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Yoshitaka Kubo1, Kuniaki Ogasawara1, Akira Kurose2, Hiroshi Kashimura1, Takahiro Koji1, Yasunari Otawara1, Jun Kamei3, Manami Akasaka3, Makoto Sasaki4, Akira Ogawa1 1Department of Neurosurgery, 2Department of Pathology, 3Department of Pediatrics, 4Department of Radiology, Iwate Medical University, Morioka, Japan Abstract: Intraparenchymal hemorrhage in the full-term neonate rarely occurs more than 2 weeks after birth, and its definitive cause remains unclear. In the present report, a case of a patient with intraparenchymal hemorrhage occurring 33 days after birth is described. Histological examination of the brain tissue obtained during hematoma evacuation through craniotomy showed hemorrhagic infarction. Patent foramen ovale may have been present and this may have led to spontaneous paradoxical cerebral embolism followed by hemorrhagic infarction. Keywords: full-term neonate, hemorrhagic cerebral infarction, patent foramen ovale, surgery

The present study addresses the distortion of the compression wave reflected from an open end of a shock tube. An experiment is carried out using the simple shock tube with an open end. Computational work is also performed to represent the experimented flows. The second-order Total Variation Diminishing scheme is employed to numerically solve the unsteady, axisy-mmetric, inviscid, compressible governing equations. Both the experimented and predicted results are in good agreement. The generation and development mechanisms of the compression wave, which is reflected from the open end of the shock tube, are obtained in detail from the present computations. The effect of size of the baffle plate at the open-end that causes the reflection of the incident expansion wave is found negligible. A good correlation is obtained for transition of the reflected compression wave to a shock wave inside the tube. The present data show that for a given wave length of the incident expansion wave the transition of the reflected compression wave to a shock wave can be predicted with good accuracy. [ABSTRACT FROM AUTHOR]

Abstract Background and Aims: Telomerase activity is thought to be necessary for cellular immortality and carcinogenesis. The mRNA that encodes the telomerase catalytic subunit (hTERT) has recently been identified, and expression of hTERT mRNA is thought to regulate activation of telomerase. To determine at what stage of carcinogenesis cells begin to express hTERT, we analysed hTERT mRNA expression in gastric carcinoma and precancerous conditions, focusing on chronic gastritis with or without intestinal metaplasia. Methods: Using reverse transcription-polymerase chain reaction, hTERT gene expression was investigated in 18 gastric cancers and 60 specimens of chronic gastritis. Telomerase activity was evaluated using telomeric repeat amplification protocol. Results: Sixteen of 18 (89%) gastric carcinomas expressed hTERT mRNA, and this expression was unrelated to histological type or depth of invasion. Telomerase activity was found in seven of eight (88%) gastric cancer tissues, all of which expressed hTERT mRNA. Expression of hTERT mRNA was positive in 14 of 60 (23%) specimens of chronic gastritis, and was most prominent in seven of 15 (47%) specimens of gastric mucosa with intestinal metaplasia. Expression of the hTERT gene was significantly more frequent in chronic gastritis with intestinal metaplasia than in gastritis without intestinal metaplasia (P = 0.030). In addition, hTERT gene expression was not correlated with age, sex, biopsy site, histological grade of inflammatory cells, glandular atrophy and lymph follicles, or infection with Helicobacter pylori. None of eight normal gastric mucosa expressed hTERT mRNA. Conclusions: Our results indicate that hTERT mRNA is expressed in precancerous conditions as well as in gastric cancer, and that hTERT gene expression is induced at an early stage of gastric carcinogenesis. [ABSTRACT FROM AUTHOR]

Celiac axis stenosis is frequently associated with pancreaticoduodenal artery aneurysms. Although the cause of stenosis was not clear in most of the reported cases, compression of the median arcuate ligament of the diaphragm was found to be responsible for the stenosis in 7 of 42 reported cases of this type of aneurysm. We report a case of aneurysm caused by compression of the median arcuate ligament of the diaphragm and celiac plexus. An asymptomatic 43-year-old Japanese man was admitted with a low echoic lesion in the uncus of pancreas. Computed tomographic scan and angiogram revealed stenosis of the celiac axis and two aneurysms in the inferior posterior pancreaticoduodenal artery. The celiac plexus and median arcuate ligament were divided surgically and normal flow was reestablished in the celiac axis. One of the aneurysms was resected and the afferent artery of the other aneurysm was ligated. In the setting of pancreaticoduodenal artery aneurysm associated with celiac axis stenosis, management of stenosis should be considered in addition to local treatment of the aneurysm. In this context, division of median arcuate ligament and celiac plexus or aorto-celiac bypass may normalize the flows in the pancreaticoduodenal arcade and could be effective in preventing aneurysm reformation. [ABSTRACT FROM AUTHOR]

We report a case of steroid-refractory ulcerative colitis, treated with cyclosporine, in a 38-year-old woman with a 13-year history of ulcerative colitis. No remission was achieved with treatments that included intravenous hyperalimentation, sulfasalazine, and intensive parenteral prednisolone therapy for 4 weeks. Intravenous infusion of cyclosporine was performed because the patient refused to undergo surgery. Her condition improved dramatically and colectomy was avoided. She has been maintained on oral cyclosporine and azathioprine since steroids were discontinued, and she has remained in clinical and endoscopic remission for 2 years. The side effects were not significant, but mild paresthesia in both hands and mild hypertension, which was controlled by anti-hypertensives. Cyclosporine seems to be an effective treatment for patients with steroid-refractory severe active ulcerative colitis in whom colectomy seems inevitable. We believe further clinical trials of the treatment are warranted. [ABSTRACT FROM AUTHOR]

