bluuebunny/crossref_metadata_2025_split huggingface dataset:
Anaphylactic Shock
Authors: Dewachter Pascale , Jouan-Hureaux Valérie , Franck Patricia , Menu Patrick , de Talancé Nicole , Zannad Faiez , Laxenaire Marie-Claire , Longrois Dan , Mertes Paul Michel 
Published: June 2005

Background
The pathophysiology of anaphylactic shock during anesthesia is incompletely characterized. It is described as distributive by analogy with septic shock (anaerobic metabolism, high tissue oxygen pressure [Ptio2] values). The Ptio2 profile and its metabolic consequences during anaphylaxis are not known.

Methods
Ovalbumin-sensitized anaphylactic shock rats (n = 11) were compared to nicardipine-induced hypotension rats (n = 12) for systemic hemodynamics, Ptio2, sympathetic nervous system activation, skeletal muscle blood flow, and interstitial lactate and pyruvate concentrations using combined microdialysis and polarographic Clark-type oxygen probes.

Results
In both groups, the time course and the magnitude of arterial hypotension were similar. The ovalbumin group but not the nicardipine group displayed decreased skeletal muscle blood flow (from 45 +/- 6.2 ml x 100 g(-1) x min(-1) to 24.3 +/- 5 ml x 100 g(-1) x min(-1); P < 0.0001) and Ptio2 values (from 42 +/- 5 to 5 +/- 2; P < 0.0001). The ovalbumin group had more intense sympathetic nervous system activation with higher plasma epinephrine and interstitial norepinephrine concentrations. For the ovalbumin group, there was skeletal muscle anaerobic metabolism (lactate concentration increased from 0.446 +/- 0.105 to 1.741 +/- 0.459 mm; P < 0.05) and substrate depletion (pyruvate concentration decreased from 0.034 +/- 0.01 mm to 0.006 +/- 0.002 mm; P < 0.05) leading to increased interstitial lactate/pyruvate ratios (from 17 +/- 6 to 311 +/- 115; P < 0.05).

Conclusions
This profile suggests decreased skeletal muscle blood flow and oxygen delivery. Persistent energy consumption results in decreased Ptio2 and substrate depletion through anaerobic glycolysis leading to complete failure of cellular energy production. This could explain rapid organ dysfunction and resuscitation difficulties.
Sevoflurane Depresses Glutamatergic Neurotransmission to Brainstem Inspiratory Premotor Neurons but Not Postsynaptic Receptor Function in a Decerebrate Dog Model
Authors: Stucke Astrid G. , Zuperku Edward J. , Tonkovic-Capin Viseslav , Krolo Mirko , Hopp Francis A. , Kampine John P. , Stuth Eckehard A. E. 
Published: June 2005

Background
Inspiratory bulbospinal neurons in the caudal ventral medulla are premotor neurons that drive motoneurons, which innervate pump muscles such as the diaphragm and external intercostals. Excitatory drive to these neurons is mediated by N-methyl-d-aspartate (NMDA) receptors and alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA) receptors and is modulated by an inhibitory gamma-aminobutyric acid type A (GABAA)ergic input. The authors investigated the effect of sevoflurane on these synaptic mechanisms in decerebrate dogs.

Methods
Studies were performed in decerebrate, vagotomized, paralyzed, and mechanically ventilated dogs during hypercapnic hyperoxia. The effect of 1 minimum alveolar concentration sevoflurane on extracellularly recorded activity of single neurons was measured during localized picoejection of the GABAA receptor blocker bicuculline and the glutamate agonists AMPA and NMDA. Complete blockade of the GABAAergic mechanism by bicuculline allowed differentiation between the effects of sevoflurane on overall GABAAergic inhibition and on overall glutamatergic excitation. The neuronal responses to exogenous AMPA and NMDA were used to estimate the anesthetic effect on postsynaptic glutamatergic neurotransmission.

Results
One minimum alveolar concentration sevoflurane depressed the spontaneous activity of 23 inspiratory premotor neurons by (mean +/- SD) 30.0 +/- 21.0% (P < 0.001). Overall glutamatergic excitation was depressed 19.2 +/- 18.5% (P < 0.001), whereas overall GABAAergic inhibition was enhanced by 11.9 +/- 25.1% (P < 0.05). The postsynaptic responses to exogenous AMPA and NMDA did not change.

