Doublecortin-immunoreactive (DCX+) cells were detected across the allo- and neo-cortical regions in the adult guinea pig cerebrum, localized to layer II specifically at its border with layer I. The density of labeled cells declined with age, whereas no apparent apoptotic activity was detectable over the cortex including layer II. DCX+ cells varied in somal size, labeling intensity, nuclear appearance, and complexity of processes. These cells were often arranged in clusters with cells of similar morphology sometimes packed tightly together. They exhibited complete colocalization with polysialylated neural cell adhesion molecule (PSA-NCAM) and neuron-specific type III beta-tubulin (TuJ1). Medium to large-sized DCX+ cells had well-developed neuritic processes, and expressed neuron-specific nuclear protein (NeuN). Large mature-looking cells with weak DCX reactivity invariably displayed heavy NeuN reactivity, implicating a transitional stage of these labeled cells. These "transitional" cells also consistently exhibited weak reactivity for gamma-aminobutyric acid (GABA), glutamate decarboxylase (GAD67), beta-nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) and neuronal nitric oxide synthase (nNOS), suggestive of them being young GABAergic/nitrinergic interneurons. Our data indicate that DCX+ cells exist widely in the adult guinea pig cerebral cortex, with a predominant localization in upper layer II. The morphological variation and differential expression of neuronal markers in these cells implicate that they might be developing neurons, and that they are probably differentiating into GABAergic interneurons. This population of cells might be involved in interneuron plasticity in the adult mammalian cerebral cortex.

DCX-immunoreactive (DCX+) cells occur in the piriform cortex in adult mice and rats, but also in the neocortex in adult guinea pigs and rabbits. Here we describe these cells in adult domestic cats and primates. In cats and rhesus monkeys, DCX+ cells existed across the allo- and neocortex, with an overall ventrodorsal high to low gradient at a given frontal plane. Labeled cells formed a cellular band in layers II and upper III, exhibiting dramatic differences in somal size (5–20 μm), shape (unipolar, bipolar, multipolar and irregular), neuritic complexity and labeling intensity. Cell clusters were also seen in this band, and those in the entorhinal cortex extended into deeper layers as chain-like structures. Densitometry revealed a parallel decline of the cells across regions with age in cats. Besides the cellular band, medium-sized cells with weak DCX reactivity resided sparsely in other layers. Throughout the cortex, virtually all DCX+ cells co-expressed polysialylated neural cell adhesion molecule. Medium to large mature-looking DCX+ cells frequently colocalized with neuron-specific nuclear protein and γ-aminobutyric acid (GABA), and those with a reduced DCX expression also partially co-labeled for glutamic acid decarboxylase, parvalbumin, calbindin, β-nicotinamide adenine dinucleotide phosphate diaphorase and neuronal nitric oxide synthase. Similar to cats and monkeys, small and larger DCX+ cells were detected in surgically removed human frontal and temporal cortices. These data suggest that immature neurons persist into adulthood in many cortical areas in cats and primates, and that these cells appear to undergo development and differentiation to become functional subgroups of GABAergic interneurons.

No abstract

(Cardiol J 2014; 21, 1: 89-95)

AIm:We present the long-term outcomes as well as their correlation with tumor size in 127 consecutive patients harboring large MSWM after microsurgical treatment. mATeRIAL and meTHods:The retrospective analysis of clinical data and follow-up data of 127 microsurgical treated patients with MSWM was performed. The mean maximum diameter of tumors was 5.2cm (ranged 1.5-10.0cm).ResuLTs: 104 cases (81.9%) achieved gross total resection. There was no operative mortality. Detailed follow-up data was available in 120 cases for a mean duration of 81.6 months (12-216 months). The permanent morbidity was 14.2%. The mean KPS score 1 year after surgery was 90.6 (ranged 60-100). Among 74 patients of preoperative visual acuity (VA) impairment, postoperative VA improved in 42 cases (56.8%), unchanged in 30 (40.5%), and deteriorated in 2 (2.7%). MR images revealed tumor recurrence after total resection in 10 cases (10.2%) and tumor progression after subtotal resection in 10 cases (45.5%).CoNCLusIoN: Tumor recurrence was the major risk in the long run, thus the initial surgery was extremely important and hence should be aggressive. The size of tumor affected the extent of tumor removal determining clinical outcomes including VA improvement and KPS score immediately after surgery; however, it was not correlated with long-term overall outcomes. BuLGuLAR: 104 olguda (%81,9) gros total rezeksiyon yapıldı. Operatif mortalite yoktu. Ayrıntılı takip verileri 120 olguda ortalama 81,6 ay (12-216 ay) için mevcuttu. Kalıcı morbidite %14,2 oranında görüldü. Cerrahiden 1 yıl sonra ortalama KPS skoru 90,6 (aralık 60-100) bulundu. Preoperatif görme keskinliği bozukluğu olan 74 hasta içinde postoperatif dönemde görme keskinliği 42 hastada (%56,8) arttı, 30'unda (%40,5) değişmedi ve 2'sinde (%2,7) kötüye gitti. MR görüntüleri total rezeksiyon sonrasında 10 olguda (%10,2) tümör reküransı ve subtotal rezeksiyon sonrasında 10 olguda (%45,5) tümör ilerlemesi gösterdi. soNuÇ: Uzun dönemde temel risk tümör reküransıydı ve bu nedenle ilk cerrahi çok önemlidir ve agresif olmalıdır. Tümör büyüklüğü, tümör çıkarma kapsamını etkileyerek ameliyattan hemen sonra görme keskinliği düzelmesi ve KPS skoru dahil klinik sonuçları etkiledi ancak uzun dönemli genel sonuçlarla korelasyon göstermedi.ANAHTAR sÖZCÜKLeR: Medial sfenoid kanat menenjiyomları, Tümör büyüklüğü, Tümör reküransı, İşlevsel sonuç

