Biomarkers for traumatic brain injury: a short review

Neurosurgical Review - Cellular response to TBI is a mixture of excitotoxicity, neuroinflammation, and cell death. Biomarkers that can track these lesions and inflammatory processes are being...     

Quantification of Pulmonary Inflammatory Processes Using Chest Radiography: Tuberculosis as the Motivating Application

The purpose of this work was to develop a quantitative method for evaluating the pulmonary inflammatory process (PIP) through the computational analysis of chest radiography exams in posteroanterior (PA) and lateral views. The quantification procedure was applied to patients with tuberculosis (TB) as the motivating application.A study of high-resolution computed tomography (HRCT) examinations of patients with TB was developed to establish a relation between the inflammatory process and the signal difference-to-noise ratio (SDNR) measured in the PA projection. A phantom essay was used to validate this relation, which was implemented using an algorithm that is able to estimate the volume of the inflammatory region based solely on SDNR values in the chest radiographs of patients.The PIP volumes that were quantified for 30 patients with TB were used for comparisons with direct HRCT analysis for the same patient. The Bland–Altman statistical analyses showed no significant differences between the 2 quantification methods. The linear regression line had a correlation coefficient of R² = 0.97 and P < 0.001, showing a strong association between the volume that was determined by our evaluation method and the results obtained by direct HRCT scan analysis.Since the diagnosis and follow-up of patients with TB is commonly performed using X-rays exams, the method developed herein can be considered an adequate tool for quantifying the PIP with a lower patient radiation dose and lower institutional cost. Although we used patients with TB for the application of the method, this method may be used for other pulmonary diseases characterized by a PIP.     

Nicotine smoking concentrations modulate GABAergic synaptic transmission in murine medial prefrontal cortex by activation of α7* and β2* nicotinic receptors

Nicotine is the major addictive component of cigarettes, reaching a brain concentration of ~300 nM during smoking of a single cigarette. The prefrontal cortex (PFC) mechanisms underlying temporary changes of working memory during smoking are incompletely understood. Here, we investigated whether 300 nM nicotine modulates γ‐aminobutyric acid (GABA) ergic synaptic transmission from pyramidal neurons of the output layer (V) of the murine medial PFC. We used patch clamp in vitro recording from C57BL/6 mice in the whole‐cell configuration to investigate the effect of nicotine on pharmacologically isolated GABAergic postsynaptic currents (IPSCs) in the absence or presence of methyllycaconitine (MLA) or dihydro‐β‐erythroidine (DHβE), selective antagonists of α7‐ and β2‐containing (α7* and β2*) nicotinic acetylcholine receptors (AChRs), respectively. Our results indicated that nicotine, alone or in the presence of MLA, decreases electrically evoked IPSC (eIPSC) amplitude, whereas in the presence of DHβE, nicotine elicited either an eIPSCs amplitude increase or a decrease. In the presence of DHβE, nicotine increased membrane conductance leaving the paired pulse ratio unchanged in all conditions, suggesting a non‐β2* mediated effect. In the presence of MLA, nicotine decreased the mean spontaneous IPSC (sIPSC) frequency but increased their rise time, suggesting a non‐α7* AChR‐mediated synaptic modulation. Also, in the presence of DHβE, nicotine decreased both eIPSC rise and decay times. No receptors other than α7* and β2* appear to be involved in the nicotine effect. Our results indicate that nicotine smoking concentrations modulate GABAergic synaptic currents through mixed pre‐ and post‐synaptic mechanisms by activation of α7* and β2* AChRs.