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Background Hypertension can be detected at the primary health-care level and low-cost treatments can effectively control hypertension. We aimed to measure the prevalence of hypertension and progress in its detection, treatment, and control from 1990 to 2019 for 200 countries and territories. Methods We used data from 1990 to 2019 on people aged 30-79 years from population-representative studies with measurement of blood pressure and data on blood pressure treatment. We defined hypertension as having systolic blood pressure 140 mm Hg or greater, diastolic blood pressure 90 mm Hg or greater, or taking medication for hypertension. We applied a Bayesian hierarchical model to estimate the prevalence of hypertension and the proportion of people with hypertension who had a previous diagnosis (detection), who were taking medication for hypertension (treatment), and whose hypertension was controlled to below 140/90 mm Hg (control). The model allowed for trends over time to be non-linear and to vary by age. Findings The number of people aged 30-79 years with hypertension doubled from 1990 to 2019, from 331 (95% credible interval 306-359) million women and 317 (292-344) million men in 1990 to 626 (584-668) million women and 652 (604-698) million men in 2019, despite stable global age-standardised prevalence. In 2019, age-standardised hypertension prevalence was lowest in Canada and Peru for both men and women; in Taiwan, South Korea, Japan, and some countries in western Europe including Switzerland, Spain, and the UK for women; and in several low-income and middle-income countries such as Eritrea, Bangladesh, Ethiopia, and Solomon Islands for men. Hypertension prevalence surpassed 50% for women in two countries and men in nine countries, in central and eastern Europe, central Asia, Oceania, and Latin America. Globally, 59% (55-62) of women and 49% (46-52) of men with hypertension reported a previous diagnosis of hypertension in 2019, and 47% (43-51) of women and 38% (35-41) of men were treated. Control rates among people with hypertension in 2019 were 23% (20-27) for women and 18% (16-21) for men. In 2019, treatment and control rates were highest in South Korea, Canada, and Iceland (treatment >70%; control >50%), followed by the USA, Costa Rica, Germany, Portugal, and Taiwan. Treatment rates were less than 25% for women and less than 20% for men in Nepal, Indonesia, and some countries in sub-Saharan Africa and Oceania. Control rates were below 10% for women and men in these countries and for men in some countries in north Africa, central and south Asia, and eastern Europe. Treatment and control rates have improved in most countries since 1990, but we found little change in most countries in sub-Saharan Africa and Oceania. Improvements were largest in high-income countries, central Europe, and some upper-middle-income and recently high-income countries including Costa Rica, Taiwan, Kazakhstan, South Africa, Brazil, Chile, Turkey, and Iran. Interpretation Improvements in the detection, treatment, and control of hypertension have varied substantially across countries, with some middle-income countries now outperforming most high-income nations. The dual approach of reducing hypertension prevalence through primary prevention and enhancing its treatment and control is achievable not only in high-income countries but also in low-income and middle-income settings. Copyright (C) 2021 World Health Organization; licensee Elsevier.

The impact of explosive load must be considered in the design of civil defense structures. An explosion occurring below ground level generates a ground-shock wave that affects buried structures in the proximity of the explosion point. Current knowledge about the spectrum of induced vibrations in buried structures is limited. The computer code FLAC offers an opportunity to model the propagation of ground shock waves as well as the interaction between soil and structures. This paper present the procedure employed to calibrate a numerical model against idealized field data for a buried exploding charge. Some of the results during the calibration process are also presented. A FLAC model was calibrated that can reproduce the idealized field data with relatively good accuracy. To make the calibrated model successful a material model exhibiting volumetric yield had to be used.

