Phospholipid and eicosanoid signaling disturbances in schizophrenia.

[1]  S. Mahadik,et al.  Oxidative injury and potential use of antioxidants in schizophrenia. , 1996, Prostaglandins, leukotrienes, and essential fatty acids.

[2]  J. Rotrosen,et al.  Niacin-induced flush as a measure of prostaglandin activity in alcoholics and schizophrenics , 1986, Biological Psychiatry.

[3]  J. Morrow,et al.  Release of markedly increased quantities of prostaglandin D2 in vivo in humans following the administration of nicotinic acid. , 1989, Prostaglandins.

[4]  G. Vankar,et al.  Association of the ban I dimorphic site at the human cytosolic phospholipase A2 gene with schizophrenia , 1998, Schizophrenia Research.

[5]  H. Fukuzako,et al.  31P magnetic resonance spectroscopy of the medial temporal lobe of schizophrenic patients with neuroleptic-resistant marked positive symptoms , 2005, European Archives of Psychiatry and Clinical Neuroscience.

[6]  O. Forlenza,et al.  Phospholipase A2 activity in rat embryonic brain and in primary cultures of cortical neurons , 2002, Journal of Neural Transmission.

[7]  J. Hauser,et al.  No association between COMT gene MET/158 /VAL polymorphism and schizophrenia , 2002 .

[8]  F. Märki,et al.  Phospholipase A2 activity in serum of neuroleptic-naive psychiatric inpatients. , 1993, Pharmacopsychiatry.

[9]  C. Kuo,et al.  Deficiency of vitamin E and selenium enhances calcium-independent phospholipase A2 activity in rat lung and liver. , 1995, The Journal of nutrition.

[10]  I. Modai,et al.  Phospholipid patterns of erythrocytes in schizophrenia: relationships to symptomatology , 2001, Schizophrenia Research.

[11]  H. Hwu,et al.  Lack of association between schizophrenia and the phospholipase-A(2) genes cPLA2 and sPLA2. , 2001, American journal of medical genetics.

[12]  Jeffrey C. Erlich,et al.  Increased phospholipid breakdown in schizophrenia. Evidence for the involvement of a calcium-independent phospholipase A2. , 1997, Archives of general psychiatry.

[13]  S. Kish,et al.  Decreased activity of brain phospholipid metabolic enzymes in human users of cocaine and methamphetamine. , 2002, Drug and alcohol dependence.

[14]  Y. Urade,et al.  The major source of endogenous prostaglandin D2 production is likely antigen-presenting cells. Localization of glutathione-requiring prostaglandin D synthetase in histiocytes, dendritic, and Kupffer cells in various rat tissues. , 1989, Journal of immunology.

[15]  C. Hudson,et al.  The niacin challenge test: Clinical manifestation of altered transmembrane signal transduction in schizophrenia? , 1997, Biological Psychiatry.

[16]  D E Hillman,et al.  New ultrastructural findings regarding a vestibular ciliary apparatus and its possible functional significance. , 1969, Brain research.

[17]  J. D. Stevens.  The Distribution of the Phospholipid Fractions in the Red Cell Membrane of Schizophrenics , 1972 .

[18]  S. Hirsch,et al.  A volumetric biochemical niacin flush-based index that noninvasively detects fatty acid deficiency in schizophrenia , 2002, Progress in Neuro-Psychopharmacology and Biological Psychiatry.

[19]  R. Hitzemann,et al.  Membrane abnormalities in the psychoses and affective disorders. , 1984, Journal of psychiatric research.

[20]  W. Gattaz,et al.  Increased platelet membrane lysophosphatidylcholine in schizophrenia , 1991, Biological Psychiatry.

[21]  P. Kinnunen,et al.  Increased plasma phospholipase-A2 activity in schizophrenic patients: Reduction after neuroleptic therapy , 1987, Biological Psychiatry.

[22]  D. V. van Kammen,et al.  Increased turnover of platelet phosphatidylinositol in schizophrenia. , 1992, Prostaglandins, leukotrienes, and essential fatty acids.

[23]  B. Ross,et al.  Reduced vasodilatory response to methylnicotinate in schizophrenia as assessed by laser Doppler flowmetry , 2004, European Neuropsychopharmacology.

[24]  J. Rybakowski,et al.  Niacin test in schizophrenia and affective illness , 1991, Biological Psychiatry.

[25]  R. Stern,et al.  Tolerance to nicotinic acid flushing , 1991, Clinical pharmacology and therapeutics.

