Cloth-covered Starr-Edwards valves.
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The widely favored hypothesis that ovarian epithelial tumors arise from the mesothelial cell layer lining the ovarian surface fails to explain the resemblance of these tumors to those arising in organs that are embryologically derived from the Müllerian ducts such as fallopian tubes, endometrium, and endocervix. In addition, this theory cannot account for the fact that tumors that are morphologically identical to ovarian carcinomas can sometimes be found outside the ovary. A suggestion is made that components of the secondary Müllerian system, which include paraovarian/paratubal cysts, rete ovarii, endosalpingiosis, endometriosis, and endomucinosis, merit some consideration as to their possible role in ovarian tumorigenesis.
Cohort analysis of cancer mortality in industrialized countries has led to the generally accepted conclusion that these populations have been exposed to increasing levels of carcinogenic influences. Age-specific cancer mortality rates in the United States from 1962 to 1988 were portrayed in both cross-sectional and cohort manners. Both representations are consistent with the Strehler-Mildvan modification of the Gompertz relationship between aging and mortality. These observations suggest that environmental cohort effects are not responsible for rising cancer mortality. The cohort mortality perspective in epidemiology is inherently biased due to the effects of competing mortality. Competing mortality, like environmental exposures, is applied in a cross-sectional manner across multiple birth cohorts. Competing mortality produces selective mortality, or differential survival, within a birth cohort. Differential survival, an underappreciated form of selection bias, alters the gene pool of surviving birth cohort members. Since cross-sectional competing mortality risks vary with age, the gene pool of different birth cohorts is not uniformly altered. Consequently, differences between birth cohorts in age-specific mortality rates with respect to a particular disorder, for example, cancer, do not specifically imply differences in environmental exposures.
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A 71-year-old patient with melena, abdominal and lower back pain was admitted to hospital under suspicion of upper gastrointestinal bleeding. He had mild anemia and an elevated C-reactive protein. Endoscopy and ultrasound failed to localize the source of bleeding. The patient died 2 1/2 days after admission on an exsanguinating hemorrhage. On pathologic examination a fistula between the small aortic aneurysm and duodenum and periaortic inflammation in contact with a spondylitis were found. When clinical presentation is subtle, with a herald bleeding followed by a period of grace, the diagnosis of aortoenteric fistula may be extremely difficult.
rhoB-crystallin (AJ245805) is a major protein component (20%) in the eye lens of the gecko Lepidodactylus lugubris. Limited peptide sequence analysis earlier revealed that it belongs to the aldo-keto reductase superfamily, as does the frog lens rho-crystallin. We have now determined the complete cDNA sequence of rhoB-crystallin and established that it is more closely related to the aldose reductase branch of the superfamily than to frog rho-crystallin. These gecko and frog lens proteins have thus independently been recruited from the same enzyme superfamily. Aldose reductase is implicated in the development of diabetic cataract in mammals, and, if active, rhoB-crystallin might be a potential risk for the gecko lens. Apart from a replacement 298 Cys --> Tyr, rhoB-crystallin possesses all amino acid residues thought to be required for catalytic activity of the aldose reductases. However, modeling studies of the rhoB-crystallin structure indicate that substrate specificity and nicotinamide cofactor affinity might be affected. Indeed, neither recombinant rhoB-crystallin nor the reverse mutant 298 Tyr --> Cys showed noticeable activity toward aliphatic and aromatic substrates, although cofactor binding was retained. Various other oxidoreductases are known to be recruited as abundant lens proteins in many vertebrate species; rhoB-crystallin demonstrates that an aldose reductase-related enzyme also can be modified to this end.
Bile concrements may remain intraperitoneally after laparoscopic cholecystectomy. Previously, this was considered harmless, a view supported by some experimental studies. Recently, however, spilled gallstones have been identified as a source of rare but potentially serious complications. We report a case of a retrohepatic abscess and dorsal fistulation after laparoscopic cholecystectomy. Healing was achieved only by repeated surgery, including abscess drainage, stone removals, and fistula excision. Since 1990, 73 cases with gallstone-related complications after laparoscopic cholecystectomy have been reported in the literature. Among these complications, intra-abdominal abscesses and transabdominal fistulas were predominant. The interval between the cholecystectomy and the appearance of complications ranged from 4 days to 29 months, with a peak incidence at 4 months. Spillage of small bile concrements or fragments is, with the exception of multiple irremovable stones, not commonly an indication for conversion to an open procedure. However, the patient needs to be warned about the risk of gallstone loss and its associated complications at the time when informed consent is obtained. Furthermore, if gallstone loss has occurred, the patient should be informed, and the occurrence should be documented.
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