The use of liquid latex for detecting traces of blood following thermal exposure

International Journal of Legal Medicine - In cases of crimes involving blood, the perpetrators often attempt to remove the traces they have left behind. Setting fire to the crime scene, aside from...     

Phase 3 evaluation of HP802‐247 in the treatment of chronic venous leg ulcers

In 2012 we reported promising results from a phase 2 clinical trial of HP802‐247, a novel spray‐applied investigational treatment for chronic venous leg ulcers consisting of human, allogeneic fibroblasts and keratinocytes. We now describe phase 3 clinical testing of HP802‐247, its failure to detect efficacy, and subsequent investigation into the root causes of the failure. Two randomized, controlled trials enrolled a total of 673 adult outpatients at 96 centers in North America and Europe. The primary endpoint was the proportion of ulcers with confirmed closure at the end of 12 weeks of treatment. An investigation into the root cause for the failure of HP802‐247 to show efficacy in these two phase 3 trials was initiated immediately following the initial review of the North American trial results. Four hundred twenty‐one patients were enrolled in the North American (HP802‐247, 211; Vehicle 210) and 252 in the European (HP802‐247, 131; Vehicle 121) trials. No difference in proportion of closed ulcers at week 12 was observed between treatment groups for either the North American (HP802‐247, 61.1%; Vehicle 60.0%; p = 0.5896) or the European (HP802‐247, 47.0%; Vehicle 50.0%; p = 0.5348) trials. Thorough investigation found no likelihood that design or execution of the trials contributed to the failure. Variability over time during the trials in the clinical response implicated the quality of the cells comprising HP802‐247. Concordance between the two separate, randomized, controlled trials with distinct, nonoverlapping investigative sites and independent monitoring teams renders the possibility of a Type II error vanishingly small and provides strong credibility for the unexpected lack of efficacy observed. The most likely causative factors for the efficacy failure in phase 3 was phenotypic change in the cells (primarily keratinocytes) leading to batch to batch variability due to the age of the cell banks.     

Nationaler Konsensus zur Wunddokumentation beim Ulcus cruris

Background

Standards in the assessment and documentation of disease processes are the basis of guideline-based care. For the treatment of chronic wounds, especially leg ulcers, no approved parameters are available.

Objectives

Against this background, our aim was to develop standards for the documentation of leg ulcer in routine care. This article presents the recommendations for the classification and characteristics of the variables.

Materials and methods

The development of the documentation standard was based on a systematic literature research and was performed in a Delphi-based consensus process. The national consensus process included meetings as well as web-based questionnaires. The Consensus Group is coordinated by the German Center for Health Services Research in Dermatology (CVderm).

Results

The documentation standards and their variables for leg ulcer routine care were developed in seven meetings of the consensus group. The consensus group consists of 38 delegates of wound care societies, health insurances, wound networks and associations.

Discussion

For each variable, recommended in routine care, a distinct response scheme (defined set of variable characteristics) was defined. As a next step, a structured implementation process is required, which was part of the resolutions of the consensus group.

     

In Vitro Confirmation of Artemisinin Resistance in Plasmodium falciparum from Patient Isolates,Southern Rwanda, 2019

Artemisinin resistance in Plasmodium falciparum is conferred by mutations in the kelch 13 (K13) gene. In Rwanda, K13 mutations have increased over the past decade, including mutations associated with delayed parasite clearance. We document artemisinin resistance in P. falciparum patient isolates from Rwanda carrying K13 R561H, A675V, and C469F mutations.