The historical development of endogenous wind （内风） is traced with time as the thread， based on the progression of factors such as syndromes， causes of disease， and pathogenesis. It is believed that the concept of wind syndrome originated in The Inner Canon of Yellow Emperor （《黄帝内经》）， encompassing both exogenous wind （外风） and endogenous wind syndrome. Over time， exogenous wind syndrome gradually evolved into mild syndromes and severe syndromes， while endogenous wind syndrome emerged from severe syndromes of exogenous wind. Endogenous wind syndrome has both syndrome and pathogenic attributes， and its theoretical system has gradually become more refined. Based on the theories of ancient and modern medical practitioners， and combining the holistic perspectives with Xiang （象） thinking， it is proposed that endogenous wind has both physiological and pathological distinctions. The physiological endogenous wind refers to the liver's moderate dispersing and regulating function， which helps to distribute qi （气）， blood， and body fluids， while pathological endogenous wind arises from abnormal liver dispersal. Therefore， in clinical practice， different treatment methods， such as tonifying， unblocking， and warming， can be applied according to the differentiation of deficiency and excess in the pathogenesis.

Objective: To explore the correlation between the composition of bone marrow lymphocyte subsets and the clinical attributes observed in de novo AML patients, as well as their influence on prognosis. Methods: A detailed study was carried out on a cohort of 191 de novo acute myeloid leukemia patients who were admitted to our medical center between October 2022 and September 2024. In addition, a group of 24 patients with iron deficiency anemia individuals was carefully chosen as the control cohort. The proportions of lymphocyte subsets within the bone marrow of de novo AML patients were analyzed. Furthermore, an in-depth analysis was performed to investigate the association between the expression levels of these subsets in de novo AML patients and their clinical attributes, as well as their prognostic implications. Results: The proportion of CD19 and CD56 lymphocytes within the bone marrow of de novo AML patients significantly diminished compared to the control cohort (8.5% vs 13.2% P<0.05, and 15.5% vs 18.0%, P<0.05). Conversely, no significant discrepancies were observed in the CD3 , CD3 CD4 , and CD3 CD8 lymphocyte percentages between the AML patients and control group (71.7% vs 72.1%, 32.5% vs 33.7% and 32.8% vs 35.7%, P>0.05). When analyzing the relationships between lymphocyte subsets within the bone marrow of de novo patients and their respective clinical characteristics, patients aged 60 years and above exhibited diminished percentages of CD3 CD8 lymphocytes in the bone marrow compared to their younger counterparts (31.6% vs 34.1%, P<0.05), while the CD56 lymphocyte subsets demonstrated an increased prevalence (17.2% vs 14.4%, P<0.05). Furthermore, patients with leukocytosis (WBC≥100×10 /L) presented lower levels of CD3 and CD3 CD4 lymphocytes in the bone marrow compared with those without it (65.3% vs 72.9% P<0.05, and 28.9% vs 33.2%, P<0.05), respectively. The AML1-ETO fusion gene-positive cohort exhibited a higher prevalence of CD3 CD8 lymphocytes in the bone marrow than in the negative group (38.2% vs 32.3%, P<0.05), whereas the FLT3-ITD mutation-positive group presented a decreased prevalence of CD56 lymphocytes compared with the negative group (12.4% vs 16.8%, P<0.05). In addition, the NPM1 mutation-positive group demonstrated lower levels of CD3 CD8 lymphocytes in the bone marrow than in the negative group (29.1% vs 33.3%, P<0.05). Variables such as tumor protein p53(TP53) mutation positive, the absence of hematopoietic stem cell transplantation, and CD3 CD4 lymphocyte proportions below 25% were identified as independent adverse prognostic indicators for AML patients (P<0.05). Conclusion: The pathogenesis of AML is closely associated with an imbalance in bone marrow lymphocyte subsets. The FLT3-ITD mutation potentially contributes to the dysregulation of CD56 lymphocyte subset expression. The AML1-ETO fusion gene and NPM1 mutation are implicated in the abnormal expression of CD3 CD8 lymphocytes within the bone marrow. Moreover, the percentage of CD3 CD4 lymphocytes in the bone marrow serves as a prognostic factor for de novo AML patients.

