Ventral Hernia Repairs: 10 year Single Institution Review at Thomas Jefferson University Hospital

Abstract Background Definitive repair of recurrent ventral hernias using abdominal wall reconstruction techniques is an essential tool in the armentarium for general and plastic surgeons. Ramirez 1 et al describes the “component separation” technique to mobilize the rectus-abdominus internal oblique and external oblique flap to correct the defect. The recurrence rate of incisional hernias increases to 20% after gastric bypass or extensive weight loss.2 The incidence of ventral hernias after failed recurrent hernia repair increases to 40%.3 It has been reported that utilizing the sliding myofascial flap repair technique, the recurrence rate was reduced to 8.5%.4 Materials and Methods This retrospective institutional study reviews 10 years of myofascial flap reconstruction 1996-2006 at TJUH. Several techniques and prosthetic materials (alloderm, permacol, vicryl, composix) were used in our institutional review by multiple surgeons in this time period. Our goal is to identify risk factors (i.e. smoking, diabetes, obesity, size of defect, peripheral vascular disease, enterocutaneous fistula, infection) that predict or categorize patients that are at increased risk for failure of primary repair, measure the complication rates (i.e. infection, recurrence, seroma, hematoma) and evaluate the techniques and long term effectiveness of several prosthetic materials. Results Three thousand twenty ventral hernia repairs were performed at TJUH between 1996 and 2006. Two thousand three hundred eighty three approximated the rectus abdominus primarily and of these 645 utilized a component separation technique. The recurrence rate for component separations was 18.5% and 83% for primary repairs. The average follow up was 5.49 years. Statistically significant risk factors (p\u3c0.05) for recurrence were obesity (BMI\u3e30 kg/m2), age\u3e65 years, male gender, preoperative infection and postoperative seroma. Conclusion Myofascial flaps are a safe, reliable therapy for recurrent ventral hernias that addresses the population of patients that have failed conventional primary closure and reduce the recurrence rates greater than 40 percent to 18.5 percent in the carefully selected patient population

Whole genome association study of brain-wide imaging phenotypes for identifying quantitative trait loci in MCI and AD: A study of the ADNI cohort

ABSTRACT A genome-wide, whole brain approach to investigate genetic effects on neuroimaging phenotypes for identifying quantitative trait loci is described. The Alzheimer's Disease Neuroimaging Initiative 1.5T MRI and genetic dataset was investigated using voxel-based morphometry (VBM) and FreeSurfer parcellation followed by genome wide association studies (GWAS). 142 measures of grey matter (GM) density, volume, and cortical thickness were extracted from baseline scans. GWAS, using PLINK, were performed on each phenotype using quality controlled genotype and scan data including 530,992 of 620,903 single nucleotide polymorphisms (SNPs) and 733 of 818 participants (175 AD, 354 amnestic mild cognitive impairment, MCI, and 204 healthy controls, HC). Hierarchical clustering and heat maps were used to analyze the GWAS results and associations are reported at two significance thresholds (p<10 -7 and p<10 -6 ). As expected, SNPs in the APOE and TOMM40 genes were confirmed as markers strongly associated with multiple brain regions. Other top SNPs were proximal to the EPHA4, TP63 and NXPH1 genes. Detailed image analyses of rs6463843 (flanking NXPH1) revealed reduced global and regional GM density across diagnostic groups in TT relative to GG homozygotes. Interaction analysis indicated that AD patients homozygous for the T allele showed differential vulnerability to right hippocampal GM density loss. NXPH1 codes for a protein implicated in promotion of adhesion between dendrites and axons, a key factor in synaptic integrity, the loss of which is a hallmark of AD. A genome wide, whole brain search strategy has the potential to reveal novel candidate genes and loci warranting further investigation and replication. Shen et al.

Proteomics of Coagulopathy Following Injury Reveals Limitations of Using Laboratory Assessment to Define Trauma-Induced Coagulopathy to Predict Massive Transfusion

Objective:. Trauma-induced coagulopathy (TIC) is provoked by multiple mechanisms and is perceived to be one driver of massive transfusions (MT). Single laboratory values using prothrombin time (INR) or thrombelastography (TEG) are used to clinically define this complex process. We used a proteomics approach to test whether current definitions of TIC (INR, TEG, or clinical judgment) are sufficient to capture the majority of protein changes associated with MT. Methods:. Eight level I trauma centers contributed blood samples from patients available early after injury. TIC was defined as INR >1.5 (INR-TIC), TEG maximum amplitude 10 units of red blood cells in 24 hours or >4 units RBC/hour during the first 4 hours. SomaLogic proteomic analysis of 1305 proteins was performed. Pathways associated with proteins dysregulated in patients with each TIC definition and MT were identified. Results:. Patients (n = 211) had a mean injury severity score of 24, with a MT and mortality rate of 22% and 12%, respectively. We identified 578 SOMAscan analytes dysregulated among MT patients, of which INR-TIC, TEG-TIC, and Clin-TIC patients showed dysregulation only in 25%, 3%, and 4% of these, respectively. TIC definitions jointly failed to show changes in 73% of the protein levels associated with MT, and failed to identify 26% of patients that received a massive transfusion. INR-TIC and TEG-TIC patients showed dysregulation of proteins significantly associated with complement activity. Proteins dysregulated in Clin-TIC or massive transfusion patients were not significantly associated with any pathway. Conclusion:. These data indicate there are unexplored opportunities to identify patients at risk for massive bleeding. Only a small subset of proteins that are dysregulated in patients receiving MT are statistically significantly dysregulated among patients whose TIC is defined based solely on laboratory measurements or clinical assessment