Isolated rupture of the left atrial appendage after blunt chest trauma

Traumatic cardiac damage is caused by penetrating or blunt injury.The majority of disruptures in blunt trauma are the result of deceleration traumas.We present the case of an 8-year-old boy who fell off his horse. Afterwards the horse stepped on his chest. He was successfully treated for pericardial tamponade due to an isolated left appendage rupture. The lesion was probably caused by a sudden elevated intra-atrial blood pressure during chest compression.     

Syntaxin 11 is required for NK and CD8+ T‐cell cytotoxicity and neutrophil degranulation

Syntaxin 11 (STX11) controls vesicular trafficking and is a key player in exocytosis. Since Stx11 mutations are causally associated with a familial hemophagocytic lymphohistio‐cytosis, we wanted to clarify whether STX11 is functionally important for key immune cell populations. This was studied in primary cells obtained from newly generated Stx11^?/? mice. Our data revealed that STX11 is not only widely expressed in different immune cells, but also induced upon LPS or IFN‐γ treatment. However, Stx11 deficiency does not affect macrophage phagocytic function and cytokine secretion, mast cell activation, or antigen presentation by DCs. Instead, STX11 selectively controls lymphocyte cytotoxicity in NK and activated CD8⁺ T cells and degranulation in neutrophils. Stx11^?/? NK cells and CTLs show impaired degranulation, despite a comparable activation, maturation and expression of the complex‐forming partners MUNC18–2 and VTI1B. In addition, Stx11^?/? CTLs and NK cells produce abnormal levels of IFN‐γ. Since functional reconstitution rescues the defective phenotype of Stx11^?/? CTLs, we suggest a direct, specific and key role of STX11 in controlling lymphocyte cytotoxicity, cytokine production and secretion. Finally, we show that these mice are a very useful tool for dissecting the role of STX11 in vesicular trafficking and secretion.     

Extinction,generalization, and return of fear: A critical review of renewal research in humans

The main behavioral signature of fear extinction is its fragility. This is exemplified by the renewal effect, where a change in the background context produces recovery of fear to a conditioned-and-extinguished stimulus. Renewal is the backbone of a widely accepted theory of extinction in animal research, as well as an important experimental model to screen novel treatment techniques. This has led to an explosion of fear renewal research in humans. However, the mere observation of return of fear in a renewal procedure is not sufficient to validate this particular theory of extinction in the tested sample/procedure. Here, we systematically outline a set of experimental tests that aid in evaluating alternative extinction/renewal mechanisms. We examine published renewal studies in human fear conditioning and conclude that the prevailing theory of extinction is often taken for granted, but critical tests are lacking. Including these tests in future research will not only reveal the fear extinction mechanism in humans, but also inspire further developments in extinction treatment research.     

Precise ablation of dental hard tissues with ultra-short pulsed lasers. Preliminary exploratory investigation on adequate laser parameters

This study aimed to evaluate the possibility of introducing ultra-short pulsed lasers (USPL) in restorative dentistry by maintaining the well-known benefits of lasers for caries removal, but also overcoming disadvantages, such as thermal damage of irradiated substrate. USPL ablation of dental hard tissues was investigated in two phases. Phase 1—different wavelengths (355, 532, 1,045, and 1,064 nm), pulse durations (picoseconds and femtoseconds) and irradiation parameters (scanning speed, output power, and pulse repetition rate) were assessed for enamel and dentin. Ablation rate was determined, and the temperature increase measured in real time. Phase 2—the most favorable laser parameters were evaluated to correlate temperature increase to ablation rate and ablation efficiency. The influence of cooling methods (air, air–water spray) on ablation process was further analyzed. All parameters tested provided precise and selective tissue ablation. For all lasers, faster scanning speeds resulted in better interaction and reduced temperature increase. The most adequate results were observed for the 1064-nm ps-laser and the 1045-nm fs-laser. Forced cooling caused moderate changes in temperature increase, but reduced ablation, being considered unnecessary during irradiation with USPL. For dentin, the correlation between temperature increase and ablation efficiency was satisfactory for both pulse durations, while for enamel, the best correlation was observed for fs-laser, independently of the power used. USPL may be suitable for cavity preparation in dentin and enamel, since effective ablation and low temperature increase were observed. If adequate laser parameters are selected, this technique seems to be promising for promoting the laser-assisted, minimally invasive approach.     

