Haematobia irritans parasitism of F1 yak × beef cattle (Bos grunniens × Bos taurus) hybrids.

The horn fly Haematobia irritans (Diptera: Muscidae) is a blood obligate ectoparasite of bovids that causes annual losses to the U.S. beef cattle industry of over US$1.75 billion. Climate warming, the anthropogenic dispersion of bovids and the cross-breeding of beef cattle with other bovid species may facilitate novel horn fly-host interactions. In particular, hybridizing yaks [Bos grunniens (Artiodactyla: Bovidae)] with beef cows (Bos taurus) for heterosis and carcass improvements may increase the exposure of yak × beef hybrids to horn flies. The present paper reports on the collection of digital images of commingled beef heifers (n = 12) and F1 yak × beef hybrid bovids (heifers, n = 7; steers, n = 5) near Laramie, Wyoming (∼ 2200 m a.s.l.) in 2018. The total numbers of horn flies on beef heifers and F1 yak × beef heifers [mean ± standard error (SE): 88 ± 13 and 70 ± 17, respectively] did not differ significantly; however, F1 yak × beef steers had greater total horn fly abundance (mean ± SE: 159 ± 39) than female bovids. The present report of this experiment is the first such report in the literature and suggests that F1 yak × beef bovids are as susceptible as cattle to horn fly parasitism. Therefore, similar monitoring and treatment practices should be adopted by veterinarians, entomologists and producers.

Routine preoperative laboratory analyses are unnecessary before elective laparoscopic cholecystectomy.

BACKGROUND: We formulated a clinical pathway (CP) for elective laparoscopic cholecystectomy (LC), which included the following preoperative evaluation: history and physical (H&P), right upper quadrant ultrasound (US), and liver function tests (LFTs). We hypothesized that routine LFTs did not alter management beyond that dictated by H&P and US, and could be excluded from the CP. METHODS: The study involved 387 consecutive patients undergoing elective LC. Abnormalities in the preoperative evaluation were compared with the finding of choledocholithiasis or other unexpected outcomes. RESULTS: In 187 (48%) patients, abnormalities were found by H&P (n = 7), US (n = 13), and LFTs (n = 177). Seven patients (2%) had documented choledocholithiasis; two had abnormal H & P; three had abnormal US; and four had abnormal LFTs. No patient with choledocholithiasis had abnormal LFTs but normal H&P and US. CONCLUSIONS: Routine LFTs before elective LC are not cost effective. Before LC H&P and US are warranted, but LFTs do not add any useful information and should not be routinely measured.

TNF receptor I mediates chemokine production and neutrophil accumulation in the lung following systemic lipopolysaccharide.

BACKGROUND: Tumor necrosis factor (TNF)-alpha is a critical effector of lipopolysaccharide (LPS)-induced acute lung injury, and its effects are mediated by two structurally related receptors, RI and RII. Cellular adhesion molecules and C-X-C chemokines (Keratinocyte chemoattractant (KC) and macrophage inflammatory protein [MIP]-2) regulate tissue neutrophil polymorphonuclear neutrophil (PMN) accumulation in a multitude of inflammatory states. We hypothesized that TNFRI signaling dictates PMN accumulation in the lung via regulation of chemokine molecule production. Therefore, the purposes of this study were to (1) delineate LPS-induced lung TNF-alpha production and (2) characterize the contribution of both TNF receptors to lung chemokine production and neutrophil influx following systemic LPS. METHODS: Wild-type or TNFRI and TNFRII knockout (KO) mice were injected with vehicle (saline) or LPS (Escherichia coli 0.5 mg/kg intraperitoneally). After 2, 4, 6, or 24 h, lungs were analyzed for TNF-alpha and chemokine (KC and MIP-2) protein expression (enzyme-linked immunosorbent assay) and PMN accumulation (myeloperoxidase assay). RESULTS: There was an increase in total lung TNF-alpha (vehicle, 5.0 +/- 1.2 pg/mg total protein vs LPS, 950 +/- 318; P < 0.05) after LPS. Lung chemokine production and PMN accumulation were also increased compared to vehicle-injected mice. Lung chemokine production and PMN accumulation were significantly lower in TNFRI KO, but not TNFRII KO, mice, despite no difference in TNF-alpha production (TNFRI KO, 925 +/- 301 vs TNFRII KO, 837 +/- 267, P = 0.82). CONCLUSIONS: Acute lung injury following systemic LPS administration is characterized by increased lung (1) TNF-alpha production, (2) C-X-C chemokine production, and (3) neutrophil accumulation. The maximal effect of LPS-induced lung neutrophil accumulation appears to be dependent upon the TNFRI receptor but not the TNFRII receptor. .