Objective: To explore the correlation between the composition of bone marrow lymphocyte subsets and the clinical attributes observed in de novo AML patients, as well as their influence on prognosis. Methods: A detailed study was carried out on a cohort of 191 de novo acute myeloid leukemia patients who were admitted to our medical center between October 2022 and September 2024. In addition, a group of 24 patients with iron deficiency anemia individuals was carefully chosen as the control cohort. The proportions of lymphocyte subsets within the bone marrow of de novo AML patients were analyzed. Furthermore, an in-depth analysis was performed to investigate the association between the expression levels of these subsets in de novo AML patients and their clinical attributes, as well as their prognostic implications. Results: The proportion of CD19 and CD56 lymphocytes within the bone marrow of de novo AML patients significantly diminished compared to the control cohort (8.5% vs 13.2% P<0.05, and 15.5% vs 18.0%, P<0.05). Conversely, no significant discrepancies were observed in the CD3 , CD3 CD4 , and CD3 CD8 lymphocyte percentages between the AML patients and control group (71.7% vs 72.1%, 32.5% vs 33.7% and 32.8% vs 35.7%, P>0.05). When analyzing the relationships between lymphocyte subsets within the bone marrow of de novo patients and their respective clinical characteristics, patients aged 60 years and above exhibited diminished percentages of CD3 CD8 lymphocytes in the bone marrow compared to their younger counterparts (31.6% vs 34.1%, P<0.05), while the CD56 lymphocyte subsets demonstrated an increased prevalence (17.2% vs 14.4%, P<0.05). Furthermore, patients with leukocytosis (WBC≥100×10 /L) presented lower levels of CD3 and CD3 CD4 lymphocytes in the bone marrow compared with those without it (65.3% vs 72.9% P<0.05, and 28.9% vs 33.2%, P<0.05), respectively. The AML1-ETO fusion gene-positive cohort exhibited a higher prevalence of CD3 CD8 lymphocytes in the bone marrow than in the negative group (38.2% vs 32.3%, P<0.05), whereas the FLT3-ITD mutation-positive group presented a decreased prevalence of CD56 lymphocytes compared with the negative group (12.4% vs 16.8%, P<0.05). In addition, the NPM1 mutation-positive group demonstrated lower levels of CD3 CD8 lymphocytes in the bone marrow than in the negative group (29.1% vs 33.3%, P<0.05). Variables such as tumor protein p53(TP53) mutation positive, the absence of hematopoietic stem cell transplantation, and CD3 CD4 lymphocyte proportions below 25% were identified as independent adverse prognostic indicators for AML patients (P<0.05). Conclusion: The pathogenesis of AML is closely associated with an imbalance in bone marrow lymphocyte subsets. The FLT3-ITD mutation potentially contributes to the dysregulation of CD56 lymphocyte subset expression. The AML1-ETO fusion gene and NPM1 mutation are implicated in the abnormal expression of CD3 CD8 lymphocytes within the bone marrow. Moreover, the percentage of CD3 CD4 lymphocytes in the bone marrow serves as a prognostic factor for de novo AML patients.

Objective:To analyze the trend of dementia mortality rate among individuals aged 60 to 94 years in China from 1982 to 2021.Methods:Utilizing data from the Global Burden of Disease Study 2021, the Joinpoint regression model was employed to analyze the trend in the dementia mortality rate among Chinese older adults from 1982 to 2021. The age-period-cohort analysis method was used to decompose the age effect, period effect and cohort effect of dementia mortality data in Chinese elderly people.Results:From 1982 to 2021, the crude mortality rate of dementia in elderly women aged 60-94 in China (133.67/100 000-214.02/100 000) was higher than that in men (70.92/100 000-119.70/100 000), and the age-standardized mortality rate of dementia in women (230.74/100 000-246.87/100 000) was also higher than that in men (132.88/100 000-140.19/100 000). The age-standardized mortality rate of dementia in both genders showed an N-shaped fluctuation trend. The average annual percent change (AAPC) of dementia mortality rate in elderly males aged 60-94 was 0.07% (95% CI: 0.01%-0.13%), and the AAPC of dementia mortality rate in elderly females was -0.01% (95% CI:-0.08%-0.07%). Age effect analysis showed that from the age of 60, the risk of dementia death in males and females increased with age, especially among elderly people aged 75-94 who experienced a rapid increase in dementia mortality rate. The period effect analysis showed that the overall risk of dementia death in elderly men and women aged 60-94 was decreasing, but it had increased from 2017 to 2021. The cohort effect analysis showed that the risk of dementia death was lower in later birth cohorts. Conclusion:From 1982 to 2021, the dementia mortality rate among Chinese older adults aged 60 to 94 years exhibited fluctuations. Particularly, there has been a notable rebound in recent years. Special attention should be directed towards female seniors and those aged 75 to 94 years.