Summary In 2006, the Canadian Integrated Program for Antimicrobial Resistance Surveillance (CIPARS) Farm Program was implemented in sentinel grower-finisher swine herds in Quebec, Ontario, Manitoba, Saskatchewan and Alberta. Herds were visited 1–3 times annually. Faecal samples were collected from pens of close-to-market (CTM) weight (>80 kg) pigs and antimicrobial use (AMU) data were collected via questionnaires. Samples were cultured for generic Escherichia coli and Salmonella and tested for antimicrobial susceptibility. This paper describes the findings of this program between 2006 and 2008. Eighty-nine, 115 and 96 herds participated in this program in 2006, 2007 and 2008 respectively. Over the 3 years, antimicrobial resistance (AMR) levels remained consistent. During this period, resistance to one or more antimicrobials was detected in 56–63% of the Salmonella spp. isolates and 84–86% of E. coli isolates. Resistance to five or more antimicrobials was detected in 13–23% of Salmonella and 12–13% of E. coli. Resistance to drugs classified as very important to human health (Category I) by the Veterinary Drug Directorate (VDD), Health Canada, was less than or equal to 1% in both organisms. AMU data were provided by 100 herds in 2007 and 95 herds in 2008. Nine herds in 2007 and five herds in 2008 reported no AMU. The most common route of antimicrobial administration (75–79% of herds) was via feed, predominantly macrolides/lincosamides (66–68% of herds). In both 2007 and 2008, the primary reasons given for macrolide/lincosamide use were disease prevention, growth promotion and treatment of enteric disease. The Category I antimicrobials, ceftiofur and virginiamycin were not used in feed or water in any herds in 2008, but virginiamycin was used in feed in two herds in 2007. Parenteral ceftiofur was used in 29 herds (29%) in 2007 and 20 herds (21%) in 2008. The reasons for ceftiofur use included treatment of lameness, respiratory disease and enteric disease.

A DNA-based one-stage technique, polymerase chain reaction with sequence-specific primers (PCR-SSP) was developed for genotyping of the platelet specific alloantigen HPA-5 (Bra/Brb). Sequence-specific primers, matching the wild type and the point mutation responsible for the HPA-5 (Bra/Brb) phenotype, were constructed. Conjointly a fragment of the gene coding for glycoprotein (GP) IIIa was amplified as an internal control of the enzyme reaction. Using these HPA-5 (Bra/Brb) sequence-specific primers the correct fragment of the GPIa gene was amplified, as evidenced by the PCR product size, the restriction map and by the nucleotide sequence. This assay was applied on 187 Swedish blood donors; 157 individuals were found to have a homozygous HPA-5a (Bra/Brb) genotype and 30 individuals a heterozygous HPA-5a,b (Bra/Brb) genotype. None of the donors was found to display a homozygous HPA-5b (Bra/Brb) genotype. Thus, the (HPA-5b) Bra antigen frequency in this population will be approximately 16.0% with a gene frequency of 8.0%. It is concluded that this assay is an attractive technique for genotyping of the HPA-5 (Bra/Brb) alloantigens on genomic DNA. The technique can replace serological alloantigen typing, especially in cases where platelets and rare human alloantisera are not available.

This test case is based on experimental data from a study of the mechanical and hydraulic reaction of a natural rough joint upon normal and shear stress loading. The test was conducted in NGI's Coupled Shear Flow Test apparatus, which allows large diameter jointed rock cores to be tested under controlled boundary stresses with multiple loading-unloading cycles. Five teams have modelled two joints, using finite and discrete element codes with different joint constitutive laws. The simulation results agree well with the experimental data during pure normal stress loading, and less well for shear displacement induced joint dilation.

The most commonly used microstructure for passive fiber alignment is the ordinary v-groove, defined by {111} planes on a (100) silicon wafer. The plane at the end of the groove, having a 54.7/spl deg/ angle to the surface, can be used as a reflecting mirror. For single-mode fiber applications, a 45/spl deg/ mirror is advantageous together with high accuracy in the position of the fiber, i.e. a smooth mirror and good control of the groove geometry is needed. Two techniques are presented to form 45/spl deg/ mirrors along with well-defined grooves in silicon, using the wet anisotropic etchants EDP and KOH. These techniques are used: (1) to reveal {110} planes on (100) silicon and (2) to make {111} mirrors on wafers that are cut 9.7/spl deg/ off the [100] axis. On (100) silicon, EDP without pyrazine gave the best result. The best mirror and groove reproducibility was found on off-axis cut silicon, using 36 wt.% KOH, with isopropyl alcohol added.

