ABSTRACT
Traumatic brain injury (TBI) causes disability and death, accelerating the progression towards Alzheimer’s disease and Parkinson’s disease (PD). TBI causes serious motor and cognitive impairments, as seen in PD that arise during the period of the initial insult. However, this has been understudied relative to TBI induced neuroinflammation, motor and cognitive decline that progress towards PD. Neuronal ubiquitin-C-terminal hydrolase- L1 (UCHL1) is a thiol protease that breaks down ubiquitinated proteins and its level represents the severity of TBI. Previously, we demonstrated the molecular action of glia maturation factor (GMF); a proinflammatory protein in mediating neuroinflammation and neuronal loss. Here, we show that the weight drop method induced TBI neuropathology using behavioral tests, western blotting, and immunofluorescence techniques on sections from wild type (WT) and GMF-deficient (GMF-KO) mice. Results reveal a significant improvement in substantia nigral tyrosine hydroxylase and dopamine transporter expression with motor behavioral performance in GMF-KO mice following TBI. In addition, a significant reduction in neuroinflammation was manifested, as shown by activation of nuclear factor-kB, reduced levels of inducible nitric oxide synthase, and cyclooxygenase- 2 expressions. Likewise, neurotrophins including brain-derived neurotrophic factor and glial-derived neurotrophic factor were significantly improved in GMF-KO mice than WT 72 h post-TBI. Consistently, we found that TBI enhances GFAP and UCHL-1 expression and reduces the number of dopaminergic TH-positive neurons in WT compared to GMF-KO mice 72 h post-TBI. Interestingly, we observed a reduction of THpositive tanycytes in the median eminence of WT than GMF-KO mice. Overall, we found that absence of GMF significantly reversed these neuropathological events and improved behavioral outcome. This study provides evidence that PD-associated pathology progression can be initiated upon induction of TBI.
ABSTRACT
To evaluate the diagnostic yield of CT guided percutaneous cutting needle biopsy [CNB] of lung lesions. Our study was a descriptive study including 63 patients who underwent CT guided percutaneous core needle [cutting needle] biopsy of lung lesions. Of the total sampling, only 53 cases were followed up. Samples taken were preserved in formalin bottle and sent for histopathology. CT scan at the level of the biopsy was taken immediately after the procedure when patient was still on CT table. X-ray chest in erect position was taken after 04 hours to look for development of pneumothorax. Hemoptysis and pneumothorax were recorded. Other complications were also noted. Out of these 53 cases, histopathology showed 32 [60.4%] cases to be malignant, 17 [32.1%] cases benign and 4 [7.5%] cases being non-representative. The histological diagnostic yield [number of correct diagnosis obtained at CNB/number of definitive diagnosis] of this procedure was found to be 92.45% [49/53]. Pneumothorax occurred in 1 out 53 [1.9%] and hemoptysis in 4 of 53 [7.45%]. There was no major complication like hemodynamic instability or death. CT guided percutaneous CNB of the lung lesions is an accurate procedure for a specific histological diagnosis and has a low rate of complications