Anomalous right coronary artery originating from the distal left circumflex artery: single coronary artery with choronic atrial fibrillation

This report describes a patient with a single coronary artery in whom the right coronary artery originated from the distal left circumflex artery. Single coronary artery is a rare congenital anomaly of the coronary circulation which is often associated with other congenital cardiac malformations. This anomaly is thought to be clinically significant especially in patients with atrial fibrillation, although no other associated cardiac anomaly was detected.     

Different mechanisms for the inhibition of progesterone secretion by ACTH and corticosterone in pregnant rats.

The present study investigated possible sites through which ACTH or corticosterone inhibit progesterone secretion in pregnant rats, and the role of placental factors in blocking the inhibitory effect. The number of conceptuses was adjusted to one (IC group) or more than ten (FC group) on day 7 of pregnancy by aspirating the desired number. Serum concentrations of progesterone, testosterone and oestradiol were significantly (P less than 0.01) lower on day 15 in the 1C group than in the FC group. Corpora lutea (CL) obtained on day 15 were incubated for 6 h with corticosterone or ACTH. Corticosterone (1 mumol/l) significantly (P less than 0.05) inhibited progesterone secretion in the 1C group but not in the FC group. The inhibitory effect of corticosterone in the 1C group was completely blocked by co-addition of 1 mumol testosterone/l or 1 mumol oestradiol/l but not by 1 mumol dihydrotestosterone/l. ACTH (1 microgram/l-1 mg/l) had no direct effect on progesterone secretion in either the 1C or the FC groups, although ACTH apparently decreases progesterone secretion in vivo. Placentae obtained from rats of the FC group on day 15 were incubated for 24 h with or without ACTH (1 mg/l). The supernatant after placental incubation without ACTH significantly (P less than 0.01) increased progesterone secretion by the CL in both the 1C and FC groups, and also eliminated the inhibitory effect of corticosterone in the 1C group. The supernatant after placental incubation with ACTH also increased progesterone secretion in the FC group as effectively as the supernatant from the control incubation, but it had no effect in the 1C group.(ABSTRACT TRUNCATED AT 250 WORDS)     

Evaluation of the depth score of type V pit patterns in crypt orifices of colorectal neoplastic lesions

Background We developed and evaluated the clinical usefulness of a scoring system that subclassified type Vi pit patterns. Methods We studied 119 colon cancer lesions (pTis, n = 26; pT1, n = 93) and 22 tubular adenoma lesions with severe atypia in which a type Vi pit pattern was visible under a stereomicroscope. Four type Vi pit pattern formation appearances (existing pits, marginal irregularities of the gland duct, narrowing of the gland duct lumen, and unclear outline of the gland duct) were defined, and the relationship between each appearance and the invasive depth of the cancer was evaluated. Results When the four type Vi pit pattern appearances were considered in a logistic regression analysis, the odds of a more invasive submucosal cancer were significantly increased by the appearance of marginal irregularities, a narrowed lumen, and an unclear outline. In the logistic regression analysis results, when 0.63 was used as the cutoff score for prediction of a more invasive submucosal cancer, 80 cases in the less invasive group were classified correctly (specificity, 1.0), whereas 53 (86.9%) of the 61 cases in the more invasive group were classified correctly (sensitivity, 0.869). Conclusions It is important first to understand the usability and limitations of objective scoring of type V pit pattern findings and then to apply this score to the determination of cancer depth in order to accurately identify lesions suitable for endoscopic treatment.     

A survival case of acute mitral regurgitation and cardiogenic shock caused by subtotal occlusion of the first diagonal branch.

An 80-year-old woman was admitted with cardiogenic shock; she arrived in a deep coma with systolic blood pressure of 44 mmHg. An electrocardiogram showed ST elevation in I, aVL, V5 and V6, suggesting myocardial infarction in the lateral area of the left ventricle. A chest roentgenogram showed right pulmonary edema without cardiomegaly. Transthoracic and transesophageal echocardiograms revealed severe mitral regurgitation and a flailing anterior mitral valve leaflet, suggesting a ruptured papillary muscle. The patient was initially treated with high-dose dopamine, dobutamine and norepinephrine. Intraaortic balloon pumping was initiated after the patient's condition stabilized. She underwent emergency mitral valve replacement with a prosthetic valve. Complete rupture of the anterior papillary muscle was confirmed. Histological examination revealed necrosis of the anterior papillary muscle with inflammatory changes. She recovered uneventfully. Postoperative coronary angiography demonstrated subtotal occlusion of the first diagonal branch, and left ventriculography demonstrated akinesis of the lateral segment. This was a rare case in which subtotal occlusion of the first diagonal branch caused rupture of an anterior papillary muscle leading to severe mitral regurgitation.     

