Pub Date : 2025-12-01eCollection Date: 2025-01-01DOI: 10.37796/2211-8039.1682
Ho Bao Chau Le, Kollawat Somsri, Thansita Bhunyakarnjanarat, Nattiya Hirankarn, Asada Leelahavanichkul
Melatonin, a hormone produced by the pineal gland, is known for regulating circadian rhythms and has emerging therapeutic potential in psychiatric disorders. This systematic review examines evidence from clinical and preclinical studies to assess melatonin's efficacy in the following conditions: depression, anxiety, bipolar disorder, and schizophrenia. Beyond its role in circadian regulation, melatonin exhibits antioxidative, anti-inflammatory, and immunomodulatory properties, which intersect with nutrition, lifestyle medicine, and psychoneuroimmunology (PNI). The review finds that melatonin improves sleep quality, restores circadian balance, and modulates stress-related neuroimmune pathways. It also supports neuroplasticity and reduces oxidative stress, contributing to resilience against psychosocial and environmental stressors. Lifestyle factors, including diet, exercise, and sleep hygiene, enhance melatonin's effects, positioning it as a valuable component of multimodal treatment strategies. Within the PNI framework, melatonin facilitates communication between the nervous and immune systems, offering potential for targeted psychiatric interventions. This synthesis underscores melatonin's promise as a therapeutic and adjunctive strategy in personalized mental health care. Future research should prioritize rigorous clinical trials, biomarker-driven patient stratification, and integrative approaches combining melatonin with lifestyle interventions and digital health tools to optimize its therapeutic impact.
{"title":"The integrative role of melatonin in psychiatric disorders: A systematic review of evidence from circadian biology, lifestyle medicine, and psychoneuroimmunology.","authors":"Ho Bao Chau Le, Kollawat Somsri, Thansita Bhunyakarnjanarat, Nattiya Hirankarn, Asada Leelahavanichkul","doi":"10.37796/2211-8039.1682","DOIUrl":"10.37796/2211-8039.1682","url":null,"abstract":"<p><p>Melatonin, a hormone produced by the pineal gland, is known for regulating circadian rhythms and has emerging therapeutic potential in psychiatric disorders. This systematic review examines evidence from clinical and preclinical studies to assess melatonin's efficacy in the following conditions: depression, anxiety, bipolar disorder, and schizophrenia. Beyond its role in circadian regulation, melatonin exhibits antioxidative, anti-inflammatory, and immunomodulatory properties, which intersect with nutrition, lifestyle medicine, and psychoneuroimmunology (PNI). The review finds that melatonin improves sleep quality, restores circadian balance, and modulates stress-related neuroimmune pathways. It also supports neuroplasticity and reduces oxidative stress, contributing to resilience against psychosocial and environmental stressors. Lifestyle factors, including diet, exercise, and sleep hygiene, enhance melatonin's effects, positioning it as a valuable component of multimodal treatment strategies. Within the PNI framework, melatonin facilitates communication between the nervous and immune systems, offering potential for targeted psychiatric interventions. This synthesis underscores melatonin's promise as a therapeutic and adjunctive strategy in personalized mental health care. Future research should prioritize rigorous clinical trials, biomarker-driven patient stratification, and integrative approaches combining melatonin with lifestyle interventions and digital health tools to optimize its therapeutic impact.</p>","PeriodicalId":51650,"journal":{"name":"BioMedicine-Taiwan","volume":"15 4","pages":"4-13"},"PeriodicalIF":2.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12788878/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145953556","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background: Depression is one of the common mental disorders worldwide, and currently used antidepressants have undesirable effects; therefore, the development of new antidepressants without side effects is urgently needed. Paeoniflorin (PF) exhibits various pharmacological activities, including anti-inflammatory, antioxidant, and neuroprotective effects. NMDA receptors in the hippocampus play a vital role in the pathophysiology of depression. Due to the scarcity of reports on the neuroprotection of PF on NMDA-induced excitotoxicity in the hippocampus, the present study aims to investigate the effects of PF on NMDA-mediated EPSP and calcium influx in the hippocampus to evaluate the potential of PF as an antidepressant.
Methods: In order to investigate the effects of PF on the NMDA receptor in the hippocampus, the hippocampal slices, primary-cultured hippocampal neurons, and in silico molecular docking analysis of PF with the NMDA receptor were used.
