SUPERVISING WEATHER STATUS BY EMPLOYING REAL TIME CYBER PHYSICAL PROCEDURE WITH ITS DESIGN AND IMPLEMENTATION

Different of your prosaic initiated utensil or the actual-year body, Cyber-Physical System (CPS) integrates esteem among environment-friendly entities, care for moderate for nipper beings to interlock plus the world in order that we continue. With the results of CPS, massed gadgets are not any scepticism undivided toward the web, for the most part within the birth of Environment Monitoring. Thus, the affair and far away manoeuvre of designs intensity subject matters for CPSs. for the indicated postpone, we spread a CPS plus the effectiveness of offering an ascendable, whippy exemplify in Environment monitoring. The shade monitoring gimmick is composed of triumvirate veneer: ultimately sensing strip, report burden stratum, proof effort thickness. Generally, sensors and sensor hub and that fact bring together sensor population density and repute powers that be to the end area gather of considerable sensing ingot. And the edict register for numbers gets rid of stretch charge sooner than sensor report to the specified crowning achievement corner. The final lump is bosom the occupy, cocky of a photocopy killer along with an information sorry. Data deriving out of sensual sensing bed might be analysed in support of the heavy computing artistry of drizzle computing. The approved symphony offer accessible deal along gadgets inured that fact every one of one's testimony of gadgets is rescued in the direction of through to indication centre the clutter. Even below the annoying job of morphology, notice performed via sensors perhaps taciturn invest stash clan; let down plenty life for the end user purposely the web irk and never the attitude of a sentimental at the surroundings monitoring

Clinical and experimental aspects of aneurysmal subarachnoid hemorrhage

Aneurysmal subarachnoid hemorrhage (aSAH) continues to be associated with significant morbidity and mortality despite advances in care and aneurysm treatment strategies. Cerebral vasospasm continues to be a major source of clinical worsening in patients. We intended to review the clinical and experimental aspects of aSAH and identify strategies that are being evaluated for the treatment of vasospasm. A literature review on aSAH and cerebral vasospasm was performed. Available treatments for aSAH continue to expand as research continues to identify new therapeutic targets. Oral nimodipine is the primary medication used in practice given its neuroprotective properties. Transluminal balloon angioplasty is widely utilized in patients with symptomatic vasospasm and ischemia. Prophylactic “triple‐H” therapy, clazosentan, and intraarterial papaverine have fallen out of practice. Trials have not shown strong evidence supporting magnesium or statins. Other calcium channel blockers, milrinone, tirilazad, fasudil, cilostazol, albumin, eicosapentaenoic acid, erythropoietin, corticosteroids, minocycline, deferoxamine, intrathecal thrombolytics, need to be further investigated. Many of the current experimental drugs may have significant roles in the treatment algorithm, and further clinical trials are needed. There is growing evidence supporting that early brain injury in aSAH may lead to significant morbidity and mortality, and this needs to be explored further.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/151874/1/cns13222_am.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/151874/2/cns13222.pd

Refractory Orthostatic Hypotension Caused by a Recurrent Hemangioblastoma: Case Report and Review of the Literature

Abstract Refractory orthostatic hypotension (OH) has been described following surgery for posterior fossa tumors. We present the case of a patient with refractory OH following attempted surgical resection. We also reviewed the available literature to describe pathophysiologic mechanisms for this rare entity. A 58-year-old female was found to have a hemangioblastoma at the cervicomedullary junction following workup for dysphagia and coordination difficulties. She underwent successful suboccipital craniotomy and gross total resection. However, the patient's symptoms returned several years later and a magnetic resonance imaging (MRI) showed tumor recurrence. A surgical resection was attempted but could not be performed due to significant scarring. Following discharge, she returned to our care with severe syncopal episodes, refractory OH, and an inability to ambulate. Aggressive medical therapy resulted in a gradual improvement in her ability to ambulate and a reduction in her orthostatic episodes. Unfortunately she died due to sepsis from aspiration pneumonia several months later. A survey of the literature yielded a total of 10 reports (14 patients) with refractory OH as a result of tumors in the cervicomedullary region. Five of fourteen patients died from complications related to OH and brainstem compression while the remainder had some improvement and were discharged. Refractory OH can rarely be a presenting sign of a tumor in the cervicomedullary junction or can manifest following surgical resection of tumors in this region. Recognition of OH and the institution of medical therapy (sodium and fluid replacement) and pharmacotherapy may curb the significant morbidity associated with this condition

