Annular pancreas associated with carcinoma in the dorsal part of pancreas divisum

Summary A carcinoma in the dorsal part of the pancreas divisum with an annular pancreas in the anterior part is reported. A 79-yr-old female was admitted in our hospital complaining of epigastralgia. Computed tomography (CT) and ultrasound (US) showed an irregular mass in the pancreatic body. A pancreatogram obtained through the major duodenal papilla demonstrated only the ventral pancreatic duct that encircled the duodenum. Contrast medium injected from the minor duodenal papilla showed Santorini’s duct obstruction at the neck portion of the pancreas without communication with the ventral pancreatic duct. The patient died with liver metastases. Autopsy confirmed annular pancreas and a 6-cm tumor in the pancreatic body extending to the pancreatic head and pancreas divisum. Pancreatic carcinoma; histologically a moderately differentiated adenocarcinoma; originated from the dorsal part of pancreas divisum. To our knowledge this is the first report of pancreatic carcinoma associated with annular pancreas coexistent with pancreas divisum.     

Involvement of Rho-kinase in prostaglandin F2alpha-stimulated interleukin-6 synthesis via p38 mitogen-activated protein kinase in osteoblasts

We have previously reported that prostaglandin F(2alpha) (PGF(2alpha)) stimulates interleukin-6 (IL-6), a potent bone resorptive agent, through p44/p42 mitogen-activated protein (MAP) kinase in osteoblast-like MC3T3-E1 cells. In the present study, we investigated whether Rho-kinase is implicated in the PGF(2alpha)-stimulated IL-6 synthesis in MC3T3-E1 cells. PGF(2alpha) time-dependently induced the phosphorylation of myosin phosphatase targeting subunit (MYPT-1), a Rho-kinase substrate. Y27632, a specific Rho-kinase inhibitor, significantly reduced the PGF(2alpha)-stimulated IL-6 synthesis as well as the MYPT-1 phosphorylation. Fasudil, another inhibitor of Rho-kinase, suppressed the PGF(2alpha)-stimulated IL-6 synthesis. Y27632 and fasudil failed to affect the PGF(2alpha)-induced phosphorylation of p44/p42 MAP kinase. SB203580 and BIRB0796, potent inhibitors of p38 MAP kinase, suppressed the IL-6 synthesis induced by PGF(2alpha). While SP600125, an inhibitor of stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK), failed to reduce the synthesis. Y27632 as well as fasudil attenuated the PGF(2alpha)-induced phosphorylation of p38 MAP kinase. These results strongly suggest that Rho-kinase regulates PGF(2alpha)-stimulated IL-6 synthesis via p38 MAP kinase activation in osteoblasts.     

Successful treatment of chronic granulomatous disease with fludarabine-based reduced-intensity conditioning and unrelated bone marrow transplantation

Allogeneic hematopoietic stem-cell transplantation (HSCT) for chronic granulomatous disease (CGD) with a reduced-intensity conditioning regimen can be expected to lead to less therapy-related mortality and late-onset impairment, whereas it has also been reported to increase the risk of unsustained mixed donor chimerism and late rejection after transplantation. Herein, we report a 4-year-old boy with CGD who was successfully treated with unrelated bone marrow transplantation with a reduced-intensity conditioning regimen (RIC). Fludarabine-based RIC, 4 Gy of total body irradiation, 120 mg/kg of cyclophosphamide, and 125 mg/m² of fludarabine, was adopted for transplantation, followed with 8.9 × 10⁸/kg mononucleated donor cells infused without T-cell depletion. Although hematopoietic engraftment was rapidly obtained by day +17, he developed unstable donor chimerism. After tacrolimus withdrawal, the patient showed grade III acute graft-versus-host disease (GVHD), and subsequently reached full donor chimerism by day +61. Twelve months post-transplant, the patient has remained well with stable and durable engraftment, 100% donor chimerism, and normal superoxide production, without the requirement of donor lymphocyte infusions (DLI).     

Transvenous shock‐only implantable cardioverter defibrillator after an atrio‐pulmonary Fontan surgery

A 42‐year‐old woman with tricuspid atresia who underwent a Fontan surgery (atrio‐pulmonary connection) was admitted to our hospital due to symptomatic ventricular tachycardia (VT). A defibrillation lead was implanted in a distal site of a coronary vein since there was no usual entry to the ventricle. Ventricular pacing was impossible due to the high threshold, however, good sensing was obtained. Three years later, she felt palpitations and a subsequent shock therapy while climbing stairs. The cardioverter data showed that an appropriate cardioversion therapy successfully converted VT to normal rhythm.     

