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Neurological disorder

Indoor air immissions of organic solvents from paints and varnishes can cause neurological [Pg.1244]

Other compounds in paints and varnishes apart from solvents can cause neurological disorders (e.g., lead). However, it is difficult to prove that solvents specifically cause neurological changes. [Pg.1244]

In earlier reviews and cross-sectional studies, various symptoms and neuro-behavioral effects were described for workers in the paint manufacturing industry, house painters, car and industry painters, and shipyard painters. Subjective symptoms (fatigue, loss of concentration, emotional instability, short-term memory disorders, headache) or effects on psychomotoric performance are examples of these symptoms. However, similar former studies did not find symptoms in house painters using mainly water-based paints.  [Pg.1244]

Different results were found concerning neuro-physiological changes and neurological diseases. Electroencephalographic changes and a slight decrease in cerebral blood flow of paint industry workers was noted by Oerbaek et al. and there were occasional cases of [Pg.1244]

Inconsistent results were reported for severe diseases of the central nervous system (nemopsychiatric diseases, encephalopathy) for painters and other persons exposed to sol-vents.- - -  [Pg.1245]

On completion of the following case study, you will be able to  [Pg.17]

Mrs Smith, a retired maths lecturer, is 69 years old. She has consulted her family doctor complaining that she feels very stiff and has developed tremor in her limbs, especially in her hands. She also reported having difficulties getting up and down the stairs at home. She mentioned that her mother remains very fit however, her father, who died at the age of 70, developed similar symptoms when he was 65 years old. Her doctor made a provisional diagnosis and referred her to a specialist clinic. The consultant prescribed levodopa (L-dopa) plus carbidopa. After finding out the [Pg.17]

Clinical Physiology and Pharmacology Farideh Javid and Janice McCurrie 2008 John Wiley Sons, Ltd [Pg.17]

Q2 What are the symptoms of Parkinson s disease Could it be hereditary  [Pg.18]

Q4 Comment on the pharmacological management of this condition. What classes of drug are available for patients with Parkinson s disease  [Pg.18]

The transcription factor that binds to the second GC-rich region (—110 to —103) has not yet been identified. Immediately downstream of this GC-rich element is an inverted MEDl element (multiple start site downstream 1, iMED), an element involved in constitutive expression of ABCBl in neuroblastoma and leukemia cell lines. It is not clear whether iMED also contributes to ABCBl induction in multidrug-resistant cells. [Pg.389]

Importantly, GC-rich elements also control constitutive expression of a number of other drug transporters. The MRPl promoter contains a GC-rich domain (—91 to +103) that has been shown to interact with SP-1 and is essential for its basal transcription. MRP3 features multiple GC-rich SP-1 binding sites (—91 to —21). BCRP, another TATA-less promoter, harbors several putative SP-1 binding sites, about 300 bp upstream ofthe transcription start site, which confer basal expression. [Pg.389]

The MRP2 promoter, which lacks GC-rich sequences, possesses a putative CCAAT box that interacts in vitro with YB-1 rather than NE-Y. In summary, constitutive expression of ABC drug transporters is conferred mainly by SP-1 binding to GC-rich sequences and by NE-Y binding to an inverted CCAAT box [6, 7]. [Pg.389]

The brain is a unique compartment shielded from the peripheral circulation by the [Pg.389]


Is the substance known to cause ctuicer or serious reproductive or neurological disorders, genetic mutations, or otlier clironic hetiltli effects ... [Pg.67]

Epilepsy is a chronic neurological disorder that affects about 0.6-0.8% of the general population worldwide. The clinical hallmark of epilepsy is... [Pg.125]

Die neurological disorder associated with severe vitamin B12 deficiency is termed funicular myelitis. Vitamin B12 deficiency leads to disturbed choline-, phospholipid-, and nucleic-acid synthesis, resulting in spinal marrow damages. Disturbed myelin synthesis finally causes irreversible neurological failure. In addition, there are psychiatric disturbances (disturbed memory, apathy). [Pg.512]

