 mice were exposed HI injected intracerebroventricularly with 0.1 μL 80 μmol necrostatin, Nec-1, 5-(1H-Indol-3-ylmethyl)-(2-thio-3-methyl) hydantoin, or vehicle. Necrostatin significantly decreased injury...
To determine if oral clonidine would reduce the duration of opioid detoxification for neonatal abstinence syndrome.Infants with intrauterine exposure to methadone or heroin and syndrome (2 consecutive modified Finnegan scores > =9) were enrolled at 2 hospitals during 2002-2005 followed until final hospital discharge. All infants (80) received diluted tincture opium according a standardized algorithm randomly assigned receive (1 microg/kg every 4 hours) (40 infants) placebo infants). Primary...
Susceptibility and progression of brain injury in the newborn is closely associated with an exacerbated innate immune response, but underlying mechanisms are often unclear. Toll-like receptors (TLRs) important sensors that may influence vulnerability developing brain. In current study, we provide novel data to show activation viral receptor TLR-3 sensitizes neonatal subsequent hypoxic–ischemic (HI) damage. Poly inosinic:poly cytidylic acid (Poly I:C), a synthetic ligand for TLR-3, was...
Neurodevelopmental disabilities persist in survivors of neonatal hypoxic-ischemic encephalopathy (HIE) despite treatment with therapeutic hypothermia. Cerebrovascular autoregulation, the mechanism that maintains cerebral perfusion during changes blood pressure, may influence outcomes. Our objective was to describe relationship between acute autoregulatory vasoreactivity and neurodevelopmental outcomes at 2 years age. In a pilot study 28 neonates HIE, we measured hemoglobin volume index (HVx)...
Background: Therapeutic hypothermia provides incomplete neuroprotection for neonatal hypoxic-ischemic encephalopathy (HIE). We examined whether hemodynamic goals that support autoregulation are associated with decreased brain injury and these relationships affected by birth asphyxia or vary anatomic region. Methods: Neonates cooled HIE received near-infrared spectroscopy monitoring to identify the mean arterial blood pressure optimized autoregulatory function (MAPOPT). Blood deviation from...
We studied microsporidiosis in human immunodeficiency virus-positive patients 2 Lima hospitals. Of 2652 patients, 66% were male, 6% received antiretroviral therapy (ART), and the median CD4 lymphocyte count was 131 cells/microL. Sixty-seven (3%) had microsporidiosis; stool specimens from 56 identified as having Enterocytozoon bieneusi of 10 different genotypes. The most common genotypes, Peru-1 Peru-2, not associated with significant increases chronic diarrhea; other genotypes a 4-fold...
Abstract The endoplasmic reticulum (ER) is tasked, among many other functions, with preventing excitotoxicity from killing neurons following neonatal hypoxia‐ischemia (HI). With the search for delayed therapies to treat HI, study of ER responses becomes relevant. We hypothesized that stress a prominent feature neuronal death via programmed necrosis after HI. Since necrostatin‐1 (Nec‐1), an inhibitor necrosis, provides neuroprotection against HI in male mice, Nec‐1 ideal tool responses. C57B6...
Therapeutic hypothermia is standard of care for infants with hypoxic ischemic encephalopathy. Murine models hypoxic-ischemic injury exist; however, a well-established mouse model therapeutic following lacking. The goal this study was to develop full-term-equivalent murine after hypoxia-ischemia and examine magnetic resonance imaging, behavior, histology in region sex specific manner. Hypoxic-ischemic induced at postnatal day 10 C57BL6 mice using modified Vannucci model. Mice were randomized...
Despite the introduction of therapeutic hypothermia, neonatal hypoxic ischemic (HI) brain injury remains a common cause developmental disability. Development rational adjuvant therapies to hypothermia requires understanding pathways cell death and survival modulated by HI. The conceptualization apoptosis-necrosis “continuum” in predicts mechanistic interactions between hydrid forms such as programmed or regulated necrosis. Many components signaling pathway regulating necrosis have been...
Delayed hippocampal injury and memory impairments follow neonatal hypoxia-ischemia (HI) despite the use of therapeutic hypothermia (TH). Death pyramidal cells occurs acutely after HI, but characterization delayed cell death interneurons (INs) is unknown. We hypothesize that INs HI is: (i) asynchronous to cells, (ii) independent severity, (iii) unresponsive TH. was induced in C57BL6 mice at p10 with unilateral right carotid ligation 45 min hypoxia (FiO2 = 0.08). Mice were randomized...
<b><i>Background:</i></b> Despite treatment with therapeutic hypothermia (TH), infants who survive hypoxic ischemic (HI) encephalopathy (HIE) have persistent neurological abnormalities at school age. Protection by TH against HI brain injury is variable in both humans and animal models. Our current preclinical model of hypoxia-ischemia displays this variability outcomes neuropathological neuroimaging end points some sexual dimorphism. The detailed behavioral phenotype...