Results: PF (2 μM) significantly depressed the NMDA-mediated EPSPs, resulting in a 50 % inhibition. The intracellular calcium level in primary-cultured hippocampal neurons was 102.67 nM, and 520.36 nM after NMDA (125 μM) treatment. With NMDA and PF co-treatment, the calcium level was 204.58 μM, showing a 60.68 % decrease. After NMDA was co-treated with 1 μM ruthenium red (RuR), the calcium level increased (from 534.58 nM to 665.68 nM). Additionally, co-treatment with PF significantly decreased the calcium level (468.05 nM, representing a 29.50 % decrease). In the presence of NMDA and 1 μM ω-conotoxin MVIIC (ω-Cono) co-treatment, the calcium level was 496.29 nM. In the presence of NMDA, ω-Cono, and RuR, the calcium level was 568.5 nM. Additionally, NMDA, ω-Cono, RuR, and PF co-treatment significantly decreased the calcium level to 270.94 nM. In silico molecular docking analysis revealed a binding energy of -48.5188 kcal/mol for PF with the NMDA receptor.
Conclusions: PF binds to the NMDA receptor, exhibits neuroprotection, and contributes to its potential as an antidepressant.
{"title":"Neuroprotection of paeoniflorin as antidepressant candidate.","authors":"Yuh-Fung Chen, Yi-Jui Chen, Jai-Sing Yang, Min-Min Lee, Huei-Yann Tsai","doi":"10.37796/2211-8039.1680","DOIUrl":"10.37796/2211-8039.1680","url":null,"abstract":"<p><strong>Background: </strong>Depression is one of the common mental disorders worldwide, and currently used antidepressants have undesirable effects; therefore, the development of new antidepressants without side effects is urgently needed. Paeoniflorin (PF) exhibits various pharmacological activities, including anti-inflammatory, antioxidant, and neuroprotective effects. NMDA receptors in the hippocampus play a vital role in the pathophysiology of depression. Due to the scarcity of reports on the neuroprotection of PF on NMDA-induced excitotoxicity in the hippocampus, the present study aims to investigate the effects of PF on NMDA-mediated EPSP and calcium influx in the hippocampus to evaluate the potential of PF as an antidepressant.</p><p><strong>Methods: </strong>In order to investigate the effects of PF on the NMDA receptor in the hippocampus, the hippocampal slices, primary-cultured hippocampal neurons, and <i>in silico</i> molecular docking analysis of PF with the NMDA receptor were used.</p><p><strong>Results: </strong>PF (2 μM) significantly depressed the NMDA-mediated EPSPs, resulting in a 50 % inhibition. The intracellular calcium level in primary-cultured hippocampal neurons was 102.67 nM, and 520.36 nM after NMDA (125 μM) treatment. With NMDA and PF co-treatment, the calcium level was 204.58 μM, showing a 60.68 % decrease. After NMDA was co-treated with 1 μM ruthenium red (RuR), the calcium level increased (from 534.58 nM to 665.68 nM). Additionally, co-treatment with PF significantly decreased the calcium level (468.05 nM, representing a 29.50 % decrease). In the presence of NMDA and 1 μM ω-conotoxin MVIIC (ω-Cono) co-treatment, the calcium level was 496.29 nM. In the presence of NMDA, ω-Cono, and RuR, the calcium level was 568.5 nM. Additionally, NMDA, ω-Cono, RuR, and PF co-treatment significantly decreased the calcium level to 270.94 nM. In silico molecular docking analysis revealed a binding energy of -48.5188 kcal/mol for PF with the NMDA receptor.</p><p><strong>Conclusions: </strong>PF binds to the NMDA receptor, exhibits neuroprotection, and contributes to its potential as an antidepressant.</p>","PeriodicalId":51650,"journal":{"name":"BioMedicine-Taiwan","volume":"15 4","pages":"50-69"},"PeriodicalIF":2.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12788882/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145953471","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Tai Chi, a traditional Chinese martial art characterized by gentle, fluid movements and deep breathing, has gained increasing recognition for its cardiovascular health benefits. This study investigated the integration of Tai Chi into contemporary cardiovascular health practices, focusing on its physiological and psychological effects. The slow, controlled movements characteristic of Tai Chi contribute to enhanced cardiovascular fitness, decreased blood pressure, and improved vascular function, while simultaneously alleviating stress and fostering emotional well-being. Through a review of clinical studies and trials, this study underscores the efficacy of Tai Chi in cardiovascular rehabilitation programs and its accessibility as a community-based intervention. Additionally, this study addresses obstacles to widespread adoption, including cultural barriers and the lack of standardized training for instructors. By integrating traditional practices with contemporary medical approaches, Tai Chi is as a valuable complementary therapy for cardiovascular health. The paper presents future research directions and advocacy strategies aimed at promoting broader acceptance and implementation of Tai Chi in health-care settings. This review underscores the continued relevance of Tai Chi as an effective intervention for cardiovascular wellness in modern therapeutic contexts.
