Publications by authors named "John Kuluz"

21 Publications

  • Page 1 of 1

Is It Possible That IV Immunoglobulin Does Not Improve Outcome in Children With Guillain-Barré Syndrome? Answer: Yes.

Authors:
John W Kuluz

Pediatr Crit Care Med 2019 07;20(7):681-682

Department of Pediatric Neurosurgery, Nicklaus Children's Hospital, Miami, FL.

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http://dx.doi.org/10.1097/PCC.0000000000001965DOI Listing
July 2019

Posttraumatic Seizures in Children with Severe Traumatic Brain Injury.

Authors:
John Kuluz

Pediatr Crit Care Med 2017 01;18(1):87-88

Pediatric Brain Injury Program Nicklaus Children's Hospital Miami, FL.

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http://dx.doi.org/10.1097/PCC.0000000000000968DOI Listing
January 2017

Emergency Neurologic Life Support: Spinal Cord Compression.

Neurocrit Care 2015 Dec;23 Suppl 2:S129-35

Division of Neurosurgery, Nicklaus Children's Hospital, Miami, FL, USA.

There are many causes of acute myelopathy including multiple sclerosis, systemic disease (SD), and acute spinal cord compression (SCC). SCC should be among the first potential causes considered given the significant permanent loss of neurologic function commonly associated with SCC. This impairment can occur over a short period of time, and may be avoided through rapid and acute surgical intervention. Patients with SCC typically present with a combination of motor and sensory dysfunction that has a distribution referable to a spinal level. Bowel and bladder dysfunction and neck or back pain may also be part of the clinical presentation, but are not uniformly present. Because interventions are critically time-sensitive, the recognition and treatment of SCC was chosen as an ENLS protocol.
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http://dx.doi.org/10.1007/s12028-015-0166-1DOI Listing
December 2015

Acute changes in systemic hemodynamics and serum vasopressin after complete cervical spinal cord injury in piglets.

Neurocrit Care 2010 Aug;13(1):132-40

Saint Louis University School of Medicine, Saint Louis, MO, USA.

Background: Spinal cord injury (SCI) produces acute hemodynamic alterations through disruption of sympathetic output of the autonomic nervous system and places individuals with SCI at high risk of secondary ischemic insult to the spinal cord as well as to other organs. The purpose of this study was to examine hemodynamics and serum vasopressin concentration in the acute period following complete cervical SCI in piglets.

Methods: We developed a new model of traumatic complete cervical SCI in piglets and measured acute hemodynamic variables and serum arginine vasopressin (AVP) concentrations at baseline and for 4 h after SCI under fentanyl anesthesia.

Results: Complete cervical SCI caused an immediate tachycardia which lasted for approximately 1 h, immediate hypotension which was sustained for the 4-h duration of the study, decreases in both systemic and pulmonary vascular resistance, and a compensatory increase in cardiac output, which resulted initially from an increase in heart rate (HR) but was later sustained after resolution of tachycardia by an increase in cardiac stroke volume. Serum AVP concentration increased significantly after SCI and did not change in the control group. Neurogenic shock did not occur due to the robust increase in cardiac output and cardiac stroke volume.

Conclusions: Complete cervical SCI produces hemodynamic alterations consistent with the withdrawal of sympathetic tone. Although mean arterial pressure (MAP) decreased significantly after SCI, the increase in serum vasopressin may have played a role in maintaining blood pressure and preventing circulatory collapse, a complication which is encountered frequently in patients with cervical and upper thoracic SCI.
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http://dx.doi.org/10.1007/s12028-010-9364-zDOI Listing
August 2010

Safety and pharmacokinetic analysis of methotrexate administered directly into the fourth ventricle in a piglet model.

J Neurooncol 2010 Dec 4;100(3):397-406. Epub 2010 May 4.

Department of Neurological Surgery, University of Miami Miller School of Medicine, and Miami Children's Hospital, Miami, FL 33155, USA.

