Microsurgery Training in Plastic Surgery.

Advances in surgical instruments, magnification technology, perforator dissection techniques, and vascular imaging over the past decades have facilitated exponential growth in the field of microsurgery. With wide application potential including but not limited to limb salvage, breast reconstruction, lymphedema treatment, and sex affirmation surgery, microsurgery represents a critical skill set that powerfully augments the reconstructive armamentarium of plastic surgeons. Accordingly, microsurgical training is now a critical component of the plastic surgery residency education curriculum. Trainees must meet minimum microsurgery case requirements in addition to the core competencies outlined by the Accreditation Council for Graduate Medical Education. Through the use of simulation models, residency programs increasingly incorporate early skills development and assessment in microsurgery in the laboratory. Beyond residency, microsurgery fellowships offer additional exposure and refinement by offering volume, complexity, autonomy, and possible focused specialization. With continued refinement in technology and advances in knowledge, new types of simulation training models will continue to be developed and incorporated into microsurgery training curricula.

Tumor cells, rather than dendritic cells, deliver antigen to the lymph node for cross-presentation.

It is widely accepted that generation of tumor specific CD8+ T-cell responses occur via cross-priming; however the source of tumor antigen for this event is unknown. We examined the source and form of tumor antigen required for cross-presentation in the local lymph node (LN) using a syngeneic mouse tumor model expressing a marker antigen. We found that cross-presentation of this model tumor antigen in the LN is dependent on continuous traffic of antigen from the tumor site, but without any detectable migration of tumor resident dendritic cells (DCs). Instead, small numbers of tumor cells metastasize to local LNs where they are exposed to a localized CTL attack, resulting in delivery of tumor antigen into the cross-presentation pathway.

Urinary proteases degrade albumin: implications for measurement of albuminuria in stored samples.

BACKGROUND: Previous studies have shown that albumin in stored urine samples degrades over time, and that albumin losses are greatest in samples with low pH conditions (pH < 5). Furthermore, the high-performance liquid chromatography (HPLC) assay for urinary albumin has been shown to be particularly susceptible to the effects of prolonged storage. METHODS: Frozen urine samples, stored for 12 months at -70 and -20 degrees C, were analysed for albumin fragmentation. Urinary protease activity was investigated in vitro in urine adjusted to pH 2.3-2.5. Albumin was measured by nephelometry, HPLC and sodium dodecyl sulphate-polyacrylamide gel electrophoresis. RESULTS: In the unadjusted samples, albumin was degraded in 11 out of 40 samples stored at -20 degrees C. In the in vitro experiments, both endogenous albumin and exogenous albumin added to urine were rapidly degraded into large fragments within minutes after adjustment to low pH. The fragments produced were consistent with those produced during digestion with pepsin and urinary degradation was completely inhibited by pepstatin. Albumin concentration measured by HPLC was most dramatically affected, with near-complete loss of albumin-sized material within one hour of incubation at pH 2.3-2.5. Sample reactivity with antiserum in a nephelometry assay initially declined then increased, possibly due to exposure of internal epitopes during albumin digestion. CONCLUSIONS: This study demonstrated that proteases are present and active in stored human urine samples. Urinary albumin digestion occurred in a manner consistent with activity of endogenous urinary proteases. Adjustment to neutral pH or addition of protease inhibitors may be useful techniques for sample preservation.