Objective:To explore the clinical characteristics of 1q21.1 microdeletion by using single nucleotide polymorphism microarrays (SNP array).Methods:Eighteen cases of 1q21.1 microdeletion syndrome diagnosed at the Longgang District Maternal and Child Health Care Hospital of Shenzhen City from June 2017 to December 2022 were selected as the study subjects. Clinical data of the patients were collected. Results of chromosomal karyotyping and SNP assay were retrospectively analyzed.Results:Among the 18 cases with 1q21.1 microdeletions, 13 had a deletion between BP3 and BP4, 4 had a deletion between BP1/BP2 and BP4, whilst 1 had a proximal 1q21.1 deletion (between BP2 and BP3) involving the Thrombocytopenia-absent radius (TAR) region. The deletions had spanned from 360 kb to 3.9 Mb, which encompassed the GJA5, GJA8, CHD1L, RBM8AB and other morbid genes. In three families, the proband child has inherited the same 1q21.1 microdeletion from their parents, whose clinical phenotype was normal or slightly abnormal. The clinical phenotypes of 1q21.1 microdeletion had included cognitive or behavioral deficits in 9 cases (9/18, 50.0%), growth retardation in 8 cases (8/18, 44.4%), craniofacial deformities in 7 cases (7/18, 38.8%), cardiovascular malformations in 5 cases (5/18, 27.8%), and microcephaly in 3 cases (3/18, 16.7%). Conclusion:1q21.1 microdeletion syndrome has incomplete penetrance and varied expression such as intellectual impairment, growth and development delay, and microcephaly, with a wide range of non-specific phenotypes.

Objective:To analyze the trend of dementia mortality rate among individuals aged 60 to 94 years in China from 1982 to 2021.Methods:Utilizing data from the Global Burden of Disease Study 2021, the Joinpoint regression model was employed to analyze the trend in the dementia mortality rate among Chinese older adults from 1982 to 2021. The age-period-cohort analysis method was used to decompose the age effect, period effect and cohort effect of dementia mortality data in Chinese elderly people.Results:From 1982 to 2021, the crude mortality rate of dementia in elderly women aged 60-94 in China (133.67/100 000-214.02/100 000) was higher than that in men (70.92/100 000-119.70/100 000), and the age-standardized mortality rate of dementia in women (230.74/100 000-246.87/100 000) was also higher than that in men (132.88/100 000-140.19/100 000). The age-standardized mortality rate of dementia in both genders showed an N-shaped fluctuation trend. The average annual percent change (AAPC) of dementia mortality rate in elderly males aged 60-94 was 0.07% (95% CI: 0.01%-0.13%), and the AAPC of dementia mortality rate in elderly females was -0.01% (95% CI:-0.08%-0.07%). Age effect analysis showed that from the age of 60, the risk of dementia death in males and females increased with age, especially among elderly people aged 75-94 who experienced a rapid increase in dementia mortality rate. The period effect analysis showed that the overall risk of dementia death in elderly men and women aged 60-94 was decreasing, but it had increased from 2017 to 2021. The cohort effect analysis showed that the risk of dementia death was lower in later birth cohorts. Conclusion:From 1982 to 2021, the dementia mortality rate among Chinese older adults aged 60 to 94 years exhibited fluctuations. Particularly, there has been a notable rebound in recent years. Special attention should be directed towards female seniors and those aged 75 to 94 years.

