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Functional near-infrared spectroscopy (fNIRS) has been increasingly employed to monitor cerebral hemodynamics in normal and diseased conditions. However, fNIRS suffers from its susceptibility to superficial activity and systemic physiological noise. The objective of the study was to establish a noise reduction method for fNIRS in a whole-head montage.

We have developed an automated denoising method for whole-head fNIRS. A high-density montage consisting of 109 long-separation channels and 8 short-separation channels was used for recording. Auxiliary sensors were also used to measure motion, respiration and pulse simultaneously. find more The method incorporates principal component analysis and general linear model to identify and remove a globally uniform superficial component. Our denoising method was evaluated in experimental data acquired from a group of healthy human subjects during a visually cued motor task and further compared with a minimal preprocessing method and three established denoising methods in the literature. Quantitative metrics including contrast-to-noise ratio, within-subject standard deviation and adjusted coefficient of determination were evaluated.

After denoising, whole-head topography of fNIRS revealed focal activations concurrently in the primary motor and visual areas.

Analysis showed that our method improves upon the four established preprocessing methods in the literature.

An automatic, effective and robust preprocessing pipeline was established for removing physiological noise in whole-head fNIRS recordings. Our method can enable fNIRS as a reliable tool in monitoring large-scale, network-level brain activities for clinical uses.

An automatic, effective and robust preprocessing pipeline was established for removing physiological noise in whole-head fNIRS recordings. Our method can enable fNIRS as a reliable tool in monitoring large-scale, network-level brain activities for clinical uses.

Non-invasive and robust identification of salvageable tissue (penumbra) is crucial for interventional stroke therapy. Besides identifying stroke injury as a whole, the ability to automatically differentiate core and penumbra tissues, using both diffusion and perfusion magnetic resonance imaging (MRI) sequences is essential for ischemic stroke treatment.

A fully automated and novel one-shot multi-view iterative random walker (MIRW) method with an automated injury seed point detection is developed for lesion delineation. MIRW utilizes the heirarchical decomposition of multi-sequence MRI physical properties of the underlying tissue within the lesion to maximize the inter-class variations of the volumetric histogram to estimate the probable seed points. These estimates are further utilized to conglomerate the lesion estimations iteratively from axial, coronal and sagittal MRI volumes for a computationally efficient segmentation and quantification of salvageable and necrotic tissues from multi-sequence MRI.

Comprehensive experimental analysis of MIRW is performed on three challenging adult(sub-)acute ischemic stroke datasets using performance measures like precision, sensitivity, specificity and Dice similarity score (DSC), which are computed with respect to the manual ground-truth.

MIRW method resulted in a high DSC of 83.5% in a very less computational time of 98.23 s/volume, which is a significant improvement on the ISLES benchmark dataset for penumbra detection, compared to the state-of-the-art techniques.

Quantitative measures demonstrate the promising potential of MIRW for computational analysis of adult stroke and quantifying penumbra in stroke patients which is essential for selecting the good candidates for recanalization.

Quantitative measures demonstrate the promising potential of MIRW for computational analysis of adult stroke and quantifying penumbra in stroke patients which is essential for selecting the good candidates for recanalization.Ulinastatin is a broad-spectrum protease inhibitor widely used for the treatment of various inflammation-related diseases owing to its recognized excellent anti-inflammatory and cytoprotective properties. However, whether ulinastatin can relieve postoperative pain remains unclear. In this study, we evaluated the analgesic effects of ulinastatin administered either as a single agent or in combination with sufentanil in a validated preclinical rat model of postoperative pain induced by plantar incision. We found that incisional surgery on the hind paw of these rats induced sustained ipsilateral mechanical pain hypersensitivity that lasted for at least 10 days. A single intraperitoneal (i.p.) injection of ulinastatin prevented the development and reversed the maintenance of incision-induced mechanical pain hypersensitivity in a dose-dependent manner. However, ulinastatin had no effect on the baseline nociceptive threshold. Moreover, repeated i.p. injections of ulinastatin persistently attenuated incision-induced mechanical pain hypersensitivity and promoted recovery from the surgery. The rats did not develop any analgesic tolerance over the course of repeated injections of ulinastatin. A single i.p. injection of ulinastatin was also sufficient to inhibit the initiation and maintenance of incision-induced hyperalgesic priming when the rats were subsequently challenged with an ipsilateral intraplantar prostaglandin E2 injection. Furthermore, the combined administration of ulinastatin and sufentanil significantly enhanced the analgesic effect of sufentanil on postoperative pain, which involved mechanisms other than a direct influence on opioid receptors. These findings demonstrated that ulinastatin had a significant analgesic effect on postoperative pain and might be a novel pharmacotherapeutic agent for managing postoperative pain either alone or as an adjuvant.Parkinson's disease (PD) is the prevalent neurodegenerative disorder characterized by the degeneration of the nigrostriatal neurons. Dynamin-related protein 1 (Drp1) is a key regulator mediating mitochondrial fission and affecting mitophagy in neurons. It has been reported that the inhibition of Drp1 may be beneficial to PD. However, the role of Drp1 and mitophagy in PD remains elusive. Therefore, in this research, we investigated the role of Drp1 and the underlying mechanisms in the mice model of PD. We used the dynasore, a GTPase inhibitor, to inhibit the expression of Drp1. We found that inhibition of Drp1 could ameliorate the motor deficits and the expression of tyrosine hydroxylase in the mice of the PD model. But Drp1 inhibition did not affect mitochondria number and morphological parameters. Moreover, suppression of Drp1 up-regulated the mitochondrial expressions of PINK1 and Parkin while not affected the expressions of NIX and BNIP3. Conclusively, our findings suggest that the inhibition of Drp1 ameliorated the mitochondrial ultrastructure at least via regulating PINK1 and Parkin in the mice of the PD model.