Electrophysiologic properties of atrial muscle in paroxysmal atrial fibrillation

The electrophysiologic properties of atrial muscle were studied by programmed atrial stimulation in 42 patients with paroxysmal atrial fibrillation (PAF) and in 53 control patients without PAF. Single premature atrial stimulation was given at the right atrial appendage following 8 basic stimuli with a basic cycle length of 500 ms. Repetitive atrial firing (RAF) was defined as the occurrence of 2 or more successive premature atrial activations following single premature atrial stimulation. Fragmented atrial activity (FAA) was defined as an increase by more than 75% of the duration of the atrial electrogram in response to a single premature stimulation. Interatrial conduction delay was defined as an increase of the conduction time by more than 50 ms in response to a single premature stimulation. RAF was induced in 26 of 42 patients (61.9%) with PAF and in 14 of 53 control patients (26A%). FAA and interatrial conduction delay were elicited in 69.0 and 80.9% of patients with PAF and in 34.0 and 56.6% of control patients, respectively. In 16 patients with PAF in whom RAF was not induced, FAA developed in 11 patients (68.8%). In 88.1% of 42 patients with PAF and in 41.5% of 53 controls, RAF or FAA, or both, were elicited by atrial premature stimulation. It is concluded that the incidence of RAF and FAA were significantly higher in patients with PAF than in the control group, and the induction of RAF or FAA, or both, was closely related to the vulnerability of the atrial muscle to atrial fibrillation.     

CD3 down-regulating factor in sera and culture supernatants of leukaemic cells from patients with adult T cell leukaemia

Immunological abnormality of T lymphocytes in patients with adult T cell leukaemia (ATL) is characterized by abnormal expression of the 55 kD chain of the receptor for interleukin 2 (IL-2R/p55) (Tac), and the down-regulation of CD 3 expression. Using serum and culture supernatants of leukaemic cells from ATL patients (Group A) whose CD 3 expression was down-regulated and those (Group B) whose CD 3 was not low, the possible mechanism of CD 3 down-regulation on ATL cells was discussed. When PBMC from normal individuals were cultured with sera from ATL patients for 24 h, CD 3 expression revealed by mean fluorescent intensity (MFI) was down-regulated by sera from ATL patients in Group A (MFI: Pt 1 = 51.6 ± 4.5, Pt 2 = 48.0 ± 6.9, control = 96.5 ± 6.6), not by sera from patients in Group B (MFI: Pt 3 = 105.5 ± 7.9, Pt 4 = 102.5 ± 8.3, control = 96.5 ± 6.6). When normal PBMC were cultured with supernatants of leukaemic cells from ATL patients in Group A, this CD 3 down-regulating activity was also detected (MFI: Pt 1 = 78.0 ± 10.2, Pt 2 = 70.6 ± 8.7, control = 94.0 ± 6.6). By using gel-chromatography, the fractionated supernatants from ATL patients in Group A decreased CD 3 expression of normal PBMC significantly (MFI: Pt 1 = 22.9 ± 5.8, Pt 2 = 28.8 ± 7.4, control = 92.1 ± 9.6). This CD 3 down-regulating activity in fractionated supernatant was not inhibited by any lymphokine antibodies, anti-IL-1α antibody (Ab), anti-IL-1B Ab, anti-IL-2 Ab, anti-IL-3 Ab, anti-IL-4 Ab, anti-IL-6 Ab, anti-TNF-α Ab and anti-IFN-γ Ab. Any known cytokines (IL-1, IL-2, IL-3, IL-4, IL-6, TNF-α and IFN-γ) could not modulate CD 3 expression of normal PBMC. These findings suggested that there are novel factor(s) with CD 3 down-regulating activity in the serum and culture supernatant of ATL patient and those factor(s) are involved in progression of ATL.     

Polymicrogyria with calcification in Pallister-Killian syndrome detected by microarray analysis

BackgroundPallister-Killian syndrome (PKS) is a rare disorder caused by the mosaic tetrasomy of chromosome 12p, and is characterized by facial dysmorphism, developmental delay, hypotonia and seizures.ResultsWe report a patient with PKS showing unique polymicrogyria with calcification. He had delayed development and dysmorphic facial features including frontal bossing, hypertelorism, and high arched palate at 6 months of age. Neuroimaging revealed unilateral polymicrogyria with spot calcifications, which predominantly affected the right perisylvian region. Chromosome G-banding showed the karyotype 46,XY, however, array-based comparative genomic hybridization analysis showed mosaic duplication of chromosome 12p, in which CCND2, which encodes cyclin D2 and is a downstream mediator of PI3K-AKT pathway, is located. Supernumerary chromosome of 12p was detected in 58% of buccal mucosa cells by the interphase fluorescence in situ hybridization analysis using chromosome 12 centromere-specific D12Z3 probe. The diagnosis of PKS was made based on distinctive clinical features of our patient and the results of cytogenetic analyses.ConclusionThis report is, to our knowledge, the first case of a patient with PKS who clearly demonstrates polymicrogyria colocalized with calcifications, as shown by CT scans and MRI, and suggests that a patient with PKS could show structural brain anomalies with calcification. We assume that somatic mosaicism of tetrasomy could cause asymmetrical polymicrogyria in our patient, and speculate that increased dosages of CCND2 at chromosome 12p might be involved in the abnormal neuronal migration in PKS.     

Characteristics of gram-negative bacteremia during febrile neutropenia among allogeneic hematopoietic stem cell transplant recipients on levofloxacin prophylaxis

European Journal of Clinical Microbiology & Infectious Diseases - The aim of this study is to clarify the characteristics of gram-negative bacteremia (GNB), including extended-spectrum...     

Gastrointestinal tract metastasis of lung cancer: The PD-L1 expression and correlated clinicopathological variables

The gastrointestinal tract is a rare site for metastatic lung cancer. Programmed cell death-ligand 1 (PD-L1) expression in lung cancer is a biomarker for the response to anti-PD-1/PD-L1 therapy. We investigated clinicopathological features and PD-L1 expression in 25 gastrointestinal metastatic tumors from the lung and primary adenocarcinoma of the small bowel. The small bowel was the most common site (16/25; 64%) of gastrointestinal tract lung cancer metastasis. A total of 19 (76%) of the gastrointestinal metastasis showed PD-L1 expression in ≥5% of tumor cells, with 14 (56%) showing high expression levels (≥50%). In contrast, 21 (84%) expressed PD-L1 in ≥5% immune cells, including 4 (16%) showing a high expression levels (≥50%). The PD-L1 expression on tumor cells and immune cells in primary lung cancer and corresponding gastrointestinal metastasis was concordant in 13 (68%) and 11 (58%) of the 19 paired cases, respectively. Small-bowel metastasis of lung cancer was characterized by a higher incidence of perforation (31% vs. 0%), ulcerated mass (83% vs. 60%), and neoplastic PD-L1 expression (75% vs. 0%) compared to primary small-bowel adenocarcinoma. Gastrointestinal metastasis from lung cancer might be a potential target for immune checkpoint inhibitor therapy, given its high expression of PD-L1.