Objective To explore the effect of pristimerin combined with cisplatin on proliferation and apoptosis of nasopharyngeal carcinoma cells.Methods CCK-8 assay was used to examine the survival rate of HNE-1 and CNE-2Z cells following treatment for 24 h with different concentrations of pristimerin,cisplatin or their combination.The changes in colony formation ability,apoptosis,and intracellular reactive oxygen species(ROS)levels of the treated cells were analyzed using colony formation assay and flow cytometry.Western blotting was performed to detect the changes in protein expressions in the cells.The effects of pre-treatment with NAC on proliferation,apoptosis,and PI3K/AKT signaling pathway were observed in pristimerin-and/or cisplatin-treated cells.Results Both pristimerin and cisplatin significantly lowered the survival rate of HNE-1 and CNE-2Z cells(P<0.05).Compared with pristimerin or cisplatin alone,their combination more strongly inhibited survival and colony formation ability of the cells,increased cell apoptosis rate and intracellular ROS levels,upregulated the protein expressions of Bax,cleaved caspase-3,and cleaved PARP,and downregulated the protein expressions of Bcl-2,Mcl-1,PARP and p-PI3K and p-AKT(P<0.05).NAC pretreatment significantly attenuated proliferation inhibition and apoptosis-promoting effects of pristimerin combined with cisplatin,and partially restored the downregulated protein expressions of p-PI3K and p-AKT in HNE-1 and CNE-2Z cells with the combined treatment(P<0.05).Conclusion Pristimerin can enhance cisplatin-induced proliferation inhibition and apoptosis in nasopharyngeal carcinoma cells,the mechanism of which may involve ROS-mediated deactivation of the PI3K/AKT signaling pathway.

Objective To investigate the effect of dihydroartemisinin(DHA)for enhancing the inhibitory effect of cisplatin(DDP)on DDP-resistant nasopharyngeal carcinoma cell line HNE1/DDP and explore the mechanism.Methods CCK-8 method was used to assess the survival rate of HNE1/DDP cells treated with DHA(0,5,10,20,40,80,and 160 μmol/L)and DDP(0,4,8,16,32,64,128 μmol/L)for 24 or 48 h,and the combination index of DHA and DDP was calculated using Compusyn software.HNE1/DDP cells treated with DHA,DDP,or their combination for 24 h were examined for cell viability,proliferation and colony formation ability using CCK-8,EdU and colony-forming assays.Flow cytometry was used to detect cell apoptosis and intracellular reactive oxygen species(ROS).The expression levels of apoptosis-related proteins cleaved PARP,cleaved caspase-9 and cleaved caspase-3 were detected by Western blotting.The effects of N-acetyl-cysteine(a ROS inhibitor)on proliferation and apoptosis of HNE1/DDP cells with combined treatment with DHA and DDP were analyzed.Results Different concentrations of DHA and DDP alone both significantly inhibited the viability of HNE1/DDP cells.The combination index of DHA(5 μmol/L)combined with DDP(8,16,32,64,128 μmol/L)were all below 1.Compared with DHA or DDP alone,their combined treatment more potently decreased the cell viability,colony-forming ability and the number of EdU-positive cells,and significantly increased the apoptotic rate,intracellular ROS level,and the expression levels of cleaved PARP,cleaved caspase-9 and cleaved caspase-3 in HNE1/DDP cells.N-acetyl-cysteine pretreatment obviously attenuated the inhibitory effect on proliferation and apoptosis-inducing effect of DHA combined with DDP in HNE1/DDP cells(P<0.01).Conclusion DHA enhances the growth-inhibitory and apoptosis-inducing effect of DDP on HNE1/DDP cells possibly by promoting accumulation of intracellular ROS.

Poor ovarian response (POR) is a pathological condition in which the ovary responds poorly to gonadotropins,and is a major constraint on the unsatisfactory outcome of in vitro fertilization-embryo transfer (IVF-ET). Follicular growth,development,maturation,and expulsion are all affected by the yin-yang balance between heart and kidney,as well as the elevation exchange. If the heart and kidney essence and blood are insufficient,water and fire are out of harmony,and qi movement is not smooth,fewer high-quality follicles will be recruited and acquired during the ovarian stimulation cycle,resulting in a low transferable embryo rate and unacceptable pregnancy result. Sympathetic treatment of heart and kidney should be based on the following principles at different stages of the IVF-ET cycle:replenishing the heart,kidney,essence,and blood before entering the cycle,in order to nourish the essence and assist in the growth of the follicles;nourishing renal water,and clearing heart fire during the pituitary down-regulation period,in order to lessen the negative effects of the down-regulation medicinals;regulating the depression of the heart,liver,spleen,and kidney meridians during the follicle's retrieval period,in order to encourage the smooth release of the ova;and warming heart and kidney fire to improve endometrial tolerance during the implantation period. The application of the theory of intercourse of heart and kidney to elucidate the pathogenesis of POR is critical to the development of clinical strategies for fertility enhancement,as well as providing new ideas for the clinical application of traditional Chinese medicine in the field of reproduction.