Biomedical subjects

J D Geiger

Publications and source records attributed to J D Geiger.

At least 55 records · Page 3Linked to original sources

PubMed1998

The association of large ovarian cysts with cloacal exstrophy.

BACKGROUND/PURPOSE: Cloacal exstrophy can now be managed with excellent survival rates and reasonable long-term outcomes with many of these patients living into their late teens and early adulthood. In this report, the authors describe for the first time the association of large ovarian cysts with cloacal exstrophy. METHODS: From 1974 to 1996, 12 patients with cloacal exstrophy have been treated at C.S. Mott Children's Hospital. Massive ovarian cysts developed in four of these. These patients represent the subjects of this study. RESULTS: All four patients have been followed up beyond puberty and massive ovarian cysts have developed, which have caused significant morbidity. Three patients have required surgical intervention. All the patients had reached menarche before the development of the cysts. In all cases, the presentation was severe pelvic pain. Urinary tract obstruction from the large pelvic cysts developed in three of the four. The cysts were bilateral in three of four patients and measured 8 to 10 cm in diameter on ultrasound scan or computed tomography (CT). Cyst aspiration was attempted in two cases and was unsuccessful. Three of the four patients have required bilateral salpingo-oophorectomy. The indications for surgery were uncontrollable pelvic pain in one and urinary obstruction and uncontrollable pelvic pain in two. Surgical findings demonstrated massive thin-walled cysts with essentially no normal ovarian tissue in association with duplicated mullerian structures. The pathology findings were corpus luteal cyst in two and mucinous cystadenoma in one. The fourth patient with an 8- x 10-cm unilateral cyst is being followed up. CONCLUSIONS: The authors have described, for the first time, the association of massive ovarian cysts with cloacal exstrophy. These cysts can lead to severe pelvic pain and urinary tract obstruction. Bilateral oophorectomy has been required in most of these patients.

Adolescent↗

PubMed1998

Latex sensitization in general pediatric surgical patients: a call for increased screening of patients.

BACKGROUND/PURPOSE: Latex sensitization is a well-documented occurrence in children with myelodysplastic and urologic anomalies. The incidence of latex allergy in general pediatric surgical patients, however, has not been previously addressed. The purpose of this study was to examine the risk of perioperative latex reactions in a general pediatric surgical practice over a 1-year period. METHODS: This study examined the occurrence of latex sensitization using two methods. First, the preoperative anesthesia records of patients that have undergone surgery from October 1995 through September 1996 at Mott Children's Hospital were reviewed retrospectively. Second, all patients who had intraoperative anaphylaxis attributable to latex sensitization, including those from three additional hospitals, were evaluated. RESULTS: During a 12-month period, 1,523 pediatric general surgical operations were performed at the C.S. Mott Children's Hospital. Of these, only 11 operations on five patients were performed under latex precautions. All of these patients had a preoperative diagnosis of latex sensitivity. During the same period, intraoperative anaphylactic reactions caused by latex allergy occurred in two of the general surgical patients (0.13%) at the C.S. Mott Hospital. Four additional cases are also reported from other study hospitals. None of these patients were suspected, based on current screening methods, of having a latex allergy before their surgery. CONCLUSIONS: Latex allergy is a potentially life-threatening condition in the pediatric general surgical population. Further study is needed to develop criteria to preoperatively identify patients at risk for latex sensitization.

Adolescent↗

PubMed1998

The lateral approach for open splenectomy.