A low level of TNF-alpha mediates hemorrhage-induced acute lung injury via p55 TNF receptor.

Acute lung injury after hemorrhagic shock (HS) is associated with the expression of tumor necrosis factor (TNF)-alpha in the lung. However, the role of TNF-alpha and its receptors in this pulmonary disorder remains obscure. This study examined the temporal relationship of pulmonary TNF-alpha production to neutrophil accumulation during HS and determined the role of TNF-alpha in neutrophil accumulation and lung leak. HS was induced in mice by removal of 30% of total blood volume. Lung TNF-alpha was measured by ELISA. Neutrophil accumulation was detected by immunofluorescent staining, and microvascular permeability was assessed using Evans blue dye. Although HS induced a slight and transient increase in lung TNF-alpha, neutrophil accumulation preceded the increase in TNF-alpha. However, lung neutrophil accumulation and lung leak were abrogated in TNF-alpha knockout mice, and both were restored by administration of recombinant TNF-alpha to TNF-alpha knockout mice before HS. Neutrophil accumulation and lung leak were abrogated in mice lacking the p55 TNF-alpha receptor, but neither was influenced by p75 TNF-alpha receptor knockout. This study demonstrates that a low level of pulmonary TNF-alpha is sufficient to mediate HS-induced acute lung injury during HS and that the p55 TNF-alpha receptor plays a dominant role in regulating the pulmonary inflammatory response to HS.

Life-threatening dog attacks: a devastating combination of penetrating and blunt injuries.

BACKGROUND/PURPOSE: Children often are the victims of dog attacks. Although bite injuries sustained in an attack characteristically are attributed to the penetrating component of the bite, the blunt nature of a bite may represent the most serious and devastating component of injury. The purpose of this study was to characterize a group of children suffering life-threatening dog bites and examine the predominant aspect of injury. METHODS: Thirty-nine children were admitted to the trauma service at a regional pediatric trauma center with the diagnosis of dog bite injury over a 6-year period (1994 through 1999). Patient demographics, site and description of injury, and surgical procedures performed were recorded from a chart review. RESULTS: Mean age of the 35 children included for analysis was 5.4 years (range, 0.8 to 17 years). Twenty-five (71%) injuries occurred in the head and neck region. Eight (23%) children sustained life-threatening injuries. Of these, blunt force was the predominant injury in 6. This resulted in 1 (20%) arterial occlusion requiring vascular reconstruction, 2 (40%) permanent neurologic injuries (stroke, spinal cord transection), and 1 (20%) death (exsanguination). CONCLUSIONS: On evaluation of a dog attack, the focus generally is on the obvious penetrating aspect of the bite. Yet, we found the blunt component of injury can have devastating consequences reflected in acute arterial, brain, and spinal cord injury. Even in the absence of significant penetrating trauma, further evaluation should be considered to exclude occult blunt arterial or neurologic injury.

Vascular cell adhesion molecule--1 expression is obligatory for endotoxin-induced myocardial neutrophil accumulation and contractile dysfunction.

BACKGROUND: Sepsis-induced cardiac dysfunction occurs commonly in critically ill patients and is associated with high mortality rates. Neutrophils play a central role in sepsis-induced lung and liver injury; however, the mechanism of sepsis-induced cardiac dysfunction remains unclear. Vascular cell adhesion molecule-1 (VCAM-1) has been implicated in neutrophil-mediated liver injury during endotoxemia and is also expressed in myocardium. The purposes of this study were to examine the temporal relationship of myocardial VCAM-1 expression with neutrophil accumulation during endotoxemia and to determine whether VCAM-1 mediates neutrophil accumulation and cardiac dysfunction during endotoxemia. METHODS: Mice were subjected to lipopolysaccharide (LPS; 0.5 mg/kg, intraperitoneally). Myocardial VCAM-1 expression and neutrophil accumulation were determined by immunofluorescence staining. Cardiac performance with or without VCAM-1 blocking antibody (5 mg/kg, intravenously) was determined by the Langendorff technique. RESULTS: LPS caused a time-dependent increase in both myocardial VCAM-1 expression and neutrophil accumulation. At 6 hours after LPS, the immunofluorescent intensity for VCAM-1 increased from 2.5 +/- 0.6 x 10(6) in saline solution controls to 19.9 +/- 3.5 x 10(6) (P <.05, analysis of variance), and neutrophil count increased from 2.4 +/- 1.7/mm(2) in saline solution controls to 13.0 +/- 2.5/mm(2) (P <.05). Left ventricular developed pressure was decreased maximally at 6 hours after LPS compared with saline solution controls (29.1 +/- 1.1 mm Hg vs 53.1 +/- 3.9 mm Hg; P <.05). Treatment with VCAM-1 monoclonal antibody abrogated both myocardial neutrophil accumulation and cardiac dysfunction during endotoxemia. CONCLUSIONS: LPS-induced myocardial dysfunction is associated with increased expression of VCAM-1 and with neutrophil accumulation. Blockade of VCAM-1 abrogates myocardial neutrophil accumulation and preserves cardiac function during endotoxemia, which supports a role for VCAM-1 as a therapeutic target for myocardial protection during sepsis.

