Neuroimaging through Sonolucent Cranioplasty: A Systematic Scoping Review Protocol

Cranioplasty is a neurosurgical procedure in which the skull bone is repaired after craniectomy. Recently, studies have suggested that sonolucent synthetic materials are safe and useful for cranioplasty. Sonolucent cranioplasty (SC) implants provide unprecedented opportunity in adult neurosurgery to monitor neuroanatomy, assess hemodynamics, view devices located within the implant, and conduct focused ultrasound treatments. Current research on SC includes proof-of-concept cadaveric studies, patient-related safety and feasibility studies, and case series demonstrating transcranioplasty ultrasonography (TCUS). The purpose of this protocol is to investigate the current literature on SC use and outcomes in TCUS. We will perform a systematic literature search following PRISMA-ScR guidelines. The search will be conducted using Ovid Embase, Ovid Medline, and Web of Science Core Collection databases. Titles, abstracts, and full texts will be screened. Joanna Briggs Institute critical appraisal tools will be utilized. Data extraction points will include subject characteristics, SC implant characteristics, ultrasound characteristics, and sonographic findings. These findings will provide a comprehensive review of the literature on sonolucent cranioplasty and directions for future research

Cervical Cancer Diagnosis Using Intelligent Living Behavior of Artificial Jellyfish Optimized With Artificial Neural Network

Cervical cancer affects nearly 4% of the women across the globe and leads to mortality if not treated in early stage. A few decades before, the mortality rate was too high when compared to the present statistics. This is achieved as nowadays most of women are aware of this disease and undergo health examination mainly for screening cervical cancer on regular basis. But only the accurate diagnosis can be helpful for further treatment. Many works are carried out for accurate diagnosis and always have some limitations in accurate predictions. In this work, an efficient algorithm is proposed for the accurate diagnosis of cervical cancer. A meta-heuristic called artificial Jellyfish search optimizer (JS) algorithm is combined with artificial neural network (ANN) to tackle this problem. The proposed algorithm is called JellyfishSearch_ANN and is employed to classify the cervical cancer dataset with four type of targets based on the examination. The JellyfishSearch_ANN provides outstanding results among other classifiers taken for comparison and mainly its classification accuracy is found to be above 98.87% for all targets

Combined Inhibition of AKT and KIT Restores Expression of Programmed Cell Death 4 (PDCD4) in Gastrointestinal Stromal Tumor

The majority of gastrointestinal stromal tumor (GIST) patients develop resistance to the first-line KIT inhibitor, imatinib mesylate (IM), through acquisition of secondary mutations in KIT or bypass signaling pathway activation. In addition to KIT, AKT is a relevant target for inhibition, since the PI3K/AKT pathway is crucial for IM-resistant GIST survival. We evaluated the activity of a novel pan-AKT inhibitor, MK-4440 (formerly ARQ 751), as monotherapy and in combination with IM in GIST cell lines and preclinical models with varying IM sensitivities. Dual inhibition of KIT and AKT demonstrated synergistic effects in IM-sensitive and -resistant GIST cell lines. Proteomic analyses revealed upregulation of the tumor suppressor, PDCD4, in combination treated cells. Enhanced PDCD4 expression correlated to increased cell death. In vivo studies revealed superior efficacy of MK-4440/IM combination in an IM-sensitive preclinical model of GIST compared with either single agent. The combination demonstrated limited efficacy in two IM-resistant models, including a GIST patient-derived xenograft model possessing an exon 9 KIT mutation. These studies provide strong rationale for further use of AKT inhibition in combination with IM in primary GIST; however, alternative agents will need to be tested in combination with AKT inhibition in the resistant setting

HMGB1 released from nociceptors mediates inflammation.

Inflammation, the body's primary defensive response system to injury and infection, is triggered by molecular signatures of microbes and tissue injury. These molecules also stimulate specialized sensory neurons, termed nociceptors. Activation of nociceptors mediates inflammation through antidromic release of neuropeptides into infected or injured tissue, producing neurogenic inflammation. Because HMGB1 is an important inflammatory mediator that is synthesized by neurons, we reasoned nociceptor release of HMGB1 might be a component of the neuroinflammatory response. In support of this possibility, we show here that transgenic nociceptors expressing channelrhodopsin-2 (ChR2) directly release HMGB1 in response to light stimulation. Additionally, HMGB1 expression in neurons was silenced by crossing synapsin-Cre (Syn-Cre) mice with floxed HMGB1 mice (HMGB1f/f). When these mice undergo sciatic nerve injury to activate neurogenic inflammation, they are protected from the development of cutaneous inflammation and allodynia as compared to wild-type controls. Syn-Cre/HMGB1fl/fl mice subjected to experimental collagen antibody-induced arthritis, a disease model in which nociceptor-dependent inflammation plays a significant pathological role, are protected from the development of allodynia and joint inflammation. Thus, nociceptor HMGB1 is required to mediate pain and inflammation during sciatic nerve injury and collagen antibody-induced arthritis