In 2006, the Canadian Integrated Program for Antimicrobial Resistance Surveillance (CIPARS) Farm Program was implemented in sentinel grower-finisher swine herds in Québec, Ontario, Manitoba, Saskatchewan and Alberta. Herds were visited 1-3 times annually. Faecal samples were collected from pens of close-to-market (CTM) weight (80 kg) pigs and antimicrobial use (AMU) data were collected via questionnaires. Samples were cultured for generic Escherichia coli and Salmonella and tested for antimicrobial susceptibility. This paper describes the findings of this program between 2006 and 2008. Eighty-nine, 115 and 96 herds participated in this program in 2006, 2007 and 2008 respectively. Over the 3 years, antimicrobial resistance (AMR) levels remained consistent. During this period, resistance to one or more antimicrobials was detected in 56-63% of the Salmonella spp. isolates and 84-86% of E. coli isolates. Resistance to five or more antimicrobials was detected in 13-23% of Salmonella and 12-13% of E. coli. Resistance to drugs classified as very important to human health (Category I) by the Veterinary Drug Directorate (VDD), Health Canada, was less than or equal to 1% in both organisms. AMU data were provided by 100 herds in 2007 and 95 herds in 2008. Nine herds in 2007 and five herds in 2008 reported no AMU. The most common route of antimicrobial administration (75-79% of herds) was via feed, predominantly macrolides/lincosamides (66-68% of herds). In both 2007 and 2008, the primary reasons given for macrolide/lincosamide use were disease prevention, growth promotion and treatment of enteric disease. The Category I antimicrobials, ceftiofur and virginiamycin were not used in feed or water in any herds in 2008, but virginiamycin was used in feed in two herds in 2007. Parenteral ceftiofur was used in 29 herds (29%) in 2007 and 20 herds (21%) in 2008. The reasons for ceftiofur use included treatment of lameness, respiratory disease and enteric disease.

Cerebrospinal fluid (CSF) levels of neurofilament triplet protein (NFL), a non-specific marker of neuronal damage, are normal in Parkinson's disease (PD) but increased after brain trauma and in several neurological disorders. Using longitudinal CSF-NFL measurements as an indicator of neuronal damage, this study investigated the impact of deep brain stimulation (DBS) of the subthalamic nucleus (STN) on the brain, directly following the surgical intervention and in chronically treated patients with PD.CSF-NFL levels were measured consecutively in eight patients with PD before and after STN-DBS treatment.CSF-NFL levels were normal prior to STN-DBS and increased sharply during the first 2 weeks post-operatively, but normalized after 12 months or more.The STN-DBS procedure leads to an acute but limited neuronal damage, as expected. However, normal CSF-NFL levels at 12 months post-operatively and beyond suggest the absence of any long-term neuronal damage caused by long-term STN-DBS stimulation.

Psychiatric and neurological symptoms are common among soldiers exposed to blast without suffering a direct head injury. It is not known whether such symptoms are direct consequences of blast overpressure.To examine if repeated detonating explosions or firing if of heavy weapons is associated with neurochemical evidence of brain damage.Three controlled experimental studies. In the first, army officers were exposed to repeated firing of a FH77B howitzer or a bazooka. Cerebrospinal fluid (CSF) was taken post-exposure to measure biomarkers for brain damage. In the second, officers were exposed for up to 150 blasts by firing a bazooka, and in the third to 100 charges of detonating explosives of 180 dB. Serial serum samples were taken after exposure. Results were compared with a control group consisting of 19 unexposed age-matched healthy volunteers.The CSF biomarkers for neuronal/axonal damage (tau and neurofilament protein), glial cell injury (GFAP and S-100b), blood-brain barrier damage (CSF/serum albumin ratio) and hemorrhages (hemoglobin and bilirubin) and the serum GFAP and S-100b showed normal and stable levels in all exposed officers.Repeated exposure to high-impact blast does not result in any neurochemical evidence of brain damage. These findings are of importance for soldiers regularly exposed to high-impact blast when firing artillery shells or other types of heavy weapons.

