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Cerebrospinal protein levels

A generalized systemic illness may accompany HIV seroconversion (Cooper et al. 1985). Guillain-Barre syndrome (GBS) (Piette et al. 1986), unilateral (Wiselka et al. 1987) or bilateral facial palsies (Wechsler and Ho 1989), bibra-chial palsy (Calabrese et al. 1987) and sensory neuropathy (Denning 1988) have been reported to occur during this process, usually within 1-2 weeks of the acute febrile illness. Spinal fluid analysis may show a mild to moderate mononuclear pleocytosis and a mild increase in protein levels. The precise relationship to HIV viral load in the cerebrospinal fluid (CSF) or plasma is unknown (Brew 2003). There is no proven therapy, but most patients recover spontaneously without any treatment. [Pg.58]

Cinque P, Vago L, Mengozzi M, Torn V, Ceresa D, Vicenzi E, Transidico P, Vagani A, Sozzani S, Mantovani A, Lazzarin A, PoU G (1998) Elevated cerebrospinal fluid levels of monocyte chemotactic protein-1 correlate with HlV-1 encephalitis and local viral rephcation. AIDS 12 1327-1332... [Pg.241]

Lithium is readily absorbed from the gastrointestinal tract, reaching a peak plasma level in 2 to 4 hours. Distribution occurs throughout the extracellular fluid with no evidence of protein binding. Passage through the blood-brain barrier is limited, so that cerebrospinal fluid levels are 50% of plasma levels at steady state. [Pg.393]

Delavirdine has an oral bioavailability of about 85%, but this is reduced by antacids or H2-blockers. It is extensively bound ( 98%) to plasma proteins and has correspondingly low cerebrospinal fluid levels. Serum half-life is approximately 6 hours. [Pg.1079]

The absolute oral bioavailability of ribavirin is 45-64%, increases with high-fat meals, and decreases with co-administration of antacids. Plasma protein binding is negligible, volume of distribution is large, and cerebrospinal fluid levels are about 70% of those in plasma. Ribavirin elimination is primarily through the urine therefore, clearance is decreased in patients with creatinine clearances less than 30 mL/min. [Pg.1086]

Hypothalamic content and mRNA levels of TNF-a peak during the early light period, when NREM sleep is maximal, in the rat (70,71). IL-1-like activity varies with the sleep-wake cycle in the cerebrospinal fluid of cats (72). IL-lp protein levels in plasma (73) and hypothalamic IL-lp mRNA levels (74) are highest during the sleep period in rats. Sleep deprivation increases IL-ip and TNF-a mRNA levels in the hypothalamus (75-77) and expression of the 55-kD TNFR is also stimulated in the brain (77). In humans, peak levels of IL-1 occur at sleep onset in the blood (78) and IL-1 blood levels also increase during sleep deprivation (79). Blood levels of TNF-a correlate with EEG slow-wave activity (80), and concentrations of circulating TNF-a and the soluble 55-kD TNFR increase after sleep deprivation in humans (81). [Pg.520]

In contrast to earlier NRTIs, abacavir is a guanosine analog. It is well absorbed following oral administration (83%), is unaffected by food, and is about 50% bound to plasma proteins. In singledose studies, the elimination half-life was 1.5 hours. Cerebrospinal fluid levels are approximately one-third those of plasma. The drug is metabolized by alcohol dehydrogenase and glucuronosyltransferase to inactive metabolites that are eliminated primarily in the urine. [Pg.1137]

The oral bioavailability of nevirapine is excellent (> 90%) and is not food-dependent. The drug is highly lipophilic, approximately 60% protein-bound, and achieves cerebrospinal fluid levels that are 45% of those in plasma. It is extensively metabolized by the CYP3 A isoform to hydroxylated metabolites and then excreted, primarily in the urine. [Pg.1139]

Mehta PD, Pirttila T, Mehta SP, Sersen EA, Aisen PS, Wisniewski HM. Plasma and cerebrospinal fluid levels of amyloid beta proteins 1-40 and 1-42 in Alzheimer disease. Arch Neurol 2000 57(1) 100-105. [Pg.127]

ScHAPiRO, M. B., Rapoport, S. L, Moller, H. J., Davies, P., Hampel, H. (2002). Differential diagnosis of Alzheimer disease with cerebrospinal fluid levels of tau protein phosphorylated at threonine 231. Arch. Neurol. 59, 1267-1272. [Pg.273]

Dependence of cerebrospinal fluid Tau protein levels on apolipoprotein E4 allele frequency in patients with Alzheimer s disease. Neurosci. Lett. 225, 213-215. [Pg.274]

Most proteomics analyses involve 2-D electrophoresis and MALDl-TOF MS steps, as this approach allows for a reliable quantification of changes in protein levels. In one study, the LC-MS/MS approach was used for the detection of proteins enriched in amyloid plaques in the AD brain (liao et al., 2004). Employing the former proteomic approach, levels of about 100 proteins were foimd to be changed in the AD brain and cerebrospinal fluid (CSF) in comparison with the control brain and CSF, respectively (Table 15.1). These proteins have various functions, mainly involved in neurotransmission, guidance, signal transduction, metabolism, detoxification, and conformational changes. The CSF proteins are plasma proteins. [Pg.284]

Matsushita S, Miyakawa T, Maesato H, Matsui T, Yokoyama A, Arai H et al (2(X)8) Elevated cerebrospinal fluid tau protein levels in Wernicke s encephtilopathy. Alcohol CHn Exp Res... [Pg.664]

