In Vivo Length Changes Between the Attachments of the Medial Patellofemoral Complex Fibers in Knees With Anatomic Risk Factors for Patellar Instability

Background: Medial patellofemoral complex (MPFC) reconstruction plays an important role in the surgical treatment of patellar instability. Anatomic reconstruction is critical in re-creating the native function of the ligament, which includes minimizing length changes that occur in early flexion. Anatomic risk factors for patellar instability such as trochlear dysplasia, patella alta, and increased tibial tuberosity to trochlear groove (TT-TG) distance have been shown to influence the function of the MPFC graft in cadaveric studies, but the native length change patterns of the MPFC fibers in knees with anatomic risk factors have not been described. Purpose: To describe the in vivo length changes of the MPFC fibers in knees with anatomic risk factors for patellar instability and identify the optimal attachment sites for MPFC reconstruction. Study Design: Controlled laboratory study. Methods: Dynamic computed tomography imaging was performed on the asymptomatic knee in patients with contralateral patellar instability. Three-dimensional digital knee models were created to assess knees between 0° and 50° of flexion in 10° increments. MPFC fiber lengths were calculated at each flexion angle between known anatomic attachment points on the extensor mechanism (quadriceps tendon, MPFC midpoint [M], and patella) and femur (1, 2, and 3, representing the proximal to distal femoral footprint). Changes in MPFC fiber length were compared for each condition and assessed for their relationships to morphologic risk factors (trochlear depth, Caton Deschamps Index [CDI], and TT-TG distance). Results: In 22 knees, native MPFC fibers were found to be longer at 0° than at 20° to 50° of flexion. Length changes observed between 0° and 50° increased with the number of risk factors present. In the central fibers of the MPFC (M-2), 1.7% ± 3.1% length change was noted in knees with no anatomic risk factors, which increased to 5.6% ± 4.6%, 17.0% ± 6.4%, and 26.7% ± 6.8% in the setting of 1, 2, and 3 risk factors, respectively. Nonanatomic patella-based attachments were more likely to demonstrate unfavorable length change patterns, in which length was greater at 50° than 0°. In patellar attachments, an independent relationship was found between increasing length changes and TT-TG distance, while in quadriceps tendon attachments, a trend toward a negative relationship between length changes and CDI was noted. All configurations demonstrated a strong relationship between percentage change in length and number of morphologic risk factors present, with the greatest influence found in patella-based attachments. Conclusion: The MPFC fibers demonstrated increased length changes in knees when a greater number of morphological risk factors for patellar instability were present, which worsened in the setting of nonanatomic configurations. This suggests that the function of the intact MPFC in patients with anatomic risk factors may not reflect previously described findings in anatomically normal knees. Further studies are needed to understand the pathoanatomy related to these changes, as well as the implications for graft placement and assessment of length changes during MPFC reconstruction techniques. Clinical Relevance: MPFC length change patterns vary based on the number of morphologic risk factors for patellar instability present and should be considered during reconstructive procedures.</p

Postulated Vasoactive Neuropeptide Autoimmunity in Fatigue-Related Conditions: A Brief Review and Hypothesis

Disorders such as chronic fatigue syndrome (CFS) and gulf war syndrome (GWS) are characterised by prolonged fatigue and a range of debilitating symptoms of pain, intellectual and emotional impairment, chemical sensitivities and immunological dysfunction. Sudden infant death syndrome (SIDS) surprisingly may have certain features in common with these conditions. Post-infection sequelae may be possible contributing factors although ongoing infection is unproven. Immunological aberration may prove to be associated with certain vasoactive neuropeptides (VN) in the context of molecular mimicry, inappropriate immunological memory and autoimmunity

Can cellular transplantation improve function in doxorubicin-induced heart failure?

International audienceBackground: Transplantation of fetal cardiomyocytes has been shown to improve function of regionally infarcted myocardium, but its effects on global heart failure are still unknown.Methods and results: Heart failure was induced in female mice by intraperitoneal injection of doxorubicin (2 mg/kg twice per week over 2 cycles of 2 weeks separated by a 2-week drug-free period). One week after the end of treatment, left ventricular function was assessed by transthoracic echocardiography (baseline). Animals were then randomized into 3 groups: The treated group (n = 12) received an intramyocardial injection of fetal cardiomyocytes (1 x 10(6) in 10 microL) harvested from transgenic mice expressing the gene of beta-galactosidase, the control group (n = 15) received an equivalent volume of culture medium alone, and 10 sham mice had no surgery. Two weeks and 1 month after transplantation, function was again assessed echocardiographically. At baseline, fractional shortening was not significantly different between the 3 groups. It then significantly increased in cell-treated mice at 2 weeks and 1 month after transplantation (P < 0.002 and P < 0.03 versus baseline, respectively), whereas it did not change in untreated animals. Transplanted cells could not be identified by beta-galactosidase activity or presence of Y chromosome (with 1 exception).Conclusions: Cellular transplantation can improve function of globally failing hearts by a mechanism that might not necessarily involve the sustained presence of transplanted cells but rather the effects of cardioprotective factors released by them