Pineal toxoplasmosis mimicking pineal tumor in an AIDS patient.

A pineal mass in a patient with acquired immunodeficiency syndrome (AIDS) is reported. Computed tomography (CT) scan revealed a nodular mass in the pineal region with foci of calcification and obstruction of the aqueduct mimicking a pineal tumor. At autopsy, the brain revealed a well-circumscribed lesion with central necrosis in the pineal region suggestive of toxoplasma and involving the periaqueductal area. Susceptibility of a patient with AIDS to opportunistic infections should be considered.     

Surface immunoglobulins mediate efficient transport of antigen to lysosomal compartments resulting in enhanced specific antigen presentation by B cells

A BCL₁ immunoglobulin (Ig) transfectant, expressing wild-type surface (s)IgM with the TEPC-15 idiotype (T15-Id) and anti-phosphorylcholine (PC) specificity, was previously shown to present PC-conjugated hen egg-white lysozyme (PC-HEL) to a HEL-specific T cell hybridoma at a lower antigen (Ag) concentration than that required for native HEL. Two variant Ig transfectants, expressing T15-Id sIgM with substitutions either in the entire spacer, transmembrane (TM) domain and cytoplasmic tail (B186 variant) or in the NH₂-terminal third of TM domain only (TM2 variant), failed to display this sIgM-mediated, enhanced presentation of PC-HEL at low concentrations. However, prolonged treatment with anti-T15-Id monoclonal antibody (mAb) led to a reduction of surface expression of the T15-Id sIgM in the wild-type and TM2 variant, but not in the B186 variant sIgM transfectants. Treatment with anti-T15-Id mAb also resulted in an increased intracellular accumulation of T15-Id sIgM in the wild-type transfectant, but not in the B186 variant. Subcellular fractionation analysis revealed that the ligands bound to the T15-Id sIgM are not efficiently transported to the dense lysosomal compartments in both B186 and TM2 transfectants, as compared to the wild-type sIgM transfectant. A significant increase in tyrosine phosphorylation after cross-linking of the T15-Id sIgM was observed only in the wild-type sIgM transfectant. These results suggest that, while the NH₂-terminal third of the TM region is not involved in the process responsible for the ligand-induced reduction of surface expression of sIgM, it appears to be essential for subsequent transport of sIgM/ligand complexes to the lysosomal compartments, as well as efficient activation of tyrosine kinases. These results strongly suggest that sIg-mediated enhancement of specific antigen presentation reflects the ability of sIg to efficiently transport antigen to the lysosomal compartments, and possibly the activation of protein tyrosine kinases.     

A deletion mutant defines DQ beta variants with DR4 positive DQw3 positive haplotypes

We describe the production of an HLA deletion mutation by radiation mutagenesis of a DR4- and DQw3-homozygous, Dw4- and Dw14-heterozygous cell line designed to analyze polymorphisms associated with DR4 and DQw3. Southern blot analysis confirms a deletion of class I and class II genes on one haplotype. Variation in DQ beta alleles associated with DQw3 was previously described by characteristic RFLP patterns for a DQ beta bene. One pattern, which correlated precisely with A-10-83 monoclonal antibody reactivity (TA10), defined an allele which we call DQ"3.1". The mutant cell line has lost the polymorphic bands on Southern blots corresponding to the DQ"3.1" allele, while the intact Dw14 haplotype retains the alternate allele at DQ beta which is DQw-3 positive. TA10-negative. These data demonstrate the segregation of two DQw3 positive DQ beta allelic variants, both associated with DR4, which can be distinguished on the basis of both RFLP and monoclonal antibody reactivity.     