BACKGROUND: Laparoscopic splenectomy (LS) has been used increasingly to treat children with hematologic disorders and has been reported to have advantages over open splenectomy performed through a standard vertical or subcostal incision. The authors perform open splenectomy (OS) through a lateral, muscle-splitting approach, and believe their approach is more reasonable in comparison with LS. METHODS: Thirty-nine consecutive open splenectomies performed between 1991 and 1995 were reviewed retrospectively and compared with recent reports of LS. The series included 24 boys and 15 girls with an average age of 9 years and average weight of 37.5 kg. Indications included immune thrombocytopenic purpura (n = 20), hereditary spherocytosis (n = 18), and sickle cell anemia (n = 1). The operation was performed with the child in the lateral decubitus position through a left upper abdominal muscle-splitting incision (off the 11th rib), sparing the rectus muscle. RESULTS: All 39 cases were completed without intraoperative complications with an average surgical time of 98.0 minutes (range, 30 to 302). The average surgical blood loss was 89 mL (range, 10 to 300). The children started feeding an average of 1.2 days (range, 0 to 4) postoperatively, were on a regular diet at an average of 2.0 days (range, 1 to 6) postoperatively, and had an average length of stay of 2.7 days (range, 1 to 6). There was no mortality or morbidity. CONCLUSIONS: Open lateral splenectomy is performed with shorter surgical times, less blood loss, an excellent cosmetic result, no complications, and a length of stay comparable to any of the published series on laparoscopic splenectomy in children. This approach provides a reasonable basis for comparison with laparoscopic splenectomy.

Adolescent↗

PubMed1998

Neuronal excitatory properties of human immunodeficiency virus type 1 Tat protein.

Neuronal dysfunction and cell death in patients with human immunodeficiency virus type-1 (HIV-1) infection may be mediated by HIV-1 proteins and products released from infected cells. Two HIV-1 proteins, the envelope glycoprotein gp120 and nonstructural protein Tat, are neurotoxic. We have determined the neuroexcitatory properties of HIV-1 tat protein using patch-clamp recording techniques. When fmoles of Tat were applied extracellularly, it elicited dose-dependent depolarizations of human fetal neurons in culture and rat CA1 neurons in slices, both in the absence and presence of tetrodotoxin. These responses were voltage-dependent, reversed at approximately 0 mV, and were significantly increased by repetitive applications with no evidence of desensitization. That these responses to Tat were due to direct actions on neurons was supported by observations that Tat dose-dependently depolarized outside-out patches excised from cultured human neurons. Removal of extracellular Ca2+ decreased the responses both in neurons and membrane patches. This is the first demonstration that an HIV-1 protein can, in the absence of accessory cells, directly excite neurons and leads us to speculate that Tat may be a causative agent in HIV-1 neurotoxicity.

Animals↗

PubMed1998

Levels of endogenous adenosine in rat striatum. I. Regulation by ionotropic glutamate receptors, nitric oxide and free radicals.

Glutamate release after ischemia, hypoxia and seizure activity plays an important role in stimulating adenosine production and release. We characterized the ionotropic glutamate receptor subtype that regulates adenosine levels in vivo and investigated the role of nitric oxide and free radicals in mediating N-methyl-D-aspartate (NMDA)-induced increases in adenosine levels. Rats received unilateral intrastriatal injections and were sacrificed 15 min postinjection by high-energy focused microwave irradiation (10 kW, 1.25 s). Adenosine levels were measured by high-performance liquid chromatography in ipsilateral and contralateral striata. NMDA and kainic acid dose-dependently increased levels of adenosine whereas (+/-)-alpha-amino-3-hydroxy-5-methyl-4-isoxazol proprionic acid had no effect. The NMDA- and kainic acid-induced increases were blocked by dizocilpine, and the kainic acid response was decreased by 6-cyano-7-nitroquinoxaline-2,3-dione. The effects of NMDA and kainic acid on levels of adenosine were not additive. Intrastriatal L-arginine decreased, and the nitric oxide synthase inhibitor, NG-nitro-L-arginine methyl ester, increased basal adenosine levels. Coadministration of NMDA with L-arginine or NG-nitro-L-arginine methyl ester did not significantly affect NMDA-induced increases in levels of adenosine. N-Tert-butyl-phenylnitrone, a free radical scavenger, reversed L-arginine-induced decreases and NMDA-induced increases in levels of adenosine. Together, these results indicate that NMDA-type ionotropic receptors play an important role in regulating in vivo levels of adenosine in rat striatum and that free radicals, but not nitric oxide, apparently are involved in NMDA-induced increases in levels of adenosine. Conversely, nitric oxide, but not free radicals, apparently exert tonic control over basal levels of endogenous adenosine.