{"title":"Tai Chi for cardiovascular wellness: Integrating an ancient practice into modern therapeutic approaches.","authors":"Chun-Han Cheng, Wen-Rui Hao, Huan-Yuan Chen, Po-Yuan Chen, Ju-Chi Liu, Tzu-Hurng Cheng","doi":"10.37796/2211-8039.1678","DOIUrl":"10.37796/2211-8039.1678","url":null,"abstract":"<p><p>Tai Chi, a traditional Chinese martial art characterized by gentle, fluid movements and deep breathing, has gained increasing recognition for its cardiovascular health benefits. This study investigated the integration of Tai Chi into contemporary cardiovascular health practices, focusing on its physiological and psychological effects. The slow, controlled movements characteristic of Tai Chi contribute to enhanced cardiovascular fitness, decreased blood pressure, and improved vascular function, while simultaneously alleviating stress and fostering emotional well-being. Through a review of clinical studies and trials, this study underscores the efficacy of Tai Chi in cardiovascular rehabilitation programs and its accessibility as a community-based intervention. Additionally, this study addresses obstacles to widespread adoption, including cultural barriers and the lack of standardized training for instructors. By integrating traditional practices with contemporary medical approaches, Tai Chi is as a valuable complementary therapy for cardiovascular health. The paper presents future research directions and advocacy strategies aimed at promoting broader acceptance and implementation of Tai Chi in health-care settings. This review underscores the continued relevance of Tai Chi as an effective intervention for cardiovascular wellness in modern therapeutic contexts.</p>","PeriodicalId":51650,"journal":{"name":"BioMedicine-Taiwan","volume":"15 4","pages":"30-39"},"PeriodicalIF":2.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12788880/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145953542","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-01eCollection Date: 2025-01-01DOI: 10.37796/2211-8039.1691
Chang Jane Pei-Chen, Su Kuan-Pin
Emerging evidence reveals that circadian rhythm, melatonin signaling, nutrition, and inflammation are intricately intertwined in shaping both mental and physical health. Circadian disruptions and lifestyle imbalances contribute to neuroinflammation, mood dysregulation, and cardiometabolic dysfunction, as seen in attention-deficit/hyperactivity disorder (ADHD), major depressive disorder (MDD), metabolic syndrome, and cardiovascular diseases. This special issue highlights interdisciplinary research that integrates circadian biology, nutrition, and psychoneuroimmunology (PNI) toward personalized and preventive psychiatry. Featured studies explore circadian and melatonin mechanisms in ADHD and MDD, the therapeutic and prophylactic potential of omega-3 polyunsaturated fatty acids (n-3 PUFAs), the neuroprotective potentical of paeoniflorin, and the role of extracellular matrix gene variants in MDD vulnerability. Additionally, evidence supporting lifestyle-based interventions such as Tai Chi underscores the value of non-pharmacological mind-body approaches. Collectively, these studies illuminate a multidimensional model linking biological rhythm, nutrition, and inflammation to mental resilience and cardiovascular well-being.
