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Endodermal sinus tumor (EST) of the vagina is extremely rare and primarily affects infants. We report on a six-month-old female infant with EST of the vagina who presented with vaginal spotting of one month's duration. Pelvic ultrasound and computerized tomography showed a 3.8 x 3.5 cm heterogeneous mass between the bladder and the rectum. The serum alpha-fetoprotein (AFP) level was high (1270 ng/mL) and the beta-human chorionic gonadotropin was undetectable. She received surgical intervention followed by chemotherapy. The patient was disease-free and serum AFP remained undetectable during the eight-month follow-up period.

A large, one-hour-old female baby was noted to have hypoglycemia immediately after birth. Although early feeding and then intravenous glucose infusion with a dose gradually increased to 30 mg/kg/min were given, the baby still had recurrent hypoglycemia 14 days after birth. High serum insulin/glucose ratios (> 2.5) were noted twice during hypoglycemic episodes. At the same time, the baby's serum growth hormone, thyroid hormone and cortisol levels were within normal ranges. Hyperinsulinism due to nesidiodysplasia was diagnosed and a near-total pancreatectomy was performed at the age of 14 days. After the operation, euglycemia was achieved and there was no episode of hypoglycemia even after fasting for eight hours. Our experience confirms that surgery is the treatment of choice for patients, including neonates, with hyperinsulinemic hypoglycemia.

A 3700-g male infant born at 37 weeks' gestation presented with cyanosis at birth. He was diagnosed as having persistent pulmonary hypertension of the newborn (PPHN) on the basis of persistent hypoxemia, despite continuous mechanical ventilatory support with 100% O2, and right-to-left shunting through the foramen ovale shown by Doppler echocardiography. Treatment with hyperventilation, and administration of tolazoline, prostaglandin E1 and MgSO4 failed to reverse his hypoxemia. High ventilator settings were required, and pneumothoraces ensued. Airway resistance increased gradually with development of hypercapnia and deterioration of hypoxemia. Bradycardia unresponsive to resuscitation occurred, and he died at eight days of age. Postmortem examination of the lungs revealed increased peripheral connective tissue and diffuse extension of medial smooth muscle to the precapillary pulmonary arteries. Excessive antenatal muscularization of the peripheral pulmonary arteries and resultant increased vasoconstriction capacity may have played an important role in the pathogenesis of PPHN in this case.

Intrauterine death of one twin in a monochorionic twin pregnancy is associated with increased mortality and morbidity of the survivor. The exact cause is usually difficult to determine even after delivery. The choice of management for the mother and the viable co-twin is difficult. We report on a case of intrauterine death of one twin with monochorionic placentation. Twin-to-twin transfusion syndrome was suggested by the sonographic findings and evidence of a vascular communication. The co-twin survived for another 39 days without complications after the diagnosis of fetal death. Postmortem examination showed severe torsion and constriction of the umbilical cord at the fetal end with focal deficiency of Wharton's jelly. It is likely that torsion and constriction of the cord was responsible for the one intrauterine fetal death; this so-called "twist amputation" of the cord, on the other hand, contributed to the favorable outcome in the surviving co-twin.

Ten cases of renal transplantations with pulmonary infection are reported. Nine cases were diagnosed by autopsy, one case clinically. Because of compromised immunological function, in these cases the causative microorganism, clinical manifestations, courses of the disease, therapies and result of the disease were different from those of ordinary pneumonia. The causative microorganisms were mainly opportunistic bacteria including virus, protozoa and fungus. During infection, symptoms were insidious and the disease disseminated rapidly, the mortality rate was high. Therefore in any case when the cause of the fever is unknown and no abnormal signs in the chest is find, it is necessary to take chest X-ray film immediately and repeatedly. Once diagnosis of pulmonary infection is established, series of bronchoscopic examination and lung biopsy are needed to find out the causative organism in order to treat the disease specifically, then the life of the patient can be saved.

Neuromuscular manifestations, including a variety of peripheral neuropathies and myopathies, can occur either as isolated clinical phenomena or concurrently with other clinical manifestations, and are common in acquired immunodeficiency syndrome (AIDS). A 33-year-old male patient had a four-year history of increasing proximal muscle weakness of the extremities. Elevated muscle enzymes, a muscle biopsy and interstitial lung disease all suggested a diagnosis of polymyositis with lung involvement. However, a transbronchial lung biopsy revealed Pneumocystis carinii pneumonia, and serology for HIV infection disclosed positive results. Zidovudine and cotrimoxazole were instituted and the patient improved. HIV-associated myopathy should be considered by practicing clinicians in cases presenting with myopathy, since the number of patients with HIV infection is increasing in Taiwan.

