Helicobacter pylori infection is associated with the development of gastric cancer. In short-term coculture with AGS gastric cells, H. pylori inhibits cell cycle progression and induces dose-dependent apoptosis. Based on the concept that an imbalance between proliferation and apoptosis may contribute to the emergence of gastric cancer, we chronically exposed AGS cells to H. pylori as a model of chronic exposure in humans. The AGS derivatives selected by this process were stably resistant not only to H. pylori-induced apoptosis but also to apoptosis induced by other enteric bacteria and by several toxic agents including radiation and cancer chemotherapy. Like the parental AGS cells, the derivatives underwent G 1 /S-phase cell cycle inhibition in response to H. pylori. The AGS derivatives displayed a marked decrease in cellular levels of the cell cycle control protein p27 kip1 . We found a similar decrease in epithelial cell p27 kip1 expression in gastric biopsy specimens from H. pylori-infected patients. These findings are consistent with observations that link decreases in the p27 kip1 level to increased susceptibility to cancer in mice with p27 kip1 deleted and to a poor prognosis of gastric cancer in humans. This is the first demonstration that bacterial infection can lead to apoptosis resistance and to cross-resistance to other inducers of apoptosis such as bacteria, chemotherapeutic agents, and radiation. The development of apoptosis resistance and downmodulation of p27 kip1 may contribute to the increased risk for gastric cancer observed in humans chronically exposed to H. pylori.
BackgroundHypertension is the prime risk factor for stroke, and primary aldosteronism (PA) is the most common cause of secondary hypertension. The prevalence of PA in stroke patients has never been reported. The aim of this study was to elucidate the prevalence of PA.MethodsA total of 427 consecutive patients with acute stroke were prospectively enrolled for this study. The screening tests were performed at the initial visit and a week after admission by measuring plasma aldosterone concentration and plasma renin activity. The rapid adrenocorticotropic hormone (ACTH) test was performed as the confirmatory test when both screening tests were positive. The primary endpoint was a final diagnosis of PA.ResultsThe sensitivity of the dual screening system for the diagnosis of PA was 88.2 %, and PA was finally diagnosed in 4.0 % of acute stroke patients and in 4.9 % of stroke patients with a history of hypertension. Patients with PA were less likely to be male and have diabetes, and they had higher blood pressure at the initial visit, lower potassium concentration, and more intracerebral hemorrhage. The rapid ACTH test was performed safely even in acute stroke patients.ConclusionsThe prevalence of PA is not low among acute stroke patients. Efficient screening of PA should be performed particularly for patients with risk factors.Trial registrationUMIN-CTR; UMIN000011021. Trial registration date: June 23, 2013 (retrospectively registered).
Background Intracranial pseudoaneurysm formation due to a ruptured non-traumatic aneurysm is extremely rare. We describe the radiological findings and management of pseudoaneurysms due to ruptured cerebral aneurysms in our case series and previously reported cases. Patients and methods Four additional and 20 reported patients presenting with subarachnoid hemorrhage (SAH) are included. Radiological findings and clinical features of these patients were reviewed. Results In our series, three-dimensional computed tomographic angiography (3D-CTA) and/or angiography showed an irregular- or snowman-shaped cavity extending from the parent artery. The radiological examination additionally revealed delayed filling and retention of contrast medium. These findings were the same as previously reported cases. One patient underwent direct clipping of the true aneurysm. For the other three patients with aneurysms at the basilar and anterior communicating arteries, the true portion of the aneurysm was embolized with platinum coils. During the procedures, care was taken not to insert the coils into the distal pseudoaneurysm portion to prevent rupture. The review of 24 cases revealed that the location of the aneurysms was most frequent in the anterior communicating artery (41.7%), and 86.7% of patients were in a severe stage of SAH (>Grade 3 in WFNS or Hunt & Kosnik grading) implying abundant SAH. Conclusions Pseudoaneurysm formation in SAH after non-traumatic aneurysm rupture is rare. However, in cases with an irregular-shaped aneurysm cavity, pseudoaneurysm formation should be taken into consideration.
The aim of this study was to analyze the pattern of magnetic resonance diffusion-weighted imaging (DWI) findings in status epilepticus in terms of clinical characteristics. Participants comprised 106 patients with status epilepticus who were admitted to our hospital and underwent DWI. Forty-five patients (42.5 %) showed abnormal findings on DWI and were divided into two groups, comprising 26 patients (24.5 %) with cortex lesions alone and 19 patients (17.9 %) with cortex and pulvinar lesions in the same hemisphere. A long duration of status epilepticus (>120 min) tended to be more prevalent among patients with cortex and pulvinar lesions (57.9 %) than among patients with cortex lesions alone (30.8 %) by univariate and multivariate analyses. Todd's palsy tended to be more frequent in patients with abnormalities on DWI (24/45, 53.3 %) than in patients with normal DWI (21/61, 34.4 %). Six of the 26 patients with cortex lesions alone (23.1 %) had taken anti-epileptic drugs before the attack compared to none of the 19 patients with both cortex and pulvinar lesions. The trend toward a longer duration of status epilepticus in patients with both cortex and pulvinar lesions favors a spreading pattern of seizure discharge from cortex to pulvinar via cortico-pulvinar pathways, and anti-epileptic drugs might, to some extent, prevent spreading of seizure discharge from cortex to pulvinar. In addition, existence of high-intensity areas on DWI at the onset of epilepsy may be a predictive factor for the occurrence of Todd's palsy.
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