We have developed a piglet model to assess chemotherapy administration directly into the fourth ventricle as a potential treatment for medulloblastoma and other malignant posterior fossa tumors. The objective of this study was to assess safety and pharmacokinetics after methotrexate infusions into the fourth ventricle. Catheters were inserted into the fourth ventricle and lumbar cistern in five piglets. Two milligrams of Methotrexate (MTX) was infused into the fourth ventricle on five consecutive days. Safety was assessed by neurological examination, 4.7 T MRI, and post-mortem pathological analysis. MTX levels in serum and cerebrospinal fluid (CSF) were measured, and area under the concentration-time curve (AUC) was calculated for CSF samples. No neurological deficits were caused by MTX infusions. One piglet died from complications of anesthesia induction for MRI scanning. MRI scans showed accurate catheter placement without signal changes in the brainstem or cerebellum. One piglet had asymptomatic ventriculomegaly. Pathological analysis demonstrated meningitis and choroid plexitis consisting predominantly of CD-3 positive T-lymphocytes in all piglets and a small focal area of subependymal necrosis in one. In all piglets, mean peak MTX level in fourth ventricular CSF exceeded that in lumbar CSF by greater than five-fold. Serum MTX levels were undetectable or negligible. Statistically significant differences between fourth ventricle and lumbar AUC were detected at peaks (P = 0.01) and at all collection time points (P = 0.01) but not at troughs (P = 0.36). MTX can be infused into the fourth ventricle without clinical or radiographic evidence of damage. An inflammatory response without clinical correlate is observed. Significantly higher peak MTX levels are observed in the fourth ventricle than in the lumbar cistern.
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http://dx.doi.org/10.1007/s11060-010-0210-0DOI Listing
December 2010

Pediatric spinal cord injury in infant piglets: description of a new large animal model and review of the literature.

J Spinal Cord Med 2010 ;33(1):43-57

Pediatric Critical Care (R-131), University of Miami School of Medicine, 1611 NW 12th Avenue, Miami, FL 33136, USA.

Objective: To develop a new, clinically relevant large animal model of pediatric spinal cord injury (SCI) and compare the clinical and experimental features of pediatric SCI.

Methods: Infant piglets (3-5 weeks old) underwent contusive SCI by controlled cortical impactor at T7. Severe complete SCI was induced in 6 piglets, defined as SCI with no spontaneous return of sensorimotor function. Eight piglets received incomplete SCI, which was followed by partial recovery. Somatosensory evoked potentials, magnetic resonance imaging, neurobehavioral function, and histopathology were measured during a 28-day survival period.

Results: Mean SCI volume (defined as volume of necrotic tissue) was larger after complete compared with incomplete SCI (387 +/- 29 vs 77 +/- 38 mm3, respectively, P < 0.001). No functional recovery occurred after complete SCI. After incomplete SCI, piglets initially had an absence of lower extremity sensorimotor function, urinary and stool retention, and little to no rectal tone. Sensory responses recovered first (1-2 days after injury), followed by spontaneous voiding, lower extremity motor responses, regular bowel movements, and repetitive flexion-extension of the lower extremities when crawling. No piglet recovered spontaneous walking, although 4 of 8 animals with incomplete injuries were able to bear weight by 28 days. In vivo magnetic resonance imaging was performed safely, yielded high-resolution images of tissue injury, and correlated closely with injury volume seen on histopathology, which included intramedullary hemorrhage, cellular inflammation, necrosis, and apoptosis.

Conclusion: Piglets performed well as a reproducible model of traumatic pediatric SCI in a large animal with chronic survival and utilizing multiple outcome measures, including evoked potentials, magnetic resonance imaging, functional outcome scores, and histopathology.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2853328PMC
http://dx.doi.org/10.1080/10790268.2010.11689673DOI Listing
May 2010

Pharmacokinetic analysis of etoposide distribution after administration directly into the fourth ventricle in a piglet model.

J Neurooncol 2010 Mar 18;97(1):25-32. Epub 2009 Aug 18.

Department of Neurological Surgery, University of Miami Miller School of Medicine and Miami Children's Hospital, Ambulatory Care Building Suite 3109, Miami, FL 33155, USA.