Identification of MEN1 gene mutations in sporadic carcinoid tumors of the lung

Lung carcinoids occur sporadically and rarely in association with multiple endocrine neoplasia type 1 (MEN1). There are no well defined genetic abnormalities known to occur in these tumors. We studied 11 sporadic lung carcinoids for loss of heterozygosity (LOH) at the locus of the MEN1 gene on chromosome 11q13, and for mutations of the MEN1 gene using dideoxy fingerprinting. Additionally, a lung carcinoid from a MEN1 patient was studied. In four of 11 (36%) sporadic tumors, both copies of the MEN1 gene were inactivated. All four tumors showed the presence of a MEN1 gene mutation and loss of the other allele. Observed mutations included a 1 bp insertion, a 1 bp deletion, a 13 bp deletion and a single nucleotide substitution affecting a donor splice site. Each mutation predicts truncation or potentially complete loss of menin. The remaining seven tumors showed neither the presence of a MEN1 gene mutation nor 11q13 LOH. The tumor from the MEN1 patient showed LOH at chromosome 11q13 and a complex germline MEN1 gene mutation. The data implicate the MEN1 gene in the pathogenesis of sporadic lung carcinoids, representing the first defined genetic alteration in these tumors.      

Impact of Dissection after Drug-Coated Balloon Treatment of De Novo Coronary Lesions: Angiographic and Clinical Outcomes

PurposeDissection after plain balloon angioplasty is required to achieve adequate luminal area; however, it is associated with a high risk of vascular events. This study aimed to examine the relationship between non-flow limiting coronary dissections and subsequent lumen loss and long-term clinical outcomes following successful drug-coated balloon (DCB) treatment of de novo coronary lesions.Materials and MethodsA total of 227 patients with good distal flow (Thrombolysis in Myocardial Infarction flow grade 3) following DCB treatment were retrospectively enrolled and stratified according to the presence or absence of a non-flow limiting dissection. The primary endpoint was late lumen loss (LLL) at 6-month angiography, and the secondary endpoint was target vessel failure (TVF, a composite of cardiac death, target vessel myocardial infarction, target vessel revascularization, and target vessel thrombosis).ResultsThe cohort consisted of 95 patients with and 132 patients without a dissection. There were no between-group differences in LLL (90.8%) returning for angiography at 6 months (0.05±0.19 mm in non-dissection and 0.05±0.30 mm in dissection group, p=0.886) or in TVF (6.8% in non-dissection and 8.4% in dissection group, p=0.799) at a median follow-up of 3.4 years. In a multivariate analysis, the presence of dissection and its severity were not associated with LLL or TVF. Almost dissections (93.9%) were completely healed, and there was no newly developed dissection at 6-month angiography.ConclusionThe presence of a dissection following successful DCB treatment of a de novo coronary lesion may not be associated with an increased risk of LLL or TVF (Impact of Drug-coated Balloon Treatment in de Novo Coronary Lesion; {"type":"clinical-trial","attrs":{"text":"NCT04619277","term_id":"NCT04619277"}}NCT04619277).     

Determination of gallium concentration in "blood-free" tissues using a radiolabeled blood marker

Radioiodinated serum albumin has been used as a blood marker to define and quantitate physiological volumes for 12 organs and tissue types. The concentration of gallium-67 in "blood-free" tissues of rats was also determined at various times after intravenous administration. Tissues were divided into two kinetically distinguishable types based on reported nonuniform distribution of the blood marker and the gallium distribution observed in the present study. Gallium distribution into the liver and spleen was observed to be slow, with a discernable accumulation phase followed by monoexponential elimination. In contrast, gallium accumulation into the stomach, small and large intestines, heart, lung, skin/adipose tissue, and muscle was rapid and elimination was monophasic.     

Levels of polychlorinated biphenyls (PCBs), DDE,and mirex in waterfowl collected in New York State, 1981–1982

The PCBs, DDE, and mirex levels were measured in the subcutaneous fat and breast muscle of fifty-five waterfowl collected in New York State during 1981 and 1982. Levels were obtained by electron capture gas chromatography (EC-GC) on wet weight, dry weight, and lipid weight bases; results were confirmed by gas chromatography-mass spectrometry (GC-MS). The mean PCB levels were 6.1 (g/g in fat and 0.25 g/g in breast muscle on a wet weight basis. The mean DDE and mirex levels were 0.10 g/g and 0.28 g/g in fat and 0.01 g/g and 0.002 g/g in breast muscle on a wet weight basis, respectively.The results of the present study confirm those of the previous study (Kimet al. 1984). The detailed comparison, however, shows that the levels of PCBs and DDE in fat continued to decline while the level of mirex increased slightly.     