Conclusion
One minimum alveolar concentration depressed the activity of inspiratory premotor neurons by a reduction of glutamatergic excitation and an increase in overall inhibition. The postsynaptic AMPA and NMDA receptor response was unchanged. These findings contrast with studies in inspiratory premotor neurons where halothane did not change overall inhibition but significantly reduced the postsynaptic glutamate receptor response.
Sevoflurane Enhances γ-Aminobutyric Acid Type A Receptor Function and Overall Inhibition of Inspiratory Premotor Neurons in a Decerebrate Dog Model
Authors: Stucke Astrid G. , Zuperku Edward J. , Krolo Mirko , Brandes Ivo F. , Hopp Francis A. , Kampine John P. , Stuth Eckehard A. E. 
Published: June 2005

Background
Inspiratory premotor neurons in the caudal ventral medulla relay excitatory drive to phrenic and inspiratory intercostal motoneurons in the spinal cord. These neurons are subject to tonic gamma-aminobutyric acid type A (GABAA)ergic inhibition. In a previous study, 1 minimum alveolar concentration (MAC) sevoflurane depressed overall glutamatergic excitatory drive and enhanced overall GABAAergic inhibitory drive to the neurons. This study investigated in further detail the effects of sevoflurane on GABAAergic inhibition by examining postsynaptic GABAA receptor activity in these neurons.

Methods
Studies were performed in decerebrate, vagotomized, paralyzed, and mechanically ventilated dogs during hypercapnic hyperoxia. The effect of 1 MAC sevoflurane on extracellularly recorded neuronal activity was measured during localized picoejection of the GABAA receptor antagonist bicuculline and the GABAA agonist muscimol. Complete blockade of GABAAergic inhibition by bicuculline allowed estimation of the prevailing overall inhibition of the neuron. The neuronal response to muscimol was used to assess the anesthetic effect on the postsynaptic GABAA receptor function.

Results
One MAC sevoflurane depressed the spontaneous activity of 21 inspiratory premotor neurons by (mean +/- SD) 32.6 +/- 20.5% (P < 0.001). Overall excitatory drive was depressed 17.9 +/- 19.8% (P < 0.01). Overall GABAAergic inhibition was enhanced by 18.5 +/- 18.2% (P < 0.001), and the postsynaptic GABAA receptor function was increased by 184.4 +/- 121.8% (n = 20; P < 0.001).

Conclusion
One MAC sevoflurane greatly enhanced GABAA receptor function on inspiratory premotor neurons and increased overall synaptic inhibition but to a smaller extent, indicating that the presynaptic inhibitory input was also reduced. Therefore, the anesthetic depression of spontaneous inspiratory premotor neuronal activity by 1 MAC sevoflurane in vivo is due to a combined effect on the two major ionotropic synaptic neurotransmitter systems with a decrease in overall glutamatergic excitation and a strong enhancement of postsynaptic GABAA receptor function.
Pyruvate Modulates Hepatic Mitochondrial Functions and Reduces Apoptosis Indicators during Hemorrhagic Shock in Rats
Authors: Sharma Pushpa , Walsh Kane T. , Kerr-Knott Kimberly A. , Karaian John E. , Mongan Paul D. 
Published: June 2005

Background
Dysfunctional mitochondria have been widely accepted as one of the key targets and a mediator of secondary cell injury and organ failure during hemorrhagic shock (HS). The liver is known to be the first organ to display the signs of injury during HS. This report describes experiments to determine whether modulation of hepatic mitochondrial dysfunctions by pharmacologic agents could prevent liver injury in rats subjected to HS.

Methods
In this study, Sprague-Dawley rats were either treated as controls or subjected to computer-controlled arterial hemorrhage (40 mmHg) for 60 min followed by resuscitation with hypertonic saline, hypertonic beta-hydroxybutyrate, or hypertonic sodium pyruvate for the next 60 min before death. During the course of the experiment, animals were continuously monitored for hemodynamic and metabolic parameters. At the end of the experiment, the liver was excised and examined for oxidative injury, mitochondrial functions, expression of nitric oxide synthase, and indicators of apoptosis.

Results
In comparison to hypertonic saline and hypertonic beta-hydroxybutyrate, pyruvate significantly protected the liver from oxidative injury, prevented the up-regulation of nitric oxide synthase, inhibited pyruvate dehydrogenase deactivation, and improved cellular energy charge and mitochondrial functions. In addition, pyruvate also reduced cleavage of poly-adenosine diphosphate ribose polymerase by preventing leakage of mitochondrial cytochrome c in the liver of HS animals.

