Lithium augmentation in treatment-resistant depression: meta-analysis of placebo-controlled studies.
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Antidepressive Agents↗
Biomedical subjects
M Bauer
Publications and source records attributed to M Bauer.
Stimulation of platelets and endothelial cells by mildly oxidized LDL proceeds through activation of lysophosphatidic acid receptors and the Rho/Rho-kinase pathway. Inhibition by lovastatin.
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Blood Platelets↗
Cell viability in optical tweezers: high power red laser diode versus Nd:YAG laser.
Viability of cultivated Chinese hamster ovary cells in optical tweezers was measured after exposure to various light doses of red high power laser diodes (lambda = 670-680 nm) and a Nd:yttrium-aluminum-garnet laser (lambda = 1064 nm). When using a radiant exposure of 2.4 GJ/cm2, a reduction of colony formation up to a factor 2 (670-680 nm) or 1.6 (1064 nm) as well as a delay of cell growth were detected in comparison with nonirradiated controls. In contrast, no cell damage was found at an exposure of 340 MJ/cm2 for both wavelengths, and virtually no lethal damage at 1 GJ/cm2 applied at 1064 nm. Cell viabilities were correlated with fluorescence excitation spectra and with literature data of wavelength dependent cloning efficiencies. Fluorescence excitation maxima of the coenzymes NAD(P)H and flavins were detected at 365 and 450 nm, respectively. This is half of the wavelengths of the maxima of cell inactivation, suggesting that two-photon absorption by these coenzymes may contribute to cellular damage. Two-photon excitation of NAD(P)H and flavins may also affect cell viability after exposure to 670-680 nm, whereas one-photon excitation of water molecules seems to limit cell viability at 1064 nm.
Absorption↗
Double-blind, placebo-controlled trial of the use of lithium to augment antidepressant medication in continuation treatment of unipolar major depression.
OBJECTIVE: Use of lithium to augment antidepressant medication has been shown to be beneficial in the acute treatment of depression. The authors examined the efficacy of lithium augmentation in the continuation treatment of unipolar major depressive disorder. METHOD: Thirty patients with a refractory major depressive episode who had responded to acute lithium augmentation during an open 6-week study participated in a randomized, parallel-group, double-blind, placebo-controlled trial of lithium augmentation during continuation treatment. After a 2-4-week stabilization period following remission, patients were randomly assigned to receive either lithium or placebo for a 4-month period. Antidepressant medication was continued throughout the study. RESULTS: Relapses (including one suicide) occurred in seven (47%) of the 15 patients who received placebo in addition to antidepressants. None (0%) of the 14 patients who received lithium augmentation with antidepressants suffered a relapse during the double-blind phase of the study. Five of the seven relapsing patients in the placebo group developed a depressive episode, and the other two experienced a manic episode. CONCLUSIONS: Lithium augmentation in the continuation phase of treatment of unipolar major depressive disorder effectively protects patients against a relapse. Patients who respond to lithium augmentation should be maintained on lithium augmentation for a minimum of 6 months or even longer.
Adolescent↗
[The "difficult" patient in community psychiatry].
The "difficult patient" does not exist in psychiatric textbooks but rather in every day practice. A solely diagnostic description is not very useful, the categorisation into three separate subgroups by Sheets et al. (1982) on the contrary helps a lot. Three case studies describes typical treatment-situations with "difficult patients" in a community psychiatric setting.
Adult↗
[Everything has a beginning. Comments on the historical development of the psychiatry enquete].
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Community Psychiatry↗
[Cloning of partial cDNA of rat connective tissue growth factor and expression of its mRNA in experimental liver fibrosis].
OBJECTIVE: To clone the partial cDNA sequence of rat connective tissue growth factor (CTGF) and investigate the mRNA expression of CTGF and transforming growth factor-beta 1 (TGF-beta 1) in rat experimental liver fibrosis. METHODS: A 430-base pair sequence of rat CTGF Cdna was cloned by reverse transcription-polymerase chain reaction. Sixteen female Wistar rats were allocated into bile duct occlusion group (n=8) and sham-operated group (n=8). The liver tissue mRNA levels of CTGF and TGF-beta 1 were measured by multiprobe ribonuclease protection assay (RPA). RESULTS: The cloned partial cDNA sequence of rat CTGF was 95% homology (at nucleic acid level) with the mouse counterpart. In the liver of rats with biliary fibrosis mRNA levels of TGF-beta 1 and CTGF were 4 and 7 times as high as in those of sham-operated rats, respectively. CONCLUSION: The mRNA expression of CTGF is remarkably upregulated in rat liver fibrogenesis.
