Sandwich Thyroplasty: A Novel Technique for Simplifying Medialization of Vocal Fold Using Silicone Implant in Paralytic Dysphonia with Modification of Thyroplasty Window.

A novel technique of thyroplasty-Sandwich thyroplasty-described, with modification of Isshiki's thyroplasty window to overcome the problems of securing and stabilising the silicone implant in the window thus simplifying the medialization of the vocal fold. Seventy five patients diagnosed with paralytic dysphonia of varied etiology, attending Sri Sathya Sai Institute of ORL, Guntur, India from January 2005 to January 2012, were subjected to this new technique. Medialization of vocal fold was achieved by sandwiching and stabilising a silicone implant between a superiorly based cartilaginous hinged door and the inner perichondrium of the modified thyroplasty window. Results were analysed based upon pre and postoperative voice handicap index, maximum phonation time readings and video-stroboscopic findings. The results were statistically significant with no untoward complications. Sandwich thyroplasty technique facilitated easier fixation and stabilization of silicone implant avoiding difficult and time consuming, techniques involving flanges or sutures.

An in vitro study to compare the transverse strength of thermopressed and conventional compression-molded polymethylmethacrylate polymers.

STATEMENT OF PROBLEM: Acrylic resins have been in the center stage of Prosthodontics for more than half a century. The flexural fatigue failure of denture base materials is the primary mode of clinical failure. Hence there is a need for superior physical and mechanical properties. PURPOSE: This in vitro study compared the transverse strength of specimens of thermopressed injection-molded and conventional compression-molded polymethylmethacrylate polymers and examined the morphology and microstructure of fractured acrylic specimens. MATERIALS AND METHODS: The following denture base resins were examined: Brecrystal (Thermopressed injection-molded, modified polymethylmethacrylate) and Pyrax (compression molded, control group). Specimens of each material were tested according to the American Society for Testing and Materials standard D790-03 for flexural strength testing of reinforced plastics and subsequently examined under SEM. The data was analyzed with Student unpaired t test. RESULTS: Flexural strength of Brecrystal (82.08 ± 1.27 MPa) was significantly higher than Pyrax (72.76 ± 0.97 MPa). The tested denture base materials fulfilled the requirements regarding flexural strength (>65 MPa). The scanning electron microscopy image of Brecrystal revealed a ductile fracture with crazing. The fracture pattern of control group specimens exhibited poorly defined crystallographic planes with a high degree of disorganization. CONCLUSION: Flexural strength of Brecrystal was significantly higher than the control group. Brecrystal showed a higher mean transverse strength value of 82.08 ± 1.27 MPa and a more homogenous pattern at microscopic level. Based on flexural strength properties and handling characteristics, Brecrystal may prove to be an useful alternative to conventional denture base resins.

Zirconium for esthetic rehabilitation: an overview.

The demand for esthetic restorations has resulted in an increased use of dental ceramics for anterior and posterior restorations. A few decades ago, all-ceramic restorations were restricted to treatment in the anterior region, but now all-ceramic restorations can be made anywhere in the dentition. The properties of traditional ceramic materials, however, have limited their use to single crowns; larger restorations have been inadvisable because of insufficient strength. In attempts to meet the requirements for dental materials and improve strength and toughness, several new ceramic materials and techniques have been developed during the past few decades The paper reviews the current literature on dental zirconia with respect to survival, properties, marginal fit, cementation, esthetics and suggests clinical recommendations for their use.

Acute toxicity and cardio-respiratory effects of 2-deoxy-D-glucose: a promising radio sensitiser.