We hypothesize that infusion of chemotherapeutic agents directly into the fourth ventricle potentially may play a role in treating malignant posterior fossa brain tumors. Accordingly, we used a piglet model developed in our laboratory to test the safety of etoposide infusions into the fourth ventricle and to study the pharmacokinetics associated with these infusions. In 5 piglets, closed-tip silicone catheters were inserted into the fourth ventricle and lumbar cistern. Five consecutive daily infusions of etoposide (0.5 mg) were administered via the fourth ventricle catheter. Serum and CSF from both catheters were sampled for measurement of etoposide level by reversed-phase high performance liquid chromatography (HPLC). For CSF samples, area under the concentration-time curve (AUC) was calculated. Piglets underwent daily neurological examinations, a 4.7 Tesla MRI scan, and then were sacrificed for post-mortem brain examination. No neurological deficits or signs of meningitis were caused by intraventricular chemotherapy infusions. MRI scans showed catheter placement within the fourth ventricle but no signal changes in the brain stem or cerebellum. In all piglets, the mean fourth ventricular CSF peak etoposide level exceeded the mean peak lumbar etoposide levels by greater than 10-fold. Statistically significant differences between fourth ventricle and lumbar AUC were noted at peaks (DeltaAUC = 3384196 ng h/ml with 95%CI: 1758625, 5009767, P = 0.0044) and at all collection time points (DeltaAUC = 1422977 ng h/ml with 95%CI: 732188, 2113766, P = 0.0046) but not at troughs (DeltaAUC = -29546 ng h/ml (95%CI: -147526, 88434.2, P = 0.5251). Serum etoposide was absent at two and four hours after intraventricular infusions in all animals. Pathological analysis demonstrated meningitis, choroid plexitis, and ependymitis in the fourth and occasionally lateral ventricles. Etoposide can be infused directly into the fourth ventricle without clinical or radiographic evidence of damage. Autopsy examination revealed ventriculitis and meningitis which did not have a clinical correlate. Etoposide does not distribute evenly throughout CSF spaces after administration into the fourth ventricle, and higher peak CSF levels are observed in the fourth ventricle than in the lumbar cistern.
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http://dx.doi.org/10.1007/s11060-009-9998-xDOI Listing
March 2010

Traumatic injury activates MAP kinases in astrocytes: mechanisms of hypothermia and hyperthermia.

J Neurotrauma 2009 Sep;26(9):1535-45

Department of Pediatrics, University of Miami, Miller School of Medicine, Miami, Florida, USA.

Hyperthermia is common following traumatic brain injury (TBI) and has been associated with poor neurologic outcome, and hypothermia has emerged as a potentially effective therapy for TBI, although its mechanism is still unclear. In this study we investigated the effects of temperature modulations on astrocyte survival following traumatic injury and the involved MAPK pathways. Trauma was produced by scratch injury of a monolayer of confluent astrocytes in culture, followed by incubation at hypothermia (308 degree C), normothermia (378 degree C), or hyperthermia (398 degree C). The activation of MAPK pathways including extracellular signal-regulated protein kinase (ERK), c-Jun NH(2)-terminal kinase ( JNK), and p38 MAPK were measured at 0, 15, 30, 60, and 120 min after traumatic injury followed by temperature modulation. Apoptosis of astrocytes was assessed by quantitation of cleaved caspase-3 expression 24 h after injury. Our findings showed that only JNK activation at 15 min after trauma was reduced by hypothermia, and this was associated with a marked reduction in apoptosis. Hyperthermia activated both ERK and JNK and increased apoptosis. The specific JNK inhibitor, SP60025, markedly reduced JNK-induced apoptosis at normothermia and hyperthermia, and showed a dose-dependent effect. In conclusion, the JNK pathway appears to mediate traumatic injury-induced apoptosis in astrocytes. Prolonged hyperthermia as a secondary insult worsens apoptosis by increasing JNK activation. Hypothermia protects against traumatic injury via early suppression on JNK activation and subsequent prevention of apoptosis. Manipulation of the JNK pathway in astrocytes may represent a therapeutic target for ameliorating the devastating progression of tissue injury and cell death after TBI.
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http://dx.doi.org/10.1089/neu.2008.0743DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6468954PMC
September 2009

Postreceptor crosstalk on PI3K/Akt between GH and insulin in non-catch-up growth rats born small for gestational age.

Horm Res 2008 21;70(1):29-35. Epub 2008 May 21.

Department of Pediatrics, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, China.

