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Hepatopulmonary syndrome (HPS) is associated with increased waitlist mortality in liver transplantation (LT) candidates. Children with HPS are granted Model for End-Stage Liver Disease (MELD)/Pediatric End-Stage Liver Disease (PELD) exception points for waitlist prioritization in the United States based on criterion developed for adults. In this study, the impact of this MELD/PELD exception policy on post-LT survival in children was examined. A retrospective cohort of patients aged younger than 18 years with a MELD/PELD exception request who underwent LT between 2007 and 2018 were identified in the Scientific Registry of Transplant Recipients. Patients were stratified by waitlist partial pressure of arterial oxygen (PaO

Describe the techniques and prove the feasibility of performing complex hepatobiliary and pancreatic surgery on a Jehovah's Witness (JW) population. 2. Describe a strategy that offsets surgical blood loss by the manipulation of circulating blood volume to create reserve whole blood upon anesthesia induction.Major liver and pancreatic resections often require operative transfusions. This limits surgical options for patients who do not accept major blood component- transfusions. There is also growing recognition of the negative impact of allogenic blood transfusions.A 23-year, single center, retrospective review of JW patients undergoing liver and pancreatic resections was performed. We describe perioperative management and patient outcomes. Acute normovolemic hemodilution (ANH) is proposed as an important strategy for offsetting blood losses and preventing the need for blood transfusion. A quantitative mathematical formula is developed to provide guidance for its use.One hundred and one major resections were analyzed (liver n=57, pancreas n=44). ANH was utilized in 72 patients (liver n=38, pancreas n=34) with median removal of 2 units that were returned for hemorrhage as needed or at the completion of operation. There were no perioperative mortalities. Morbidity classified as Clavien grade 3 or higher occurred in 7.0% of liver resection and 15.9% of pancreatic resection patients.Deliberate perioperative management makes transfusion-free liver and pancreatic resections feasible. Intraoperative whole blood removal with ANH specifically preserves red cell mass, platelets, and coagulation factors for timely reinfusion. Application of the described JW transfusion-free strategy to a broader general population could lessen blood utilization costs and morbidities.

Although pediatric liver transplantation (LT) results in excellent long-term outcomes, a high incidence of early acute cellular rejection and late graft fibrosis persists. Routine measurement of allograft enzymes may not reliably detect rejection episodes, identify candidates for immunosuppression minimization, or indicate allograft fibrosis. Surveillance biopsies (SBs) can provide valuable information in this regard, but their role in pediatric LT is not fully established. A retrospective cohort of 236 pediatric LT recipients from a high-volume center was studied to characterize the risks and benefits of SB versus for-cause biopsies (FCBs). The study population was 47.1% male and 54.7% Hispanic, and 31% received living donor grafts. Our data suggest that patients in the SB group had better transplant outcomes (rejection-free, graft, and patient survival) compared with patients who had FCBs or who never underwent biopsy. Among 817 biopsies obtained from 236 patients, 150 (18.4%) were SBs. Only 6 patients had a biopsy-related complication, and none were observed in the SB subset. Graft biochemical blood tests did not accurately predict rejection severity on biopsy, with aspartate aminotransferase area under the receiver operating characteristic curve (AUROC) 0.66, alanine aminotransferase AUROC 0.65 (very poor predictions), and gamma-glutamyltransferase AUROC 0.58 (no prediction). SBs identified subclinical rejection in 18.6% of biopsies, whereas 63.3% of SBs had evidence of fibrosis. SBs prompted changes in immunosuppression including dose reduction. Our experience suggests that SB in pediatric LT is safe, offers valuable information about subclinical rejection episodes, and can guide management of immunosuppression, including minimization. Improved outcomes with SB were likely multifactorial, potentially relating to a more favorable early posttransplant course and possible effect of management optimization through SB. Further multicenter studies are needed to examine the role of SBs on long-term outcomes in pediatric LT.

