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Relationship of the abdomen-sole deep body temperature difference (DBT) to the hemodynamics was examined in patients with congenital heart disease. Hemodynamic data were obtained by routine cardiac catheter examination, and DBT was measured during the catheterization. Significant positive correlation was found between DBT and systemic-pulmonary flow ratio (Qp/Qs) (r = 0.85, p = 0.001). DBT was maintained below 2 C degrees in almost every patient when the Qp/Qs was less than 2, whereas DBT rose rapidly when the Qp/Qs was more than 2. Furthermore, systemic blood flow and arterial-venous oxygen difference ranged widely within the normal values when DBT was less than 2 C degrees. On the other hand, when DBT was more than 2 C degrees, systemic blood flow and arterial-venous oxygen difference tended to show fixed values which were around the normal upper or lower limits. This means that systemic circulation is marginally adapted when the Qp/Qs is more than 2. The measurement of deep body temperature difference is noninvasive, easy and useful as a circulatory monitor in pediatric patients with congenital heart disease.

We examined strain differences in neoplastic response to DMBA-induced uterine vascular tumors in mice. Female BALB/c, C57BL, C3H, SWR/J, GRS/A and DDD/1-Mtv-2 mice were treated with a single intraperitoneal injection (ip) of 1 mg of 7,12-dimethylbenz(a)anthracene (DMBA) at 4 weeks of age, and observed until they were 32 weeks of age. The BALB/c, C57BL, C3H strains showed a high incidence of uterine vascular tumors (87%, 93%, and 90%, respectively), while in contrast, the SWR/J, GRS/A, and DDD/1-Mtv-2 strains showed a low incidence (17%, 11% and 15%, respectively); these differences were striking. The mice of American origin (BALB/c, C57BL and C3H) appeared to be susceptible to DMBA, while those of European origin (SWR/J, GRS/A and DDD/1-Mtv-2) were resistant to the induction of uterine vascular tumors.

Female 6-week-old shrews were given a solution of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) at a concentration of 50 micrograms/ml or 100 micrograms/ml in the drinking water. All 11 shrews receiving 100 micrograms/ml MNNG died 8-13 days after the beginning of carcinogen administration and 6 of the 20 shrews receiving 50 micrograms/ml MNNG died after 10-54 days. When animals were between 43 and 54 weeks of age, multiple esophageal lesions were evoked in all 14 that had received 50 micrograms/ml MNNG for 30 weeks. All shrews developed a protruding, ulcerative, or superficial type of squamous-cell carcinoma of the esophagus, accompanied by papillomas. Local invasion was seen in squamous-cell carcinoma but no distant metastasis was noted. None of the 5 control shrews developed any esophageal abnormality. No gastric adenocarcinoma, intestinal sarcoma, or other tumors were induced with MNNG. It can be concluded that MNNG has a carcinogenic effect on shrew esophageal epithelium.

Our recent experiences of the autogenous pericardial patch augmentation of Blalock-Taussig anastomotic orifice are reported. In Case 1, the direct suture between the left subclavian artery and the left pulmonary artery was difficult on the anterior wall because of the shortness of the left subclavian artery. Therefore, a piece of the patient's own pericardium was excised and sutured anteriorly between the two vessels by interrupted 7-0 polypropylene sutures. A 19 months postoperative angiogram showed so-called parrot-beaking of the subclavian artery probably due to tension, but there was no distortion or stenosis of the pulmonary artery. In Case 2, the right subclavian artery distal to the bifurcation of the vertebral artery was longitudinally split measuring approximately 2.5 cm in length, and widened by a piece of the autogenous pericardium in a wedge shape. Then, it was anastomosed to the right pulmonary artery without undue tension. Seven months postoperatively the patient died from severe AV valve regurgitation. The autopsy showed widely patent anastomosis and good healing as well as slight expansion of the pericardial patch but without aneurysm formation. In Case 3, the same operation as in Case 2 was performed. A 6 months postoperative angiogram showed no stenosis or distortion of either the subclavian or the pulmonary artery. Although it is premature to draw any conclusion, the use of the autogenous pericardium may be indicated to widen the anastomotic orifice of Blalock-Taussig shunt without sacrificing the length of the subclavian artery even in small infants or neonates.

To prevent extraction of lipids during a double staining procedure for electron microscopy, the tissue slices, double fixed with glutaraldehyde and osmium tetroxide to preserve microvesicular lipid droplets in the cytoplasm, were immersed for 2 hr in veronal buffer (pH 9.0) containing 0.5% p-phenylenediamine and 0.5% imidazole immediately after postfixation. The stained sections of the immersed tissue slice showed blackened, well circumscribed lipid droplets similar to those in corresponding unstained sections. Moreover, highly contrasting features of the cellular architecture could be visualized with the double stained, as well as routinely prepared sections.