Impact of sex differences on thrombin-induced hydrocephalus and white matter injury: the role of neutrophils

Abstract Background Thrombin has been implicated in playing a role in hydrocephalus development following intraventricular hemorrhage (IVH). However, the mechanisms underlying the sex differences to the detrimental effects of thrombin post-IVH remain elusive. Method Three-month old male and female Sprague-Dawley rats underwent unilateral intracerebroventricular (ICV) injections of 3U or 5U thrombin, or saline, to examine differences in thrombin-induced hydrocephalus and white matter injury. Mortality, and lateral ventricle volume and white matter injury were measured on magnetic resonance imaging evaluation at 24 h post-injection. In addition, male rats were pretreated with 17-β estradiol (E2, 5 mg/kg) or vehicle at 24 and 2 h prior to ICV injection of 3U thrombin. All rats were euthanized at 24 h post-injection for histology and immunohistochemistry. Results ICV injection of 5U thrombin caused 100 and 0% mortality in female and male rats, respectively. 3U of thrombin resulted in significant ventricular dilation and white matter damage at 24 h in both male and female rats, but both were worse in females (p < 0.05). Furthermore, neutrophil infiltration into choroid plexus and periventricular white matter was enhanced in female rats and may play a critical role in the sex difference in brain injury. Pre-treating male rats with E2, increased thrombin (3U)-induced hydrocephalus, periventricular white matter injury and neutrophil infiltration into the choroid plexus and white matter. Conclusions ICV thrombin injection induced more severe ventricular dilation and white matter damage in female rats compared to males. Estrogen appears to contribute to this difference which may involve greater neutrophil infiltration in females. Understanding sex differences in thrombin-induced brain injury may shed light on future interventions for hemorrhagic stroke.http://deepblue.lib.umich.edu/bitstream/2027.42/173753/1/12987_2021_Article_273.pd

A timeline of oligodendrocyte death and proliferation following experimental subarachnoid hemorrhage

AimsWhite matter (WM) injury is a critical factor associated with worse outcomes following subarachnoid hemorrhage (SAH). However, the detailed pathological changes are not completely understood. This study investigates temporal changes in the corpus callosum (CC), including WM edema and oligodendrocyte death after SAH, and the role of lipocalin-2 (LCN2) in those changes.MethodsSubarachnoid hemorrhage was induced in adult wild-type or LCN2 knockout mice via endovascular perforation. Magnetic resonance imaging was performed 4 hours, 1 day, and 8 days after SAH, and T2 hyperintensity changes within the CC were quantified to represent WM edema. Immunofluorescence staining was performed to evaluate oligodendrocyte death and proliferation.ResultsSubarachnoid hemorrhage induced significant CC T2 hyperintensity at 4 hours and 1 day that diminished significantly by 8 days post-procedure. Comparing changes between the 4 hours and 1 day, each individual mouse had an increase in CC T2 hyperintensity volume. Oligodendrocyte death was observed at 4 hours, 1 day, and 8 days after SAH induction, and there was progressive loss of mature oligodendrocytes, while immature oligodendrocytes/oligodendrocyte precursor cells (OPCs) proliferated back to baseline by Day 8 after SAH. Moreover, LCN2 knockout attenuated WM edema and oligodendrocyte death at 24 hours after SAH.ConclusionsSubarachnoid hemorrhage leads to T2 hyperintensity change within the CC, which indicates WM edema. Oligodendrocyte death was observed in the CC within 1 day of SAH, with a partial recovery by Day 8. SAH-induced WM injury was alleviated in an LCN2 knockout mouse model.Lipocalin-2 deficiency attenuates corpus callosum T2 hyperintensity and oligodendrocyte death after SAH induction.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/172271/1/cns13812.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/172271/2/cns13812_am.pd

Tip60 HAT activity mediates APP induced lethality and apoptotic cell death in the CNS of a Drosophila Alzheimer's disease model.