T-helper type 1/T-helper type 2 balance in malignant pleural effusions compared to tuberculous pleural effusions

STUDY OBJECTIVES: Malignant and tuberculous pleurisies are two major causes of lymphocyte-dominant pleurisy. Several studies have already reported that tuberculous pleurisy is a T-helper type 1(Th1)-dominant disease. In this study, we sought to examine the Th1/T-helper type 2 (Th2) balance, especially focusing on the polarizing status of T-cells to Th1/Th2 in malignant pleural effusions by measuring cytokines in pleural effusions and by evaluating the polarizing status of T-cells on the point of stimulation with interleukin (IL)-12 and/or IL-18. Furthermore, we evaluated inhibitors of interferon (IFN)-gamma production in effusions to rule out the possibility of direct inhibition of T-cell polarization. PATIENTS: Effusion samples were collected from 19 patients with malignant pleurisy caused by lung cancer and from 7 patients with tuberculous pleurisy. MEASUREMENTS: Concentrations of pleural fluid IFN-gamma, IL-12, and IL-4 were measured. IFN-gamma production of T-cells enriched from malignant pleural effusions in the presence of IL-12 and/or IL-18 was also examined. We further compared the inhibitory activity of malignant pleural effusions against IFN-gamma production and analyzed the expression of T-cell immunoglobulin mucin, mucin domain (Tim-3), a Th1-specific molecule in pleural fluid T-cells. RESULTS: Although malignant pleural effusions showed low levels of Th1 and Th2 cytokines and ratios of IFN-gamma and IL-12 to IL-4 were low, isolated T-cells produced a significant level of IFN-gamma in the presence of IL-12 and IL-18. Soluble factors were not found to inhibit IFN-gamma production in malignant pleural effusions. In tuberculous pleural effusion, ratios of IFN-gamma and IL-12 to IL-4 were significantly higher, and T-cells showed the expression of Tim-3 messenger RNA. CONCLUSIONS: We confirmed that T-cells in the malignant pleural effusions are mainly na?ve or not definitely polarized to Th1. Moreover, malignant tumor does not actively distort the cytokine condition through production of soluble inhibitors within effusions. The present study indicates that antitumor immunity may be enhanced by restored IFN-gamma activity through combination of IL-12 and IL-18, and that it will lead to new therapies for malignant effusion.     

A New Ultrasonographic “Fluttering Sign” for Hepatic Hemangioma

The aim of the study described here was to clarify the diagnostic value of the fluttering sign, a new sign that characterizes hepatic hemangiomas in gray-scale ultrasonography (US). It refers to a phenomenon in which the speckled echogenicity inside the hemangioma changes continuously and seems to be moving. A total of 172 hemangiomas diagnosed with contrast-enhanced US were evaluated. The fluttering sign was found in 123 of 172 hemangiomas (71.5%). Its prevalence was significantly higher than that of the marginal strong echo (89/172, 51.7%, p < 0.001), posterior acoustic enhancement (103/172, 59.9%, p = 0.031) and chameleon sign (100/172, 58.1%, p = 0.013). In addition, the fluttering sign was observed significantly more frequently in mixed or hypo-echoic tumors than in hyper-echoic tumors (p < 0.001), relatively large tumors (p < 0.001) and tumors that were less than 5 cm from the body surface (p = 0.015). The fluttering sign in gray-scale US has great potential to be a new complementary sign for the diagnosis of hemangioma.     

Ablation of the microglial protein DOCK2 reduces amyloid burden in a mouse model of Alzheimer's disease

Alzheimer's disease (AD) neuropathology is characterized by innate immune activation primarily through prostaglandin E2 (PGE₂) signaling. Dedicator of cytokinesis 2 (DOCK2) is a guanyl nucleotide exchange factor expressed exclusively in microglia in the brain and is regulated by PGE₂ receptor EP2. DOCK2 modulates microglia cytokine secretion, phagocytosis, and paracrine neurotoxicity. EP2 ablation in experimental AD results in reduced oxidative damage and amyloid beta (Aβ) burden. This discovery led us to hypothesize that genetic ablation of DOCK2 would replicate the anti-Aβ effects of loss of EP2 in experimental AD. To test this hypothesis, we crossed mice that lacked DOCK2 (DOCK2 −/−), were hemizygous for DOCK2 (DOCK2 +/−), or that expressed two DOCK2 genes (DOCK2 +/+) with APPswe-PS1Δe9 mice (a model of AD). While we found no DOCK2-dependent differences in cortex or in hippocampal microglia density or morphology in APPswe-PS1Δe9 mice, cerebral cortical and hippocampal Aβ plaque area and size were significantly reduced in 10-month-old APPswe-PS1Δe9/DOCK2 −/− mice compared with APPswe-PS1Δe9/DOCK2 +/+ controls. DOCK2 hemizygous APPswe-PS1Δe9 mice had intermediate Aβ plaque levels. Interestingly, soluble Aβ₄₂ was not significantly different among the three genotypes, suggesting the effects were mediated specifically in fibrillar Aβ. In combination with earlier cell culture results, our in vivo results presented here suggest DOCK2 contributes to Aβ plaque burden via regulation of microglial innate immune function and may represent a novel therapeutic target for AD.