Analysis techniques for blob properties from gas puff imaging data.

Filamentary structures, also known as blobs, are a prominent feature of turbulence and transport at the edge of magnetically confined plasmas. They cause cross-field particle and energy transport and are, therefore, of interest in tokamak physics and, more generally, nuclear fusion research. Several experimental techniques have been developed to study their properties. Among these, measurements are routinely performed with stationary probes, passive imaging, and, in more recent years, Gas Puff Imaging (GPI). In this work, we present different analysis techniques developed and used on 2D data from the suite of GPI diagnostics in the Tokamak à Configuration Variable, featuring different temporal and spatial resolutions. Although specifically developed to be used on GPI data, these techniques can be employed to analyze 2D turbulence data presenting intermittent, coherent structures. We focus on size, velocity, and appearance frequency evaluation with, among other methods, conditional averaging sampling, individual structure tracking, and a recently developed machine learning algorithm. We describe in detail the implementation of these techniques, compare them against each other, and comment on the scenarios to which these techniques are best applied and on the requirements that the data must fulfill in order to yield meaningful results.

Hepatocellular transferrin receptor expression in secondary siderosis.

We investigated the hepatocellular transferrin receptor expression in 55 human liver specimens with secondary siderosis, with an indirect immunoperoxidase technique on frozen sections using 3 monoclonal anti-transferrin receptor antibodies. For comparison, specimens were also stained with the monoclonal antibody BK19.9, recognizing an antigen which is biochemically similar to the transferrin receptor, and with a monoclonal antibody against the epidermal growth factor receptor. The degree of iron overload was estimated semi-quantitatively, taking into account hepatocellular and Kupffer cell iron deposition. In 47 out of 55 specimens hepatocellular transferrin receptor expression was present. The positivity was predominantly localized on hemosiderin-free hepatocytes. With increasing hepatocellular iron deposition, the proportion of cases with absent transferrin receptor immunoreactivity increased. This supports the previously reported disappearance of hepatocellular transferrin receptor expression in primary hemochromatosis cases with severe iron deposition. However, the transferrin receptor negative cases included four specimens in which Kupffer cell iron deposition clearly exceeded hepatocyte iron load. This finding suggests that in addition to hepatocellular iron load other factors may regulate the expression of parenchymal transferrin receptors in iron overload diseases. These may include plasma levels of various iron sources and/or Kupffer cell iron load. The iron deposition did not influence the staining of the hepatocellular epidermal growth factor receptor nor the Kupffer cell staining by the BK19.9 antibody. This confirms the specificity of the findings concerning the behaviour of the transferrin receptor in secondary siderosis.

Hepatic injury associated with the use of nitrofurans: a clinicopathological study of 52 reported cases.

Fifty cases of nitrofurantoin-associated hepatic injury and two cases of nifurtoinol (hydroxymethylnitrofurantoin)-associated hepatic injury reported to the Netherlands Centre for Monitoring of Adverse Reactions to Drugs were analyzed in detail. In 38 cases, a causal relationship was considered likely [i.e., "highly probable" (n = 4), "probable" (n = 23) or "possible" (n = 11)]. In 25 cases, hepatic injury was of the acute type whereas 13 cases presented a chronic type of reaction. Both types were more common in the elderly. Eighty per cent of the acute reactions appeared within the first 6 weeks of treatment and were sometimes accompanied by fever (28%), rash (12%) and eosinophilia (16%). Biochemically, the pattern was mainly hepatocellular (32%), whereas mixed cholestatic-hepatocellular (4%) and cholestatic (4%) patterns were uncommon. Although mild to moderate liver enzyme elevations (60%) were common, these were primarily symptomatic. The reaction was fatal in one "acute" and one "chronic" case. In the chronic cases, nuclear (82%) and smooth muscle (73%) antibodies and LE cells (50%) were frequently present. HLA typing showed no increase of the HLA B8 or HLA DRw3 haplotype. HLA DR2 (56%) and HLA DRw6 (56%) were more frequent than in controls (both 29%), but this was not statistically significant. Histology showed mainly necrosis, varying from spotty to massive, in the acute cases and a pattern consistent with chronic active hepatitis in the chronic cases.(ABSTRACT TRUNCATED AT 250 WORDS)

Sicca syndrome with iron deposition in the salivary glands.

