To better understand the role of irisin in humans, we examined the effects of irisin in human primary adipocytes and fresh human subcutaneous white adipose tissue (scWAT). Human primary adipocytes derived from 28 female donors' fresh scWAT were used to examine the effects of irisin on browning and mitochondrial respiration, and preadipocytes were used to examine the effects of irisin on adipogenesis and osteogenesis. Cultured fragments of scWAT and perirenal brown fat were used for investigating signal transduction pathways that mediate irisin's browning effect by Western blotting to detect phosphorylated forms of p38, ERK, and STAT3 as well as uncoupling protein 1 (UCP1). Individual responses to irisin in scWAT were correlated with basal expression levels of brown/beige genes. Irisin upregulated the expression of browning-associated genes and UCP1 protein in both cultured primary mature adipocytes and fresh adipose tissues. It also significantly increased thermogenesis at 5 nmol/l by elevating cellular energy metabolism (OCR and ECAR). Treating human scWAT with irisin increased UCP1 expression by activating the ERK and p38 MAPK signaling. Blocking either pathway with specific inhibitors abolished irisin-induced UCP1 upregulation. However, our results showed that UCP1 in human perirenal adipose tissue was insensitive to irisin. Basal levels of brown/beige and FNDC5 genes correlated positively with the browning response of scWAT to irisin. In addition, irisin significantly inhibited adipogenic differentiation but promoted osteogenic differentiation. We conclude that irisin promotes "browning" of mature white adipocytes by increasing cellular thermogenesis, whereas it inhibits adipogenesis and promotes osteogenesis during lineage-specific differentiation. Our findings provide a rationale for further exploring the therapeutic use of irisin in obesity and exercise-associated bone formation.
Brown-Sequard syndrome (BSS) produced by hemisection of the spinal cord will lead to ipsilateral motor weakness, proprioceptive and vibratory sensation loss and is associated with contralateral deficit in sensation of pain and temperature. BSS is most commonly caused by injuries and neoplasms in the cervical and thoracic region.1-5 BSS induced by disc disorders is rare; since the first published case in 1928, only 50 cases have been reported in English language literatures. 6-10This case is the 51st published discogenic BSS, which is produced by calcified herniated C4-C5 disc and posterior vertebral osteophyte. Contrast to previous cases with acute progression, features of BSS took place 7 years after the onset of initial radicular symptom in a quite chronic manner.This 53-year-old male patient had a 7-year history of mild pain and numbness in the left arm. During the 6 months before admission, he had experienced progressive weakness in the left arm and leg, along with contralateral deficit in sensation of pain and temperature below T11.Upon physical examination, features of BSS were shown, including ipsilateral weakness in the left arm and leg (MRC Grade 3/5), hypertonia and hyperreflexia in left lower extremity, as well as reduced contralateral sensation of pain and temperature below T11. In addition, Hoffmann sign, Babinski sign and ankle clonus test of the left side were positive.CT scan showed calcifications of herniated C4-C5 disc and posterior vertebral osteophyte of C5 (Fig. 1). MRI showed a large central left-sided C4-C5 disc herniation, compressing the spinal cord, leading to increased signal intensity on T2WI (Fig. 2). MRI of thoracic spine showed no positive result, eliminating disorders in the thoracic region (Fig. 3). j o u r n a l o f o r t h o p a e d i c s 1 2 ( 2 0 1 5 ) s 2 6 0 -s 2 6 3 a r t i c l e i n f o
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