Isolated ovarian polyarteritis nodosa

Polyarteritis nodosa is a rare disorder and a form of systemic vasculitis. A 48 year-old female was admitted to the hospital because menorrhagia and pelvic pain in February 1993. The patient underwent exploratory laparotomy resulting in a total hysterectomy and bilateral salpingo-oophorectomy for myoma of uterus and a right adnexal cystic mass. Histopathologic examination revealed left ovarian periarteritis nodosa. Further investigation and 9 months follow-up failed to show any systemic involvement. To our knowledge the isolated ovarian polyarteritis nodosa is the first case in the literature.     

Temporal order and functional analysis of mutations within the Fli-1 and p53 genes during the erythroleukemias induced by F-MuLV

The erythroleukemias induced by Friend murine leukemia virus (F-MuLV) result from the accumulation of a number of genetic changes, including activation of the Fli-1 proto-oncogene and inactivation of the p53 tumor suppressor gene. We have determined the temporal order of mutation of the genes involved in this multistage malignancy, by serial in vivo transplantation of F-MuLV induced primary erythroleukemias into syngenic Balb/c mice. These primary tumors are capable of growing when transplanted into syngenic mice, but die after several days of in vitro culture. From the transplanted tumors grown in syngenic mice, erythropoietin-dependent cell lines were established in culture that are clonally related to cells in the primary tumors. We show that retroviral insertional activation of the Fli-1 ets family member is the first detectable genetic event in F-MuLV induced primary erythroleukemias. Mutations in the p53 gene were observed in the Epo-dependent cell lines but not in the transplanted erythroleukemias used to establish these cell lines in culture. These data suggest that activation of Fli-1 plays an important role in the early stages of F-MuLV-induced leukemia, perhaps by altering the self-renewal probabilities of erythroid progenitor cells and that p53 mutations immortalize these cells, enabling them to grow in vitro in the presence of Epo.     

Scanning electron microscopy of the myosin-coated surface of polystyrene beads in a force-movement assay system for ATP-dependent actin-myosin sliding

An outbreak of Cryptosporidiosis occurred over three months in a British Columbia community, peaking in December 1990. Results of the case-control study and illness surveys support the hypothesis that transmission occurred in a public children's pool at the local recreation centre. Analysis using lab-confirmed cases revealed a matched odds ratio of 4.5 [95% CI 0.97, 20.83], and using clinical cases an unmatched odds ratio of 12.8 [95% CI 3.68, 46.77], associated with swimming in the children's pool within two weeks prior to onset of illness. Other risk factors were not significant. Attack rates in various groups of children's pool users ranged from 8% to 78%. The children's pool was closed for steam cleaning and disinfection. Unusually frequent defecations including liquid stools had occurred before and during the outbreak. Improvements were instituted for removal of feces and superchlorination of pool water.     

Liquid viscosities and densities of HFC-134a+glycol mixtures

Liquid viscosity and density of six binary mixtures of HFC-134a with glycols [ethylene glycol, diethylene glycol, triethylene glycol, polyethylene glycol (400), and polypropylene glycol (2000)] have been measured in the temperature range from 273 to 333 K. The viscosity was measured by a rolling-ball viscometer calibrated with standard liquids of viscosities and densities (JS5, JS10, JS20, and JS50). The density was measured with a glass pycnometer. The uncertainties of the measurements were estimated to be less than 3.4 % for viscosity and 0.04 % for density, respectively. An equation is given to represent the obtained viscosity values as a function of weight fraction and temperature.     

Fetal heart rate following coelocentesis

For psychological reasons, coelocentesis was performed in 20 women prior to termination of pregnancy, at 6-11 weeks of gestation. The fetal heart rate (FHR) was measured immediately before the procedure and at 1, 5, and 10 min afterward. There was no significant difference between FHR before coelocentesis compared to the values at 1 min (mean = 158, range 114-178; z = -0.629, P = 0.529), 5 min (mean = 160, range 121-179; z = -0.191, P = 0.848), or 10 min (mean 159, range 117-183; z = -0.214, P = 0.83) after the procedure. These findings suggest that coelocentesis does not have a major effect on the fetal cardiovascular system.     

cGMP-stimulated cyclic nucleotide phosphodiesterase regulates the basal calcium current in human atrial myocytes

