[Pulmonary venous obstruction after the Williams procedure for partial anomalous pulmonary venous connection].

A 54-year-old man was admitted to our hospital because of chest discomfort. Cardiac catheterization revealed partial anomalous pulmonary venous connection with an intact atrial septum. The right upper pulmonary vein (RUPV) drained into the upper segment of the superior vena cava (SVC). Using the Williams procedure, an atrial septal defect (ASD) was created and a fresh autologous pericardial patch was used to fashion a new pulmonary vein return route from SVC to the ASD. Although the patient was stable after the procedure, he was admitted again 6 months later because of obstruction of RUPV. At reoperation, it was found that the previous pulmonary vein route was obstructed and that the pericardial baffle had adhered to the atrial septum above the ASD. The shrunken and thickened pericardial baffle was removed and the orifice of the ASD was extensively enlarged, after which an expanded polytetrafluoroethylene (ePTFE) patch was used as a new baffle. After the reoperation, the patient's condition improved.

An experimental study of chondrogenesis and osteogenesis in rat submandibular gland induced by implantation of demineralized dentin.

Demineralized dentin pieces were implanted in 18 rat submandibular glands to examine the chondrogenesis and osteogenesis in pleomorphic adenoma of the salivary gland. After 7 days of implantation, a large amount of cartilage tissue was found next to the inner portions of the implanted pieces, and small amounts of the osteoid and cartilage tissues were detected next to the outer portions. A small amount of bone tissue was found in contact with the cartilage 10 days after the implantation. In the inner portions, invasions of capillaries and a small amount of osteoid tissue were noted. These histological findings resembled those of endochondral ossification. Large amounts of bone tissue and resorption of the implant were observed after 14 days. It has been suggested that cartilage and bone are produced by bone morphogenetic proteins (BMP) in demineralized dentin resulting in chondrogenesis followed by osteogenesis in submandibular gland. Apparently, undifferentiated mesenchymal cells are produced by implantation, undergo dedifferentiation, and are redifferentiated into chondroblasts and osteoblasts in the presence of BMP. These results suggest that chondrogenesis and osteogenesis in the submandibular gland are induced by BMP. It is possible that the chondroid tissues in pleomorphic adenoma of the salivary glands are induced by proteins such as BMP.

Ameloblastoma and its relationship to ameloblastic fibroma: their histogenesis based on an unusual case and review of the literature.

The present paper describes the relationship between ameloblastoma and ameloblastic fibroma deduced from a case diagnosed as "ameloblastoma combined with ameloblastic fibroma" arising in the mandible of a 5-year-old boy. Histologically, the tumor consisted of ameloblastoma in the central area and ameloblastic fibroma in the peripheral area; it clinically fits the characteristics of ameloblastic fibroma based on predominant age, manner of growth, and encapsulation. We reviewed the literature and discussed the relationship between ameloblastoma a ameloblastic fibroma in terms of tumorigenesis. It is assumed that ameloblastic fibroma can also be transformed into ameloblastoma, if the succeeding hard tissues are not formed, and the collagenous connective tissue substituting for the stromal mesenchymal tissue is formed by the inductive effect of the epithelial strands or other unknown factors. Several possibilities relative to the pathogenesis of ameloblastoma have been proposed by oral pathologists; however, to our knowledge, "ameloblastic fibroma can be transformed into ameloblastoma" has not hitherto been reported. The case we experienced here may be thought as an intermediate tumor pattern between ameloblastic fibroma and ameloblastoma.

[Statistical study of epulis, especially in general pathology].

This report contains a statistical study of 874 cases of epulis diagnosed by the Department of Pathology of Tokyo Dental College from 1966 to 1986. 1. Of the 874 cases, 344 were epulis fibrosa, 217 were epulis granulomatosa, 78 were epulis fibromatosa, 74 were epulis fibrosaosteoplastica, 51 were epulis hemangiomatosa, 43 were epulis fibrosa teleangiectaticum, 15 were epulis cementoplastica, 14 were epulis osteomatosa, 3 were congenital epulis, 2 were giant cell epulis, and 1 was epulis cementomatosa. 2. As has been reported in other literature, there is a marked tendency for this condition to occur in females (331 male cases and 539 female cases). 3. Our data indicate a higher occurrence rate in people in their fifties, although the occurrence rates were similar in people in their twenties and in people in their sixties. 4. The epulis was observed most frequently in the maxillary incisor region.