OBJECTIVE: To evaluate the acute toxicity of 2-deoxy-D-glucose (2DG) by oral (p.o.) and intravenous (i.v.) routes, and also the cardio-respiratory effects following high doses of 2DG in animal models. METHODS: The LD50 of 2DG (in water) was determined in rats and mice by p.o. route and in mice by i.v. route. The effect of 2-DG (250 mg/kg, 500 mg/kg, and 1000 mg/kg, i.v.) was studied on various cardio-respiratory parameters viz., mean arterial blood pressure, heart rate and respiratory rate in anaesthetised rats. The effect of 2DG (500 mg/kg, 1000 mg/kg, and 2000 mg/kg, p.o.) was also studied on various respiratory parameters viz., respiratory rate and tidal volume in conscious rats and mice using a computer program. RESULTS: The p.o. LD50 of 2DG was found to be >8000 mg/kg in mice and rats, and at this dose no death was observed. The LD50 in mice by i.v. route was found to be 8000 mg/kg. At this dose 2 out of 4 mice died and the death occurred within 6 h. A significant increase in the body weight was observed after p.o. administration of 2DG in rats at 500 mg/kg, 1000 mg/kg, and 2000 mg/kg doses. There was no significant change in the body weight at 4000 mg/kg and 8000 mg/kg by the p.o. route in rats and up to 8000 mg/kg by p.o. as well as i.v. routes in mice. Intravenous administration of 2DG (250 mg/kg, 500 mg/kg, and 1000 mg/kg) in anaesthetised rats showed a time-dependent decrease in the mean arterial blood pressure. There was no change in the heart rate in any of the treatment groups. The tidal volume was not changed significantly by p.o administration in conscious rats, but a significant decrease in the respiratory frequency at 500 mg/kg and 1000 mg/kg doses was observed. In the mice also there was no change in the tidal volume after p.o, administration, but the respiratory frequency decreased significantly at 2000 mg/kg dose. CONCLUSION: 2DG is a safe compound but can cause a fall in the blood pressure and a decrease in respiratory frequency at high doses.

Enhancement of radionuclide induced cytotoxicity by 2-deoxy-D-glucose in human tumor cell lines.

The efficacy of targeted radiotherapy can be enhanced by selective delivery of radionuclide to the tumors and/or by differentially enhancing the manifestation of radiation damage in tumors. Our earlier studies have shown that the 2-deoxy-D-glucose (2-DG), an inhibitor of glucose transport and glycolytic ATP production, selectively enhances the cytotoxicity of external beam radiation in tumor cells. Therefore, it is suggested that 2-DG may also enhance the cytotoxic effects of radionuclides selectively in tumor cells, thereby improving the efficacy of radionuclide therapy. In vitro studies on breast carcinoma (MDA-MB-468) and glioma (U-87) cell lines, has been carried out to verify this proposition. Clonogenicity (macrocolony assay), cell proliferation, cytogenetic damage (micronuclei formation) and apoptosis were investigated as parameters of radiation response. Mean inactivation dose D (dose required to reduce the survival from 1 to 0.37), was 48 MBq/ml and 96 MBq/ml for 99 mTc, treated MDA-MB-468 and U-87, respectively. The dose response of growth inhibition, induction of micronuclei formation and apoptosis observed under these conditions, were correlated well with the changes in cell survival. Presence of 2-DG (5 mM) during radionuclide exposure (24 hrs), reduced the survival by nearly 2 folds in MDA-MB-468 (from 48.5 MBq to 18.5 MBq) and by 1.6 folds in U-87 cells (from 96 MBq to 66 Mbq). These results clearly show that the presence of 2-DG during radionuclide exposure, significantly enhances the cytotoxicity, by increasing mitotic as well as interphase death. Further studies to understand the mechanisms of radio-sensitization by 2-DG and preclinical studies using tumor-bearing animals, are required for optimizing the treatment schedule.

Stem cell fate specification: role of master regulatory switch transcription factor PU.1 in differential hematopoiesis.

PU.1 is a versatile hematopoietic cell-specific ETS-family transcriptional regulator required for the development of both the inborn and the adaptive immunity, owing to its potential ability to regulate the expression of multiple genes specific for different lineages during normal hematopoiesis. It functions in a cell-autonomous manner to control the proliferation and differentiation, predominantly of lymphomyeloid progenitors, by binding to the promoters of many myeloid genes including the macrophage colony-stimulating factor (M-CSF) receptor, granulocyte-macrophage (GM)-CSF receptor alpha, and CD11b. In B cells, it regulates the immunoglobulin lambda 2-4 and kappa 3' enhancers, and J chain promoters. Besides lineage development, PU.1 also directs homing and long-term engraftment of hematopoietic progenitors to the bone marrow. PU.1 gene disruption causes a cell-intrinsic defect in hematopoietic progenitor cells, recognized by an aberrant myeloid and B lymphoid development. It also immortalizes erythroblasts when overexpressed in many cell lines. Although a number of reviews have been published on its functional significance, in the following review we attempted to consolidate information about the differential participation and role of transcription factor PU.1 at various stages of hematopoietic development beginning from stem cell proliferation, lineage commitment and terminal differentiation into distinct blood cell types, and leukemogenesis.

