In vivo occupancy of the striatal dopamine uptake complex by various inhibitors does not predict their effects on locomotion

We have recently found that allogenic bone marrow transplantation (BMT) can be used to treat lupus nephritis in NZB x NZW F1 (B/W F1) and BXSB mice. To elucidate why and how glomerular damage is repaired, serial renal biopsies were carried out using B/W F1 mice before, and after BMT. Donor-derived B cells and macrophages with normal functions developed two weeks after BMT, whereas donor-derived functional T cells were generated after seven weeks of BMT. Visceral epithelial cells as well as macrophages in the glomeruli were activated (probably by T cell-derived lymphokines) at this time; they showed marked phagocytic activity, resulting in clearance of immune complexes (ICs) and repair of damaged basement membranes. These results suggest that normal T cell functions, which have the capacity to activate macrophages and epithelial cells, are essential in repairing IC-mediated glomerular damage.     

Incomplete inversion and double-valued fundamental linewidth ofinfrared HeNe and HeXe lasers

We have measured the quantum-limited linewidths of small HeNe 3.39 μm and HeXe 3.51 μm lasers. In contrast to the expected Schawlow-Townes behaviour strong deviations from the inverse power dependence are observed, leading to a double-valued relation between the linewidth and the output power. This phenomenon is analyzed in terms of the increase of spontaneous emission, by a factor N_sp, due to incompleteness of the inversion. Our analysis shows that typically N_sp has a value ranging from 1-10. Combining existing models for the pump power dependence of the level populations with measurements of the small signal gain, we are able to explain the observed double-valued linewidth behaviour in a quantitative way     

Glucagon-like peptide I enhances the insulinotropic effect of glibenclamide in NIDDM patients and in the perfused rat pancreas

OBJECTIVE: To investigate the acute effects of glibenclamide and glucagon-like peptide I (GLP-I) and their combination in perfused isolated rat pancreas and in patients with secondary failure to sulfonylureas. RESEARCH DESIGN AND METHODS: Rat islets were perfused with 10 nmol/l GLP-I in combination with 2 mumol/l glibenclamide. In human experiments, GLP-I (0.75 pmol. kg-1.min-1) was given as a continuous infusion during 240 min, while glibenclamide (3.5 mg) was administered orally. Eight patients participated in the study (age 57.6 +/- 2.7 years, BMI 28.7 +/- 1.5 kg/m2, mean +/- SE). In all subjects, blood glucose was first normalized by insulin infusion administered by an artificial pancreas (Biostator). RESULTS: GLP-I increased the insulinotropic effect of glibenclamide fourfold in the perfused rat pancreas. In human experiments, treatment with GLP-I alone and in combination with glibenclamide significantly decreased basal glucose levels (5.1 +/- 0.4 and 4.5 +/- 0.1 vs. 6.0 +/- 0.3 mmol/l, P < 0.01), while with only glibenclamide, glucose concentrations remained unchanged. GLP-I markedly decreased total integrated glucose response to the meal (353 +/- 60 vs. 724 +/- 91 mmol.l-1. min-1, area under the curve [AUC] [-30-180 min], P < 0.02), whereas glibenclamide had no effect (598 +/- 101 mmol.l-1. min-1, AUC [-30-180 min], NS). The combined treatment further enhanced the glucose lowering effect of GLP-I (138 +/- 24 mmol. l-1.min, AUC [-30-180 min], P < 0.001). GLP-I, glibenclamide, and combined treat-stimulated meal-induced insulin release as reflected by insulinogenic indexes (control 1.44 +/- 0.4; GLP-I 6.3 +/- 1.6, P < 0.01; glibenclamide 6.8 +/- 2.1, P < 0.01; combination 20.7 +/- 5.0, P < 0.001). GLP-I inhibited basal but not postprandial glucagon responses. Using paracetamol as a marker for gastric emptying rate of the test meal, treatment with GLP-I decreased gastric emptying at 180 min by approximately 50% compared with the control subjects (P < 0.01). CONCLUSIONS: In acute experiments on overweight patients with NIDDM, GLP-I exerted a marked antidiabetogenic action on the basal and postprandial state. The peptide stimulated insulin, suppressed basal glucagon release, and prolonged gastric emptying. The glucose-lowering effect of GLP-I was further enhanced by glibenclamide. This action may be at least partially accounted for by a synergistic effect of these two compounds on insulin release. Glibenclamide per se enhanced postprandial but not basal insulin release and exerted a less pronounced antidiabetogenic effect compared with GLP-I.     

Is there a myofascial, temporomandibular disorder personality?

It is widely accepted that abnormal personality factors play an important role in the etiology and maintenance of myofascial-type temporomandibular disorder, or M/TMD. However, the foundation on which this belief rests is based largely on clinical lore, rather than on any evidence. The continued belief in the stress theory has important implications. Clinicians continue to be trained in unproven but traditionally sanctioned treatments. Such approaches not only may lead to problems of patient care, they may forge an unstable foundation for future research. Two theories are examined in this article: the psychosomatic and psychophysiological models. The findings show that both theories lack evidence, and further research is warranted because definitive studies are unavailable. The data from this study do not support the contention that M/TMD cases are characterized by a specific premorbid personality.     

Mine operating accurate stability control with optical fibersensing and Bragg grating technology: the European BRITE/EURAM STABILOSproject

Recent developments of stability control in mines, essentially based on Ge-doped fiber Bragg gratings (FBG) are reported including results about the different aspects of the system: accurate characterizations of FBG, sensor network topology and multiplexing method, user interface design and sensor packaging     

Theory for passive mode-locking in semiconductor laser structuresincluding the effects of self-phase modulation, dispersion, and pulsecollisions

We present a theory for passive mode-locking in semiconductor laser structures using a semiconductor laser amplifier and absorber. The mode-locking system is described in terms of the different elements in the semiconductor laser structure. We derive mode-locking conditions and show how other mode-locking parameters, like pulse width and pulse energy, are determined by the mode-locking system. System parameters, like bandwidth, dispersion, and self-phase modulation are shown to play an important role in mode-locking conditions and results. We also discuss the effects of pulse collisions and positions of the mode-locking elements inside the cavity on mode-locking stability and show that these effects can be easily included in the presented model. Finally, we give a number of design rules and recommendations for fabricating passively mode-locked lasers