The effectiveness of exercise and physical activity programs on fatigue and sleep in people with arthritis - A systematic review with meta-analysis.

This systematic review aimed to systematically investigate the literature on the effectiveness of exercise and physical activity programs on fatigue and sleep in people with arthritis. For that, seven databases were searched for relevant randomized controlled trials. After the searches, 36 studies investigating 2281 participants were included. Risk of bias assessments were done by two independent reviewers using the Cochrane Risk of Bias tool 2. Random-effects meta-analyses were performed, and the Grading of Recommendations Assessment, Development and Evaluation framework was used to judge the certainty of evidence. The evidence on benefits of exercise and physical activity programs on fatigue and sleep parameters in people with osteoarthritis and psoriatic arthritis was either lacking or inconclusive. There was very low to low certainty evidence for a slight benefit of exercise and physical activity programs on fatigue at short-term in people with ankylosing spondylitis and rheumatoid arthritis. However, the evidence was very uncertain for the medium- and long-term as well as for any sleep parameters. The results indicate that exercise and physical activity programs may offer some benefits on fatigue for people with arthritis in the short-term, although the best type of exercise remains uncertain. The available evidence on improvements in sleep was insufficient to draw strong conclusions.

Adult human progenitor cells from the temporal lobe: another source of neuronal cells.

OBJECTIVES: In the adult human brain, neurogenesis occurs in the SVZ and the dentate gyrus of the hippocampus, but it is still unclear whether persistent neural progenitor/stem cells are also present in other brain areas. The present work studies the possibility of obtaining neural progenitor/stem cells from the temporal lobe and investigates their potential to differentiate into neuronal cells. METHODS: Human biopsies from the temporal lobe of epileptic patients were used to isolate potential neural progenitors. Differentiation was induced in the presence of different agents (NGF, NT3, RA) and immunocytochemistry was then performed for quantitative analysis. RESULTS: It was shown that a significant number of cells in the temporal lobe are also capable of expansion and multi-potency. These cells can be amplified as neurospheres and have the potential to differentiate naturally in vitro into neurons, astrocytes and oligodendrocytes. Quantitative analyses show that the progenitor cells of the temporal lobe exhibit a better rate of neuronal differentiation in vitro than the cells from the SVZ, particularly in the presence of NGF. CONCLUSION: This study indicates that neural progenitors are also present in the human temporal lobe. Studying them could be of great interest for cell therapy in neurological disorders.

Blockade of cannabinoid receptors by SR141716 selectively increases Fos expression in rat mesocorticolimbic areas via reduced dopamine D2 function.

The present study investigated, in rats, whether blockade of cannabinoid CB1 receptors may alter Fos protein expression in a manner comparable to that observed with antipsychotic drugs. Intraperitoneal administration of the selective CB1 receptor antagonist, SR141716, dose-dependently (1.0, 3.0 and 10 mg/kg) increased Fos-like immunoreactivity in mesocorticolimbic areas (prefrontal cortex, ventrolateral septum, shell of the nucleus accumbens and dorsomedial caudate-putamen), while motor-related structures such as the core of the nucleus accumbens and the dorsolateral caudate-putamen were unaffected. In the ventrolateral septum, taken as a representative structure, the Fos-inducing effect of SR141716 (10 mg/kg) was maximal 2 h after injection and returned to near control levels by 4 h. Within the prefrontal cortex, SR141716 increased the number of Fos-positive cells predominantly in the infralimbic and prelimbic cortices, presumptive pyramidal cells being the major cell types in which Fos was induced. The D1-like receptor antagonist, SCH23390 (0.1 mg/kg), did not prevent the Fos-inducing effect of SR141716 in any brain region examined (prefrontal cortex, nucleus accumbens, ventrolateral septum and dorsomedial caudate-putamen), although SCH23390 significantly reduced Fos expression induced by cocaine (20 mg/kg) in all these regions. By contrast, the dopamine D2-like agonist, quinpirole (0.25 mg/ kg), counteracted SR141716-induced Fos-like immunoreactivity in the ventrolateral septum, the nucleus accumbens and the dorsomedial caudate-putamen, while no antagonism was observed in the prefrontal cortex. Microdialysis experiments in awake rats indicated that SR141716, at doses which increased Fos expression (3 and 10 mg/kg), did not alter dopamine release in the shell of the nucleus accumbens. Finally, SR141716 increased the levels of neurotensin-like immunoreactivity in the nucleus accumbens, but not in the caudate-putamen. Collectively, the present results show that blockade of cannabinoid receptors increases Fos- and neurotensin-like immunoreactivity with characteristics comparable to those reported for atypical neuroleptic drugs.

Effect of the neuroprotective compound SR57746A on nerve growth factor synthesis in cultured astrocytes from neonatal rat cortex.

