The neural plate specifies somite size in the Xenopus laevis gastrula.

The organizer has traditionally been considered the major source of somite-inducing signals. We show here that signaling from the neural plate specifies somite tissue and regulates somite size in the Xenopus gastrula. Ectopic undifferentiated neural tissue induces massive somite expansion at the expense of intermediate and lateral plate mesoderm. Although the early expanded somite expresses muscle-specific markers, only a portion terminally differentiates, suggesting that myotome development requires additional signals. Explant assays demonstrate that neural tissue induces somite-specific marker expression even in the absence of the organizer. Finally, we demonstrate that neural tissue is required for proper somite development because elimination of neural precursors results in pronounced somite reduction. Thus, an important reciprocal interaction exists between somite and neural tissue that is mutually reinforcing and critical for normal embryonic patterning.

Bilateral primary renal non-Hodgkin's lymphoma presenting with acute renal failure: successful treatment with systemic chemotherapy.

Primary renal non-Hodgkin's lymphoma (NHL) with acute renal failure is a very rare condition, which frequently occurs in bilateral renal involvement. We report a 26-year-old male with primary bilateral renal NHL presenting with acute renal failure. A CT scan of the abdomen showed markedly enlarged kidneys with multinodularity and para-aortic lymphadenopathy. A percutaneous renal biopsy demonstrated 'follicular center lymphoma, diffuse, small cell'. Thirteen cycles of systemic chemotherapy with cyclophosphamide-doxorubicin-vincristine-prednisolone (CHOP) and ifosfamide-methotrexate-etoposide-bleomycin (IMVP-Bleo) regimens were administered, which resulted in normalization of renal function with improvement of renal lymphoma. Since there was no further change of renal lesions after initial partial remission, a follow-up renal biopsy was performed 10 months after diagnosis, and no residual lymphoma was found.

Changes in intracellular Ca2+ concentration of rabbit coronary artery smooth muscle cell during ischemic cardioplegic period.

To elucidate the possibility whether an elevation of intracellular Ca2+ concentration ([Ca2+]i) in rabbit coronary artery myocytes during ischemic cardioplegic period may serve as one of the mechanisms of the "no-reflow' phenomenon or not, the changes in [Ca2+]i were measured under ischemic cardioplegia conditions using a fluorescent Ca2+ indicator, fura 2/AM. When single cells were perfused with cardioplegic or ischemic cardioplegic solutions, [Ca2+]i was significantly increased and the degree of [Ca2+]i elevation was further augmented by the ischemic cardioplegic solution. Pretreatment of a sarcoplasmic reticulum emptying agent, 20 mM caffeine, had no effect on ischemic cardioplegia-induced [Ca2+]i changes, but application of a Ca2+ channel blocker, 5 x 10 (-1)M nifedipine, or an antagonist of Na+/Ca2+ exchange, 5 mM Ni2+, significantly inhibited the [Ca2+]i elevation, respectively. The magnitude of ischemic cardioplegia-induced [Ca2+]i elevation was dependent on the Ca2+ concentration of perfusate in the range of 0 and 25 mM. When Ni2+ was added to the reperfusion solution, recovery of ischemic cardioplegia-induced [Ca2+]i elevation was very rapid compared with the controls. It is concluded that ischemic cardioplegia-induced [Ca2+]i elevation may serve as one of the mechanisms of the "no-reflow' phenomenon in rabbit coronary artery smooth muscle cells. We propose that Na+/Ca2+ exchange may serve as a key function in ischemic cardioplegia-induced [Ca2+]i elevation.