Antagonistic effect of butyrate on hexamethylene bisacetamide induced differentiation of murine erythroleukemia cells.

Butyrate, at concentrations greater than 0.75 mM, induces hemoglobin accumulation in murine erythroleukemia cells (MELC). At concentrations below 0.75 mM, butyrate inhibits hemoglobin accumulation induced by hexamethylene bisacetamide (HMBA) as well as HMBA induced commitment to terminal cell division. The blocking of HMBA induced differentiation does not result from growth inhibition. When cells were exposed to HMBA and butyrate for 4 days and then both inducers were removed, the cells did not terminally divide. On the other hand, cells exposed to HMBA for 4 days, with subsequent removal of HMBA, did go on to terminally divide. Thus, butyrate blocks the ability of HMBA to accumulate the intracellular signals for terminal cell division. A 48-h pretreatment of cells with butyrate did not inhibit the ability of subsequent HMBA treatment, after butyrate removal, to induce terminal cell division. These results might suggest that cells do not generate a memory of exposure to HMBA in the presence of butyrate or a memory of exposure to butyrate when used as a pretreatment under these conditions. HMBA, at concentrations below 1.0 mM, does not induce MELC differentiation, but such concentrations actually enhance dimethyl sulfoxide induced differentiation of MELC. Equimolar concentrations of short chain fatty acids (1 to 7 carbons) were tested for their ability to block HMBA induced differentiation of MELC. Butyrate and valerate (4 and 5 carbons, respectively) had blocking activities similar to each other, whereas the other fatty acids exhibited little or no blocking of HMBA induced differentiation.

Selenium in rheumatic diseases.

Selenium is involved in several important biochemical pathways relevant to rheumatic diseases. Experimental and clinical studies suggest that selenium modulates the inflammatory and immune responses. Patients suffering from inflammatory rheumatic diseases often have low selenium levels, but this finding does not correlate with disease severity. Selenium supplementation needs stricter selection criteria and better ascertainment of dose to obtain a stimulatory or inhibitory effect relevant to the disease state. Prevention of marginal selenium deficiency by moderate supplementation might enhance host defense mechanisms.

The internal bony architecture of the sacrum.

STUDY DESIGN: Radiographic and direct quantitative measurements were made of the cortical and the trabecular anatomy of the sacrum. OBJECTIVES: To define the trabecular patterns and the cortical thickness of the sacrum. SUMMARY OF BACKGROUND DATA: The sacrum is a frequent site of internal fixation. In previous anatomic studies, investigators have focused on specific dimensional measurements of the sacrum, whereas others have described the anatomic course of the anterior sacral neurovascular or visceral structures. Computed tomographic imaging also has been used to quantify the sacral trabecular bone density. The internal architecture of the sacrum has yet to be described in detail. METHODS: Seventeen cadaveric sacra were studied by computed tomographic imaging and then were sectioned at 3-mm intervals in the axial or sagittal plane. The cortical thickness of each section was measured under microscopic visualization. The sections were radiographed with high-resolution imaging to delineate their trabecular patterns. RESULTS: The trabecular bone was densest adjacent to the endplates. The sacral body trabeculae were arranged in a cruciate pattern, and bony atrophy occurred in a systematic fashion. An alar void was a consistent finding in all specimens with definable boundaries. The cortical thickness was uniform throughout the surface of each specimen. The computed tomographic images correlated with the anatomy observed in the cadaveric sections. CONCLUSION: The internal bony architecture of the sacrum has several consistent features. The relatively uniform cortical thickness seen in each sacral specimen may have clinical significance in the internal fixation of this region.

Evolution of osteocalcin, alkaline phosphatase and parathyroid hormone after parathyroidectomy in patients receiving chronic maintenance hemodialysis.

Parathyroid hormone (PTH), osteocalcin and alkaline phosphatase (AP) were investigated before and after parathyroidectomy in 12 patients receiving hemodialysis. Early post-parathyroidectomy, PTH decreased (p less than 0.001), AP increased (p less than 0.05), but osteocalcin remained unchanged. At 3 months, osteocalcin and AP declined. A negative correlation was observed between aluminum staining and post-parathyroidectomy osteocalcin. In conclusion, early post-parathyroidectomy, osteocalcin and AP reflect persistent osteoblastic activity, which declined after 3 months. In patients receiving hemodialysis both variables may represent different aspects of osteoblastic activity and osteocalcin allows mixed uremic osteodystrophy after parathyroidectomy.