2-deoxy-D-glucose enhances the cytotoxicity of topoisomerase inhibitors in human tumor cell lines.

Resistance of tumors due to restricted drug accumulation and reversal of DNA lesions in tumor cells as well as normal tissue toxicity limit the efficacy of topoisomerase inhibition based anticancer drugs. It has been proposed that selective inhibition of energy dependent repair processes and enhanced retention of drug in cancer cells can significantly improve the therapeutic efficacy. The purpose of these studies was to verify this proposition by investigating the effects of 2-deoxy-D-glucose (2-DG) an inhibitor of the glycolytic ATP production on the cytotoxicity of certain topoisomerase inhibitors in human tumor cell lines. Human glioma (BMG-1 and U-87) and squamous carcinoma (4197 and 4451) cell lines were investigated with topo-poisons like etoposide (topo II inhibitor), camptothecin (topo I inhibitor) and hoechst-33342 (topo I and II inhibitor). DNA damage induction (halo assay), cell survival (macro colony assay), cytogenetic damage (micronuclei) and apoptosis (morphological analysis) were investigated. Presence of 2-DG for 2 h following exposure to the topoisomerase inhibitors enhanced the cell death (macro colony assay) in a concentration dependent manner and a 2-3-fold increase was observed at 5 mM (equimolar with glucose). Halo assay revealed that 2-DG inhibited the reversal of cleavable complex leading to the accumulation of DNA strand breaks. Under these conditions 2-DG enhanced the drug-induced micronuclei formation by nearly 2 folds with etoposide and hoechst-33342 and a 4-fold increase in delayed apoptosis was observed in case of etoposide. These results clearly demonstrate that presence of 2-DG for a few hours following exposure to topo-inhibitors enhances the cytotoxicity, primarily by increasing the cytogenetic damage.

Alterations in radiation induced cell cycle perturbations by 2-deoxy-D-glucose in human tumor cell lines.

In the present studies, effects of glucose analogue, 2-deoxy-D-glucose (2-DG) on radiation-induced cell cycle perturbations were investigated in human tumor cell lines. In unirradiated cells, the levels of cyclin B1 in G2 phase were significantly higher in both the glioma cell lines as compared to squamous carcinoma cells. Upon irradiation with Co60 gamma-rays (2 Gy), the cyclin B1 levels were reduced in U87 cells, while no significant changes could be observed in other cell lines, which correlated well with the transient G2 delay observed under these conditions by the BrdU pulse chase measurements. 2-DG (5 mM, 2 hr) induced accumulation of cells in the G2 phase and a time-dependent increase in the levels of cyclin B1 in both the glioma cell lines, while significant changes could not be observed in any of the squamous carcinoma cell lines. 2-DG enhanced the cyclin B1 level further in all the cell lines following irradiation, albeit to different extents. Interestingly, an increase in the unscheduled expression of B1 levels in G1 phase 48 hr after irradiation was observed in all the cell lines investigated. 2-DG also increased the levels of cyclin D1 at 24 hr in BMG-1 cell line. These observations imply that 2-DG-induced alterations in the cell cycle progression are partly responsible for its radiomodifying effects.

Sepsis-induced alteration in T-cell Ca(2+) signaling in neonatal rats.