Terzi M, Birinci A, Cetinkaya E, Onar MK (2007) Cerebrospinal fluid total tau protein levels in patients with multiple sclerosis. Acta Neurol Scand 115 325-330 Tolnay M, Probst A (1999) REVIEW tau protein pathology in Alzheimer s disease and related disorders. Neuropathol Appl Neurobiol 25 171-187 Trojanowski JQ, Lee VM (2002) The role of tau in Alzheimer s disease. Med CUn North Am 86 615-627... [Pg.666]

DJI does not appear to be an essential component of LBs in sporadic cases (Bandopadhyay et al., 2004). DJI mutations are rare in sporadic PD but recent studies suggest that DJI may play an important role in common forms of the disease. Sporadic PD brain exhibits DJI with oxidative damage (Choi et al., 2006). Sporadic PD patients also demonstrate a significant increase in total cerebrospinal fluid DJI protein levels compared to normal controls (Waragai et al., 2006). [Pg.725]

A consequence of the development of the large number of cephalosporins is that the molecular structures have become more and more complex. Alterations in the cephalosporin molecule have resulted in differences between cephalosporins in spectrum of activity, protein binding, peak serum level, serum half-life, route of excretion, cerebrospinal fluid levels and toxicity. Cephalosporins are semi-synthetic antibiotics derived from 7-aminocephalosporanic acid, which is also called the cephalosporin nucleus. The cephem ring ( nucleus") is composed of a (3-lactam ring fused with a dihydrothiazine ring (Figure 1). [Pg.299]

Nephelometry, immunoturbidimetry, electroimmunodiffu-sion, and RID are most often used for measurements of albumin and IgG in cerebrospinal fluid. Apparent absence of IgG may be due to its. degradation by proternases in the specimen. RIA is required for determination of specific pro-teins present in very low concentrations (e.g., IgM). The reference interval for albumin levels in lumbar CSF by RID is 17.7 to 25.1 mg/dL. IgA, IgD, and IgM, measured by RIA, are each normally less than 0.2 mg/dL. Reference intervals for IgG are age related their means increase from 3.5 mg/dL in the 15- to 20-year-old group to 5.8 in adults aged 60 or older. The usual reference interval for CSF IgG in adults is 0.8 to 4.2 mg/dL for total protein, 15 to 45 mg/dL. Total protein levels are considerably higher in neonates, and in healthy elderly adults, concentrations up to 60 mg/dL are considered normal. [Pg.590]

Han MR, Schellenberg GD, Wang LS, Initiative A s D N (2010) Genome-wide association reveals genetic effects on human A(142 and x protein levels in cerebrospinal fluids A case control study. BMC Neurol 10 90. doi 10.1186/1471-2377-10-90... [Pg.525]

The patient was treated for 10 days with ceftriaxone and remained afebrile after the second day. At completion of therapy, cerebrospinal fluid was sterile, CIE was negative, and the white cell count and protein levels were returning tow ard the normal range. [Pg.453]

During the first phase of the disease, the most common laboratory abnormalities are a low white blood cell count (leukopenia) and a low platelet count (thrombocytopenia). Liver enzymes in the serum may also be mildly elevated. After the onset of neurological disease during the second phase, an increase in protein levels, an increase in the number of white blood cells or a decrease in the glucose levels in the cerebrospinal fluid (CSF) is usually found. [Pg.105]

Since the preparation of this manuscript, a recent paper has reported total tau protein levels in cerebrospinal fluid were elevated in acute WE, but declined at follow up. This may suggest that neuronal cell death occurs transiently in acute WE. [Pg.297]

Serum and Cerebrospinal Fluid Bilirubin and Protein Levels in Relation TO Tocopherol Administration... [Pg.566]

Cinque, P., Vago, L., Mengozzi, M., Torri, V., Ceresa, D., Vicenzi, E., Transidico, P., Vagani, A., Sozzani, S., Mantovani, A., Lazzarin, A., and Poli, G. (1998). Elevated cerebrospinal fluid levels of monocyte chemotactic protein-1 correlate with HIV-1 encephalitis and local viral replication. AIDS 12, 1327 1332. [Pg.25]

The cerebrospinal fluid protein is elevated in all cases of HAP, while the cell count is normal. Protein levels usually range from 100 to 700 mg per 100 ml, but may be higher in some cases. Frequently there is some correlation between the severity of the clinical picture and the protein concentration in the cerebrospinal fluid. [Pg.362]

Hyperammonemia Type 2. A deficiency of ornithine transcarbamoylase (reaction 2, Figure 29-9) produces this X chromosome-linked deficiency. The mothers also exhibit hyperammonemia and an aversion to high-protein foods. Levels of glutamine are elevated in blood, cerebrospinal fluid, and urine, probably due to enhanced glutamine synthesis in response to elevated levels of tissue ammonia. [Pg.247]

Hyperargininemia. This defect is characterized by elevated blood and cerebrospinal fluid arginine levels, low erythrocyte levels of arginase (reaction 5, Figure 29-9), and a urinary amino acid pattern resembling that of lysine-cystinuria. This pattern may reflect competition by arginine with lysine and cystine for reabsorption in the renal tubule. A low-protein diet lowers plasma ammonia levels and abolishes lysine-cystinuria. [Pg.248]


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