Using a High-Speed Movie Camera to Evaluate Slice Dropping in Clinical Image Interpretation with Stack Mode Viewers

The purpose of this study is to verify objectively the rate of slice omission during paging on picture archiving and communication system (PACS) viewers by recording the images shown on the computer displays of these viewers with a high-speed movie camera. This study was approved by the institutional review board. A sequential number from 1 to 250 was superimposed on each slice of a series of clinical Digital Imaging and Communication in Medicine (DICOM) data. The slices were displayed using several DICOM viewers, including in-house developed freeware and clinical PACS viewers. The freeware viewer and one of the clinical PACS viewers included functions to prevent slice dropping. The series was displayed in stack mode and paged in both automatic and manual paging modes. The display was recorded with a high-speed movie camera and played back at a slow speed to check whether slices were dropped. The paging speeds were also measured. With a paging speed faster than half the refresh rate of the display, some viewers dropped up to 52.4 % of the slices, while other well-designed viewers did not, if used with the correct settings. Slice dropping during paging was objectively confirmed using a high-speed movie camera. To prevent slice dropping, the viewer must be specially designed for the purpose and must be used with the correct settings, or the paging speed must be slower than half of the display refresh rate.     

Risk factors associated with late aneurysmal sac expansion after endovascular abdominal aortic aneurysm repair

PURPOSE

We aimed to identify the risk factors associated with late aneurysmal sac expansion after endovascular abdominal aortic aneurysm repair (EVAR).

METHODS

We retrospectively reviewed contrast-enhanced computed tomography (CT) images of 143 patients who were followed for ≥6 months after EVAR. Sac expansion was defined as an increase in sac diameter of 5 mm relative to the preoperative diameter. Univariate and multivariate analyses were performed to identify associated risk factors for late sac expansion after EVAR from the following variables: age, gender, device, endoleak, antiplatelet therapy, internal iliac artery embolization, and preprocedural variables (aneurysm diameter, proximal neck diameter, proximal neck length, suprarenal neck angulation, and infrarenal neck angulation).

RESULTS

Univariate analysis revealed female gender, endoleak, aneurysm diameter ≥60 mm, suprarenal neck angulation >45°, and infrarenal neck angulation >60° as factors associated with sac expansion. Multivariate analysis revealed endoleak, aneurysm diameter ≥60 mm, and infrarenal neck angulation >60° as independent predictors of sac expansion (P < 0.05, for all).

CONCLUSION

Our results suggest that patients with small abdominal aortic aneurysms (<60 mm) and infrarenal neck angulation ≤60° are more favorable candidates for EVAR. Intraprocedural treatments, such as prophylactic embolization of aortic branches or intrasac embolization, may reduce the risk of sac expansion in patients with larger abdominal aortic aneurysms or greater infrarenal neck angulation.The aim of endovascular abdominal aortic aneurysm repair (EVAR) is to prevent rupture of an abdominal aortic aneurysm (AAA) by depressurizing the aneurysm and excluding it from the systemic circulation using a stent-graft. Aneurysmal sac reduction is a reliable marker for the long-term prognosis after EVAR. Although most aneurysmal sacs shrink after EVAR, some sacs continue to expand. A relationship between aneurysm size and endoleaks was previously reported (1, 2). Most type II endoleaks spontaneously disappear over time, but 10%–25% persist for more than six months after EVAR (3–6). Persistent endoleaks with aneurysmal sac expansion are at high risk of rupture because of the continuously elevated intra-aneurysmal pressure and require a second intervention, such as embolization (7–11). However, it is difficult to predict sac expansion and persistent endoleak before performing EVAR. Although intraoperative intrasac thrombin injection and prophylactic embolization of aortic branches such as the inferior mesenteric artery and lumbar artery are reported to reduce the incidence of type II endoleak, the efficacy and clinical benefit of these procedures in terms of late postoperative aneurysm shrinkage have not been fully evaluated (12–15). Therefore, the purpose of this study was to identify the risk factors associated with late aneurysmal sac expansion after EVAR to determine possible indications for intrasac embolization and prophylactic embolization of aortic branches.     

Generation and characterization of a novel shoulder contracture mouse model

Frozen shoulder is a relatively common disorder that leads to severe pain and stiffness in the shoulder joint. Although this disorder is self‐limiting in nature, the symptoms often persist for years, resulting in severe disability. Recent studies using human specimens and animal models have shown distinct changes in the gene expression patterns in frozen shoulder tissue, indicating that novel therapeutic intervention could be achieved by controlling the genes that are potentially involved in the development of frozen shoulder. To achieve this goal, it is imperative to develop a reliable animal joint contracture model in which gene expression can be manipulated by gene targeting and transgenic technologies. Here, we describe a novel shoulder contracture mouse model. We found that this model mimics the clinical presentation of human frozen shoulder and recapitulates the changes in the gene expression pattern and the histology of frozen shoulder and joint contracture in humans and other larger animal models. The model is highly reproducible, without any major complications. Therefore, the present model may serve as a useful tool for investigating frozen shoulder etiology and for identifying its potential target genes. © 2015 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 33:1732–1738, 2015.