Bilateral Multiligamentous Knee Injuries: A Case Report and Technique Review.

Bilateral knee dislocations are rare musculoskeletal injuries. We report a case of a patient who sustained traumatic bilateral knee dislocations resulting in multiligamentous injuries to both knees. The patient subsequently underwent acute ligamentous reconstructions of both knees performed at 2 weeks and 3 weeks after the initial injury. One year after these procedures, the patient has achieved excellent functional outcomes and has returned to recreational sports.

Lateral Collateral Ligament Injury About the Knee: Anatomy, Evaluation, and Management.

The lateral collateral ligament is the primary varus stabilizer of the tibiofemoral joint. Diagnosing an injury to this ligament can be challenging in the setting of multiligamentous trauma; however, failure to recognize these injuries can result in instability of the knee and unsatisfactory outcomes after cruciate ligament reconstruction. Recent literature exploring the anatomy and biomechanics of the lateral collateral ligament has enhanced our understanding and improved diagnosis and management of these injuries. Physical examination and imaging studies also are important in diagnosis and can facilitate classification of lateral collateral ligament tears, which affects treatment decisions. Nonsurgical, reparative, and reconstructive techniques can all be used to manage lateral collateral ligament injury about the knee; the optimal treatment is selected on the basis of injury severity.

Growth factor independent-1 maintains Notch1-dependent transcriptional programming of lymphoid precursors.

Growth factor independent 1 (Gfi1) is a transcriptional repressor originally identified as a gene activated in T-cell leukemias induced by Moloney-murine-leukemia virus infection. Notch1 is a transmembrane receptor that is frequently mutated in human T-cell acute lymphoblastic leukemia (T-ALL). Gfi1 is an important factor in the initiation and maintenance of lymphoid leukemias and its deficiency significantly impedes Notch dependent initiation of T-ALL in animal models. Here, we show that immature hematopoietic cells require Gfi1 to competently integrate Notch-activated signaling. Notch1 activation coupled with Gfi1 deficiency early in T-lineage specification leads to a dramatic loss of T-cells, whereas activation in later stages leaves development unaffected. In Gfi1 deficient multipotent precursors, Notch activation induces lethality and is cell autonomous. Further, without Gfi1, multipotent progenitors do not maintain Notch1-activated global expression profiles typical for T-lineage precursors. In agreement with this, we find that both lymphoid-primed multipotent progenitors (LMPP) and early T lineage progenitors (ETP) do not properly form or function in Gfi1(-/-) mice. These defects correlate with an inability of Gfi1(-/-) progenitors to activate lymphoid genes, including IL7R, Rag1, Flt3 and Notch1. Our data indicate that Gfi1 is required for hematopoietic precursors to withstand Notch1 activation and to maintain Notch1 dependent transcriptional programming to determine early T-lymphoid lineage identity.