AMPA receptors and seizures mediate hippocampal radial glia-like stem cell proliferation.

Neurogenesis is sustained throughout life in the mammalian brain, supporting hippocampus-dependent learning and memory. Its permanent alteration by status epilepticus (SE) is associated with learning and cognitive impairments. The mechanisms underlying the initiation of altered neurogenesis after SE are not understood. Glial fibrillary acidic protein-positive radial glia (RG)-like cells proliferate early after SE, but their proliferation dynamics and signaling are largely unclear. We have previously reported a polarized distribution of AMPA receptors (AMPARs) on RG-like cells in vivo and postulated that these may signal their proliferation. Here, we examined the acute effects of kainate on hippocampal precursor cells in vitro and in kainate-induced SE on proliferating and quiescent clones of 5-bromo-2-deoxyuridine prelabeled hippocampal precursors in vivo. In vitro, we found that 5 μM kainate shortened the cell cycle time of RG-like cells via AMPAR activation and accelerated cell cycle re-entry of their progeny. It also shifted their fate choice expanding the population of RG-like cells and reducing the population of downstream amplifying neural progenitors. Kainate enhanced the survival of all precursor cell subtypes. Pharmacologically, kainate's proliferative and survival effects were abolished by AMPAR blockade. Functional AMPAR expression was confirmed on RG-like cells in vitro. In agreement with these observations, kainate/seizures enhanced the proliferation and expansion predominantly of constitutively cycling RG-like cell clones in vivo. Our results identify AMPARs as key potential players in initiating the proliferation of dentate RG-like cells and unravel a possible receptor target for modifying the radial glia-like cell response to SE

Resolving solitary osteolytic lumbar tuberculosis in young adult.

Lumbar vertebral tuberculosis presenting with a focal solitary osteolytic lesion is rare in spinal tuberculosis (TB) and the English literature describing this entity is scant. The differential diagnosis includes primary and secondary malignancies. In this report, we describe a case of 35-year-old woman who presented with low back pain and was found to have a focal L4 vertebral lytic lesion on MRI and CT. Whole body CT was carried out as a potential malignancy staging procedure and demonstrated lung lesions suggestive of TB. Her neurological and general examination were entirely normal. Her blood test was positive for QuantiFERON Gold. She was managed conservatively with anti-TB medications and serial imaging which showed evidence of resolution of the osteolytic lesion. Although it is unusual for TB to present as an isolated osteolytic vertebral body lesion, the possibility should always be considered in the differential diagnosis, along with neoplastic processes. Conservative medical management, in the absence of neurological deficits and deformity, is the main stay of management with a very good outlook

Malignant middle cerebral artery infarction following subacute subdural hematoma: A case report and literature review

Background: Subacute subdural hematomas (ASDH) are only treated surgically when they cause mass effect significant enough to give symptoms. Rarely, sub-ASDH may cause enough pressure to result in a malignant middle cerebral artery (MCA) territory infarction. Decompressive craniectomy (DC) is the last resort to reduce intracranial pressure following malignant MCA infarction. Herein, we review the literature and describe a case of MCA/posterior cerebral artery (PCA) territories infarction following drainage of a sub-ASDH that was treated with DC with good outcome. Case Description: We report a case of malignant right-sided MCA/PCA infarction in a 62-year-old man who presented with progressive headache following a cycling incident leading to a head injury. Initial CT head demonstrated a small right ASDH. He had no neurological deficit, headache settled on analgesia, and there was no expansion of the SDH on the repeat CT; therefore, he was managed conservatively. He was admitted 6-days later with worsening headaches and hyponatremia. Repeat CT revealed an increase in size of the hematoma and mass effect leading to a mini-craniotomy and evacuation of hematoma. He developed left-sided hemiplegia, slurred speech and hyponatremia, and CT head demonstrated a right-sided MCA/PCA infarction with significant mass effect. He underwent emergent DC and subsequent cranioplasty and ultimately recovered to mRS of 2. Conclusion: SDH are frequent neurosurgical entities. Malignant MCA/PCA strokes following mini-craniotomies are rare but need to be considered especially during the consent process

Eosinophilic Granuloma of the Skull Presenting as Non-Traumatic Extradural Haematoma in Children.