Conduction tissue in congenital heart surgery

The anatomy of the cardiac conduction system in normal and malformed hearts reconstructed from histological serial sections is reviewed. The sinus node and its arterial supply are located in the right superior cavoatrial junction except in hearts with left-sided juxtaposition of the atrial appendages, mirror-image, and isomeric arrangements of the atria. In the presence of normally positioned atrial and ventricular septal structures, the triangle of Koch is a useful guide to the location of the atrioventricular node and the penetrating bundle. In hearts with isolated ventricular septal defects, it is necessary to distinguish between a perimembranous defect and a muscular inlet defect. The conduction axis runs in the area of fibrous continuity at the posteroinferior edge of a perimembranous defect but in the anterosuperior rim of a muscular inlet defect. In most hearts with tetralogy of Fallot, the danger area is the region of aortic-mitral-tricuspid fibrous continuity where the axis penetrates. In hearts with atrioventricular septal defects, the lack of contiguity between atrial and ventricular septum results in a posterior displacement of the nodal triangle and coronary sinus and an elongation of the nonbranching bundle. Hearts with abnormally located atrioventricular nodes and conduction axes are mainly those with atrioventricular discordance, ambiguous atrioventricular connection in presence of left-hand pattern ventricular topology, hearts with univentricular atrioventricular connection to a morphologically left or indeterminate ventricle, and hearts with a straddling tricuspid valve. The location of the atrioventricular node is governed by the orientation of the ventricular septum and by the pattern of ventricular topology.

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Resumen Se revisa la anatomía del sistema de conducción cardiaca en los corazones normales y con malformaciones a la luz de la reconstrucción a partir de cortes histológicos seriados. El nódulo sinusal y su irrigación arterial está ubicado en la unión cavoatrial derecha, excepto en corazones con yuxtaposición izquierda de las auriculillas o con alteraciones en imagen en espejo e isoméricas de las aurículas. En presencia de estructuras septales atriales y ventriculares normalmente ubicadas, el tríangulo de Koch es una guía útil para la localización del nódulo atrioventricular y la penetración del haz. En corazones con defectos septales ventriculares aislados es necesario distinguir entre un defecto perimembranoso y un defecto del tracto muscular de entrada. El haz de conducción avanza en el área de continuidad fibrosa sobre el borde posteroinferior de un defecto perimembranoso, en el filo anterosuperior de un defecto del tracto muscular de entrada. En la mayoría de los corazones con tetralogía de Fallot el área de peligro se encuentra en la región del trígono fibroso aórticomitral y tricuspídeo sobre el cual penetra el haz de conducción. En corazones con defectos septales atrioventriculares la falta de continuidad entre el septo atrial y el ventrícular resulta en un desplazamiento posterior del triángulo de Koch y del seno coronario y en una elongación del haz no ramificado. Corazones con nódulos atrioventriculares y haces de conducción anormalmente ubicados son principalmente aquellos con discordancia atrioventricular, con conexión atrioventricular ambigua en presencia de un patrón izquierdo de arquitectura ventricular, corazones con conexión atrioventricular univentricular a un ventrículo morfológicamente izquierdo o indeterminado y corazones con válvula tricuspídea cabalgante. La ubicación del nódulo atrioventricular está determinada por la orientación del septo ventricular y por el patrón de la arquitectura ventricular.

