Tumor or Hematoma?: An Unusual Case of an Extradural Lesion of the Lumbar Spine

Purpose: Spinal epidural hematoma is a rare clinical entity. We present a case of atypical contrast enhancement pattern in a chronic epidural hematoma of the lumbar spine mimicking an extradural tumor. Case Report: A 76-year-old man on treatment with oral anticoagulants presented with a 1-month history of lower back pain radiating into his right upper thigh accompanied by spinal claudication. Preoperative MRI showed a posterior epidural lesion compressing the cauda equina with almost homogeneous contrast enhancement. Surgery was performed under the presumptive diagnosis of spinal extradural neoplasm. Intraoperative and histological findings were consistent with a chronic spinal epidural hematoma. Postoperatively, the patient had instant relief of his symptoms. Conclusion: Chronic spinal epidural hematoma may resemble an extradural tumor, requiring surgery for histological confirmation and decompressio

The mechanical and electronic properties of spinel oxides VX2O4 (X = Mn and Fe) by first principle calculations

We have performed first-principles density functional theory calculations within generalized-gradient approximation to obtain the mechanical properties and the electronic behavior of Vanadium based Spinel Oxides VX2O4 (X=Mn and Fe) which conform Fm-3m space group with 225 space number and are promising good candidates for spintronic applications due to their half-metallic band gaps (Eg=1.71 eV for VFe2O4 and Eg = 0.53 eV for VMn2O4) in the plotted spin-polarized electronic band structure. Also, the calculated negative formation enthalpies indicate that these materials have thermodynamic stability and structural synthesizability. Additionally, the calculated elastic constants by using stress-strain approach indicate mechanical stability of above-mentioned materials. © 2019 Author(s)

Structural and lattice dynamical properties of Zintl NaIn and NaTl compounds

The first-principles calculations based on the density-functional theory have been performed using both the generalized-gradient approximation (GGA) and the local-density approximation (LDA) to investigate many physical properties of NaIn and NaTl compounds. Specifically, the structural (lattice constant, bulk modulus, pressure derivative of bulk modulus, phase transition pressure (P-t)), mechanical (second-order elastic constants (C-ij), Young's modulus, isotropic shear modulus, Zener anisotropy factor, Poisson's ratio, sound velocities), thermo dynamical (cohesive energy, formation enthalpy, Debye temperature), and the vibrational properties (phonon dispersion curves and one-phonon density of states) are calculated and compared with the available experimental and other theoretical data. Also, we have presented the temperature variations of various thermo dynamical properties such as free energy, internal energy, entropy and heat capacity for the same compounds. (C) 2010 Elsevier B.V. All rights reserved

Ultrastructural changes in the circumventricular organs after experimental subarachnoid hemorrhage

Objectives: Circumventricular organs (CVOs) are fine, periventricular, neurotransmitter-rich structures that are devoid of a Blood-brain barrier and are known for their secretory role controlling fluid and electrolyte balance, thirst and even reproduction. Common pathologies of the brain such as trauma or bleeding affect CVOs, and hence their function. However, at what stage of these disease processes are CVOs affected and the time sequence of their recovery is still not clear. The aim of this study was to detect the morphological changes in CVOs using electron microscopy after experimental subarachnoid hemorrhage (SAH). Methods: Experimental SAH was induced by transclival puncture of the basilar artery. Both scanning and transmission electron microscopic examination of the representive sections from each CVO was undertaken. Results: Electron microscopy has shown that after SAH, the cells that form the CVOs exhibit signs of cellular necrosis with margination of the nucleus as well as cytoplasmic, mitochondrial and axonal edema. The subfornicial organ and organum vasculosum lamina terminalis appear to be more vulnerable to the effects of SAH than the median eminence or area postrema. Discussion: Considering the fact that the experimental SAH model we have used is very similar to the momentary rupture of an aneurysm with secondary reflex spasm to seal the hole, it will not be unrealistic to consider that similar effects may also take place in the clinical setting. © 2005 W. S. Maney & Son Ltd

Novel CCM1, CCM2, and CCM3 mutations in patients with cerebral cavernous malformations: in-frame deletion in CCM2 prevents formation of a CCM1/CCM2/CCM3 protein complex

Cerebral cavernous malformations (CCM) are prevalent cerebrovascular lesions predisposing to chronic headaches, epilepsy, and hemorrhagic stroke. Using a combination of direct sequencing and MLPA analyses, we identified 15 novel and eight previously published CCM1 (KRIT1), CCM2, and CCM3 (PDCD10) mutations. The mutation detection rate was >90% for familial cases and >60% for isolated cases with multiple malformations. Splice site mutations constituted almost 20% of all CCM mutations identified. One of these proved to be a de novo mutation of the most 3' acceptor splice site of the CCM1 gene resulting in retention of intron 19. A further mutation affected the 3' splice site of CCM2 intron 2 leading to cryptic splice site utilization in both CCM2 and its transcript variant lacking exon 2. With the exception of one in-frame deletion of CCM2 exon 2, which corresponds to the naturally occurring splice variant of CCM2 on the RNA level and is predicted to result in the omission of 58 amino acids (CCM2:p.P11_K68del), all mutations lead to the introduction of premature stop codons. To gain insight into the likely mechanisms underlying the only known CCM2 in-frame deletion, we analyzed the functional consequences of loss of CCM2 exon 2. The CCM2:p.P11_K68del protein could be expressed in cell culture and complexed with CCM3. However, its ability to interact with CCM1 and to form a CCM1/CCM2/CCM3 complex was lost. These data are in agreement with a loss-of-function mechanism for CCM mutations, uncover an N-terminal CCM2 domain required for CCM1 binding, and demonstrate full-length CCM2 as the essential core protein in the CCM1/CCM2/CCM3 complex