Staging and its use in the determination of treatment modalities for Kienb?ck's disease

For more than 80 years, surgeons have staged an unsuccessful search for a universally acceptable treatment for Kienb?ck's disease. It is our contention that no single treatment will be universally successful. Treatment choice must be based on a number of variables, including the experience of the surgeon, the desires and activity level of the patient, the anatomic variation of the ulna, and most importantly, on the stage of the disease. In the early stages, efforts should be made to salvage the lunate and prevent loss of normal architecture. In the later stages, efforts should be made to restore that architecture. In end stage, normal architecture must be sacrificed to restore function. Currently we recommend immobilization with possible equalization procedures for patients with ulnar-minus variance and stage I disease. In a patient with stage I disease and ulnar-positive variance, we recommend immobilization with consideration for a revascularization procedure. For stages II or IIIA disease with ulnar-minus variance, we attempt an equalization procedure. For stages II or IIIA disease with ulnar-positive variance, we recommend revascularization as performed by Hori. In stage IIIB disease, we prefer a triscaphe fusion to restore carpal stability and prevent further degeneration. In stage IV disease, proximal row carpectomy or wrist arthrodesis is indicated.     

Effects of nonoxynol-9 on vaginal microflora and chlamydial infection in a monkey model

A 58-year-old male with left renal cell carcinoma and prostatic carcinoma occurring synchronously, is reported. He visited our hospital, because of the high level of serum prostate-specific antigen (PSA) pointed out in a health screening by his company. Prostatic cancer was detected in both lobes of the prostate by needle biopsy specimens and histopathology represented moderately > poorly differentiated adenocarcinoma. Magnetic resonance imaging (MRI) and computed tomography (CT) revealed no cancer invasion beyond the prostate and no lymph node metastasis. Bone scintigram showed no abnormal RI accumulation to bone. Therefore, his prostatic cancer was considered to be at stage B2. Abdominal ultrasound echogram showed the mass lesion in the left kidney. CT and angiogram also demonstrated a left renal tumor. Left radical nephrectomy was performed and histopathology showed a mixed subtype of renal cell carcinoma (stage: pT2b, pN0, pM0). Although 94 cases of double cancers associated with genitourinary organs have been reported in the Japanese literature, only 4 cases of double cancers of renal cell carcinoma and prostatic cancer have been reported.     

Pancreatic polypeptide stimulates corticosterone secretion by isolated rat adrenocortical cells

Pancreatic polypeptide (PP) dose-dependently enhanced both basal and submaximally ACTH-stimulated corticosterone production by dispersed zona fasciculata/reticularis cells of the rat adrenal gland. Conversely PP did not affect either basal or ACTH- and angiotensin-II-stimulated aldosterone and corticosterone secretion of zona glomerulosa cells. These findings could throw light on the physiological significance of the marked increase in the pancreatic release of PP during stresses.     

(+)-Anatoxin-a is a potent agonist at neuronal nicotinic acetylcholine receptors

The effects of the nicotinic agonist (+)-anatoxin-a have been examined in four different preparations, representing at least two classes of neuronal nicotinic receptors. (+)-Anatoxin-a was most potent (EC50 = 48 nM) in stimulating 86Rb+ influx into M10 cells, which express the nicotinic receptor subtype comprising alpha 4 and beta 2 subunits. A presynaptic nicotinic receptor mediating acetylcholine release from hippocampal synaptosomes was similarly sensitive to (+)-anatoxin-a (EC50 = 140 nM). alpha-Bungarotoxin-sensitive neuronal nicotinic receptors, studied using patch-clamp recording techniques, required slightly higher concentrations of this alkaloid for activation: Nicotinic currents in hippocampal neurons were activated by (+)-anatoxin-a with an EC50 of 3.9 microM, whereas alpha 7 homooligomers reconstituted in Xenopus oocytes yielded an EC50 value of 0.58 microM for (+)-anatoxin-a. In these diverse preparations, (+)-anatoxin-a was between three and 50 times more potent than (-)-nicotine and approximately 20 times more potent than acetylcholine, making it the most efficacious nicotinic agonist thus far described.     

The mechanism of local tumor irradiation combined with interleukin 2 therapy in murine renal carcinoma: histological evaluation of pulmonary metastases

We have demonstrated that tumor irradiation enhanced the therapeutic effect of interleukin 2 (IL-2) on pulmonary metastases from a murine renal adenocarcinoma, Renca. To investigate the mechanism of interaction between tumor irradiation and IL-2 therapy, we have histologically evaluated the effects of each therapy alone or in combination on Renca pulmonary metastases. Following treatment of established lung metastases with irradiation and IL-2 therapy, lung sections were processed for H&E or immunohistochemical staining. We found that tumor irradiation or IL-2 therapy locally induced vascular damage, resulting in multifocal hemorrhages and mononuclear cell mobilization in the lung tissue. This effect was amplified in lungs treated with the combined therapy. Immunohistochemistry showed that irradiation produced a macrophage influx into irradiated tumor nodules, and systemic IL-2 therapy induced T-cell infiltration in tumor nodules. Lungs treated with the combined therapy exhibited massive macrophage, T-cell, and natural killer cell mobilization in disintegrating tumor nodules and in the lung tissue. This combined therapy caused a decrease in the number of proliferating tumor cells and an increase in the number of apoptotic cells, which were more marked than with either therapy alone. We suggest that the macrophages mobilized by radiation-induced tissue injury could play a role in phagocytosis of apoptotic tumor cells, processing and presenting of tumor antigens for a systemic immune response activated by IL-2. Tumor destruction may result from the concomitant action of activated T cells, natural killer cells, and macrophages infiltrating the tumor nodules.     

The development of sexual dimorphism in natural killer cell activity and resistance to tumor metastasis in the Fischer 344 rat

The development of sexual dimorphism in the number and activity level of natural killer (NK) cells was studied in the inbred Fischer 344 rat from prepubescence to maturity. Additionally, in view of the biological significance of NK cells in controlling cancer, especially the metastatic process, we used a syngeneic mammary tumor (MADB106) to assess the host anti-metastatic activity. This tumor model was used because NK cells control the lung clearance of i.v.-injected MADB106 tumor cells, a process that critically affects the metastatic colonization of these tumor cells in the lungs. The results indicated that although prepubescent (36 days of age) males and females exhibited greater NK cytotoxicity (assessed in vitro) and higher anti-metastatic activity, evidenced by fewer tumor cells retained in the lungs. On the other hand, the mature males (140-170 days of age) displayed greater LGL/NK number and activity per ml blood, retained fewer tumor cells, and developed fewer lung tumor colonies compared to the females. During early postpubescence (63 days of age), a transitional stage between prepubescence and maturity, females and males exhibited equivalent numbers of circulating LGL/NK cells, and females displayed slightly greater NK cytotoxicity per ml blood yet retained somewhat greater numbers of tumor cells compared to the males. Overall, whereas the males exhibited increasing levels of NK number and activity throughout the age span tested, the females, despite displaying greater NK function compared to the males at prepubescence and slight improvement at postpubescence, fell behind the males in these indices of NK function at maturity.