Prototype foamy virus encodes a transactivator called Bel1 that enhances viral gene transcription and is essential for PFV replication. Nuclear localization of Bel1 has been reported to rely on two proximal basic motifs R(199)H(200) and R(221)R(222)R(223) that likely function together as a bipartite nuclear localization signal. In this study, we report that mutating R(221)R(222)R(223), but not R(199)H(200), relocates Bel1 from the nucleus to the cytoplasm, suggesting an essential role for R(221)R(222)R(223) in the nuclear localization of Bel1. Although not affecting the nuclear localization of Bel1, mutating R(199)H(200) disables Bel1 from transactivating PFV promoters. Results of EMSA reveal that the R(199)H(200) residues are vital for the binding of Bel1 to viral promoter DNA. Moreover, mutating R(199)H(200) in Bel1 impairs PFV replication to a much greater extent than mutating R(221)R(222)R(223). Collectively, our findings suggest that R(199)H(200) directly participate in Bel1 binding to viral promoter DNA and are indispensible for Bel1 transactivation activity.

The rate of UGIB incidence was higher than the estimated rate in neurocritical care patients in China, suggesting the need for better management and treatment for stress-related mucosal disease in China. History of UGIB, mechanical ventilation and/or anticoagulants significantly affected UGIB. ClinicalTrials registry number: NCT02316990.

Background. Previous studies showed that a decline in BP can reverse pressure-overloaded left ventricular hypertrophy in the long term. Whether this structural remodeling and improved cardiac function were due to reduced BP levels or sympathetic tone is unclear. The aim of this study was to evaluate the efficacy of renal denervation (RDN) on cardiac function and left ventricular hypertrophy in patients diagnosed with resistant hypertension with systolic and diastolic dysfunction. Methods. Thirteen patients diagnosed with resistant hypertension underwent bilateral RDN (RDN group), and 13 patients were selected as the control group (drug group) who received regular antihypertensive drugs for the first time. Demographic analysis and hematologic tests were performed to determine renal function as well as BNP levels. Echocardiogram was performed at baseline and 12 months after RDN. Results. All the baseline characteristics are comparable in two groups. Both RDN and drug regiments resulted in significant reduction from baseline in SBP/DBP at 12-month follow-up (all P values < 0.01), and the decline due to two interventions showed no statistically significant difference ( F = 1.64 , P = 0.213 and F = 0.124 , P = 0.853 for SBP and DBP, respectively). RDN significantly reduced mean LV mass index (LVMI) from 151.43 ± 46.91  g/m2 to 136.02 ± 37.76  g/m2 ( P = 0.038 ) and ejection fraction (LVEF) increased from 57.15 ± 5.49 % at baseline to 59.54 ± 4.18 % at 12 months ( P = 0.039 ). No similar changes were detected in the drug group ( P values, 0.90 for EF and 0.38 for LVMI). Renal parameters including BUN, Cr, UA, and eGFR at baseline, 3 months, and 12 months showed no marked difference ( P = 0.497 , 0.223 , 0.862 , 0.075 , respectively). Conclusions. Our findings show that in addition to hypertension and its progression, elevated sympathetic hyperactivity is related to left ventricular hypertrophy and cardiac function.