Cases were presented to describe the clinical manifestations, histological features, and diagnostic criteria about the current classification of ovarian tumors. They included peritoneal serous borderline tumor, endocervical-like the intestinal-type mucinous borderline tumor, transitional cell carcinoma of ovarian surface epithelial-stromal tumors and juvenile granulosa cell tumor, sclerosing stromal tumor, hepatoid yolk sac tumor, and primary mucinous carcinoid tumor of non-surface epithelial ovarian tumors. Cases were also presented for discussing the significance of structures and features of some ovarian tumors which have been reevaluated and newly classified. For instance, tumor cell of granulosa cell tumor gives vimentin expression, but is unable to express cytokeratin in all the cases detected with monoclonal antibody of CK-2. Based on the clinical manifestations, exact locating site in the ovary, as well as the histology and histochemistry features, it is possible to identify the stromal luteoma, leydig cell tumor, and non-specific steroid cell tumor respectively in the family of steroid cell tumors. Additionally, the diagnostic significance of the occurrence of basal membrane-like substance and intestinal cells in some yolk sac tumors is also discussed.

A series of 56 cases of prostatic adenocarcinoma and 48 cases of benign prostate hyperplasia were studied with histochemical, immunohistochemical methods and Feulgen-Image Analysis Technique. Duct-acinar dysplasia (DAD) was found in 81.8% of the prostate adenocarcinoma cases collected, but only in 47.9% of the benign hyperplasia cases. The frequency and extent of disruption of basal cell layer increased coincidently with the progressive increase of DAD grading. Intraluminal acid mucin and metachromasia stained with toluidine blue around the acini were identified in DAD. Immunohistochemical staining for prostatic acid phosphatase, cytokeratin, vimentin and UEA-1 receptor changed in DAD cells. The nuclear areas, DNA content and ploidy, mean numbers of AgNOR in DAD cells were higher than those in benign hyperplasia of the prostates and lower than those in adenocarcinomas, which indicates the possession of premalignant behavior of prostatic carcinoma.

Interleukin 2 (IL-2) at a dose of 10,000 to 20,000 U/kg/q 8 hr was given for 9-12 days to six patients with cases of severe atopic dermatitis (AD) which were refractory to conventional therapy. After IL-2 therapy, the clinical symptoms and signs of eczema including pruritus, scratching, papulovesicles, and lichenification were much improved, but all of them recurred 2-6 weeks after stopping treatment. Adverse reactions were similar to those reported previously, but all of them subsided after discontinuation of therapy. Laboratory findings showed decreased T-cell subsets, especially CD4+ cells, and increased IL-2R+ (CD25) cells, but there was no significant change in serum IL-2, serum IgE, or in vitro IgE production. Immunopathological studies of the skin biopsies showed decreased mononuclear-cell infiltration, depletion of CD4+ cells, and enhanced expression of CD25 and HLA-DR antigens. As lymphokine-activated killer (LAK)-cell activity against cultured fibroblasts was similar in patients with AD and in normals and CD1+ Langerhans cells were not decreased after IL-2 therapy, we speculate that the depletion of helper/inducer CD4+ cells and hence abrogation of the exaggerated antigen processing and cellular activation in diseased skin are the explanation for the transient efficacy of IL-2 in the treatment of atopic dermatitis.

The content and acyl group composition of phosphatidylinositol, poly-phosphoinositides, diacylglycerols, phosphatidic acids, and free fatty acids in rat brain homogenates of cerebral cortex and subcellular fractions were examined with respect to a 2 min post-decapitative ischemic treatment. With the exception of free fatty acids, these lipids are involved in the cyclic event associated with the receptor-mediated poly-phosphoinositide turnover. The ischemic treatment elicited a decrease in poly-phosphoinositide level in brain homogenates, synaptosomes, plasma membranes, and microsomes but not in myelin, and an increase in diacylglycerols, which was observed in brain homogenates and synaptosomes but not in other subcellular fractions. On the other hand, the level of phosphatidylinositol was not altered. The acyl groups of phosphoinositides are enriched in stearic and arachidonic acids. The diacylglycerols and free fatty acids that accumulated during the ischemic treatment are also enriched with the same fatty acids. There is a decrease in phosphatidic acid level after the ischemic treatment, but the change was only found in brain homogenates and synaptosomes. Therefore, the diacylglycerols increased during the ischemic treatment may be derived from hydrolysis of poly-phosphoinositides and phosphatidic acids. However, the amount of poly-phosphoinositides degraded is not enough to account for both diacylglycerols and free fatty acid increase.