TNF is a pleiotropic cytokine exerting a wide range of cellular responses, that affect biological processes such as lipid metabolism, coagulation, and insulin resistance and the function of endothelial cells. As a major proinflammatory cytokine TNF is also involved in progression of diseases like cancer, Alzheimer, Diabetes type II, cardiovascular, pulmonary or neurological disorders, and many autoimmune diseases. Blocking the action of TNF clearly reduces its inflammatory potential on various autoimmune disorders like Crohn s disease, rheumatoid arthritis (RA), and psoriasis. [Pg.1249]

Whether supplementation of vitamin B12 is useful in the therapy of a number of neurological disorders is still subject to discussion and further investigations. [Pg.1293]

Meisler MH, Kearney JA (2005) Sodium channel mutations in epilepsy and other neurological disorders. J Clin Invest 115 2010-2017. [Pg.1308]

The barbiturates are contraindicated in patients with known hypersensitivity to the drugs. The barbiturates are used cautiously in patients with liver or kidney disease and those with neurological disorders. The barbiturates (eg, phenobarbital) are used with caution in patients with pulmonary disease and in hyperactive children. When barbiturates are used with other CNS depressants (eg, alcohol, narcotic analgesics, and antidepressants), an additive CNS depressant effect may occur. See Chapter 26 for additional information on the barbiturates. [Pg.257]

Item 19 List any pre-existing physician-diagnosed allergies, birth defects, medical conditions (including developmental and/or neurologic disorders) for the patient. [Pg.670]

Thus, in diseases resulting from mutations of mtDNA, an affected mother would in theory pass the disease to all of her children but only her daughters would transmit the trait. However, in some cases, deletions in mtDNA occur during oogenesis and thus are not inherited from the mother. A number of diseases have now been shown to be due to mutations of mtDNA. These include a variety of myopathies, neurologic disorders, and some cases of diabetes mellitus. [Pg.323]

The reported risk factors for HIV-associated sensory neuropathy are varied and may have changed since the availability of HAART. In the pre-HAART era, age, nutritional deficiencies, alcohol exposure, higher HIV viral load, and low CD4 counts (Moyle and Sadler 1998 Childs et al. 1999), as well as mood, other neurologic disorders and functional abnormalities (Schifitto et al. 2002) were neuropathy risk factors. In the HAART era, the use of NRTI (Cherry et al. 2006 Pettersen et al. 2006) and exposure to protease inhibitor (PI) medication (Pettersen et al. 2006 Smyth et al. 2007) are considered additional risk factors. Although hepatitis C mono-infection has been associated with peripheral nerve disease, and there is... [Pg.55]

NfNDS rt-PA Study Group. Tissue plasminogen activator for acute ischemic stroke. The National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group. N EnglJMed 1995 333 1581-1587. [Pg.29]

This section will review the phase III clinical trials of IV thrombolytic agents for acute ischemic stroke, organized by the type of agent and the time window from stroke onset to study drug delivery (Table 3.1). The 1995 National Institute of Neurological Disorders and Stroke (NINDS) rt-PA trial is presented first because it showed that IV rt-PA, given within 3 hours of stroke onset, reduced stroke-related disability. This trial was the basis for the United States Food and Drug Administration (FDA) approval for rt-PA for use in acute ischemic stroke. [Pg.41]

Dr. Smith is supported by grant funding from the National Institute of Neurological Disorders and Stroke (K23 NS-046327). [Pg.55]

Kwiatkowski TG, Libman RB, Frankel M, Tilley BC, Morgenstem LB, Lu M, Broderick JP, Lewandowski CA, Marler JR, Levine SR, Brott T. Effects of tissue plasminogen activator for acute ischemic stroke at one year. National Institute of Neurological Disorders and Stroke Recombinant Tissue Plasminogen Activator Stroke Study Group. New England Journal of Medicine. 1999 340 1781-1787. [Pg.56]

The severity of the neurological deficit at the time of stroke onset is a major predictor of stroke outcome. In an analysis of the placebo-treated patients in the National Institute of Neurological Disorders and Stroke (NINDS) recombinant tissue-plasminogen activator (rt-PA) study, the best acute predictor of a poor outcome at 1 year was an National Institute of Health Stroke Scale (NIHSS) score >17 for patients over 70 years. These criteria had a high specificity (98%), but sensitivity was only 31%. The low sensitivity of the acute NIHSS score alone in predicting... [Pg.198]


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