Immunohistochemical studies in the differential diagnosis of small round cell soft tissue tumors.

In this review the authors focus on the differential diagnosis of small round cell tumors of soft tissue origin, giving emphasis on their specific immunohistochemical profiles. The sources of diagnostic errors and misinterpretations of the results of immunohistochemical staining are discussed in detail. It is thorough knowledge of specific characteristics of each tumor and appropriate interpretation of different staining techniques that will lead to precise classification of any given tumor, thus allowing accurate determination of prognosis and implementation of the optimal treatment.

The effects of ethidium bromide induced loss of mitochondrial DNA on mitochondrial phenotype and ultrastructure in a human leukemia T-cell line (MOLT-4 cells).

Mitochondrial DNA-deficient (rho(0)) cells were generated following a 26-day incubation of MOLT-4 lymphoblastoid T cells in ethidium bromide (3,8-diamino-5-ethyl-6-phenylphenanthridinium bromide). The absence of mitochondrial DNA (mtDNA) in the resultant MOLT-4 rho(0) cells was confirmed by Southern analysis and quantitative polymerase chain reaction (PCR). MOLT-4 rho(0) cells proliferated more slowly than parental cells (wild type) and produced significantly more lactate (approximately fourfold increase; P < 0.001) with concomitantly reduced oxygen consumption (12.3% vs. 100%; P < 0.001) compared with the wild type. MOLT-4 rho(0) cells also showed reduced cytochrome c oxidase activity and a reduced cytochrome c oxidase/citrate synthase activity ratio compared to parental wild-type MOLT-4 cells (P < 10(-11)). Electron microscopy showed elongated mitochondria with parallel cristae in MOLT-4 cells although the mitochondria in MOLT-4 rho(0) cells appeared enlarged, some were vacuolated with either an absent or a grossly distorted cristae pattern. Vital staining with 5,5',6,6'-tetrachloro-1,1',3,3'-tetraethylbenzimidazolyl-carbocyanine iodide (JC-1) was used to image mitochondria in intact cells and study mitochondrial transmembrane potential (Deltapsi(m)). Flow cytometry using JC-1 indicated that MOLT-4 rho(0) had a lower Deltapsi(m) than MOLT-4. Sodium fluoride (an inhibitor of the glycolytic pathway) at a concentration of 20 mM further reduced the Deltapsi(m) in MOLT-4-rho(0) cells. This data suggested that a glycolytic pathway product, possibly ATP, was required for the maintenance of Deltapsi(m) in MOLT-4 rho(0) cells.

Adrenal cortical adenoma with excess black pigment deposition, combined with myelolipoma and clinical Cushing's syndrome.

We report a case of a functional adenoma with excess black pigment deposition and myelolipoma in the same adrenal gland in a 58-year-old woman. The patient presented with gastrointestinal bleeding, and after being diagnosed with colonic diverticulosis, underwent a total colectomy. An abdominal computerized tomographic (CT) scan during her work-up showed a right adrenal mass consistent with myelolipoma. Postoperatively, the patient was diagnosed with Cushing's syndrome and underwent a right adrenalectomy. The adrenalectomy specimen consisted of a dark brown and golden-yellow adrenal adenoma, myelolipoma, and atrophic adrenal gland. Immunostains indicated that the dark brown adenoma component was responsible for the patient's hypercortisolism. Co-occurrence of a functional black adenoma and a well-developed myelolipoma has not been reported in the literature. We describe the significant findings of this case, together with a review of the literature.

Treating coagulopathy in trauma patients.

Coagulopathy in patients with severe trauma is related to platelet and coagulation factor loss, consumption, and dysfunction. It is exacerbated by dilution, acidosis, and hypothermia. Hemorrhage control, warming, and appropriate blood product support are lifesaving. Further improvements in hemorrhage control will save additional lives and resources.

Oxygen consumption rates and oxygen concentration in molt-4 cells and their mtDNA depleted (rho0) mutants.

Respiratory deficient cell lines are being increasingly used to elucidate the role of mitochondria and to understand the pathophysiology of mitochondrial genetic disease. We have investigated the oxygen consumption rates and oxygen concentration in wild-type (WT) and mitochondrial DNA (mtDNA) depleted (rho(0)) Molt-4 cells. Wild-type Molt-4 cells have moderate oxygen consumption rates, which were significantly reduced in the rho(0) cells. PCMB (p-chloromercurobenzoate) inhibited the oxygen consumption rates in both WT and rho(0) cells, whereas potassium cyanide decreased the oxygen consumption rates only in WT Molt-4 cells. Menadione sodium bisulfite (MSB) increased the oxygen consumption rates in both cell lines, whereas CCCP (carbonyl cyanide m-chlorophenylhydrazone) stimulated the oxygen consumption rates only in WT Molt-4 cells. Superoxide radical adducts were observed in both WT and rho(0) cells when stimulated with MSB. The formation of this adduct was inhibited by PCMB but not by potassium cyanide. These results suggest that the reactive oxygen species (ROS) induced by MSB were at least in part produced via a mitochondrial independent pathway. An oxygen gradient between the extra- and intracellular compartments was observed in WT Molt-4 cells, which further increased when cells were stimulated by CCCP and MSB. The results are consistent with our earlier findings suggesting that such oxygen gradients may be a general phenomenon found in most or all cell systems under appropriate conditions.