1.Practical study on the application of “BRAND”pharmaceutical care model in advanced NSCLC patients with positive driver genes
Jiankang YU ; Wei GONG ; Jinfang SHI ; Jie TANG ; Yinhua GONG
China Pharmacy 2026;37(5):655-659
OBJECTIVE To establish a “BRAND” pharmaceutical care model for advanced non-small cell lung cancer (NSCLC) patients with positive driver genes, providing theoretical and practical references for the clinical implementation of precise and individualized oncology pharmaceutical care. METHODS One hundred patients admitted to the department of pulmonary and critical care medicine in our hospital from January 2023 to May 2024 were collected meeting the inclusion and exclusion criteria. Patients were randomly divided into control group and intervention group, with 50 patients in each group. The control group received routine pharmaceutical care, while the intervention group received pharmaceutical care under the “BRAND” model (collecting patients’ basic information, reviewing disease treatment-related information, conducting precise medication assessments, formulating individualized pharmaceutical care plans for the next steps, and implementing medication guidance and follow-up management). The study was conducted in a 3-week cycle for a total of 4 cycles. The medication compliance, quality of life, laboratory test indicators, incidence of drug-related adverse events and satisfaction of patients in both groups were compared before and after the intervention to evaluate the effects. RESULTS After 12 weeks of intervention, compared with the control group, the medication compliance, cognitive function, social function and satisfaction of patients in the intervention group were improved significantly ( P <0.05); the severity of fatigue and constipation and the incidence of drug-related adverse events were significantly reduced ( P <0.05), and there was no statistically significant difference in laboratory test indicators ( P >0.05). CONCLUSIONS The “BRAND” pharmaceutical care model can effectively improve the medication compliance of patients with advanced NSCLC with positive driver genes and improve their quality of life. This study can provide a feasible path for clinical pharmacists to carry out standardized and high-quality pharmaceutical care.
2.Shank3 Overexpression Leads to Cardiac Dysfunction in Mice by Disrupting Calcium Homeostasis in Cardiomyocytes
Tae Hee KO ; Yoonhee KIM ; Chunmei JIN ; Byeongil YU ; Minju LEE ; Phuong Kim LUONG ; Tran Nguyet TRINH ; Yeji YANG ; Hyojin KANG ; Yinhua ZHANG ; Ruiying MA ; Kwangmin YOO ; Jungmin CHOI ; Jin Young KIM ; Sun-Hee WOO ; Kihoon HAN ; Jong-Il CHOI
Korean Circulation Journal 2025;55(2):100-117
Background and Objectives:
SH3 and multiple ankyrin repeat domains 3 (Shank3) proteins play crucial roles as neuronal postsynaptic scaffolds. Alongside neuropsychiatric symptoms, individuals with SHANK3 mutations often exhibit symptoms related to dysfunctions in other organs, including the heart. However, detailed insights into the cardiac functions of Shank3 remain limited. This study aimed to characterize the cardiac phenotypes of Shank3-overexpressing transgenic mice and explore the underlying mechanisms.
Methods:
Cardiac histological analysis, electrocardiogram and echocardiogram recordings were conducted on Shank3-overexpressing transgenic mice. Electrophysiological properties, including action potentials and L-type Ca2+ channel (LTCC) currents, were measured in isolated cardiomyocytes. Ca2+ homeostasis was assessed by analyzing cytosolic Ca2+transients and sarcoplasmic reticulum Ca2+ contents. Depolarization-induced cell shortening was examined in cardiomyocytes. Immunoprecipitation followed by mass spectrometrybased identification was employed to identify proteins in the cardiac Shank3 interactome.Western blot and immunocytochemical analyses were conducted to identify changes in protein expression in Shank3-overexpressing transgenic cardiomyocytes.
Results:
The hearts of Shank3-overexpressing transgenic mice displayed reduced weight and increased fibrosis. In vivo, sudden cardiac death, arrhythmia, and contractility impairments were identified. Shank3-overexpressing transgenic cardiomyocytes showed prolonged action potential duration and increased LTCC current density. Cytosolic Ca2+ transients were increased with prolonged decay time, while sarcoplasmic reticulum Ca2+ contents remained normal. Cell shortening was augmented in Shank3-overexpressing transgenic cardiomyocytes. The cardiac Shank3 interactome comprised 78 proteins with various functions. Troponin I levels were down-regulated in Shank3-overexpressing transgenic cardiomyocytes.
