Palatability and physicochemical properties of sausages prepared via lactic acid fermentation and drying at low temperature.

The present study aimed to assess the palatability of sausages undergoing low-temperature fermentation and drying process. Lactobacillus sakei D-1001 or Lactobacillus salivarius A001 were used as starter cultures for fermentation, and the following properties of the sausages were investigated: colony-forming units of lactic acid bacteria; concentrations of lactic acid, protein, peptides, and free amino acids; distribution of protein; composition of free amino acids; and physical properties and taste. Alterations in the composition of proteins, peptides, and free amino acids as well as in various physical properties were caused by fermentation by lactic acid bacteria. A sensory test indicated that the palatability of the fermented sausages was greater than that of the non-fermented sausages, particularly in terms of hardness and juiciness. This was considered to be due to protein degeneration and changes in the physical properties of the sausages as a result of fermentation by lactic acid bacteria. However, the taste of the fermented sausages was sourer than that of the non-fermented sausages, and therefore, inferior. Our study revealed that the palatability of the sausages in terms of hardness and juiciness were increased by low-temperature fermentation by lactic acid bacteria and the drying process.

Accumulation of carboxy-terminal fragments of APP increases phosphodiesterase 8B.

The long-standing "amyloid hypothesis" that Alzheimer's disease is caused by the production and aggregation of amyloid-ß faces serious challenges by data recently obtained from neuroimaging studies and amyloid-ß amyloid-focused clinical trials. Meanwhile, accumulation of carboxy-terminal fragments (CTFs) of the amyloid precursor protein (APP) may be neurotoxic and may impair synaptic plasticity and long-term memory in Alzheimer's disease, as suggested in murine models. To clarify these issues, we carried out a proteomic analysis of Chinese hamster ovary cells expressing APP CTFs and found that APP-CTF accumulation induced an increase in the level of phosphodiesterase 8B, suggesting that the hydrolysis of cyclic AMP was enhanced.

Neural stem cell-like gene expression in a mouse ependymoma cell line transformed by human BK polyomavirus.

Ependymomas often show characteristics similar to those of neural stem cells in vivo and in vitro. However, few ependymoma cell lines that exhibit neural stem cell-like properties have been reported. In this study, we have characterized a novel cell line, designated Vn19, established from ependymoma that arose in mice inoculated intracerebrally with human BK polyomavirus. Transplanted Vn19 cells in nude mice ubiquitously expressed viral large T antigen in the nucleus and coexpressed neuronal and glial marker proteins in vivo. Remarkably, individual Vn19 cells in dispersed cultures simultaneously expressed marker proteins of neural stem cells (nestin, Bmi1, CD133), neurons (ßIII tubulin, neurofilament-M) and glial cells (glial fibrillary acidic protein, A2B5, S100ß, O4). Ubiquitous and homogenous expression of these multilineage marker proteins was also observed in cloned Vn19 cells. The Vn19 cells formed neurosphere-like aggregates when cultured in the presence of growth factors. Quantitative RT-PCR analysis revealed that expression of mRNA for nestin, neurofilament-H and glial fibrillary acidic protein significantly increased in Vn19 cells cultured under growth factor-deprived conditions. Among MAGE (melanoma antigen) family genes, MAGE-A (A1-8), MAGE-B (B1-3), MAGE-D1, MAGE-E1, MAGE-G1 (necdin-like 2) and MAGE-H1 were expressed in the Vn19 cells, in which neither necdin nor MAGEL2 was detectable. These results suggest that this murine ependymoma cell line recapitulates the gene expression profile in ependymal cells undergoing malignant transformation.

Enhanced carbonyl stress in a subpopulation of schizophrenia.

CONTEXT: Various factors are involved in the pathogenesis of schizophrenia. Accumulation of advanced glycation end products, including pentosidine, results from carbonyl stress, a state featuring an increase in reactive carbonyl compounds (RCOs) and their attendant protein modifications. Vitamin B(6) is known to detoxify RCOs, including advanced glycation end products. Glyoxalase I (GLO1) is one of the enzymes required for the cellular detoxification of RCOs. OBJECTIVES: To examine whether plasma levels of pentosidine and serum vitamin B(6) are altered in patients with schizophrenia and to evaluate the functionality of GLO1 variations linked to concomitant carbonyl stress. DESIGN: An observational biochemical and genetic analysis study. SETTING: Multiple centers in Japan. PARTICIPANTS: One hundred six individuals (45 schizophrenic patients and 61 control subjects) were recruited for biochemical measurements. Deep resequencing of GLO1 derived from peripheral blood or postmortem brain tissue was performed in 1761 patients with schizophrenia and 1921 control subjects. MAIN OUTCOME MEASURES: Pentosidine and vitamin B(6) concentrations were determined by high-performance liquid chromatographic assay. Protein expression and enzymatic activity were quantified in red blood cells and lymphoblastoid cells using Western blot and spectrophotometric techniques. RESULTS: We found that a subpopulation of individuals with schizophrenia exhibit high plasma pentosidine and low serum pyridoxal (vitamin B(6)) levels. We also detected genetic and functional alterations in GLO1. Marked reductions in enzymatic activity were associated with pentosidine accumulation and vitamin B(6) depletion, except in some healthy subjects. Most patients with schizophrenia who carried the genetic defects exhibited high pentosidine and low vitamin B(6) levels in contrast with control subjects with the genetic defects, suggesting the existence of compensatory mechanisms. CONCLUSIONS: Our findings suggest that GLO1 deficits and carbonyl stress are linked to the development of a certain subtype of schizophrenia. Elevated plasma pentosidine and concomitant low vitamin B(6) levels could be the most cogent and easily measurable biomarkers in schizophrenia and should be helpful for classifying heterogeneous types of schizophrenia on the basis of their biological causes.