6-Cyano-7-nitroquinoxaline-2,3-dione↗

PubMed1998

Levels of endogenous adenosine in rat striatum. II. Regulation of basal and N-methyl-D-aspartate-induced levels by inhibitors of adenosine transport and metabolism.

Selective inhibitors of adenosine production, degradation and transport were used to potentiate in vivo levels of adenosine and to determine the source of both basal and N-methyl-D-aspartate (NMDA)-induced increases in levels of endogenous adenosine in vivo. Male Sprague-Dawley rats receiving unilateral intrastriatal injections of pharmacological agents were sacrificed 15 min postinjection by high-energy focused microwave irradiation (10 kW, 1.25 s). Ipsilateral and contralateral striata were dissected, and adenosine levels were measured by high-performance liquid chromatography. Inhibition of 5'-nucleotidase by alpha, beta-methylene ADP dose-dependently decreased adenosine levels under basal as well as NMDA-stimulated conditions. Inhibition of nucleoside transport by dilazep and adenosine deaminase by 2'-deoxycoformycin each dose-dependently increased basal adenosine levels. 2'-Deoxycoformycin potentiated NMDA-induced increases in adenosine levels. Inhibition of adenosine kinase by 5'-amino-5'-deoxyadenosine increased basal levels of adenosine, but did not significantly affect NMDA-induced increases in adenosine. 2'-Deoxycoformycin combined with 5'-amino-5'-deoxyadenosine produced a greater enhancement of NMDA-induced increases in levels of adenosine than when either drug was administered separately. Endogenous adenosine in vivo apparently originates from release of adenosine as well as from release and extracellular breakdown of a nucleotide under both basal and NMDA-stimulated conditions. Furthermore, inhibitors of adenosine kinase and adenosine deaminase work best to increase levels of endogenous adenosine under basal and NMDA-stimulated conditions, respectively.

5'-Nucleotidase↗

PubMed1997

Antioxidants and dipyridamole inhibit HIV-1 gp120-induced free radical-based oxidative damage to human monocytoid cells.

Reactive oxygen species (ROS) may play an important role in HIV-1 pathogenesis and HIV-1 gp120-induced neurotoxicity. Our studies determined the extent to which gp120 increased ROS production in human monocytic U937 cells and the effectiveness of various agents, including dipyridamole (DPR), in blocking these responses. The thiobarbituric acid-reactive substances (TBARS) assay was used as a measure of recombinant gp120 (HIV-1[3B])-induced oxidative damage to U937 cells. As a control, TBARS production was measured using a hypoxanthine/xanthine superoxide generating system. There was gp120-induced oxidative damage in U937 cells with a concentration that produces 50% of maximal effect (apparent EC50 value) of 11 pM. Polyclonal antiserum to gp120 significantly (p < 0.05) inhibited gp120-induced oxidative damage. gp120-induced oxidative damage was significantly inhibited 81% (p < 0.01) by catalase/superoxide dismutase, 53% (p < 0.05) by (+/-)-alpha-tocopherol, 78% (p < 0.01) by desferrioxamine, and 82% (p < 0.01) by ethylene diamine tetraacetic acid (EDTA). These results indicate that gp120 is capable of promoting iron-based oxygen free radical damage to U937 cells. DPR potently (p < 0.05) inhibited both hypoxanthine/xanthine- and gp120-induced oxidative damage with concentrations that produce 50% inhibition (apparent IC50 values) of 1.3 microM for hypoxanthine/xanthine and 1.0 microM for gp120. Therapeutic intervention against ROS production may prevent HIV-1 neurotoxicity.