Conclusions
These data suggest that modulation of mitochondrial metabolic functions is likely to be one of the important mechanisms by which pyruvate exerts its protective effects on the liver during HS and resuscitation in rats.
A Comparative Study of Sequential Epidural Bolus Technique and Continuous Epidural Infusion
Authors: Ueda Kenichi , Ueda Wasa , Manabe Masanobu 
Published: June 2005

Background
In this randomized, double-blind study, the authors compared the effectiveness of a sequential epidural bolus (SEB) technique versus a standard continuous epidural infusion (CEI) technique of local anesthetic delivery. Both techniques used the same hourly dose of local anesthetic.

Methods
Sixteen gynecologic patients undergoing abdominal surgery received postoperative epidural analgesia using 0.75% ropivacaine at a dose of 22.5 mg (3 ml) per hour. Patients were randomly assigned to one of two groups. In the SEB group (n = 8), patients received one third of the hourly dose every 20 min as a bolus. In the CEI group (n = 8), the hourly dose was administered as a continuous infusion. Analgesia was assessed by rest pain scored by a visual analog scale and pinprick to determine the number of separately blocked spinal segments on each side of the body. Doses of rescue medication for pain were also recorded.

Results
The median number of blocked spinal segments was 19.5 (range, 18-24) in the SEB group and 11.5 (range, 10-18) in the CEI group (P < 0.001). The median difference in the number of blocked segments between the right and left sides was 0 (range, 0-1) in the SEB group and 2 (range, 0-6) in the CEI group (P < 0.04). No patients in the SEB group but one patient in the CEI group required rescue medication for pain. The visual analog scale pain score was 0 in both groups except for one patient in the CEI group during the study period.

Conclusion
The SEB technique with ropivacaine provides superior epidural block compared with an identical hourly dose administered as a continuous infusion.
Remifentanil-induced Postoperative Hyperalgesia and Its Prevention with Small-dose Ketamine
Authors: Joly Vincent , Richebe Philippe , Guignard Bruno , Fletcher Dominique , Maurette Pierre , Sessler Daniel I. , Chauvin Marcel 
Published: June 2005

Background
Remifentanil-induced secondary hyperalgesia has been documented experimentally in both animals and healthy human volunteers, but never clinically. This study tested the hypotheses that increased pain sensitivity assessed by periincisional allodynia and hyperalgesia can occur after relatively large-dose intraoperative remifentanil and that small-dose ketamine prevents this hyperalgesia.

Methods
Seventy-five patients undergoing major abdominal surgery were randomly assigned to receive (1) intraoperative remifentanil at 0.05 microg x kg(-1) x min(-1) (small-dose remifentanil); (2) intraoperative remifentanil at 0.40 microg x kg(-1) x min(-1) (large-dose remifentanil); or (3) intraoperative remifentanil at 0.40 microg x kg(-1) x min(-1) and 0.5 mg/kg ketamine just after the induction, followed by an intraoperative infusion of 5 microg x kg(-1) x min(-1) until skin closure and then 2 microg x kg(-1) x min(-1) for 48 h (large-dose remifentanil-ketamine). Pain scores and morphine consumption were recorded for 48 postoperative hours. Quantitative sensory tests, peak expiratory flow measures, and cognitive tests were performed at 24 and 48 h.

Results
Hyperalgesia to von Frey hair stimulation adjacent to the surgical wound and morphine requirements were larger (P < 0.05) and allodynia to von Frey hair stimulation was greater (P < 0.01) in the large-dose remifentanil group compared with the other two groups, which were comparable. There were no significant differences in pain, pressure pain detection threshold with an algometer, peak flow, cognitive tests, or side effects.

Conclusion
A relatively large dose of intraoperative remifentanil triggers postoperative secondary hyperalgesia. Remifentanil-induced hyperalgesia was prevented by small-dose ketamine, implicating an N-methyl-d-aspartate pain-facilitator process.
Financial Implications of a Hospital’s Specialization in Rare Physiologically Complex Surgical Procedures
Authors: Wachtel Ruth E. , Dexter Franklin , Lubarsky David A. 
Published: June 2005

Background
The authors previously identified a hospital that has a unique role in its region for surgical care. In children aged 0-2 yr, the hospital performed 64% of all physiologically complex procedures statewide (>or= 8 American Society of Anesthesiologists Relative Value Guide basic units). For all age groups combined, 48% of the physiologically complex procedures performed at that hospital were rare, defined as < 1/workday statewide.

Methods
The authors tested the hypothesis that financially important differences can result from performing relatively large numbers of such specialized procedures. Methods were developed to compare contribution margin (revenue from facility and professional fees minus variable costs) per operating room hour (CM/OR hour) between patient groups and different types of surgical procedures.