Background/aims: Children born small for gestational age (SGA) are at increased risk for short stature and type 2 diabetes mellitus as a result of growth hormone (GH) resistance and insulin resistance. The mechanisms of multiple hormone resistance remain unclear. This study was designed to investigate the relationship between GH resistance and insulin resistance in non-catch-up growth (NCU-SGA) rats, and how their signaling pathways are related based on their crosstalk on the insulin receptor substrate-1 phosphatidylinositol 3'-kinase (IRS-1-PI3K) pathway.

Methods: NCU-SGA rat model was developed by restricting prenatal food intake in pregnant dams. Activated levels of IRS-1 and Akt in liver protein extracts were compared between NCU-SGA and age- and sex-matched controls born appropriate for gestational age rats at baseline, after insulin stimulation, and after pretreatment with AG490 (GH-JAK2 pathway inhibitor) followed by insulin stimulation.

Results: GH secretion was positively related to markedly increased insulin levels in NCU-SGA rats. There was no difference of IRS-1 phosphorylation in response to insulin between two groups, however, insulin-stimulated Akt phosphorylation was attenuated in NCU-SGA rats compared to appropriate for gestational age rats. Pretreatment with AG490 restored the Akt response to insulin demonstrated by significantly increased Akt phosphorylation.

Conclusion: GH plays a role in inducing insulin resistance via signaling crosstalk with insulin at the level of PI3K/Akt in NCU-SGA rats.
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http://dx.doi.org/10.1159/000129675DOI Listing
August 2008

Chemotherapy administration directly into the fourth ventricle in a new piglet model. Laboratory Investigation.

J Neurosurg Pediatr 2008 May;1(5):373-80

Department of Neurological Surgery, University of Miami Miller School of Medicine and Miami Children's Hospital, Miami, Florida 33155, USA.

Object: The authors hypothesized that chemotherapy infusions directly into the fourth ventricle may potentially play a role in treating malignant posterior fossa tumors. In this study the safety and pharmacokinetics of etoposide administration into the fourth ventricle was tested using an indwelling catheter in piglets.

Methods: A closed-tip silicone lumbar drain catheter was inserted into the fourth ventricle via a posterior fossa craniectomy and 5 daily infusions of etoposide (0.5 mg in 5 animals) or normal saline (in 2 animals) were instilled. Piglets (10-18 kg, 2-3 months of age) underwent daily neurological examinations and 4.7-T magnetic resonance (MR) imaging after the final infusion and were then killed for postmortem examination. Pharmacokinetics were studied using reversed-phase high-performance liquid chromatography on cerebrospinal fluid (CSF) samples at 0.25, 1, 2, 4, 8, 12, and 24 hours after etoposide infusion. Peak and trough CSF etoposide levels were measured for each subsequent infusion. Serum etoposide levels were obtained at 2 and 4 hours after infusion.

Results: All piglets remained neurologically intact, and MR images demonstrated catheter placement within the fourth ventricle without signal changes in the brainstem or cerebellum. Serum etoposide was absent at 2 and 4 hours after intraventricular infusions. When adequate samples could be obtained for analysis, CSF etoposide levels peaked 15 minutes after infusion and progressively decreased. Cytotoxic levels (> 0.1 microg/ml) were maintained for 5 consecutive peak and trough measurements with 1 exception. Etoposide-related neuropathology included moderate-to-severe T-lymphocytic meningitis and fourth and lateral ventricular choroid plexitis with associated subependymal inflammation.

Conclusions: Etoposide can be infused directly into the fourth ventricle without clinical or imaging evidence of damage. Cytotoxic CSF etoposide levels can be maintained for 24 hours with a single daily infusion into the fourth ventricle using an indwelling catheter. Intraventricular etoposide elicits an inflammatory response, the long-term effects of which are as yet undetermined.
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http://dx.doi.org/10.3171/PED/2008/1/5/373DOI Listing
May 2008

Post traumatic brain perfusion SPECT analysis using reconstructed ROI maps of radioactive microsphere derived cerebral blood flow and statistical parametric mapping.

BMC Med Imaging 2008 Feb 29;8. Epub 2008 Feb 29.

Department of Biomedical Engineering, Florida International University, 10555 West Flagler Street, EC 2671, Miami, FL 33199, USA.

