TY - JOUR. T1 - Platinum-induced peripheral neurotoxicity. T2 - From pathogenesis to treatment. AU - Staff, Nathan P.. AU - Cavaletti, Guido. AU - Islam, Badrul. AU - Lustberg, Maryam. AU - Psimaras, Dimitri. AU - Tamburin, Stefano. N1 - Funding Information: The study was supported by National Institutes of Health/National Cancer Institute: R01 CA 211887 (NPS). Publisher Copyright: © 2019 Peripheral Nerve Society. PY - 2019/10/1. Y1 - 2019/10/1. N2 - Platinum-induced peripheral neurotoxicity (PIPN) is a common side effect of platinum-based chemotherapy that may cause dose reduction and discontinuation, with oxaliplatin being more neurotoxic. PIPN includes acute neurotoxicity restricted to oxaliplatin, and chronic non-length-dependent sensory neuronopathy with positive and negative sensory symptoms and neuropathic pain in both upper and lower limbs. Chronic sensory axonal neuropathy manifesting as stocking-and-glove distribution is also frequent. Worsening of neuropathic symptoms after ...
Acrylamide (ACR), a type-2 alkene, may lead to a synaptopathy characterized by ataxia, skeletal muscles weakness and numbness of the extremities in exposed human and laboratory animals. Currently, only the mildly affected patients undergo complete recovery, and identification of new molecules with therapeutic bioactivity against ACR acute neurotoxicity is urgently needed. Here, we have generated a zebrafish model for ACR neurotoxicity by exposing 5 days post-fertilization zebrafish larvae to 1 mM ACR for 3 days. Our results show that zebrafish mimics most of the pathophysiological processes described in humans and mammalian models. Motor function was altered, and specific effects were found on the presynaptic nerve terminals at the neuromuscular junction level, but not on the axonal tracts or myelin sheath integrity. Transcriptional markers of proteins involved in synaptic vesicle cycle were selectively altered, and the proteomic analysis showed that ACR-adducts were formed on cysteine residues ...
Do You Have Neurotoxicity Syndromes? Join friendly people sharing true stories in the I Have Neurotoxicity Syndromes group. Find support forums, advice and chat with groups who share this life experience. A Neurotoxicity Syndromes anonymous support g...
Peripheral neurotoxicity is a debilitating condition that afflicts up to 90% of patients with colorectal cancer receiving oxaliplatin-containing therapy. Although emerging evidence has highlighted the importance of various solute carriers to the toxicity of anticancer drugs, the contribution of these proteins to oxaliplatin-induced peripheral neurotoxicity remains controversial. Among candidate transporters investigated in genetically engineered mouse models, we provide evidence for a critical role of the organic cation transporter 2 (OCT2) in satellite glial cells in oxaliplatin-induced neurotoxicity, and demonstrate that targeting OCT2 using genetic and pharmacological approaches ameliorates acute and chronic forms of neurotoxicity. The relevance of this transport system was verified in transporter-deficient rats as a secondary model organism, and translational significance of preventive strategies was demonstrated in preclinical models of colorectal cancer. These studies suggest that ...
Platinum-based drugs, such as cisplatin and oxaliplatin, are well-known for inducing chronic sensory neuropathies but their acute and motor neurotoxicities are less well characterised. Use was made of nerve conduction studies and needle electromyography (EMG) to assess motor nerve excitability in cancer patients during their first treatment cycle with platinum-based chemotherapy in this study. Twenty-nine adult cancer patients had a neurophysiological assessment either before oxaliplatin plus capecitabine, on days 2 to 4 or 14 to 20 after oxaliplatin plus capecitabine, or on days 2 to 4 after carboplatin plus paclitaxel or cisplatin, undertaken by a neurophysiologist who was blinded to patient and treatment details. Patients completed a symptom questionnaire at the end of the treatment cycle. Abnormal spontaneous high frequency motor fibre action potentials were detected in 100% of patients (n = 6) and 72% of muscles (n = 22) on days 2 to 4 post-oxaliplatin, and in 25% of patients (n = 8) and 13% of
Oxaliplatin can induce peripheral neuropathy (OXIPN) as an adverse side effect in cancer patients. Until now, no effective preventive or therapeutic drug has b...
In the section of Developmental Neurotoxicity: An Update of the Pediatric Anesthesia Neurodevelopmental Assessment (PANDA) symposium 2018 the speakers presented the current literature in translational and clinical research. Dr. Brambrink spoke about translational research in anesthetic neurotoxicity, beginning with discovery in the rodent model, then focusing on evidence from nonhuman primates. Dr. Waspe applied the methodology of Adverse Outcome Pathways from the field of toxicology to developmental neurotoxicity of anesthetics. Dr. OLeary presented relevant clinical studies that were published in 2017 divided by a focus on academic performance, clinical outcomes or diagnoses, or neuropsychological testing.. Read More. ...
