Reverse second dorsal metacarpal artery vascularized bone flap for index distal bone loss: A case report.

Fingertip trauma with resultant bony loss is optimally reconstructed with an autologous bone substitute, offering a unique opportunity for use of a local vascularized bone graft. The second dorsal metacarpal artery is well-described for use in soft tissue and bony reconstruction, with recent cadaveric studies suggesting a reverse-flow second dorsal metacarpal artery bone flap could reach defects in the distal phalanx. The aim of the current report is to illustrate the use of this technique in reconstructing the distal digit in a traumatized index finger with bony loss of the middle third of the distal phalanx. A 49-year-old man presented with a traumatic circular saw injury to his left index finger, with the unique finding of distal phalanx bony loss to the middle third of this bone, with no associated disruption of palmar or dorsal structures. Reconstructive goals were solely that of bony reconstruction, with no soft tissue coverage required. A reverse SDMA vascularized bone flap was successfully used for reconstruction, with the vascularized bone flap mobilized on its reverse SDMA pedicle and pivoted at the level of the distal anastomoses between the palmar and dorsal metacarpal arteries. There was uncomplicated donor and recipient site closures, and good functional outcomes with the ability to retain full distal interphalangeal joint motion and force on distal pinch grip. This case shows that the reverse second dorsal metacarpal artery vascularized bone flap may be undertaken to reconstruct bony loss in the distal phalanx.

IL-2 receptor gamma chain cytokines differentially regulate human CD8+CD127+ and CD8+CD127- T cell division and susceptibility to apoptosis.

Expression of IL-7 receptor alpha (CD127) is associated with naive and memory (i.e. non-effector) CD8+ T cell phenotypes. Effector CD8+ T cells are predominantly CD127- and most die by apoptosis. Therefore, CD127 appears to be a marker for CD8+ T cell differentiation, yet its role in CD8+ T cell survival and memory development is unclear. To address this, we investigated the cell death and cell division of isolated CD8+CD127+ and CD8+CD127- T cells in response to common IL-2 receptor gamma chain (gamma(C)) cytokines other than IL-7. We show here that (i) memory cells (CD127+CD45RA-) divide frequently in response to either IL-2, -4 or -15; (ii) IL-2 and -15 enhance cell division in effector-memory-like cells (CD127-CD45RA+) while IL-4 enhances the cell division of effector cells (CD127-CD45RA-); (iii) CD8+CD127+ T cells are more sensitive to the anti-apoptotic effects of IL-2 or IL-15 than CD8+CD127- T cells and (iv) CD8+CD127+ T cell produce more Bcl-2 in response to IL-2 or IL-15 compared with CD8+CD127- T cells. Therefore, CD8+CD127+ and CD8+CD127- T cells differ in their responsiveness to cell division and anti-apoptotic signals from IL-2, -4 and -15. This suggests a role for gamma(C) cytokines in the pathogenesis of diseases in which CD127 expression is altered on CD8+ T cells such as in progressive viral infections and cancer.

Treating gynecologic malignancies in elderly patients.

AIM: To determine the relative benefits of full and partial treatment for gynecologic malignancies in elderly patients. METHODS: A retrospective cohort study of all consecutive patients (n=169) aged 79 and older (median age 82 y; range, 79 to 94 y), diagnosed between 1971 and 2007 with various types of gynecologic malignancies (endometrial, 52%; ovarian, 26%; vulvar, 11%; cervical, 5%; other, 6%) was conducted. Stages were I to II (47%), III to IV (35.5%), and unknown (17.5%). Major comorbidities were hypertension (51%), diabetes (17%), cardiac diseases (34%), and other malignancy (12%). Regardless of age or chronic illnesses, patients were grouped on the basis of having been treated optimally (100 patients; 59.2%), defined as the accepted standard for each diagnosis and stage including surgery and adjuvant radiation or chemotherapy as indicated; or suboptimally (69 patients; 40.8%), that is, no or only partial treatment. Kaplan-Meier survival analysis and Cox proportional hazard models, univariate and multivariable were conducted. RESULTS: For all patients with suboptimal treatment, the age-and-stage-adjusted hazard ratio for death was 1.76 (95% CI, 1.203-2.570; P=0.004) compared with optimal treatment. Age-adjusted hazard ratio was 2.15 (95% CI, 1.127-4.114; P=0.02) and 2.3 (95% CI, 1.415-3.779; P=0.001) for ovarian and endometrial cancer patients, respectively. Age-adjusted and stage-adjusted hazard ratio was 2.8 (95% CI, 1.099-5.157; P=0.028) and 1.53 (95% CI, 0.867-2.702; P=0.1420) for ovarian and endometrial cancer patients, respectively. CONCLUSIONS: Optimal treatment in patients with gynecologic malignancies evidently improves survival in elderly patients at any age, and in patients with ovarian cancer at any stage. Regardless of chronological age, the aim should be to deliver optimal treatment.

A novel duplication confirms the involvement of 5q23.2 in autosomal dominant leukodystrophy.

OBJECTIVE: To identify the underlying locus and disease-causing mutation for adult-onset autosomal dominant leukodystrophy (ADLD). DESIGN: Previously, an adult-onset ADLD locus on chromosome 5q23 was mapped between markers D5S1495 and CTT/CCT15. This region contains 13 known and putative candidate genes. A 2-point linkage analysis confirmed linkage of a large multigenerational French Canadian family to chromosome 5q23. In addition, screening of the 13 genes within the candidate interval as well as 5 neighboring genes was completed, followed by comparative genomic hybridization. SUBJECTS: A multigenerational French Canadian family with ADLD mimicking progressive multiple sclerosis was identified and studied. Eight affected family members were available for the study and presented with autonomic dysfunction as well as upper motorneuron signs affecting gait. RESULTS: The thorough candidate gene approach did not identify any mutation. Consequently, a whole-chromosome comparative genomic hybridization for chromosome 5 identified a 280-kilobase duplication within the chromosomal band 5q23.2 in 2 affected individuals. This duplication contains 3 genes: LMNB1, FLJ36242, and MARCH3. CONCLUSION: We have identified a novel duplication on chromosomal band 5q23.2 in a French Canadian family with ADLD that supports the implication of duplicated LMNB1 as the disease-causing mutation. However, additional functional studies of lamin B1 overexpression are necessary to elucidate the involvement of lamin B1 in myelination and in degenerative disorders such as ADLD and multiple sclerosis.