White matter lesions (WMLs) caused by small vessel disease are common in elderly people and contribute to cognitive impairment. There are no established biochemical markers for WMLs. We aimed to study the relation between degree of WMLs rated on magnetic resonance imaging of the brain and cerebrospinal fluid (CSF) levels of structural biomarkers associated with Alzheimer's disease (AD) and subcortical vascular dementia.Fifty-three non-demented elderly individuals with WMLs were subjected to lumbar puncture. Degree of WMLs was rated using the Fazekas scale. Volumetric assessment of WMLs was performed. CSF samples were analyzed for the 40 and 42 amino acid fragments of amyloid beta, alpha- and beta-cleaved soluble amyloid precursor protein, total tau (T-tau), hyperphosphorylated tau (P-tau(181)), neurofilament light protein (NFL), sulfatide and CSF/Serum-albumin ratio.Fifteen subjects had mild, 23 had moderate and 15 had severe degree of WMLs. CSF-NFL levels differed between the groups (P0.001) and correlated with the volume of WMLs (r = 0.477, P0.001). CSF sulfatide concentration displayed similar changes but less strongly. T-tau, P-tau(181) and the different amyloid markers as well as CSF/S-albumin ratio did not differ significantly between the groups.The association of increased CSF-NFL levels with increasing severity of WMLs in non-demented subjects suggests that NFL is a marker for axonal damage in response to small vessel disease in the brain. This manifestation may be distinct from or earlier than the neurodegenerative process seen in AD, as reflected by the lack of association between WMLs and AD biomarkers.

Traumatic brain injury (TBI) is one of the most common causes of death and dismal outcome among children and young adults. The morbidity and mortality differ but more aggressive monitoring and more designated neuro intensive care units have improved the results. Studies have demonstrated a connection between apolipoprotein E (APOE) genotype and outcome after TBI, but few are prospective and none is from northern Europe. APOE has three alleles: epsilon2, epsilon3 and epsilon4.A total of 96 patients with Glasgow coma score (GCS)or =8 were prospectively and consecutively included. APOE genotypes were all analyzed at the same laboratory from blood samples by polymerase chain reaction-restriction fragment length polymorphism.All patients were assessed at 1 year with Glasgow outcome scale extended (GOSE), National Institute of Health Stroke Scale (NIHSS) and the Barthel daily living index. The genotype was available in all patients. Twenty-six patients expressed APOE epsilon4 while 70 patients did not. Outcome demonstrated that patients with APOE epsilon4 had worse outcome vs. those lacking this allele. When subdividing patients into gender, males with APOE epsilon4 did worse, a difference not detected among female patients.APOE epsilon4 correlated to worse outcome in TBI patients. We also found that males with APOE epsilon4 had poor outcome while females did not. Thus, the results indicate that genetic polymorphism may influence outcome after TBI.

We explored the relationship between adiposity factors measured during mid-life and blood-brain barrier (BBB) integrity measured via the cerebrospinal fluid/serum (CSF/S) albumin ratio in late life. Adiposity factors included body mass index and blood levels of sex hormone binding globulin (SHBG) and leptin. Design. Retrospective analyses over 24 years within a longitudinal study.Population-based sample. Subjects. Eighty-one women.CSF/S albumin ratio.The CSF/S albumin ratio measured at age 70-84 years was higher amongst women who were overweight or obese (6.50 +/- 2.79 vs. 5.23 +/- 1.61, age-adjusted P = 0.012), and was inversely correlated with SHBG (age-adjusted r = -0.321, P0.005) at age 46-60 years. In stepwise regression models, SHBG predicted the CSF/S albumin ratio (beta = -0.017, R2 = 0.107, P = 0.007). The best model (R2 = 0.187) predicting CSF/S albumin ratio included SHBG, age group (age 46 years versus46), overweight or obesity, and an age group by SHBG interaction.Lower levels of SHBG in mid-life were related to worse BBB integrity in women after 24 years in late life, even considering other adiposity factors. SHBG may be important for understanding sex hormone-mediated mechanisms in brain health or as an independent marker of adipose tissue, the largest endocrine organ.

