Cystic teratoma of the ovary: CT detection

Computed tomography (CT) was performed in 38 patients with 41 benign cystic teratomas of the ovary and two patients with malignant transformation. CT depicted all tumors. The presence of fat in 40 of 43 cases (93%), tooth or calcification in 24 of 43 (56%), Rokitansky protuberance in 35 of 43 (81%), tufts of hair in 28 of 43 (65%), and a fat-fluid level in five of 43 (12%) allowed a definite diagnosis of ovarian cystic teratoma in 42 of 43 cases (98%). In the two cases of malignancy, single large (greater than 10 cm) plugs (with uptake of contrast medium in one) with a cauliflower appearance and an irregular border forming an obtuse angle with the inner wall of the cyst suggested malignant transformation. In three cases of benign cystic teratoma, a mucinous tumor (one benign, one borderline, one malignant) arising in the same ovary was seen at pathologic examination but was only diagnosed with the help of CT in two of three cases. Thickening of the tube was noted in two cases of torsion of the adnexa. CT findings were compared with findings at radiography of the abdomen and hysterosalpingography in 30 cases, ultrasound in 31, and magnetic resonance imaging in three. This study demonstrated that CT was the best procedure for imaging cystic teratomas of the ovary.     

Complicated cholesteatomas: CT findings in inner ear complications of middle ear cholesteatomas

Patients with facial palsy and middle ear disease, which may be chronic but clinically occult, may have a cholesteatoma with extension medially along the facial canal. In two patients, axial computed tomographic (CT) scans demonstrated involvement of the medial petrous bone. Patients with vertigo and chronic middle ear disease may have a cholesteatoma with a "fistula" between the middle and inner ears. Although the fistula usually involves the lateral semicircular canal, the cholesteatoma may pass through the oval window. In two patients, coronal CT scans showed extension to the oval window in one and through it in the other.     

Temporal sequence of mammary intraductal proliferations, ductal carcinomas in situ and adenocarcinomas induced by 1-methyl-1- nitrosourea in rats

An experimental model for mammary carcinogenesis has been described in which intraductal proliferations, ductal carcinomas in situ and adenocarcinomas can be readily detected and the frequency of their occurrence quantified. The objective of the experiment reported in this study was to determine the latency period between carcinogen administration and the occurrence of each of these types of lesion. A total of 150 female Sprague-Dawley rats were injected i.p. with 50 mg 1- methyl-1-nitrosourea (MNU)/kg body wt at 21 days of age. Groups of 30 rats each were killed at 7, 14, 21, 28 and 35 days post-carcinogen. Mammary intraductal proliferations were the first detected lesions and were observed in 20% of the animals at 14 days following carcinogen administration. At 21 days post-carcinogen ductal carcinomas in situ and adenocarcinomas were observed. The number of each type of lesion increased with time post-carcinogen, but the temporal pattern of occurrence was different among lesion types. The pattern of lesion occurrence was consistent with intraductal proliferations being a precursor lesion for ductal carcinomas in situ and adenocarcinomas. Furthermore, the data imply that ductal carcinomas in situ represent one pathway of morphological progression by which intraductal proliferations evolve into invasive carcinomas, but that this lesion type, as currently defined histologically, may not be an obligatory intermediate in morphologic progression. These findings are consistent with emerging evidence of multiple but distinct pathogenetic pathways leading to mammary carcinomas that display different morphological patterns and biological activities.      

Wilms' tumor and gonadal dysgenesis in a child with the 2q37.1 deletion syndrome

Here we report Wilms' tumor, gonadal dysgenesis and a bifid uterus in an 18-month-old female with a terminal deletion of the long arm of chromosome 2 [46, XX, del(2)(q37.1)]. Since Wilms' tumor has been previously reported in the 2q37 deletion syndrome, the present observation raises the question of whether a tumor susceptibility gene maps to chromosome 2q37 and suggests giving consideration to the possible occurrence of Wilms' tumor in the course of disease.     

Tinidazole in treatment of amoebic liver abscess in children

Tinidazole as a single drug therapy given in a single dose daily for 5 or 3 days was put to rigorous test in malnourished children. Of 25 children with amoebic liver abscess, 23 were cured. The 2 remaining cases required surgical drainage followed by other amoebicides, one subsequently dying from complicating bronchopneumonia.     

Molecular internalization of a region of myelin basic protein

The conformation of myelin encephalitogenic or basic protein (BP) was investigated with a double-antibody radioimmunoassay by studying the reaction of BP or its fragments with antibodies produced in two rabbits against peptide 43-88 linked to rabbit serum albumin. Both antisera reacted well with peptide 43-88 but showed little or no reaction with BP. Absorption of these antisera with a BP-immunoadsorbent did not remove the antibody activity against peptide 43-88. Within the region of peptide 43- 88 it was shown that peptides 68-88 and 79-88 gave an equivalent or better reaction than peptide 43-88, whereas peptides 43-67 and 64-73 had very little reactivity. In the BP fragments containing region 43-88, peptide 1-88 showed the best reactivity, peptide 20-166 showed minimal reactivity, while peptide 1-115 showed none. These data document the internal position of at least a portion of peptide 43-88 and all of residues 79-88 in the BP molecule. The much greater reactivity of peptide 1-88 as compared to peptide 1-115 suggests that the region or a portion of the region of BP containing residues 89- 115 participates in the conformational alignment of BP restricting access to peptide 79-88. After absorption with BP, neither of the antisera prepared to peptide 43-88 reacted with PNS myelin in fixed tissue sections but continued to react with CNS myelin in similarly treated sections. The present findings demonstrate the need to consider the role of shielded antigenic determinants in the investigation of antigens or of immune responses.