Summary of Background Data. Limited evidence on complications in double-level X-Stop surgery is available.
Methods. Three men, 47, 63, and 75 years old, respectively, underwent surgery with insertion
of X-Stop at L3-L4 and L4-L5 because of low back pain and neurogenic claudication due to degenerative lumbar spine conditions. Two 10 mm devices were implanted in the first patient and two 16 mm distractors in the second man. One 10 mm X-Stop at L3-L4 and one 12 mm at L4-L5, respectively, were implanted in the third patient. No intraoperative complications occurred and the postoperative course was uneventful, with symptoms relief.
Results. The first 2 patients presented because of recurrent symptoms 4 and 6 months after surgery, respectively. Imaging revealed “”spontaneous”" fracture of the L4 SP in both of them. Revision surgery MK-4827 concentration was required, with removal of the interspinous devices, decompression and fixation. In the third patient the L4 SP fracture was detected when this website the patient presented because of recurrent back pain 18 months after the index surgery, but revision surgery was not consented.
Conclusion. To our knowledge this is the first
report describing the “”sandwich phenomenon,”" i.e., the atraumatic fracture of the intervening SP in patients with adjacent, double-level X-Stop. Possible underlying theories and anatomic peculiarities which may predispose to this rare event are discussed.”
“A reduction in fatty acid ( FA) oxidation has been associated with lipid accumulation and insulin resistance in skeletal muscle of obese individuals. Numerous reports suggest that the reduction in FA oxidation may result from intrinsic mitochondrial defects, although little direct evidence has been offered Quizartinib to support this conclusion. This brief review summarizes recent
work from our laboratory that reexamined whether this decrease in skeletal muscle FA oxidation with obesity was attributable to a dysfunction in FA oxidation within mitochondria or simply to a reduction in muscle mitochondrial content. Whole-muscle mitochondrial content and FA oxidation was reduced in the obese, but there was no decrease in the ability of isolated mitochondria to oxidize FA. The mitochondrial content of the transport protein, FA translocase ( FAT/CD36), did not differ between lean and obese women but was correlated with mitochondrial FA oxidation. It was concluded that the reduced FA oxidation in obesity is attributable to decreased muscle mitochondrial content and not intrinsic defects in mitochondrial FA oxidation, and that mitochondrial FAT/CD36 is involved in regulating FA oxidation in human skeletal muscle. The reduced skeletal muscle mitochondrial content with obesity may result from impaired mitochondrial biogenesis.