{"title":"From rhythm to resilience: The interplay of circadian rhythm, melatonin, lifestyle, nutrition in psychoneuroimmunology (PNI).","authors":"Chang Jane Pei-Chen, Su Kuan-Pin","doi":"10.37796/2211-8039.1691","DOIUrl":"10.37796/2211-8039.1691","url":null,"abstract":"<p><p>Emerging evidence reveals that circadian rhythm, melatonin signaling, nutrition, and inflammation are intricately intertwined in shaping both mental and physical health. Circadian disruptions and lifestyle imbalances contribute to neuroinflammation, mood dysregulation, and cardiometabolic dysfunction, as seen in attention-deficit/hyperactivity disorder (ADHD), major depressive disorder (MDD), metabolic syndrome, and cardiovascular diseases. This special issue highlights interdisciplinary research that integrates circadian biology, nutrition, and psychoneuroimmunology (PNI) toward personalized and preventive psychiatry. Featured studies explore circadian and melatonin mechanisms in ADHD and MDD, the therapeutic and prophylactic potential of omega-3 polyunsaturated fatty acids (n-3 PUFAs), the neuroprotective potentical of paeoniflorin, and the role of extracellular matrix gene variants in MDD vulnerability. Additionally, evidence supporting lifestyle-based interventions such as Tai Chi underscores the value of non-pharmacological mind-body approaches. Collectively, these studies illuminate a multidimensional model linking biological rhythm, nutrition, and inflammation to mental resilience and cardiovascular well-being.</p>","PeriodicalId":51650,"journal":{"name":"BioMedicine-Taiwan","volume":"15 4","pages":"1-3"},"PeriodicalIF":2.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12788877/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145953945","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-01eCollection Date: 2025-01-01DOI: 10.37796/2211-8039.1677
Halliru Zailani, Daniel Tzu-Li Chen, Sheng-Che Lin, Jia-Hau Lee, Mei-Ling Li, Jane Pei-Chen Chang, Kuan-Pin Su
Dysregulation of extracellular matrix (ECM) degradation pathways has been increasingly implicated in major depressive disorder (MDD), yet its genetic basis remains unclear. This study investigated the relationship between ECM-related genetic polymorphisms and MDD susceptibility. In a case-control study, we analyzed 317 MDD patients and 1268 sexmatched controls from the Taiwan Biobank (TWB). Genomic DNA was analyzed using the Affymetrix TWB array, targeting single nucleotide polymorphisms (SNPs) in 140 ECM degradation genes (Reactome database). Full-model association tests identified significant SNPs, validated with 5000 max(T) permutations and adjusted via logistic regression for age, body mass index, education level, and marital status. We identified 12 SNPs across 10 ECMrelated genes significantly associated with MDD, including ADAM metallopeptidase domain 17 (ADAM17, rs55820761), brevican (BCAN, rs11264511), CD44 molecule (CD44, rs12270356), collagen type XVII alpha 1 chain (COL17A1; rs2282436 and rs10883962), collagen type III alpha 1 chain (COL3A1; rs16830979 and rs10883962), collagen type VI alpha 6 chain (COL6A6, rs16830219), cathepsin L (CTSL, rs2274611), Kallikrein-related peptidase 2 (KLK2, rs2664156), matrix metallopeptidase 11 (MMP11, rs738791), and nicastrin (NCSTN, rs3753391). This study provides the first genetic evidence linking ECM degradation pathways to MDD susceptibility, identifying novel biomarkers for early diagnosis and precision therapy. Further research and cross-population studies are needed to confirm these findings.
{"title":"Genetic variations in extracellular matrix degradation pathways linking to major depressive disorder: Evidence from a large-scale genetic association study.","authors":"Halliru Zailani, Daniel Tzu-Li Chen, Sheng-Che Lin, Jia-Hau Lee, Mei-Ling Li, Jane Pei-Chen Chang, Kuan-Pin Su","doi":"10.37796/2211-8039.1677","DOIUrl":"10.37796/2211-8039.1677","url":null,"abstract":"<p><p>Dysregulation of extracellular matrix (ECM) degradation pathways has been increasingly implicated in major depressive disorder (MDD), yet its genetic basis remains unclear. This study investigated the relationship between ECM-related genetic polymorphisms and MDD susceptibility. In a case-control study, we analyzed 317 MDD patients and 1268 sexmatched controls from the Taiwan Biobank (TWB). Genomic DNA was analyzed using the Affymetrix TWB array, targeting single nucleotide polymorphisms (SNPs) in 140 ECM degradation genes (Reactome database). Full-model association tests identified significant SNPs, validated with 5000 max(T) permutations and adjusted via logistic regression for age, body mass index, education level, and marital status. We identified 12 SNPs across 10 ECMrelated genes significantly associated with MDD, including ADAM metallopeptidase domain 17 (<i>ADAM17</i>, rs55820761), brevican (<i>BCAN</i>, rs11264511), CD44 molecule (<i>CD44</i>, rs12270356), collagen type XVII alpha 1 chain (<i>COL17A1</i>; rs2282436 and rs10883962), collagen type III alpha 1 chain (<i>COL3A1</i>; rs16830979 and rs10883962), collagen type VI alpha 6 chain (<i>COL6A6</i>, rs16830219), cathepsin L (<i>CTSL</i>, rs2274611), Kallikrein-related peptidase 2 (<i>KLK2</i>, rs2664156), matrix metallopeptidase 11 (<i>MMP11</i>, rs738791), and nicastrin (<i>NCSTN</i>, rs3753391). This study provides the first genetic evidence linking ECM degradation pathways to MDD susceptibility, identifying novel biomarkers for early diagnosis and precision therapy. Further research and cross-population studies are needed to confirm these findings.