PURPOSE OF REVIEW: Due to a persistent shortage of donor livers, attention has turned toward ways of utilizing marginal grafts, particularly those with steatosis, without incurring inferior outcomes. Here we review the evaluation and utilization of steatotic liver allografts, highlight recently published data, and discuss novel methods of graft rehabilitation. RECENT FINDINGS: While severe liver allograft (>60%) steatosis has been associated with inferior graft and recipient outcomes, mild (

Background Trauma and sepsis both increase the risk for secondary infections. Injury mobilizes mitochondrial (MT) danger-associated molecular patterns (mtDAMPs) directly from cellular necrosis. It is unknown, however, whether sepsis can cause active MT release and whether mtDAMPs released by sepsis might affect innate immunity. Methods Mitochondrial release from human monocytes (Mo) was studied after LPS stimulation using electron microscopy and using fluorescent video-microscopy of adherent Mo using Mito-Tracker Green (MTG) dye. Release of MTG+ microparticles was studied using flow cytometry after bacterial stimulation by size exclusion chromatography of supernatants with polymerase chain reaction (PCR) for mitochondrial DNA (mtDNA). Human neutrophil (PMN), chemotaxis, and respiratory burst were studied after PMN incubation with mtDNA. Results LPS caused Mo to release mtDAMPs. Electron microscopy showed microparticles containing MT. mtDNA was present both in microvesicles and exosomes as shown by PCR of the relevant size exclusion chromatography bands. In functional studies, PMN incubation with mtDNA suppressed chemotaxis in a dose-dependent manner, which was reversed by chloroquine, suggesting an endosomal, toll-like receptor-9-dependent mechanism. In contrast, PMN respiratory burst was unaffected by mtDNA. Conclusion In addition to passive release of mtDAMPs by traumatic cellular disruption, inflammatory and infectious stimuli cause active mtDAMP release via microparticles. mtDNA thus released can have effects on PMN that may suppress antimicrobial function. mtDAMP-mediated "feed-forward" mechanisms may modulate immune responses and potentially be generalizable to other forms of inflammation. Where they cause immune dysfunction the effects can be mitigated if the pathways by which the mtDAMPs act are defined. In this case, the endosomal inhibitor chloroquine is benign and well tolerated. Thus, it may warrant study as a prophylactic antiinfective after injury or prior sepsis.

Objectives To determine neuroprotective effects and mechanism of the combination therapy of niacin and selenium in cardiac arrest rats. Design Prospective laboratory study. Setting University laboratory. Subjects Rat cortex neurons and male Sprague-Dawley rats (n = 68). Interventions In rat cortex neurons underwent 90 minutes of oxygen-glucose deprivation and 22.5 hours of reoxygenation, effects of the combination therapy of niacin (0.9 mM) and selenium (1.5 μM) were investigated. The role of DJ-1 was determined using DJ-1 knockdown cells. In cardiac arrest rats, posttreatment effects of the combination therapy of niacin (360 mg/kg) and selenium (60 μg/kg) were evaluated. Measurements and main results In oxygen-glucose deprivation and 22.5 hours of reoxygenation cells, combination therapy synergistically activated the glutathione redox cycle by a niacin-induced increase in glutathione reductase and a selenium-induced increase in glutathione peroxidase activities and reduced hydrogen peroxide level. It increased phosphorylated Akt and intranuclear Nuclear factor erythroid 2-related factor 2 expression and attenuated neuronal injury. However, these benefits were negated by DJ-1 knockdown. In cardiac arrest rats, combination therapy increased DJ-1, phosphorylated Akt, and intranuclear nuclear factor erythroid 2-related factor 2 expression, suppressed caspase 3 cleavage, and attenuated histologic injury in the brain tissues. It also improved the 7-day Neurologic Deficit Scales from 71.5 (66.0-74.0) to 77.0 (74.-80.0) (p = 0.02). Conclusions The combination therapy of clinically relevant doses of niacin and selenium attenuated brain injury and improved neurologic outcome in cardiac arrest rats. Its benefits were associated with reactive oxygen species reduction and subsequent DJ-1-Akt signaling up-regulation.