Anti-HIV Agents↗

PubMed1997

Diadenosine polyphosphates inhibit adenosine kinase activity but decrease levels of endogenous adenosine in rat brain.

Findings in peripheral tissues that diadenosine polyphosphates (Ap(n)As) activate 5'-nucleotidase activity and inhibit adenosine kinase activity in vitro led us to test the hypothesis that Ap(n)As and analogues thereof, through such actions on purine enzymes, increase brain levels of endogenous adenosine in vivo. Accordingly, we tested Ap(n)As for their effects on the in vitro activities of adenosine kinase, adenosine deaminase, AMP deaminase and 5'-nucleotidase and, following unilateral microinjections in rat striatum, on in vivo levels of endogenous adenosine. Adenosine kinase activity was not affected significantly by 5',5'''-P1,P2-diadenosine pyrophosphate (Ap2A) or by 5',5'''-P1,P3-diadenosine triphosphate (Ap3A), but was inhibited by 5',5'''-P1,P4-diadenosine tetraphosphate (Ap4A), 5',5'''-P1,P5-diadenosine pentaphosphate (Ap5A) and 5',5'''-P1,P6-diadenosine hexaphosphate (Ap6A); apparent IC50 values were 5.0, 3.3 and 500 microM, respectively. Inhibition of adenosine kinase activity by Ap4A and the four metabolically stable analogues of Ap4A tested was uncompetitive. Following unilateral intrastriatal injections, adenosine levels, relative to uninjected contralateral striatum, were decreased significantly (P < 0.05) by 48% with Ap4A and by 37% with AppCH2ppA, a metabolically stable analogue of Ap4A. Striatal levels of adenosine were not affected significantly by Ap5A or Ap6A. Cytosolic, but not particulate 5'-nucleotidase activity was inhibited and AMP deaminase activity was increased by some Ap(n)As. Although adenosine kinase inhibitors increase levels of endogenous adenosine and we showed here that Ap(n)As were potent inhibitors of this enzyme, these particular actions of Ap(n)As were not consistent with their effects on levels of endogenous adenosine.

5'-Nucleotidase↗

PubMed1997

Conservative management of mesenchymal hamartoma of the liver.

The natural history of mesenchymal hamartoma of the liver is poorly understood. This case demonstrates the course of a biopsy-proven mesenchymal hamartoma using sequential computed tomography (CT) examinations. These CT scans show initial expansion of the lesion with subsequent involution. The spontaneous resolution in this patient suggests the possibility of conservative management of asymptomatic mesenchymal hamartomas. The case is presented, and the literature on mesenchymal hamartoma is reviewed.

Hamartoma↗

PubMed1997

Pediatric blunt abdominal trauma: role of computed tomography vascular blush.

Nonoperative management of blunt abdominal trauma is widely accepted in pediatric patients. There are few factors prospectively available to predict reliably which children will not respond to nonoperative treatment. Computed tomography scans demonstrating a vascular contrast blush are associated with arterial bleeding and the failure of nonoperative management of splenic injuries in adults. The authors describe five hemondynamically stable pediatric patients who have intraabdominal injury and a characteristic vascular contrast blush who acutely did not respond to nonoperative treatment. Vascular blush may be an indication for early laparotomy in pediatric trauma patients.

Abdominal Injuries↗

PubMed1997

Caffeine stimulates amyloid beta-peptide release from beta-amyloid precursor protein-transfected HEK293 cells.