Background: Assessment of cerebral blood flow (CBF) by SPECT could be important in the management of patients with severe traumatic brain injury (TBI) because changes in regional CBF can affect outcome by promoting edema formation and intracranial pressure elevation (with cerebral hyperemia), or by causing secondary ischemic injury including post-traumatic stroke. The purpose of this study was to establish an improved method for evaluating regional CBF changes after TBI in piglets.

Methods: The focal effects of moderate traumatic brain injury (TBI) on cerebral blood flow (CBF) by SPECT cerebral blood perfusion (CBP) imaging in an animal model were investigated by parallelized statistical techniques. Regional CBF was measured by radioactive microspheres and by SPECT 2 hours after injury in sham-operated piglets versus those receiving severe TBI by fluid-percussion injury to the left parietal lobe. Qualitative SPECT CBP accuracy was assessed against reference radioactive microsphere regional CBF measurements by map reconstruction, registration and smoothing. Cerebral hypoperfusion in the test group was identified at the voxel level using statistical parametric mapping (SPM).

Results: A significant area of hypoperfusion (P < 0.01) was found as a response to the TBI. Statistical mapping of the reference microsphere CBF data confirms a focal decrease found with SPECT and SPM.

Conclusion: The suitability of SPM for application to the experimental model and ability to provide insight into CBF changes in response to traumatic injury was validated by the SPECT SPM result of a decrease in CBP at the left parietal region injury area of the test group. Further study and correlation of this characteristic lesion with long-term outcomes and auxiliary diagnostic modalities is critical to developing more effective critical care treatment guidelines and automated medical imaging processing techniques.
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http://dx.doi.org/10.1186/1471-2342-8-4DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2311288PMC
February 2008

Neuron-like differentiation of adipose-derived stem cells from infant piglets in vitro.

J Spinal Cord Med 2007 ;30 Suppl 1:S35-40

University of Miami School of Medicine, Miami, Florida, USA.

Background/objective: Adipose-derived stem cells (ADSCs) are mesenchymal stem cells (MSCs) that can be extracted from adipose tissue and obtained by a less invasive method and in larger quantities compared with bone marrow-derived MSCs. The objective of this study was to harvest ADSCs from piglets and to explore their neuronal differentiation potential.

Methods: Adipose tissue from piglet facial or abdominal fat was digested with collagenase type XI, followed by filter and centrifugation; the isolated adipose stromal cells were cultured in dishes. MSC markers were measured by flow cytometry; 2 to 5 passage cells were used for in vitro differentiation. Adipogenic, chondrogenic, osteogenic, and neuronal differentiation was induced by incubation of the ADSCs with different induction media.

Results: ADSCs were easily expanded to beyond 15 passages, maintaining the undifferentiated state and exhibiting MSC characteristics and markers CD29, CD44, and CD90. ADSCs differentiated into other mesodermal cells including adipocytes, chondrocytes, and osteocytes. These cells were induced to differentiate into neuron-like cells as evidenced by neuronal morphology and the presence of neuronal markers including microtubule-associated protein 2, neuronal nuclear antigen, and beta-tubulin III.

Conclusions: ADSCs can be readily obtained from a small amount fat tissue and expanded in culture. Adipose tissue may be an alternative source of stem cell therapy for nervous system injury.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2031970PMC
http://dx.doi.org/10.1080/10790268.2007.11753967DOI Listing
October 2007

New pediatric model of ischemic stroke in infant piglets by photothrombosis: acute changes in cerebral blood flow, microvasculature, and early histopathology.

Stroke 2007 Jun 26;38(6):1932-7. Epub 2007 Apr 26.

Department of Pediatrics, University of Miami School of Medicine, Miami, Florida, USA.

Background And Purpose: The etiology and pathophysiology of acute ischemic stroke in children differ greatly from those in adults. The purpose of this study was to establish a new pediatric model of ischemic stroke in infant piglets for use in future studies of the response of the developing brain to focal ischemic injury.

Methods: Ischemic stroke was produced in male infant piglets (2 to 4 weeks old) by photothrombotic occlusion of the middle cerebral artery. Regional cerebral blood flow was measured with radiolabeled microspheres up to 4 hours after occlusion. Early histopathology, including caspase-3 immunohistochemistry for apoptosis, was examined 4 hours after ischemia. The nature of the thrombus and its interaction with vascular endothelium were assessed by electron microscopy.

