Chronic wounds affect over 4 million individuals and pose a significant burden to the US healthcare system. Diabetes, venous stasis, radiation or paralysis are common risk factors for chronic wounds. Unfortunately, the current standard of care (SOC) has a high relapse rate and these wounds continue to adversely affect patients' quality of life. Fortunately, advances in tissue engineering have allowed for the development of cell-based wound dressings that promote wound healing by improving cell migration and differentiation. As the available options continue to increase in quantity and quality, physicians should have a user-friendly guide to reference when deciding which dressing to use. The objective of this review is to identify the currently available biologic dressings, describe their indications, and provide a framework for integration into clinical practice. This review included 53 studies consisting of prospective and retrospective cohorts as well as several randomized control trials. Three general categories of cell-based biologic dressings were identified and nine brands were included. Cell-based biologic dressings have shown efficacy in a broad range of scenarios, and studies examining their efficacy have improved our understanding of the pathophysiology of chronic wounds. Amniotic and placental membranes have the widest scope and can be used to treat all subtypes of chronic wounds. Human skin allografts and bioengineered skin substitutes can be used for chronic ulcers but generally require a vascularized wound bed. Autologous platelet rich plasma (PRP) has shown promise in venous stasis ulcers and decubitus ulcers that have failed conventional treatment. Overall, more research is necessary to determine if these novel therapeutic options will change the current SOC, but current studies demonstrate encouraging results in the treatment of chronic wounds.

Latinos in the United States experience numerous alcohol-related health disparities. There is accumulating evidence that pre-immigration factors are associated with post-immigration alcohol use, but the explanation for health disparities remains unclear. The present study is a secondary analysis of data from the Recent Latino Immigrant Study (RLIS), the first community-based cohort study to examine the pre- to post-immigration alcohol use trajectories of young adult Latino immigrants during their initial years in the United States. Exploratory analysis and hierarchical multiple logistic regression were performed to assess associations between various pre- and post-immigration factors and alcohol misuse among young adult Latino immigrants early in the immigration process. Using an ecodevelopmental approach, we examined potential social and environmental determinants across multiple levels of influence associated with post-immigration alcohol misuse in this population. The study sample consisted of 474 young adult Latino immigrants between the ages of 18–34. The sample was comprised of the following national/regional origins: Cuban (43%), South American (28.7%), and Central American (28.3%). Approximately half of the sample (49.6%) reported a family history of substance use problems (FHSUP+). Participants who reported FHSUP+ and who engaged in alcohol misuse prior to immigrating to the US were more likely to engage in post-immigration alcohol misuse. Results revealed various social and environmental factors associated with pre-immigration alcohol misuse in this population. Study findings can inform culturally tailored prevention interventions aimed at mitigating problem drinking behaviors among young adult recent Latino immigrants.

Background: The fibroblast growth factor receptor (FGFR) family includes transmembrane receptors involved in a wide range of developmental and postdevelopmental biologic processes as well as a wide range of human diseases. In particular, FGFR3 has been implicated in the mechanism by which 9-cis retinoic acid (9-cisRA) induces lymphangiogenesis and improves lymphedema. The purpose of this study was to validate the efficacy of a novel small peptide FGFR3 inhibitor, peptide P3 (VSPPLTLGQLLS), and to elucidate the role of FGFR3 in 9-cisRA-induced lymphangiogenesis using this peptide. Methods and Results: Peptide P3 effectively inhibited FGFR3 phosphorylation. In vitro, peptide P3-mediated FGFR3 inhibition did not decrease lymphatic endothelial cell (LEC) proliferation, migration, or tubule formation. However, peptide P3-mediated FGFR3 inhibition did block 9-cisRA-stimulated LEC proliferation, migration, and tubule formation. In vivo, peptide P3-mediated FGFR3 inhibition was sufficient to inhibit 9-cisRA-induced tracheal lymphangiogenesis. Conclusion: FGFR3 does not appear to be essential to nonpromoted LEC proliferation, migration, and tubule formation. However, FGFR3 may play a key role in LEC proliferation, migration, tubule formation, and postnatal in vivo lymphangiogenesis when pharmacologically induced by 9-cisRA. P3 may have the potential to be used as a precise regulatory control element for 9-cisRA-mediated lymphangiogenesis.

Vascularized lymph node transfer (VLNT) is a promising treatment modality for lymphedema; however, how lymphatic tissue responds to ischemia has not been well defined. This study investigates the cellular changes that occur in lymph nodes in response to ischemia and reperfusion. Lymph node containing superficial epigastric artery-based groin flaps were isolated in Prox-1 EGFP rats which permits real time identification of lymphatic tissue by green fluorescence during flap dissection. Flaps were subjected to ischemia for either 1, 2, 4, or 8 hours, by temporarily occluding the vascular pedicle. Flaps were harvested after 0 hours, 24 hours, or 5 days of reperfusion. Using EGFP signal guidance, lymph nodes were isolated from the flaps and tissue morphology, cell apoptosis, and inflammatory cytokines were quantified and analyzed via histology, immunostaining, and rtPCR. There was a significant increase in collagen deposition and tissue fibrosis in lymph nodes after 4 and 8 hours of ischemia compared to 1 and 2 hours, as assessed by picrosirius red staining. Cell apoptosis significantly increased after 4 hours of ischemia in all harvest times. In tissue subject to 4 hours of ischemia, longer reperfusion periods were associated with increased rates of CD3 + and CD45 + cell apoptosis. rtPCR analysis demonstrated significantly increased expression of CXCL1/GRO-α with 2 hours of ischemia and increased PECAM-1 and TNF-α expression with 1 hour of ischemia. Significant cell death and changes in tissue morphology do not occur until after 4 hours of ischemia; however, analysis of inflammatory biomarkers suggests that ischemia reperfusion injury can occur with as little as 2 hours of ischemia.

The free transverse rectus abdominis myocutaneous (fTRAM) flap is a frequently used option for autologous breast reconstruction, typically based on deep inferior epigastric vessels anastomosed to either the axillary or internal mammary systems. The distal portion of the fTRAM flap is routinely discarded prior to anastomosis, due to tenuous blood supply in the vascular territory most distal to the pedicle. This becomes problematic in cases that require use of the entire flap, such as in thin patients with large soft-tissue defects. We report a case where an additional "supercharged" venous microsurgical anastomosis was successfully performed to minimize adverse events while utilizing the entire fTRAM flap.