TNF receptor I is required for induction of macrophage heat shock protein 70.

Expression of heat shock proteins (HSP) is an adaptive response to cellular stress. Stress induces tumor necrosis factor (TNF)-alpha production. In turn, TNF-alpha induces HSP70 expression. However, osmotic stress or ultraviolet radiation activates TNF-alpha receptor I (TNFR-I) in the absence of TNF-alpha. We postulated that TNF-alpha receptors are involved in the induction of HSP70 by cellular stress. Peritoneal Mphi were isolated from wild-type (WT), TNF-alpha knockout (KO), and TNFR (I or II) KO mice. Cells were cultured overnight and then heat stressed at 43 +/- 0.5 degrees C for 30 min followed by a 4-h recovery at 37 degrees C. Cellular HSP70 expression was induced by heat stress or exposure to endotoxin [lipopolysaccharide (LPS)] as determined by immunoblotting. HSP70 expression induced by either heat or LPS was markedly decreased in TNFR-I KO Mphi, whereas TNFR-II KO Mphi exhibited HSP70 expression comparable to that in WT mice. Expression of HSP70 after heat stress in TNF-alpha KO Mphi was also similar to that in WT mice, suggesting that induction of HSP70 by TNFR-I occurs independently of TNF-alpha. In addition, levels of steady-state HSP70 mRNA were similar by RT-PCR in WT and TNFR-I KO Mphi despite differences in protein expression. Furthermore, the effect of TNFR-I appears to be cell specific, since HSP70 expression in splenocytes isolated from TNFR-I KO was similar to that in WT splenocytes. These studies demonstrate that TNFR-I is required for the synthesis of HSP70 in stressed Mphi by a TNF-independent mechanism and support an intracellular role for TNFR-I.

L-arginine attenuates lipopolysaccharide-induced lung chemokine production.

Chemokines stimulate the influx of leukocytes into tissues. Their production is regulated by nuclear factor-kappaB (NF-kappaB), an inducible transcription factor under the control of inhibitory factor kappaB-alpha (IkappaB-alpha). We have previously demonstrated that L-arginine (L-Arg) attenuates neutrophil accumulation and pulmonary vascular injury after administration of lipopolysaccharide (LPS). We hypothesized that L-Arg would attenuate the production of lung chemokines by stabilizing IkappaB-alpha and preventing NF-kappaB DNA binding. We examined the effect of L-Arg on chemokine production, IkappaB-alpha degradation, and NF-kappaB DNA binding in the lung after systemic LPS. To block nitric oxide (NO) production, a NO synthase inhibitor was given before L-Arg. LPS induced the production of chemokine protein and mRNA. L-Arg attenuated the production of chemokine protein and mRNA, prevented the decrease in IkappaB-alpha levels, and inhibited NF-kappaB DNA binding. NO synthase inhibition abolished the effects of L-Arg on all measured parameters. Our results suggest that L-Arg abrogates chemokine protein and mRNA production in rat lung after LPS. This effect is dependent on NO and is mediated by stabilization of IkappaB-alpha levels and inhibition of NF-kappaB DNA binding.

Removal of an intrathoracic migrated fixation pin by thoracoscopy.

Migration of orthopedic fixation pins into the thoracic cavity can result in perforation of pulmonary vasculature, aorta, bronchus, atrium, or ventricle. Prompt diagnosis and treatment is tantamount in preventing devastating consequences. A patient who had fixation of a right humeral fracture weeks later had intrathoracic migration of a fixation pin, found by routine postoperative radiographic examination. Because the patient was asymptomatic, we removed the pin with a thoracoscopic operation. The foreign body was retrieved successfully without intraoperative or postoperative complication.