</p>","PeriodicalId":51650,"journal":{"name":"BioMedicine-Taiwan","volume":"15 4","pages":"70-78"},"PeriodicalIF":2.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12788879/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145953975","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-01eCollection Date: 2025-01-01DOI: 10.37796/2211-8039.1679
Ayesha Zafar Iqbal, Patricia Marest Suwindi, Sunny Yin-Shan Chen, Lindsay Liang-Tien Cho, Kuan-Pin Su, Jane Pei-Chen Chang
Attention-deficit hyperactivity disorder (ADHD) is a common neurodevelopmental condition often accompanied by circadian rhythm disturbances, particularly delayed sleep phase. These involve suprachiasmatic nucleus (SCN) dysregulation, altered melatonin secretion, and hypothalamic-pituitary-adrenal (HPA) axis activity, which may be exacerbated by artificial light exposure. Genetic studies further implicate circadian mechanisms, linking ADHD with polymorphisms in clock genes such as PER and CLOCK. Nutraceuticals, particularly omega-3 polyunsaturated fatty acids (n-3 PUFAs), have been proposed as modulators of circadian rhythms. N-3 PUFAs are essential for brain health and may influence melatonin synthesis and sleep-wake regulation. Preclinical and clinical findings suggest that supplementation can improve cognitive and behavioral outcomes in ADHD, possibly through circadian pathways, though direct clinical evidence remains limited. This review integrates findings on melatonin and cortisol dysregulation in ADHD and evaluates n-3 PUFAs as potential non-photic zeitgebers. N-3 PUFAs may modulate circadian clock genes in the SCN, restore rhythm synchronization, normalize melatonin secretion, stabilize HPA axis activity, and reduce systemic inflammation. Future research should focus on well-designed trials to clarify the circadian effects of n-3 supplementation in ADHD.
{"title":"Circadian rhythms and neuroendocrine dysregulation in ADHD: Therapeutic insights from omega-3 fatty acids.","authors":"Ayesha Zafar Iqbal, Patricia Marest Suwindi, Sunny Yin-Shan Chen, Lindsay Liang-Tien Cho, Kuan-Pin Su, Jane Pei-Chen Chang","doi":"10.37796/2211-8039.1679","DOIUrl":"10.37796/2211-8039.1679","url":null,"abstract":"<p><p>Attention-deficit hyperactivity disorder (ADHD) is a common neurodevelopmental condition often accompanied by circadian rhythm disturbances, particularly delayed sleep phase. These involve suprachiasmatic nucleus (SCN) dysregulation, altered melatonin secretion, and hypothalamic-pituitary-adrenal (HPA) axis activity, which may be exacerbated by artificial light exposure. Genetic studies further implicate circadian mechanisms, linking ADHD with polymorphisms in clock genes such as <i>PER</i> and <i>CLOCK</i>. Nutraceuticals, particularly omega-3 polyunsaturated fatty acids (n-3 PUFAs), have been proposed as modulators of circadian rhythms. N-3 PUFAs are essential for brain health and may influence melatonin synthesis and sleep-wake regulation. Preclinical and clinical findings suggest that supplementation can improve cognitive and behavioral outcomes in ADHD, possibly through circadian pathways, though direct clinical evidence remains limited. This review integrates findings on melatonin and cortisol dysregulation in ADHD and evaluates n-3 PUFAs as potential non-photic zeitgebers. N-3 PUFAs may modulate circadian clock genes in the SCN, restore rhythm synchronization, normalize melatonin secretion, stabilize HPA axis activity, and reduce systemic inflammation. Future research should focus on well-designed trials to clarify the circadian effects of n-3 supplementation in ADHD.</p>","PeriodicalId":51650,"journal":{"name":"BioMedicine-Taiwan","volume":"15 4","pages":"14-29"},"PeriodicalIF":2.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12788881/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145953929","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-01eCollection Date: 2025-01-01DOI: 10.37796/2211-8039.1667
Ikbal Andrian Malau, Cheng-Ho Chang, Wei-Jen Chen, Wen-Chun Liu, Halliru Zailani, Hsien-Feng Liao, Jane Pei-Chen Chang, Wei-Che Chiu, Kuan-Pin Su
Background: Omega-3 polyunsaturated fatty acids (n-3 PUFAs) have demonstrated efficacy as adjunctive treatment for MDD. In fact, fewer studies assessed the prophylactic properties of n-3 PUFAs as monotherapy on the recurrence of MDD.