A case of iron deposition in the labial accessory salivary glands associated with prominent xerostomy and xerophtalmy is reported. Suffering from a myelodysplastic syndrome with refractory anaemia, this patient received multiple transfusions over the past 7 years. A transfusional haemosiderosis gradually developed. Histopathologic examination of accessory salivary glands demonstrated haemosiderin deposition in the serous alveoli and in the epithelial cells of intercalated and interlobular ducts. A relationship between the iron deposition in the salivary glands and the development of the sicca syndrome is suggested. The literature related to iron deposition in salivary glands and sicca syndrome is reviewed.

Lymph node architecture in Hodgkin's disease: evidence for the role of the composite nodule in nodular sclerosing Hodgkin's disease.

The presence or absence of composite nodules, corresponding to recently described structural and functional units in the human reactive lymph node, was investigated in 22 lymph nodes involved by Hodgkin's disease using in situ immuno- and enzymehistochemical techniques. In 10/13 cases of nodular sclerosing subtype, typical composite nodules composed of adjacent B- and T-domains and surrounded by a rim of high endothelial venules were recognized. In association with these venules, a concentrical rim of fusiform shaped Alk Phase+ fibroblastic reticulum cells was observed. Reed-Sternberg cells and their morphological variants were exclusively found in the T-area of these composite nodules. In 5/6 cases of mixed cellularity Hodgkin's disease, B lymphoid follicles were apparent. No vascular relationship with the tumourally involved areas was noticed. In the remaining cases, including all cases of lymphocytic depletion Hodgkin's disease only scattered B cell clusters were recognized. Our observations indicate the persistence of an organoid structure, i.e. the composite nodule in nodular sclerosing Hodgkin's Disease (HD).

Ketoconazole-induced hepatitis: a case with a definite cause-effect relationship.

We present the case of a female patient in whom acute hepatitis developed after 180 days of ketoconazole administration (200 mg/day). A prompt renewed hepatic injury after an unintentional rechallenge 6 months later provided definitive evidence for a causative relationship between ketoconazole and acute liver disease. The clinical and biochemical parameters of the case are reported. Histological examination revealed the picture of acute hepatitis with possible transition to chronicity. A prominent accumulation of perisinusoidal lipocytes (Ito cells) was observed.

Ketoconazole-associated hepatic injury. A clinicopathological study of 55 cases.

Fifty-five cases of ketoconazole-associated hepatic injury, reported to the Netherlands Centre for Monitoring of Adverse Reactions to Drugs, were analysed in detail. In 50 cases a causal relationship was considered likely, i.e. 'probable' (27 cases) or 'possible' (23 cases). Eighty-four % of individuals were women. Forty-six % of patients were over 50 years of age which suggests that, considering the lower prescription rate in this age group, the elderly are more vulnerable to ketoconazole. In 60% of all cases hepatic injury appeared within the first 6 weeks of therapy but in the group of 'probable'-cases the onset was mostly later. Jaundice was present in 44% of all cases but in 63% of the group of 'probable'-cases. Eosinophilia (10%), fever (6%) and rash (2%) were uncommon. Biochemically the pattern was hepatocellular in 54%, cholestatic in 16% and mixed cholestatic-hepatocellular in 30%. Histology (14 cases) showed a predominantly hepatocellular pattern in 57% with extensive centrilobular necrosis and mild to moderate bridging. In 43% cholestasis predominated. None of the cases had a fatal course. The incidence of symptomatic hepatic injury may be estimated at approximately 1:2000 but is probably higher. The mechanism of ketoconazole-induced hepatic injury seems to be based on metabolic idiosyncrasy although it is not excluded that in some patients an immunoallergic mechanism is causative.