Animals↗
Chromosome 17 loss-of-heterozygosity studies in benign and malignant tumors in neurofibromatosis type 1.
Neurofibromatosis type 1 (NF1) is a common autosomal dominant condition characterized by benign tumor (neurofibroma) growth and increased risk of malignancy. Dermal neurofibromas, arising from superficial nerves, are primarily of cosmetic significance, whereas plexiform neurofibromas, typically larger and associated with deeply placed nerves, extend into contiguous tissues and may cause serious functional impairment. Malignant peripheral nerve sheath tumors (MPNSTs) seem to arise from plexiform neurofibromas. The NF1 gene, on chromosome segment 17q11.2, encodes a protein that has tumor suppressor function. Loss of heterozygosity (LOH) for NF1 has been reported in some neurofibromas and NF1 malignancies, but plexiform tumors have been poorly represented. Also, the studies did not always employ the same markers, preventing simple comparison of the frequency and extent of LOH among different tumor types. Our chromosome 17 LOH analysis in a cohort of three tumor types was positive for NF1 allele loss in 2/15 (13%) dermal neurofibromas, 4/10 (40%) plexiform neurofibromas, and 3/5 (60%) MPNSTs. Although the region of loss varied, the p arm (including TP53) was lost only in malignant tumors. The losses in the plexiform tumors all included sequences distal to NF1. No subtle TP53 mutations were found in any tumors. This study also reports the identification of both NF1 "hits" in plexiform tumors, further supporting the tumor suppressor role of the NF1 gene in this tumor type.
Adolescent↗
Hirudin monitoring using the TAS ecarin clotting time in patients with heparin-induced thrombocytopenia type II.
OBJECTIVE: To assess the reliability of the TAS/ecarin clotting time (ECT) for on-line monitoring of r-hirudin in cardiovascular surgery with and without cardiopulmonary bypass (CPB). DESIGN: Samples were spiked with r-hirudin (0 to 5 microg/mL) and calibration curves constructed. Reproducibility was evaluated by measurement of the sample five times at each concentration. The influence of variations in hematocrit, plasma factors, and platelet count on the test results was examined. Samples were obtained from patients during cardiovascular surgery with CPB (n = 8), without CPB (n = 3), and from volunteers (n = 5) and compared with the laboratory reference tests. All tests were performed in duplicate. SETTING: Deutsches Herzzentrum Berlin. PARTICIPANTS: Five healthy volunteers and 11 patients undergoing cardiovascular surgery. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: The TAS/ECT showed linearity and reliability to an r-hirudin concentration of 5 microg/mL and was not influenced (p < 0.005) by the varying conditions of the in vitro setup. The correlation to the laboratory method was 0.74 for the CPB group and 0.87 for the non-CPB group. CONCLUSIONS: The TAS/ECT is a reliable assay for monitoring r-hirudin at the point of care. With this information, the use of r-hirudin during surgery or angioplasty should become more effective and safer.
Adult↗
Phosphorylation-dependent proline isomerization catalyzed by Pin1 is essential for tumor cell survival and entry into mitosis.
Pin1, a member of the parvulin family of peptidyl-prolyl cis-trans isomerases (PPIases) has been implicated in the G2-M transition of the mammalian cell cycle. Pin1 interacts with a series of mitotic phosphoproteins, including Polo-like kinase-1, Cdc25C, and Cdc27, and is thought to act as a phosphorylation-dependent PPIase for these target molecules. Pin1 recognizes phosphorylated serine-proline or threonine-proline peptide-bonds in test substrates up to 1300-fold better than in the respective unphosphorylated peptides. To test directly whether Pin1 regulates the G2-M transition and/or progression through mitosis by catalyzing phosphorylation-dependent prolyl isomerization of essential mitotic targets, we examined the consequences of Pin1 depletion, achieved by (a) overexpression of Pin1 antisense RNA, (b) overexpression of dominant-negative Pin1, and (c) by a known small-molecule Pin1-PPIase inhibitor, juglone. The results of all of the three lines of investigation show that the catalytic activity of Pin1 is essential for tumor cell survival and entry into mitosis.
Antineoplastic Agents, Phytogenic↗
[Expression of collagen XVIII mRNA in rat liver fibrosis].
