Minimizing Ionizing Radiation in Evaluating Suspected Appendicitis in Children Before and After the Release of the ACEP Clinical Policy.

STUDY OBJECTIVE: The aim of this study was to examine the impact of the ACEP (American College of Emergency Physicians) clinical policy regarding diagnosis of suspected appendicitis on changing practice in the pediatric emergency department (ED) in the absence of a formal departmental protocol. METHODS: This was a retrospective chart review in a pediatric ED in which patients aged 2 to 18 years were evaluated for appendicitis via ultrasound, computed tomography (CT), or both, over a 7-year study period. We compared rates of CT utilization in the period before the release of the ACEP clinical policy regarding diagnosis and treatment of appendicitis (2008-2009) and the period after (2010-2014). Other metrics of interest were ultrasound results and physician response to results, as well as surrogate markers for quality of care. RESULTS: Seven hundred pediatric ED visits were included, with 200 prepolicy release and 500 postrelease. Computed tomography utilization decreased significantly postpolicy release from 43.5% (95% confidence interval [CI], 36.6%-50.3%) to 22.2% (95% CI, 18.5%-25.8%). The proportion of ultrasounds with indeterminate results also decreased, with 71.5% (95% CI, 65.1%-77.9%) and 55.1% (95% CI, 50.7%-59.5%) in the pre and post groups, respectively. Physicians ordered fewer CTs after indeterminate ultrasounds, decreasing from 63.7% (95% CI, 56.9%-70.5%) to 48.3%% (95% CI, 43.9%-52.7%). CONCLUSIONS: After the release of the clinical policy, CT utilization decreased significantly suggesting possible effectiveness of the policy in bringing about change in practice. Subsequently, there was an increase in the definitiveness in the ultrasound results. Physicians also evolved in their response to indeterminate ultrasound results, with fewer CTs ordered reflexively after indeterminate results.

Host attraction and biting behaviour of Anopheles mosquitoes in South Halmahera, Indonesia.

BACKGROUND: Indonesia is home to a variety of malaria vectors whose specific bionomic traits remain largely uncharacterized. Species-specific behaviours, such as host feeding preferences, impact the dynamics of malaria transmission and the effectiveness of vector control interventions. METHODS: To examine species-specific host attraction and feeding behaviours, a Latin square design was used to compare Anopheles mosquitoes attracted to human, cow, and goat-baited tents. Anopheles mosquitoes were collected hourly from the inside walls of each baited tent. Species were morphologically and then molecularly identified using rDNA ITS2 sequences. The head and thorax of individual specimens were analysed for Plasmodium DNA using PCR. Bloodmeals were identified using a multiplex PCR. RESULTS: A total of 1024, 137, and 74 Anopheles were collected over 12 nights in cow, goat, and human-baited tents, respectively. The species were identified as Anopheles kochi, Anopheles farauti s.s., Anopheles hackeri, Anopheles hinesorum, Anopheles indefinitus, Anopheles punctulatus, Anopheles tessellatus, Anopheles vagus, and Anopheles vanus, many of which are known to transmit human malaria. Molecular analysis of blood meals revealed a high level of feeding on multiple host species in a single night. Anopheles kochi, An. indefinitus, and An. vanus were infected with Plasmodium vivax at rates comparable to primary malaria vectors. CONCLUSIONS: The species distributions of Anopheles mosquitoes attracted to human, goat, and cow hosts were similar. Eight of nine sporozoite positive samples were captured with animal-baited traps, indicating that even predominantly zoophilic mosquitoes may be contributing to malaria transmission. Multiple host feeding and flexibility in blood feeding behaviour have important implications for malaria transmission, malaria control, and the effectiveness of intervention and monitoring methods, particularly those that target human-feeding vectors.

MicroRNAs associated with small bowel neuroendocrine tumours and their metastases.

Novel molecular analytes are needed in small bowel neuroendocrine tumours (SBNETs) to better determine disease aggressiveness and predict treatment response. In this study, we aimed to profile the global miRNome of SBNETs, and identify microRNAs (miRNAs) involved in tumour progression for use as potential biomarkers. Two independent miRNA profiling experiments were performed (n=90), including primary SBNETs (n=28), adjacent normal small bowel (NSB; n=14), matched lymph node (LN) metastases (n=24), normal LNs (n=7), normal liver (n=2) and liver metastases (n=15). We then evaluated potentially targeted genes by performing integrated computational analyses. We discovered 39 miRNAs significantly deregulated in SBNETs compared with adjacent NSB. The most upregulated (miR-204-5p, miR-7-5p and miR-375) were confirmed by qRT-PCR. Two miRNAs (miR-1 and miR-143-3p) were significantly downregulated in LN and liver metastases compared with primary tumours. Furthermore, we identified upregulated gene targets for miR-1 and miR-143-3p in an existing SBNET dataset, which could contribute to disease progression, and show that these miRNAs directly regulate FOSB and NUAK2 oncogenes. Our study represents the largest global miRNA profiling of SBNETs using matched primary tumour and metastatic samples. We revealed novel miRNAs deregulated during SBNET disease progression, and important miRNA-mRNA interactions. These miRNAs have the potential to act as biomarkers for patient stratification and may also be able to guide treatment decisions. Further experiments to define molecular mechanisms and validate these miRNAs in larger tissue cohorts and in biofluids are now warranted.

Glucagon receptor gene mutations with hyperglucagonemia but without the glucagonoma syndrome.