[26]  A. Douglass,et al.  Niacin skin flush is not diagnostic of schizophrenia , 1986, Biological Psychiatry.

[27]  M Takigawa,et al.  Changes in levels of phosphorus metabolites in temporal lobes of drug-naive schizophrenic patients. , 1999, The American journal of psychiatry.

[28]  J. Morrow,et al.  Identification of skin as a major site of prostaglandin D2 release following oral administration of niacin in humans. , 1992, The Journal of investigative dermatology.

[29]  M. Keshavan,et al.  Alterations in brain high-energy phosphate and membrane phospholipid metabolism in first-episode, drug-naive schizophrenics. A pilot study of the dorsal prefrontal cortex by in vivo phosphorus 31 nuclear magnetic resonance spectroscopy. , 1991, Archives of general psychiatry.

[30]  J. Rotrosen,et al.  Elevated PLA2 activity in schizophrenics and other psychiatric patients , 1993, Biological Psychiatry.

[31]  D. Blackwood,et al.  Red cell membrane fatty acids, cytosolic phospholipase-A2 and schizophrenia , 1998, Schizophrenia Research.

[32]  B. Ross,et al.  Clinical subtyping reveals significant differences in calcium-dependent phospholipase A2 activity in schizophrenia , 1999, Biological Psychiatry.

[33]  D. Horrobin,et al.  Degradation of specific polyunsaturated fatty acids in red blood cells stored at -20 degrees C proceeds faster in patients with schizophrenia when compared with healthy controls. , 2003, Prostaglandins, leukotrienes, and essential fatty acids.

[34]  M. Keshavan,et al.  Frontal lobe metabolism and cerebral morphology in schizophrenia: 31P MRS and MRI studies , 1993, Schizophrenia Research.

[35]  P. Ward,et al.  Niacin skin flush in schizophrenia: a preliminary report , 1998, Schizophrenia Research.

[36]  Horrobin Df.  Schizophrenia: a biochemical disorder? , 1980 .

[37]  T. Asakura,et al.  Study of chronic schizophrenics using 31P magnetic resonance chemical shift imaging , 1992, Acta psychiatrica Scandinavica.

[38]  S. Kish,et al.  Phospholipase A2 Activity Is Selectively Decreased in the Striatum of Chronic Cocaine Users , 1996, Journal of neurochemistry.

[39]  D. Horrobin,et al.  A red cell membrane abnormality in a subgroup of schizophrenic patients: evidence for two diseases , 1994, Schizophrenia Research.

[40]  L. Demisch,et al.  Incorporation of 14C-arachidonic acid into platelet phospholipids of untreated patients with schizophreniform or schizophrenic disorders , 1987, Psychiatry Research.

[41]  P. Williamson,et al.  An in vivo study of the prefrontal cortex of schizophrenic patients at different stages of illness via phosphorus magnetic resonance spectroscopy. , 1995, Archives of general psychiatry.

[42]  D. St. Clair,et al.  Lack of association between schizophrenia and a polymorphism close to the cytosolic phospholipase A2 gene , 1997, Psychiatric genetics.

[43]  B. Thelma,et al.  Association studies of cytosolic phospholipase A2 polymorphisms and schizophrenia among two independent family-based samples , 2001, Psychiatric genetics.

[44]  B. Ross,et al.  Chronic cocaine administration reduces phospholipase A(2) activity in rat brain striatum. , 2002, Prostaglandins, leukotrienes, and essential fatty acids.

[45]  P. Kinnunen,et al.  Increased serum phospholipase A2 activity in schizophrenia: a replication study. , 1990, Biological psychiatry.

[46]  D. Braus,et al.  Effects of antipsychotic treatment on membrane phospholipid metabolism in schizophrenia , 2001, Journal of Neural Transmission.

[47]  S. Kish,et al.  Differential alteration of phospholipase A2 activities in brain of patients with schizophrenia , 1999, Brain Research.

[48]  H. Meltzer,et al.  Genetic variant near cytosolic phospholipase A2 associated with schizophrenia , 1996, Schizophrenia Research.

[49]  D. Swanson,et al.  Calcium-independent phospholipase A2 and schizophrenia. , 1998, Archives of general psychiatry.

[50]  R. Rao.  Depression after transient ischemic attack: a clinically distinct subtype of vascular depression? , 1998, Archives of general psychiatry.

[51]  D. Horrobin.  The membrane phospholipid hypothesis as a biochemical basis for the neurodevelopmental concept of schizophrenia , 1998, Schizophrenia Research.