Extracellular amyloid beta-peptide (A beta) deposition is a pathological feature of Alzheimer's disease and the aging brain. Intracellular A beta accumulation is observed in the human muscle disease, inclusion body myositis. A beta has been reported to be toxic to neurons through disruption of normal calcium homeostasis. The pathogenic role of A beta in inclusion body myositis is not as clear. Elevation of intracellular calcium following application of calcium ionophore increases the generation of A beta from its precursor protein (betaAPP). A receptor-based mechanism for the increase in A beta production has not been reported to our knowledge. Here, we use caffeine to stimulate ryanodine receptor (RYR)-regulated intracellular calcium release channels and show that internal calcium stores also participate in the genesis of A beta. In cultured HEK293 cells transfected with betaAPP cDNA, caffeine (5-10 mM) significantly increased the release of A beta fourfold compared with control. These actions of caffeine were saturable, modulated by ryanodine, and inhibited by the RYR antagonists ruthenium red and procaine. The calcium reuptake inhibitors thapsigargin and cyclopiazonic acid potentiated caffeine-stimulated A beta release. NH4Cl and monensin, agents that alter acidic gradients in intracellular vesicles, abolished both the caffeine and ionophore effects. Immunocytochemical studies showed some correspondence between the distribution patterns of RYR and cellular betaAPP immunoreactivities. The relevance of these findings to Alzheimer's disease and inclusion body myositis is discussed.

Amyloid beta-Peptides↗

PubMed1997

Use of abdominal ultrasonography to assess pediatric splenic trauma. Potential pitfalls in the diagnosis.

OBJECTIVE: The purpose of this study was to evaluate the accuracy of abdominal ultrasonography (US) for screening and grading pediatric splenic injury. SUMMARY BACKGROUND DATA: The use of abdominal US has increased rapidly as a method of evaluating organ damage after blunt abdominal trauma. Despite US's increasing use, little is known about its accuracy in children with splenic injury. METHODS: Children (N = 32) suffering blunt abdominal trauma who were diagnosed with splenic injury by computerized tomography (CT) scan prospectively were enlisted in this study. Degree of splenic injury was evaluated by both CT and US. The ultrasounds were evaluated by an initial reading as well as by a radiologist who was blinded as to the results of the CT. RESULTS: Twelve (38%) of the 32 splenic injuries found on CT were missed completely on the initial reading of the US. When the ultrasounds were graded in a blinded fashion, 10 (31%) of the splenic lacerations were missed and 17 (53%) were downgraded. Seven (22%) of the 32 splenic fractures were not associated with any free intraperitoneal fluid on the CT scan. CONCLUSIONS: This study has shown that US has a low level of sensitivity (62% to 78%) in detecting splenic injury and downgrades the degree of injury in the majority of cases. Reliance on free intraperitoneal fluid may be inaccurate because not all patients with splenic injury have free intra-abdominal fluid. Based on these findings, US may be of limited use in the initial assessment, management, and follow-up of pediatric splenic trauma.

Abdomen↗

PubMed1996

Nucleoside transporter-mediated uptake and release of [3H]L-adenosine in DDT1 MF-2 smooth muscle cells.

[3H]L-Adenosine, an enantiomer of the physiological D-adenosine, was shown previously to be taken up and released, at least in part, through nucleoside transporters in rat brain preparations. In the present study, we used clonal smooth muscle DDT1 MF-2 cells that contain almost exclusively equilibrative inhibitor-sensitive (es) nucleoside transporters to test the hypothesis that L-adenosine is a permeant for these bidirectional nucleoside transporters. DDT1 MF-2 cells accumulated approximately 3 times more [3H]D- than [3H]L-adenosine; 10 microM nitrobenzylthioinosine significantly (P < 0.01) inhibited the accumulation of [3H]D-adenosine by 86% and of [3H]L-adenosine by 63%. The IC50 values for the nitrobenzylthioinosine-sensitive portions of [3H]L- and [3H]D-adenosine accumulation were 1.6 and 2.0 nM, respectively. [3H]D-Adenosine accumulation was significantly (P < 0.05) inhibited by up to 72% with L-adenosine and [3H]L-adenosine accumulation was significantly (P < 0.01) inhibited by up to 52% with D-adenosine. Release of accumulated [3H]L-adenosine was temperature- and time-dependent, and was significantly (P < 0.05) reduced by 47% with dipyridamole, 39% with dilazep, and 45% with nitrobenzylthioinosine; the apparent IC50 value for nitrobenzylthioinosine was < 1 nM. These data indicate that a significant proportion of [3H]L-adenosine uptake and release in DDT1 MF-2 cells is mediated by es nucleoside transporters.

