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酒精使用障礙症合併憂鬱情緒患者接受認知行為治療之個案研究

為了解決CNS1336的問題，作者葉育修 這樣論述：

摘要：本研究以個案報告記錄三位「酒精使用障礙症」(Alcohol use disorder, AUD)合併「憂鬱症」(Major depressive disorder, MDD)患者接受「認知行為治療」(Cognitive Behavior Therapy, CBT) 的歷程。本研究分為四個階段，第一階段於身心科門診或病房收案；第二階段在病患充分知情同意後納入研究，並施行心理測驗評估病患的認知功能可接受「認知行為治療」(Cognitive Behavior Therapy, CBT)。第三階段，病患會接受12次CBT治療，並在最後一次治療時，接受心理測驗。第四階段在結案後一個月再進行追蹤訪

談與評估CBT療效。研究結果發現，個案在接受認知行為治療時，有助於療效因子分為內在因素與外在因素。內在因素包括：病患能修改失功能的信念與負面的自動化思考，提升回家作業遵從性，並且在渴求時採取有效因應策略。外在因素為正向積極的社交支持力量。無助於療效的因子，包括：在治療時，病患不願意揭露實際飲酒情況與憂鬱情緒，無法與治療師建立合作同盟的治療關係，回家作業遵從性不佳與欠缺社群支持。此外，本研究建議酒精使用障礙症合併有憂鬱情緒與述情障礙特質者，認知行為治療重點應著重於教導病患辨識在高風險情境中促進飲酒的信念，並且使用行為活化技巧對應渴求與憂鬱情緒。最後，本研究結果為相關領域提供更近一步量化研究基礎，

並且提供該族群接受更有效評估與臨床介入方式。

牙齦卟啉單胞菌造成腦部內皮細胞死亡之機制探討

為了解決CNS1336的問題，作者VICHUDA CHAROENSAENSUK 這樣論述：

Emerging studies have shown the interconnection between the brain-oral axis, especially for the pathophysiology of brain disorders and oral pathogens. Porphyromonas gingivalis (P. gingivalis), a prominent microorganism responsible for periodontal disease, has been reported to increase the risk of d

eveloping cerebrovascular damage. A previous study from the master’s thesis has shown that P. gingivalis adhered and invaded bEnd.3 cells, thus triggering cell death by upregulating pro-inflammatory cytokines proteins tumor necrosis factor alpha (TNF-α) and interleukin 1 beta (IL-1β). However, the u

nderlying mechanisms of the effect of this periodontal bacterium on brain vascular endothelial cell death remain unknown. The purpose of this work was to explore the regulatory mechanisms of P. gingivalis on the inflammation and death of bEnd.3 and primary mouse brain endothelial cells (MBECs). More

over, the therapeutic effects of THSG (2,3,5,4ʹ-Tetrahydroxystilbene-2-O-β-glucoside), a Chinese herbal medicine extract, in P. gingivalis-stimulated brain endothelial cells were examined in this study. Results revealed that the viable form of P. gingivalis but not heat-inactivated caused apoptosis

in bEnd.3 cells. Moreover, P. gingivalis elevated intracellular reactive oxygen species (ROS) and promoted the activation of the nuclear factor kappa B (NF-κB) p65 transcription factor. The toxicity effect of P. gingivalis was reversed by treatment with antioxidant agents N-Acetyl-L-cysteine (NAC),

thereby confirming that P. gingivalis provoked cytokine expression and induced cell death via the oxidative stress pathway in brain endothelial cells. MBECs were further exploited to examine the impact of P. gingivalis on brain endothelial cell death. Moreover, THSG offered anti-inflammatory and ant

i-apoptosis in bEnd.3 and MBECs stimulated with P. gingivalis with a comparable efficacy as the well-established nicotinamide adenine dinucleotide phosphate (NADPH) inhibitor apocynin. To conclude, this study has proven that P. gingivalis stimulates the expression of TNF-α and IL-1β proteins, thereb

y inducing apoptotic cell death in brain endothelial cells via the ROS/NF-κB pathway. This study strongly supports the hypothesis that a periodontal infection increases the risk of developing a cerebrovascular disease. We further reported the therapeutic effects of THSG in preventing brain endotheli

al cell death from periodontal pathogen infection.