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative syndrome with familial and sporadic forms. Most ALS-associated mutations are found in the superoxide dismutase 1 (SOD1) gene. We conducted a study including 60 sporadic and 19 familial ALS patients, 206 reference patients with other neurological disorders and 40 age- and sex-matched healthy controls to test the hypothesis that cerebrospinal fluid (CSF) levels of neurofilament light (NF-L) protein, a marker of axonal degeneration, might provide diagnostic and prognostic information on the disease. All ALS patients were screened for SOD1 mutations. Ten of the familial and five of the sporadic cases carried SOD1 mutations. NF-L concentration [median (range)] was strongly elevated in ALS [2110 (255-10 800) ng/l] compared with reference patients and healthy controls [277 (125-15 506) and 175 (125-710) ng/l, respectively, P0.001] and correlated inversely with disease duration (Spearman R = -0.518, P = 0.001). NF-L levels were lower in SOD1 mutation-associated ALS compared with SOD1 wild-type (wt) ALS (P = 0.03). In conclusion, CSF NF-L levels may provide both diagnostic and prognostic information, particularly in SOD1 wt ALS.

A technique for controlling the tip–sample distance in near-field optical microscopes is presented. It consists of mechanically exciting a fiber tip inserted without any adhesive between the two prongs of a high Q-piezoelectric tuning fork. The detection of the shear forces is classically achieved by measuring the decrease of the dithering amplitude when the tip approaches the surface. This simple setup greatly simplifies tip replacement and its resonance frequency tuning.

GFAP levels in the CSF were highly elevated in three genetically confirmed cases of Alexander disease clinically conforming with infantile, early and late juvenile forms. No other CSF abnormalities were detected. Assay of CSF-GFAP may prove to be a rapid and cost-effective screening test in clinical variants of Alexander disease and an indicator of GFAP gene mutations.

In a previous study we found that nine of 47 siblings to multiple sclerosis (MS) patients with a normal neurological examination carry an intrathecal oligoclonal immunopathy with limited specificity, a condition we termed MS immunopathic trait. The purpose of this study is to further characterize the MS immunopathic trait phenotype. We found that the neurofilament light protein (NFL) and glial fibrillary acidic protein (GFAp) concentrations were increased in the group of patients with clinically definite MS (n = 47) in latent or slowly progressive phases. There was no increase in GFAp and NFL in cerebrospinal fluid in the healthy siblings of MS patients (n = 47), nor in the subgroup of these siblings with MS immunopathic trait (n = 9) compared with a group of healthy control subjects (n = 50). Thus, there was no indication of presymptomatic CNS parenchymal involvement in MS immunopathic trait.

The objective of this study was to compare cerebrospinal fluid (CSF) levels of the light subtype of the neurofilament proteins (NFL), tau, and beta-amyloid42 (Abeta42) in individuals with moderate or severe white matter changes (WMC) and in those with mild or no WMC. Twenty-two patients with Alzheimer's disease (AD), nine patients with subcortical vascular dementia (SVD), and 20 normal controls were included in the study. The occurrence of WMC was evaluated by a neuroradiologist using the Blennow-Wallin scale. Thirty-seven subjects had no or only punctate WMC; 14 had moderate to severe WMC. Both diagnostic group and WMC, but not gender or apolipoproteinE E4 inheritance, contributed to the variance in the CSF levels of tau, NFL, and Abeta42. In patients with moderate to severe WMC, CSF NFL (P0.01), but not CSF tau or CSF Abeta42, was increased also after correction for age, gender, and degree of cognitive impairment. A comparison between patients and controls with any signs of WMC and those without such signs yielded a similar result: CSF NFL (P0.001) was increased in the group with signs of WMC. As in numerous previous studies, we found that CSF tau was increased in AD (P0.001) compared with controls. Furthermore, CSF NFL was increased in both AD and SVD compared with controls (P0.001 for both). Although diagnostic group seems to be a stronger predictor of the variance found in CSF NFL, a clear association between the presence of WMC and increased CSF NFL was found. Because NFL is located mainly in large myelinated axons, increased CSF NFL in individuals with WMC probably reflects axonal degeneration.

