Independence of Peripheral Brain-Derived Neurotrophic Factor from Depression and Anxiety Symptoms in Cocaine Use Disorder: An Initial Description

Cocaine use disorder (CUD) presents high comorbidity with mood symptoms that impair recovery processes and facilitate relapses. Peripheral brain-derived neurotrophic factor (BDNF) is negatively correlated with mood symptoms in depressive disorders. However, whether a correlation exists between BDNF and mood in CUD is still unknown. Thus, in this cross-sectional study, we explored the potential relationship between peripheral BDNF levels and depression and anxiety symptoms in CUD. Serum peripheral BDNF was determined by the ELISA method. Standardized Hamilton Depression (HDRS) and Anxiety (HARS) inventories were administered. Twenty-nine seeking-treatment CUD participants under stable medication (female = 3) were enrolled. According to the mood severity, 34.48% of participants were classified as normal, 24.14% as moderate, and 41.38% as severe symptoms (p < 0.001). Peripheral BDNF was similar between the different mood severity groups (p > 0.05). No correlation between BDNF and HDRS and BDNF and HARS was detected regardless of the severity of mood symptoms (p > 0.05). Different from what has been observed in depressive disorders, independence between peripheral BDNF levels and mood symptoms in CUD was observed. This finding suggests a singular, intricate regulation of peripheral BDNF and mood as part of CUD-related maladaptations that might disrupt the expected antidepressant response and perpetuate mood symptoms in CUD

Fibrogenic polymorphisms (TGF-β, PAI-1, AT) in Mexican patients with established liver fibrosis. Potential correlation with pirfenidone treatment

Background/Aim: The aim of this work was to establish a potential correlation between specific polymorphisms and presence of hepatic fibrosis in Mexican patients with established liver fibrosis (ELF). Second, necroinflammatory index improvement was correlated with Pirfenidone (PFD) treatment response and the same polymorphisms. Methods: We analyzed TGF-β polymorphisms in codon 25, a single basepair guanine insertion-deletion polymorphism (4G/5G) for PAI-1 and angiotensin AT-6 single nucleotide polymorphism located in -6 promoter region. Twenty patients infected with either hepatitis C virus (HCV) (n = 13) or affected by alcohol consumption (n = 7) were included. Thirty subjects with no hepatic damage were included in control group. Blood samples for genomic DNA were obtained and plasminogen activator inhibitor-1 polymorphisms were done by polymerase chain reaction-artificial introduction of a restriction site, TGF-β by polymerase chain reaction-amplification refractory mutation system and AT by polymerase chain reaction-restriction fragment length polymorphisms. Liver biopsies were obtained at baseline and after 12 months of PFD treatment. Results: Established liver fibrosis patients had the homo-zygote G/G TGF-β genotype, which has been associated with increased development of fibrosis. None of our patients had the G/C genotype. All pure HCV and pure alcohol abuse subjects carried G/G TGF-β genotype (100% vs 37% control) (P = 0.0006). The odds of having β G/G genotype was 19.5 for HCV patients and 10.83 for alcohol consumption patients as compared with healthy subjects (P < 0.001). Established liver fibrosis patients had an improvement in necroinflammatory index after PFD treatment when correlated with plasminogen activator inhibitor-1 and angiotensinogen-6 genotypes. Conclusion: Our data suggested that a combination of inherited polymorphisms increased the risk of advanced fibrosis in ELF patients. Pure HCV and pure alcohol consumption patients which were homozygous G/G carriers had 19.5- and 10.8-fold higher risk to develop advanced fibrosis respectively. © 2008 by The American Federation for Medical Research

Nuclear genome size and cytotype analysis in Agave cupreata Trel. & Berger (Agavaceae)

Background/Aim: The aim of this work was to establish a potential correlation between specific polymorphisms and presence of hepatic fibrosis in Mexican patients with established liver fibrosis (ELF). Second, necroinflammatory index improvement was correlated with Pirfenidone (PFD) treatment response and the same polymorphisms. Methods: We analyzed TGF-? polymorphisms in codon 25, a single basepair guanine insertion-deletion polymorphism (4G/5G) for PAI-1 and angiotensin AT-6 single nucleotide polymorphism located in -6 promoter region. Twenty patients infected with either hepatitis C virus (HCV) (n = 13) or affected by alcohol consumption (n = 7) were included. Thirty subjects with no hepatic damage were included in control group. Blood samples for genomic DNA were obtained and plasminogen activator inhibitor-1 polymorphisms were done by polymerase chain reaction-artificial introduction of a restriction site, TGF-? by polymerase chain reaction-amplification refractory mutation system and AT by polymerase chain reaction-restriction fragment length polymorphisms. Liver biopsies were obtained at baseline and after 12 months of PFD treatment. Results: Established liver fibrosis patients had the homo-zygote G/G TGF-? genotype, which has been associated with increased development of fibrosis. None of our patients had the G/C genotype. All pure HCV and pure alcohol abuse subjects carried G/G TGF-? genotype (100% vs 37% control) (P = 0.0006). The odds of having ? G/G genotype was 19.5 for HCV patients and 10.83 for alcohol consumption patients as compared with healthy subjects (P < 0.001). Established liver fibrosis patients had an improvement in necroinflammatory index after PFD treatment when correlated with plasminogen activator inhibitor-1 and angiotensinogen-6 genotypes. Conclusion: Our data suggested that a combination of inherited polymorphisms increased the risk of advanced fibrosis in ELF patients. Pure HCV and pure alcohol consumption patients which were homozygous G/G carriers had 19.5- and 10.8-fold higher risk to develop advanced fibrosis respectively. " 2008 by The American Federation for Medical Research.",,,,,,,,,"http://hdl.handle.net/20.500.12104/41497","http://www.scopus.com/inward/record.url?eid=2-s2.0-58149171859&partnerID=40&md5=2d9bdf46f3633f1bdbec471aff3ce07