Acute NT was reported in 95 of 1,218 (7.8%) eligible patients treated on POG 9005. The incidence by regimen was regimen A, 46 of 543 patients (8.3%); regimen B, 13 of 354 patients (3.7%); and regimen C, 36 of 321 patients (11.2%) (P , .001). The majority of events were seizures and the median number of days to first occurrence of symptomatic NT after ITM or TIT was 10 to 11 days. Computed tomography (CT) or magnetic resonance imaging (MRI) evidence consistent with leukoencephalopathy (LE), with or without the presence of cerebral calcifications, was observed in 75% and 77.1 % of symptomatic patients treated on regimens A and C, respectively, but in only 15.4% of symptomatic patients treated on regimen B (P , .001). Factors associated with an increased incidence of NT included increased cumulative exposure with repeated i.v. MTX (regimens A and C v B), increased MTX-leucovorin (LCV) ratio (regimens A and C v B), and choice and timing of TIT therapy. The use of i.v. MP during intensification did ...
In 1998, EPA published Guidelines for Neurotoxicity Risk Assessment as the basis for interpreting neurotoxicity results. At that time, the focus was on traditional toxicity testing and human clinical /epidemiological data. More recently, a change in approach to toxicity testing was proposed in A 21st Century Update on Neurotoxicity Risk Assessment (NRC, 2007), stating that traditional toxicity testing was too slow and expensive to develop information on the potential toxicity of the large number of untested chemicals already used in commerce. In addition, new technologies have compounded the problem as new materials, such as engineered nanomaterials, are introduced at a rate exceeding traditional testing capacity. There is currently much effort to develop higher throughput neurotoxicity testing capabilities, especially for developmental neurotoxicity, but there is no general consensus regarding how alternative testing data should be interpreted for neurotoxicity risk assessment. The ...
CIPN is the main dose-limiting toxicity caused by various chemotherapeutic agents. PTX is a chemotherapeutic drug, and it has been widely used in various solid tumors. However, peripheral neuropathic pain caused by PTX leads to loss of body function, a significant decline in quality of life, and even a delay in treatment. The peripheral neurotoxicity caused by PTX is rarely disabling, but it often lasts for several months to years after stopping the drug, causing inconvenience and impacting the patients quality of life (Kiya et al., 2011). PTX-induced peripheral neurotoxicity usually occurs within 24-72 hours of administration, which is dose-accumulating with an incidence of 59%-78% (Wilkes, 2007).. With the proposal of the mechanism of PIPN, some prevention and treatment methods have emerged accordingly. Although there are many clinical trials on the treatment of PIPN, there is no unified standard in clinical treatment. To date, there have been 42 randomized controlled clinical trials of drug ...
In view of the neurotoxic properties of 1-methyl-4-phenylpyridinium (MPP+), the monoamine oxidase-B-generated metabolite of the Parkinsonian agent 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (Kalgutkar et al., 2001), the identification of MPP+-like HPP+ and RHPP+ metabolites in significant quantities in the urine (Subramanyam et al., 1991b), plasma (Avent et al., 1997), and post-mortem brain samples (Eyles et al., 1997) in schizophrenic patients treated with HP is of neurotoxicological importance especially in the pathogenesis of HP-induced TD. Additional support for this proposal is evident from the observations that HPP+ displays MPP+-like neurotoxicity in vivo as well as in vitro (Bloomquist et al., 1994).. Although glucuronidation and reduced HP formation constitute the major routes of HP clearance in humans, the wide interindividual variations in HP oral clearance have been mainly attributed to the minor P450-catalyzed biotransformation pathways (30% of overall HP metabolism) (Kudo and ...
The State fashions itself as our protector from pollution. Yet in the name of efficiency and opposition to pollution a new additive , methyl t-butyl ether (MTBE) is imposed on our environemt through our gasoline.MTBE is now known to have both carcinogenic and neurotoxicological effects in mammals. The time has come to expose the blatant disregard for public well-being that MTBE represents and call for the impeachment or defeat of any politician who supports it. This is an excellent opportunity for libertarians to expose the hypocrisy and malevolence of statism! The government viciously and stubbornly refuses to acknowledge its mistake and continues to pollute our bodies to coverup their incompetence. H R Olson, MA Bioethicist ...
Acute and chronic neurologic disorders associated with the various neurologic effects of ethanol. Primary sites of injury include the brain and peripheral nerves.
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highest risk for acute (accidental) poisoning, easy to catch and treat, chronic poisoning is harder to detect because the person is exposed to low levels of drug and sings may not show toxicity immediately ...
Chemotherapy-induced peripheral neuropathy (CIPN), a debilitating major side-effect of malignancy treatment, is definitely seen as a pain and sensory loss at hand and feet. mitochondrial accumulation of p53 in dorsal root ganglia (DRG), spinal cord, and peripheral nerve without evidence for apoptosis. Cisplatin-treatment also reduced mitochondrial membrane potential and lead to abnormal mitochondrial morphology and impaired mitochondrial function in DRG neurons. Pre-treatment with PFT- prevented the early cisplatin-induced increase in mitochondrial p53 and the reduction in mitochondrial membrane potential. Inhibition of the early mitochondrial p53 accumulation by PFT- also prevented the abnormalities buy 936563-96-1 in mitochondrial morphology and mitochondrial bioenergetics (reduced oxygen consumption rate, maximum respiratory capacity, and adenosine triphosphate synthesis) that develop in DRG and peripheral nerve after cisplatin-treatment. Functionally, inhibition of mitochondrial p53 ...