Adenosine↗

PubMed1996

[3H]adenosine transport in DDT1 MF-2 smooth muscle cells: inhibition by metabolites of propentofylline.

Adenosine receptor signal transduction mechanisms have previously been characterized in Syrian hamster smooth muscle DDT1 MF-2 cells but adenosine transport in these cells has not. DDT1 MF-2 cells possess a high density (370,000 sites/cell) of high affinity (Kd value of 0.26 nM) binding sites for [3H]nitrobenzylthioinosine, a marker for the equilibrative and inhibitor-sensitive subtype of nucleoside transporters. Transport of [3H]adenosine was insensitive to Na+ and was inhibited by the nucleoside transport inhibitors nitrobenzylthioinosine, dilazep and dipyridamole with IC50 values of 1, 13 and 270 nM, respectively. Propentofylline, a neuroprotective compound that can inhibit nucleoside transporters, is rapidly metabolized in vivo to the racemate (+/-)-A720287. Based on recent findings that some transport inhibitors exhibit marked stereoselectivity, we tested the degree to which individual stereoisomers of (+/-)-A720287 affect adenosine transport. Propentofylline inhibited [3H]adenosine transport in DDT1 MF-2 cells with an IC50 value of 24 microM. (+/-)-A720287 and the individual stereoisomers (+)-833791 and (-)-844261 had similar potency to propentofylline for inhibition of [3H]adenosine transport in DDT1 MF-2 cells as well as in clonal mouse leukemia L1210/B23.1 cells, cells which possess only the equilibrative and inhibitor-sensitive subtype of nucleoside transporters. Thus, the neuroprotective effects of propentofylline may be due, in part, to the primary metabolites of propentofylline.

Adenosine↗

PubMed1996

Subcellular localization of ryanodine receptors in rat brain.

Subcellular fractions of rat brain were used to determine the subcellular localization of ryanodine receptors. [3H]Ryanodine binding in purified cortical, cerebellar and hippocampal synaptosomes was up to 3.6-fold higher compared with mitochondrial fractions. The density of sites (Bmax) in hippocampal mossy fiber synaptosomes (249 fmol/mg protein) was 3.7-fold greater than in cortical synaptosomes (67 fmol/mg protein) and binding affinity was approximately 2-fold greater in the former (KD, 6.1 nM) than the latter (KD, 3.1 nM). At single sub-saturating concentrations of [3H]ryanodine, binding was 1.6-fold higher in mossy fibers compared with total hippocampal synaptosomes. [3H]Ryanodine binding sites were distributed similarly in subfractions of cortical synaptosomes and microsomes from discontinuous sucrose density gradients. An enrichment of sites was found in the lightest fractions containing the lowest activities of plasma membrane (5'-nucleotidase) and endoplasmic reticulum (glucose 6-phosphatase) enzyme markers when data for microsomal and synaptosomal subfractions were expressed as activity/binding per mg protein and when data for synaptosomal subfractions were expressed as a percentage of total activity/binding in collected fractions. Thus, ryanodine receptors appear to be concentrated in presynaptic terminals where they may play a major role in neurotransmitter release, and appear to be localized either in a specialized endoplasmic reticulum subcompartment or a distinct subcellular organelle.

Animals↗

PubMed1996

Prophylactic surgery for multiple endocrine neoplasia type IIa after genetic diagnosis: is parathyroid transplantation indicated?