Sepsis-induced suppression in T-cell proliferation follows deranged Ca(2+) signaling in adult rats. In preliminary studies, we observed suppression in T-cell proliferation in septic neonatal rats as well. In this study, we assessed splenic T-cell cytosolic Ca(2+) concentration, [Ca(2+)](i), as its elevation plays an important role in T-cell proliferation. Also, we investigated the role of PGE(2) in sepsis-related changes in T-cell [Ca(2+)](i) in animals pretreated with cyclooxygenase-1 (COX-1) inhibitor (resveratrol) and cyclooxygenase-2 (COX-2) inhibitor (NS-398). Sepsis was induced in 15-day-old rat pups by intraperitoneal implantation of fecal pellets containing Escherichia coli and Bacteroides fragilis. The sham group consisted of pups implanted with sterile fecal pellets. Septic and sham pups were sacrificed 24 h after implantation and their spleens were removed. The spleens from sham and septic pups, along with spleens from unoperated control pups, were processed for single cell suspensions, and T cells were isolated using nylon wool columns. Fura-2 fluorophotometry was employed for the measurement of [Ca(2+)](i) (in nM units) in T cells stimulated with concanavalin A (ConA). Our results show that ConA-mediated T-cell [Ca(2+)](i) response is significantly suppressed in septic neonatal rats. Pretreatment of pups with COX-2, but not COX-1 inhibitor, prevented the decrease in the [Ca(2+)](i) response. These findings suggest that PGE(2) might induce the attenuation in T-cell Ca(2+) signaling during sepsis in neonatal rats.

PGE2 suppresses intestinal T cell function in thermal injury: a cause of enhanced bacterial translocation.

Increased gut bacterial translocation in burn and trauma patients has been demonstrated in a number of previous studies, however, the mechanism for such an increased gut bacterial translocation in injured patients remains poorly understood. Utilizing a rat model of burn injury, in the present study we examined the role of intestinal immune defense by analyzing the T cell functions. We investigated if intestinal T cells dysfunction contributes to bacterial translocation after burn injury. Also our study determined if burn-mediated alterations in intestinal T cell functions are related to enhanced release of PGE2. Finally, we examined whether or not burn-related alterations in intestinal T cell function are due to inappropriate activation of signaling molecule P59fyn, which is required for T cell activation and proliferation. The results presented here showed an increase in gut bacterial accumulation in mesenteric lymph nodes after thermal injury. This was accompanied by a decrease in the intestinal T cell proliferative responses. Furthermore, the treatments of burn-injured animals with PGE2 synthesis blocker (indomethacin or NS398) prevented both the decrease in intestinal T cell proliferation and enhanced bacterial translocation. Finally, our data suggested that the inhibition of intestinal T cell proliferation could result via PGE2-mediated down-regulation of the T cell activation-signaling molecule P59fyn. These findings support a role of T cell-mediated immune defense against bacterial translocation in burn injury.

Omega-3 polyunsaturated fatty acid enriched diet attenuates stress-induced lactacidemia in 10-day-old rats.

BACKGROUND: Lactacidemia is often seen under stress conditions including septic shock in the newborn. Under stress conditions, plasma catecholamine concentrations are increased and play an important role in lactate metabolism. Our previous study shows that perinatal feeding of omega-3 polyunsaturated fatty acid enriched diet (omega-3PUFA) attenuates lactacidemia of endotoxic shock in 10-day-old rats. In the omega-6 fatty acids series, decosapentanoic acid, two series prostaglandins and four series leukotrienes are synthesized through linoleic acids. As plasma lactate concentration correlates with the outcome of septic shock in the newborn, it is important to understand the effects of omega-3PUFA on lactate metabolism. Thus, we tested the hypothesis that perinatal feeding of omega-3 polyunsaturated fatty acid enriched diet (omega-3PUFA) alters responses to catecholamines and attenuates the stress-induced lactacidemia in 10-day-old rats. METHODS: Ten-day-old rats which perinatally fed omega-3PUFA. Lactacidemia was induced by swimming for 5 min. Ten-day-old rats which perinatally fed omega-6PUFA were controls. Omega-6 fatty acids series are contained in animal fats and corn oil. Adrenergic blockers were used to assess roles of catecholamines in swimming-induced lactacidemia. RESULTS: Swimming increased plasma lactate concentration less (P<0.05) in rats fed omega-3PUFA than rats fed omega-6PUFA. Swimming increased plasma concentrations of glucose and glucagon, cyclic adenosine monophosphate (cAMP) concentration and phosphoenolypruvate carboxykinase mRNA in the liver, and cAMP concentration in the hindlimb muscle more (P<0.05) in rats fed omega-3PUFA than in rats fed omega-6PUFA. Phentolamine and propranolol enhanced swim-induced lactacidemia in the omega-3PUFA group, while they decreased the lactacidemia in the omega-6PUFA group. Propranolol enhanced swimming-induced hyperglycemia in the omega-6PUFA group more than in the omega-3PUFA group. CONCLUSIONS: Omega-3PUFA might increase beta-adrenergic response in the liver and increase gluconeogenesis in response to stress, resulting in decreased lactacidemia.