Changes in expression of the proto-oncogene Bcl-2 are well known in the developing brain, with a high expression level in young post-mitotic neurons that are beginning the outgrowth of processes. The physiological significance of the Bcl-2 up-regulation in these neurons is not fully understood. We used a differentiation model for human CNS neurons to study the expression and function of Bcl-2. NT2/D1 human neuronal precursor cells differentiated into a neuronal phenotype in the presence of 10 microM retinoic acid for 3-5 weeks. This concentration of retinoic acid was not toxic to undifferentiated NT2/D1 cells but was sufficient to up-regulate the BCL-2 protein in 6 days. The BCL-2 levels increased further after 3 weeks, i.e. when the cells started to show neuronal morphology. Inhibition of the accumulation of endogenous BCL-2 with vectors expressing the antisense mRNA of Bcl-2 caused extensive apoptosis after 3 weeks of the retinoic acid treatment. The loss of neuron-like cells from differentiating cultures indicated that the dead cells were those committed to neuronal differentiation. Death was related to the presence of retinoic acid since withdrawal of retinoic acid after 16 days of treatment dramatically increased cell surviving. The ability of BCL-2 to prevent retinoic acid-induced cell death was also confirmed in undifferentiated NT2/D1 cells that were transfected with a vector containing Bcl-2 cDNA in sense orientation and exposed to toxic doses (40-80 microM) of retinoic acid. Furthermore, down-regulation of BCL-2 levels by an antisense oligonucleotide in neuronally differentiated NT2/D1 cells increased their susceptibility to retinoic acid-induced apoptosis. These results indicate that one function of the up-regulation of endogenous BCL-2 during neuronal differentiation is to regulate the sensitivity of young post-mitotic neurons to retinoic acid-mediated apoptosis.

Several studies indicate that systemic GH influences various brain functions. Connexin-43 forms gap junctions that mediate intercellular communication and establish the astroglial syncytium. We investigated the effects of peripheral administration of bovine GH (bGH) and recombinant human insulin-like growth factor I (rhIGF-I) on the expression of connexin-43 in the rat brain. Hypophysectomized female Sprague Dawley rats were substituted with cortisol (400 microg/kg x day) and L-T4 (10 microg/kg x day) and treated with either bGH (1 mg/kg x day) or rhIGF-I (0.85 mg/kg x day) for 19 days. The abundance of connexin-43 messenger RNA (mRNA) and protein in the brainstem, cerebral cortex, hippocampus, and hypothalamus was quantified by means of ribonuclease protection assays and Western blots. Treatment with bGH increased the amounts of connexin-43 mRNA and protein in the cerebral cortex and hypothalamus. No changes were found in the brainstem or hippocampus. Infusion of rhIGF-I did not affect connexin-43 mRNA or protein levels in any of the brain regions studied. These results show that administration of bGH increases the abundance of cx43 in specific brain regions, suggesting that GH may influence gap junction formation and thereby intercellular communication in the brain.

