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T1-weighted images showed low signal masses with foci of high signal intensity in 73% of cases. Tumors enhanced in a variety of patterns after the administration of Gd. Soft tissue masses extending anteriorly were seen in all cases with posterior extension in 77% of cases. The posterior masses involved the surrounding muscles and extended toward the greater sciatic notch, appearing with pseudopodia (87%). Sacroiliac joints were involved in 23% of cases. Four lesions showed intraspinal extension and involvement of the posterior spinal muscles above the level of bony involvement. In 6 patients recurrent tumors were found at or around the surgical margin of the tumor 6 months to 5 years after resection of the sacral tumor. In two of the patients, nodular metastases to the pelvic bones and femur were found 1-4 years after initial examination. In conclusion, MR imaging is useful in the diagnosis and preoperative assessment of sacrococcygeal chordoma. Characteristic findings included sacral mass with heterogeneously high signal intensity with crisscrossing septa on long-repetition-time imaging, well-encapsulated pseudopodia-like or lobulated appearance, and gluteal muscle infiltration. Follow-up MR imaging is helpful to assess for recurrent or metastatic lesions of chordomas.

ObjectiveWe wanted to demonstrate the temporal changes of the magnetic resonance imaging (MRI) findings in experimentally-induced intramuscular hematomas in rats and to correlate these data with the concurrent pathologic observations.Materials and MethodsIntramuscular hematoma was induced in 30 rats. The MR images were obtained at 1, 4, 7 and 10 days and at 2, 3, 4, 6 and 8 weeks after muscle injury. The characteristic serial MRI findings were evaluated and the relative signal intensities were calculated. Pathologic specimens were obtained at each time point.ResultsOn the T1-weighted imaging (T1WI), the intramuscular hematomas exhibited isointensity compared to that of muscle or the development of a high signal intensity (SI) rim on day one after injury. The high SI persisted until eight weeks after injury. On the T2-weighted imaging (T2WI), the hematomas showed high SI or centrally low SI on day one after injury, and mainly high SI after four days. A dark signal rim was apparent after seven days, which was indicative of hemosiderin on the pathology. The gradient echo (GRE) imaging yielded dark signal intensities at all stages.ConclusionUnlike brain hematomas, experimentally-induced intramuscular hematomas show increased SI on both the T1WI and T2WI from the acute stage onward, and this is pathologically correlated with a rich blood supply and rapid healing response to injury in the muscle. On the T2WI and GRE imaging, high SI with a peripheral dark signal rim is apparent from seven days to the chronic stage.

Zn deficiency reduces food intake and growth rate in rodents. To determine the relationship between Zn deficiency and the regulation of food intake, we evaluated leptin gene expression in epididymal white adipose tissue (eWAT), and hypothalamic corticotropin-releasing hormone (hCRH) and hypothalamic neuropeptide Y (hNPY) of rats Zn-deficient only to show reduced food intake and growth rate but not food intake cycling. Growing male Sprague-Dawley rats (240 g) were randomly assigned to one of four dietary groups: Zn-adequate (ZA; 30 mg/kg diet), Zn-deficient (ZD; 3 mg/kg diet), pair-fed with ZD (PF; 30 mg/kg diet) and Zn-sufficient (ZS; 50 mg/kg diet) (n 8), and were fed for 3 weeks. Food intake and body weight were measured, as were blood mononuclear cells and pancreas Zn levels. eWAT leptin, hCRH and hNPY mRNA levels were determined. Food intake was decreased by about 10 % in ZD and PF rats compared to ZA and ZS rats. Growth and eWAT leptin mRNA levels were unaffected in PF rats but were significantly (P, 0·05) decreased in ZD rats. However, hNPY showed a tendency to increase, and hCRH significantly (P, 0·05) decreased, in both ZD and PF rats. These results suggest that while leptin gene expression may be directly affected by Zn, hNPY and hCRH are likely responding to reduced food intake caused by Zn deficiency.Zinc deficiency: Corticotrophin-releasing hormone: Leptin: Food intake: Growth Zn is an essential component of numerous enzymes and transcription factors and influences many biological processes including the control of food intake and growth 1,2 . Zn deficiency in experimental animals and in man causes anorexia, poor appetite, weight loss and growth retardation. Food intake is controlled by appetite and satiety centres in the central nervous system involving systemic hormonal and nervous feedback of fat reserves and food ingestion 3 . Leptin, a 16 kDa protein secreted primarily by white adipocytes, targets receptors in neurons of hypothalamic nuclei, informing the central nervous system about fat reserves and regulating the expression and signalling of orexigenic and anorexigenic neuropeptides 3 . Leptin negatively and positively regulates the release of neuropeptide Y (NPY) and corticotropinreleasing hormone (CRH), respectively, from the hypothalamic paraventricular nucleus 4 . NPY is a potent stimulator of appetite whereas CRH inhibits food intake, and so in starved animals, NPY expression is increased and CRH decreased due principally to decreased circulating leptin levels 4 .Zn may be a mediator of leptin production in human subjects 5,6 and rodents 7 -9 . Circulating leptin levels and white adipose tissue leptin mRNA levels are decreased in Zn deficiency 7,8 . Also, Zn supplementation of obese mice 10 and diabetic mice 11 increased circulating leptin levels. As would be expected, in acute Zn deficiency where food intake is reduced, body adipose tissue diminishes resulting in reduced leptin synthesis and secretion. Hypothalamic NPY mRNA and protein levels increase in Zn deficiency 12 , although the r...