TNFalpha decreases gluconeogenesis in hepatocytes isolated from 10-day-old rats.

Gluconeogenesis decreases during septic shock, but its mechanism is not well known. Tumor necrosis factor alpha (TNF-alpha), which is a key cytokine in septic shock, can increase GLUT1 gene expression and glucose uptake in muscles and fatty tissues. TNF-alpha does not alter the metabolism of hepatocytes in which GLUT2 is the predominant glucose transporter. However, GLUT1 is the predominant glucose transporter in hepatocytes of 10-d-old rats. Thus, we hypothesized that TNF-alpha might increase glucose uptake and glycolysis in those cells, and decrease gluconeogenesis. In the present study, hepatocytes isolated from 10-d-old rats were incubated with TNF-alpha at the concentrations of 0, 0.98, 9.8, 98, and 980 ng/mL to evaluate TNF-alpha effects on gluconeogenesis and glucose uptake. TNF-alpha increased glucose uptake (41.1 +/- 8 to 114 +/- 21.4 micromol/10(6) cells at the concentration of 980 ng/mL of TNF-alpha) in a dose-dependent manner, and decreased gluconeogenesis (98.2 +/- 8.2 to 1.1 +/- 3.2 micromol/10(6) cells at the concentration of 980 ng/mL of TNF-alpha) in a dose-dependent manner. The decrease of glucokinase mRNA and GLUT1 mRNA abundance correlated with glucose uptake (r = 0.988 and 0.997, respectively), and the decrease of phosphoenolpyruvate carboxykinase mRNA abundance correlated with the decrease of gluconeogenesis (r = 0.972). The decrease of gluconeogenesis by TNF-alpha correlated with the increase of glucose uptake (r = -0.988). We concluded that TNF-alpha reciprocally suppressed gluconeogenesis in hepatocytes isolated from 10-d-old rats.

Effects of burn with and without Escherichia coli infection in rats on intestinal vs. splenic T-cell responses.

OBJECTIVE: To evaluate the effect of burn injury with and without an Escherichia coliseptic complication on T-cell proliferation, interleukin-2 production, and Ca(2+) signaling responses in intestinal Peyer's patch and splenic T cells. DESIGN: Prospective, randomized, sham-controlled animal study. SETTING: University medical center research laboratory. SUBJECTS: Adult male Sprague-Dawley rats. INTERVENTIONS: Rats were subjected to a 30% total body surface area, full skin thickness burn. Infection in rats was induced via intraperitoneal inoculation of E. coli, 10(9) colony forming units/kg, with or without a prior burn. MEASUREMENTS AND MAIN RESULTS: Rat Peyer's patch and splenic T lymphocytes were isolated by using a nylon wool cell purification protocol. T-cell proliferation, interleukin-2 production, and Ca(2+) signaling responses were measured after stimulation of cells with the mitogen, concanavalin A. T-cell proliferation was determined by measuring incorporation of (3)H-thymidine into T-cell cultures. Interleukin-2 production by T-cell cultures was measured by using enzyme-linked immunosorbent assay. Intracellular T-cell Ca2(+ )concentration, [Ca(2+)](i), was measured by the use of Ca(2+)-specific fluorescent label, fura-2, and its fluorometric quantification. [Ca(2+)](i) was also evaluated by the use of digital video imaging of fura-2 loaded individual T cells. T-cell proliferation and interleukin-2 production were suppressed substantially in both Peyer's patch and splenic T cells 3 days after either the initial burn alone or burn followed by the E. coli inoculation at 24 hrs after the initial burn. There seemed to be no demonstrable additive effects of E. coli infection on the effects produced by burn injury alone. The T-cell proliferation and interleukin-2 production suppressions with burn or burn-plus-infection insults were correlated with attenuated Ca(2+) signaling. E. coli infection alone suppressed T-cell proliferation in Peyer's patch but not in splenic T cells at 2 days postbacterial inoculation; E. coli infection had no effect on Peyer's patch or splenic T cells at 1 day postinjury. On the other hand, burn injury alone caused a substantial T-cell proliferative suppression at 2 days postburn in both Peyer's patch and splenic cells and a significant suppression in T-cell proliferation on day 1 postburn in Peyer's patch but not in the spleen. CONCLUSION: An initial burn injury suppressed T-cell proliferation at a level that it would not be further affected by a subsequent infection even if the infection by itself has the potential of suppressing T-cell proliferation. An earlier onset of T-cell suppression in Peyer's patch cells than in the spleen with burn could be attributable to an initial hypoperfusion-related intestinal mucosal tissue injury. Overall, our study supports the concept that burn injury per se can significantly suppress T-cell mediated immunity and that the intestine is an early tissue site of such suppression.