Multivitamin supplements may reduce incidence of chemotherapy-induced peripheral neuropathy among women undergoing treatment with paclitaxel for breast cancer, according to results of a study led by researchers at Roswell Park Comprehensive Cancer Center.“Our study showed that use of multivitamin supplements, but not specific vitamins, was associated with less neurotoxicity,”
Chemotherapy-induced peripheral neuropathy (CIPN) is one of the most challenging and complex complications of cancer chemotherapy.
Chemotherapy-induced peripheral neuropathy (CIPN) is the most frequent cause of dose reduction or treatment discontinuation in patients treated for cancer with...
TY - JOUR. T1 - A new approach to prevent the chemotherapy-induced peripheral neuropathy. AU - Kawashiri, Takehiro. PY - 2019/1/1. Y1 - 2019/1/1. UR - http://www.scopus.com/inward/record.url?scp=85064722410&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=85064722410&partnerID=8YFLogxK. U2 - 10.1254/fpj.153.200. DO - 10.1254/fpj.153.200. M3 - Comment/debate. C2 - 30971662. AN - SCOPUS:85064722410. VL - 153. JO - Folia Pharmacologica Japonica. JF - Folia Pharmacologica Japonica. SN - 0015-5691. IS - 4. ER - ...
Cytokine release symptoms (CRS) and immune effector cellCassociated neurotoxicity syndrome (ICANS) are major limitations of chimeric antigen receptor (CAR) T-cell therapy. 71-year-old man with chemorefractory diffuse large B-cell lymphoma (DLBCL) received second-generation 41BB CD3 anti-CD19 anti-CD20 (LV20.19) bispecific CAR T cells on a phase 1 clinical trial (type:clinical-trial,attrs:text:NCT03019055″,term_id:NCT03019055″NCT03019055). On day time +5 post-LV20.19 CAR infusion, the patient developed grade 2 CRS that resolved with tocilizumab. On day time +7, he developed grade 2 neurotoxicity by Common Terminology Criteria for Adverse Events v5. Treatment with dexamethasone, 10 mg every 6 hours, was initiated. With quick improvement, his dexamethasone was tapered. Regrettably, he progressed with grade 3 neurotoxicity on day time +13 that was manifested by tremor, mutism, and nonresponsiveness. Lumbar puncture (LP) was performed, and cerebrospinal fluid (CSF) analysis exposed a ...
High-level Technology Service (STAN). Description:. A tissue can be sliced into thin sections with a freezing microtome (30-60 microns) or in a cryostat (10-50 microns). The advantage of using the freezing microtome is that it performs quick cuts and, therefore, plenty of material can be processed daily. Moreover, in the cryostat the tissue does not undergo temperature fluctuations and also, the machine performs thinner cuts which are placed directly on the microscope slide for later analysis.. Methodology: The sample is placed on the microtome base and then a quick freezing is carried out with carbon dioxide. On a following stage, the suggested thickness is cut and the material is collected in corresponding solutions.. NEUROTOXICOLOGY. High-level Technology Service (STAN). Description: Neuronal death detection with the use of neurohistological techniques for evaluation in the field of Neurotoxicology.. Methodology: The Silver Staining technique is of great value for neurotoxicological studies ...
This study has demonstrated that metabolism and pharmacokinetic behaviour of BPAU and m-DNB significantly modified their neurotoxicity. Three metabolites of BPAU, 3-hydroxy-5-(4-bromophenyl)-1,3 -diazapentane-2,4-dione (M1), 4-4-bromo-phenyl)-3-oxapyrrolidine-2,5-dione (M2) and 3-methyl-5-(4-bromophenyl)-1,3-diaza- pentane-2,4-dione (M3), were identified and characterised in this study. Phenylmethanesulfonyl fluoride (PMSF) which can intensify BPAU-induced neuropathy signiflcandy delayed BPAU elimination, increased M1 levels in tissues and decreased M2 concentration in serum This metabolic interaction and neurotoxic synergy between the two compounds represent a distinct model in the mechanistic studies of the promotion of delayed neuropathy. The present study also showed that 1-year old rats which are more susceptible to BPAU-induced neuropathy produced more M1 and less M2 than 6-week old rats ...
Dublin, Dec. 05, 2018 (GLOBE NEWSWIRE) -- The Chemotherapy-Induced Peripheral Neuropathy (CIPN) - Market Insights, Epidemiology and Market Forecast...
international medical journal (ISSN:13412051) is a peer reviewed medical journal that aims to publish the quality of medical, pharmaceutical and health science research paper
Choosing to participate in a study is an important personal decision. Talk with your doctor and family members or friends about deciding to join a study. To learn more about this study, you or your doctor may contact the study research staff using the contacts provided below. For general information, Learn About Clinical Studies. ...
