10 research outputs found
Hybrid SPECT/CT for the assessment of a painful hip after uncemented total hip arthroplasty
Background The diagnosis of hip pain after total hip replacement (THR)
represents a highly challenging question that is of increasing concern to
orthopedic surgeons. This retrospective study assesses bone scintigraphy with
Hybrid SPECT/CT for the diagnosis of painful THR in a selected cohort of
patients. Methods Bone SPECT/CT datasets of 23 patients (mean age 68.9 years)
with a painful hip after THR were evaluated. Selection of the patients
required an inconclusive radiograph, normal serum levels of inflammatory
parameters (CRP and ESR) or a negative aspiration of the hip joint prior to
the examination. The standard of reference was established by an
interdisciplinary adjudication-panel using all imaging data and clinical
follow-up data (>12 month). Pathological and physiological uptake patterns
were defined and applied. Results The cause of pain in this study group could
be determined in 18 out of 23 cases. Reasons were aseptic loosening (nâ=â5),
spine-related (nâ=â5), heterotopic ossification (nâ=â5), neuronal (nâ=â1),
septic loosening (nâ=â1) and periprosthetic stress fracture (nâ=â1). In (nâ=
5) cases the cause of hip pain could not be identified. SPECT/CT imaging
correctly identified the cause of pain in (nâ=â13) cases, in which the
integrated CT-information led to the correct diagnosis in (nâ=â4) cases,
mainly through superior anatomic correlation. Loosening was correctly assessed
in all cases with a definite diagnosis. Conclusions SPECT/CT of THA reliably
detects or rules out loosening and provides valuable information about
heterotopic ossifications. Furthermore differential diagnoses may be detected
with a whole-body scan and mechanical or osseous failure is covered by CT-
imaging. SPECT/CT holds great potential for imaging-based assessment of
painful prostheses
A peptide inhibitor of c-Jun N-terminal kinase protects against excitotoxicity and cerebral ischemia.
Neuronal death in cerebral ischemia is largely due to excitotoxic mechanisms, which are known to activate the c-Jun N-terminal kinase (JNK) pathway. We have evaluated the neuroprotective power of a cell-penetrating, protease-resistant peptide that blocks the access of JNK to many of its targets. We obtained strong protection in two models of middle cerebral artery occlusion (MCAO): transient occlusion in adult mice and permanent occlusion in 14-d-old rat pups. In the first model, intraventricular administration as late as 6 h after occlusion reduced the lesion volume by more than 90% for at least 14 d and prevented behavioral consequences. In the second model, systemic delivery reduced the lesion by 78% and 49% at 6 and 12 h after ischemia, respectively. Protection correlated with prevention of an increase in c-Jun activation and c-Fos transcription. In view of its potency and long therapeutic window, this protease-resistant peptide is a promising neuroprotective agent for stroke