Manop Huntrakoon

Misalignment of lung vessels and alveolar capillary dysplasia: a cause of persistent pulmonary hypertension.

Two infants with fatal persistent pulmonary hypertension are described. Morphologically there was misalignment of the lung vessels, with the veins and the arterioles anomalously related, often sharing the same adventitial sheet. The capillaries did not make contact with the alveolar epithelium. The arterioles had increased medial muscle, and there was extension of the arteriolar muscularization to the precapillary level. The fraction of the parenchyma that was septal and connective tissue was increased. The acini had a decreased complexity, with immature alveoli and with a decreased radial alveolar count. The cause appeared to be related to abnormal capillary and venous plexus formation and migration. This syndrome seems to be identical with that described in three previous reports and probably represents a specific cause of persistent pulmonary hypertension.

Oncocytic carcinoma of the pancreas

A large firm 12.5 cm mass at the tail of pancreas was surgically resected in a 73‐year‐old white man. The tumor was composed of solid sheets of cells with abundant finely granular eosinophilic cytoplasm. Electron microscopic study revealed tumor cells which were packed with mitochondria, a feature characteristic of the oncocyte. Perineural invasion and direct extension into the parenchyma of the spleen was present, as well as metastasis to a lymph node. There appears not to be a report of a similar case.

Muscular hamartoma of the breast

A rare case of muscular hamartoma of the breast was presented. An electron microscopic study confirmed that the proliferating spindle cells were of smooth muscle cell origin.

Isolated perfused lung histamine release, lipid peroxidation, and tissue superoxide dismutase from rats exposed to normobaric hyperoxia

Female Sprague-Dawley inbred rats were exposed to either 1 atm of 100% O2 for 24 h, or 65% O2 for 5 days, with or without pretreatment with disulfiram, an inhibitor of lung CuZn-SOD. After O2 exposure, the rats were killed, the lungs removed, and isolated perfused lungs (IPLs) prepared. The IPLs were perfused with modified Krebs-Henseleit buffer, and perfusate histamine, malondialdehyde (MDA), and lung tissue CuZn-SOD activity examined. Disulfiram administration decreased the LT50 of O2-exposed rats from 65 to 36 h. Histamine and MDA in the perfusate from the IPL prepared from rats exposed to 100% O2 for 24 h were markedly increased. When rats were pretreated with disulfiram and exposed to 100% O2 for 24 h, histamine and MDA were increased an additional 77% and 45%, respectively. In separate experiments, 100% O2 exposure significantly decreased lung CuZn-SOD activity by 40% while IPL histamine and MDA were significantly increased. However, exposure of rats to 65% O2 for 5 days decreased lung CuZn-SOD by 69% but did not affect IPL histamine release or perfusate MDA. These studies suggest that IPL histamine release and/or MDA may be an early biochemical marker for pulmonary O2 toxicity, that lung CuZn-SOD activity may not be the only determinant in O2 toxicity, and other defense mechanisms may play a vital protective role during sublethal O2 exposures.

Bilateral Choroidal Neonatal Neuroblastoma

We treated a bilateral, well-differentiated neuroblastoma of the choroid in a patient who had congenital abdominal neuroblastoma. Although orbital metastasis of neuroblastoma is common, intraocular metastasis is not. In our patient, there was no amplification of the N-myc oncogene in the tumor of either eye. This is consistent with early-stage primary neuroblastoma. Histologically, the tumors were identical in each eye and well differentiated with Homer Wright rosettes; most neuroblastoma metastases have few rosettes and are composed of more undifferentiated, anaplastic cells. We believe that our patient had bilateral primary tumors and not metastatic tumors.

Superficial spreading malignant melanoma with neurosarcomatous metastasis

&NA; Summary A case of neurosarcomatous nodal metastasis of superficial spreading malignant melanoma, without primary site desmoplasia or sarcomatous changes, is reported. Of particular interest regarding the metastasis are: the ultrastructural demonstration of numerous cytoplasmic microtubules, absence of premeianosomes, intense immunohistochemical reaction with S‐100 protein antibody, and the presence, at the light microscopic level, of extranodal fibrosis. The primary lesion shows a preexisting benign nevus and features suggestive of lamellar fibroplasia. The origin and histogenesis of melanocytic desmoplasia, in the context of a neural crest progenitor cell, and of lamellar fibroplasia, are discussed.

Immunocytochemical studies of subtypes of pulmonary endocrine cells in diethylnitrosamine-treated rabbits

SummaryNew Zealand White rabbits were injected subcutaneously with 20 mg/kg body weight of diethylnitrosamine (DEN), twice per week, starting when they were 1 week old. The animals were sacrificed 6 to 12 months after the first injection and lung tissues were processed for light microscopy. Using serotonin (5HT) and neuron specific enolase (NSE) as markers for the endocrine cells, tissue sections were stained immunocytochemically by the avidin-biotin complex method. Numerous neuroepithelial bodies (NEBs) positive for 5HT, but negative for NSE, were seen in the alveolar duct regions of DENtreated rabbits. On the other hand, an increased number of solitary endocrine cells immunoreactive for NSE was found in bronchial or bronchiolar epithelia. The results indicate that DEN induced increases in two distinct types of endocrine cells: the component cells of NEBs are positive for 5HT and solitary cells are positive for NSE.