Factors affecting the biodiversity of historical landscape elements: detailed analyses from three case studies in Slovakia.

A direct, positive correlation between biodiversity and the traditional agricultural landscape is evident on the national or regional scale. It is mostly conditioned by higher landscape diversity and less intensive farming. We have carried out research on a detailed scale at plot level (productive plots of arable lands, grasslands, vineyards, orchards, and unproductive agrarian landforms (mostly field margins) such as terraced slopes, terraced steps, heaps, mounds, and unconsolidated walls) in three traditional agricultural landscapes: the mountain village Liptovská Teplicka, the vineyard landscape in Svätý Jur, and dispersed settlements in a submontane area in Hrinová. We determined the statistical significance of the impact of the selected landscape ecological factors (a set of factors concerning land use and management, agrarian landforms and relief properties) on the distribution of vegetation and selected invertebrate groups (spiders, millipedes, grasshoppers, and crickets). We also explored whether maintaining traditional land use and traditional management helped to enhance the biodiversity. We found that the management regime is the most important factor determining the species composition of vascular plants and all studied animal groups. Also, present land use and agrarian landforms character (type, skeleton content, continuity) are significant factors. Our expectation of a positive relationship between biodiversity and the maintaining traditional land use and traditional management was, in general, not confirmed: such a relation was only found in Svätý Jur for biodiversity of spiders.

Gender-related differences observed among immune cells in synovial fluid in knee osteoarthritis.

OBJECTIVE: There is no existing comprehensive report on the cellular composition of synovial fluids (SFs) from knee osteoarthritis (OA). We therefore aimed to characterise the immune cell composition in SFs from knee OA (KOA) and in subgroups according to gender. DESIGN: The immunophenotyping of monocyte/macrophage lineage cells, T and B cells, NK cells, neutrophils, dendritic and mast cells (MC) present in SFs from 53 patients (24 males/29 females) with KOA was performed using 6-colour flow cytometry. RESULTS: SFs from patients with OA contained 90% hematopoietic cells. Lymphocytes were the predominant cell population (44.8%) in the SFs of OA patients, with CD4+ T lymphocytes being more prevalent than CD8+ T cells (CD4+/CD8+ ratio = 1.3). Within the monocyte/macrophage lineage gating, monocytes accounted for 33.9%, macrophages 14.8%, myeloid dendritic cells 16.4%. The rest of the hematopoietic cells were comprised of neutrophils (8%), NK cells (3.8%), T regulatory cells (1.2%), plasmacytoid dendritic cells (1.1%), mast cells (0.3%). In OA females, a higher percentage of CD4+ T cells (P = 0.023), macrophages (P = 0.012), and a lower percentage of monocytes (P = 0.008) and CD8+ T cells (P = 0.002) were detected in comparison to OA males. CONCLUSIONS: Based on the immune cell composition of SFs, data mining analysis revealed distinct phenotypes (monocyte- and lymphocyte-predominant) within each gender group. This first study on the cellular complexity of SFs in KOA showed marked differences between male and female patients. The findings give a rational starting point for patient stratification according to their phenotypes, as is required for phenotype-specific treatment strategies.

Investigation on the origin of hot electrons in laser plasma interaction at shock ignition intensities.

Shock Ignition is a two-step scheme to reach Inertial Confinement Fusion, where the precompressed fuel capsule is ignited by a strong shock driven by a laser pulse at an intensity in the order of [Formula: see text] W/cm[Formula: see text]. In this report we describe the results of an experiment carried out at PALS laser facility designed to investigate the origin of hot electrons in laser-plasma interaction at intensities and plasma temperatures expected for Shock Ignition. A detailed time- and spectrally-resolved characterization of Stimulated Raman Scattering and Two Plasmon Decay instabilities, as well as of the generated hot electrons, suggest that Stimulated Raman Scattering is the dominant source of hot electrons via the damping of daughter plasma waves. The temperature dependence of laser plasma instabilities was also investigated, enabled by the use of different ablator materials, suggesting that Two Plasmon Decay is damped at earlier times for higher plasma temperatures, accompanied by an earlier ignition of SRS. The identification of the predominant hot electron source and the effect of plasma temperature on laser plasma interaction, here investigated, are extremely useful for developing the mitigation strategies for reducing the impact of hot electrons on the fuel ignition.

Alterations in allocation and composition of lipid classes in Euonymus fruits and seeds.