Background The aim of this study was to investigate whether a nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (Nox) inhibitor, apocynin, reduces reactive oxygen species (ROS) production, suppresses the nuclear factor κB (NF-κB) pathway, attenuates lung injury, and improves survival in rat hemorrhagic shock (HS) model. Methods Blood was drawn from male Sprague-Dawley rats (290-340 g) to maintain a mean arterial pressure of 20-25 mm Hg for 40 minutes. The rats were resuscitated with the drawn blood, and a vehicle (HS), a low dose of apocynin (20 mg/kg, LD-Apo), or a high dose of apocynin (40 mg/kg, HD-Apo) was administered intraperitoneally. The survival of the rats was observed for 72 hours. Then, a separated set of rats was euthanized at 6 hours post-HS induction. We measured gp91-phox (Nox2) expression, Nox activity, cytoplasmic phosphorylated inhibitor κB-α (p-IκB-α) expression, NF-κB p65 DNA-binding activity, tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) gene expressions, malondialdehyde (MDA) level, myeloperoxidase (MPO) activity, and histological damage in the lung tissues. Results The survival rates of the sham, HS, HS + LD-Apo, and HS + HD-Apo groups were 100% (5/5), 30% (3/10), 40% (4/10), and 70% (7/10), respectively. A high dose of apocynin decreased gp91-phox expression, Nox activity, and MDA level in the lung tissues during HS and resuscitation. It also decreased p-IκB-α expression, NF-κB p65 DNA-binding activity, TNF-α and IL-6 gene expressions, and MPO activity in the lung tissues and attenuated histological lung injuries. However, a low dose of apocynin failed to show these benefits. Conclusions The administration of a high dose of apocynin inhibited Nox2 expression and Nox activity, reduced lipid peroxidation, suppressed the NF-κB pathway and subsequent pro-inflammatory cytokines transcription in the lung tissues, and attenuated lung injury during HS and resuscitation in rats.

Copyright © 2019 by the Society of Critical Care Medicine and Wolters Kluwer Health, Inc. All Rights Reserved. Objectives: Trauma predisposes to systemic sterile inflammation (systemic inflammatory response syndrome) as well as infection, but the mechanisms linking injury to infection are poorly understood. Mitochondrial debris contains formyl peptides. These bind formyl peptide receptor-1, trafficking neutrophils to wounds, initiating systemic inflammatory response syndrome, and wound healing. Bacterial formyl peptides, however, also attract neutrophils via formyl peptide receptor-1. Thus, mitochondrial formyl peptides might suppress neutrophils antimicrobial function. Also, formyl peptide receptor-1 blockade used to mitigate systemic inflammatory response syndrome might predispose to sepsis. We examined how mitochondrial formyl peptides impact neutrophils functions contributing to antimicrobial responses and how formyl peptide receptor-1 antagonists affect those functions. Design: Prospective study of human and murine neutrophils and clinical cohort analysis. Setting: University research laboratory and level 1 trauma center. Patients: Trauma patients, volunteer controls. Animal Subjects: C57Bl/6, formyl peptide receptor-1, and formyl peptide receptor-2 knockout mice. Interventions: Human and murine neutrophils functions were activated with autologous mitochondrial debris, mitochondrial formyl peptides, or bacterial formyl peptides followed by chemokines or leukotrienes. The experiments were repeated using formyl peptide receptor-1 antagonist cyclosporin H, “designer” human formyl peptide receptor-1 antagonists (POL7178 and POL7200), or anti-formyl peptide receptor-1 antibodies. Mouse injury/lung infection model was used to evaluate effect of formyl peptide receptor-1 inhibition. Measurements and Main Results: Human neutrophils cytosolic calcium, chemotaxis, reactive oxygen species production, and phagocytosis were studied before and after exposure to mitochondrial debris, mitochondrial formyl peptides, and bacterial formyl peptides. Mitochondrial formyl peptide and bacterial formyl peptides had similar effects on neutrophils. Responses to chemokines and leukotrienes were suppressed by prior exposure to formyl peptides. POL7200 and POL7178 were specific antagonists of human formyl peptide receptor-1 and more effective than cyclosporin H or anti-formyl peptide receptor-1 antibodies. Formyl peptides inhibited mouse neutrophils responses to chemokines only if formyl peptide receptor-1 was present. Formyl peptide receptor-1 blockade did not inhibit neutrophils bacterial phagocytosis or reactive oxygen species production. Cyclosporin H increased bacterial clearance in lungs after injury. Conclusions: Formyl peptides both activate and desensitize neutrophils. Formyl peptide receptor-1 blockade prevents desensitization, potentially both diminishing systemic inflammatory response syndrome and protecting the host against secondary infection after tissue trauma or primary infection.

