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신상호,Jung Wi Hoon,Robert McCutcheon,Mattia Veronese,Katherine Beck,Lee Jae Sung,Lee Yun-Sang,Oliver D. Howes,Kim Euitae,Kwon Jun Soo 대한신경정신의학회 2022 PSYCHIATRY INVESTIGATION Vol.19 No.7
Objective Striatal dopamine dysfunction caused by cortical abnormalities is a leading hypothesis of schizophrenia. Although prefrontal cortical pathology is negatively correlated with striatal dopamine synthesis, the relationship between structural frontostriatal connectivity and striatal dopamine synthesis has not been proved in patients with schizophrenia with different treatment response. We therefore investigated the relationship between frontostriatal connectivity and striatal dopamine synthesis in treatment-responsive schizophrenia (non-TRS) and compared them to treatment-resistant schizophrenia (TRS) and healthy controls (HC).Methods Twenty-four patients with schizophrenia and twelve HC underwent [<sup>18</sup>F] DOPA PET scans to measure dopamine synthesis capacity (the influx rate constant K<sub>i</sub><sup>cer</sup>) and diffusion 3T MRI to measure structural connectivity (fractional anisotropy, FA). Connectivity was assessed in 2 major frontostriatal tracts. Associations between K<sub>i</sub><sup>cer</sup> and FA in each group were evaluated using Spearman’s rho correlation coefficients.Results Non-TRS showed a negative correlation (r=-0.629, p=0.028) between connectivity of dorsolateral prefrontal cortex-associative striatum (DLPFC-AST) and dopamine synthesis capacity of associative striatum but this was not evident in TRS (r=-0.07, p=0.829) and HC (r=-0.277, p=0.384).Conclusion Our findings are consistent with the hypothesis of dysregulation of the striatal dopaminergic system being related to prefrontal cortex pathology localized to connectivity of DLPFC-AST in non-TRS, and also extend the hypothesis to suggest that different mechanisms underlie the pathophysiology of non-TRS and TRS.
Metabolic effects of recombinant ovine placental lactogen and growth hormone in pregnant ewes
Min, S H,Mackenzie, D D S,Breier, B H,McCutcheon, S N,Gluckman, P D 中央大學校 食糧資源硏究所 1998 食糧資源硏究所 論文集 Vol.10 No.1
The effects of recombinant ovine placental lactogen (oPL) and bovine growth hormone (bGH) on maternal metabolism, mammary gland development and fetal growth were examined in singleton bearing ewes at day 101 of gestation. Ewes were treated by twice daily subcutaneous injection for 7 days with oPL(n=7) or bGH (n=8) at a dose of 0.15 mg/kg LW/day or with saline (n=8). Jugualr blood samples were taken on days 1 and 7 of treatment. Relative to those of salinetreated ewes, bGH treatment significantly (P<0.01) reduced maternal plasma concentrations of oPL at day 7 of treatment. Administration of bGH also increased maternal circulating concentrations of insulinlike growth factor (IGF)Ⅰ (P<0.001), insulin (P<0.01), glucose (P<0.01) and nonesterified fatty acids (NEFA) (P<0.10) and decreased IGFⅡ (P<0.001) and urea (P<0.05) concentrations relative to those in oPL or salinetreated ewes. None of these parameters was affected by oPL treatment (vs saline treatment) except for maternal circulating oPL concentration which was increased by 50%(P<0.001). Neither bGH nor oPL had significant effects on dimension or trimmed weight of the mammary gland. Similarly, oPL treatment had no effects on weights of uterine components, whereas treatment with bGH increased the total weight of the gravid uterus (P<0.05) and weights of the uterine fluids, fetal membranes and myoendometrium (P<0.05). oPL, but not bGH treatment, also reduced maternal spleen (P<0.05) and heart (P<0.10) weights relative to those in salinetreated ewes. These results suggest that oPL acts in a distinctly different manner from bGH and that effects of oPL in the ewe are not mediated via changes in circulating concentrations of either IGFI or IGFII.