Resolving the origin of the petrogenic hydrocarbon background in Prince William Sound, Alaska.

The dominant sources of the petrogenic hydrocarbon background in benthic sediments of Prince William Sound, AK (PWS), site of the 1989 Exxon-Valdez oil spill, are eroding Tertiary shales and residues of natural oil seepage. Mass balance considerations and statistical analyses of hydrocarbon fingerprints independently indicate that coal contributes generally less than 1% of the polycyclic aromatic hydrocarbons (PAH) and chemical biomarkers in this background. This is environmentally significant because of presumed differences in the bioavailability of PAH in coal, seep oil residues, and shales. Coal particles are present in PWS sediments, but their PAH and chemical biomarker contributions are overwhelmed by those of seep oil residues and organic particles from shales of low-to-high thermally maturity. In the late Tertiary or early Quaternary, the currently exposed and eroding shale formations were heated into the oil-generation window and, consequently, are now relatively rich in extractable PAH and chemical biomarkers. The exposed and eroding coals in the area, in contrast, experienced long hot burial and are now thermally overmature with respect to oil generation. The concentrations of thermally sensitive PAH and biomarker compounds in PWS sediments are not consistent with a mature coal origin but are consistent with the low-to-high maturity shales and seep oils in the area.

Dietary ferric vs. ferrous iron in copper-deficient rats fed fructose-based diets.

OBJECTIVE: This preliminary study was undertaken to determine whether the valence state of dietary iron affects signs associated with copper deficiency in rats fed fructose. METHODS: Rats were fed either copper-deficient or adequate diets containing 62% fructose as the sole dietary carbohydrate for 5 weeks. The mineral mixture contained equal concentration of either ferric or ferrous iron. RESULTS: Copper deficiency resulted in growth retardation, anemia, heart hypertrophy but pancreatic atrophy. The consumption of ferrous iron resulted in increased hematocrit and pancreas size. The combination of ferrous iron with copper deficiency reduced heart size. CONCLUSIONS: Copper deficiency had a major impact on each parameter measured. Although the valence state of iron did not protect the rats against the pathological consequence of copper deficiency it did have some positive effects. It may be that ferrous iron is a more available form than ferric iron.

Effect of coenzyme Q10 supplementation on cardiac hypertrophy of male rats consuming a high-fructose, low-copper diet.

Administration of coenzyme Q10 to humans and animals has a beneficial effect on a number of cardiac diseases. The purpose of the present study was to determine if coenzyme Q10 treatment could ameliorate cardiac abnormalities associated with the carbohydrate x copper interaction in rats. Weanling male rats were provided with a copper-deficient diet (0.6 microgram Cu/g) containing either 62.7% starch (S-Cu) or fructose (F-Cu) for 5 wk. Half of the rats provided with the F-Cu diet were given daily oral supplements of 300 mg coenzyme Q10/kg body weight (F-Cu + Q). Heart hypertrophy, liver enlargement, or pancreatic atrophy were not affected by, nor was body growth or anemia improved by, supplementation with coenzyme Q10 when compared to rats fed only the F-Cu diet. Hearts from rats fed the F-Cu diet had severe inflammation, degeneration, fibrosis, and giant mitochondria with abnormal cristae. Hearts from F-Cu + Q rats had similar mitochondrial changes as the F-Cu rat hearts but without any apparent degenerative changes. None of the F-Cu + Q rats, but 30% of the F-Cu rats, died during the study as a result of heart rupture. These observations show that whereas coenzyme Q10 treatment did not prevent the cardiac hypertrophy of the carbohydrate x copper interaction, it did play a role in maintaining the integrity of the heart.

Low dietary iron prevents free radical formation and heart pathology of copper-deficient rats fed fructose.

Two studies were conducted to determine whether hepatic iron overload in rats fed fructose plays a role in the exacerbation of the signs associated with copper deficiency. When fed the adequate iron diet (50 micrograms Fe/g), copper-deficient rats fed either fructose or starch exhibited hepatic iron overload of similar magnitude. However, only livers of copper-deficient rats fed fructose exhibited the presence of high peaks associated with an iron compound detected by electron spin resonance. In addition, only copper-deficient rats fed fructose developed anemia, pancreatic atrophy, and heart hypertrophy with histopathologic changes, and they died prematurely of heart-related abnormalities. Lowering dietary iron from 50 micrograms/g to 30 micrograms/g was not sufficient to protect the animals against the pathologic consequences of copper deficiency. In contrast, the consumption of a fructose diet inadequate in both copper (0.6 micrograms/g) and iron (17 micrograms/g) resulted in the reduction of hepatic iron, which in turn caused the amelioration of the deficiency, compared with rats fed the adequate iron (50 micrograms/g) diet. None of these rats developed pancreatic atrophy, none exhibited myocardial lesions, and none died of the deficiency. Electron spin resonance spectra of their livers did not show the presence of free radicals. The data suggest that hepatic iron overload plays a role in the exacerbation of copper deficiency only when fructose diets are consumed.

The severity of copper deficiency can be ameliorated by deferoxamine.