Results
CM/OR hour was significantly larger by a financially important amount (> 250 dollars/OR hour) for pediatric versus geriatric patients (P <or= 0.002), primarily because of higher professional reimbursements, with no difference in hospital reimbursements. Unexpectedly, CM/OR hour was also significantly greater by at least 250 dollars when a rare procedure was involved (P < 0.001 for all ages combined), primarily because of greater hospital reimbursements. For cases involving implant charges of 10,000 dollars or greater, overall CM/OR hour was negative because increased revenues did not compensate for the high variable costs.

Conclusions
Other hospitals can use these methods to perform a similar analysis of the financial impact of those patient populations or surgical procedures that are unique to their own roles in their regional healthcare systems, and to identify the sources of financial losses and gains experienced by the hospital.
Interphase fluorescence in situ hybridization with an IGH probe is important in the evaluation of patients with a clinical diagnosis of chronic lymphocytic leukaemia
Authors: Nowakowski G. S. , Dewald G. W. , Hoyer J. D. , Paternoster S. F. , Stockero K. J. , Fink S. R. , Smoley S. A. , Remstein E. D. , Phyliky R. L. , Call T. G. , Shanafelt T. D. , Kay N. E. , Zent C. S. 
Published: June 2005

SummaryTranslocations involving IGH are common in some lymphoid malignancies but are believed to be rare in chronic lymphocytic leukaemia (CLL). To study the clinical utility of fluorescence in situ hybridization (FISH) for IGH translocations, we reviewed 1032 patients with a presumptive diagnosis of CLL. Seventy‐six (7%) patients had IGH translocations. Pathology and clinical data were available for the 24 patients evaluated at the Mayo Clinic. Ten (42%) patients had IGH/cyclin D1 fusion and were diagnosed with mantle cell lymphoma (MCL). The immunophenotype was typical of MCL in three of these patients and atypical for MCL in seven patients. One patient had biclonal disease with typical MCL and CLL with IGH/BCL‐2. Eleven (46%) patients had IGH/BCL‐2 fusion including the patient with biclonal disease. Two of these patients had leukaemic phase follicular lymphoma and nine patients had CLL. The median progression‐free survival of patients with CLL and IGH/BCL‐2 translocation was 20·6 months. The two patients with IGH/BCL‐3 fusion (one of these also had IGH/BCL‐11a) had rapid disease progression. The IGH partner gene was not identified in two patients. We conclude that use of an IGH probe in FISH analysis of monoclonal B‐cell lymphocytosis improves diagnostic precision and could have prognostic value in patients with CLL.
Low‐dose cyclophosphamide conditioning for haematopoietic cell transplantation from HLA‐matched related donors in patients with Fanconi anaemia
Authors: Zanis‐Neto J. , Flowers M. E. D. , Medeiros C. R. , Bitencourt M. A. , Bonfim C. M. , Setúbal D. C. , Funke V. , Sanders J. , Deeg H. J. , Kiem H. P. , Martin P. , Leisenring W. , Storb R. , Pasquini R. 
Published: June 2005

SummaryAllogeneic haematopoietic cell transplantation (HCT) is effective therapy for Fanconi anaemia (FA). FA patients do not tolerate conditioning with 200 mg/kg of cyclophosphamide (Cy), typically used in aplastic anaemia. We previously published results of studies in which Cy doses were gradually reduced from 200 to 100 mg/kg. Here we update results of the initial studies and report data on 30 new patients conditioned with Cy either at 80 mg/kg (n = 7) or at 60 mg/kg (n = 23), given over 4 days before HCT from human leucocyte antigen‐matched related donors. Methotrexate and cyclosporine were given for graft‐versus‐host disease (GVHD) prophylaxis. All seven patients given Cy at 80 mg/kg and 21 of 23 given Cy at 60 mg/kg had sustained engraftment, while two patients, both with clonal cytogenetics abnormalities, experienced graft failure. Grades 2–3 acute GVHD rates were 57% and 14% for patients given the higher and lower Cy doses, respectively (P = 0·001). Four patients given Cy at 80 mg/kg and 22 given Cy at 60 mg/kg were alive at a median of 47 (44–58) months and 16 (3–52) months, respectively. Cy at 60 mg/kg has acceptable toxicities, low rates of GVHD, and is sufficient for engraftment of related grafts in most FA patients.
CD34+ cell selection is required to assess HOXA9 expression levels in patients with myelodysplastic syndrome
Authors: Heinrichs Stefan , Berman Jason N. , Ortiz Taylor M. , Kornblau Steven M. , Neuberg Donna S. , Estey Elihu H. , Thomas Look A. 
Published: June 2005