Pancreatic neoplasms producing exclusively glucagon associated with glucagon cell hyperplasia of the islets and not related to hereditary endocrine syndromes have been recently described. They represent a novel entity within the panel of non-syndromic disorders associated with hyperglucagonemia. This case report describes a 36-year-old female with a 10 years history of non-specific abdominal pain. No underlying cause was evident despite extensive diagnostic work-up. More recently she was diagnosed with gall bladder stones. Abdominal ultrasound, computerised tomography and magnetic resonance imaging revealed no pathologic findings apart from cholelithiasis. Endoscopic ultrasound revealed a 5.5 mm pancreatic lesion. Fine needle aspiration showed cells focally expressing chromogranin, suggestive but not diagnostic of a low grade neuroendocrine tumor. OctreoScan(®) was negative. Serum glucagon was elevated to 66 pmol/L (normal: 0-50 pmol/L). Other gut hormones, chromogranin A and chromogranin B were normal. Cholecystectomy and enucleation of the pancreatic lesion were undertaken. Postoperatively, abdominal symptoms resolved and serum glucagon dropped to 7 pmol/L. Although H and E staining confirmed normal pancreatic tissue, immunohistochemistry was initially thought to be suggestive of alpha cell hyperplasia. A count of glucagon positive cells from 5 islets, compared to 5 islets from 5 normal pancreata indicated that islet size and glucagon cell ratios were increased, however still within the wide range of normal physiological findings. Glucagon receptor gene (GCGR) sequencing revealed a heterozygous deletion, K349_G359del and 4 missense mutations. This case may potentially represent a progenitor stage of glucagon cell adenomatosis with hyperglucagonemia in the absence of glucagonoma syndrome. The identification of novel GCGR mutations suggests that these may represent the underlying cause of this condition.

Does the use of biopatch devices at drain sites reduce perioperative infectious complications in patients undergoing immediate tissue expander breast reconstruction?

BACKGROUND: To decrease the rate of infectious complications, surgeons have begun to use Biopatch (Ethicon, Somerville, N.J.) disks at drain exit sites. The authors investigated whether use of a Biopatch disk could convey a reduction in perioperative infections in patients undergoing immediate tissue expander breast reconstruction. METHODS: A retrospective review was conducted of all patients undergoing tissue expander/implant breast reconstruction from November of 2010 to November of 2012 at a single institution. Breasts were divided into two cohorts: controls with traditional adhesive dressings and those with Biopatch disks at drain sites. Breasts were compared based on demographics, complications, drain duration, and antibiotic type. RESULTS: A total of 1211 breasts met inclusion criteria. The control group (November of 2010 to October of 2011) included 606 breasts. The Biopatch cohort (November of 2011 to October of 2012) included 605 breasts. When comparing breasts with disks to controls, there were no statistical differences in overall infection (6.2 versus 7.4 percent; p = 0.4235), major infection (4.0 versus 4.3 percent; p = 0.8853), need for explantation (2.2 versus 1.8 percent; p = 0.5372), and mastectomy skin flap necrosis (12.6 versus 14.6 percent; p = 0.3148). However, age greater than 50 years, diabetes mellitus, hypertension, hypercholesterolemia, obesity, history of prior breast irradiation, and mastectomy skin flap necrosis were independent predictors of infectious complications. CONCLUSIONS: Biopatch disks do not reduce the rate infectious complications in patients undergoing immediate tissue expander breast reconstruction. Other conventional risks, including medical comorbidities, obesity, and mastectomy skin flap necrosis, remain significantly associated with infectious complications. CLINICAL QUESTION/LEVEL OF EVIDENCE: Therapeutic, III.

CCL11 blocks IL-4 and GM-CSF signaling in hematopoietic cells and hinders dendritic cell differentiation via suppressor of cytokine signaling expression.

The chemokine eotaxin/CCL11 is an important mediator of leukocyte migration, but its effect on inflammatory cytokine signaling has not been explored. In this study, we find that CCL11 induces suppressor of cytokine signaling (SOCS)1 and SOCS3 expression in murine macrophages, human monocytes, and dendritic cells (DCs). We also discover that CCL11 inhibits GM-CSF-mediated STAT5 activation and IL-4-induced STAT6 activation in a range of hematopoietic cells. This blockade of cytokine signaling by CCL11 results in reduced differentiation and endocytic ability of DCs, implicating CCL11-induced SOCS as mediators of chemotactic inflammatory control. These findings demonstrate cross-talk between chemokine and cytokine responses, suggesting that myeloid cells tracking to the inflammatory site do not differentiate in the presence of this chemokine, revealing another role for SOCS in inflammatory regulation.

Medical treatment at Louis Armstrong New Orleans International Airport after hurricane Katrina: the experience of disaster medical assistance teams WA-1 and OR-2.

In the week following Hurricane Katrina, over 3000 patients were evacuated by air from a triage and medical treatment station at the Louis Armstrong New Orleans International Airport. This represents the largest air evacuation in history. Over 24,000 additional evacuees were transported from the airport to shelters. Disaster Medical Assistance Teams (DMATs) from several US states were deployed to the Louis Armstrong New Orleans International Airport to provide medical care to those evacuated from New Orleans. Despite warning from the US National Weather Service of catastrophic damage to New Orleans, adequate medical staffing was not attained at the airport triage station until 6 days after the hurricane struck. Organizational lapses, including inadequate medical and operational planning, understaffing of medical personnel, and failure to utilize Incident Command System, diminished the effectiveness of the Hurricane Katrina New Orleans Medical Operation.