The microscopical and ultrastructural findings in twenty-five prolactin-secreting pituitary adenomas removed by transsphenoidal surgery have been analyzed and compared with previously published cases. Under the light microscope, these adenomas could easily be confused with chromophobe adenomas. However, in eight cases a small number of cells contained erythrosinophilic granules of the type found in prolactin cells. Electron microscopical study of the tumor cells showed scarce secretory granules frequently undergoing exocytosis, a prominent rough endoplasmic reticulum, and a large Golgi area containing immature granules. Cytoplasmic bundles and aggregates of filaments, as well as myelin figures and glycogen within the mitochondria were occasionally found. Comparison with prolactin cells during lactation, in pituitary autografts, and under in vitro stimulation shows that the tumor cells are actively secreting.

A 56-year-old woman had pseudoxanthoma elasticum (PXE). Ultrastructural findings in the endocardium showed increased collagenogenesis and elastogenesis. The newly formed elastic fibers appeared morphologically normal, but showed a notable propensity to become calcified. The internal structure of the calcified areas was essentially similar to that of the adjacent uninvolved portions of the elastic fibers. Some of the heavily calcified fibers showed loss of internal structure and fragmentation. These findings support the concept that in PXE, calcification involves morphologically unaltered elastic fibers that subsequently may undergo secondary degenerative changes, such as loss of internal structure and fragmentation.

Among the morphological features of an oncocytic mucoepidermoid carcinoma of the parotid salivary gland in a 78-year-old man, the oncocytes had granular eosinophilic cytoplasm that was characterized ultrastructurally by large numbers of mitochondria that displayed minimal abnormalities. Complex cell-to-cell relationship, well-developed junctival complexes, and microvillous-like surface projections suggestive of ductal differentiation were present; epidermoid features in the form of dense focal aggregates of cytoplasmic fibrils were also seen.

Administration of D-serine to rats induced acute necrosis of the proximal straight tubules, proteinuria, glucosuria, and aminoaciduria. Proteinuria and glucosuria developed at the onset of tubular necrosis and disappeared when the tubules were completely relined by new epithelium. Our findings suggest (1) that abnormal loss of protein and glucose in urine is due to diffusion of these substances from interstitium to tubular fluid across the denuded permeable basement membranes of the necrotic tubules, and (2) that tubular cells normally are a barrier to diffusion of certain solutes betweeen interstitial and tubular fluids. Amino-aciduria preceded the onset of tubular necrosis and increased excretion of some amino acids persisted after tubular repair. Thus, D-serine-induced aminoaciduria may be due to impaired reabsorption of amino acids by the injured proximal straight tubules, as well as by backward diffusion of amino acids from the interstitium.

Rats were infused for three hours with doses of calcium gluconate to elevate serum calcium level and were killed either immediately after infusion or after 24 hours. Necrosis of proximal tubular cells was observed when serum calcium level was 16.0 mg/dl or higher. Above 16.0 mg/dl, an additional 5% of renal tubular profiles contained damaged cells for each 1 mg/dl in serum calcium. No difference in extent of damage was found in rats killed immediately or after 24 hours. Initial changes were formation of granular dense bodies in mitochondria, cell swelling, rupture, and extensive mitochondrial calcification. Renal tubular basement membrane changes appeared to be initiated by protrusion of cytoplasmic buds, forming ovoid bodies, which became embedded in the basement membrane. These ovoid bodies then appeared to serve as a nidus for further extensive basement membrane calcification.

Three cases of Hodgkin disease with renal manifestations were studied with electron microscopy and immunofluorescence. The first patient had lipoid nephrosis that disappeared after chemotherapy for Hodgkin disease. Immune-complex nephritis was observed in the second patient who also had Sjogren syndrome. The third patient developed amyloid nephrosis five years after the onset of Hodgkin disease. Apparently, diverse lesions and mechanisms are involved in the development of the nephrotic syndrome in Hodgkin disease and the diagnosis can only be established by appropriate studies of kidney specimens.

Pancreatic tissues from 22 patients with a wide variety of types of shock were obtained within minutes of somatic death for light and electron microscopy and for cytochemical studies. By light microscopy, it was difficult to ascertain any differences between the shock groups; however, electron microscopy disclosed subcellular alterations that could be correlated well with the type, severity, and duration of shock. Mild cases of shock or shock of short duration showed mild cell damage, while extreme cases of hemorrhagic or septic shock showed cell death and necrosis. No morphological evidence for lysosomal initiation of damage was seen, but it is clear that the pancreas can undergo severe cell injury during shock that could result in release of further damaging enzymes, most probably from zymogen granules rather than from lysosomes.

During a recent outbreak of Lassa fever in Sierre Leone, a 20-year-old woman developed an acute febrile disease with tonsillar exudates and hemorrhagic manifestations. Lassa virus was isolated in cell cultures from pharyngeal secretions and pleural fluid and was identified by complement fixation. Typical arenavirus particles were observed in these infected cell cultures. In a liver biopsy specimen, diffuse hepatocellular damage and focal necroses were evident, with a spectrum of liver cell change, ranging from slight vacuolizaiton to frank lysis. Virus was frequently observed in nearby extracellular spaces and was clearly associated with hepatocytes rather than sinusoidal cells. The demonstration for the first time of Lassa virus particules in human tissue provides direct evidence that the virus is responsible for the observed pathologic changes.