OBJECTIVE: To measure and study quantitatively the collagen XVIII mRNA in normal and fibrotic rat livers. METHODS: We used ribonuclease protection assay to investigate the collagen XVIII mRNA expression in rat liver fibrosis induced by complete bile duct occlusion (BDO). The expression level of procollagen 1 (XVIII) mRNA was compared with that of procollagen 1 (I) and tissue inhibitor of metalloproteinase 1 (TIMP1). RESULTS: mRNA levels of procollagen and TIMP 1 increased 20- and 4-fold in BDO rat livers, respectively. In contrast, hepatic procollagen 1 mRNA level increased only 1.8-fold in fibrotic rat livers. CONCLUSION: C XVIII mRNA is upregulated slightly in liver fibrosis, which is probably correlated with the fact that CXVIII is mainly expressed by hepatocytes.
Animals↗
[Cost control in anesthesiology--regulating net costs exemplified by anesthetics].
German hospitals are beginning to feel more and more pressure due to rising costs in health care. These are due to continuous increase in health care expenditure and decrease in state insurance contributions. A change in the state insurance system (GKV) is well and truly overdue; the source of income needs to be increased by either raising the compulsory insurance wage base or making other forms of income liable for insurance contributions. Unfortunately, the government is still reluctant to take action. The ruling coalition feels that it is better to limit the increase in expenditure on hospital care by introducing a case-related payment system. Unfortunately, they do not recognize that the main reason for the increase in health care expenditure is the growing medical potential and the higher morbidity of an, on average, older population. These cuts in financial means demand an efficient allocation of the available funds. As far as hospital in-patient care is concerned, this means that hospitals need to reconsider their expenditure and that economic success is dependent on their potential to recognize ways of reducing overall costs. This article illustrates that before the "Diagnosis Related Groups" (DRG) become effective in 2003, one needs to establish the cost price of individual hospital cases. The economic principles of cost-benefit ratios and methods to prevent cost inflation are presented. The methods of making a cost-effectiveness analysis of anaesthetic costs are explained in detail. The aim of this paper is to give the clinician a better understanding of cost management and to motivate staff to initiate cost-control studies.
Anesthesiology↗
Dimension reduction for highdimensional online-monitoring data in intensive care.
Nowadays high dimensional data in intensive care medicine can be captured, stored, and retrieved with the help of clinical information systems. Intelligent alarm systems are needed for an adequate bedside decision support, in the course of which the detection of qualitative patterns in physiologic monitoring data such as outliers, level changes, or trends aims at a proper classification of the patients state. Statistical time series techniques have already been applied successfully to the analysis of single physiological variables. The simultaneous online analysis of the multivariate patient curve yields further challenges. We describe methods for reducing the dimension and for keeping the computational efforts necessary for monitoring low. We present preliminary results of an ongoing study on monitoring critically ill patients.
Adult↗
[Anesthesia with remifentanil combined with desflurane or sevoflurane in lumbar intervertebral disk operations].
Recovery characteristics, haemodynamic profile, analgesic requirement and costs were evaluated and compared in patients undergoing elective lumbar discectomy with remifentanil-based anaesthesia using either desflurane or sevoflurane as the volatile anaesthetic agent. Sixty-two patients (ASA I/II status) were randomly assigned to receive either desflurane and remifentanil or sevoflurane and remifentanil (in oxygen/air) for anaesthesia. After induction with 0.5 microgram/kg/min remifentanil, 4 to 5 mg/kg thiopentone and 0.5 mg/kg atracurium, the patients received 0.25 microgram/kg/min remifentanil and 0.5 +/- 0.05 MAC of one of the volatile anaesthetic agents for further maintenance of anaesthesia. At the end of surgery, early emergence from anaesthesia was recorded by assessing the time to sufficient spontaneous respiration, eye opening and tracheal extubation. The total demand of piritramide in the postoperative period was determined using patient-controlled analgesia (PCA device). Quality of pain therapy was assessed via a verbal ranking scale (VRS). Side-effects such as postoperative nausea, vomiting or shivering were recorded in the postanaesthetic care unit. In both groups, the haemodynamic profile was nearly identical. Mean arterial pressure (-18%) and heart rate (-23%) were significantly reduced throughout anaesthesia in both groups. All recovery parameters were significantly shorter in the desflurane group in comparison with the sevoflurane group (e.g. time to tracheal extubation: 8.5 +/- 3.0 min vs. 11.9 +/- 4.6 min). No significant differences between the groups were observed concerning the amount of piritramide required, side-effects such as nausea and vomiting or the total cost of anaesthesia. In conclusion, both anaesthetic techniques provide adequate haemodynamic stability and postoperative pain control in a surgical procedure with minimal trauma. Incidence and severity of side-effects such as nausea, vomiting or shivering did not differ between the groups and were acceptable under clinical conditions. Costs for desflurane were significantly higher than those for sevoflurane, but total costs were not different between the groups. Concerning recovery profile, desflurane/remifentanil seems to have small advantages over sevoflurane/remifentanil in patients undergoing lumbar vertebral disc resection.
