Rarely, the ophthalmic artery (OA) arises from the cavernous segment of the internal carotid artery (ICA) inferolaterally and enters into the orbit via the superior orbital fissure. This anomalous OA that originates from the inferolateral trunk is regarded as a persistent dorsal OA. Extremely rarely, both normal OA and persistent dorsal OA arise from the ICA. We report the first case of such double OAs, one of which arose from the cavernous segment of the ICA superolaterally and we believe that it originated from the meningohypophyseal trunk rather than the inferolateral trunk. 相似文献
We report a case of type 1 proatlantal intersegmental artery (PIA) associated with multiple anomalies of the aortic arch, and discuss the possible embryonic mechanism and clinical importance of the multiple cerebrovascular variants in this patient.
Methods
A 65-year-old woman with dizziness underwent cerebral magnetic resonance (MR) imaging and head and neck MR angiography using a 3-tesla scanner and computed tomography (CT) angiography using a 64-slice multidetector CT scanner.
Results
MR and CT angiography demonstrated an aneurysm of the distal end of the azygos anterior cerebral arteries and hypoplasia of the proximal right vertebral artery (VA) with an anastomotic artery, between the right internal carotid artery (ICA) and distal right VA that passed through the foramen magnum, indicating a type 1 PIA. She also demonstrated an aberrant right subclavian artery (ARSA) with hypoplasia of the right VA, and the left VA arose directly from the aortic arch.
Conclusion
To our knowledge, this is the first report of a type 1 PIA associated with multiple vascular anomalies of the aortic arch, such as ARSA and origin of the left VA from the arch. In cases of persistent anastomoses between the carotid and vertebrobasilar arteries, such as PIAs, imaging examination should include the aortic arch to identify associated vascular variations. 相似文献
Pregnant women are highly susceptible to malaria infection because of their low immunity and are at increased risk of maternal illness or death, in addition to spontaneous abortion, stillbirth, premature delivery, and low birth weight. However, the detailed pathogenesis of maternal malaria remains unclear. In this study, we evaluated a mouse model that shows similar severe pathological features of pregnant women during Plasmodium falciparum infection and investigated the pathogenesis of maternal malaria. Pregnant mice immunized by infection with an attenuated parasite, Plasmodium berghei XAT, were more susceptible to virulent P. berghei NK65 challenge/infection than were nonpregnant mice and showed high levels of parasitemia and a poor pregnancy outcome associated with placental pathology, such as accumulation of parasitized red blood cells, in the late phase of pregnancy. Notably, the pregnant immune mice challenged/infected with P. berghei NK65 developed liver injury associated with microvesicular fatty infiltration in late pregnancy. The pathological features were similar to acute fatty liver of pregnancy. Higher levels of gamma interferon and nitric oxide (NO) were found in plasma from pregnant immune mice infected with P. berghei NK65 than in plasma from nonpregnant mice. These findings suggest that development of liver injury and placental pathology in pregnant immune mice challenged/infected with P. berghei NK65 is accompanied by enhanced production of proinflammatory cytokines. 相似文献
ObjectiveThe correlation between enhancement of the vestibulocochlear nerves on gadolinium-enhanced magnetic resonance imaging (MRI) and vestibulocochlear functional deficits was examined in patients with Ramsay Hunt syndrome (RHS).MethodsNineteen patients with RHS who showed herpes zoster oticus, peripheral facial palsy, and vertigo were enrolled. Canal paresis (CP) in the caloric test, abnormal response to ocular and cervical vestibular myogenic potentials (oVEMP and cVEMP), and refractory sensorineural hearing loss were evaluated. MRI images perpendicular to the internal auditory canal were reconstructed to identify the superior (SVN) and inferior vestibular nerves (IVN) and the cochlear nerve (CV). The signal intensity increase (SIinc) of the four-nerve enhancement was calculated as an index.ResultsAmong RHS patients, 79%, 53%, 17% and 26% showed CP in the caloric test, abnormal responses to oVEMP and cVEMP, and refractory sensorineural hearing loss, respectively. SIinc rates of the SVN were significantly increased in RHS patients with CP in the caloric test, and with abnormal responses to oVEMP and cVEMP. SIinc rates of the SVN tended to increase in RHS patients with refractory sensorineural hearing loss (p = 0.052). SIinc rates of the IVN were significantly increased in RHS patients with abnormal responses to oVEMP and cVEMP, and refractory sensorineural hearing loss, but not in those with CP in the caloric test. SIinc rates of the CN were significantly increased in RHS patients with CP in the caloric test, abnormal response to oVEMP and refractory sensorineural hearing loss, but not in those with abnormal response to cVEMP.ConclusionIn patients with RHS, the origin of vertigo may be superior vestibular neuritis, which is affected by reactive varicella-zoster virus from the geniculate ganglion of the facial nerve through the faciovestibular anastomosis. The results also suggested that in some RHS patients, inferior vestibular neuritis contributes to the development of vertigo and that the origin of refractory sensorineural hearing loss is cochlear neuritis. 相似文献
Recently we reported that macrophage colony-stimulating factor (M-CSF) can mobilize endothelial progenitor cells (EPCs) from the bone marrow into the peripheral blood, resulting in an increase in the number of blood vessels and augmentation of blood flow in the ischemia-induced legs. M-CSF accelerates neovascularization of ischemic lesions resulting from the mobilization of EPCs. In the present paper, we analyze the mechanisms underling the mobilization of EPCs by M-CSF. M-CSF augments the production of vascular endothelial growth factor (VEGF) from the bone marrow cells, especially from myeloid lineage cells. In vivo administration of anti-VEGF antibody abrogates both the acceleration of the recovery of blood flow in the ischemia-induced limbs by M-CSF and the augmentation of the mobilization of EPCs induced by M-CSF. These results suggest that the M-CSF contributes to rapid recovery of blood flow in ischemic lesions by mobilization of EPCs from the bone marrow through augmentation of VEGF production in the bone marrow and that the VEGF is mainly produced by myeloid lineage cells. 相似文献
Axenfeld-Rieger syndrome is inherited in an autosomal dominant pattern and is characterized by anomalies of the anterior segment of the eye and systemic signs including craniofacial dysmorphic features and cardiac defects. The disorder is genetically heterogeneous and one causative gene, FOXC1, is located on chromosome 6p25. Persistent hyperplastic primary vitreous (PHPV) is a congenital ocular disorder in which there is a failure of the normal regression of the primary vitreous and a proliferation of fibrous tissue from the remnants of the primary vitreous. Deletions of chromosome 6p25 have been reported in a small number of patients with Axenfeld-Rieger syndrome; however, no case of chromosome 6p25 deletion has been reported with PHPV. We report a newborn girl who had both Axenfeld-Rieger syndrome and the combined type of PHPV, in whom the G-banding and spectral karyotyping revealed a 6p monosomy of terminal deletion with a breakpoint at chromosome 6p25.1. The karyotype was 46,XX,del(6)(p25.1). We conclude that PHPV in the context of Axenfeld-Rieger syndrome can be caused by 6p25 terminal deletion. 相似文献
We have established an agonistic monoclonal antibody, UT12, that induces stimulatory signals comparable to those induced by lipopolysaccharide (LPS) through Toll-like receptor 4 and MD-2. UT12 activated nuclear factor kappaB and induced the production of proinflammatory cytokines such as tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6) in peritoneal exudative cells. In addition, mice injected with UT12 rapidly fell into endotoxin shock concomitant with the augmentation of serum TNF-alpha and IL-6 levels, followed by death within 12 h. On the other hand, when the mice were pretreated with a sublethal dose of UT12, the mice survived the subsequent lethal LPS challenges, with significant suppression of serum TNF-alpha and IL-6, indicating that UT12 induced tolerance against LPS. This effect of UT12 was maintained for at least 9 days. In contrast, the tolerance induced by LPS continued for less than 3 days. These results illuminate a novel potential therapeutic strategy for endotoxin shock by the use of monoclonal antibodies against the Toll-like receptor 4/MD-2 complex. 相似文献
Background: The local anesthetic lidocaine affects neuronal excitability in the central nervous system; however, the mechanisms of such action remain unclear. The intracellular sodium concentration ([Na+]i) and sodium currents (INa) are related to membrane potential and excitability. Using an identifiable respiratory pacemaker neuron from Lymnaea stagnalis, the authors sought to determine whether lidocaine changes [Na+]i and membrane potential and whether INa is related to these changes.