Impact of Early Parenteral Nutrition on Metabolism and Kidney Injury

A poor nutritional state and a caloric deficit associate with increased morbidity and mortality, but a recent multicenter, randomized controlled trial found that early parenteral nutrition to supplement insufficient enteral nutrition increases morbidity in the intensive care unit, including prolonging the duration of renal replacement therapy, compared with withholding parenteral nutrition for 1 week. Whether early versus late parenteral nutrition impacts the incidence and recovery of AKI is unknown. Here, we report a prespecified analysis from this trial, the Early Parenteral Nutrition Completing Enteral Nutrition in Adult Critically Ill Patients (EPaNIC) study. The timing of parenteral nutrition did not affect the incidence of AKI, but early initiation seemed to slow renal recovery in patients with stage 2 AKI. Early parenteral nutrition did not affect the time course of creatinine and creatinine clearance but did increase plasma urea, urea/creatinine ratio, and nitrogen excretion beginning on the first day of amino acid infusion. In the group that received late parenteral nutrition, infusing amino acids after the first week also increased ureagenesis. During the first 2 weeks, ureagenesis resulted in net waste of 63% of the extra nitrogen intake from early parenteral nutrition. In conclusion, early parenteral nutrition does not seem to impact AKI incidence, although it may delay recovery in patients with stage 2 AKI. Substantial catabolism of the extra amino acids, which leads to higher levels of plasma urea, might explain the prolonged duration of renal replacement therapy observed with early parenteral nutrition.The development of AKI is a frequent and devastating condition in patients admitted to the intensive care unit (ICU). Short-term mortality is high and increases with worsening AKI stages.¹ In AKI survivors, renal recovery is often incomplete, progression to ESRD may be accelerated, and longer-term mortality rates are increased compared with non-AKI patients.^2,3 Patient management consists of maximal prevention of additional renal damage by hemodynamic stabilization and prevention of (iatrogenic) nephrotoxicity. A curative strategy for established AKI is currently unavailable.⁴Observational studies, finding associations between a poor nutritional state and increased morbidity and mortality of AKI patients⁵ and between accumulation of a caloric deficit and poor renal and survival outcome of ICU patients,^6,7 have led to the hypothesis that feeding could ameliorate kidney injury and improve survival of ICU patients. However, nutrition, especially parenteral nutrition (PN), also has potential complications.^8–11 Because of the lack of adequately designed studies, nutritional guidelines are largely based on expert opinion.^12–14 These opinions invariably recommend the early initiation of enteral feeding but substantially differ in their recommendation on when to start supplemental PN.The Early Parenteral Nutrition Completing Enteral Nutrition in Adult Critically Ill Patients (EPaNIC) study was the first large, multicenter, randomized controlled trial (RCT) addressing this important question. The study showed that early initiation of PN increased dependency on intensive care compared with withholding supplemental PN for 1 week (hereafter labeled early PN and late PN, respectively).¹⁵ Indeed, early PN prolonged the ICU and hospital length of stay (LOS), increased the incidence of new infections, and prolonged the need for mechanical ventilation. Renal harm was suggested by a clear prolongation of the duration of renal replacement therapy (RRT) in ICU and a trend for more AKI (defined as a doubling or more of ICU admission plasma creatinine). However, the number of patients requiring RRT was unaltered, and recovery to premorbid kidney function was not investigated.It was preplanned to study the detailed impact of early versus late PN on the incidence and recovery of AKI and the time course of blood/urine markers of renal function during ICU stay.¹⁶ A priori, we hypothesized that early PN would attenuate kidney injury. However, the original study findings suggested that AKI incidence and renal recovery could be aggravated by increased macronutrient provision in the acute phase of critical illness.     

Fundamentals of randomized clinical trials in wound care: Reporting standards

In wound care research, available high‐level evidence according to the evidence pyramid is rare, and is threatened by a poor study design and reporting. Without comprehensive and transparent reporting, readers will not be able to assess the strengths and limitations of the research performed. Randomized clinical trials (RCTs) are universally acknowledged as the study design of choice for comparing treatment effects. To give high‐level evidence the appreciation it deserves in wound care, we propose a step‐by‐step reporting standard for comprehensive and transparent reporting of RCTs in wound care. Critical reporting issues (e.g., wound care terminology, blinding, predefined outcome measures, and a priori sample size calculation) and wound‐specific barriers (e.g., large diversity of etiologies and comorbidities of patients with wounds) that may prevent uniform implementation of reporting standards in wound care research are addressed in this article. The proposed reporting standards can be used as guidance for authors who write their RCT, as well as for peer reviewers of journals. Endorsement and application of these reporting standards may help achieve a higher standard of evidence and allow meta‐analysis of reported wound care data. The ultimate goal is to help wound care professionals make better decisions for their patients in clinical practice.