The spindle tree (Euonymus europaeus L.) is a much-branched deciduous shrub or small tree. Its fruit capsules contain seeds with remarkably high content of oil interesting for industry, especially the 3-acetyl-1,2-diacyl-sn-glycerols (AcDAG) synthesized by a specific acetyl-CoA diacylglycerol acetyltransferase. The distribution and amount of individual triacylglycerols (TAG) and especially acetyl-triacylglycerols (AcDAG) in Euonymus fruit have previously been assigned to specific tissues. Using anatomical and microscopical observations, we studied the fruit morphology, and for the first time, we identified a more detailed allocation of oil bodies in individual tissue structures. Thin layer chromatography separation of extracts from immature and mature fruits confirmed TAG and AcDAG as the most abundant lipid classes in both endosperm and embryo, followed by fatty acids and polar lipids. The abundance of fatty acids was further studied in the TAG and AcDAG fractions using gas chromatography. Data revealed particular FAs in both fractions allocated in tissue-specific manner and/or as indicators of maturation of E. europaeus seeds. While the abundance of cis-vaccenic-, linoleic as well as α-linolenic acids in the AcDAG structures generally drop with maturation in both embryo and endosperm, content of oleic acid increases. Abundance of cis-vaccenic acid in TAG was recorded in immature endosperm. For embryo, the abundance of stearic acid in AcDAG and oleic acid in TAG fraction was distinctive. Deeper understanding of underlying metabolic processes will be essential for targeted metabolic engineering and/or application for oilseed crops.

The effects of short-term norepinephrine up-titration on hemodynamics in cardiogenic shock.

A higher mean arterial pressure (MAP) achieved by norepinephrine up-titration may improve organ blood flow in critically ill, whereas norepinephrine-induced afterload rise might worsen myocardial function. Our aim was to assess the effects of norepinephrine dose titration on global hemodynamics in cardiogenic shock. We prospectively evaluated 12 mechanically ventilated euvolemic patients (aged 67 +/- 12 years) in cardiogenic shock (10 patients acute myocardial infarction, 1 patient dilated cardiomyopathy, 1 patient decompensated aortic stenosis). Hemodynamic monitoring included arterial and Swan-Ganz catheters. The first data were obtained at MAP of 65 mm Hg, then the norepinephrine dose was increased over 40 min to achieve MAP of 85 mm Hg. Finally, the norepinephrine-dose was tapered over 40 min to achieve MAP of 65 mm Hg. Norepinephrine up-titration increased MAP to the predefined values in all patients with concomitant mild increase in filling pressures and heart rate. Systemic vascular resistance increased, whereas cardiac output remained unchanged. During norepinephrine down-titration, all hemodynamic parameters returned to baseline values. We observed no changes in lactate levels and mixed venous oxygen saturation. Our data suggest that short-term norepinephrine dose up-titration in cardiogenic shock patients treated or pretreated with inotropes was tolerated well by the diseased heart.

Intravenous immunoglobulin for myasthenia gravis.

BACKGROUND: Myasthenia gravis is an autoimmune disease in which autoantibodies interfere with neuromuscular transmission. As with other autoimmune diseases, people with myasthenia gravis would be expected to benefit from intravenous immunoglobulin (IVIg). OBJECTIVES: The objective of this review was to examine the efficacy of intravenous immunoglobulin for treating exacerbations of myasthenia gravis or for chronic myasthenia gravis. SEARCH STRATEGY: We searched the Cochrane Neuromuscular Disease GroupTrials Register (April 2007) and MEDLINE (January 1966 to May 2007) using 'myasthenia gravis' and 'intravenous immunoglobulin' as the search terms. SELECTION CRITERIA: We included all randomised or quasi-randomised trials in which intravenous immunoglobulin was compared with no treatment, placebo or plasma exchange, in people with myasthenia gravis. DATA COLLECTION AND ANALYSIS: One review author extracted the data and two others checked these data and the source from which they were derived. For methodological reasons, no formal meta-analysis was performed. MAIN RESULTS: We identified six randomised controlled trials, all of which investigated short-term benefit. A trial of IVIg compared with placebo including 51 patients provided evidence for the effectiveness of IVIg in myasthenia gravis worsening. A study of 87 participants with exacerbation found no statistically significant difference between immunoglobulin and plasma exchange after two weeks. A study of 12 participants with moderate or severe myasthenia gravis treated in a crossover design trial found no statistically significant difference in the efficacy of immunoglobulin and plasma exchange after four weeks. A study with 15 participants with mild or moderate myasthenia gravis found no statistically significant difference in efficacy of IVIg and placebo after six weeks. A study included 33 participants with moderate exacerbations of myasthenia gravis and showed no statistically significant difference in the efficacy of IVIg and methylprednisolone. The last trial including 173 people with myasthenia gravis exacerbations, showed no superiority of IVIg 1 g/kg on two consecutive days over IVIg 1 g/kg on a single day. AUTHORS' CONCLUSIONS: In exacerbation of myasthenia gravis, one randomised controlled trial of IVIg versus placebo demonstrated the efficacy of IVIg and another did not show a significant difference between IVIg and plasma exchange. Another showed no significant difference in efficacy between 1 g/kg and 2 g/kg of IVIg. A further, but underpowered, trial showed no significant difference between IVIg and oral methylprednisolone. In chronic myasthenia gravis, there is insufficient evidence from randomised trials to determine whether IVIg is efficacious. More research is needed to determine whether IVIg reduces the need for corticosteroids as suggested by two case series.