Sixty-six benign and malignant skin appendage tumors were studied for the expression and localization of the glycoproteins identified by the monoclonal antibodies (MoAbs) GCDFP-15, CU18, B72.3, and VU-1D9. Formalin-fixed, paraffin-embedded tissue was processed by the avidin-biotin complex method. In normal eccrine and apocrine sweat glands, GCDFP-15, CU18, B72.3, and VU-1D9 staining was localized differently (intracellular, membranous, or intraluminal), whereas eccrine glands showed no B72.3 staining. There were various patterns of positive staining of tumors arising from sweat glands, but no immunoreactivity for B72.3 was found in eccrine-derived tumors. CU18 and VU-1D9 labeled mature sebocytes in a vacuolar fashion and stained sebaceous carcinomas. VU-1D9 labeled membranes of the secondary germ cells in early anagen of a hair follicle bulb as well as the basaloid cells of trichoepitheliomas and basal cell carcinomas. These MoAbs appear to be valuable markers for the study of normal skin appendages and their tumors.

Immunoreactivities in 25 cases of prostatic adenocarcinoma and 10 normal/hyperplastic prostates were investigated in methacarn-fixed, paraffin-embedded serial sections using a panel of nine anti-keratin monoclonal antibodies (mAbs); 34 beta E12, CK8.12, 312C8-1, CK4.62, RPN1165, RPN1162, 35 beta H11, CK5, M20, and one of anti-actin mAb, HHF35. In normal/hyperplastic prostates, RPN1162, 35 beta H11, CK5 and M20 stained luminal cells without staining basal cells, and 34 beta E12, CK8.12 and 312C8-1 stained basal cells but not luminal cells. Other mAbs, CK4.62 and RPN1165, stained basal cells as well as luminal cells. All of the mAbs labelling luminal cells stained cancer cells with variable frequencies in a manner unrelated to the grade of tumour differentiation. Of the prostate cancer cases 92% were scored positive with M20, 84% with 35 beta H11, 80% with CK5, 68% with CK4.62, 60% with RPN1165 and 4% with RPN1162. However, basal cell-specific keratins labelled with 34 beta E12, CK8.12 and 312C8-1 were totally negative in the cancer cells. HHF35 showed no labelling in normal, hyperplastic or neoplastic epithelial cells of the prostate. Our findings indicate that the major part of the cells of prostatic adenocarcinomas have keratin phenotypes similar to luminal cells but not basal cells, and that no myoepithelial differentiation can be detected in epithelial cell of the prostate. Thus, mAbs for keratins facilitate the identification of epithelial cell phenotypes in normal, benign and malignant conditions of the prostate.

The patient was a 46-year-old male hemophiliac who died of acute mycobacterial meningitis associated with AIDS (acquired immune deficiency syndrome). Autopsy revealed severe basal meningitis which was characterized by an infiltration of numerous polymorphonuclear leukocytes. Severe mural inflammation of the subarachnoid arteries was noted, and innumerable acid-fast bacilli were demonstrated. Epithelioid cell granulomas were not found in the meningeal lesion. The lungs, liver, spleen, and bone marrow contained many epithelioid cell granulomas with caseous necrosis. Massive proliferation of swollen histiocytes could not be identified in any organ. The absence of epithelioid cell granulomas in the meningeal lesion indicate a severe impairment of cell-mediated immunity in the patient; this anergic type of lesion is one of the characteristics of tuberculosis occurring in association with terminal AIDS.

The carcinogenic effect of 7,12-dimethylbenz[a]anthracene (DMBA) was examined in the virgin female Japanese house musk shrew, Suncus murinus (family: Soricidae, order: Insectivora). Leukemia, musk gland tumors, pilosebaceous tumors and sarcomas were induced in the DMBA-treated shrews, whereas none of the controls developed any tumors up to 50 weeks of age. DMBA emulsion was administered i.p. at a dose of 1.25 or 2.5 mg once a week, with either four or eight doses being given from 8 weeks of age. Leukemia developed in 100% (9/9), 50% (5/10), 56% (5/9) and 0% (0/10) of the animals treated with a total dose of 20 mg (8 x 2.5 mg), 10 mg (8 x 1.25 mg), 10 mg (4 x 2.5 mg) and 5 mg (4 x 1.25 mg) of DMBA respectively. Leukemia was of the lymphatic and/or mast cell type, and the spleen was the organ invariably involved. A dose-dependent effect of DMBA was not observed for pilosebaceous and musk gland tumors. When 1 mg of DMBA powder was dusted into the subcutaneous tissue at 4 weeks of age, sarcomas developed at the dusted site (69%; 9/13).

The immunohistochemical reactivities of 69 cases of breast carcinoma were examined on methacarn-fixed, paraffin-embedded sections using eight different monoclonal antibodies which recognize one or a few keratin polypeptides. In the normal breast, the monoclonal antibodies RPN1162, RPN1165 and AE1 stained almost all the luminal cells but not the basal (myoepithelial) cells. The monoclonal antibodies 35BH11, M20, CK5 and CK8.12 stained only a subset of the luminal cells. In contrast, 312C8-1 stained basal cells but not luminal cells. All the tumour specimens reacted with AE1, while over 80% of them also reacted with 35BH11 (57/69), CK5 (57/69) and RPN1165 (55/69); 30% reacted with CK8.12 (21/69) and 16% with RPN1162 (11/69). Basal cell-specific keratin, as defined by 312C8-1, was detected in only 1% of cases (1/69). Monoclonal antibodies to different keratin polypeptides may be of use in the characterization and subdivision of breast cancer.