Differential cardiopulmonary recruitment of neutrophils during hemorrhagic shock: a role for ICAM-1?

Hemorrhagic shock and subsequent resuscitation can result in acute lung injury and cardiac dysfunction. Previous studies have demonstrated that tissue neutrophil accumulation contributes to cardiopulmonary injury associated with trauma. Thus, suppression of tissue neutrophil recruitment in an early therapeutic window after hemorrhagic shock may protect the cardiopulmonary system. It is unclear whether hemorrhagic shock induces cardiopulmonary recruitment of neutrophils before resuscitation. Intercellular adhesion molecule-1 (ICAM-1) is one of the important factors that mediate tissue neutrophil recruitment. The physiologic significance of ICAM-1 expression after hemorrhage before resuscitation is not well delineated. The present study examined the role of ICAM-1 in neutrophil accumulation in the heart and lung after severe hemorrhage without resuscitation. Mice were subjected to hemorrhagic shock by removal of 30% of total blood volume. Lung neutrophil number as determined by immunofluorescent staining increased by 1 h after hemorrhage and was maximal at 4 h whereas myocardial neutrophil number was not changed. Lung neutrophil accumulation was not associated with an up-regulation of ICAM-1 expression or an alteration in ICAM-1 subcellular distribution. Surprisingly, deletion of the ICAM-1 gene enhanced hemorrhagic shock-induced lung neutrophil accumulation. These results suggest that hemorrhagic shock induces preferential neutrophil accumulation to the lung that appears to occur independent of ICAM-1-expression.

Clinical applications of cardiovascular angiogenesis.

Angiogenesis is fundamental to both normal physiologic (wound healing) and pathologic (cancer) processes. Manipulation of divergent angiogenic signals promises effective therapy of atherosclerotic cardiovascular disease. Positive proangiogenic strategies promise collateral circulation to ischemic territories, while negative antiangiogenic strategies starve the fibromuscular proliferation within the atherosclerotic lesion. Indeed, recent phase 1 trials suggest that delivering DNA or recombinant protein to the site of vascular occlusion may stimulate physiologically significant collateral circulation in chronically ischemic myocardium. While symptomatic and functional improvement has been documented, toxicity profiles and effects on long-term patient survival are still unclear. The purposes of this article are as follows: (1) to review the pathophysiologic basis for pro- and antiangiogenic strategies in the treatment of cardiovascular disease, (2) to examine the clinical trials of proangiogenic gene or recombinant protein delivery into ischemic beds, and conversely, (3) to explore antiangiogenic strategies in the prevention and treatment of intimal neovascularization and smooth muscle proliferation within the vessel wall.

Cervical spine trauma in the injured child: a tragic injury with potential for salvageable functional outcome,.

BACKGROUND/PURPOSE: Cervical spine injuries are uncommon in children, and, therefore, presumptive immobilization and diagnosis remain controversial. The purpose of this study was to review the author's experience with cervical spine injuries in children to determine the incidence, injury mechanism, pattern of injury, and subsequent functional outcome. METHODS: Fifty-two children over a 6-year period (1994 to 1999) with a cervical spine injury secondary to blunt trauma were identified (1.3% incidence). The functional independent measure (FIM) was assessed at the time of discharge in each of 3 categories: communication, feeding, and locomotion. RESULTS: Mean age of the study children was 10.7 +/- 0.7 years. Eight children (15%) were less than 5 years old, and 4 (8%) were less than 2 years old. The mechanism of injury included motor vehicle crash (52%), falls (15%), bicycle accidents (11%), sports-related injuries (10%), pedestrian accidents (8%), and motorcycle crashes (4%). Seven patients died yielding an overall mortality rate of 13%. Injuries were distributed along the cervical spinal cord as follows: 5 atlanto-occipital dislocations, 28 C1 to C3 injuries, 17 C4 to C7 injuries, and 2 ligamentous injuries. FIM scores were recorded for 18 patients. Seventeen communicated independently, 14 fed themselves independently, and 12 had independent locomotive function. CONCLUSIONS: Cervical spine injuries occur in children across a spectrum of ages. Although atlanto-occipital dislocation is a highly lethal event, children with C1 to C7 injuries have a high likelihood of reasonable independent functioning.

Selective mitochondrial KATP channel opening controls human myocardial preconditioning: too much of a good thing?

