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Objective: To compare length of stay and total hospital costs among patients admitted to hospital under the care of family physicians who were their usual health care providers in the community (group A) and patients admitted to the same inpatient service under the care of family physicians who were not their usual health care providers (group B)., Design: Retrospective observational study., Setting: A large urban hospital in Vancouver, BC., Participants: All adult admissions to the family practice inpatient service between April 1, 2006, and June 30, 2008., Main Outcome Measures: Ratio of length of stay to expected length of stay and total hospital costs per resource intensity weight unit. Multivariate linear regression was performed to determine the effect of admitting group (group A vs. group B) on the natural logarithm transformations of the outcomes., Results: The median acute length of stay was 8.0 days (interquartile range [IQR] 4.0 to 13.0 days) for group A admissions and 8.0 days (IQR 4.0 to 15.0 days) for group B admissions. The median (IQR) total hospital costs were $6498 ($4035 to $11,313) for group A admissions and $6798 ($4040 to $12,713) for group B admissions. Aftera djustment for patient characteristics, patients admitted to hospital under the care of their own family physicians did not significantly differ in terms of acute length of stay to expected length of stay ratio (percent change 0.6%, P = .942)or total hospital costs per resource intensity weight unit (percent change -2.0%, P = .722) compared with patients admitted under the care of other family physicians., Conclusion: These findings suggest that having networks of family physicians involved in hospital care for patients is not less efficient than having family physicians provide care for their own patients.

Objective: Coxsackievirus infections have long been associated with the induction of type 1 diabetes. Infection with coxsackievirus B4 (CB4) enhances type 1 diabetes onset in NOD mice by accelerating the presentation of beta-cell antigen to autoreactive T-cells. It has been reported that a progressive defect in regulatory T-cell (Treg) function is, in part, responsible for type 1 diabetes onset in NOD mice. This defect may contribute to susceptibility to viral-induced type 1 diabetes. We asked whether the immune response after CB4 infection could be manipulated to reestablish peripheral tolerance while maintaining the immune response to virus., Research Design and Methods: NOD mice expressing transforming growth factor-beta (TGF-beta) specifically in the beta-cells were infected with CB4, and the functional role of Tregs in disease protection was measured. Systemic treatments with TGF-beta were used to assess its therapeutic potential., Results: Here, we report that Tregs induced after CB4 infection in the presence of TGF-beta prevented type 1 diabetes. The capacity to directly infect pancreatic beta-cells correlated with increased numbers of pancreatic Tregs, suggesting that presentation of beta-cell antigen is integral to induction of diabetogenic protective Tregs. Furthermore, the presence of these viral induced Tregs correlated with protection from type 1 diabetes without altering the antiviral response. Finally, when TGF-beta was administered systemically to NOD mice after infection, the incidence of type 1 diabetes was reduced, thereby signifying a potential therapeutic role for TGF-beta., Conclusions: We demonstrate manipulations of the immune response that result in Treg-mediated protection from type 1 diabetes without concomitant loss of the capacity to control viral infection.