Association between polymorphisms in the promoter region of the sialyltransferase 8B (SIAT8B) gene and schizophrenia.

BACKGROUND: Sialyltransferase 8B (SIAT8B) and 8D (SIAT8D) are two polysialyltransferases that catalyze the transfer of polysialic acid (PSA) to the neural cell adhesion molecule 1 (NCAM1). PSA modification of NCAM1 plays an important role in neurodevelopment of the brain and disruption of this process is postulated as an etiologic factor in psychiatric disorders. Altered levels of the PSA-NCAM1 in the brain of schizophrenics have been reported, suggesting a role for this molecule in the disorder. METHODS: We performed an association study of single nucleotide polymorphisms (SNPs) within SIAT8B and SIAT8D, using 188 schizophrenics and 156 age and gender matched controls. All genotypes were determined by polymerase chain reaction (PCR) amplification and direct sequencing. RESULTS: Two polymorphisms, -1126T > C and -851T > C, located in the promoter region of SIAT8B showed nominally significant association with schizophrenia (allelic associations, p = .014 and p = .007, respectively), and haplotypes constructed from three additional SNPs located in the same linkage disequilibrium block were associated with schizophrenia. Furthermore an in vitro promoter assay revealed that a reporter construct containing a risk haplotype for SIAT8B had significantly higher transcriptional activity compared with one containing a protective haplotype (p = .021). In contrast, no significant association was observed between any variations in SIAT8D and schizophrenia. CONCLUSIONS: The present study suggests that functional promoter SNPs of SIAT8B could confer a risk for schizophrenia in the Japanese population.

Association of neural cell adhesion molecule 1 gene polymorphisms with bipolar affective disorder in Japanese individuals.

BACKGROUND: Although the pathogenesis of mood disorders remains unclear, heritable factors have been shown to be involved. Neural cell adhesion molecule 1 (NCAM1) is known to play important roles in cell migration, neurite growth, axonal guidance, and synaptic plasticity. Disturbance of these neurodevelopmental processes is proposed as one etiology for mood disorder. We therefore undertook genetic analysis of NCAM1 in mood disorders. METHODS: We determined the complete genomic organization of human NCAM1 gene by comparing complementary deoxyribonucleic acid and genomic sequences; mutation screening detected 11 polymorphisms. The genotypic, allelic, and haplotype distributions of these variants were analyzed in unrelated control individuals (n = 357) and patients with bipolar disorder (n = 151) and unipolar disorder (n = 78), all from central Japan. RESULTS: Three single nucleotide polymorphisms, IVS6+32T>C, IVS7+11G>C and IVS12+21C>A, displayed significant associations with bipolar disorder (for allelic associations, nominal p =.04, p =.02, and p =.004, respectively, all p >.05 after Bonferroni corrections). Furthermore, the haplotype located in a linkage disequilibrium block was strongly associated with bipolar disorder (the p value of the most significant three-marker haplotype is .005). CONCLUSIONS: Our results suggest that genetic variations in NCAM1 or nearby genes could confer risks associated with bipolar affective disorder in Japanese individuals.

Association between a novel polymorphism in the promoter region of the neuropeptide Y gene and schizophrenia in humans.

Hypoactivity of neuropeptide Y (NPY) is thought to be involved in the pathophysiology of schizophrenia, because post-mortem brain studies revealed a decrease of the NPY in schizophrenia, and antipsychotic treatments increase the NPY in animal brains and in cerebrospinal fluid of patients. We performed genetic analysis of the NPY gene in schizophrenia. Mutation screening of the gene detected nine single nucleotide polymorphisms, of which we typed a -485C>T variation from potential functional relevance. The -485T allele was overly represented in the disease group (P=0.0043). An in vitro promoter assay revealed that a C to T change at nt -485 significantly reduced transcriptional activity. These results suggest that the -485T allele in NPY may confer susceptibility to schizophrenia by decreasing the neuropeptide in brains.