SummaryOverexpression of HOXA9 is linked to the molecular pathogenesis of acute myeloid leukaemia (AML) and myelodysplastic syndrome (MDS), conferring a poor prognosis. HOXA9 expression levels were analysed in the diagnostic bone marrow (BM) samples of 13 MDS patients. HOXA9 was expressed by CD34+ BM cells at median levels 3·1‐fold higher than in CD34− cells from the same patient and at median levels 4·3‐fold higher than in CD34+ cells from healthy donors. These results indicate that CD34+ cell selection is required to accurately assess the expression levels of HOXA9 and related genes in the multipotential malignant progenitor cells of MDS patients.
Impaired bradykinin response to ischaemia and exercise in patients with mild congestive heart failure during angiotensin‐converting enzyme treatment. Relationships with endothelial function, coagulation and inflammation
Authors: Cugno Massimo , Agostoni Piergiuseppe , Mari Daniela , Meroni Pier Luigi , Gregorini Luisa , Bussotti Maurizio , Anguissola Gian Battista , Donatelli Francesco , Nussberger Jürg 
Published: June 2005

SummaryInflammation and endothelial dysfunction play important roles in the pathophysiology of congestive heart failure (CHF), and the peptide bradykinin, generated during inflammation, may act as a defence mechanism by inducing vasodilation. Plasma bradykinin levels are increased in experimental heart failure but low in patients with advanced chronic CHF despite treatment with angiotensin‐converting enzyme (ACE) inhibitors. It is not currently known how bradykinin behaves in less severe phases of CHF controlled by long‐term ACE inhibitor treatment. We studied 10 male patients with clinically stable chronic CHF [New York Heart Association (NYHA) class II] on long‐term ACE inhibitor treatment and 10 normal sex‐ and age‐matched control subjects. High performance liquid chromatography/radioimmunoassay methods were used to evaluate plasma levels of bradykinin in relation to an array of parameters of endothelial function, coagulation and inflammation before and after stimuli of forearm arterial occlusion and physical exercise. CHF patients had higher levels of bradykinin (P = 0·008), activated factor XII (P = 0·049), interleukin‐6 (P = 0·050) and tumour necrosis factor receptor II (sTNFRII) (P = 0·026) than controls. Arterial occlusion and exercise significantly increased bradykinin and von Willebrand factor levels in controls but not in CHF patients. The increase in brachial artery diameter after arterial occlusion was less in CHF patients (P = 0·036) and inversely related to baseline plasma levels of bradykinin (r = −0·855, P = 0·002) and sTNFRII (r = −0·780, P = 0·008). NYHA class II CHF patients during long‐term treatment with ACE inhibitors have increased bradykinin levels and signs of inflammation. They are unable to respond adequately to stimuli of ischaemia and physical exercise which both require vasodilation.
Osteosclerosis in advanced chronic idiopathic myelofibrosis is associated with endothelial overexpression of osteoprotegerin
Authors: Bock Oliver , Loch Gero , Schade Ulrika , Büsche Guntram , von Wasielewski Reinhard , Wiese Birgitt , Kreipe Hans 
Published: June 2005

SummaryAdvanced chronic idiopathic myelofibrosis (IMF) with osteosclerosis and increase and thickening of bone trabeculae is typically contrasted by the absence or sparse presence of osteoclasts. Because osteoclast formation can be inhibited by osteoprotegerin (OPG) we investigated OPG expression in IMF with severe fibrosis and osteosclerosis, which expressed significantly higher (up to 71‐fold) OPG mRNA levels when compared with prefibrotic cellular IMF and control cases. The receptor activator of nuclear factor kappaB ligand (RANKL), a positive regulator of osteoclast differentiation and putative antagonist of OPG was overexpressed by up to 34‐fold exclusively in advanced IMF. Case‐specific calculation of the RANKL/OPG ratio in advanced IMF showed a wide range without significant differences when compared with the prefibrotic IMF and non‐neoplastic haematopoiesis. Immunohistochemical detection of OPG protein revealed strong labelling of endothelial cells within proliferating vessels in fibrotic IMF and heterogeneously labelled megakaryocytes, and fibroblasts. Osteosclerosis and impaired osteoclast function in IMF appears to be associated with upregulated endothelial OPG expression but concomitant reduction of the antagonist RANKL could not be demonstrated. We conclude that osteosclerosis in IMF is associated with increased endothelial OPG expression without concomitant RANKL downregulation.