EHNA (Erythro-9-[2-hydroxy-3-nonyl]adenine) is a wellknown inhibitor of adenosine deaminase. Recently, EHNA was shown to block the activity of purified soluble cGMPstimulated phosphodiesterase (PDE2) from frog, human, and porcine heart with an apparent Ki value of approximately 1 microM and with negligible effects on Ca2+/calmodulin PDE (PDE1), cGMP-inhibited PDE (PDE3), and low Km cAMP-specific PDE (PDE4) (Méry, P.F., C. Pavoine, F. Pecker, and R. Fischmeister. 1995. Mol. Pharmacol. 48:121-130; Podzuweit, T., P. Nennstiel, and A. Muller. 1995. Cell. Signalling. 7:733- 738). To investigate the role of PDE2 in the regulation of cardiac L-type Ca2+ current (ICa), we have examined the effect of EHNA on ICa in freshly isolated human atrial myocytes. Extracellular application of 0.1-10 microM EHNA induced an increase in the amplitude of basal ICa ( approximately 80% at 1 microM) without modification of the current-voltage or inactivation curves. The maximal stimulatory effect of EHNA on ICa was comparable in amplitude with the maximal effect of isoprenaline (1 microM), and the two effects were not additive. The effect of EHNA was not a result of adenosine deaminase inhibition, since 2'-deoxycoformycin (1-30 microM), another adenosine deaminase inhibitor with no effect on PDE2, or adenosine (1-10 microM) did not increase ICa. In the absence of intracellular GTP, the substrate of guanylyl cyclase, EHNA did not increase ICa. However, under similar conditions, intracellular perfusion with 0.5 microM cGMP produced an 80% increase in ICa. As opposed to human cardiomyocytes, EHNA (1-10 microM) did not modify ICa in isolated rat ventricular and atrial myocytes. We conclude that basal ICa is controlled by PDE2 activity in human atrial myocytes. Both PDE2 and PDE3 may contribute to keep the cyclic nucleotides concentrations at minimum in the absence of adenylyl and/or guanylyl cyclase stimulation.     

Ambulatory subcutaneous internal sphincterectomy]

The internal anal sphincterotomy operation represents the best therapy for the treatment of those anal lesions, above all anal fissures, which cause hypertrophy and spasms of the internal anal sphincter. The Authors report their experience of 253 operations of internal subcutaneous sphincterotomy carried out between 1989 and 1995 under local anaesthesia in the outpatient clinic. The excellent results achieved prove that the procedure can easily be carried out under local anaesthesia in an outpatient clinic and, therefore, it is preferable to the surgical technique of isolation of the internal sphincter, not only for its practicality but also for the improved results.     

Association of angiotensin-converting enzyme gene I/D polymorphism with change in left ventricular mass in response to physical training

PURPOSE: To determine the radiologic characteristics of cystic dystrophy of the duodenal wall. MATERIALS AND METHODS: Ten patients with cystic dystrophy of the duodenal wall and chronic pancreatitis underwent ultrasonography (US) (n = 10), computed tomography (CT) (n = 10), endoscopic US (n = 5), and endoscopic retrograde cholangiopancreatography (ERCP) (n = 9). Cystic dystrophy of the duodenal wall was classified as either cystic or solid. The imaging findings were retrospectively analyzed and compared with findings at pancreatoduodenectomy (n = 10). RESULTS: The more frequent cystic type (n = 7) of cystic dystrophy of the duodenal wall was characterized by the presence of easily recognizable cystic lesions (diameter, more than 1 cm), located within the thickened wall of the second portion of the duodenum. The solid type (n = 3) of cystic dystrophy of the duodenal wall demonstrated fibrous thickening of the duodenal wall within which small cysts (diameter, less than 1 cm) were present. The intraduodenal cysts were usually elongated or bilobate with a thick wall. The thickening of the duodenal wall appeared as a solid layer between the duodenal lumen and the pancreas, hypoechoic at US, isoattenuating at unenhanced CT, and hypoattenuating in the early phase (after initiation of infusion of contrast material) and isoattenuating in the late phase (after completion of infusion) at contrast material-enhanced CT. Findings at retrospective analysis of CT and endoscopic US images were characteristic. CONCLUSION: Imaging modalities, notably CT and endoscopic US, helped establish the diagnosis of cystic dystrophy of the duodenal wall.