Results: Severe ischemia (0 to 15 mL/100 g per min) occurred rapidly in 1.4+/-0.2 g of tissue at 15 minutes and increased to 2.4+/-0.7 g at 4 hours. Similarly, moderate ischemia (16 to 30 mL/100 g per min) was measured in 1.2+/-0.3 g of tissue at 15 minutes and increased to 2.0+/-0.6 g at 4 hours. These regional cerebral blood flow values represent ischemic levels of blood flow in 20% to 25% of the volume of the ischemic hemisphere at 4 hours after ischemia. Ischemic infarction occurred in both gray and white matter, and cerebral microvessels in the ischemic hemisphere contained large numbers of inflammatory leukocytes. Caspase-3-positive cells were few in number and were found in the periphery of the infarct; cell death appeared to occur primarily by necrosis rather than apoptosis at 4 hours. Electron microscopy revealed a pure platelet thrombus firmly attached to the vascular endothelium, which in some areas appeared to be detached from the basement membrane.

Conclusions: Ischemic stroke can be produced in infant piglets by middle cerebral artery photothrombosis. The stroke involved both gray and white matter and exhibited a robust inflammatory component. The mean infarct volume determined histopathologically amounted to 9.6+/-2.4% of the affected (ipsilateral) hemisphere, which was correlated well with the mass equivalent of tissue (12.0+/-3.5%), in which severe declines in regional cerebral blood flow were observed at 4 hours.
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http://dx.doi.org/10.1161/STROKEAHA.106.475244DOI Listing
June 2007

Snoezelen: a controlled multi-sensory stimulation therapy for children recovering from severe brain injury.

Brain Inj 2006 Jul;20(8):879-88

DeWitt Daughtry Family Department of Surgery, Division of Trauma and Surgical Critical Care, Ryder Trauma Center, Miami, FL 33136, USA.

Objective: To investigate the effects of Snoezelen therapy on physiological, cognitive and behavioural changes in children recovering from severe traumatic brain injury (TBI).

Methods: An observational study was conducted to assess the physiological, cognitive and behavioural changes of children recovering from severe TBI while receiving Snoezelen therapy. Fifteen subjects completed the pre- and post-Snoezelen treatment measurements computed over 10 consecutive sessions. Physiological, cognitive and behavioural measures were administered. Data was collected prospectively on each session in the Snoezelen room and were analysed by calculating the difference between pre- and post-treatment measurements for each Snoezelen session.

Results: Results revealed significant changes on physiological measures. Heart rates decreased for each subject in each treatment session and were found to be significant (p = 0.032). Muscle tone was decreased in all the affected extremities (right upper extremity p = 0.009, left upper extremity p = 0.020, right lower extremity p = 0.036 and left lower extremity p = 0.018). Agitation levels decreased over time and the overall cognitive outcome measures showed significant improvement when comparing the beginning of treatment with the end.

Conclusion: This study revealed a beneficial use of Snoezelen therapy with children recovering from severe brain injury. However, there continues to be a critical need for evidenced-based research for this patient population and others in this multi-sensory environment.
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http://dx.doi.org/10.1080/02699050600832635DOI Listing
July 2006

Parents' reactions at 24-48 hrs after a preschool child's head injury.

Pediatr Crit Care Med 2005 Sep;6(5):550-6

School of Nursing, Florida International University, USA.

Objectives: Our objectives were, first, to compare mothers' and fathers' early reactions (stressors, concerns) to the preschool child's head injury, their perceptions of the child's injury severity, and their social support and mental health; second, to compare families with a child in the pediatric intensive care unit (PICU) vs. general care unit (GCU) on these variables; and third, to describe the relationships between parents' early reactions and perceived and objective injury severity, their social support, and mental health.

Design: Analysis of data collected in the hospital 24-48 hrs after the child's admission as part of a longitudinal study of parent and family functioning after a preschool child's head injury.

Setting: Seven tertiary care centers: three free-standing children's hospitals and four comprehensive hospitals.