Nanoparticles (NPs) have been shown to accumulate in organs, cross the blood-brain barrier and placenta, and have the potential to elicit developmental neurotoxicity (DNT). Here, we developed a human embryonic stem cell (hESC)-derived 3-dimensional (
This report reviews neurotoxicological principles relevant to situations of hazardous waste disposal. Some of the diagnostic techniques currently used for field assessment of nervous system dysfunction are critically evaluated. These include nerve conduction velocity, evoked potentials, neuropsychological testing and use of the Optacon ...
In this item we try to elucidate the mechanisms involved in methamphetamine-induced neurotoxicity, in particular in dopaminergic neurons. ...
Background. The majority of patients receiving the platinum-based chemotherapy drug oxaliplatin develop peripheral neurotoxicity. Because this neurotoxicity involves ROS production, we investigated the efficacy of mangafodipir, a molecule that has antioxidant properties and is approved for use as an MRI contrast enhancer.. Methods. The effects of mangafodipir were examined in mice following treatment with oxaliplatin. Neurotoxicity, axon myelination, and advanced oxidized protein products (AOPPs) were monitored. In addition, we enrolled 23 cancer patients with grade ≥2 oxaliplatin-induced neuropathy in a phase II study, with 22 patients receiving i.v. mangafodipir following oxaliplatin. Neuropathic effects were monitored for up to 8 cycles of oxaliplatin and mangafodipir.. Results. Mangafodipir prevented motor and sensory dysfunction and demyelinating lesion formation. In mice, serum AOPPs decreased after 4 weeks of mangafodipir treatment. In 77% of patients treated with oxaliplatin and ...
TY - JOUR. T1 - Oxaliplatin-induced neuropathy. T2 - a tale of two electrolytes. AU - Babiker, Hani M.. AU - Green, Myke R.. AU - Nelson, Mark A. AU - Elquza, Emad -. PY - 2015/6/1. Y1 - 2015/6/1. KW - Calcium/magnesium. KW - Oxaliplatin. KW - Sensory neurotoxicity. UR - http://www.scopus.com/inward/record.url?scp=84940006306&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=84940006306&partnerID=8YFLogxK. U2 - 10.1007/s00520-015-2702-0. DO - 10.1007/s00520-015-2702-0. M3 - Article. C2 - 25801447. AN - SCOPUS:84940006306. VL - 23. SP - 1483. EP - 1485. JO - Supportive Care in Cancer. JF - Supportive Care in Cancer. SN - 0941-4355. IS - 6. ER - ...
This category includes neurological diseases that are caused by toxins, poisons or overdoses of medications. Examples include heavy metal poisoning, botulism, etc.
Another feature review covers the difficult-to-manage syndrome of chemotherapy-induced peripheral neuropathy (CIPN), which is poorly understood physiologically and is clinically manifested in variable fashion in terms of onset and chronicity. Drs Trivedi, Hershman, and Crew provide a very helpful overview on the physiology and clinical spectrum of CIPN, with strategies on surveillance and grading-an approach that should become standard practice. The difficulty in managing CIPN is highlighted, with a review of approaches with demonstrated benefit, but an acknowledgment that responses are variable and far from adequate, highlighting the need for more research and awareness of this common treatment side effect ...
Condition: Chemotherapy-induced Peripheral Neuropathy Intervention: Sponsors: Carsten Dahl Mørch; Aalborg University Hospital Not yet recruiting...
Environmental toxicants such as mercury, manganese, pesticides and others; contaminants in designer drugs of abuse such as MPTP; and a vast and growing inventory of industrial chemicals have been linked to neurological damage and a significant number of progressive neurological diseases such as Parkinsons and other CNS degenerative syndromes. In addition, attrition due to neurotoxicity represents a significant issue in all stages of drug development. Traditionally, neurotoxicity testing has relied on composite data sets of functional assessments (e.g., behavior, activity, seizures) and conventional neuropathological evaluations (e.g., organ weights, gross observations, histopathology of neural tissue). Current histopathologic analyses often suffer from constrained spatial sampling and limited translational capability and microscopic findings often do not correlate with the functional and/or neurochemical evidence typically collected. In addition, most neurotoxicants produce very specific ...
Read this review article to examine reported cases of reversible lithium neurotoxicity and its clinical profile. Plus, discover precipitating factors with probable mechanisms and the preventive measures to avoid lithium neurotoxicity.
The possibility of anesthetic neurotoxicity was first suggested more than 15 years ago with findings of apoptosis in the brains of rodents after ethanol exposure during critical periods of neurodevelopment. A similar neuroapoptotic effect was soon identified in anesthetic agents and linked to long-term functional consequences. Since then, nearly all commonly used N-methyl-D-aspartate (NMDA) antagonists and γ-amino butyric acid (GABA) agonists have been evaluated and were found to result in neurotoxic effects in a variety of animal species, including non-human primates.1 Hundreds of preclinical studies have now been published demonstrating effects with anesthetic doses relevant to humans and using monitoring standards similar to those used for clinical care in children. Despite the presence of this robust body of preclinical data, however, the clinical evidence is much sparser ...