Ultrastructure of basal cell adenoma in the parotid gland.

Basal cell adenoma of the parotid gland was studied with electron microscopy. The cells constituting this tumor were divided into three types of epithelial cells; ductal, myoepithelial, and squamous cells. The ductal cells, which were polygonal and cuboidal in shape, formed a sometimes distinct lumen. Glycogen were recognized in the cytoplasm of these cells. The myoepithelial cells appeared as plasmacytoid cells which contained abundant microfilaments. The squamous cells were characterized by the presence of well-developed tonofilaments and desmosomes. However, no secretory cells could be found, although small, electron dense granules were detected in the cytoplasm of the ductal cells. The granules were unlike secretory granules in their size, number and location. In consideration of the presence of secretory and myoepithelial cells, we reviewed previously reported literature and discussed the identification of secretory granules. From our and other reported results, we tentatively concluded that the electron dense granules described as secretory granules are not intrinsic secretory granules. Further, we suggested that the cell types and the histogenesis of basal cell adenoma are analogous to those of both pleomorphic and clear cell adenomas.

Cardiac sensitivity to hyperkalemia in adrenalectomized dogs.

In dogs with bilateral adrenalectomy loaded with K by infusion of 2 mEq KCI/kg/hr there is a marked increase of cardiac sensitivity to hyperkalemia. Typical ECG changes begin at lower serum K levels (5-6 mEq/l) and the prelethal arrhythmias that signal the imminent onset of fatal when mean serum K is 7.6 mEq/l, 2.9 mEq/l above the average pre-infusion level. In control dogs, ECG changes start above 8 mEq K/liter, and prelethal arrhythmias appear between 9.5 and 10.2 mEq/l, a mean increase of 5.6 mEq/l above the average preinfusion level.

Kaluresis and cardiac sensitivity to hyperkalaemia in intact and adrenalectomized rabbits.

Rabbits K loaded by infusion of 2 meq KCl/kg/hr excrete over 55% of the administered K in the urine and do not develop prelethal ECG changes until mean serum K attains to 14.9 meq/liter, i.e., 11.8 meq/liter above the average preinfusion level. Four hours after bilateral adrenalectomy there is a profound diminution of urinary K loss in K loaded rabbits--less than 7% of the infused K is excreted. There is, however, no significant change in cardiac sensitivity to hyperkalemia. K loaded dogs lose only about 20% of infused K in the urine and develop prelethal ECG changes at similar to 10.2 meq/liter, i.e., 5.6meq/liter above the mean of the preinfusion levels. After adrenalectomy, urinary K loss is only moderately diminished (12% of infused K is still found in the urine), but cardiac sensitivity to K is markedly increased: prelethal ECG changes appear at a serum K level of similar to 7.6 meq/liter--about 2.9 meg/liter above the preinfusion value.

Kaluresis and diuresis after administration of antidiuretic hormone to hyperkalemic dogs.

Dogs infused with 2 meq KCl/kg per h exhibit electrocardiographic evidence of prelethal cardiotoxicity in about 3 h when serum potassium reaches a level between 10.2-10.5 meq/liter. During this time, their urine output of 30 ml/h is equal to the volume of KCl infused. Studies of the potassium distribution in these animals indicate that 20 percent of the infused ion is added to the extracellular fluid and red blood cell mass, 20 percent is excreted in the urine, while the remaining 60 percent is unaccounted for and presumably transferred to intracellular fluid. Dogs treated with moderately large doses of antidiuretic hormone intramuscularly before and during KCl infusion delay development of prelethal cardiotoxicity for about 5 h, with serum potassium levels comparable to those of untreated dogs. In addition, treated animals display a considerable diuresis and kaluresis with urine volumes nearly 4 times that of the volume infused. The potassium ion distribution in animals given antidiuretic hormone is much different from that of untreated dogs, with 55 percent of the infused ion found in the urine, about 15 percent in extracellular fluid and red blood cell mass, and only 30 percent presumably transferred to intracellular fluid. Transfer of potassium to intracellular fluid was calculated to be 3.1 plus or minus 0.7 meq/kg in antidiuretic-hormone-treated animals and 3.8 plus or minus 0.7 meq/kg in untreated (control) animals. Since these values are, within experimental error, quite comparable, it is possible that antidiuretic-hormone-induced kaluresis and diuresis are involved in protecting some animals from the effects of hyperkalemia by delaying the attainment of cardiotoxic blood levels.