Conclusions
This study revealed cardiac dysfunction in Shank3-overexpressing transgenic mice, potentially attributed to changes in Ca2+ homeostasis and contraction, with a notable reduction in troponin I.
3.Shank3 Overexpression Leads to Cardiac Dysfunction in Mice by Disrupting Calcium Homeostasis in Cardiomyocytes
Tae Hee KO ; Yoonhee KIM ; Chunmei JIN ; Byeongil YU ; Minju LEE ; Phuong Kim LUONG ; Tran Nguyet TRINH ; Yeji YANG ; Hyojin KANG ; Yinhua ZHANG ; Ruiying MA ; Kwangmin YOO ; Jungmin CHOI ; Jin Young KIM ; Sun-Hee WOO ; Kihoon HAN ; Jong-Il CHOI
Korean Circulation Journal 2025;55(2):100-117
Background and Objectives:
SH3 and multiple ankyrin repeat domains 3 (Shank3) proteins play crucial roles as neuronal postsynaptic scaffolds. Alongside neuropsychiatric symptoms, individuals with SHANK3 mutations often exhibit symptoms related to dysfunctions in other organs, including the heart. However, detailed insights into the cardiac functions of Shank3 remain limited. This study aimed to characterize the cardiac phenotypes of Shank3-overexpressing transgenic mice and explore the underlying mechanisms.
Methods:
Cardiac histological analysis, electrocardiogram and echocardiogram recordings were conducted on Shank3-overexpressing transgenic mice. Electrophysiological properties, including action potentials and L-type Ca2+ channel (LTCC) currents, were measured in isolated cardiomyocytes. Ca2+ homeostasis was assessed by analyzing cytosolic Ca2+transients and sarcoplasmic reticulum Ca2+ contents. Depolarization-induced cell shortening was examined in cardiomyocytes. Immunoprecipitation followed by mass spectrometrybased identification was employed to identify proteins in the cardiac Shank3 interactome.Western blot and immunocytochemical analyses were conducted to identify changes in protein expression in Shank3-overexpressing transgenic cardiomyocytes.
Results:
The hearts of Shank3-overexpressing transgenic mice displayed reduced weight and increased fibrosis. In vivo, sudden cardiac death, arrhythmia, and contractility impairments were identified. Shank3-overexpressing transgenic cardiomyocytes showed prolonged action potential duration and increased LTCC current density. Cytosolic Ca2+ transients were increased with prolonged decay time, while sarcoplasmic reticulum Ca2+ contents remained normal. Cell shortening was augmented in Shank3-overexpressing transgenic cardiomyocytes. The cardiac Shank3 interactome comprised 78 proteins with various functions. Troponin I levels were down-regulated in Shank3-overexpressing transgenic cardiomyocytes.
Conclusions
This study revealed cardiac dysfunction in Shank3-overexpressing transgenic mice, potentially attributed to changes in Ca2+ homeostasis and contraction, with a notable reduction in troponin I.
4.Shank3 Overexpression Leads to Cardiac Dysfunction in Mice by Disrupting Calcium Homeostasis in Cardiomyocytes
Tae Hee KO ; Yoonhee KIM ; Chunmei JIN ; Byeongil YU ; Minju LEE ; Phuong Kim LUONG ; Tran Nguyet TRINH ; Yeji YANG ; Hyojin KANG ; Yinhua ZHANG ; Ruiying MA ; Kwangmin YOO ; Jungmin CHOI ; Jin Young KIM ; Sun-Hee WOO ; Kihoon HAN ; Jong-Il CHOI
Korean Circulation Journal 2025;55(2):100-117
Background and Objectives:
SH3 and multiple ankyrin repeat domains 3 (Shank3) proteins play crucial roles as neuronal postsynaptic scaffolds. Alongside neuropsychiatric symptoms, individuals with SHANK3 mutations often exhibit symptoms related to dysfunctions in other organs, including the heart. However, detailed insights into the cardiac functions of Shank3 remain limited. This study aimed to characterize the cardiac phenotypes of Shank3-overexpressing transgenic mice and explore the underlying mechanisms.
Methods:
Cardiac histological analysis, electrocardiogram and echocardiogram recordings were conducted on Shank3-overexpressing transgenic mice. Electrophysiological properties, including action potentials and L-type Ca2+ channel (LTCC) currents, were measured in isolated cardiomyocytes. Ca2+ homeostasis was assessed by analyzing cytosolic Ca2+transients and sarcoplasmic reticulum Ca2+ contents. Depolarization-induced cell shortening was examined in cardiomyocytes. Immunoprecipitation followed by mass spectrometrybased identification was employed to identify proteins in the cardiac Shank3 interactome.Western blot and immunocytochemical analyses were conducted to identify changes in protein expression in Shank3-overexpressing transgenic cardiomyocytes.