Objectives To determine whether the combination therapy of niacin and selenium attenuates lung injury and improves survival during sepsis in rats and whether its benefits are associated with the activation of the glutathione redox cycle and up-regulation of nuclear factor erythroid 2-related factor 2. Design Prospective laboratory study. Setting University laboratory. Subjects Human lung microvascular endothelial cells and male Sprague-Dawley rats (n = 291). Intervention In lipopolysaccharide-exposed cells, the dose-related effects of niacin and selenium were assessed, and the therapeutic effects of the combination therapy of niacin (0.9 mM) and selenium (1.5 μM) were evaluated. The role of nuclear factor erythroid 2-related factor 2 was determined using nuclear factor erythroid 2-related factor 2 knockdown cells. In endotoxemic and cecal ligation and puncture with antibiotics rats, the therapeutic effects of the posttreatments of clinically relevant doses of niacin (360 mg/kg) and selenium (60 μg/kg) were evaluated. Measurements and main results Combination therapy reduced the hydrogen peroxide level via the synergistic activation of the glutathione redox cycle, which involves niacin-induced increases in glutathione reductase activity, and reduced the glutathione level and a selenium-induced increase in glutathione peroxidase activity. Combination therapy contributed to the up-regulation of nuclear factor erythroid 2-related factor 2, enhancement of glutathione synthesis, and down-regulation of nuclear factor κB signaling, but nuclear factor erythroid 2-related factor 2 knockdown inhibited the enhancement of glutathione synthesis and down-regulation of the nuclear factor κB pathway. The therapeutic effects of combination therapy on endotoxemic rats were consistent with those on lipopolysaccharide-exposed cells. In addition, the posttreatment of combination therapy attenuated lung injury and improved survival in endotoxemic and cecal ligation and puncture with antibiotics rats. However, individual therapies of niacin or selenium failed to achieve these benefits. Conclusions The combination therapy of niacin and selenium attenuated lung injury and improved survival during sepsis. Its therapeutic benefits were associated with the synergistic activation of the glutathione redox cycle, reduction of hydrogen peroxide level, and up-regulation of nuclear factor erythroid 2-related factor 2.