CINC blockade prevents neutrophil Ca(2+) signaling upregulation and gut bacterial translocation in thermal injury.

In this study, we have evaluated the role of cytokine-induced neutrophil chemoattractant (CINC), in the upregulation of neutrophil Ca(2+) signaling in neutrophils from thermally injured rats treated with anti-CINC antibody. Additionally, we have determined the effect of the treatment with CINC antibody on the accumulation of activated neutrophils in the intestinal wall, and the effect of such accumulation on gut bacterial translocation. Measurements of myeloperoxidase (MPO) activity and immunohistochemical localization of neutrophils determined neutrophil sequestration in the rat intestine. Agar culture analyses and a specific Escherichia coli beta-galactosidase gene polymerase chain reaction was carried out to detect gut indigenous bacterial invasion into intestinal wall and extraintestinal mesenteric lymph nodes (MLN). The results showed that pretreatment of rats with anti-CINC antibody attenuated the thermal injury-induced enhancement in [Ca(2+)](i) responses in neutrophils both in the basal and Formyl-Met-Leu-Phe stimulated conditions. Moreover, treatment with the CINC antibody decreased neutrophil infiltration into the gut and attenuated thermal injury-caused translocation of bacteria into the MLN.

Insulin tolerance during endotoxic shock in 10-day-old rats.

PURPOSE: The purpose was to investigate insulin tolerance during endotoxic shock in 10-day-old rats. MATERIALS AND METHODS: [(14)C]Deoxy-glucose (2DG) with or without insulin (1 unit/kg) was injected to 10-day-old and 6-week-old rats 3 h after an injection of endotoxin (lipopolysaccharide: LPS). Plasma concentrations of glucose and 2DG were serially measured for 45 min. Gluconeogenesis was measured in hepatocytes isolated from control and endotoxic 10-day-old rats to evaluate effects of insulin on gluconeogenesis. RESULTS: In endotoxic 10-day-old rats, plasma glucose concentration at 45 min was 48 +/- 3% (P < 0.05) of value at 0 min, and when insulin was injected with 2DG, it was 29 +/- 4% (P < 0.05) after insulin injection. Plasma 2DG disappearance was enhanced by insulin injection in the control (t(1/2) = 17.9 vs 20.5 min, P < 0.05), but not in the endotoxic rats (t(1/2) = 17.9 vs 18.4 min), indicating the presence of insulin tolerance in septic rats. Insulin decreased gluconeogenesis (P < 0.05) in hepatocytes from both control and endotoxic 10-day-old rats. In endotoxic 6-week-old rats, plasma glucose concentration was decreased to 46 +/- 10% at 45 min and further decreased to 38 +/- 4% (P < 0.05) by insulin injection. Plasma 2DG disappearance was enhanced by insulin injection in the control (t(1/2) = 11.8 vs 17.4 min, P < 0.05) and in the septic rats (t(1/2) = 14.8 vs 12.2 min). However, the enhancement of plasma 2DG disappearance by insulin was less (P < 0.05) in the septic rats than in the control, confirming reports of other investigators which showed insulin tolerance in septic shock. CONCLUSION: Although hepatocytes from endotoxic rats retained insulin sensitivity, insulin tolerance which was evaluated by 2DG disappearance occurred during septic shock in newborn rats.