Results:
The hearts of Shank3-overexpressing transgenic mice displayed reduced weight and increased fibrosis. In vivo, sudden cardiac death, arrhythmia, and contractility impairments were identified. Shank3-overexpressing transgenic cardiomyocytes showed prolonged action potential duration and increased LTCC current density. Cytosolic Ca2+ transients were increased with prolonged decay time, while sarcoplasmic reticulum Ca2+ contents remained normal. Cell shortening was augmented in Shank3-overexpressing transgenic cardiomyocytes. The cardiac Shank3 interactome comprised 78 proteins with various functions. Troponin I levels were down-regulated in Shank3-overexpressing transgenic cardiomyocytes.
Conclusions
This study revealed cardiac dysfunction in Shank3-overexpressing transgenic mice, potentially attributed to changes in Ca2+ homeostasis and contraction, with a notable reduction in troponin I.
5.Shank3 Overexpression Leads to Cardiac Dysfunction in Mice by Disrupting Calcium Homeostasis in Cardiomyocytes
Tae Hee KO ; Yoonhee KIM ; Chunmei JIN ; Byeongil YU ; Minju LEE ; Phuong Kim LUONG ; Tran Nguyet TRINH ; Yeji YANG ; Hyojin KANG ; Yinhua ZHANG ; Ruiying MA ; Kwangmin YOO ; Jungmin CHOI ; Jin Young KIM ; Sun-Hee WOO ; Kihoon HAN ; Jong-Il CHOI
Korean Circulation Journal 2025;55(2):100-117
Background and Objectives:
SH3 and multiple ankyrin repeat domains 3 (Shank3) proteins play crucial roles as neuronal postsynaptic scaffolds. Alongside neuropsychiatric symptoms, individuals with SHANK3 mutations often exhibit symptoms related to dysfunctions in other organs, including the heart. However, detailed insights into the cardiac functions of Shank3 remain limited. This study aimed to characterize the cardiac phenotypes of Shank3-overexpressing transgenic mice and explore the underlying mechanisms.
Methods:
Cardiac histological analysis, electrocardiogram and echocardiogram recordings were conducted on Shank3-overexpressing transgenic mice. Electrophysiological properties, including action potentials and L-type Ca2+ channel (LTCC) currents, were measured in isolated cardiomyocytes. Ca2+ homeostasis was assessed by analyzing cytosolic Ca2+transients and sarcoplasmic reticulum Ca2+ contents. Depolarization-induced cell shortening was examined in cardiomyocytes. Immunoprecipitation followed by mass spectrometrybased identification was employed to identify proteins in the cardiac Shank3 interactome.Western blot and immunocytochemical analyses were conducted to identify changes in protein expression in Shank3-overexpressing transgenic cardiomyocytes.
Results:
The hearts of Shank3-overexpressing transgenic mice displayed reduced weight and increased fibrosis. In vivo, sudden cardiac death, arrhythmia, and contractility impairments were identified. Shank3-overexpressing transgenic cardiomyocytes showed prolonged action potential duration and increased LTCC current density. Cytosolic Ca2+ transients were increased with prolonged decay time, while sarcoplasmic reticulum Ca2+ contents remained normal. Cell shortening was augmented in Shank3-overexpressing transgenic cardiomyocytes. The cardiac Shank3 interactome comprised 78 proteins with various functions. Troponin I levels were down-regulated in Shank3-overexpressing transgenic cardiomyocytes.
Conclusions
This study revealed cardiac dysfunction in Shank3-overexpressing transgenic mice, potentially attributed to changes in Ca2+ homeostasis and contraction, with a notable reduction in troponin I.