Lee, G. C., Lin, C. H., Tao, Y. C., Yang, J. M., Hsu, K. C., Huang, Y. J., Huang, S. H., Kung, P. J., Chen, W. L., Wang, C. M., Wu, Y. R., Chen, C. M., Lin, J. Y., Hsieh-Li, H. M. & Lee-Chen, G. J., 五月 1 2015, 於 : NeuroToxicology. 48, p. 120-130 11 p.. 研究成果: 雜誌貢獻 › 文章 ...
The IPEG is an association of scientists and researchers actively involved in electrophysiological brain research in preclinical and clinical pharmacology, neurotoxicology and related areas of interest
Background Oxaliplatin is effective in adjuvant and first-line colorectal cancer chemotherapy. Oxaliplatin-induced severe chronic neurotoxicity is the main dose-limiting adverse event. No standard treatment for oxaliplatin-induced chronic neurotoxicity has been identified.. Materials and methods We conducted a prospective pilot clinical trial to explore whether neurotropin has neuroprotective effects on chronic neurotoxicity. From May 1 2010 to July 1 2011, 80 stage II and III colorectal cancer patients who were eligible to receive oxaliplatin-based chemotherapy voluntarily enrolled in the trial. The patients were randomly divided into 2 groups, one of which received neurotropin treatment.. Results The patients in the control group experienced significantly ≥ grade 2 and ≥ grade 3 neurotoxicity (by NCI CTCAE grading) than did those in the neurotropin group (60.9% vs. 38%, for at least grade 2 neurotoxicity, P = 0.001; 39% vs. 2.7%, for at least grade 3 neurotoxicity, P < 0.001). If ...
TY - JOUR. T1 - Prevention and management of chemotherapy-induced peripheral neuropathy in survivors of adult cancers. T2 - American society of clinical oncology clinical practice guideline. AU - Hershman, Dawn L.. AU - Lacchetti, Christina. AU - Dworkin, Robert H.. AU - Lavoie Smith, Ellen M.. AU - Bleeker, Jonathan. AU - Cavaletti, Guido. AU - Chauhan, Cynthia. AU - Gavin, Patrick. AU - Lavino, Antoinette. AU - Lustberg, Maryam B.. AU - Paice, Judith. AU - Schneider, Bryan. AU - Smith, Mary Lou. AU - Smith, Tom. AU - Terstriep, Shelby. AU - Wagner-Johnston, Nina. AU - Bak, Kate. AU - Loprinzi, Charles L.. PY - 2014/6/20. Y1 - 2014/6/20. N2 - Purpose: To provide evidence-based guidance on the optimum prevention and treatment approaches in the management of chemotherapy-induced peripheral neuropathies (CIPN) in adult cancer survivors. Methods: A systematic literature search identified relevant, randomized controlled trials (RCTs) for the treatment of CIPN. Primary outcomes included incidence and ...
Title: Role of Sigma Receptors in Methamphetamine-Induced Neurotoxicity. VOLUME: 9 ISSUE: 1. Author(s):Nidhi Kaushal and Rae R. Matsumoto. Affiliation:Department of Basic Pharmaceutical Sciences, School of Pharmacy, West Virginia University, Morgantown, WV 26506, USA.. Keywords:Methamphetamine, sigma receptors, oxidative stress, endoplasmic reticulum, mitochondria, neurotoxicity, dopamine, glutamate, opamine, Hperthermia, Psychosis, Depression, Protein Kinase, Apoptic Death Cell, ER Stress, Excitotoxicity. Abstract: Methamphetamine (METH) is a widely abused substance world over. Currently, there is no effective pharma- cotherapy to treat its effects. This necessitates identification of potential novel therapeutic targets. METH interacts with sigma (σ) receptors at physiologically relevant micromolar concentrations. In addition, σ receptors are present in organs like the brain, heart, and lungs at which METH acts. Additionally, σ receptors have been implicated in various acute and subchronic ...
We aimed at validating the role of genetic variants identified by a recent genome-wide association study (GWAS) as determinants of chronic oxaliplatin-induced peripheral neurotoxicity (OXAIPN). Eight polymorphisms (rs10486003, rs2338, rs843748, rs797519, rs4936453, rs12023000, rs17140129, and rs6924 …
To update the ASCO guideline on the recommended prevention and treatment approaches in the management of chemotherapy-induced peripheral neuropathy (CIPN) in adult cancer survivors.An Expert Panel conducted targeted systematic literature reviews to identify new studies.The search strategy identified 257 new references, which led to a full-text review of 87 manuscripts. A total of 3 systematic reviews, 2 with meta-analyses, and 28 primary trials for prevention of CIPN in addition to 14 primary trials related to treatment of established CIPN, are included in this update.The identified data reconfirmed that no agents are recommended for the prevention of CIPN. The use of acetyl-l-carnitine for the prevention of CIPN in patients with cancer should be discouraged. Furthermore, clinicians should assess the appropriateness of dose delaying, dose reduction, substitutions, or stopping chemotherapy in patients who develop intolerable neuropathy and/or functional impairment. Duloxetine is the only agent ...