Aims: This study aimed to assess the prophylactic effect of n-3 PUFAs monotherapy against recurrent MDD.
Methods: We conducted a 6-month randomized controlled trial to assess the prophylactic effect of n-3 in preventing recurrent MDD. We assigned 60 remitted MDD patients to the n-3 group (n = 30) and placebo (n = 30). Furthermore, we assessed the difference in depression severity and MDD recurrence based on the 21-item Hamilton Rating Scale for Depression (HRSD) at months 1, 2, 3, 4, and 6 between groups. The recurrent event of MDD was defined as an HRSD score >20. Furthermore, biochemical parameters in plasma were assessed as the secondary outcomes.
Results: There was no significant difference in the HRSD score between the n-3 group and placebo each month ( p-value >0.05). However, our findings have implicated that omega-3 monotherapy for MDD contributed to a lower recurrence rate compared to the placebo group at month 6 ( p-value = 0.035). Omega-3 supplementation was superior to placebo to preventing recurrent MDD analyzed using Kaplan-Meier survival analysis over a 6-month study period ( p-value = 0.041). In comparison, the eicosapentaenoic acid (EPA) plasma level of the n-3 group at the end point of study was significantly higher than the placebo ( p-value = 0.023), but not for docosahexaenoic acid (DHA) ( p-value = 0.119).
Conclusion: Our study concluded that n-3 PUFAs monotherapy demonstrated a prophylactic effect on the recurrence of MDD.
{"title":"Prophylactic effect of omega-3 polyunsaturated fatty acids monotherapy in preventing recurrent major depressive disorder: A randomized controlled trial.","authors":"Ikbal Andrian Malau, Cheng-Ho Chang, Wei-Jen Chen, Wen-Chun Liu, Halliru Zailani, Hsien-Feng Liao, Jane Pei-Chen Chang, Wei-Che Chiu, Kuan-Pin Su","doi":"10.37796/2211-8039.1667","DOIUrl":"10.37796/2211-8039.1667","url":null,"abstract":"<p><strong>Background: </strong>Omega-3 polyunsaturated fatty acids (n-3 PUFAs) have demonstrated efficacy as adjunctive treatment for MDD. In fact, fewer studies assessed the prophylactic properties of n-3 PUFAs as monotherapy on the recurrence of MDD.</p><p><strong>Aims: </strong>This study aimed to assess the prophylactic effect of n-3 PUFAs monotherapy against recurrent MDD.</p><p><strong>Methods: </strong>We conducted a 6-month randomized controlled trial to assess the prophylactic effect of n-3 in preventing recurrent MDD. We assigned 60 remitted MDD patients to the n-3 group (n = 30) and placebo (n = 30). Furthermore, we assessed the difference in depression severity and MDD recurrence based on the 21-item Hamilton Rating Scale for Depression (HRSD) at months 1, 2, 3, 4, and 6 between groups. The recurrent event of MDD was defined as an HRSD score >20. Furthermore, biochemical parameters in plasma were assessed as the secondary outcomes.</p><p><strong>Results: </strong>There was no significant difference in the HRSD score between the n-3 group and placebo each month ( <i>p-</i>value >0.05). However, our findings have implicated that omega-3 monotherapy for MDD contributed to a lower recurrence rate compared to the placebo group at month 6 ( <i>p</i>-value = 0.035). Omega-3 supplementation was superior to placebo to preventing recurrent MDD analyzed using Kaplan-Meier survival analysis over a 6-month study period ( <i>p-</i>value = 0.041). In comparison, the eicosapentaenoic acid (EPA) plasma level of the n-3 group at the end point of study was significantly higher than the placebo ( <i>p</i>-value = 0.023), but not for docosahexaenoic acid (DHA) ( <i>p</i>-value = 0.119).</p><p><strong>Conclusion: </strong>Our study concluded that n-3 PUFAs monotherapy demonstrated a prophylactic effect on the recurrence of MDD.</p>","PeriodicalId":51650,"journal":{"name":"BioMedicine-Taiwan","volume":"15 4","pages":"40-49"},"PeriodicalIF":2.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12788876/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145953450","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-01eCollection Date: 2025-01-01DOI: 10.37796/2211-8039.1650
Abdulmohsen I Algefare, Manal A Alfwuaires