The extracellular fluid of two cortical regions was investigated in eight patients who underwent surgery for subarachnoid hemorrhage within 7-96 h after the rupture of an arterial aneurysm. Microdialysis samples, collected from the cortex of the ipsilateral gyrus rectus and temporal lobe for 52-127 h, were analyzed with respect to amino acids and the glial fibrillary acidic protein. In agreement with a previous study, an inverse relation was observed between total amino acid concentration and the level of consciousness. We also found that the concentration of glial fibrillary acidic protein was higher close to the bleeding site. Furthermorel we observed specific changes in the concentration of the protein and certain amino acids which coincided with clinical events such as increased intracranial pressure, vasospasm, ischemia and infarction. Finally, the concentrations of taurine may corroborate its function as an osmoequivalent. [Neural Res 1997; 19: 361-368]

The clinical application of a newly developed highly sensitive ELISA method (20) to assay glial fibrillary acidic protein (GFAP) in the cerebrospinal fluid (CSF) was investigated in children and adolescents with neurological disorders. GFAP analysis was explored as a tool to differentiate disorders with ongoing astrocytosis. A consecutive series of 34 subjects, 17 boys and 17 girls, with nonprogressive and progressive neurological encephalopathies was compared to 10 healthy controls. The mean CSF GFAP concentration of the controls was 60.6 ± 54 ng/l (SD). The group of 24 subjects (12 boys and 12 girls) with progressive neurologic disorders had higher mean CSF GFAP levels than the group of 10 subjects (5 boys and 5 girls) with non-progressive disorders, 222.6 ± 186 and 127.5 ± 86 ng/l, respectively. The progressive encephalopathies differed significantly from controls (p < 0.01) while the non-progressive did not. The mean GFAP concentration of the epilepsy cases (n = 18) and non-epilepsy cases (n = 16) was 212.9 ± 196 and 174.0 ± 132 ng/l, respectively. The epilepsy cases differed significantly from controls which could be explained by the dominance of progressive cases (15 out of 18). Six subjects with known gliotic progressive disorders (glutaric aciduria Type 1, Unverricht-Lundborg disease, Hallervorden-Spatz disease, Jansky-Bielschowsky disease and juvenile Huntington disease) differed significantly, as expected, from controls with a mean CSF GFAP concentration of 326.2 ± 132.5 ng/l, p < 0.001. The group with Lennox-Gastaut syndrome (3 boys and 3 girls) also differed significantly from controls (205.0 ± 107.6, p

Median neurofilament and glial fibrillary acidic protein concentrations in the cerebrospinal fluid of 18 infants with posthaemorrhagic ventricular dilatation were 20-200 times higher than control values. S-100 protein in cerebrospinal fluid was four times higher than control values. Glial fibrillary acidic protein concentrations correlated with death or disability and with parenchymal lesions but not with shunt dependence.

Brain specific proteins in the cerebrospinal fluid: markers of damage to the periventricular white matter and prognosis after intraventricular haemorrhage

The immunohistochemical distribution of S-100, a protein originally isolated from the brain, has been investigated at the light and electron microscopic levels in rat and man urinary systems. In both species the antigen essentially exhibited the same location, restricted, with different degrees of staining, to certain cells in the kidney, i.e. collecting tubules, thin limbs of Henle's loop and renal papillae.

Zimelidine, a specific 5-HT uptake inhibitor, reduced peroral morphine consumption by morphine-addicted adult male and female Sprague-Dawley rats and old male rats in choice tests. The effect was dose dependent in male rats. Thus, the availability of central 5-HT appears to be important for the regulation of morphine preference in rat. The results are discussed in relation to recent literature where ethanol preference has been found to be attenuated by zimelidine. The results may provide insights into the complex cellular mechanisms underlying opiate addiction.

Young adult rats were fed an isocaloric diet for 28 days. The diet consisted of either 22% casein, or protein-restricted food consisting of a 5% mixture of soy and whey protein, or a synthetic amino acid mixed diet devoid of the essential amino acids tryptophan, valine, lysine, and threonine. The level of the nervous tissue-specific S-100 protein was quantified immunoelectrophoretically in 9 different brain areas. A marked decrease of S-100 was observed in hippocampus and posterior part of the cerebellar vermis per g wet weight in protein-restricted rats. An additional lowering was noticed in sensory motor cortex per mg soluble protein. This effect was potentiated with the amino acid-deficient diet. The in vitro incorporation of 3H-leucine into cerebellar proteins was slightly decreased in the low-protein-fed rats, and more markedly decreased in those receiving an amino acid-restricted diet.