6.Research on the clinical medical humanities teaching system from the perspective of medical-literature integration
Yinhua ZHOU ; Yu CHENG ; Changjie CUI ; Xiaohui TIAN ; Longwen FU ; Chan FANG ; Xiaoxing LIAO ; Qikun CHEN
Chinese Medical Ethics 2024;37(7):860-866
Aiming at the current situation of insufficient integration of medical humanities teaching and clinical practice,as well as the need for further research and improvement in the teaching system,guided by the concept of medicine and humanistic literacy integration advocated by the new medical science,this paper deeply discussed the construction of clinical medical humanities teaching system from four aspects,including the selection of clinical medical humanities teachers and team building;the teaching path that combines theoretical education,narrative medicine,and clinical skill training infused with medical humanities content;curriculum ideological and political construction with the goal of establishing the core concept and value orientation of"patient-centered";the teaching assessment and evaluation method characterized by formative evaluation.The clinical medical humanities teaching system emphasizes the practicality,experiential,and emotional aspects of medical humanities teaching,deeply integrating medical humanities with clinical practice teaching content throughout the clinical internship period of medical education,with a view to enhancing the humanistic practice ability and literacy of medical students.
7.Progress on the relationship between environmental risk factors during maternal pregnancy and childhood allergic diseases
International Journal of Pediatrics 2024;51(8):537-542
Allergic diseases are one of the most common chronic non-infectious diseases in childhood,primarily resulting from genetic and environmental interactions.Evidence suggests that maternal exposure to risk factors during pregnancy can impact the fetus through the placenta,leading to immune dysregulation,disruptions in gut microbiota composition,and ultimately contributing to the development of allergic diseases in children.Therefore,maternal pregnancy represents a critical period for preventing allergic diseases in children.This article provides an overview of research advancements regarding the influence of environmental risk factors during pregnancy on allergic diseases in children,focusing on aspects such as maternal diet,medication usage,maternal illnesses during pregnancy,and allergen exposure,so as to provide new strategies for preventing childhood allergic diseases.
8.Application value of a Nomogram model established on clinical and ultrasound features in modifying classification results of the Chinese Thyroid Imaging Reporting and Data System by ultrasound physicians
Yinhua ZHAO ; Yu LIANG ; Yunhan WANG ; Li YANG ; Tong XU ; Erxi FAN ; Xuan LI
Journal of Clinical Medicine in Practice 2024;28(11):18-22
Objective To analyze the application value of a Nomogram model established on clinical and ultrasound features of thyroid in modifying classification results of the Chinese Thyroid Imaging Reporting and Data System (C-TI-RADS) by ultrasound physicians. Methods The clinicopathological ultrasound materials of patients with surgical resection for thyroid nodules in Sichuan Provincial People's Hospital (training set,
9.Meta synthesis of qualitative research on cognitive experience of physical restraint among nursing assistants in nursing homes
Haixu PU ; Liangchu LUO ; Yiwen SUN ; Qian YU ; Yinhua ZHANG
Chinese Journal of Modern Nursing 2022;28(25):3412-3417
Objective:To systematically evaluate the attitudes and experiences of nursing assistants in nursing homes on physical restraint, so as provide a reference for regulating and reducing the physical restraint.Methods:Cochrane Library, PubMed, Embase, EBSCO, Web of Science, China Biology Medicine (CBM) , China National Knowledge Infrastructure, WanFang Data, VIP and other domestic and foreign databases were searched by computer. The retrieval time limit was from the establishment of the database to June 2021. The quality of the article was evaluated using the quality evaluation criteria for qualitative research of the Joanna Briggs Institute Evidence-Based Health Care Center in Australia, and the Meta synthesis was used to summarize and interpret the results.Results:A total of 7 articles were included, and 58 results, 11 categories and four synthesis results were extracted. That was, the factors that affected the implementation of physical restraint (the elderly's own factors, the factors of nursing assistants, the influence of other personnel, the factors of elderly care institutions) , the attitude towards physical restraint (support attitude, opposition attitude and neutral attitude) , emotional experience and release methods (emotional experience and ways of release) , existing deficiencies and suggestions for restraint use (existing deficiencies, related suggestions) .Conclusions:The use of physical restraint in elderly care institutions is the result of many factors. Nursing assistants have positive, negative and neutral attitudes and emotional experiences in the implementation of physical restraint, and based on their rich clinical experience, they can find existing problems in restraint use and make relevant suggestions. Relevant departments need to fully consider the interests of all parties when formulating physical restraint norms and restraint reduction strategies, and effectively solve the problem of physical restraint abuse from the root cause.
10. Analysis of influence factors of voriconazole trough concentration in patients with hematopoietic stem cell transplantation
Min PENG ; Yinhua DENG ; Wen LIU ; Panhao HUANG ; Zhen YU ; Qing XIA ; Yueliang XIE ; Wei LI
Chinese Journal of Clinical Pharmacology and Therapeutics 2021;26(6):640-646
AIM: To study the distribution characteristics of steady-state trough concentration (C


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