Background The purpose of the current study was to investigate the protective effect of niacin on acute lung injury by the down-regulation of the nuclear factor κB (NF-κB) pathway in hemorrhagic shock (HS) rats. Methods HS was induced in male Sprague-Dawley rats by withdrawing blood to maintain a mean arterial pressure of 20 mm Hg to 25 mm Hg for 40 minutes. The rats were resuscitated by the reinfusion of the drawn blood, and a vehicle (HS), a low-dose of niacin (360 mg/kg, HS + LD-NA), or a high dose of niacin (1,080 mg/kg, HS + HD-NA) were administered orally. The survival of the subjects was observed for 72 hours, and a separate set of animals was killed at 6 hours after HS induction. We measured cytoplasmic phosphorylated inhibitor κB-α and inhibitor κB-α expressions, nuclear NF-κB p65 expression, NF-κB p65 DNA-binding activity, MEK partner 1 activity, tumor necrosis factor α (TNF-α), interleukin 6 (IL-6), IL-8, nicotinamide adenine dinucleotide (NAD+), reduced nicotinamide adenine dinucleotide phosphate, reduced glutathione, glutathione disulfide, malondialdehyde levels, and histologic damage in the lung tissue. We also measured TNF-α, IL-6, and IL-8 levels in the serum. Results The survival rates of the sham, HS, HS + LD-NA, and HS + HD-NA groups were 6 of 6 (100%), 0 of 9 (0%), 1 of 9 (11.1%), and 3 of 9 (33.3%), respectively. A high dose of niacin increased lung NAD+, nicotinamide adenine dinucleotide phosphate levels, and glutathione-glutathione disulfide ratios; decreased lung malondialdehyde levels; down-regulated the NF-κB pathway; suppressed TNF-α, IL-6, and IL-8 levels in the lung tissue and serum; and attenuated histologic lung damage. Conclusion A high dose of niacin attenuated lung inflammation, suppressed proinflammatory cytokine release, reduced histologic lung damage, and improved survival after HS in rats. Its therapeutic benefits were associated with the down-regulation of the reactive oxygen species-dependent NF-κB pathway.

Objectives: To investigate whether 48 hours of therapeutic hypothermia is more effective to attenuate brain apoptosis than 24 hours and to determine whether the antiapoptotic effects of therapeutic hypothermia are associated with the suppressions of the cleavage of protein kinase C-δ, the cytosolic release of cytochrome c, and the cleavage of caspase 3 in a swine cardiac arrest model. Design: Prospective laboratory study. Setting: University laboratory. Subjects: Male domestic pigs (n = 24). Interventions: After 6 minutes of no-flow time that was induced by ventricular fibrillation, cardiopulmonary resuscitation was provided, and the return of spontaneous circulation was achieved. The animals were randomly assigned to the following groups: sham, normothermia, 24 hours of therapeutic hypothermia, or 48 hours of therapeutic hypothermia. Therapeutic hypothermia (core temperature, 32–34°C) was maintained for 24 or 48 hours post return of spontaneous circulation, and the animals were rewarmed for 8 hours. At 60 hours post return of spontaneous circulation, the animals were killed, and brain tissues were harvested. Measurements and Main Results: We examined cellular apoptosis and neuronal damage in the brain hippocampal cornu ammonis 1 region. We also measured the cleavage of protein kinase C-δ, the cytosolic release of cytochrome c, and the cleavage of caspase 3 in the hippocampus. The 48 hours of therapeutic hypothermia attenuated cellular apoptosis and neuronal damage when compared with normothermia. There was also a decrease in the cleavage of protein kinase C-δ, the cytosolic release of cytochrome c, and the cleavage of caspase 3. However, 24 hours of therapeutic hypothermia did not significantly attenuate cellular apoptosis or neuronal damage. Conclusions: We found that 48 hours of therapeutic hypothermia was more effective in attenuating brain apoptosis than 24 hours of therapeutic hypothermia. We also found that the antiapoptotic effects of therapeutic hypothermia were associated with the suppressions of the cleavage of protein kinase C-δ, the cytosolic release of cytochrome c, and the cleavage of caspase 3.