Intravenous immunoglobulin for myasthenia gravis.

BACKGROUND: Myasthenia gravis is an autoimmune disease in which autoantibodies interfere with neuromuscular transmission. As with other autoimmune diseases, people with myasthenia gravis would be expected to benefit from intravenous immunoglobulin. OBJECTIVES: The objective of this review was to examine the efficacy of intravenous immunoglobulin for treating exacerbations of myasthenia gravis or for chronic myasthenia gravis. SEARCH STRATEGY: We searched the Cochrane Neuromuscular Disease Group trials register (March 2005) and MEDLINE (January 1966 to March 2005) using 'myasthenia gravis' and 'intravenous immunoglobulin' as the search terms. SELECTION CRITERIA: We included all randomised or quasi-randomised trials in which intravenous immunoglobulin was compared with no treatment, placebo or plasma exchange, in people with myasthenia gravis. DATA COLLECTION AND ANALYSIS: One author extracted the data and the two others checked these data and the source from which they were derived. For methodological reasons, no formal meta-analysis was performed. MAIN RESULTS: We identified five randomised controlled trials, all of which investigated short-term benefit. The first study of 87 participants with exacerbation found no statistically significant difference between immunoglobulin and plasma exchange after two weeks. The second study of 12 participants with moderate or severe myasthenia gravis treated in a crossover design trial found no statistically significant difference in the efficacy of immunoglobulin and plasma exchange after four weeks. The third study with 15 participants with mild or moderate myasthenia gravis found no statistically significant difference in efficacy of intravenous immunoglobulin and placebo after six weeks. The fourth study terminated early. It included 33 participants with moderate exacerbations of myasthenia gravis and showed no statistically significant difference in the efficacy of intravenous immunoglobulin and methylprednisolone. The fifth trial including 173 people with myasthenia gravis exacerbations, showed no superiority of intravenous immunoglobulin 1 g/kg on two consecutive days over intravenous immunoglobulin 1 g/kg on a single day. AUTHORS' CONCLUSIONS: In severe exacerbations of myasthenia gravis, one randomised controlled trial did not show a significant difference between intravenous immunoglobulin and plasma exchange. Another showed no significant difference in efficacy between 1 g/kg and 2 g/kg of intravenous immunoglobulin. A further trial showed no significant difference between intravenous immunoglobulin and oral methylprednisolone. In chronic myasthenia gravis, there is insufficient evidence from randomised trials to determine whether intravenous immunoglobulin is efficacious. More research is needed to determine whether intravenous immunoglobulin reduces the need for steroids as suggested by two case series.

Corticosteroids for myasthenia gravis.