Chemotherapy-induced peripheral neuropathy (CIPN) is a progressive, enduring, and often irreversible condition featuring pain, numbness, tingling and sensitivity to cold in the hands and feet (sometimes progressing to the arms and legs) that afflicts between 30% and 40% of patients undergoing chemotherapy. Chemotherapy drugs associated with CIPN include thalidomide, the epothilones such as ixabepilone, the vinca alkaloids vincristine and vinblastine, the taxanes paclitaxel and docetaxel, the proteasome inhibitors such as bortezomib, and the platinum-based drugs cisplatin, oxaliplatin and carboplatin. Whether CIPN arises, and to what degree, is determined by the choice of drug, duration of use, the total amount consumed and whether the patient already has peripheral neuropathy. Though the symptoms are mainly sensory - pain, tingling, numbness and temperature sensitivity - in some cases motor nerves are affected, and occasionally, also, the autonomic nervous system. CIPN often follows the first ...
INTRODUCTION: Chemotherapy-induced peripheral neuropathy (CIPN) is a prevalent and clinically meaningful side effect of cancer treatment. CIPN is induced by neurotoxic agents, causing severe sensory and/or motor deficits, resulting in disability and poor recovery, reducing patients quality of life and limiting medical therapy. To date, effective treatment options are lacking. Whole-body vibration (WBV) training can attenuate motor and sensory deficits. We are conducting a two-armed, multicentre, assessor-blinded, randomised controlled trial, to investigate the effects of WBV on relevant symptoms of CIPN and determine the training characteristics. METHODS AND ANALYSIS: In this ongoing study, 44 patients who have completed therapy in the past 3 months, with a neurologically confirmed CIPN are assessed before and after a 12-week intervention and follow-up. The intervention group receives WBV twice a week. Exercises are individually tailored according to the initially determined optimal ...
Rapid advances have been made in the diagnosis and treatment of neurological disease over the last two decades. Over that period, major developments have also occurred in other fields of medicine, most notably in the management of cancer. Two-thirds of all cancer patients now survive at 5-years post-diagnosis, with over 28 million cancer survivors worldwide.1 As cancer outcomes improve, there has been increased focus on the long-term quality of life in cancer survivors. Not unexpectedly, neurological complications are a prevalent and potentially disabling long-term side effect of cancer treatment. Chemotherapy-induced peripheral neuropathy (CIPN), in particular, is the dose-limiting toxicity of many chemotherapeutic agents, … ...
ASCO has released a clinical practice guideline on prevention and treatment of chemotherapy-induced peripheral neuropathy in adult cancer patients, published in the Journal of Clinical Oncology.1. The guidelines resulted from the efforts of an expert panel, with representation from the fields of medical oncology, community oncology, nursing, pain research, genetics, neurology, pharmacology, patient representation, and guideline methodology. Charles Loprinzi, MD, of the Mayo Clinic, Rochester, Minnesota, and Dawn Hershman, MD, of Columbia University Medical Center, New York, were the panel co-chairs.. The overall incidence of the condition is estimated at close to 40% in patients treated with multiple agents, with reported rates varying according to chemotherapy regimens, duration of exposure, and assessment methods. Regimens associated with higher risk are those including platinum drugs, vinca alkaloids, bortezomib (Velcade), and taxanes.. Clinical Question. The clinical question addressed by ...
Although neurochemical and behavioral changes associated with near-total losses of DA in striatum have been well characterized, little is known about the long-term consequences on basal ganglia function of the partial monoamine loss associated with METH-induced neurotoxicity. The present data show that 3 weeks after administration of a neurotoxic regimen of METH, SP mRNA in striatum was decreased and CO activity in the EPN and the SNr was increased. However, ENK mRNA in the striatum and neuronal activity in the GP and STN were unaltered. These data suggest that such exposure to METH results in a selective decrease in striatonigral pathway function.. Numerous studies indicate that the DA innervation of striatum is compromised following administration of high doses of METH (Hotchkiss and Gibb, 1980; Wagner et al., 1980). In the present study, dose-dependent decreases in DA tissue content and TH immunoreactivity in striatum were seen 3 weeks after administration of multiple doses of METH. At ...
Exposure to high doses of methamphetamine (METH), a major drug of abuse, may cause neuronal damage. Previous studies have implicated the role of peroxynitrite, produced by nitric oxide (NO) and reactive oxygen species, in dopaminergic neurotoxicity produced by METH in mice. The present article was undertaken to investigate if a neurotoxic regimen of METH is associated with changes in tissue levels of nitrate and nitrite, which are the stable products of NO. Administration of METH (5 mg/kg x 3) to Swiss Webster mice resulted in marked depletion of dopamine (DA) and DA transporter (DAT) binding sites but no change in 5-hydroxytryptamine (5-HT) and 5-HT transporter (5-HTT) binding sites in the striatum, amygdala, frontal cortex, and hippocampus, suggesting that METH causes selective neurotoxicity to DA nerve terminals. The concentration of nitrate in the striatum was increased by about two-fold after METH administration; however, no changes in nitrate concentration were detected in other brain ...