Histone acetylation of chromatin promotes dynamic transcriptional responses in neurons that influence neuroplasticity critical for cognitive ability. It has been demonstrated that Tip60 histone acetyltransferase (HAT) activity is involved in the transcriptional regulation of genes enriched for neuronal function as well as the control of synaptic plasticity. Accordingly, Tip60 has been implicated in the neurodegenerative disorder Alzheimer's disease (AD) via transcriptional regulatory complex formation with the AD linked amyloid precursor protein (APP) intracellular domain (AICD). As such, inappropriate complex formation may contribute to AD-linked neurodegeneration by misregulation of target genes involved in neurogenesis; however, a direct and causative epigenetic based role for Tip60 HAT activity in this process during neuronal development in vivo remains unclear. Here, we demonstrate that nervous system specific loss of Tip60 HAT activity enhances APP mediated lethality and neuronal apoptotic cell death in the central nervous system (CNS) of a transgenic AD fly model while remarkably, overexpression of Tip60 diminishes these defects. Notably, all of these effects are dependent upon the C-terminus of APP that is required for transcriptional regulatory complex formation with Tip60. Importantly, we show that the expression of certain AD linked Tip60 gene targets critical for regulating apoptotic pathways are modified in the presence of APP. Our results are the first to demonstrate a functional interaction between Tip60 and APP in mediating nervous system development and apoptotic neuronal cell death in the CNS of an AD fly model in vivo, and support a novel neuroprotective role for Tip60 HAT activity in AD neurodegenerative pathology

Anticoagulation vs Antiplatelet Treatment in Patients with Carotid and Vertebral Artery Dissection: A Study of 370 Patients and Literature Review

Dissection of the carotid and vertebral arteries is an important cause of stroke in young patients. The objective of this study is to compare antithrombotic treatments in patients with carotid and vertebral dissections. Three hundred seventy patients with carotid and vertebral artery dissections were included. Univariate and multivariate analyses were conducted to analyze the association between treatment and new or recurrent events and clinical outcome. Mean follow-up was 24.3 months. In patients with spontaneous dissection, 55% received antiplatelets, 29.4% anticoagulation, and 12.6% combined treatment. New or recurrent ischemic and hemorrhagic events occurred in 9.6% of patients on antiplatelets, 10.4% on anticoagulation, and 13.3% on combined treatment. For traumatic dissection, 58.3% received antiplatelets, 26.9% anticoagulation, and 10.2% combined treatment. New or recurrent ischemic and hemorrhagic events occurred in 6.9% on antiplatelets, 11.1% on anticoagulation, and 20% on combined treatment. In patients with intracranial dissection, 63.1% were started on antiplatelets, 19.7% on anticoagulation, and 14.5% on combined treatment. Ischemic and hemorrhagic events occurred in 8.5% on antiplatelet treatment, 15.4% on anticoagulation, and 18.2% on combined treatment. In patients with extracranial dissection, 54.4% were on antiplatelets, 28.9% on anticoagulation, and 11.2% on combined treatment. Ischemic and hemorrhagic events occurred in 10.1% on antiplatelet treatment, 9.3% on anticoagulation, and 13.8% on combined treatment. The association between antithrombotic treatment and ischemic/hemorrhagic events and clinical outcome was not significant for all subtypes of dissection. The rate of new or recurrent events is similar with antiplatelet and anticoagulation treatment in treating intracranial and extracranial carotid and vertebral artery dissection

Decreased CSF output as a clinical indicator of cerebral vasospasm following aneurysmal subarachnoid hemorrhage

Vasospasm is a significant cause of morbidity and mortality among those with aneurysmal subarachnoid hemorrhage (aSAH). Treating increased intracranial pressure by drainage of cerebral spinal fluid through an external ventriculostomy is routine practice. The objective of this study is to evaluate the trends of CSF output in patients who experience vasospasm. Electronic medical charts were reviewed to identify two groups of patients with aSAH, 75 consecutive patients who developed vasospasm and 75 matched patients who did not develop vasospasm. CSF output was recorded within 3 days before and 3 days after the occurrence of vasospasm. CSF output was recorded for the same days after SAH in matched patients with no vasospasm. Total CSF output was lower in patients with vasospasm as compared to patients without vasospasm matched for the same day (p<0.001). In patients with vasospasm, CSF output recordings were significantly higher prior to the occurrence of vasospasm (438ml/day) than the period following vasospasm (325.7ml/day), with a consistent decrease in CSF drainage from day 3 before vasospasm to day 3 after vasospasm (p=0.012). Decreasing CSF output was significantly associated with the occurrence of vasospasm (p=0.017). Youden indices demonstrated that daily CSF drainage <160ml was significantly associated with the occurrence of vasospasm. The sensitivity of this test was 64.79% and the specificity was 55.38%. In addition to clinical exam findings, observation of a CSF output decline to less than 160ml/day may be used as additional support for the diagnosis of vasospasm