BACKGROUND: Although widely accepted as an appropriate immunosuppressive therapy, the efficacy of glucocorticosteroid treatment has only rarely been tested in controlled studies. OBJECTIVES: To assess the efficacy of glucocorticosteroids or adrenocorticotrophic hormone (ACTH) medication in autoimmune myasthenia gravis. SEARCH STRATEGY: We searched the Cochrane Neuromuscular Disease Group Trials Register in July 2004, MEDLINE (from January 1966 to June 2004) and EMBASE (from January 1980 to June 2004). We also checked the bibliographies in reviews and the randomised trials and contacted their authors to identify additional published and unpublished data. SELECTION CRITERIA: From the articles identified we selected those open or controlled studies which allowed us to assess the outcome of treated and untreated patients at definite endpoints. Types of studies: quasi-randomised or randomised controlled trials. TYPES OF PARTICIPANTS: patients with myasthenia gravis of all ages and all degrees of severity. Types of interventions: any form of glucocorticosteroids or adrenocorticotrophic hormone treatment. Types of outcome measures:Primary outcome(1) improvement after at least three months in either the weakest muscles or all muscles. Secondary outcomes(1) proportion of patients improved after at least six months(2) proportion of patients in remission(3) number of episodes of worsening during the first six months(4) acetylcholine receptor antibody titres after at least three months of therapy. DATA COLLECTION AND ANALYSIS: Three authors extracted the data from the selected articles and one other checked them. MAIN RESULTS: A trial of adrenocorticotrophic hormone (43 patients) did not show any advantage compared with placebo for the treatment of ocular myasthenia gravis. Two double-blind trials compared prednisone with placebo for generalised myasthenia gravis. In the first (13 patients), the improvement was slightly greater in the prednisone group at six months. In the second (20 patients) which was a short-term trial, the improvement was significantly greater at two weeks. Two trials compared glucocorticosteroids with azathioprine (41 and 10 patients respectively). In one of these the rate of treatment failure was greater in the prednisone group. In a trial of glucocorticosteroids versus intravenous immunoglobulin (33 patients) no differences in treatment responses were encountered during a treatment period of 14 days. An open trial (39 patients) evaluating different corticosteroid doses revealed a shorter time to improvement in the high-dose group. However only limited evidence can be drawn from the available randomised controlled trials due to numerous and important methodological flaws. AUTHORS' CONCLUSIONS: Limited evidence from randomised controlled trials suggests that corticosteroid treatment offers significant short-term benefit in myasthenia gravis compared with placebo. This supports the conclusions of observational studies and expert opinion. Limited evidence from randomised controlled trials does not show any difference in efficacy between corticosteroids and either azathioprine or intravenous immunoglobulin.

Anti-titin antibodies in myasthenia gravis: tight association with thymoma and heterogeneity of nonthymoma patients.

BACKGROUND: Titin is the major autoantigen recognized by anti-striated muscle antibodies, which are characteristic of generalized myasthenia gravis (MG). OBJECTIVE: To seek a correlation between anti-titin antibodies and other features of MG patients, including histopathology, age at diagnosis, anti-acetylcholine receptor (anti-AChR), autoantibody titers, and clinical severity. METHODS: A novel, highly specific radioligand assay was performed on a large group of 398 patients with generalized MG. RESULTS: Among thymectomized patients, anti-titin antibodies were present in most patients with thymoma (56/70 [80%]), contrasting with only a minority of patients with thymus atrophy or hyperplasia (17/165 [10%]). They were also present in 64 (41%) of 155 nonthymectomized patients who had a radiologically normal thymus. In these patients and in those who had a histologically normal thymus, anti-titin antibodies were associated with a later age at onset of disease and with intermediate titers of anti-AChR antibodies. After controlling for these 2 variables, disease severity was not significantly influenced by anti-titin antibodies. CONCLUSIONS: Anti-titin antibodies are a sensitive marker of thymoma associated with MG in patients 60 years and younger, justifying the insistent search for a thymoma in MG patients of this age group who have these antibodies. In nonthymoma patients, anti-titin antibodies represent an interesting marker complementary to the anti-AChR antibody titer, identifying a restricted subset of patients. These clinical correlations should prompt further studies to examine the mechanisms leading to the production of anti-titin antibodies.

Beneficial effects of dantrolene in the treatment of neuroleptic malignant syndrome: a report of two cases.

Two schizophrenic patients developed muscular rigidity, stupor, and hyperpyrexia consistent with neuroleptic malignant syndrome, 8 to 10 days after starting haloperidol therapy. Muscle rigidity was not affected by etybenzatropine or diazepam, but dantrolene, a direct-acting skeletal muscle relaxant, provided muscle relaxation with a concomitant decrease of fever and serum creatine kinase. Neuroleptic malignant syndrome and malignant hyperthermia are clinically similar, and dantrolene is effective in both; suggesting a muscular origin of fever in these two diseases.

Linkage of HLA to myasthenia gravis and genetic heterogeneity depending on anti-titin antibodies.