Intraatrial mitral valve insertion with native valve preservation in children.

Two patients underwent intraatrial mitral valve insertion for an unsuccessful valvotomy for severe mitral stenosis and left-sided atrioventricular valve insufficiency associated with corrected transposition utilizing a porcine valve from a valved conduit with preservation of the native valve. The valves were inserted using continuous suture distally at the mitral annulus and proximally at the pulled atrial wall distal to the pulmonary veins. Both patients had uneventful hospital course and are doing well at up to 6 months postoperatively. This approach provides a viable option for congenital mitral stenosis or insufficiency in children.

Effects of hydrazine sulfate on galactosamine-sensitized endotoxic shock in ten-day-old rats.

Patients who have liver diseases are susceptible to septic shock. Galactosamine induces liver damage and increases endotoxin-sensitivity. Hydrazine stimulates pituitary-adrenal axis and decreases mortality in galactosamine-sensitized endotoxic shock in the adult. However, as pituitary-adrenal function in the newborn is immature, the effects of hydrazine on galactosamine-sensitized endotoxic shock in the newborn remained unclear. In the present study, galactosamine-sensitized endotoxic shock was induced and treated with hydrazine in ten-day-old rats. Galactosamine (600 mg/kg) plus Salmonella enteritidis lipopolysaccharide (LPS; 0.01 mg/kg) induced hypoglycemia, lactacidemia and resulted in high mortality. Hydrazine at the dose of 20, 50 or 80 mg/kg did not alter the hypoglycemia, lactacidemia or morality. Dexamethasone ameliorated the hypoglycemia and lactacidemia (p < 0.05) and decreased the morality (p < 0.05). The lack of beneficial effects of hydrazine in galactosamine-sensitized endotoxic shock in ten-day-old rats may be related to immature pituitary-adrenal function and suppression of gluconeogenesis by hydrazine.

Endotoxemia following enteral refeeding in children.

Plasma endotoxin-like activity, tumor necrosis factor alpha (TNFalpha) concentrations, core body temperature, and liver functions were measured before and after enteral feeding in children who had been deprived of enteral feeding for 5 days because of their illness. Transient endotoxemia and elevations in plasma TNFalpha concentrations occurred. Core body temperature, aspartate aminotransferase, alamine aminotransferase, and bilirubin concentrations were normal in patients who had elevated plasma endotoxin-like activity. Transient endotoxemia following enteral feeding may be due to the translocation from the gastrointestinal (GI) tract as a result of increased mesenteric circulation and peristalsis. No clinical consequences were noted despite transient endotoxemia. The transient endotoxemia is not due to the immature GI tract; instead, it results from enteral feeding following the deprivation of enteral feeds.

Galactosamine alters glucose regulation in ten-day-old rats treated with a low dose of endotoxin.

Hypoglycemia develops rapidly during septic shock and is a common and life-threatening problem in the human newborn. In adult animals, galactosamine alter glucose metabolism and increases mortality of endotoxic shock. Galactosamine may alter tissue glucose uptake and induce hypoglycemia in ten-day-old rats. The present study showed that galactosamine induced hypoglycemia and a high mortality without an increase in plasma insulin concentration in ten-day-old rats treated with a low dose of endotoxin. Galactosamine decreased tissue glucose uptake in endotoxin-treated animals. Hypoglycemia induced by galactosamine could be due to decreased gluconeogenesis.

Ventilatory support for infants in emergency and in the intensive care unit.

Pediatric anesthesia and intensive care management has improved dramatically over the past two decades. Improved understanding of the pathophysiology underlying newborn surgical emergencies, new medications and new modes of ventilatory support have all contributed to better patient outcome. The authors have reviewed the anatomy and physiology of the infant airway, indications for and principles of endotracheal intubation, the management of newborn surgical emergencies, indications for post-operative ventilatory support, different modes of mechanical ventilation available, complications of mechanical ventilation with weaning parameters and extubation criteria. The introduction of nitric oxide and the implications of extracorpreal membrane oxygenation in the management of newborn emergency refractory to conventional ventilation are discussed.