Evolving concepts in intracranial pressure monitoring - from traditional monitoring to precision medicine.

A wide range of acute brain injuries, including both traumatic and non-traumatic causes, can result in elevated intracranial pressure (ICP), which in turn can cause further secondary injury to the brain, initiating a vicious cascade of propagating injury. Elevated ICP is therefore a neurological injury that requires intensive monitoring and time-sensitive interventions. Patients at high risk for developing elevated ICP undergo placement of invasive ICP monitors including external ventricular drains, intraparenchymal ICP monitors, and lumbar drains.

Neuromonitoring in the ICU - what, how and why?

Purpose Of Review: We selectively review emerging noninvasive neuromonitoring techniques and the evidence that supports their use in the ICU setting. The focus is on neuromonitoring research in patients with acute brain injury.

Recent Findings: Noninvasive intracranial pressure evaluation with optic nerve sheath diameter measurements, transcranial Doppler waveform analysis, or skull mechanical extensometer waveform recordings have potential safety and resource-intensity advantages when compared to standard invasive monitors, however each of these techniques has limitations.

Coagulopathy in Isolated Traumatic Brain Injury: Myth or Reality.

Introduction: Traumatic Brain Injury (TBI) has been shown to be associated with altered hemostasis and coagulopathy, that correlates with worsening secondary injury and clinical outcomes. Isolated Traumatic Brain Injury (iTBI), that is TBI without significant extracranial injuries, has also been shown to be associated with systemic coagulopathy and derangements in hemostasis.

Methods: Literature Review.

Picking the optimal target for antibody-drug conjugates.

Antibody-drug conjugates (ADCs) combine the cytotoxic potential of chemotherapeutic drugs with the specificity of monoclonal antibodies (mAbs). After many years of unfulfilled promise, the field of ADCs is experiencing resurgence as more is learned about each of the components of an ADC and how these components need to be combined to produce a successful therapeutic agent. Choosing an appropriate target for ADCs is a critical parameter that effects the efficacy, therapeutic window, and toxicity profile of ADCs.

Neuroprotective drug riluzole amplifies the heat shock factor 1 (HSF1)- and glutamate transporter 1 (GLT1)-dependent cytoprotective mechanisms for neuronal survival.

Heat shock factor 1 (HSF1) mediates the cellular response to stress to increase the production of heat shock protein (HSP) chaperones for proper protein folding, trafficking, and degradation; failure of this homeostatic mechanism likely contributes to neurodegeneration. We show that the neuroprotective drug riluzole increased the amount of HSF1 in NG108-15 neuroprogenitor cells by slowing the specific turnover of HSF1 and supporting a more robust and sustained activation of HSF1. Using Hsp70-luciferase as a functional readout of the activity of HSF1, we show that riluzole amplified the heat shock induction of the reporter gene with an optimal increase at 1 μM.