In this work, we consider a two-level hierarchical MIMO antenna array system, where each antenna of the upper level is made up of a subarray on the lower one. The concept of spatial multiplexing is applied twice in this situation: Firstly, the spatial multiplexing of a Line-of-Sight (LoS) MIMO system is exploited. It is based on appropriate (sub-)array distances and achieves multiplexing gain due to phase differences among the signals at the receive (sub-)arrays. Secondly, one or more additional reflected paths of different angles (separated from the LoS path by different spatial beams at the subarrays) are used to exploit spatial multiplexing between paths.By exploiting the above two multiplexing kinds simultaneously, a high dimensional system with maximum spatial multiplexing is proposed by jointly using 'phase differences' within paths and 'angular differences' between paths. The system includes an advanced hybrid beamforming architecture with large subarray separation, which could occur in millimeter wave backhaul scenarios. The possible gains of the system w.r.t. a pure LOS MIMO system are illustrated by evaluating the capacities with total transmit power constraints.
Abstract:We report the neuropathological findings in a patient with Parkinson's disease (PD) associated with Basque R1441G-LRRK2/dardarin mutation. The patient was a man with disease onset at 68 years of age, with unilateral rest tremor; the Parkinsonism was well controlled with medication for 15 years. He died at the age of 86, after 18 years of evolution. The neuropathological examination disclosed mild neuronal loss in the substantia nigra pars compacta without a-synuclein, tau, LRRK2, or ubiquitin cytoplasmic inclusions. Lewy bodies and Lewy neurites were absent. This is the first neuropathological study of PD associated with brain with the R1441G mutation in LRRK2. Movement Disorder SocietyKey words: Parkinson's disease; LRRK2; dardarin; neuropathology Pathogenic mutations in the leucine-rich repeated kinase 2 (LRRK2-PARK 8) gene have been identified as the most common currently known cause of familial autosomal dominant Parkinson's disease (PD). 1,2 Patients with PD associated with the LRRK2 mutations have a clinical phenotype similar to other patients with PD without detected mutations. The R1441G-LRRK2/ dardarin mutation is frequent in the Basque country, representing 16% of the familial and 4% of apparently sporadic PD cases. 3 Patients with this mutation belonging to the same family have rather homogenous symptoms and clinical course, but differences are seen between patients with this mutation in different families.The neuropathological changes in patients with PD associated with LRRK2 mutations seem to be heterogeneous. 1 In some cases, the presence of neuronal loss in the substantia nigra (SN) and a-synuclein-positive Lewy bodies (LBs) is consistent with classic PD. In other cases, the neuropathological study shows the presence of nonspecific neuronal loss with ubiquitinreactive cytoplasmic and nuclear inclusions, tau pathology reminiscent of progressive supranuclear palsy, or pure nigral degeneration without specific a-synuclein, tau, or ubiquitin inclusions. 1 We report here a patient with the R1441G-LRRK2/ dardarin mutation with neurological symptoms consistent with classic PD. The neuropathological examination disclosed nonspecific nigral degeneration in the SN without a-synuclein, tau, LRRK2, or ubiquitin inclusions. CASE REPORTA 69-year-old man presented with a 1-year history of rest tremor in his right hand. Two years before, he had an angina episode and since then had been taking 100 mg aspirin daily. Although his family history for PD was negative, the sister of the patient explained that their mother, of Basque origin (Durango-Bizcay), had suffered from upper limb tremor and clumsiness at an older age. The mother did not know their origin because she had been brought up in an orphanage. The father of the patient was of Castilian origin. The patient had no children and had one sister and one Vol. 24, No. 13, 2009, pp. 1998-2019 2009 Movement Disorder Society brother without neurological symptoms at the age of 83 and 73 years, respectively, and so they were not tested for the mutation...
BackgroundElevated serum uric acid (SUA) levels can enhance its antioxidant prosperities and reduce the occurrence of cerebral infarction. Significantly elevated SUA levels have been associated with a better prognosis in patients with cerebral infarction; however, the results from some studies on the relationship between SUA and the prognosis of patients with cerebral infarction remain controversial.MethodsWe analyzed the relationship between SUA and clinical prognosis of 585 young Chinese adults with acute ischemic stroke as determined by the modified Rankin Scale at discharge. Using multivariate logistic regression modeling, we explore the relationship between SUA levels and patient's clinical prognosis.ResultsLower SUA levels at time of admission were observed more frequently in the lowest quintile for patients with severe stroke (P = 0.02). Patients with cerebral infarction patients caused by small-vessel blockage had higher SUA concentrations (P = 0.01) and the lower mRS scores (P < 0.01) were observed in, while the lowest SUA concentrations and the highest mRS scores were seen in patients with cardiogenic cerebral infarction patients. Logistic regression analysis adjusted for confounders confirmed the following independent predictors for young cerebral infarction: uric acid (-0.003: 95%CI 0.994 to 0.999) and platelet (0.004, 95%CI 0.993 to 0.996).ConclusionElevated SUA is an independent predictor for good clinical outcome of acute cerebral infarction among young adults.
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