BACKGROUND: MG is an autoimmune disease of the neuromuscular junction. MG with thymus hyperplasia has been associated with, but not genetically linked to, the HLA-DR3 haplotype. OBJECTIVE: To re-evaluate the association of HLA with MG in 656 patients with generalized disease and to test linkage of HLA to MG with thymus hyperplasia. METHOD: Patients were genotyped for HLA-DRB1. Data analysis included case-control comparisons after subgrouping patients by thymus histopathology. The transmission of parental alleles to MG offspring with thymus hyperplasia was studied in simplex families using the transmission/disequilibrium test (TDT) as a test of linkage. RESULTS: MG with thymus hyperplasia was positively associated with DR3 (OR = 4.5, p = 1 x 10(-6)) and negatively associated with DR7 (OR = 0.28, p = 1 x 10(-6)), based on both case-control comparisons and TDT. No association was detected with thymomas. Conversely, patients who lacked thymus anomalies but expressed anti-titin antibodies (ATA) had an increase of DR7 (OR = 2.08, p = 4 x 10(-3)) and a decrease of DR3 (OR = 0.33, p = 9 x 10(-3)). CONCLUSIONS: The authors established linkage of HLA to MG and thymus hyperplasia, defining the MYAS1 locus. Moreover, DR3 and DR7, or closely linked genes, have opposing effects on MG phenotypes. Nonthymomatous patients with ATA may be a pathogenetically distinct subset of MG patients.

Impaired cerebral glucose metabolism in myotonic dystrophy: a triplet-size dependent phenomenon.

Myotonic dystrophy (DM) is caused by an expansion of a CTG triplet repeat sequence in the 3'-noncoding region of a protein kinase gene, yet the mechanism by which the triplet repeat expansion causes disease remains unknown. Impaired glucose penetration into brain tissues has been described in DM patients and is a phenomenon that remains unexplained. The present study shows that altered brain glucose metabolism is triplet repeat dependent. We studied brain glucose metabolism (CMRGlu, mumol/100 g/min) by the use of positron emission tomography and 18F-fluoro-2-deoxy-D-glucose in 11 ambulatory non-obese DM patients and in 11 age and sex matched healthy subjects. All subjects underwent a glucose tolerance test with plasma insulin determinations. The expansion of CTG triplet repeats was analyzed in patients with the probe cDNA25 after EcoRI digestion. As compared to controls, in DM patients, the CMRGlu was significantly decreased (26.26 +/- 5.05 vs. 33.43 +/- 2.18, mumol/100 g/min, P = 0.004), and after oral glucose loading, plasma insulin levels were significantly higher and plasma glucose levels remained unchanged (respectively, F = 11.21, P = 0.004 and F = 0.20, P = 0.66). Subsequently, the glucose/insulin ratio was significantly lower in DM patients (F = 6.25, P = 0.02). The length of the expansion of the CTG repeats correlated negatively with the CMRGlu (r2 = 0.63, P = 0.003) and positively with the area under the curve for insulin changes over time after oral glucose (r2 = 0.49, P = 0.016). We conclude that, in DM patients, the brain metabolism of glucose is impaired in a repeat dependent manner.

Association of Km3 allotype with increased serum levels of autoantibodies against muscle acetylcholine receptor in myasthenia gravis.

Association of immunoglobulin allotypes with myasthenia gravis was examined in a set of 84 patients presenting autoantibodies against muscle acetylcholine receptor (AChR). Km and G1m(f)/G1m(z) allotypes were determined by PCR-amplification followed by hybridization with allele-specific oligonucleotides. The Km3 kappa light chain allotype was found to be associated with significantly increased serum levels of anti-AChR autoantibodies in myasthenic patients (P = 0.014). We hypothesize that an allelic polymorphism of a regulatory (enhancer) sequence closely linked to the C kappa gene segment could account for our finding.

Human IgG monoclonal autoantibodies against muscle acetylcholine receptor: direct evidence for clonal heterogeneity of the antiself humoral response in myasthenia gravis.