Objectives To determine whether niacin attenuates brain injury and improves neurological outcome after cardiac arrest in rats and if its therapeutic benefits are associated with suppression of the mitogen-activated protein kinase pathway. Design Prospective laboratory study. Setting University laboratory. Subjects Male Sprague-Dawley rats (n=77). Interventions After 6 minutes of no flow time induced by ventricular fibrillation, cardiopulmonary resuscitation was provided and return of spontaneous circulation was achieved. Animals were then administered vehicle, single low dose (360 mg/kg; at 1 hr postreturn of spontaneous circulation), single high dose (1080 mg/kg; at 1 hr), or repeated low dose of niacin (360 mg/kg/d for 3 d; at 1, 24, and 48 hr) through an orogastric tube. Measurements and main results Neurologic deficit scales were scored at 24 hours, 72 hours, and 7 days postreturn of spontaneous circulation. Single high dose of niacin improved neurologic deficit scales at 48 hours and 7 days, and repeated low dose of niacin improved neurologic deficit scales at 7 days. Then, a separate set of animals were killed at 72 hours postreturn of spontaneous circulation, and brain tissues were harvested. Single high dose and repeated low dose of niacin attenuated cellular apoptosis and neuronal damage in hippocampal cornu ammonis 1 and decreased axonal injury and microglial activation in corpus callosum. They increased nicotinamide adenine dinucleotide, reduced nicotinamide adenine dinucleotide phosphate and reduced glutathione levels, and decreased malondialdehyde level in brain tissues. Furthermore, they suppressed the phosphorylations of p38 and c-Jun N-terminal kinase/stress-activated protein kinase and the cleavage of caspase 3. However, they failed to enhance extracellular signal-regulated kinases 1/2 phosphorylation. Conclusions Single high dose and repeated low dose of niacin attenuated brain injury and improved neurological outcome after cardiac arrest in rats. Their therapeutic benefits were associated with suppressions of the phosphorylations of p38 and c-Jun N-terminal kinase/stress-activated protein kinase and the cleavage of caspase 3.

The aim of this study was to report the treatment results and complications of cranial bone reconstruction in patients with craniosynostosis at the Seoul National University Children's Hospital over the 14-year period from 1996 to 2009. A retrospective study was undertaken on 96 cases of 94 consecutive patients diagnosed with craniosynostosis, operated on between 1996 and 2009. The authors collected the data regarding age at surgery, operative time, duration of hospitalization, and follow-up period. Surgical results including the amount of blood loss, signs related to increased intracranial pressure, aesthetic results, cranial index, and complications were evaluated. The authors compared these results with those of the past 10-year period from 1986 to 1995 at the same hospital. There were 81 patients with single synostosis and 13 patients with multiple synostoses. The age of patients ranged from 3 months to 130 months (mean, 27.9 months). The mean operative time was 7.54 ± 1.77 hours. The duration of hospital stay ranged from 5 to 70 days with a mean period of 8.97 days. The intraoperative loss of hemoglobin ranged from 0 to 9.2 g/dL (mean, 2.35 g/dL). The symptoms of increased intracranial pressure were improved after cranioplasty. With regard to aesthetic results, 94 patients were classified into category I and 2 into category IV. The cranial index decreased from 88.0% ± 1.2% to 86.9% ± 1.1% on average. There were 34 minor complications in 28 operations (29.2%). There were statistically significant differences in age at surgery, operative time, duration of hospital stay, and reoperation rate between the recent 14-year study and the past 10-year study. We observed good surgical results and low complications of cranial bone reconstruction in patients with craniosynostosis. The results of the recent 14-year operations were better than those of the past 10-year operations.

Background 4F, apolipoprotein AI mimetic peptide, mimics anti-inflammatory properties of high-density lipoprotein (HDL). The aim of this study was to investigate whether 4F attenuates acute lung injury and improves survival in endotoxemic rats and to determine whether the therapeutic benefits of 4F are associated with the stimulation of sphingosine-1-phosphate receptor 1 (S1P1), the activation of Akt, the down-regulation of the nuclear factor-κB (NF-κB) pathway, and the suppression of cell adhesion molecules. Methods To induce endotoxemia in rats, lipopolysaccharide (LPS, 10 mg/kg) was injected into a tail vein and 10 minutes later, vehicle or 4F (10 mg/kg) was administered intraperitoneally, respectively. We observed the survival of subjects for 72 hours. At 6-hour post-LPS, we killed animals and measured S1P1 expression, phosphorylated Akt/Akt ratio, cytoplasmic phosphorylated inhibitor κB-α/inhibitor κB-α ratio, nuclear NF-κB p65 expression and DNA-binding activity, endothelial leukocyte adhesion molecule-1 (E-selectin) and intercellular adhesion molecule-1 expression, myeloperoxidase activity, and histologic damages in lung tissues. We also measured serum HDL cholesterol level. Results 4F improved survival in endotoxemic rats. 4F restored LPS-induced diminution of serum HDL cholesterol level and increased lung S1P1 expression and phosphorylated Akt/Akt ratio in LPS-treated rats. Furthermore, 4F suppressed inhibitor κB-α degradation, NF-κB activation, E-selectin and intercellular adhesion molecule-1 expression, and myeloperoxidase activity, and attenuated histologic damages in lung tissues. Conclusions 4F attenuated acute lung injury and improved survival in endotoxemic rats. The therapeutic benefits of 4F were found to be associated with the stimulation of S1P1, the activation of Akt, the down-regulation of the NF-κB pathway, and the suppression of cell adhesion molecules.