30 cases of autopsies of patients who died after human renal allografts were studied. The incidence of infection was 60% and the lethal infectious complications amounted to 43%. The most common infectious agents were bacteria, including mycobacterium tuberculosis. In addition, some opportunistic agents, such as Cryptococcus, Aspergillus, mucormycosis, Pneumocystis carinii and cytomegalovirus were also found. All these patients had a history of receiving large dosage of immunosuppressive drugs such as cyclophosphamide, azathioprine, prednisone and dexamethasone after renal allografts. Pathological changes showed marked atrophy of lymphoid tissue and it was compatible with the histologic appearance of immunodeficiency. It is concluded that overuse of immunosuppressive drugs impairs the function of the immune system causing acquired immunodeficiency. Pathological features of lesions caused by the aforementioned infectious agents are also described in this paper.

Metabolic changes in brain phosphoinositides with respect to post-decapitative ischemic treatment were examined with rats labeled after i.p. injection of (32)Pi and intracerebral injection of [(3)H]inositol. The ischemic treatment resulted in a large and rapid decrease (40% in 2 min) in labeled polyphosphoinositide (poly-Pl), regardless of the source of the labeling. The rapid disappearance of poly-PI labeling can be similarly detected in the synaptosomes and plasma membrane fractions. On the other hand, the ischemic treatment resulted in an increase (10%) in [(32)P]-labeling of phosphatidylinositol, indicating possible contribution due to the poly-PI phosphomonoesterase pathway. In addition to the decrease in labeling of poly-PI, there was a decrease in radioactivity of phosphatidic acids in brain homogenates and plasma membranes due to the ischemic treatment. The labeling pattern of other phospholipids was not altered by the ischemic treatment. With rats prelabeled with [(3)H]inositol, the amount of labeled inositol monophosphate in brain increased 4-fold after pretreatment with LiCl (8 meq/kg). While no obvious change in labeling of inositol bisphosphate and inositol monophosphate was observed, there was a 40% decrease in labeled inositol trisphosphate after 2 min ischemic treatment. Discussions were made regarding the advantage and disadvantages in labeling brain phosphoinositides with these two types of labeled precursors.

Heterotopic oral gastrointestinal cyst, also called enterocystoma, is a rare choristoma composed of gastric and intestinal mucosa. Its origin is thought to be derived from misplaced embryonal rests. Clinically, it often causes swallowing and speaking difficulties. Surgical excision is the treatment of choice. Our reported case was a 16-month-old boy. He was noted to have a sublingual mass since birth, and was brought to our out-patient clinic due to gradual enlargement of the mass in the past month with swallowing and phonation difficulties. Surgical excision of the cyst was performed and microscopic examination revealed gastric mucosa and a variety of epithelial linings along the cyst wall. The patient had a good recovery after the operation.

Normal rat tracheal epithelial cells require exogenous pyruvate to survive in culture while carcinogen-altered cells do not. The aims of our study were, (i) to utilize this loss of requirement for pyruvate by carcinogen-altered cells as a way of selecting out and quantitating the numbers of altered cell populations induced in tracheas exposed to 200 micrograms 7,12-dimethylbenz[a]-anthracene (DMBA)-beeswax pellets for different lengths of time, (ii) to determine the constancy of these numbers at increasing time intervals after the exposure, (iii) to look for distinctive growth properties in cell populations that may be related to the exposure conditions. Tracheal implants were exposed for 2 weeks, 4 weeks or continuously to the 200 micrograms DMBA. At 2, 6 and 9 months after the start of exposure, the tracheas were cut into pieces and primary cultures established from outgrowths in an enriched Waymouth's medium. After 2 weeks, pyruvate and insulin were removed from the medium for 2 weeks to kill the normal cells and leave the altered, i.e., the selected cell populations (SPC). The pyruvate and insulin were then returned to the medium to stimulate rapid expansion of the SPC. The length of DMBA exposure had a marked effect on the number of SPC induced in the tracheas. There were 1.8 SPC/trachea 2 months after the 2 weeks exposure, while 5.0 and 7.2 SPC were obtained from the 4 weeks and continuously exposed tracheas, respectively, at this time. The numbers of SPC did not increase with time after exposure indicating that the maximal number of initiation sites was fixed. Between 2 and 9 months the number of subculturable SPC increased from 67 to 88% in the 2 week exposed group, while 93-100% of the SPC were subculturable after the longer DMBA exposures. Only the SPC from the 2 week DMBA--2 month group were distinguished by smaller numbers of cells surviving the selection medium and by a slower average growth rate compared to all the other experimental conditions.