Prolonged exposure to inorganic arsenic is commonly linked to brain damage via oxidative and apoptotic processes. The compound garcinol (GCL) has garnered significant interest because of its beneficial effects on human health. However, the protective ability of GCL against arsenic-induced toxicity in the brain remains unexplored. Therefore, our study aimed to examine the neuroprotective effect of GCL against the adverse impact of sodium arsenite (SA) on behavioral patterns, molecular mechanisms, apoptotic markers, and oxidative stress parameters in the brain, liver, and kidneys of mice. The mice were categorized into four distinct groups for 28 days: Group I, referred to as the Control group, received a 5 % v/v solution of dimethyl sulfoxide (DMSO); Group II, referred to as the SA group, received a dosage of 20 mg/kg of SA; Group III, referred to as the SA + GCL group, received a combined dosage of 20 mg/kg of SA and 50 mg/kg of GCL; and Group IV, referred to as the GCL group, received a dosage of 50 mg/kg of GCL. Following drug administration, the behavior of the animals was evaluated and analyzed. Additionally, the levels of acetylcholinesterase (AChE), ATP hydrolysis, and angiotensin I-converting enzyme (ACE), which are associated with cognitive function, were examined. Our study demonstrated that the administration of GCL enhanced cognitive behavior. Additionally, GCL mitigated cholinergic deficits as evidenced by a reduction in AChE activity. Furthermore, GCL increased the signaling of glycogen synthase kinase 3 beta (GSK3β) and cAMP response element-binding protein (CREB) in SA-treated mice, enhanced redox equilibrium, and protected against oxidative damage caused by SA in the brains of mice. This effect was mediated by the activation of nuclear factor erythroid 2-related factor 2 (NRF2)/heme oxygenase-1 (HO-1) proteins, resulting in a significant decrease in malondialdehyde concentration. Thus, this preclinical study showed that treatment with GCL ameliorated neurobehavior, modulated cognitive function-associated biomarkers, and protected mice from SA-induced neurotoxicity.
{"title":"Effect of garcinol against arsenic-induced neurobehavioral alterations and liver and kidney dysfunction in albino mice.","authors":"Abdulmohsen I Algefare, Manal A Alfwuaires","doi":"10.37796/2211-8039.1650","DOIUrl":"10.37796/2211-8039.1650","url":null,"abstract":"<p><p>Prolonged exposure to inorganic arsenic is commonly linked to brain damage via oxidative and apoptotic processes. The compound garcinol (GCL) has garnered significant interest because of its beneficial effects on human health. However, the protective ability of GCL against arsenic-induced toxicity in the brain remains unexplored. Therefore, our study aimed to examine the neuroprotective effect of GCL against the adverse impact of sodium arsenite (SA) on behavioral patterns, molecular mechanisms, apoptotic markers, and oxidative stress parameters in the brain, liver, and kidneys of mice. The mice were categorized into four distinct groups for 28 days: Group I, referred to as the Control group, received a 5 % v/v solution of dimethyl sulfoxide (DMSO); Group II, referred to as the SA group, received a dosage of 20 mg/kg of SA; Group III, referred to as the SA + GCL group, received a combined dosage of 20 mg/kg of SA and 50 mg/kg of GCL; and Group IV, referred to as the GCL group, received a dosage of 50 mg/kg of GCL. Following drug administration, the behavior of the animals was evaluated and analyzed. Additionally, the levels of acetylcholinesterase (AChE), ATP hydrolysis, and angiotensin I-converting enzyme (ACE), which are associated with cognitive function, were examined. Our study demonstrated that the administration of GCL enhanced cognitive behavior. Additionally, GCL mitigated cholinergic deficits as evidenced by a reduction in AChE activity. Furthermore, GCL increased the signaling of glycogen synthase kinase 3 beta (GSK3β) and cAMP response element-binding protein (CREB) in SA-treated mice, enhanced redox equilibrium, and protected against oxidative damage caused by SA in the brains of mice. This effect was mediated by the activation of nuclear factor erythroid 2-related factor 2 (NRF2)/heme oxygenase-1 (HO-1) proteins, resulting in a significant decrease in malondialdehyde concentration. Thus, this preclinical study showed that treatment with GCL ameliorated neurobehavior, modulated cognitive function-associated biomarkers, and protected mice from SA-induced neurotoxicity.</p>","PeriodicalId":51650,"journal":{"name":"BioMedicine-Taiwan","volume":"15 3","pages":"44-59"},"PeriodicalIF":2.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12513395/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145281647","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
We report the case of a 70-year-old woman who sustained complex traumatic injuries in a motor vehicle accident, including cervical spine fractures and a high suspicion of traumatic vertebral artery injury (VAI). Initial digital subtraction angiography (DSA) revealed no evidence of vertebral artery (VA) involvement. She subsequently underwent anterior cervical discectomy and fusion (ACDF); however, an iatrogenic injury to the right VA occurred intra-operatively, necessitating emergent endovascular stenting for vascular repair. This case underscores the importance of comprehensive preoperative imaging, intraoperative vigilance, and coordinated multidisciplinary management in cervical spine trauma with potential vascular involvement.