We have reported that endothelin-1 induces gastric ulcer characterized by a potent long-lasting vasoconstriction of the regional microvasculature. Nitric oxide synthesized from L-arginine has been shown to regulated gastric mucosal blood flow, and inhibition of its synthesis has been shown to delay the healing of gastric ulcers. We examined the effect of exogenous L-arginine and the inhibition of nitric oxide synthesis on the development of endothelin-1-induced gastric ulcers. In rats anesthetized with urethane, a continuous intravenous infusion of L- or D-arginine (10 mg.kg-1.min-1) was followed, 15 min later, by a submucosal injection of endothelin-1 (200 pmol/kg) in the anterior wall of the gastric body. In another group, rats were intravenously pretreated with N omega-nitro-L-arginine-methyl ester (1-10 mg/kg), a nitric oxide synthesis inhibitor, and then injected with endothelin-1 (40 pmol/kg). Twenty-four h later, L-arginine, but not D-arginine, had significantly reduced the extent and the severity of the endothelin-1-induced ulcer (mucosal wall damage, 18.11 +/- 4.79% and 88.14 +/- 7.06%, respectively; mean +/- SD, P < 0.001), and the nitric oxide synthesis inhibitor (10 mg/kg) had increased the endothelin-1-induced mucosal damage (ulcer length, 3.8 +/- 1.2 mm and 1.1 +/- 0.2 mm, respectively, P < 0.01). Continuous gastric mucosal blood flow measurements showed that L-arginine antagonized the endothelin-1-induced vasoconstriction. L-arginine protected the gastric mucosa from the ulcerogenic action of endothelin-1 and antagonized its vasoconstrictive action. The inhibition of endogenous nitric oxide potentiated the ulcerogenic effect of endothelin-1 on rat gastric mucosa. [ABSTRACT FROM AUTHOR]

We investigated the role of an endogenous vasoconstrictor peptide endothelin-1 (ET-1) and free radicals in local gastric ischemia-reperfusion injury in rats. Local gastric ischemia was induced by clamping the left gastric artery for 15 min and reperfusion was done for 10-30 min in the presence of 150 mM exogenous HCl intragastrically. Local gastric ischemia and reperfusion resulted in significant macroscopic and microscopic gastric mucosal damage together with elevation of gastric tissue ET-1 concentration. Gastric tissue ET-1 was found to increase after 15 min of ischemia alone and also with 30 min of reperfusion. A novel nonpeptide endothelin receptor antagonist, bosentan, or a combination of radical scavengers (superoxide dismutase, catalase, and deferoxamine) both attenuated gastric mucosal injury. However, the greater protection observed with bosentan than with radical scavengers might reflect a preferential role of endothelin-1 in this type of injury. [ABSTRACT FROM AUTHOR]

Thrombus migration is a well-known clinical condition that occurs before mechanical thrombectomy and after intravenous thrombolysis in patients with anterior circulation strokes. Although thrombus migration from the vertebral artery (VA) can result in life-threatening basilar artery (BA) occlusion, its occurrence in the posterior circulation has rarely been discussed. Two patients with secondary BA occlusion caused by spontaneous thrombus migration from the VA are presented. A 60-year-old man with a left cerebellar infarction secondary to ipsilateral VA occlusion was admitted to our hospital 8 hours after onset, with a National Institute of Health Stroke Scale (NIHSS) score of 4. The patient became comatose 3.5 hours after arrival owing to subsequent BA occlusion. He was successfully treated with mechanical thrombectomy. A 74-year-old man with right cerebellar infarction secondary to ipsilateral VA occlusion was admitted to our hospital 26 hours after onset, with an NIHSS score of 3. He became comatose 1 hour after arrival owing to BA occlusion and was treated with thrombectomy, followed by internal and external decompression. Despite the mild symptoms of VA occlusion and consequently delayed admission to the hospital, stroke physicians should be aware that spontaneous thrombus migration from the VA to the BA can result in a life-threatening presentation., (© 2024 The Authors. Published by Elsevier Inc. on behalf of University of Washington.)

Background: Temporal changes in the volume of chronic subdural hematoma (CSDH) following middle meningeal artery (MMA) embolization vary. We aimed to determine whether CSDH density on computed tomography is related to hematoma resolution following particle MMA embolization., Methods: Patients who underwent MMA embolization for CSDH were enrolled. The CSDHs were quantitatively divided into 2 hematoma groups based on the hematoma density at 1-week postembolization: low-density or high-density. The temporal change in the volume of CSDHs was then analyzed between the groups., Results: Thirty patients were enrolled in this study. Three patients with high-density hematomas required rescue surgery. The hematoma volume was significantly lower in low-density hematomas than in high-density hematoma at 1-week (P = 0.006), 1-month (P = 0.003), and 2-month (P = 0.004) postembolization; although the volume converged to a similar value at 3-month (P > 0.05). There was a positive correlation between hematoma density at 1-week postembolization and percentage hematoma volume at 1-week and 1-month postembolization (P = 0.004 and P < 0.001, respectively), but no correlation was observed between hematoma density before MMA embolization and percentage hematoma volume at 1-week and 1-month postembolization (P = 0.54 and P = 0.17, respectively)., Conclusions: Rapid resolution of CSDH following MMA embolization was associated with low hematoma density at 1-week postembolization. Based on hematoma density on computed tomography at 1-week postembolization, a 1-month follow-up would be sufficient in cases of low density, but a 3-month follow-up would be required in cases of high-density hematoma. Larger studies and clinical trials are needed to confirm our findings., (Copyright © 2023 Elsevier Inc. All rights reserved.)