The purpose of this study was to determine whether there are any relationships between the morphological expressions of the progression of neoplasia in tracheal epithelium in vivo, and the increased in vitro growth autonomy expressed by carcinogen-altered cell populations isolated from the same tracheas. Rat tracheal implants were exposed for 2 weeks or 4 weeks to 200 micrograms 7,12-dimethylbenz[a]anthracene (DMBA)-beeswax pellets. In the first phase of this study reported earlier (1), the numbers of carcinogen-altered cell populations, identified by their lack of need for exogenous pyruvate and insulin for survival in cell culture, were quantitated 2, 6 and 9 months after the start of the exposures. Before generating the cell cultures, lesions on the pieces of pre-exposed tracheal implants were identified by placing them in organ culture for 24 h and collecting the exfoliated cells from the medium for diagnostic cytopathology. Although the pieces of 2-week DMBA-exposed tracheas had not developed any markedly atypical lesions by 9 months, there was a progressive increase in the growth autonomy of the small number of subculturable cell populations (approximately 1/trachea) obtained from this exposure group. This was seen in the decreased time needed in culture to expand the population for testing anchorage-independent growth and tumorigenicity in nude mice. Also, anchorage-independent growth was markedly enhanced from 25 to 80% between 2 and 6 months and then to 100% at 9 months. Tumorigenicity did not show an increase. In the 4-week DMBA-exposed group, 74% of the large number of subculturable cell populations (approximately 5.0/trachea) already showed anchorage-independent growth at 2 months. This percentage increased to 94-100% at 6 and 9 months. A progressive increase in tumorigenic cell populations was also clearly seen. At 2 months, 26% of the cell populations inoculated into nude mice formed tumors. This number increased from 45 to 61% at 6 and 9 months, respectively. The pieces of tracheas taken at 2 months after the start of the 4-week DMBA exposure had no markedly atypical lesions. At 6 months one marked atypia was detected, and at 9 months five markedly atypical lesions and two carcinomas in situ were present. The cell populations derived from the explants harboring these lesions showed a high incidence of growth autonomy, e.g. anchorage-independent growth and tumor formation, indicating a close relationship between these properties and the evolving morphological manifestations of tumor development.

Lysophospholipase activity in brain subcellular fractions was measured by the release of myristic acid from 1-myristoylglycerophosphocholine or through the formation of [32P]glycerophosphocholine from [32P]lysophosphatidylcholine. Although the lysophospholipase activity was highest in microsomes, considerable enzyme activity was also found in other subcellular membrane fractions. The pH optimum for the microsomal enzyme was around 7, whereas the synaptosomes and non-synaptic plasma membranes exhibited a pH maximum around 8. Although the enzyme did not require divalent cations for activity, divalent cations (1 mM) such as Hg2+, Cu2+, and Zn2+ inhibited potently the enzyme activity. Enzyme activity was also partially inhibited by both saturated and polyunsaturated fatty acids (25-200 microM), and the inhibition seemed to be greater in the membrane than in the cytosolic fractions. Ionic detergents such as deoxycholate and taurocholate inhibited the lysophospholipase. On the other hand, the effect of Triton X-100 was biphasic, i.e., stimulation at concentrations below 100 micrograms/mg protein and inhibition at higher concentrations. Addition of cholesterol (50-250 micrograms/ml), but not cholesteryl esters, also potently inhibited enzyme activity. The presence of active lysophospholipase(s) in brain is probably an important mechanism for preventing unnecessary accumulation of lysophospholipids which may exert a deleterious effect on the membranes because of their detergent properties.