The present study was undertaken in order to determine whether hepatic iron overload plays a role in the exacerbation of copper deficiency. Weanling male Sprague-Dawley rats were fed a copper-deficient (0.6 microgram Cu/g) diet containing 62% fructose for 5 weeks. Some of the copper-deficient rats were injected daily with deferoxamine (DFX), an iron chelator that has been widely used to reduce iron overload. DFX reduced hepatic iron concentrations, which in turn ameliorated the pathology of copper deficiency when compared with nontreated copper-deficient animals. It is suggested that hepatic iron overload in a reduced environment plays a major role in the exacerbation of copper deficiency. Once the concentration of hepatic iron is reduced, the severity of the deficiency should be improved.

Plastic sections and ultrastructural techniques in the evaluation of bone marrow pathology.

Discussion in this article is focused on the advantages and applications of plastic-embedded bone marrow biopsy sections in the evaluation of bone marrow pathology. Routine processing of bone marrow biopsy specimens for plastic embedding and electron microscopy is also briefly described.

Squamous cell carcinoma of the splenic flexure of the colon.

A partially obstructing lesion of the splenic flexure was discovered during a barium enema examination, and subsequent colonoscopy and biopsy demonstrated a squamous cell carcinoma. This is the first reported instance of squamous cell carcinoma of the colon in which the splenic flexure has been involved. The case is discussed, and the recent literature on this entity is reviewed.

Embedding in large plastic blocks. Diagnostic light and potential electron microscopy on the same block.

Specimens destined for light and electron microscopy were fixed in a modified buffered formalin, postosmicated, dehydrated, and embedded in a mixture of epoxy resins (Epon-araldite) in large plastic molds. These blocks were sectioned at 0.5 to 1 micron on a JB-4 microtome and stained with a combined nuclear and cytoplasmic stain (Paragon). The sections were examined by light microscopy for diagnostic evaluation. If ultrastructural examination was also desired, the selected area was isolated using the "mesa" technique. The trimmed block was then sectioned on an ultramicrotome, picked up on grids, stained, and examined in the electron microscope. We think these techniques offer the diagnostic pathologist the potential of viewing 1-micron sections at a light microscopy level with the option of subsequent electron microscopy of the same area of the same block.

Lipolytic activity of human lingual glands (Ebner).

Human tongue preparations contain lipolytic activity similar to that present in human esophageal and gastric aspirates and in serous glands of rat tongue. The activity is present in homogenates of the glandular region (Ebner) beneath the cirumvallate papillae, and in secretions collected from the trough of the papillae. The lipolytic enzyme hydrolyzes long chain triglycerides to partial glycerides (di- and monoglyceride), glycerol, and free fatty acids at pH optimum 5.4. Lipolytic activity, expressed as nanomoles of triglyceride hydrolyzed per minute was in the range of 0 to 500 per gm. of tongue homogenate and 78 to 277 per ml. of aspirate from the vallate papillae. There was a 50% inhibition of the lipolytic activity by 4 mM sodium taurodeoxycholate. Specimens obtained from the region of the vallate papillae were examined by light and electron microscopy. Electron-dense granules similar to secretory granules present in rat Ebner's gland and in serous acini of human submaxillary glands were detected. Our findings suggest that in man, as previously reported in the rat, the lingual serous glands secrete a lipase that acts in the stomach where it initiates the digestion of dietary fat.

Quinidine hepatotoxicity. A report of a case and review of the literature.

A case is described of presumed quinidine hepatotoxicity, characterized by the development of fever, abnormal serum transaminase values, which improved after cessation of the drug but recurred after a challenge dose, and centrizonal hepatocellular necrosis detected on liver biopsy. Morphological changes on electron microscopy, consistent with a drug reaction, are also described. Pertinent features of previous case reports are analyzed, and the histological findings by light microscopy of the present and past cases are discussed. It is suggested that the development of unexplained fever within 1 month of quinidine administration should lead to consideration of possible hepatotoxicity.

Education and training in electron microscopy.

There is currently a need for diagnostic electron microscopy in both autopsy and surgical pathology. As more information emerges from the research laboratories, applied electron microscopy will grow in depth, and all large medical centers will need the expertise provided by a diagnostic electron microscopy laboratory. Many physicians other than electron microscopists find it essential to have an understanding of the contributions and limitations of electron microscopy. Education and training programs therefore must encompass not only paramedical personnel who prepare the electron micrographs and pathologists who are thoroughly trained in interpret the electron micrographs, but also other physicians and scientists who utilize the information obtained therefrom. Medical students should obtain sufficient background in normal and abnormal ultrastructure to enable them to interpret the medical literature, and the means to obtain this background should be available within the medical school curriculum. Some medical students will also desire more thorough training obtained by elective courses in electron microscopy. Pathology residents should obtain sufficient expertise during their residency to enable them to utilize the information produced by the electron microscopy laboratory. Certain pathology residents and some pathologists in practice prefer fellowships for more specialized training in electron microscopy. Four representative training programs in electron microscopy from Veterans Administration hospitals have been selected for presentation. Each emphasizes a different approach and different objectives.

The clinician's view of diagnostic electron microscopy.

From the clinician's standpoint, it has become increasingly evident that use of the electron microscope should no longer be confined to research institutes, but should be applied as an adjunct to clinical diagnosis, a guide to therapy, and a means of elucidating pathogenetic mechanisms. The usefulness of electron microscopy is stressed in relation to hematology, nephrology, virology, gastroenterology, and the study of miscellaneous metabolic conditions such as the storage diseases.