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Résumé L'anatomie du système de conduction du coeur normal et du coeur siège de malformations reconstituée à partir de coupes sériées histologiques est exposée. Le sinus nodal et sa vascularisation sont situés au niveau de la partie supérieure de la jonction auriculo-ventriculaire droite sauf dans certains cas: coeur avec juxtaposition des auricules du côté gauche, image en miroir et dispositions isomères des oreillettes. Lorsque les cloisons auriculaire et ventriculaire occupent une situation normale, le triangle de Koch constitue un repère utile pour localiser le noyau auriculo-ventriculaire et le faisceau de His. En cas de défects septaux ventriculaires isolés, il est nécessaire de distinguer les défects périmembraneux et les défects musculaires. L'axe nerveux conducteur chemine dans la zone de continuité fibreuse au bord postéroinférieur du défect périmembraneux mais il chemine au bord antéro-supérieur du défect musculaire. En cas de tétralogie de Fallot, le danger se situe souvent au niveau de la zone fibreuse de continuité aortique-mitrale-tricuspide où pénètre l'axe conducteur. En cas de coeur porteur d'un défect septal auriculo-ventriculaire, le défaut de continuité entre la cloison ventriculaire et la cloison auriculaire entraîne le déplacement postérieur du triangle nodal et du sinus coronaire ainsi que l'élongation du faisceau. Les coeurs qui présentent une anomalie du siège des noyaux auriculo-ventriculaires et des nerfs conducteurs sont principalement ceux qui sont le siège d'une anomalie auriculo-ventriculaire, d'une connexion auriculo-ventriculaire ambiguë en cas d'une disposition ventriculaire de type gauche, d'une connexion auriculo-ventriculaire univentriculaire avec une morphologie ventriculaire gauche ou indeterminée, d'une valve tricuspide en fourche. Le siège du noyau auriculo-ventriculaire est fonction de l'orientation du septum ventriculaire et de l'architecture ventriculaire.

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Supported by the British Heart Foundation.     

Subtyping lymphocytes in peripheral blood by immunoperoxidase labeling and light scatter/absorption flow cytometry

Lymphocyte subpopulations in a whole-blood sample can be detected by adapting mouse monoclonal antibodies (MAbs) and peroxidase (EC 1.11.1.7) labeling to a flow cytometer equipped with a tungsten-halogen light source and scatter/absorption optics (Technicon H6000). In the optimized cytochemical conditions each cell population generates a distinct, well-separated cluster, for accurate "thresholding" of the surface-antigen negative and positive lymphocyte populations in the presence of other leukocytes. After reaction with MAb, the erythrocytes are lysed, and the lymphocytes and other leukocytes are fixed. Biotinylated anti-mouse IgG, used as a bridge, amplifies the response from the avidin-peroxidase label. Granulocytes and monocytes, which have high endogenous peroxidase activity, and the labeled lymphocytes are stained in a specific amount of hydrogen peroxide plus 4-chloro-1-naphthol in 4-(2-hydroxyethyl)-1-piperazine-ethanesulfonic acid buffer. Accuracy and precision are equivalent to those of flow cytometers that measure immunofluorescence (e.g., Ortho Spectrum III), as demonstrated with OKT3, OKT4, OKT8, OKT11, and Leu 12 MAbs.     

An explanation of renal hemodynamics in acute renal failure based on sequential CT in patients with Korean hemorrhagic fever

The pattern of renal enhancement and washout of contrast medium was observed on sequential follow-up CT in 12 patients with Korean hemorrhagic fever, in which acute renal failure is one of the most important clinical features. Renal contrast enhancement and contrast medium washout were delayed longer in patients with severe oliguric renal failure. The delayed washout peaked at 4-5 days and did not return to normal until 8-9 days in the patients with severe oliguria; in the patients without severe oliguria the times were 1-2 days and 3-4 days, respectively. A characteristic "cart-wheel" pattern was observed during the washout stage in patients without severe oliguria. This "cart-wheel" pattern of washout is thought to result from relief of vasoconstriction and repair of tubular function. Multifocal "wedge-shaped" nonenhanced areas of the kidney, seen on the 2 week follow-up postcontrast CT, are thought to be ischemic zones due to persistent vasoconstriction. On the 6 week follow-up postcontrast CT in one patient, scarring of the kidney was detected in the same area that did not enhance on the 2 week CT. This scarring is thought to be a result of permanent vasoconstriction.