Unilateral absence of the pulmonary artery incidentally found after an episode of hemoptysis

A 29-year-old woman was admitted to our hospital because of hemoptysis and dyspnea. A chest radiographic study revealed an enlargement of the right lung hilum, and the left pulmonary artery could not be clearly visualized on contrast-enhanced CT scan. Both perfusion scintigraphy and pulmonary angiography confirmed the absence of the left pulmonary artery, and agenesis of the right upper pulmonary artery. Her clinical status has been stable for the previous two years of follow-up, even though she required long-term oxygen therapy. This is a rare case of a young woman with the unilateral absence of the left pulmonary artery incidentally found after an episode of hemoptysis.     

Accordion effect during carotid artery stenting

Introduction The term “accordion effect” is used to describe a mechanical distortion of tortuous arteries mimicking spasm or dissection. This phenomenon has been reported in patients undergoing percutaneous coronary intervention. To our knowledge, this is the first documentation of the accordion effect during carotid artery intervention. Methods Two patients who developed the accordion effect during carotid artery stenting (CAS) are described. Results Angiograms obtained just after CAS showed a stenosing lesion with wall irregularity at the distal part of the stent. This lesion disappeared and tortuosity of the internal carotid artery developed after withdrawing the guidewire until its floppy segment rested equally on the lesion. In another patient, the lesion did not disappear completely until the guiding catheter had been withdrawn to the proximal portion of the common carotid artery. We conclude that these stenosing lesions reflected the accordion effect. Conclusion It is essential to differentiate the accordion effect from dissection, spasm, and thrombosis because the management is importantly different. We report our findings and present a review of the literature.     

Involvement of a dysfunctional dopamine-D1/N-methyl-d-aspartate-NR1 and Ca2+/calmodulin-dependent protein kinase II pathway in the impairment of latent learning in a model of schizophrenia induced by phencyclidine

Continuous ingestion of phencyclidine (PCP) in humans produces long-lasting schizophrenic-like cognitive dysfunction. Although a malfunction of dopaminergic and/or glutamatergic neurotransmission is implicated in the etiology of schizophrenia, involvement of the dopaminergic-glutamatergic neurotransmission in the cognitive dysfunction induced by repeated PCP treatment is minor. We demonstrated that mice treated with PCP (10 mg/kg/day s.c.) for 14 days displayed an impairment of latent learning in a water-finding task and of learning-associated phosphorylation of Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) and NR1 in the prefrontal cortex even after drug withdrawal. The infusion of a CaMKII inhibitor and NR1 antisense oligonucleotide into the prefrontal cortex produced an impairment of latent learning and decrease of learning-associated phosphorylation of CaMKII, which were observed in the PCP-treated mice. Exogenous NMDA-induced CaMKII activation was not observed in slices of the prefrontal cortex prepared from mice treated repeatedly with PCP. The potentiation of NMDA receptor function by the infusion of glycine into the prefrontal cortex ameliorated these impairments in mice treated repeatedly with PCP. The high potassium-stimulated release of dopamine from the prefrontal cortex was less extensive in the PCP-treated than saline-treated mice. The infusion of a dopamine-D1 receptor agonist into the prefrontal cortex attenuated the impairment of latent learning and decrease of learning-associated NR1 phosphorylation in the PCP-treated mice, suggesting a functional linkage between glutamatergic and dopaminergic signaling. These findings indicate that repeated PCP treatment impairs latent learning through a prefrontal cortical dysfunction of NMDA-CaMKII signaling, which is associated with dopaminergic hypofunction.     

Rebleeding after endovascular embolization of ruptured cerebral aneurysms

This study retrospectively reviewed 227 patients with ruptured solitary cerebral aneurysm who underwent endovascular embolization with detachable coils between March 1997 and March 2006 to establish the incidence of rebleeding after endovascular treatment for ruptured cerebral aneurysm and identify the risk factors. The site and size of the aneurysm, the interval between treatment and rebleeding, and the outcome were investigated in six of the 227 patients (2.6%) who rebled after treatment. Four patients had large or giant aneurysms located on the internal carotid artery at the origin of the posterior communicating artery. The interval between treatment and rebleeding was less than 1 year in four patients (mean 394.2 days). Two patients died, and the survivors had modified Rankin Scale scores of 0, 2, 3, and 4. Re-embolization was performed in four patients and no further bleeding occurred during the mean follow-up period of 1.9 years after re-treatment. Patients with giant aneurysms of the internal carotid artery are at increased risk for rebleeding. Re-treatment should be considered if there is conventional and/or magnetic resonance angiographic evidence of dome filling. Patients with ruptured cerebral aneurysms must be followed up with diagnostic imaging closely during the first 12 months post-embolization because rebleeding frequently occurs within 1 year after initial treatment. Re-embolization is safe and effective in patients with recurrent hemorrhage from aneurysms previously embolized with detachable coils.     

Semaphorin 3A controls allergic and inflammatory responses in experimental allergic conjunctivitis

AIM: To assess the efficacy of topical Semaphorin-3A (SEMA3A) in the treatment of allergic conjunctivitis. METHODS: Experimental allergic conjunctivitis (EAC) mice model induced by short ragweed pollen (SRW) in 4-week-old of BALB/c mice, mice were evaluated using haematoxylin and eosin (H&E) staining, immunofluorescence and light microscope photographs. Early phase took the samples in 24h after instillation and late phase took the samples between 4 to 14d after the start of treatment. The study use of topical SEMA3A (10 U, 100 U, 1000 U) eye drops and subconjunctival injection of SEMA3A with same concentration. For comparison, five types of allergy eyedrops were quantified using clinical characteristics. RESULTS: Clinical score of composite ocular symptoms of the mice treated with SEMA3A were significantly decreased both in the immediate phase and the late phase compared to those treated with commercial ophthalmic formulations and non-treatment mice. SEMA3A treatment attenuates infiltration of eosinophils entering into conjunctiva in EAC mice. The score of eosinophil infiltration in the conjunctiva of SEMA3A 1000 U-treated group were significantly lower than low-concentration of SEMA3A treated groups and non-treated group. SEMA3A treatment also suppressed T-cell proliferation in vitro and decreased serum total IgE levels in EAC mice. Moreover, Treatment of SEMA3A suppressed Th2-related cytokines (IL-5, IL-13 and IL-4) and pro-inflammatory cytokines (IFN-γ, IL-17 and TNF-α) release, but increased regulatory cytokine IL-10 concentration in the conjunctiva of EAC mice. CONCLUSIONS: SEMA3A as a biological agent, showed the beneficial activity in ocular allergic processes with the less damage to the intraocular tissue. It is expected that SEMA3A may be contributed in patients with a more severe spectrum of refractory ocular allergic diseases including allergic conjunctivitis in the near future.     

Direct Intraesophageal Growth from Metastatic Mediastinal Lymphadenopathy in Thymic Carcinoma

We herein report a case of thymic carcinoma that initially exhibited dysphagia and an intraesophageal mass lesion. A 68-year-old man was admitted to our hospital because of dysphagia. An endoscopic examination revealed a mass on the middle esophagus. Chest computed tomography (CT) showed a huge anterior mediastinal mass and subcarinal lymph node swelling, directly invading into the esophageal lumen. An immunohistological examination of the esophageal and anterior mediastinal masses revealed squamous cell carcinoma originating from the thymus. This is the first report of a thymic carcinoma spreading into the esophageal lumen and forming a mass lesion.