The neurotrophic factor promoting activity of the neuroprotective compound SR57746A was evaluated in primary cultures of neonatal rat cortical astrocytes by studying the synthesis of nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF). A concentration- and time-dependent increase of nerve growth factor mRNA was induced by SR57746A (10 nM-1 microM). In these astrocytes, BDNF mRNA contents were increased to a significant but smaller extent, and beta-actin mRNA showed no variation. SR57746A (1 microM) induced increases of both de novo protein translation after 6 h of incubation and NGF release into the extracellular medium after 6-24 h. These effects were preceded by a transient augmentation of junB, c-fos and c-jun mRNA contents. These increases of AP-1 family mRNA were associated with increased nuclear AP-1 binding activity. The results show that SR57746A can increase the synthesis and release of NGF in rat cortical astrocytes. Such effects may contribute to the drug's previously described neuroprotective effects.

SR146131: a new potent, orally active, and selective nonpeptide cholecystokinin subtype 1 receptor agonist. I. In vitro studies.

SR146131 inhibited the binding of [125I]-Bolton Hunter (BH)-sulfated cholecystokinin octapeptide (CCK-8S) for the human recombinant cholecystokinin subtype 1 (CCK1) receptor (IC50 = 0.56 nM) with high (300-fold) selectivity to the CCK2 receptor. The biological activity of SR146131 was characterized in vitro in a NIH-3T3 cell line expressing the human recombinant CCK1 receptor (3T3-hCCK1). Measuring intracellular calcium release, SR146131 behaved as a full agonist with an efficacy comparable with that of CCK-8S (EC50 = 1.38 +/- 0.06 nM). On individual cells, SR146131 induced, like CCK-8S, Ca2+ oscillations at subnanomolar concentrations and sustained responses at higher concentrations. Like CCK-8S, SR146131 also fully stimulated inositol monophosphate formation (EC50 = 18 +/- 4 nM). SR146131 partially activated mitogen-activated protein kinase and enhanced the expression of the immediate early gene krox 24. In the human CHP212 and IMR32 neuroblastoma cell lines, which constitutively express the CCK1 receptor, SR146131 behaved as a partial agonist on intracellular calcium release and inositol monophosphate formation. All of these effects of SR146131 were inhibited by the CCK1 receptor antagonists SR27897B and devazepide, suggesting that the effects of SR146131 were entirely mediated by the CCK1 receptor. In contrast, high concentrations (>1 microM) of SR146131 had only minimal effects on CCK-8S-stimulated and unstimulated Chinese hamster ovary (CHO) cells expressing the human CCK2 receptor, indicating that SR146131 is functionally inactive on the CCK2 receptor. In conclusion, these in vitro experiments show that SR146131 is a highly potent and selective agonist of the CCK1 receptor.

Effects of the sigma receptor ligand SR 31742A on neurotensin biosynthesis in rat basal ganglia.

The effects of SR 31742A, a specific sigma ligand, were investigated on neurotensin (NT) biosynthesis in the basal ganglia of the rat. Both single and repeated treatments with either SR 31742A (20 mg/kg i.p.) or haloperidol (1 mg/kg i.p.) increased the concentration of NT-like immunoreactivity (NT-li) in the nucleus accumbens. In contrast to haloperidol, the administration of SR 31742A failed to increase the concentration of NT-li in the caudate-putamen. We have further investigated drug-induced variations in NT biosynthesis by studying NT/neuromedin N (NT/NN) mRNA levels in the nucleus accumbens and the ventral tegmental area of the rat following SR 31742A administration. The NT/NN mRNA levels in the ventral tegmental area were increased by a maximum of fifteen fold (7 h at 20 mg/kg i.p.). A lower increase in NT/NN mRNA levels was elicited in the nucleus accumbens. These results suggest that the increase in NT-li observed after SR 31742A treatment, like that produced by haloperidol, may result from an increase of NT biosynthesis. Furthermore, the effects of SR 31742A on NT metabolism are similar to those of atypical antipsychotics, since they appear to be selective for the limbic system.

The sigma receptor ligand SR 31742A increases neurotensin in the nucleus accumbens but not in the caudate-putamen of the rat.

The effects of SR 31742A, a specific sigma site ligand, were investigated on regional neurotensin concentrations in rat brain. Both acute and chronic (21-day) treatment with either SR 31742A (20 mg/kg i.p.) or haloperidol (1 mg/kg i.p.) increased the neurotensin-like immunoreactivity in the nucleus accumbens. In contrast to haloperidol, the administration of SR 31742A failed to increase the concentration of neurotensin-like immunoreactivity in the caudate-putamen. Thus, the effects of SR 31742A appear to be selective for the limbic system.

Minicell-forming mutants of Escherichia coli: suppression of both DicB- and MinD-dependent division inhibition by inactivation of the minC gene product.

We have determined the nucleotide sequence of the minB operon of 10 min mutants of Escherichia coli, characterized by impaired inhibition of polar divisions. These mutants were either sensitive or resistant to the division inhibitor DicB. All the mutations were found to lie in minC or minD, confirming the requirement of both gene products in the process of inhibition of polar sites. Mutations conferring resistance to inhibitor DicB were found exclusively in minC. In agreement with de Boer et al. (P. A. J. de Boer, R. E. Crossley, and L. I. Rothfield, Proc. Natl. Acad. Sci. USA 87:1129-1133, 1990), these results provide evidence that, in addition to promoting division inhibition with MinD, protein MinC acts in concert with DicB to inhibit division by a second, MinD-independent process.