Identification of germline mutations in the RET proto-oncogene predisposing to multiple endocrine neoplasia type IIa (MEN-IIa) has allowed a DNA-based approach to diagnosis and treatment by prophylactic thyroidectomy in children testing genetically positive. Although total thyroidectomy is the accepted operation for C cell disease, the necessity of routine total parathyroidectomy and autotransplantation as previously described in these asymptomatic children is questionable, particularly given the low occurrence of hyperparathyroidism in MEN-IIa (10-20%). Thirty-six children (ages 1 month to 12 years) from four MEN-IIa kindreds at risk for disease underwent genetic testing. Mutational analysis was done using a highly sensitive PCR-based denaturing gradient gel electrophoresis technique. Parathyroid or serum calcium concentrations were determined preoperatively. Of the 36 children at risk, 18 were found to have a MEN-IIa mutation; 11 have undergone prophylactic thyroidectomy at ages ranging from 2 to 12 years (mean 7.5 years). In each case, there was no biochemical evidence of hypercalcemia preoperatively, and all parathyroid glands were identified and were found to be grossly normal at exploration. Glands were carefully dissected and left in situ. Postoperatively, 10 of the 11 children maintained normocalcemia, allowing discharge within 24 to 36 hours. Resected thyroid glands contained C cell hyperplasia in nine, medullary carcinoma in one, and normal histology in one. We conclude that an alternative to routine parathyroidectomy may be desirable for prophylactic treatment of MEN-IIa. In situ parathyroid preservation can be safely achieved without compromising the completeness of the thyroid resection. This conservative approach obviates the potential morbidity associated with total parathyroidectomy and autotransplantation.

Calcium↗

PubMed1996

Brain regional levels of adenosine and adenosine nucleotides in rats killed by high-energy focused microwave irradiation.

A high-energy focused microwave system for killing experimental animals was used to rapidly inactivate enzymes and prevent postmortem breakdown of adenine nucleotides and adenosine, thereby enabling accurate measurements of AMP, ADP, ATP and adenosine in rat brain. For comparison, purine levels were measured in brains of rats killed by decapitation, decapitation into liquid nitrogen, or in situ freezing of the brain with liquid nitrogen. Of the three microwave irradiation power levels used, 10, 6.0 or 3.5 kW, rats killed by 10 kW had the highest ATP levels (28.8 nmol/mg protein) and cellular energy charge value (0.8), and the lowest levels of AMP (2.2 nmol/mg protein) and adenosine (19.7 pmol/mg protein). Of the 6 brain regions studied, adenosine levels (pmol/mg protein) ranged from 10 in cerebral cortex to 170 in cerebellum of rats killed using 10 kW microwave irradiation and, for comparison, ranged from 840 in cerebral cortex to 2498 in striatum of rats killed by decapitation. Focused microwave killing permits precise and accurate measurements of purines in discrete regions of rat brain.

Adenine Nucleotides↗

PubMed1996

Effect of very delayed repair of congenital diaphragmatic hernia on survival and extracorporeal life support use.

BACKGROUND: Since November 1992, operative repair in neonates with congenital diaphragmatic hernia (CDH) at this institution was delayed until respiratory insufficiency had resolved. METHODS: A retrospective analysis was performed (n = 33) comparing delayed repair with our previously reported institutional experience with immediate repair from January 1988 to October 1992 (n = 66). Infants with severe genetic defects or moribund conditions or who were premature were not considered candidates for repair or extracorporeal life support (ECLS), but they were included in the survival analysis. Survival was defined as hospital discharge. Data were compared with an independent t test or Pearson chi-squared test. RESULTS: Mean age at repair was 8.9 +/- 4.5 days (range, 3 to 20 days). Eleven infants in the study group were placed on ECLS (33% versus 68% in the comparison group; p = 0.001). Six of these infants survived (55% versus 58% in the comparison group; p = 0.846). Of these survivors, one patient was repaired while on ECLS, and the remainder underwent repair after decannulation from ECLS. All 20 of the remaining candidates for repair survived without need for ECLS. Overall survival was 79% versus 56% in the comparison group (p = 0.027). CONCLUSIONS: Our current data suggest that very delayed repair of newborns with CDHs is associated with an increase in the overall survival and a decrease in the use of ECLS when compared with previous experience at this institution.

Extracorporeal Membrane Oxygenation↗