Cranial extradural haematoma (EDH) is a neurosurgical emergency that can be caused by traumatic or non-traumatic causes with the former being more prevalent. Non-traumatic causes are variable and can include infection, vascular malformation and haematological disorders. This paper will address an extremely rare non-traumatic cause of EDH. More specifically, eosinophilic granuloma (EG), the localized form of Langerhans histiocytosis, may involve the skull and has rarely been reported to present with EDH. The case that will be presented is that of a three-year-old male patient, who presented with progressive vomiting and drowsiness, associated with left parietal swelling. CT scan of the brain showed an extradural haematoma and an osteolytic parietal lesion. He underwent emergent craniectomy, evacuation of the haematoma and dura resection as the lesion was infiltrating the dura. Histopathological examination of the dura and the bone edges showed eosinophilic granuloma (EG). The mechanism of a haemorrhage in this situation is poorly understood and the literature is extremely scarce. In conducting a thorough literature review, only 11 case reports of EG causing non-traumatic EDH were found. The details of these 11 cases will be reviewed and discussed in this paper, in addition to our illustrative case

DETECTING GENETIC DIVERSITY AMONG BARLEY LANDRACES GROWN IN THE WEST-BANK, PALESTINE IN 2010-2011

ABSTRACT Fifteen barley landraces were collected from different localities in the West-Bank,-Palestine during 2009. A field experiment was conducted at the Faculty of Agriculture-An Najah National University to evaluate several agronomical traits of these landraces in 2010-2011 growing season. Cluster analysis was performed using the complete-linkage method, genotypic coefficient of variation (GCV), phenotypic coefficient of variation (PCV), broad sense heritability (H 2 ), and genetic advance (GA) were calculated for the quantitative traits. Significant diversity was exhibited among the landraces regarding days to 90% heading, 100-grain weight, number of grains per spike, spike length, and awns length. The Cluster analysis showed high genetic diversity among the collected landraces with dissimilarity ranging from 0.26 to 0.75. The fifteen landraces were grouped into four clusters. Genotypic coefficient of variation ranged from 6.1 to 22.9, whereas phenotypic coefficient of variation ranged from 6.6 to 41.8 with maximum phenotypic and genotypic variability observed for number of fertile tellers, number of grains per spike and spike length. Moderate to high heritability (broad sense) estimates (70-87%) were found for most of the characters. The genetic advance was highest for number of grains per spike (39.4%), followed by spike length (37.2%). High positive significant correlations were found among the different studied traits with correlation coefficient ranging from 0.395 to 0.536. The results of this study indicated high genetic diversity among barley landraces in Palestine, which make them potential sources for selection and hybridization programmes

Vascular Collagen Type-IV in Hypertension and Cerebral Small Vessel Disease.

BACKGROUND: Cerebral small vessel disease (SVD) is common in older people and causes lacunar stroke and vascular cognitive impairment. Risk factors include old age, hypertension and variants in the genes COL4A1/COL4A2 encoding collagen alpha-1(IV) and alpha-2(IV), here termed collagen-IV, which are core components of the basement membrane. We tested the hypothesis that increased vascular collagen-IV associates with clinical hypertension and with SVD in older persons and with chronic hypertension in young and aged primates and genetically hypertensive rats. METHODS: We quantified vascular collagen-IV immunolabeling in small arteries in a cohort of older persons with minimal Alzheimer's pathology (N=52; 21F/31M, age 82.8±6.95 years). We also studied archive tissue from young (age range 6.2-8.3 years) and older (17.0-22.7 years) primates (M mulatta) and compared chronically hypertensive animals (18 months aortic stenosis) with normotensives. We also compared genetically hypertensive and normotensive rats (aged 10-12 months). RESULTS: Collagen-IV immunolabeling in cerebral small arteries of older persons was negatively associated with radiological SVD severity (ρ: -0.427, P=0.005) but was not related to history of hypertension. General linear models confirmed the negative association of lower collagen-IV with radiological SVD (P<0.017), including age as a covariate and either clinical hypertension (P<0.030) or neuropathological SVD diagnosis (P<0.022) as fixed factors. Reduced vascular collagen-IV was accompanied by accumulation of fibrillar collagens (types I and III) as indicated by immunogold electron microscopy. In young and aged primates, brain collagen-IV was elevated in older normotensive relative to young normotensive animals (P=0.029) but was not associated with hypertension. Genetically hypertensive rats did not differ from normotensive rats in terms of arterial collagen-IV. CONCLUSIONS: Our cross-species data provide novel insight into sporadic SVD pathogenesis, supporting insufficient (rather than excessive) arterial collagen-IV in SVD, accompanied by matrix remodeling with elevated fibrillar collagen deposition. They also indicate that hypertension, a major risk factor for SVD, does not act by causing accumulation of brain vascular collagen-IV