Participants: Participants were 182 mothers and 64 fathers of 183 preschool children (ages 3-6) hospitalized for head injury, half in a PICU.

Interventions: Data collection.

Measurements And Main Results: We measured parents' early reactions (stressors, concerns), influenced by parent mental health, social support, and objective and perceived injury severity. Mothers reported more stress than fathers regarding the child's behavior and emotions, communication with staff, and their parental role. Mothers in the PICU group reported more concern about the child's future and more stress regarding the child's appearance, sights and sounds of the unit, and procedures done to the child than mothers in the GCU group. Fathers in the PICU and GCU groups reported similar levels of stress and concern. Mothers' reactions were influenced by objective and perceived injury severity, social support, and psychological distress. Fathers' reactions were influenced by objective injury severity and psychological distress.

Conclusions: Although mother-father couples rated their child's injury severity similarly, mothers experienced more stress than fathers. Social support decreased the stress for mothers but not for fathers. The experience of pediatric head trauma was more stressful for mothers of children in the PICU than mothers of children in the GCU.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2614927PMC
http://dx.doi.org/10.1097/01.pcc.0000163283.27419.e9DOI Listing
September 2005

Computer phantom study of brain PET glucose metabolism imaging using a rotating SPECT/PET camera.

Comput Biol Med 2005 Jul;35(6):511-31

Department of Biomedical Engineering, Florida International University, EAS 3405, 10555 West Flagler Street, EC 2671, Miami, FL 33199, USA.

Positron emission tomography (PET) with [18F] fluoro-deoxy-glucose (FDG) provides information about glucose metabolism and is used to measure tissue glucose kinetics in the brain. The recent interest in hybrid SPECT/PET systems emerged as a practical approach to reduce the high cost of purchasing a dedicated ring-detector PET system. We have implemented interpolation methods for processing the projection data that could potentially reduce artifacts when reconstructing a dynamic imaging sequence in a PET study from a dual-head rotating SPECT/PET system. The computer simulations predict that parameter estimates from the dedicated PET system will be superior to results using the rotating camera system. However, the rotating camera system using projection interpolation may approach the accuracy of the dedicated PET system if the data noise is below 20%.
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http://dx.doi.org/10.1016/j.compbiomed.2004.03.005DOI Listing
July 2005

Alterations of CaMKII after hypoxia-ischemia during brain development.

J Neurochem 2004 Oct;91(2):429-37

Department of Neurology, University of Miami School of Medicine, Miami, Florida 33136, USA.

Transient brain hypoxia-ischemia (HI) in neonates leads to delayed neuronal death and long-term neurological deficits. However, the underlying mechanisms are incompletely understood. Calcium-calmodulin-dependent protein kinase II (CaMKII) is one of the most abundant protein kinases in neurons and plays crucial roles in synaptic development and plasticity. This study used a neonatal brain HI model to investigate whether and how CaMKII was altered after HI and how the changes were affected by brain development. Expression of CaMKII was markedly up-regulated during brain development. After HI, CaMKII was totally and permanently depleted from the cytosol and concomitantly deposited into a Triton-insoluble fraction in neurons that were undergoing delayed neuronal death. Autophosphorylation of CaMKII-Thr286 transiently increased at 30 min of reperfusion and declined thereafter. All these changes were mild in P7 pups but more dramatic in P26 rats, consistent with the development-dependent CaMKII expression in neurons. The results suggest that long-term CaMKII depletion from the cytosolic fraction and deposition into the Triton-insoluble fraction may disable synaptic development, damage synaptic plasticity, and contribute to delayed neuronal death and long-term synaptic deficits after transient HI.
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http://dx.doi.org/10.1111/j.1471-4159.2004.02733.xDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3518056PMC
October 2004

Reversal of acute tacrolimus-induced renal vasoconstriction by theophylline in rats.

Pediatr Crit Care Med 2003 Jul;4(3):358-62

Department of Pediatrics, University of Miami School of Medicine, Miami, FL 33101, USA.

Objective: To determine whether theophylline, a nonselective adenosine receptor antagonist and phosphodiesterase inhibitor, reverses the acute declines in renal blood flow and glomerular filtration rate induced by high-dose tacrolimus in rats.