[Morphology of renal structures in the dog after prolonged administration of Plasmacair]. / Etude de la morphologie des structures rénales du chien après administration prolongée de Plasmacair.

Infusion of 10% Dextran 40,000 (Dextran 40) solute was reported to induce acute renal failure with oligoanuria in some patients and in animals during experimental pharmacological studies. Dogs were infused daily with 40 ml.kg-1 a large volume (twice the dose intended in human clinical practice) of a 3,5% dextran 40 solute, associated with electrolytes Plasmacair After 30 days of administration, no differences in creatinine clearance and renal structures were noted between control and treated animals.

Isolation and mapping of Escherichia coli mutations conferring resistance to division inhibition protein DicB.

Temperature-sensitive dicA mutants of Escherichia coli, dicA1(Ts), are blocked for cell division, owing to derepressed expression of a division inhibition gene, dicB. We isolated mutants which survived a high temperature in the dicA1 background and which survived induced expression of dicB carried by a high-copy-number plasmid. Most of the mutations conferred very slow growth on the cells. Two were mapped to the 90-min cluster of genes involved in translation and transcription, in or very close to gene rpoB. The majority of the other mutations were found to cause variable degrees of minicell formation and to map within or very close to the minB locus. Contrary to these mutations, the canonical min-1 mutation did not confer resistance to DicB.

Antiviral Substances in Raw Bovine Milk Active Against Bovine Rotavirus and Coronavirus.

After experimental contamination of bovine raw and heat-treated milks with bovine rotavirus and coronavirus strains, we observed a strong viral inhibition only with raw milks, from which virus recovery was 5 × 10-4%. Between 30% and 80% of the virus was recovered from the heat-treated milks, depending on the level of inoculation. The antiviral substance is heat-labile (destroyed within 30 min at 100°C), precipitated by ammonium sulfate and filtrable (0.45 µm Millipore membrane). It also has neutralizing activity on tissue culture.

[Experimental study of diarrhea induced by a strain of Escherichia coli (serogroup O-103) in growing rabbits]. / Reproduction expérimentale chez le lapin en engraissement d'une diarrhée provoquée par une souche de Escherichia coli de sérogroupe O-103.

The experimental infection by mouth of weaned, 6 week old rabbits was performed with Escherichia coli strain O-103/10 without any adjuvant. The quantities of E. coli for the 3 experimental treatments were - none (control) - 10(4) or 10(7) per animal. The 142 rabbits were divided into 2 groups, each including the 3 treatments: A - observation of weight and eventual diarrhea during 25 days after infection; B - killing during the same period of some healthy and diarrheic animals every 2 or 3 days, for physiological, bacteriological, and histological observations. In the A group, mortality after 25 days was 0/24 in the control, 12 and 15/24 for 10(4) and 10(7) treatments respectively, but it was observed earlier for the 10(7) one. Diarrhea has been observed for 90% of infected and 20% of control rabbits, at first on day 7, 12 and 20 post-infection for the 10(7), 10(4) and control treatments respectively. The mean duration of diarrhea was 4 days in infected and only 2 in control rabbits. Always, diarrhea and weight lost were observed before death. Although the slowing down of growth rate during the experimental period, at the end, mean live weight was quite the same for animals surviving in the 3 treatments. Necropsy of killed rabbits of the B group, revealed hemorrhagic damages mainly on cecal and colonic wall, associated with high counts for E. coli (10(7) to 8 X 10(9] in the cecal content. In rabbits with highest counts (9/15), E. coli was also observed in blood. In diarrheic rabbits cecal pH was higher (6.61 vs 5.82) and cecal VFA concentration lower (53 vs 98 mM/l) than in healthy ones; but the proportions of acetic, propionic and butyric acids were not significantly affected. At constant VFA concentration in the cecum, pH and E. coli counts were correlated (r = + 0.35). Histology revealed first, attachment of bacteria to the apex of villi cells, and furthermore destruction of the epithelium with hemorrhages and necrosis. Thus the strain O-103/10 of E. coli is confirmed to be pathogenic and will provide a good experimental model for studies of diarrhea due to E. coli.

Study of the teratogenic activity of ribosomal vaccine.

The investigation on the possible teratogenic activity of a vaccinal formula of ribosomes of Klebsiella pneumoniae, Streptococcus pneumoniae, Streptococcus pyogenes A12 and Haemophilus influenzae (D 53) was carried out in three animal species: rats, mice, rabbits. The trials were performed on two generatins of rats and mice, and on one single generation of rabbits. D 53 was given in s.c. injections (6 days a week) for 8 days before mating the females, and then until the females dropped (or were sacrificed when foetuses had to be removed by Caesarean operation). The possible teratogenic or embryotoxic effects of D 53 were evaluated using the following checks: fertility rates in the mated females; rates of placenta-foetal resorptions; abnormalites in foetuses and offspring (dissection and skeletal staining). In the above experimental conditions, D 53 had no embryotoxic and teratogenic activity in the 3 animal species used.