BACKGROUND: In previous animal studies, induction of therapeutic hypothermia (HT) in hemorrhagic shock (HS) had beneficial effects on the hemodynamic and metabolic parameters and on the survival. However, the effect of induced HT on acute lung injury (ALI) in HS has not been investigated. We sought to determine the effects of HT on ALI in HS. METHODS: Male Sprague-Dawley rats (350-390 g; n = 8 per group) were randomized to the normothermia (NT; 36-37 degrees C) group or the moderate HT (27-30 degrees C) group and were subjected to volume-controlled (2 mL/100 g weight) HS (90 minutes) followed by 90 minutes of resuscitation. ALI score, lung malondialdehyde content, and myeloperoxidase activity were measured. The expression of glycogen synthase kinase 3beta (GSK-3beta), phosphorylated GSK-3beta, inducible nitric oxide synthase (iNOS), heat shock protein (HSP) 72, and nuclear factor-kappaB (NF-kappaB) in the lung were compared. RESULTS: ALI score, lung malondialdehyde content, and myeloperoxidase were lower in the HT group. GSK-3beta and iNOS gene expressions in lung tissue were significantly decreased in the HT group (p < 0.05). On the contrary, the expression of phosphorylated GSK-3beta was increased in the HT group (p < 0.001). HSP 72 was expressed in the HT group but not in the NT group. The activated p65 NF-kappaB levels in lung nuclear extract were significantly lower in the NT group (p = 0.03). CONCLUSIONS: HT attenuates HS-induced ALI in rats by the modulation of GSK, HSP 72, iNOS, and NF-kappaB.

To present the effects of subnasale (SN) flap on the correction of deviated columella base in patients with secondary unilateral cleft lip nasal (UCLN) deformity.The patients were 6 adult Koreans with cleft cases (mean age, 29.1 y; range, 20-43 y; 1 man and 5 women; secondary UCLN deformity with columella base deviation). After the open rhinoplasty with the Padovan incision had been completed for correction of the secondary UCLN deformity, the SN flap was used for correction of the deviated columella base. The design of the SN flap started from the central portion of the SN region that will be the reconstructed columella and extended to the nasal floor in the larger nostril site. Then, the SN flap was transposed into the smaller nostril site. The columella skin was also elevated and placed into the larger nostril site with the distal end inserting into the donor site. The patients' follow-up period was 16 to 40 months.The SN flap after the open rhinoplasty with the Padovan incision resulted in minimal scarring on the donor and recipient sites. The deviated columella base was straightened in all cases. During the surgical follow-up period, there was no recurrence of the columella base deviation in any patient and no other noteworthy complications were found.For correction of the columella base deviation in patients with secondary UCLN deformity, the SN flap can be a viable treatment option.