BACKGROUND: Paradoxically, patients with noninsulin-dependent diabetes mellitus experience a higher cardiovascular mortality rate than patients with insulin-dependent diabetes mellitus. We have shown that K(ATP) channel inhibition, with oral sulfonylureas, prevents myocardial preconditioning and may explain the paradox of cardiovascular death in patients with noninsulin-dependent diabetes mellitus. Cardiac preconditioning is an attractive protective strategy against any elective ischemia/reperfusion (I/R) injury. The relationship between the K(ATP) channels and human myocardial preconditioning has not previously been elucidated. METHODS: Human atrial trabeculae were harvested, placed in organ baths, and paced (1 Hz). Developed force was recorded during simulated 37 degrees C I/R (30/45 or 45/60 minutes). Before I/R, trabeculae were treated transiently with a selective mitochondrial K(ATP) channel opener for 5 minutes, followed by a 10-minute washout, or were exposed to the channel opener throughout ischemia. Recovery of function is expressed as percentage of baseline developed force. Conserved creatine kinase activity (units per gram of wet tissue) was measured at the end of reperfusion as an indicator of cellular protection. RESULTS: Transient mitochondrial K(ATP) channel opening provided protection from both I/R insults. Surprisingly, there was no protection afforded by continuous mitochondrial K(ATP) channel opening. CONCLUSIONS: Transient selective mitochondrial K(ATP) channel opening protects both viability and function of human myocardium against I/R injury, although prolonged opening of the mitochondrial K(ATP) channel does not. These results reinforce the concept of preconditioning as a transient event that must be completed before the onset of ischemia.

Isolated rupture of the cisterna chyli after blunt trauma.

An 8-year-old boy was evaluated for blunt abdominal trauma after a motor vehicle crash. In the course of his workup, a computed tomography (CT) scan of the abdomen was suspicious for a duodenal injury. At surgery, the duodenum was found to be normal; however, a rupture of the cisterna chyli was identified. This injury was repaired, and the boy made an uneventful recovery. This report is one of few in the literature describing isolated injury to the cisterna chyli after blunt abdominal trauma.

Cost analysis in the management of esophageal coins: endoscopy versus bougienage.

PURPOSE: The aim of this study was to compare the safety, efficiency, and overall cost effectiveness of esophageal bougienage versus endoscopy in the retrieval of ingested coins. METHODS: Retrospective review of patients treated for esophageal coin ingestion at Children's Hospital of Wisconsin over a 1-year period using bougienage or endoscopic retrieval was conducted. (inclusion criterion) RESULTS: Twenty-seven patients were evaluated over the 1-year study period. Two patients spontaneously passed the coins before arrival and needed no further treatment. Twelve patients met criteria for bougienage, and this treatment was successful in 10 of the 12 patients. Mean length of hospital stay was 2.15 hours, and the mean cost was $546. Thirteen patients were treated successfully with endoscopy. The mean length of hospital stay was 22.7 hours, and the mean cost was $5,230. There were no complications in any of the 25 patients. CONCLUSIONS: Bougienage is equally safe, more efficient, and much less expensive than endoscopy for treatment of esophageal coins in properly selected patients. Nearly half of the patients were excluded from bougienage because of delayed presentation alone. Education of parents and physicians regarding symptoms of coin ingestion would allow primary treatment with bougienage in the majority of cases.

Human anatomical science and illustration: the origin of two inseparable disciplines.

From the early wall paintings of ancient Egyptians to the recent advent of computer graphics, medical illustrators have employed a variety of techniques and materials to enrich the art of medicine. Over the centuries, medical illustrators have captured the variety of physical findings observed in the clinical, surgical, or postmortem settings and transferred them to a permanent medium. Specifically, the study of human anatomy has enjoyed a historically popular courtship with medical artistry since 1543, when Andreas Vesalius published his now legendary work entitled De Humani Corporis Fabrica. However, the development and subsequent advancement of human anatomical illustration are indebted to individuals whose lifetimes span several centuries prior to Vesalius. The scientific achievements in anatomy manifest not only an advancement of knowledge, but also are a reflection of cultural, political, and religious beliefs. With respect to the development of human anatomic illustration, three elements were essential: the recognition of anatomy as a distinct branch of medical science, the acceptance of human dissection as a scientific method to advance understanding of anatomical structure, and the advancement in printing such that illustrations could be included alongside descriptive text. This brief study will examine these milestones while highlighting the origin of anatomical illustration in its historical context and its relationship to the development of human anatomy as a recognized medical science.