Fragment reconstruction and bone plate fixation versus bridging plate fixation for treating highly comminuted femoral fractures in dogs: 35 cases (1987-1997)

OBJECTIVE: To compare fragment reconstruction and bone plate fixation versus bridging plate fixation for treating highly comminuted (> 4 fragments) femoral fractures in dogs. DESIGN: Retrospective study. ANIMALS: 35 dogs with highly comminuted fractures of the femur. PROCEDURE: Medical records of all dogs included in this study were reviewed. Dogs had been treated with fragment reconstruction and bone plate application (n = 20) or major fragment alignment and bridging plate fixation (15). Postoperative and follow-up radiographs were evaluated. Operating and hospitalization times, bone alignment, bone healing, and complications were considered. RESULTS: There were no differences in hospitalization times, limb alignment, and complications between dogs with fractures treated with fragment reconstruction and dogs with fractures treated with bridging plate fixation. Dogs with fractures treated with bridging plate fixation had shorter operative times and faster times to radiographic evidence of bone healing. CLINICAL IMPLICATIONS: Bridging plate fixation is quicker to perform and results in faster healing than fragment reconstruction and bone plate fixation when used to treat comminuted femoral fractures.     

Bullous erythema multiforme following topical diphenylcyclopropenone application

A 68 year-old woman underwent replacement of the descending thoracic aorta with a cryopreserved aortic homograft for the treatment of a Stanford B dissecting aneurysm. After surgery, the patient made an uneventful recovery without recurrent infection. In such cases, the use of aortic homografts to replace aortic segments is a promising and effective therapeutic option.     

Mtv-1 superantigen trafficks independently of major histocompatibility complex class II directly to the B-cell surface by the exocytic pathway

Presentation of the Mtv-1 superantigen (vSag1) to specific Vbeta-bearing T cells requires association with major histocompatibility complex class II molecules. The intracellular route by which vSag1 trafficks to the cell surface and the site of vSag1-class II complex assembly in antigen-presenting B lymphocytes have not been determined. Here, we show that vSag1 trafficks independently of class II to the plasma membrane by the exocytic secretory pathway. At the surface of B cells, vSag1 associates primarily with mature peptide-bound class II alphabeta dimers, which are stable in sodium dodecyl sulfate. vSag1 is unstable on the cell surface in the absence of class II, and reagents that alter the surface expression of vSag1 and the conformation of class II molecules affect vSag1 stimulation of superantigen reactive T cells.     

Prospective psychosocial, interpersonal, and behavioral predictors of handgun carrying among adolescents

OBJECTIVES: This study identified behavioral and psychosocial/interpersonal factors in young adolescence that are associated with handgun carrying in later adolescence. METHODS: A sample of 2200 high school students was surveyed at 9th grade and again at 12th grade. RESULTS: Multivariate logistic regression analyses indicated that measures of risk-taking preference, depression, stress, temper, and drug use assessed while the students were in 9th grade were predictive of handgun carrying in 12th grade for both male and female students. CONCLUSIONS: These findings suggest the need for a comprehensive approach to prevention that focuses on both individual and interpersonal factors associated with adolescents' decision to carry a handgun.     

Localized in vivo 1H nuclear MR spectroscopy for evaluation of human uterine cervical carcinoma

Spontaneous abortion occurs in 15% to 20% of all human pregnancies. Since the late 1800s, the management of incomplete spontaneous abortion has focused on using curettage to empty the uterus as quickly as possible. This practice began to reduce blood loss and infection and has been unquestioned for 4 decades. In today's medical climate, few spontaneous abortions are the resuslt of illegal manipulation, given the availability of legal pregnancy termination. Antibiotics and transfusions are available, should complications arise in conservatively managed cases. Two prospective randomized trials suggest that conservative management may be advantageous for women who have stable vital signs without evidence of infection. They will have fewer perforations and, possibly, fewer infections and uterine synechiae with expectant or medical management. Larger trials should be undertaken to critically assess surgical evacuation compared to medical management, factoring in the psychologic impact of treatment. We believe that medical management will prove to be the most appropriate treatment for uncomplicated spontaneous incomplete abortion in the 21st century.     

Mechanisms of innate resistance to Toxoplasma gondii infection

The interaction of protozoan parasites with innate host defences is critical in determining the character of the subsequent infection. The initial steps in the encounter of Toxoplasma gondii with the vertebrate immune system provide a striking example of this important aspect of the host-parasite relationship. In immuno-competent individuals this intracellular protozoan produces an asymptomatic chronic infection as part of its strategy for transmission. Nevertheless, T. gondii is inherently a highly virulent pathogen. The rapid induction by the parasite of a potent cell-mediated immune response that both limits its growth and drives conversion to a dormant cyst stage explains this apparent paradox. Studies with gene-deficient mice have demonstrated the interleukin-12 (IL-12)-dependent production of interferon gamma (IFN-gamma) to be of paramount importance in controlling early parasite growth. However, this seems to be independent of nitric oxide production as mice deficient in inducible nitric oxide synthase (iNOS) and tumour necrosis factor receptor were able to control early growth of T. gondii, although, they later succumbed to infection. Nitric oxide does, however, seem to be important in controlling persistent infection; treating chronic infection with iNOS metabolic inhibitors results in disease reactivation. Preliminary evidence implicates neutrophils in effector pathways against this parasite distinct from that described for macrophages. Once initiated, IL-12-dependent IFN-gamma production in synergy with other proinflammatory cytokines can positively feed back on itself to induce 'cytokine shock'. Regulatory cytokines, particularly IL-10, are essential to down-regulate inflammation and limit host pathology.     

Heart and neural tube defects in transgenic mice overexpressing the Cx43 gap junction gene

Transgenic mice were generated containing a cytomegaloviral promoter driven construct (CMV43) expressing the gap junction polylpeptide connexin 43. RNA and protein analysis confirmed that the transgene was being expressed. In situ hybridization analysis of embryo sections revealed that transgene expression was targeted to the dorsal neural tube and in subpopulations of neural crest cells. This expression pattern was identical to that seen in transgenic mice harboring other constructs driven by the cytomegaloviral promoter (Kothary, R., Barton, S. C., Franz, T., Norris, M. L., Hettle, S. and Surani, M. A. H. (1991) Mech. Develop. 35, 25-31; Koedood, M., Fitchel, A., Meier, P. and Mitchell, P. (1995) J. Virol. 69, 2194-2207), and corresponded to a subset of the endogenous Cx43 expression domains. Significantly, dye injection studies showed that transgene expression resulted in an increase in gap junctional communication. Though viable and fertile, these transgenic mice exhibited reduced postnatal viability. Examination of embryos at various stages of development revealed developmental perturbations consisting of cranial neural tube defects (NTD) and heart malformations. Interestingly, breeding of the CMV43 transgene into the Cx43 knockout mice extended postnatal viability of mice homozygote for the Cx43 knockout allele, indicating that the CMV43 trangsene may partially complement the Cx43 deletion. Both the Cx43 knockout and the CMV43 transgenic mice exhibit heart defects associated with malformations in the conotruncus, a region of the heart in which neural crest derivatives are known to have important roles during development. Together with our results indicating neural-crest-specific expression of the transgene in our CMV-based constructs, these observations strongly suggest a role for Cx43-mediated gap junctional communication in neural crest development. Furthermore, these observations indicate that the precise level of Cx43 function may be of critical importance in downstream events involving these migratory cell populations. As such, the CMV43 mouse may represent a powerful new model system for examining the role of extracardiac cell populations in cardiac morphogenesis and other developmental processes.