[New points of view on the origin of pial lipoma. A contribution to the clinical course, pathology, manner of formation and origin of the fatty tumors of the central nervous system].
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Anatomical variations of the celiac trunk and superior mesenteric artery are not infrequent. Knowledge of the existing aberrations is important in planning and conducting surgical or radiological procedures. A case of right hepatic artery arising independently from the aorta supplying an hepatocellular carcinoma was identified, through which transarterial chemoembolization was successfully performed. A second case is presented with a common splenomesenteric trunk branching into the splenic and superior mesenteric arteries. These two cases represent exceptional arterial variations in the upper abdomen.
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1. In order to evaluate possible non-salivary contributions to the content of salivary-type amylase in the circulation, parotid glands--the only salivary source of amylase in rats--have been totally removed and the effects on serum amylase have been assessed, after fasting and at different times after feeding. 2. Despite the parotidectomy the resting level of salivary-type amylase remained the same and an increase was still found to occur on feeding. 3. Isoelectric focusing has identified additional isoforms of amylase in serum and liver distinct from those occurring in parotid saliva. 4. The liver therefore may be contributing to the fasting levels of serum amylase and to the increases that occur on feeding, in rats.
RATIONALE AND OBJECTIVES: The objective is to compare three different ultrasmall superparamagnetic iron oxides (USPIOs) for magnetic resonance (MR) imaging of normal bone marrow in rodents. MATERIALS AND METHODS: Femoral bone marrow in 18 Sprague-Dawley rats was examined by using MR imaging before and up to 2 and 24 hours postinjection (PI) of 200 mumol of Fe/kg of SHU555C (n = 6), ferumoxtran-10 (n = 6), or ferumoxytol (n = 6), using T1-weighted (50 ms/1.7 ms/60 degrees = repetition time [TR]/echo time [TE]/flip angle) and T2*-weighted (100 ms/15 ms/38 degrees = TR/TE/flip angle) three-dimensional spoiled gradient recalled echo sequences. USPIO-induced bone marrow was evaluated qualitatively and quantified as signal-to-noise ratio (SNR) and change in signal intensity (DeltaSI) values. A mixed-effect model was fitted to the SNR and DeltaSI values, and differences among USPIOs were tested for significance by using F tests. RESULTS: At 2 hours PI, all three USPIOs showed marked positive signal enhancement on T1-weighted images and a corresponding marked signal loss on T2*-weighted images. At 24 hours PI, the T1 effect of all three USPIOs disappeared, whereas T2*-weighted images showed persistent signal loss on SHU555C and ferumoxytol-enhanced MR images, but not ferumoxtran-10-enhanced MR images. Corresponding SNR and DeltaSI values on T2*-weighted MR images at 24 hours PI were significantly different from baseline for SHU555C and ferumoxytol, but not ferumoxtran-10. CONCLUSION: All three USPIO contrast agents, ferumoxtran-10, ferumoxytol, and SHU555C, can be applied for MR imaging of bone marrow. Ferumoxtran-10 apparently reveals a different kinetic behavior in bone marrow than ferumoxytol and SHU555C.
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The phytopathogen Rhizoctonia leguminicola has previously been shown to incorporate pipecolic acid into the piperidine alkaloids 1-acetoxy-6-aminooctahydroindolizine (slaframine) and 3,4,5-trihydroxyoctahydro-1-pyrindine. In the experiments described here, resting cultures of R. leguminicola were incubated with [1-14C]- and [2-14C]malonic acid and with [1-14C]- and [2-2H]acetic acid. Both acids were incorporated into the ring systems of both alkaloids. Mass spectrometric analysis of 2H-enriched slaframine showed that the label resides in the five-membered ring and that the methyl carbon of acetate is joined to the carboxyl carbon of pipecolate. A pipecolate-dependent decarboxylation of [1-14C]malonate was demonstrated in cell-free extracts of R. leguminicola. The results account for previously unattributed carbons in the two alkaloids and suggest the formation of an eight-carbon intermediate common to both alkaloids by acylation of malonate with pipecolic acid.
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It is widely accepted that natural gas is formed from thermal decomposition of both oil in reservoirs and, to a lesser extent, the organic matter in shales from which the oil was derived. But laboratory pyrolysis experiments on shales do not reproduce the methane-rich composition typical of most gas reservoirs, leading to suggestions that other mechanisms, such as transition-metal catalysis, may be important. The discrepancy might, however, instead arise because gas (and oil) deposits have migrated from their source rocks, so that the reservoir composition might not be representative of the composition in the source rocks where the hydrocarbons were generated. To address this question, we have analysed gas samples coproduced with oils directly from a source rock (the Bakken shales, North Dakota, USA) where the local geology has prevented significant hydrocarbon migration. The methane contents of these Bakken-shale gases are much lower than that of conventional gas reservoirs, but are consistent with that from pyrolysis experiments on these shales. Thus, because these Bakken gases form with (rather than from) oils, we argue that compositional differences between gases from source rocks and conventional gas deposits result from fractionation processes occurring after hydrocarbon expulsion from the source rock.