Methods: Intracellular recording and sodium imaging were used simultaneously to measure membrane potentials and [Na+]i, respectively. Measurements for [Na+]i were made in normal, high-Na+, and Na+-free salines, with membrane hyperpolarization, and with tetrodotoxin pretreatment trials. Furthermore, changes of INa were measured by whole cell patch clamp configuration.
Results: Lidocaine increased [Na+]i in a dose-dependent manner concurrent with a depolarization of the membrane potential. In the presence of high-Na+ saline, [Na+]i increased and the membrane potential was depolarized; the addition of lidocaine further increased [Na+]i, and the membrane potential was further depolarized. In Na+-free saline or in the presence of tetrodotoxin, lidocaine did not change [Na+]i. Similarly, hyperpolarization of the membrane by current injections also prevented the lidocaine-induced increase of [Na+]i. In the patch clamp configuration, membrane depolarization by lidocaine led to an inward sodium influx. A persistent reduction in membrane potential, resulting from lidocaine, brings the cell within the window current of INa where sodium channel activation occurs. 相似文献
Despite facet joints being three-dimensional structures, previous computed tomography and magnetic resonance imaging studies have evaluated facet joint orientation in only the axial plane. Facet joint orientation in the sagittal plane has rarely been studied using these imaging techniques. The aim of this study was to elucidate facet joint orientation in both the axial and sagittal planes on computed tomography.
Methods
A total of 568 patients (343 men, 225 women) (excluding orthopedic outpatients) for whom abdominal and pelvic computed tomography scans were obtained at our hospital between September 2010 and October 2012 were included. Mean age was 63 (range 21–90) years. Patients were divided into a degenerative spondylolisthesis group (67 patients; 30 men, 37 women) and a control group (313 patients; 313 men, 188 women). Facet joint orientation was evaluated in the control group according to patient age (≤50, 51–60, 61–70, or ≥71 years). The findings in the control group were then compared with those in the degenerative spondylolisthesis group. The orientation of the lumbar facet joints at each level was measured in the axial and sagittal planes on computed tomography images.
Results
Facet joint angles decreased with age at L4/5 and L5/S1 in women in the axial plane and at L4/5 in men and L3/4 and L4/5 in women in the sagittal plane. The variation in facet joint angle was greatest at L4/5 in women. Patients with degenerative spondylolisthesis showed more sagittally and horizontally oriented facet joints in the axial and sagittal planes; facet tropism showed an association with degenerative spondylolisthesis in the axial plane.
Conclusions
The axial and sagittal orientation of facet joints in the lower lumbar vertebra, especially L4/5, was negatively correlated with age. This finding could help to explain why older people are more prone to degenerative spondylolisthesis. 相似文献
Balloon kyphoplasty or vertebroplasty is widely performed as a surgical intervention for osteoporotic vertebral fracture (OVF) and the effects have been investigated in many previous studies. However, the influence of the timing of the procedure on patient outcomes has not been studied formally. The purpose of this study was to investigate differences in the surgical outcomes of OVFs according to the timing of balloon kyphoplasty.
Methods
This was a multicenter cohort study. Participants comprised 72 consecutive patients who underwent balloon kyphoplasty between January 2012 and January 2016. Patients were analyzed in two groups according to the timing of kyphoplasty after onset (Early group: ≤2 months; Late group: >2 months). Follow-up continued for more than 6 months.
Results
A total of 72 patients were effectively analyzed. Of these, 27 (38%) patients underwent kyphoplasty within 2 months after symptom onset. The Late group showed greater angular motion of fractured vertebrae (p = 0.005) and compression of anterior vertebral height (p = 0.001) before surgery. Final outcomes adjusted for age and preoperative outcome showed lower visual analog scale (VAS) scores for low back pain in the Early group than in the Late group (19.9 vs. 30.4, p = 0.049). Final relative anterior vertebral height and kyphotic angle were more preserved in the Early group than in the Late group (p = 0.002 and p = 0.020, respectively), although absolute differences were not significant.
Conclusions
Vertebral height and kyphotic angle before and after balloon kyphoplasty were greater in patients who underwent kyphoplasty within 2 months after onset, and the VAS score for low back pain at final follow-up was better. Our results support kyphoplasty within 2 months. 相似文献