Single-Use Negative Pressure Wound Therapy Applied on Various Wound Types: An Interventional Case Series.

PURPOSE: The purpose of this study was to determine whether a single-use negative pressure wound therapy (NPWT) system achieves individualized goals of therapy when used to treat patients with a variety of wound types. DESIGN: Multiple case series. SUBJECTS AND SETTING: The same comprised 25 participants; their mean age was 51.2 years (SD: 18.2; range: 19-79 years); 14 were male (56%) and 11 were female (44%). Seven study participants withdrew from study participation. Wound etiologies vary; 4 had diabetic foot ulcers; 1 had a full-thickness pressure injury; 7 were treated for management of an abscess or cyst; 4 had necrotizing fasciitis, 5 had nonhealing postsurgical wounds, and 4 had wounds of other etiologies. Data were collected at 2 ambulatory wound care clinics located in the Southeastern United States (Augusta and Austell, Georgia). METHODS: A single-outcome measure was selected for each participant by his or her attending physician at a baseline visit. Selected end points were (1) decrease in wound volume, (2) decrease in size of the tunneling area, (3) decrease in size of the undermining, (4) decrease in the amount of slough, (5) increase in granulation tissue formation, (6) decrease in periwound swelling, and (7) wound bed progression toward transition to another treatment modality (such as standard dressing, surgical closure, flap, or graft). Progress toward the individualized goal was monitored until the goal was achieved (study end point) or a maximum of 4 weeks following initiation of treatment. RESULTS: The most common primary treatment goal was to achieve a decrease in wound volume (22 of 25 study participants), and the goal to increase granulation tissue was chosen for the remaining 3 study participants. A majority of participants (18 of 23, 78.3%) reached their individualized treatment outcome. The remaining 5 participants (21.7%) were withdrawn during the study (for reasons not related to the therapy). The median (interquartile range [IQR]) duration of NPWT therapy was 19 days (IQR: 14-21 days). Between baseline and the final assessment, median reductions in wound area and volume were 42.7% (IQR: 25.7-71.5) and 87.5% (IQR: 30.7-94.6). CONCLUSIONS: The single-use NPWT system achieved multiple individualized treatment objectives in a variety of wound types. Individually selected goals of therapy were met by all study participants who completed the study.

Examining the Role of Antimicrobial Irrigation and Capsular Contracture: A Systematic Review and Meta-analysis.

PURPOSE: The purpose of this study was to conduct a meta-analysis to determine if irrigation of breast implant pockets with antibiotics reduces the rate of capsular contracture (CC). Capsular contracture is the most common complication after primary augmentation mammoplasty, yet its etiology remains cryptogenic. METHODS: PubMed was searched for publications from January 1 of 2000 through October of 2015. Studies with the following criteria were included: primary breast augmentation with implants, use of antimicrobial irrigation (AMI), and documentation of CC. The primary outcome studied was incidence of CC. The quality of included studies was assessed independently. Studies were meta-analyzed to obtain a pooled odds ratio (OR) describing the effect of AMI on CC. RESULTS: The meta-analysis included 8 studies and 10,923 patients. A total of 5348 patients received AMI, and 5575 patients did not. Our analysis revealed that the combined AMI, the antibiotic irrigation subgroup, and the iodine subgroup were associated with an increased propensity for CC [OR, 2.60; 95% confidence interval (CI), 2.3-2.94, I = 97%, P < 0.00001; OR, 1.42; 95% CI, 1.14-1.78, I = 89%, P < 0.00001; OR, 0.54; 95% CI, 0.24-1.22, P = 0.05; I = 73], respectively. CONCLUSIONS: Antimicrobial irrigation of implant pockets fails to reduce the propensity for CC. The authors recommend that further prospective multicenter trials be conducted to further elucidate the role of antibiotic irrigation in CC.

Rabbit polyclonal mouse antithymocyte globulin administration alters dendritic cell profile and function in NOD mice to suppress diabetogenic responses.

Mouse antithymocyte globulin (mATG) prevents, as well as reverses, type 1 diabetes in NOD mice, through mechanisms involving modulation of the immunoregulatory activities of T lymphocytes. Dendritic cells (DC) play a pivotal role in the generation of T cell responses, including those relevant to the autoreactive T cells enabling type 1 diabetes. As Abs against DC are likely generated during production of mATG, we examined the impact of this preparation on the phenotype and function of DC to elucidate novel mechanisms underlying its beneficial activities. In vivo, mATG treatment transiently induced the trafficking of mature CD8(-) predominant DC into the pancreatic lymph node of NOD mice. Splenic DC from mATG-treated mice also exhibited a more mature phenotype characterized by reduced CD8 expression and increased IL-10 production. The resultant DC possessed a potent capacity to induce Th2 responses when cultured ex vivo with diabetogenic CD4(+) T cells obtained from BDC2.5 TCR transgenic mice. Cotransfer of these Th2-deviated CD4(+) T cells with splenic cells from newly diabetic NOD mice into NOD.RAG(-/-) mice significantly delayed the onset of diabetes. These studies suggest the alteration of DC profile and function by mATG may skew the Th1/Th2 balance in vivo and through such actions, represent an additional novel mechanism by which this agent provides its beneficial activities.

Kidney-derived stromal cells modulate dendritic and T cell responses.

Multipotent mesenchymal stromal cells from the bone marrow ameliorate acute kidney injury through a mechanism other than transdifferentiation into renal tissue. Stromal cells exert immunoregulatory effects on dendritic and T cells, both of which are important in the pathophysiology of immune-mediated kidney injury. We hypothesized that similar cells with immunoregulatory function exist within the adult kidney. We isolated murine kidney-derived cells with morphologic features, growth properties, and an immunophenotype characteristic of mesenchymal stromal cells. These cells lacked lineage markers and could be differentiated into mesodermal cell lineages, including osteocytes and adipocytes. Furthermore, these kidney-derived cells induced the generation of bone marrow-derived dendritic cells with significantly reduced MHC II expression, increased CD80 expression, increased IL-10 production and the inability to stimulate CD4+ T cell proliferation in allogeneic and nominal antigen-specific cultures. Experiments in mixed and transwell cultures demonstrated that the production of soluble immune modulators, such as IL-6, was responsible for these effects on dendritic cell differentiation and maturation. Contact-dependent mechanisms, however, inhibited mitogenic T cell proliferation. In summary, kidney-derived cells may suppress inflammation in the kidney in vivo; a better understanding of their biology could have therapeutic implications in a wide variety of immune-mediated kidney diseases.

Lymphocytes and ischemia-reperfusion injury.

Ischemia reperfusion injury (IRI) is a common and important clinical problem in many different organ systems, including kidney, brain, heart, liver, lung, and intestine. IRI occurs during all deceased donor organ transplants. IRI is a highly complex cascade of events that includes interactions between vascular endothelium, interstitial compartments, circulating cells, and numerous biochemical entities. It is well established that the innate immune system, such as complement, neutrophils, cytokines, chemokines, and macrophages participate in IRI. Recent data demonstrates an important role for lymphocytes, particularly T cells but also B cells in IRI. Lymphocytes not only participate in augmenting injury responses after IRI, but could also be playing a protective role depending on the cell type and stage of injury. Furthermore, lymphocytes appear to be participating in the healing response from IRI. These new data open the possibility for lymphocyte targeted therapeutics to improve the short and long term outcomes from IRI.