Murine skin flap survival may not be affected by underlying fat viability.

One problem in the treatment of degloving injuries is the accurate prediction of the survivability of the avulsed tissue. Initial evaluation frequently underestimates the degree of eventual flap loss, and in many cases, there is a progressive necrosis that continues over the ensuing days. The pathophysiology of this phenomenon is unclear. We undertook this study to test the theory that underlying devascularised fat contributes to overlying skin necrosis. A dorsal random skin flap model was used in the rat. Sixty-six rats were divided into three groups: flaps with viable fat and silicone sheeting underneath, flaps with devascularised fat and silicone sheeting underneath and control flaps with only silicone sheeting underneath. Flap necrosis (% area+/-SEM) was evaluated at one week, and found to be 27.1+/-4% in the live fat group, 33.2+/-4% in the dead fat group and 33.6+/-5% in the control group. One-way analysis of variance showed no statistically significant difference between the three groups at a power of 80%. In this study, we have shown that neither live nor dead fat has a significant influence on the survival of an overlying random skin flap in the rat.     

Levodopa-induced hyperactivity in mice treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine.

The present study examines the motor responses of 10- to 12-month-old, male C57 mice that were either given intraperitoneal (IP) injections of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP; 30 mg/kg per day) or vehicle for 10 consecutive days, followed by IP injections of levodopa (200 mg/kg) plus carbidopa (25 mg/kg). Five days of MPTP exposure resulted in the Straub tail phenomenon and pronounced hypokinesia. However, during the next 5 days, motor activity returned to baseline, even with continued MPTP treatment. After 10 to 14 days of rest, all mice were then treated with levodopa/carbidopa twice daily for multiple, consecutive days. However, only the previously MPTP-treated animals became hyperkinetic, as compared to levodopa-treated control animals that were not previously exposed to MPTP. Abnormal activity included scratching, running, gnawing, and jumping movements. Hyperactivity lasted for approximately 2 hours after each levodopa injection and then returned to baseline, but the amount of hyperkinesia increased with additional days of levodopa treatment, even though the daily levodopa dose was not changed. These results demonstrate that levodopa can cause reproducible hyperactivity in mice that were previously exposed to MPTP.     

Minimal Acute Rejection after Lung Transplantation: A Risk for Bronchiolitis Obliterans Syndrome

Bronchiolitis obliterans syndrome (BOS) is a major cause of lung allograft dysfunction. Although previous studies have identified mild to severe rejection (grade>or=A2) as a risk factor for BOS, the role of minimal rejection (grade A1) remains unclear. To determine if A1 rejection by itself is a risk factor for BOS, we performed a retrospective cohort study on 228 adult lung transplant recipients over a 7-year period. Cohorts were defined by their most severe rejection episode (none, A1 only, and >or=A2) and analyzed for the subsequent development and progression of BOS using univariate and multivariate time-dependent Cox regression analysis. In the univariate model, the occurrence of isolated minimal rejection was a risk factor for all stages of BOS. Similarly, multivariate models that included HLA mismatch, cytomegalovirus pneumonitis, community acquired viral infection, underlying disease and type of transplant demonstrated that A1 rejection was a distinct risk factor for BOS. Furthermore, the associated risk with A1 rejection was slightly greater than the risk from >or=A2 and treatment of A1 rejection decreased the risk for subsequent BOS stage 1. We conclude that minimal rejection is associated with an increased risk for BOS development and progression that is comparable to A2 rejection.     

Adhesive small bowel obstruction: epidemiology, biology and prevention

Intraabdominal adhesions develop after abdominal surgery as part of the normal healing processes that occur after damage to the peritoneum. Over the last 2 decades, much research has gone into understanding the biochemical and cellular processes that lead to adhesion formation. The early balance between fibrin deposition and degradation seems to be the critical factor in adhesion formation. Although adhesions do have some beneficial effects, they also cause significant morbidity, including adhesive small bowel obstruction, infertility and increased difficulty with reoperative surgery. Several strategies have been employed over the years to prevent adhesion formation while not interfering with wound healing. This article summarizes much of our current understanding of adhesion formation and strategies that have been employed to prevent them.     

Antibiotic prescribing for chronic skin wounds in primary care

The aim of this study was to describe and quantify systemic antibiotic prescribing for patients with chronic skin wounds presenting at the primary care, nonspecialist setting. Data for 1 year were extracted from a general practice morbidity database comprising approximately 185,000 patients attending family medical practitioners in Wales. Patients with chronic wounds (PCW) were identified using Read Codes and compared with nonwound patients who were randomly selected after matching for age-band, sex, and general practice. PCW received a significantly greater number of antibiotic courses than nonwound patients (p<0.001). This increased level of prescribing was evident for flucloxacillin, co-amoxiclav, cefaclor, cefalexin, erythromycin, trimethoprim, metronidazole, and ciprofloxacin (p<0.01 for all). While PCW also had a significantly higher prevalence of diabetes (16.5% compared with 6.6%, p<0.001), and attended at general practice significantly more frequently than nonwound patients (median (interquartile range) of 25 (17-40) visits per year compared with 12 (4-20), p<0.001), importantly, exclusion of diabetic patients and analysis of the proportion of visits on which patients received antibiotics did not affect the significance of the difference in antibiotic consumption. These data show a strong association between occurrence of chronic wounds and prescribing of antibiotics in primary health care, and wide variation in the type and duration of antibiotic therapy for chronic wounds. Further work is now indicated to rationalize this prescribing and determine the role that this exposure to antibiotics plays in the prevalence of antibiotic resistance in this at-risk elderly population.     

RE: Histoplasmosis in a child with JRA on low-dose methotrexate

SIR, We appreciate the comments of Kleiman et al., which serveto     

A study of the freeze-drying conditions of calixarene based solid lipid nanoparticles.

In this note, we report a study of cryoprotectant carbohydrate (glucose, fructose, mannose and maltose) effects on the reconstitution of calixarene based solid lipid nanoparticle (SLN) suspensions after freeze-drying, studied by atomic force microscopy and photon correlation spectroscopy. All carbohydrates tested showed excellent cryoprotection and redispersion properties with the calixarene based SLNs.     

The human CD40 gene lies within chromosome 20q deletions associated with myeloid malignancies

Deletions of chromosome 20q are associated with myeloid malignancies and have been previously shown to arise in a multipotent progenitor of both myeloid and B cells. However, B-cell differentiation from the abnormal progenitor was impaired. The CD40 antigen is a surface glycoprotein which is expressed in B cells and haemopoietic stem cells and is important for B-cell growth and development. Following the recent mapping of CD40 to chromosome 20q we sought to determine its position relative to 20q deletions. Analysis of lymphoblastoid cell lines carrying 20q deletions placed CD40 within a 19–21 cM interval which is almost coincidental with the common deleted region defined by previous analysis of patient samples. Our results raise the possibility that genetic alteration of this locus may contribute to the pathogenesis of myeloid disorders associated with 20q deletions.