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Evaluation of effects of copper histidine on copper transporter 1-mediated accumulation of platinum and oxaliplatin-induced neurotoxicity in vitro and in vivo
Chemotherapy-induced peripheral neuropathy (CIPN) is a major dose-limiting side effect of many chemotherapeutic agents including vincristine, paclitaxel, cisplatin, oxaliplatin, bortezomib and ixabepilone. Chemotherapy-induced peripheral neuropathy commonly occurs in greater than 40% of patients. To improve the peripheral neuropathy, the chemotherapy dosing is often either decreased or discontinued potentially affecting tumor responsiveness, prognosis, and survival.. There is an unmet medical need for treatment of cancer patients with chemotherapy induced neuropathic pain (CINP) and the proposed study will investigate the efficacy and safety of multiple dose levels of tetrodotoxin (TTX) versus placebo in moderate to severe neuropathic pain caused by chemotherapy. ...
A recent study evaluated the efficacy of cryotherapy for chemo-induced peripheral neuropathy; study participants wore frozen gloves and socks on the dominant side for 90 minutes, including the entire duration of drug infusion.
The USF College of Nursing is pleased to host Ellen M. Lavoie Smith, PhD, APRN, AOCN®, FAAN, who will present Bedside to Bench to Bedside: Managing Painful Chemotherapy-Induced Peripheral Neuropathy at noon on Tuesday, March 5, in MDN 2005. Dr. Smith is an associate professor and director of the PhD program at the University of Michigan School of Nursing. Her program of research is focused on improving the assessment and treatment of chronic, cancer-related neuropathic pain, with a specialty focus in painful chemotherapy-induced peripheral neuropathy. She has received independent research funding from the National Institutes of Health, the Oncology Nursing Society, the American Cancer Society, Dartmouth, and the University of Michigan. Dr. Smith conducted a cross-sectional study evaluating the clinimetric properties of peripheral neuropathy and neuropathic pain measurement approaches. She also completed an Oncology Nursing Society-funded study focused on utilizing quality improvement ...
The USF College of Nursing is pleased to host Ellen M. Lavoie Smith, PhD, APRN, AOCN®, FAAN, who will present Bedside to Bench to Bedside: Managing Painful Chemotherapy-Induced Peripheral Neuropathy at noon on Tuesday, March 5, in MDN 2005. Dr. Smith is an associate professor and director of the PhD program at the University of Michigan School of Nursing. Her program of research is focused on improving the assessment and treatment of chronic, cancer-related neuropathic pain, with a specialty focus in painful chemotherapy-induced peripheral neuropathy. She has received independent research funding from the National Institutes of Health, the Oncology Nursing Society, the American Cancer Society, Dartmouth, and the University of Michigan. Dr. Smith conducted a cross-sectional study evaluating the clinimetric properties of peripheral neuropathy and neuropathic pain measurement approaches. She also completed an Oncology Nursing Society-funded study focused on utilizing quality improvement ...
Chemotherapy can impact or damage the bodys peripheral nerves. Peripheral nerves carry sensations (or neurological messages) to and from the brain and spine, to control feeling and movement in different parts of the body including arms, legs, hands and feet. They also control the bowel and bladder. Damage to peripheral nerves that is caused by chemotherapy is called
TY - CHAP. T1 - Disruption of cholesterol homeostasis in developmental neurotoxicity. AU - Guizzetti, Marina. AU - Costa, Lucio G.. N1 - Publisher Copyright: © 2017 Elsevier Inc. All rights reserved. Copyright: Copyright 2021 Elsevier B.V., All rights reserved.. PY - 2017/1/1. Y1 - 2017/1/1. N2 - Cholesterol (a major component of brain membranes as well as of membrane microdomains called lipid rafts that are involved in the transduction of morphogenic signaling pathways) plays a pivotal role in fetal development and, in particular, brain development. Cholesterol levels in the brain are regulated through its biosynthesis and through its trafficking and elimination. Genetic syndromes caused by mutations in enzymes in the cholesterol biosynthesis pathways leading to reduced levels of cholesterol cause severe neurodevelopmental abnormalities, underscoring the importance of cholesterol during brain development. Additional neurodevelopmental disorders have been recently associated with altered ...
3-Fluoromethamphetamine (3-FMA) is an illegal designer drug of methamphetamine (MA) derivative. Up to date, little is known about the neurotoxic potential of 3-FMA. In the present study, we investigated the role of dopamine receptors in neurotoxicity induced by 3-FMA in comparison with MA (35 mg/kg, i.p.) as a control drug. Here we found that 3-FMA (40, 60 or 80 mg/kg, i.p.) produced mortality in a dose-dependent manner in mice. Treatment with 3-FMA (40 mg/kg, i.p.) resulted in significant hyperthermia, oxidative stress and microgliosis (microglial differentiation into M1 phenotype) followed by pro-apoptotic changes and the induction of terminal deoxynucleotidyl transferase dUDP nick end labeling (TUNEL)-positive cells ...