Human hybridomas were established from myasthenia gravis (MG) patients and screened using a fast and sensitive cell ELISA with the rhabdomyosarcoma cell line TE671. In a first series of 14 fusions using a standard protocol, 36 positive clones were detected and maintained for three passages. The number of clones in each fusion was correlated with in vivo titers of anti-acetylcholine receptor (AChR) autoantibodies. In a second series of four experiments, fusions were immediately followed by cell plating under limiting dilution conditions ('fusion cloning') providing eight stable hybridomas. These hybridomas produced monoclonal antibodies (mAbs) of IgG isotype reactive with TE671 cells, but not with AChR in solution using the radioimmunoprecipitation assay. Fine analysis of antigen specificity of these mAbs was performed using solid-phase ELISA against purified AChR from Torpedo (T-AChR) and immunoblot against recombinant chimaeric human AChR produced in bacteria. Five of the eight mAbs derived from the few patients whose antibodies showed cross-reactivity with T-AChR reacted against T-AChR. Of these five mAbs, two also reacted against chimaeric human AChR by immunoblotting. Furthermore, at least one of these two mAbs was capable of inducing antigenic modulation of labeled AChR with [125I]alpha-bungarotoxin from the surface of TE671 cells. These mAbs provide useful tools to explore the molecular basis of the structural and functional heterogeneity of the humoral anti-AChR response in myasthenia gravis.

Identification by genomic typing of non-DR3 HLA class II genes associated with myasthenia gravis.

HLA association with myasthenia gravis (MG) has been studied in a series of 114 patients using class I and class II genotyping after PCR amplification. Positive association was found with DR3, particularly in women (RR = 2.6) and in early MG onset (RR = 3.4). DRB1, DRB3, DQB1, DQA1 and B (B8 and B18) genotyping revealed that the association was predominantly with the B8 DRB1*03 DRB3*0101 DQB1*0201 DQA1*0501 ancestral haplotype. This haplotype frequency was also increased in patients with thymic hyperplasia (RR = 3.5) and was greatly reduced in patients with thymoma (RR = 0.35). Sixteen out of 48 patients carrying this 8.1 ancestral haplotype showed absence of B8 (n = 4) or of DR3 (n = 12). HLA class II genotyping further revealed the existence of two other significant associations. MG was positively associated with the DQB1*0604 allele (RR = 3.4), particularly in patients with thymoma (RR = 5.7). Furthermore, the disease was negatively associated with DR1 in females (RR = 0.32). These data suggest that MG is placed under the control of at least three distinct genes: (1) a class II predisposing gene in the 8.1 ancestral haplotype; (2) a thymoma-associated class II allele on the DQB1*0604 haplotype; and (3) a protective allele DR1.

No evidence for an association of AChR beta-subunit gene (CHRNB1) with myasthenia gravis.

Using a polymorphic dinucleotide repeat, we have investigated the contribution of the gene encoding the beta-subunit of the muscle acetylcholine receptor (CHRNB1), the target autoantigen, to the susceptibility to myasthenia gravis (MG). We have combined a case-control study (comparing 143 patients and 162 controls) and a transmission-disequilibrium test bearing on 35 simplex families with heterozygous parents. There was no evidence for an association of CHRNB1 with MG, even after subgrouping patients according to thymus histology, or other clinical criteria. Interestingly however, the shortest four variants of the CHRNB1 microsatellite were seen only in patients with thymus hyperplasia and in none of the control subjects (P < 0.0025).

Rapid shift in peak melatonin secretion associated with improved performance in short shift work schedule.

We studied the performance and adaptability of 40 nurses (median age 35 years), 20 on permanent day shift and 20 on permanent night shift with fast rotation of work and days off, matched for age, gender, and socio-familial responsibilities. For 15 days prior to the study, subjects maintained sleep logs and trained for performance tests. Questionnaires were administered to evaluate adaptability to shift work. During the experimental phase, sleep/wake patterns were monitored using sleep logs and activity/inactivity with wrist actigraphy. Performance levels were measured with the four choice reaction time and memory test for seven letters, eight times/day during the wake period, days on and off. On the last day of work and first day off, 6-sulfatoxy-melatonin levels were assayed from urine samples collected every 2 hours. Estimated total sleep time during the 15-day experimental period was not significantly different in the dayshift and nightshift nurses. Night nurses shifted regularly to daytime activities on days off and, as a group, were significantly sleep deprived on work days with napping on the job in 9 of the 20 night shift nurses (mean of 114+/-45 minutes per shift) and a significant performance decrement during the work period. Further analysis revealed two subgroups of night nurses: The majority (14 nurses) had a mean peak of 6-sulfatoxy-melatonin at 0718 hours on days off and no peak during night work while the other 6 night shift nurses presented a fast melatonin shift with two clear peaks on both work and days off. Comparison of performance scores revealed that all nurses performed similarly on days off. Daytime nurses and fast-shifting night nurses had similar scores on work days, while nonshifting night nurses had significantly lower scores at work. Despite similar gender, age, social conditions, and light exposure levels, a minority of the nurses studied possessed the physiological ability to adapt to a fast-shifting sleep-wake schedule of more than 8 hours and were able to perform appropriately in both conditions. This shift was associated with a change in the acrophase of 6-sulfatoxy-melatonin.

