The influence of lifestyle (smoking and body mass index) on wound healing and long-term recurrence rate in 534 primary pilonidal sinus patients

Purpose

With pilonidal sinus disease (PSD) incidence increasing, lifestyle issues have been suspected to be responsible to worsen the results of PSD surgery at the same time. The influence of smoking and body mass index (BMI) on long-term recurrence rate in primary PSD surgery has not been investigated yet.

Methods

A total of 534 patients (German military cohort) were analyzed, comparing the wound healing rates of non-smoker with smoker, as well as recurrence rates in either groups. Simultaneously, the impact of BMI on wound healing and recurrence was studied. Recurrence rate was determined by Kaplan–Meier calculation following up to 20 years after primary PSD surgery.

Results

Using primary open surgery, smokers’ and non-smokers’ recurrence rates did not differ statistically (p?=?0.83; log rank). Comparable rates occurred following the primary midline closure technique (p?=?0.14; log rank). A BMI of 25 and higher was not associated with adverse wound healing neither in the primary midline closure (p?=?0.14) nor in the primary open treatment group (p?=?0.3); nevertheless, a trend may be seen that a BMI of 25 and above could assist a favorable wound healing rate.

Conclusions

The lifestyle parameter smoking and body weight statistically do not complicate wound healing or long-term recurrence rates for the first 20 years following primary PSD surgery in this study. As the BMI of 25 and above may have a beneficial influence on wound healing in primary open and primary midline closure, this observation has to be investigated for the today’s surgical procedures of elective first choice-asymmetrical and flap procedures.     

Intraspinal administration of human spinal cord‐derived neural progenitor cells in the G93A–SOD1 mouse model of ALS delays symptom progression,prolongs survival and increases expression of endogenous neurotrophic factors

Neural stem or progenitor cells are considered to be a novel therapeutic strategy for amyotrophic lateral sclerosis (ALS), based on their potential to generate a protective environment rather than to replace degenerating motor neurons. Following local injection to the spinal cord, neural progenitor cells may generate glial cells and release neurotrophic factors. In the present study, human spinal cord‐derived neural progenitor cells (hscNPCs) were injected into the lumbar spinal cord of G93A–SOD1 ALS transgenic mice. We evaluated the potential effect of hscNPC treatment by survival analysis and behavioural/phenotypic assessments. Immunohistological and real‐time PCR experiments were performed at a defined time point to study the underlying mechanisms. Symptom progression in hscNPC‐injected mice was significantly delayed at the late stage of disease. On average, survival was only prolonged for 5 days. Animals treated with hscNPCs performed significantly better in motor function tests between weeks 18 and 19. Increased production of GDNF and IGF‐1 mRNA was detectable in spinal cord tissue of hscNPC‐treated mice. In summary, treatment with hscNPCs led to increased endogenous production of several growth factors and increased the preservation of innervated motor neurons but had only a small effect on overall survival. Copyright © 2015 John Wiley & Sons, Ltd.     

The academic nursing practice dean: an emerging role

This article describes the contributions of academic nursing practice to nursing education; delineates the role characteristics and competencies needed by academic practice deans; and provides examples of the challenges and issues academic practice deans face related to nursing education, research, and practice. While schools' missions vary from a strong focus on education to multiple emphases on education, research, and practice, academic nursing practice has the potential to facilitate achievement in each of these areas. Academic nursing practice deans play important roles in advancing the missions of their schools through the clinical practice activities within the schools. Strong academic nursing practice programs can serve as catalysts for the development and refinement of new models of care delivery and for the development of future nursing leaders who are comfortable with innovation.     

Tumor-associated macrophages express lymphatic endothelial growth factors and are related to peritumoral lymphangiogenesis

Formation of lymphatic metastasis is the initial step of generalized spreading of tumor cells and predicts poor clinical prognosis. Lymphatic vessels generally arise within the peritumoral stroma, although the lymphangiopoietic vascular endothelial growth factors (VEGF)-C and -D are produced by tumor cells. In a carefully selected collection of human cervical cancers (stage pT1b1) we demonstrate by quantitative immunohistochemistry and in situ hybridization that density of lymphatic microvessels is significantly increased in peritumoral stroma, and that a subset of stromal cells express large amounts of VEGF-C and VEGF-D. The density of cells producing these vascular growth factors correlates with peritumoral inflammatory stroma reaction, lymphatic microvessel density, and indirectly with peritumoral carcinomatous lymphangiosis and frequency of lymph node metastasis. The VEGF-C- and VEGF-D-producing stroma cells were identified in situ as a subset of activated tumor-associated macrophages (TAMs) by expression of a panel of macrophage-specific markers, including CD68, CD23, and CD14. These TAMs also expressed the VEGF-C- and VEGF-D-specific tyrosine kinase receptor VEGFR-3. As TAMs are derived from monocytes in the circulation, a search in peripheral blood for candidate precursors of VEGFR-3-expressing TAMs revealed a subfraction of CD14-positive, VEGFR-3-expressing monocytes, that, however, failed to express VEGF-C and VEGF-D. Only after in vitro incubation with tumor necrosis factor-alpha, lipopolysaccharide, or VEGF-D did these monocytes start to synthesize VEGF-C de novo. In conclusion VEGF-C-expressing TAMs play a novel role in peritumoral lymphangiogenesis and subsequent dissemination in human cancer.     

Distinct Roles for Signals Relayed through the Common Cytokine Receptor γ Chain and Interleukin 7 Receptor α Chain in Natural T Cell Development

The commitment, differentiation, and expansion of mainstream α/β T cells during ontogeny depend on the highly controlled interplay of signals relayed by cytokines through their receptors on progenitor cells. The role of cytokines in the development of natural killer (NK)1⁺ natural T cells is less clearly understood. In an approach to define the role of cytokines in the commitment, differentiation, and expansion of NK1⁺ T cells, their development was studied in common cytokine receptor γ chain (γc) and interleukin (IL)-7 receptor α (IL-7Rα)–deficient mice. These mutations block mainstream α/β T cell ontogeny at an early prethymocyte stage. Natural T cells do not develop in γc-deficient mice; they are absent in the thymus and peripheral lymphoid organs such as the liver and the spleen. In contrast, NK1⁺ T cells develop in IL-7Rα–deficient mice in the thymus, and they are present in the liver and in the spleen. However, the absolute number of NK1⁺ T cells in the thymus of IL-7Rα–deficient mice is reduced to ~10%, compared to natural T cell number in the wild-type thymus. Additional data revealed that NK1⁺ T cell ontogeny is not impaired in IL-2– or IL-4–deficient mice, suggesting that neither IL-2, IL-4, nor IL-7 are required for their development. From these data, we conclude that commitment and/or differentiation to the NK1⁺ natural T cell lineage requires signal transduction through the γc, and once committed, their expansion requires signals relayed through the IL-7Rα.