Neurotoxicology and Teratology provides a forum for publishing new information regarding the effects of chemical and physical agents on the...
Wilhelmina Childrens Hospital, UMC Utrecht, Utrecht, Netherlands. Background:. An increasing number of animal- and human studies indicate a potential harmful effects of general anesthesia during critical stage of neurodevelopment. Experimental and clinical studies emphasize that younger age (, 3 yr), higher dose (,1 MAC) and longer duration (,1 hr) of anesthesia are potential risk factors for anesthetic neurotoxicity. However, the translation of these risk factor to procedures potentially at risk has not been performed yet. Therefore, we tried to identify number and type of procedures potentially at risk for the anesthetic neurotoxicity.. Objective:. To quantify and to identify the type of procedures potentially at risk for the anesthetic neurotoxicity. From experimental studies we defined that the children younger than 3 years receiving 300%min sevoflurane are at risk.. Design:. We analyzed a retrospective cohort study of all patients between 0 and 18 years of age anesthetized between January ...
Chemotherapy-induced peripheral neuropathy (CIPN) is one of the most common and incapacitating complications of tumor treatment. outcomes the group of studies revealed essential lessons which have up to date subsequent function. Some examples of the include the usage of patient-reported indicator metrics the eradication of traditional-yet unsubstantiated-practice techniques as well as the breakthrough of molecular hereditary predictors of neuropathy. Current inquiry has been guided with the outcomes from these large-scale studies and therefore stands better potential for identifying long lasting solutions because of this treatment-limiting toxicity. = 0.003). The magnitude of the power from duloxetine was humble and were even more prominent with neuropathy due to oxaliplatin in comparison to paclitaxel within a subset evaluation. There is a considerably higher occurrence of CTCAE quality 2 or better exhaustion in the duloxetine arm but in any other case the medicine was well-tolerated. Organic ...
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In this online course, the Canadian Physiotherapy Association is assessing Chemotherapy-Induced Peripheral Neuropathy in the pediatric population.
Duvigneau, S.; Kettner, A.; Carius, L.; Griehl, C.; Findeisen, R.; Kienle, A.: Fast, inexpensive, and reliable HPLC method to determine monomer fractions in poly(3-hydroxybutyrate-co-3-hydroxyvalerate). Applied Microbiology and Biotechnology 105, pp. 4743 - 4749 (2021 ...
How is encephalopathy diagnosed?blood tests to detect diseases, bacteria, viruses, toxins, hormonal or chemical imbalance, or prions.spinal tap (your doctor will take a sample of your spinal fluid to look for diseases, bacteria, viruses, toxins, or prion)CT or MRI scan of your brain to detect abnormalities or damage.More items ...
Current evidence for solvent neurotoxicity is discussed. Exposure, absorption, distribution, and excretion of organic solvents are summarized. The effects of organic solvents on the peripheral nervous system are reviewed. A characteristic distal, symmetrical sensorimotor peripheral neuropathy has been clearly demonstrated following exposure of humans and animals to solvents such as n-hexane (110
Semantic Scholar extracted view of [Experimental studies on neurotoxicity of ethambutol and chloramphenicol - pathological and macroautoradiographic studies]. by Nobuo Wakata et al.
Pranita Tamma, MD, MHS, from The Johns Hopkins Medical Institution, Baltimore, MD, reported that colistin use in children has been associated primarily with nephrotoxicity and to a lesser extent neurotoxicity, at IDWeek 2012.
Fluoxetine neurotoxicity - Fast order processing. All payment cards. ED Drugs Without a Prescription. Best Online Quality. Only Quality Drugs.
Alle on koottu tukiasemasäteilyn haittoja osoittavia tutkimuksia. Näiden lisäksi on olemassa pienempi joukko tutkimuksia, joissa haittoja ei ole havaittu. Tiedossani ei ole yhtäkään tutkimusta, jossa tukiasemien läheisyys olisi yhdistynyt vähäisempään määrään oireita tai pienempään syöpäriskiin. Lista on päivitetty 29.3.2016. Abdel-Rassoul G, et al. Neurobehavioral effects among inhabitants around mobile phone base stations. Neurotoxicology. 2007;28:434-440. Ackermann…
RATIONALE: Studying samples of blood in the laboratory from patients receiving oxaliplatin for cancer may help doctors learn more about changes that occ
Images: Polycaspase Assay Kit, green was used to assess cell death in primay rat hippocampal neurons.Cells were plated on 25-mm poly-l-lysine-coated coverslips at 300,000 cells per coverslip. Cells were used at 4 or 8 days in vitro. Composite imagae (A) 3 out of 4 cells are apoptotic (green). No cells were necrotic as both of the PI-positive cells were FLICA-positive; they had compromised membranes and were probably in the late stages of apoptosis rather than necrosis. (B) 3 Caspase-positive cells fluoresce green ...
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