We modified the posterior approach by preserving the external rotator muscles to enhance joint stability after primary THA. We asked whether this modified posterior approach would have a lower dislocation rate than the conventional posterior approach, with and without a repair of external rotator muscles. We retrospectively divided 557 patients (670 hips) who had undergone primary THA into three groups based on how the external rotator muscles had been treated during surgery: (1) not repaired after sectioning, (2) repaired after sectioning, or (3) not sectioned and preserved. The minimum followup was 1 year. In the group with preserved external rotator muscles, we observed no dislocations; in comparison, the dislocation rates for the repaired rotator group and the no-repair group were 3.9% and 5.3%, respectively. This modified posterior approach, which preserves the short external rotator muscles, seemed effective in preventing early dislocation after primary THA.Level III, therapeutic study. See the Guidelines for Authors for a complete description of levels of evidence.

This article reports the use of a customized surgical guide for simple and precise C-tube plate placement with minimized incision.Patients who were planning to have orthodontic miniplate treatment because of narrow interradicular space were recruited for this study. A combined silicone and stainless steel wire surgical guide for the C-tube was fabricated on the cast model. The taller wire of the positioning guide is used to accurately start the incision. The incision guide-wire position is verified by placing the miniplate on the coronal horizontal wire to confirm that the incision will coordinate with the screw holes. Because the miniplate is firmly held in place, there is no risk of the miniplate anchoring screws (diameter, 1.5 mm; length, 4 mm) sliding on the bone surface during placement with a manual hand driver.The surgical guide was placed on the clinical site, and it allowed precise placement of the miniplate with minimum incision and preventing from slippage or path-of-insertion angulation errors that might interfere with accurate placement.Customized surgical guide enables precise planning for miniplate positions in anatomically complex sites.

Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal neoplasms of the gastrointestinal tract. Often discovered incidentally, GISTs can present with nonspecific abdominal symptoms or more overt symptoms of bleeding, obstruction, or perforation. Despite a myriad of clinical presentations, bacteremia associated with a GIST has not been described. In this report, we present an unusual clinical case that illustrates how GISTs can become infected, and demonstrate the importance of Streptococcus milleri bacteremia as an indicator of possible underlying gastrointestinal neoplasm.

Patients in whom good intertransverse fusion had been achieved were selected for the volumetric study of the fusion mass using sequential computed tomography scans.To assess the natural volumetric change of intertransverse fusion mass and the effect of the disease entity and spinal instrumentation on the fusion mass volume.The magnitude of volumetric change of the graft bone after intertransverse fusion is still inconclusive.Fifteen adult patients who underwent decompression surgery with single-level lumbar and lumbosacral intertransverse fusion were selected for this study. Preoperative diagnoses were degenerative spondylolisthesis in nine patients and isthmic spondylolisthesis in six. Seven of the 15 patients received pedicle screw fixation. They were categorized into two major groups: 1) instrumented and noninstrumented groups and 2) isthmic and degenerative groups. To assess the volumetric change of the graft bone, sequential computed tomography scans were obtained 2 weeks after surgery and again 18 months after surgery.The overall initial mean graft volume was 6251 mm3, which decreased to 2842 mm3 by 18 months after surgery (P0.001). The overall mean volume loss between the two periods was 54.8% of the initial graft volume. Although there was no significant difference in the mean graft volume between the groups at either 2 weeks or 18 months after surgery (P0.05 in all comparisons), the mean graft volume in each group decreased significantly during the observation period (P0.01 in all comparisons). There was no significant difference in the mean volume loss or in the ratio of residual volume to the initial graft volume between the groups during the study period (P0.05 in all comparisons). The initial graft volume correlated positively with the graft volume at 18 months after surgery (r = 0.612, P0.01) and volume loss (r = 0.949, P0.01), but negatively with the residual volume ratio (r = -0.507, P0.01).These results showed that more than one half of the initial graft bone volume was being absorbed during the consolidation processes of the graft bone, and that the volume loss during the period was not significantly affected by the spinal instrumentation or by the disease entity. It was also found that the greater the amount of the initial graft bone, the larger the fusion mass at 18 months after surgery. The volume loss, however, increased proportionally to an increase in the initial graft bone volume. The efficiency (ratio of residual volume to the initial graft volume) of the intertransverse fusion also tended to decline as the initial graft volume increased.