Combination therapy of long-term tumor treating fields with temozolomide and bevacizumab prolongs survival in multifocal glioblastoma diagnosed patient: a case report

The multifocal glioblastomas (GBM) are tumors with multiple discrete areas of contrast enhancing tumors which have considerably poorer prognosis than solitary GBM. Median overall survival of diagnosed patients almost twice as less than solitary presentation. We present a case report of multifocal GBM. A 72-year old right-handed male was evaluated at the Neuro-Oncology Clinic of Baylor Scott and White Hospital (Central Division). Patient presented at this hospital because of persistent progressive headaches, confusion, and an incident of fall. Physical evaluation revealed neurological impairments. Brain magnetic resonance imaging (MRI) revealed heterogeneous contrast enhancing lesions with associated vasogenic oedema. Patient underwent a stereotactic biopsy analysis of the larger lesion and pathology evaluation concluded an isocitrate dehydrogenase 1 and 2 wild type GBM with unmethylated O-6-methylguanine- DNA methyltransferase. Treatment remedies: Patient received 4 weeks concurrent radiation therapy along with combination of temozolomide at dose of 75 mg/m^2 followed adjuvant temozolomide for 10 cycles with bevacizumab at 10 mg/kg every 2 weeks and Optune treatment. Post treatment evaluation: Repeat MRIs showed near complete resolution of the tumors at 26 months of treatment along with improvement of neurological status. Conclusion: Due to limitations of surgical manipulations in multifocal GBM diagnosed patients, combinational chemo and radiation therapy is the treatment of choice for most cases. Using additional novel treatment with non-invasive therapeutic device proven to be effective is another excellent approach to the established practice. Therefore, combination therapy of Optune plus temozolomide and bevacizumab might be a promising remedy for newly diagnosed multifocal glioblastomas.

小胶质细胞在卒中中的作用

小胶质细胞在缺血后的炎症反应和受损组织的清除中扮演关键角色,它们对缺血引起的干扰反应迅速,致力于恢复失去的稳态。然而,被修改的环境,包括离子失衡、关键的神经元-小胶质细胞相互作用的中断、去极化传播以及来自坏死神经元的危险信号的产生,诱导了小胶质细胞的形态和表型转变。这导致它们表现为促炎表型并增加吞噬活动。从缺血后的第3天开始,巨噬细胞渗透到坏死组织核心,而小胶质细胞则在病灶周边聚集。此外,炎症促使代谢转向有利于糖酵解、戊糖磷酸途径和脂质合成。这些转变与吞噬脂质的摄入相结合,促进了脂滴生成、合成代谢,并使小胶质细胞增殖。增殖的小胶质细胞释放营养因子,有助于神经保护和修复。然而,一些小胶质细胞持续积累脂质,并转变为功能失调且可能有害的泡沫细胞。研究还表明,有些小胶质细胞要么清除凋亡细胞能力的受损,要么消除突触、活神经元或内皮细胞。然而,阐明被吞噬细胞的生存能力、局部环境特征、组织损伤程度和时间序列将是至关重要的。缺血为小胶质细胞提供了丰富多样的、依赖于区域和损伤的刺激,随着时间演变导致出现不同的小胶质细胞表型,包括表现为促炎性或功能失调特征的细胞,以及显示出促进修复功能的细胞。准确分析小胶质细胞表型,以及更精确地了解相关的缺血后组织条件,是对卒中进行针对性干预的必要步骤。

Are mitochondria the key to reduce the age-dependent decline in axon growth after spinal cord injury?

Spinal cord injury(SCI) is a debilitating condition resulting in varying degrees of functional impairment and exhibits only limited repair.Currently there is no cure for SCI, and no proven treatment to promote restoration of function.