Severe community-acquired pneumonia. Etiology, epidemiology, and prognosis factors. French Study Group for Community-Acquired Pneumonia in the Intensive Care Unit.

A prospective study of 132 patients with severe community-acquired pneumonia (CAP) treated in the ICU was carried out to determine the causative agents, the value of the clinical, biological, and radiologic features in predicting the etiology, and to define prognostic factors. The study group included 98 men and 34 women (mean age: 58 +/- 18 years). The most frequent underlying condition was COPD (51 patients, 39 percent). On admission, 35 patients were in shock, 71 were mentally confused, and 81 (61 percent) required mechanical ventilation during their hospitalization. The clinical, laboratory, and radiologic parameters were of little value for predicting the etiology in patients with severe CAP. An etiologic diagnosis was made in 95 (72 percent) patients. The most frequent pathogens were Streptococcus pneumoniae (43 cases [45 percent]), Gram-negative bacilli (14 cases [15 percent]), and Haemophilus influenzae (14 cases [15 percent]) Mortality was 24 percent. It was significantly associated with a age more than 60 years, septic shock, impairment of alertness, mechanical ventilation requirement, bacteremic pneumonia, and S pneumoniae or Enterobacteriaceae as the causes of the pneumonia. Recommendations for antibiotic chemotherapy in patients with severe CAP admitted to the ICU are included.

Long-term effects of nasal intermittent positive-pressure ventilation on pulmonary function and sleep architecture in patients with neuromuscular diseases.

STUDY OBJECTIVE: This article evaluates the long-term clinical and physiologic effects of nocturnal nasal intermittent positive-pressure ventilation (NIPPV) in patients with neuromuscular disease. METHODS: Before and after 18 +/- 2 months of NIPPV, we measured during the daytime arterial blood gases, lung mechanics, and respiratory muscle strength in 8 patients (51 +/- 5 years; mean +/- SEM). Sleep parameters were also evaluated at 10 +/- 2 months. RESULTS: All patients tolerated NIPPV and none required hospitalization during follow-up. After NIPPV, daytime arterial PO2 increased (71 +/- 4 to 81 +/- 2 mm Hg; p < 0.05) and arterial PCO2 decreased (46 +/- 3 to 41 +/- 1 mm Hg; p < 0.05). The change of PaO2 after NIPPV was related to its baseline value (r2 = 0.78, p < 0.05). Vital capacity (50 +/- 6% predicted), total lung capacity (63 +/- 4% predicted), alveolar-arterial oxygen gradient (20 +/- 3 mm Hg), and maximal inspiratory (39 +/- 9% predicted) or expiratory (32 +/- 5% predicted) pressures did not change after NIPPV. The apnea-hypopnea index fell from 22 +/- 6 to 1 +/- 1 (p < 0.05), and both sleep architecture and sleep efficiency (from 59 +/- 8% to 83 +/- 5%; p < 0.05) were enhanced. The time spent with an arterial oxygen saturation (SaO2) value below 90% decreased from 160 +/- 53 min to 8 +/- 4 min (p < 0.05). Mean (88 +/- 3 to 95 +/- 1%; p < 0.05) and minimal nocturnal SaO2 (67 +/- 5 to 89 +/- 1%; p < 0.001) improved after NIPPV. CONCLUSIONS: In patients with neuromuscular disease, long-term NIPPV is well tolerated and easy to implement clinically. In these patients, long-term NIPPV improves daytime arterial blood gas values and sleep-disordered breathing. However, it does not modify lung mechanics or respiratory muscle strength.

Standards of measurements in myasthenia gravis.

Valid and reliable measurements of muscle impairment are needed to assess therapeutic efficacy in patients with generalized myasthenia gravis. Several muscle scoring systems have been proposed for assessing muscle strength in such patients. The aim of the present study is to assess the validity and interobserver agreement of these muscle scores.