Characterisation of barley resistance to rhynchosporium on chromosome 6HS

Key Message: Major resistance gene to rhynchosporium, Rrs18, maps close to the telomere on the short arm of chromosome 6H in barley. Rhynchosporium or barley scald caused by a fungal pathogen Rhynchosporium commune is one of the most destructive and economically important diseases of barley in the world. Testing of Steptoe × Morex and CIho 3515 × Alexis doubled haploid populations has revealed a large effect QTL for resistance to R. commune close to the telomere on the short arm of chromosome 6H, present in both populations. Mapping markers flanking the QTL from both populations onto the 2017 Morex genome assembly revealed a rhynchosporium resistance locus independent of Rrs13 that we named Rrs18. The causal gene was fine mapped to an interval of 660 Kb using Steptoe × Morex backcross 1 S₂ and S₃ lines with molecular markers developed from Steptoe exome capture variant calling. Sequencing RNA from CIho 3515 and Alexis revealed that only 4 genes within the Rrs18 interval were transcribed in leaf tissue with a serine/threonine protein kinase being the most likely candidate for Rrs18.Max Coulter, Bianca Büttner, Kerstin Hofmann, Micha Bayer, Luke Ramsay, Günther Schweizer, Robbie Waugh, Mark E. Looseley, Anna Avrov

Vascular collagen type-IV in hypertension and cerebral small vessel disease

Cerebral small vessel disease (SVD) is common in older people and causes lacunar stroke and vascular cognitive impairment. Risk factors include old age, hypertension and variants in the genes encoding collagen alpha-1(IV) and alpha-2(IV), here termed collagen-IV, which are core components of the basement membrane. We tested the hypothesis that increased vascular collagen-IV associates with clinical hypertension and with SVD in older persons and with chronic hypertension in young and aged primates and genetically hypertensive rats. We quantified vascular collagen-IV immunolabeling in small arteries in a cohort of older persons with minimal Alzheimer's pathology (N=52; 21F/31M, age 82.8±6.95 years). We also studied archive tissue from young (age range 6.2-8.3 years) and older (17.0-22.7 years) primates ( ) and compared chronically hypertensive animals (18 months aortic stenosis) with normotensives. We also compared genetically hypertensive and normotensive rats (aged 10-12 months). Collagen-IV immunolabeling in cerebral small arteries of older persons was negatively associated with radiological SVD severity (ρ: -0.427, =0.005) but was not related to history of hypertension. General linear models confirmed the negative association of lower collagen-IV with radiological SVD ( &lt;0.017), including age as a covariate and either clinical hypertension ( &lt;0.030) or neuropathological SVD diagnosis ( &lt;0.022) as fixed factors. Reduced vascular collagen-IV was accompanied by accumulation of fibrillar collagens (types I and III) as indicated by immunogold electron microscopy. In young and aged primates, brain collagen-IV was elevated in older normotensive relative to young normotensive animals ( =0.029) but was not associated with hypertension. Genetically hypertensive rats did not differ from normotensive rats in terms of arterial collagen-IV. Our cross-species data provide novel insight into sporadic SVD pathogenesis, supporting insufficient (rather than excessive) arterial collagen-IV in SVD, accompanied by matrix remodeling with elevated fibrillar collagen deposition. They also indicate that hypertension, a major risk factor for SVD, does not act by causing accumulation of brain vascular collagen-IV