{"title":"Covered stent salvage for iatrogenic vertebral artery injury in traumatic cervical spine injury: A case report and literature review.","authors":"Tzu-Hao Yen, Wei-Liang Chen, Ying-Lin Tseng, You-Pen Chiu, Hui-Ru Ji, Jeng-Hung Guo, Cheng-Di Chiu","doi":"10.37796/2211-8039.1670","DOIUrl":"10.37796/2211-8039.1670","url":null,"abstract":"<p><p>We report the case of a 70-year-old woman who sustained complex traumatic injuries in a motor vehicle accident, including cervical spine fractures and a high suspicion of traumatic vertebral artery injury (VAI). Initial digital subtraction angiography (DSA) revealed no evidence of vertebral artery (VA) involvement. She subsequently underwent anterior cervical discectomy and fusion (ACDF); however, an iatrogenic injury to the right VA occurred intra-operatively, necessitating emergent endovascular stenting for vascular repair. This case underscores the importance of comprehensive preoperative imaging, intraoperative vigilance, and coordinated multidisciplinary management in cervical spine trauma with potential vascular involvement.</p>","PeriodicalId":51650,"journal":{"name":"BioMedicine-Taiwan","volume":"15 3","pages":"66-72"},"PeriodicalIF":2.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12513394/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145281675","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-01eCollection Date: 2025-01-01DOI: 10.37796/2211-8039.1662
Hafeez Sohaib Ahmad Warraich, Zirwa Younis, Jawairia Warraich, Khizra Warraich
Renal duplication anomalies are one of the most frequent congenital urological conditions in the general population all over the world. Bilateral incomplete duplication, however, is exceedingly rare. We present a case of a 29-year-old female with bilateral incomplete duplex kidneys complicated by mid-ureteric stenosis on the right side and calculi in the left ureter and upper moiety of the left duplex kidney. Diagnostic imaging, including ultrasound, computed tomography (CT), and intravenous urography (IVU) confirmed these findings. The patient underwent successful bilateral ureteroscopy (URS) and left-sided retrograde intra-renal surgery (RIRS) for management of the above mentioned complications related to the duplex kidneys in this patient. Postoperative recovery was uneventful, and a further right-sided percutaneous nephrolithotomy (PCNL) was planned. This case underscores the importance of comprehensive diagnostic evaluation and individualized therapeutic strategies in managing complex urological anomalies.
{"title":"Endoscopic management of ureteric stenosis and calculi in bilateral incomplete renal duplication: A case study.","authors":"Hafeez Sohaib Ahmad Warraich, Zirwa Younis, Jawairia Warraich, Khizra Warraich","doi":"10.37796/2211-8039.1662","DOIUrl":"10.37796/2211-8039.1662","url":null,"abstract":"<p><p>Renal duplication anomalies are one of the most frequent congenital urological conditions in the general population all over the world. Bilateral incomplete duplication, however, is exceedingly rare. We present a case of a 29-year-old female with bilateral incomplete duplex kidneys complicated by mid-ureteric stenosis on the right side and calculi in the left ureter and upper moiety of the left duplex kidney. Diagnostic imaging, including ultrasound, computed tomography (CT), and intravenous urography (IVU) confirmed these findings. The patient underwent successful bilateral ureteroscopy (URS) and left-sided retrograde intra-renal surgery (RIRS) for management of the above mentioned complications related to the duplex kidneys in this patient. Postoperative recovery was uneventful, and a further right-sided percutaneous nephrolithotomy (PCNL) was planned. This case underscores the importance of comprehensive diagnostic evaluation and individualized therapeutic strategies in managing complex urological anomalies.</p><p><strong>Categories: </strong>Urology, Radiology.</p>","PeriodicalId":51650,"journal":{"name":"BioMedicine-Taiwan","volume":"15 3","pages":"60-65"},"PeriodicalIF":2.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12513393/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145281672","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}