Myxoid adrenocortical tumors are extremely rare neoplasms with only nine adenomas and eleven carcinomas reported in the literature. They occasionally have a pseudoglandular component resembling metastatic mucinous adenocarcinoma in the adrenal gland. However the cytological features of this unusual tumor have not been previously described. We report here the first cytopathological study of a myxoid adrenocortical adenoma with a pseudoglandular component, contributing especially to the differential diagnosis from metastatic mucinous adenocarcinoma. Two major cytopathological features distinguishing myxoid adrenocortical adenoma from metastatic mucinous adenocarcinoma in the adrenal gland are: (1) the myxoid material is found only in the extracellular space, and not in the cytoplasm; and (2) nuclei are usually located in the central portion of the cytoplasm, and not compressed to the periphery. Careful observation of these cytological features and positive immunoreactivity to Melan A, alpha-inhibin and synaptophysin can lead to the correct diagnosis.
The value of autotransfusion is widely recognized in the surgical community and may be of increasing importance in prevention of acquired immunodeficiency syndrome and hepatitis. The concern of possible contamination of the blood with urine, bacteria in urine or viable tumor cells has limited the wide use of intraoperative autotransfusion (IAT) in urological operation. There have been no experimental reports about protection of the blood from such contamination. To investigate separation of the blood from a contaminated mixture by using an autotransfusion machine, Haemonetic Cell Saver, a study composed of three experiments was performed. First, 200 ml of blood was mixed 200 ml of urine, and thereafter, the mixture was processed by the machine and the concentration erythrocytes were collected in a bag. Biochemical analysis of the collected erythrocyte solution (CES) was performed. Second, 200 ml of blood was mixed with 200 ml of urine that was adjusted to contain each 10(7)/ml of four bacterial strains. The bacteriological study of the CES was performed. Third, 200 ml of blood was mixed with 200 ml of urine that was adjusted to contain 10(7) cancer cells. Two cell lines, KK47 originated from human bladder cancer and ACHN originated from human renal cell carcinoma was used. The cytological study of the CES was performed. The results of these experiments were: Urine constituents were completely removed from the mixture. However, all strains of bacteria could not be separated, although the number of bacteria decreased. Cancer cells were found in the CES. In conclusion IAT should be done at urological operation in selected patients that have sterile urine and do not have tumor cells in the operation field.
Prolactin-induced protein (PIP) has been shown to bind to CD4 and is speculated to block CD4-HLA-DR interaction. However, the immunomodulatory effect of PIP on chronic allergic contact dermatitis (ACD) remains to be elucidated. The aim of this work was to define the role of PIP during the immunoresponse. Using an oxazolone-induced mouse chronic ACD model, expression of PIP was immunohistologically examined. Furthermore, effects of continued exposure of a peptide mimicking the major binding site of PIP (amino acids 106-132) for CD4 was examined in a mouse chronic ACD model. We clarified that keratinocytes and dermal infiltrating cells are positively stained with anti-PIP antibody. The PIP peptide significantly downregulated oxazolone-induced mouse ACD compared to the controls. We also found that inflammation of PIP-non-applied control ear was also suppressed in a synchronized manner in the late phase of the PIP peptide applied mouse. These findings suggest that PIP might have an immunosuppressive effect in mouse chronic ACD.
Human prolactin-induced protein (PIP) is a major protein found in exocrine fluids such as saliva and sweat. Intriguingly, PIP possesses residues (human PIP (hPIP): PIP (29-63)) that display similarity to the aspartic peptidase candidapepsin. Here, we aimed to determine the effect of PIP as a protease on normal skin structure. Using an adhesive tape-stripping technique, we applied hPIP peptide on the corneocytes of normal-appearing facial skin from infants with eczema and healthy infants and then analyzed the morphological structure of corneocytes with Nile Red fluorescence. We also repeatedly applied the hPIP peptide onto the surface of a three-dimensional (3-D) human skin model and then analyzed any changes to the stratum corneum and epidermis using light microscopy and scanning electron microscopy. In both infant groups, a decrease in hydrophobic lipids from the cornified envelope was observed after treatment with hPIP. The peptide hPIP appeared to digest the fine structure of the stratum corneum and induce a proliferation of epidermal keratinocytes within the 3-D human skin model. Our results suggest that aspartic peptidase of PIP found in sweat or saliva deteriorates the skin barrier in a de novo manner, which potentially leads directly to the proliferation of epidermal keratinocytes without any external antigenic factors.
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