In the recent Dover trial, and elsewhere, the 'Intelligent Design' movement has championed the bacterial flagellum as an irreducibly complex system that, it is claimed, could not have evolved through natural selection. Here we explore the arguments in favour of viewing bacterial flagella as evolved, rather than designed, entities. We dismiss the need for any great conceptual leaps in creating a model of flagellar evolution and speculate as to how an experimental programme focused on this topic might look.
The aim of the study was to review published evidence on whether blood pressure (BP) levels and the prevalence of hypertension are higher in adult populations of African descent living in the UK as compared to the white population. A systematic literature review was carried out using MEDLINE 1966-2002 and EMBASE 1980-2002 and citations from references. In all, 14 studies were identified. Nearly all studies were carried out in the London area. The data showed important differences between studies in terms of age and sex of samples, definition of African/black and methods of evaluating BP. A total of 10 studies reported higher mean systolic BPs, while 11 studies reported higher mean diastolic BPs in men from African descent compared to white men. In women, 10 of 12 studies reported higher systolic, and 10 of 12 studies reported higher diastolic BPs. For prevalence of hypertension, eight of 10 studies reported higher rates in men from African descent; eight of nine studies showed higher rates of hypertension in women from African descent. Overall, the most representative sample and up-to-date data came from the Health Survey for England '99. Ethnic group differences in BP were not present in the younger age groups. Women of African descent had higher BP and higher body mass index (BMI). In men of African descent high BP did not coincide with higher BMI. In conclusion, the reported higher rates of hypertension in people from African descent in the UK are confirmatory of the USA African-American and white comparisons. Variations in study methods, size and body composition, and in the mix of Afro-Caribbean and West African groups explain much of the inconsistent results in the UK studies.
Epstein-Barr nuclear antigen 1 (EBNA-1) is the only viral protein required to support replication of Epstein-Barr virus during the latent phase of its life cycle. The DNA segment required for latent replication, oriP, contains two essential binding regions for EBNA-1, termed FR and DS, that are separated by 1 kilobase pair. The FR site appears to function as a replicational enhancer providing for the start of replication at the DS site. We have used electron microscopy to visualize the interaction of EBNA-1 with its binding sites and to study the mechanism for communication between the FR and DS sites. We have found that DNA-bound EBNA-1 forms a DNA loop between the FR and DS sites. From these results, we suggest that EBNA-1 bound to the replicational enhancer acts by a DNA-looping mechanism to facilitate the initiation of DNA replication. Occupancy of the DS site alone is highly sensitive to competition with nonspecific DNA. In contrast, occupancy of the DS site by looping from FR is largely resistant to the competitor DNA. These experiments support the concept that enhancers act in cis from nearby sites to provide a high local concentration of regulatory proteins at their target sites and to stabilize regulatory interactions.
Macropinocytosis refers to the formation of primary large endocytic vesicles of irregular size and shape, generated by actin-driven evaginations of the plasma membrane, whereby cells avidly incorporate extracellular fluid. Macropinosomes resemble "empty" phagosomes and show no difference with the "spacious phagosomes" triggered by the enteropathogenic bacteria Salmonella and Shigella. Macropinosomes may fuse with lysosomes or regurgitate their content back to the extracellular space. In multiple cell types, macropinocytosis is a transient response to growth factors. When amoebas are cultured under axenic conditions, macropinocytosis is induced so as to fulfil nutritional requirements. In immature dendritic cells, macropinocytosis allows for extensive sampling of soluble antigens; after a few days of maturation, this activity vanishes as processed peptides are being presented. Macropinosomes are also formed at the leading edge of motile leukocytes or neurons. In all these examples, macropinocytosis appears tightly regulated. Transformation of fibroblasts by Src or Ras also results in constitutive formation of macropinosomes at "ruffling" zones, that could be related to accelerated cell motility. Like phagocytosis, macropinocytosis depends on signalling to the actin cytoskeleton. We have explored this signalling in transformed cells. v-Src and K-Ras activate PI3K and PLC, as demonstrated by in situ production of the corresponding lipid products. Pharmacological inhibitors of PI3K and PLC and stable transfection leading to a dominant-negative PI3-kinase construct in transformed fibroblasts abolish macropinocytosis, demonstrating that both enzyme activities are essential. Conversely, stable transfection leading to a dominant-positive P13K in non-transformed fibroblasts is sufficient to induce macropinocytosis. Combination of experiments allows to conclude that P13K and PLC act in sequential order. In non-polarized cells expressing a thermosensitive v-Src mutant, v-Src kinase activation accelerates fluid-phase endocytosis. In polarized MDCK cells, this stimulation occurs selectively at the apical domain and the response is selectively abrogated by pharmacological inhibitors of P13K and PLC. Thus, two paradigmatic oncogenes cause constitutive macropinocytosis. For v-Src, this response is polarized at the apical membrane. It is suggested that, in enterocytes that do not normally phagocytose, the P13K-PLC signalling pathway leading to selective induction of macropinocytosis at the luminal surface has been subverted by enteropathogenic bacteria to penetrate via "spacious phagosomes".