Design: Prospective, randomized, placebo-controlled experimental study.

Setting: University-based basic science research laboratory.

Subjects: Adult male Sprague-Dawley rats.

Interventions: After mechanical ventilation and instrumentation under isoflurane and nitrous oxide anesthesia, animals received either tacrolimus 0.5 mg/kg intravenously or vehicle and 1 hr later either theophylline 4 mg/kg intravenously or vehicle.

Measurements And Main Results: By using radiolabeled microspheres, renal blood flow was measured in three groups: control (n = 5), tacrolimus plus vehicle (n = 6), and tacrolimus plus theophylline (n = 6) at four time points-baseline and 60, 75, and 90 mins after tacrolimus or vehicle (the latter two time points being 15 and 30 mins after theophylline or vehicle, respectively). Whole blood tacrolimus and serum theophylline concentrations were measured. In a separate group of animals, by using (51)Cr-EDTA, glomerular filtration rate was measured in two groups: tacrolimus plus vehicle (n = 5) and tacrolimus plus theophylline (n = 5) at baseline and over two consecutive 20-min time periods beginning 61 mins posttacrolimus. Urine flow rate also was measured. Following tacrolimus, both renal blood flow and glomerular filtration rate declined in parallel by approximately 33% and 50% from baseline after 75 and 90 mins, respectively (p <.05 by two-way repeated-measures analysis of variance). Theophylline completely reversed these tacrolimus-induced decreases in renal blood flow and glomerular filtration rate. Urine flow rate also increased in response to theophylline.

Conclusions: Low-dose theophylline reverses tacrolimus-induced declines in renal blood flow and glomerular filtration rate observed in an acute model of tacrolimus toxicity. Theophylline's effect in chronic toxicity remains to be determined.
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http://dx.doi.org/10.1097/01.PCC.0000074269.30004.7EDOI Listing
July 2003

New research in the field of stroke: therapeutic hypothermia after cardiac arrest.

Stroke 2003 04 20;34(4):1051-3. Epub 2003 Mar 20.

Department of Neurological Surgery, University of Miami School of Medicine, FL 33136-1060, USA.

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http://dx.doi.org/10.1161/01.STR.0000061885.90999.A9DOI Listing
April 2003

Epidermal growth factor reduces ischemia-reperfusion injury in rat small intestine.

Crit Care Med 2002 Jul;30(7):1576-80

Department of Pediatrics, University of Miami School of Medicine, Miami, FL, USA.

Objective: To measure the effect of pre-ischemic administration of intraluminal epidermal growth factor on the changes in intestinal permeability induced by 30 mins of superior mesenteric artery occlusion, followed by 2 hrs of reperfusion.

Design: Prospective, randomized, placebo-controlled experimental study.

Setting: University basic science research laboratory.

Subjects: Healthy, young, adult, male Sprague-Dawley rats.

Interventions: A 10-cm segment of small intestine was isolated and studied in situ in rats that were anesthetized with fentanyl and mechanically ventilated. Intestinal ischemia-reperfusion injury was induced by temporary occlusion of the superior mesenteric artery for 30 mins, followed by 2 hrs of reperfusion. Three groups were studied: time controls with a sham operation, saline-treated ischemia-reperfusion, and epidermal growth factor-treated ischemia-reperfusion. Epidermal growth factor, 100 ng/min, was infused intraluminally, beginning 30 mins before and continued until 40 mins after ischemia.

Measurements And Main Results: Intestinal permeability was measured for each 10-min time period by using chromium-labeled EDTA. Histopathologic injury was assessed by light microscopy. After superior mesenteric artery occlusion, intestinal permeability increased approximately ten-fold and was sustained for 2 hrs of reperfusion in saline-treated rats. Pretreatment with epidermal growth factor significantly reduced the permeability changes during reperfusion by >60% compared with saline-treated animals (p <.05). Histopathologic sections revealed apparently more extensive loss of epithelial cells and mucosal disruption in saline-treated intestine compared with epidermal growth factor-treated intestine.

Conclusion: Pre-ischemic administration of intraluminal epidermal growth factor significantly protects against intestinal ischemia-reperfusion injury.
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http://dx.doi.org/10.1097/00003246-200207000-00030DOI Listing
July 2002