Female BALB/c mice treated with a single intraperitoneal injection of 1 mg of 7, 12-dimethylbenz(a)anthracene (DMBA) at 4, 8 and 20 weeks of age showed a high incidence of uterine vascular tumors. Bilateral ovariectomy preceding DMBA treatment almost completely inhibited the induction of vascular tumors, while ovariectomy following DMBA treatment resulted in endometrial gland atrophy and a high incidence of vascular tumors. Vascular tumors were also induced when DMBA was given to neonatal androgenized mice, whereas among neonatal androgenized and normal female mice not treated with DMBA the incidence was 0%. Histological examinations revealed benign hemangiomas or angiosarcomas. In contrast, DMBA-treated male BALB/c mice and orchiectomized mice, and DMBA-untreated males showed no vascular tumors. A striking ovarian dependence of induction of uterine vascular tumors was observed.

Discussed is the case of a 41-year-old Japanese man dead at 4 months after start of his clinical course of multiple myeloma of the Bence-Jones protein lambda type of the skull. Autopsy findings revealed that atypical plasmacytes had infiltrated extensively into the testes, the retroperitoneum, including the pancreas and the renal pelvis, the bilateral pleura, the right subclavian soft tissue, and the meningism, but not to the liver, spleen, and lymph nodes. In both testes, which weighted 120 g and 100 g, respectively, myeloma cells were found disseminated throughout the testicular tissue. Such a testicular involvement in cases of a multiple myeloma is extremely rare. The pertinent literature also is reviewed.

Presented is the case of a 63-year-old woman who developed a cutaneous angiosarcoma of the hip after receiving adjuvant radiation therapy for a squamous cell carcinoma of the uterine cervix after a hysterectomy. The time lapse between the radiation therapy and the occurrence of the angiosarcoma was 15 years, and its systemic metastasis was seen on autopsy. This autopsy was carried out 26 years after the patient had received the initial irradiation and no recurrence of the uterine cancer was found. Factor involved in the etiology of an angiosarcoma are discussed, and 34 previously reported cases of a postirradiation angiosarcoma are reviewed.

To produce an animal model of Reye's syndrome (RS), 20 adult male Wistar rats were given 10 repeated i.p. injections of 50 mg/kg 4-pentenoic acid (PA) each separated by an 8-h interval. Then, 90 min after the tenth dose, they were given a final i.p. injection of 150 mg/kg PA. Thirteen control animals were injected with vehicle only using the same time schedule. More than half the animals in each group were fed a common diet, but the others were fasted during the terminal 10-h stage. All rats were sacrificed 30 min after the last injection. At the terminal stage, in comparison with the vehicle-injected controls, hypolipemia, hypoglycemia and high titers of serum ammonia and urea N were estimated significantly in the PA-treated rats fed throughout the whole period. Hypolipemia and hypoglycemia were more prominent in the terminally fasted group than the group fed continuously. Only in the PA-treated rats fed throughout the whole period moderate morphological signs of microvesicular fatty liver were exhibited. Ultracytochemical findings and biochemical determinations showed that the major lipids in the microvesicular fatty livers were triglycerides. Morphometric analysis revealed distinct hepatic mitochondrial swelling in the PA-treated rats. Therefore, the above treatment with PA was able to induce microvesicular fatty liver in rats with resembling RS, which were fed throughout the treatment procedure, but not in the terminally fasted rats.

Using immunoperoxidase staining of monoclonal antibody 312C8-1 against 51,000 dalton human keratin polypeptide, immunolocalization was observed in frozen sections of normal tissue and mammary tumours of adult female mice and rats. In normal tissue, the epitope was recognized in myoepithelial cells of the mammary, sweat and salivary glands, and in basal and suprabasal cells of the epidermis. However, the antibody did not react with luminal epithelial cells of the above glands or with mesenchymal cells. In spontaneous mammary tumours of mice, marker-positive tumour cells were distributed only in the outer layer of adenocarcinoma Type A, while they were scattered in some foci of adenocarcinoma Type B, and encircled the epithelial foci of pregnancy dependent tumours (plaque). All layers of epidermoid structures in adenoacanthoma revealed positivity. In rat mammary tumours induced by local dusting with 7, 12-dimethylbenz(a)anthracene (DMBA) powder, the staining pattern of benign tumours was comparable to that of the normal mammary gland. But, in addition to basally situated cells, marker-positive tumour cells were found scattered in the foci of adenocarcinoma, and were not restricted to basal cells in squamous cell carcinoma. The marker was not found in sarcomatous tissue. This antibody can therefore also be applied to rodents, and the staining pattern can be used to identify the epithelial subclass specific marker in normal tissue and in mammary tumours.