Adult↗
Mildly oxidized low density lipoprotein induces contraction of human endothelial cells through activation of Rho/Rho kinase and inhibition of myosin light chain phosphatase.
Mildly oxidized low density lipoprotein (mox-LDL) is critically involved in the early atherogenic responses of the endothelium and increases endothelial permeability through an unknown signal pathway. Here we show that (i) exposure of confluent human endothelial cells (HUVEC) to mox-LDL but not to native LDL induces the formation of actin stress fibers and intercellular gaps within minutes, leading to an increase in endothelial permeability; (ii) mox-LDL induces a transient decrease in myosin light chain (MLC) phosphatase that is paralleled by an increase in MLC phosphorylation; (iii) phosphorylated MLC stimulated by mox-LDL is incorporated into stress fibers; (iv) cytoskeletal rearrangements and MLC phosphorylation are inhibited by C3 transferase from Clostridium botulinum, a specific Rho inhibitor, and Y-27632, an inhibitor of Rho kinase; and (v) mox-LDL does not increase intracellular Ca(2+) concentration. Our data indicate that mox-LDL induces endothelial cell contraction through activation of Rho and its effector Rho kinase which inhibits MLC phosphatase and phosphorylates MLC. We suggest that inhibition of this novel cell signaling pathway of mox-LDL could be relevant for the prevention of atherosclerosis.
ADP Ribose Transferases↗
Dichotomous regulation of myosin phosphorylation and shape change by Rho-kinase and calcium in intact human platelets.
Both Rho-kinase and the Ca(2+)/calmodulin-dependent myosin light chain (MLC) kinase increase the phosphorylation of MLC. We show that upon thrombin receptor stimulation by low-dose thrombin or the peptide ligand YFLLRNP, or upon thromboxane receptor activation by U46619, shape change and MLC phosphorylation in human platelets proceed through a pathway that does not involve an increase in cytosolic Ca(2+). Under these conditions, Y-27632, a specific Rho-kinase inhibitor, prevented shape change and reduced the stimulation of MLC-phosphorylation. In contrast, Y-27632 barely affected shape change and MLC-phosphorylation by adenosine diphosphate (ADP), collagen-related peptide, and ionomycin that were associated with an increase in cytosolic Ca(2+) and inhibited by BAPTA-AM/EGTA treatment. Furthermore, C3 exoenzyme, which inactivates Rho, inhibited preferentially the shape change induced by YFLLRNP compared with ADP and ionomycin. The results indicate that the Rho/Rho-kinase pathway is pivotal in mediating the MLC phosphorylation and platelet shape change by low concentrations of certain G protein-coupled platelet receptors, independent of an increase in cytosolic Ca(2+). Our study defines 2 alternate pathways, Rho/Rho-kinase and Ca(2+)/calmodulin-regulated MLC-kinase, that lead independently of each other through stimulation of MLC-phosphorylation to the same physiological response in human platelets (ie, shape change).
15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
[Laser therapy of the eye for correction of refractive errors. A risk severe myopia?].
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Follow-Up Studies↗
Lysophosphatidic acid mediates the rapid activation of platelets and endothelial cells by mildly oxidized low density lipoprotein and accumulates in human atherosclerotic lesions.
Oxidized low density lipoprotein (LDL) is a key factor in the pathogenesis of atherosclerosis and its thrombotic complications, such as stroke and myocardial infarction. It activates endothelial cells and platelets through mechanisms that are largely unknown. Here, we show that lysophosphatidic acid (LPA) was formed during mild oxidation of LDL and was the active compound in mildly oxidized LDL and minimally modified LDL, initiating platelet activation and stimulating endothelial cell stress-fiber and gap formation. Antagonists of the LPA receptor prevented platelet and endothelial cell activation by mildly oxidized LDL. We also found that LPA accumulated in and was the primary platelet-activating lipid of atherosclerotic plaques. Notably, the amount of LPA within the human carotid atherosclerotic lesion was highest in the lipid-rich core, the region most thrombogenic and most prone to rupture. Given the potent biological activity of LPA on platelets and on cells of the vessel wall, our study identifies LPA as an atherothrombogenic molecule and suggests a possible strategy to prevent and treat atherosclerosis and cardiocerebrovascular diseases.
Arteriosclerosis↗