Stimulation of the hepatoportal nerve plexus with focused ultrasound restores glucose homoeostasis in diabetic mice, rats and swine

Peripheral neurons that sense glucose relay signals of glucose availability to integrative clusters of neurons in the brain. However, the roles of such signalling pathways in the maintenance of glucose homoeostasis and their contribution to disease are unknown. Here we show that the selective activation of the nerve plexus of the hepatic portal system via peripheral focused ultrasound stimulation (pFUS) improves glucose homoeostasis in mice and rats with insulin-resistant diabetes and in swine subject to hyperinsulinemic-euglycaemic clamps. pFUS modulated the activity of sensory projections to the hypothalamus, altered the concentrations of metabolism-regulating neurotransmitters, and enhanced glucose tolerance and utilization in the three species, whereas physical transection or chemical blocking of the liver-brain nerve pathway abolished the effect of pFUS on glucose tolerance. Longitudinal multi-omic profiling of metabolic tissues from the treated animals confirmed pFUS-induced modifications of key metabolic functions in liver, pancreas, muscle, adipose, kidney and intestinal tissues. Non-invasive ultrasound activation of afferent autonomic nerves may represent a non-pharmacologic therapy for the restoration of glucose homoeostasis in type-2 diabetes and other metabolic diseases

Stimulation of the hepatoportal nerve plexus with focused ultrasound restores glucose homoeostasis in diabetic mice, rats and swine

Peripheral neurons that sense glucose relay signals of glucose availability to integrative clusters of neurons in the brain. However, the roles of such signalling pathways in the maintenance of glucose homoeostasis and their contribution to disease are unknown. Here we show that the selective activation of the nerve plexus of the hepatic portal system via peripheral focused ultrasound stimulation (pFUS) improves glucose homoeostasis in mice and rats with insulin-resistant diabetes and in swine subject to hyperinsulinemic-euglycaemic clamps. pFUS modulated the activity of sensory projections to the hypothalamus, altered the concentrations of metabolism-regulating neurotransmitters, and enhanced glucose tolerance and utilization in the three species, whereas physical transection or chemical blocking of the liver-brain nerve pathway abolished the effect of pFUS on glucose tolerance. Longitudinal multi-omic profiling of metabolic tissues from the treated animals confirmed pFUS-induced modifications of key metabolic functions in liver, pancreas, muscle, adipose, kidney and intestinal tissues. Non-invasive ultrasound activation of afferent autonomic nerves may represent a non-pharmacologic therapy for the restoration of glucose homoeostasis in type-2 diabetes and other metabolic diseases

Abstract 049: Effect of the ICA Lesion Severity in Outcomes after Endovascular Treatment of Acute Tandem LVO

Introduction Tandem Lesions (TLs) pose unique challenges in the endovascular management of acute ischemic stroke.(1) The absence of anterograde blood flow in the carotid occluded segment may limit the effectiveness of endovascular interventions, resulting in delayed reperfusion or suboptimal recanalization.(2,3) Thus, the presence of unpaired blood flow through the ICA in the context of TLs is believed to exacerbate the extension of ischemic lesions. (4,5) This study compared the clinical and procedural outcomes of patients with TLs and extracranial internal carotid artery occlusion versus those with stenosis. Methods A retrospective analysis was performed on a multicenter cohort of patients with TLs who underwent endovascular treatment. The patients were categorized into two groups: those with extracranial ICA stenosis and those with occlusion. Clinical outcomes, including functional independence, hemorrhagic events, and procedural time metrics including puncture to reperfusion time were assessed. Sensitivity analyses were conducted to evaluate these differences segregating patients according to varying degrees of stenosis, and in pre‐specified subgroups. Results A total of 513 patients with TLs were included in the study. 281 (54.8%) presented with ICA occlusion, and 232 (45.2%) presented stenosis >=70% (Table 1). The comparison between the stenosis and occlusion groups revealed no significant differences in the main outcomes, including mTICI 2c‐3 (47.5% vs. 50.6%, aOR 1.07, 95% CI 0.70‐1.64, p=.751) (Figure 1), mRS 0‐2 at 90 days (43.6% vs. 48.9%, aOR 0.79, 95% CI 0.52‐1.20, p=.271), sICH rates (4.7% vs. 5.6%, aOR 0.72, 95% CI 0.31‐1.71, p=.458), and puncture to reperfusion time (58 [40‐80.5] vs. 52.5 [35.2‐80], ratio 1.04, 95% CI 0.88‐1.23, p=.64). Similar analyses performed comparing different degrees of stenosis and occlusion, and in patients treated with the antegrade approach only, did not show significant differences either. Conclusion Our findings indicate that although more severe degrees of stenosis or occlusion of the ICA prolong the time from puncture to reperfusion, no significant differences in clinical outcomes exist. The clinical implications of these findings need to be further evaluated to fully comprehend the specific needs of patients affected by TLs