Objective To explore the risk factors of prehypertension and the relationship between blood pressure and atherosclerosis.Methods The data of 456 cases in the Department of General Medicine were cross-sectional analyzed,including 174 subjects with normotension and 282 with prehypertension.The information was consisted of demographic characteristics,blood pressure,blood biochemical metabolism index,brachia-ankle pulse wave velocity (baPWV),ankle-brachial index (ABI) and carotid intima media thickness (CIMT).Results Compared to normotension group,the levels of systolic pressure,diastolic pressure,pulse pressure,body mass index,fasting blood glucose,glycosylated hemoglobin,triglyceride,uric acid,and C-reactive protein in prehypertension group were significantly increased (P ＜ 0.05) ; and high-density lipoprotein cholesterol was significantly decreased (P ＜0.05) ; the body mass index(OR =1.185),triglyceride(OR =1.302),and fasting blood sugar (OR =1.690) were the independent risk factors of prehypertension ; baPWV and CIMT in prehypertension group were higher,but ABI and artery atheromatous plaque rate were not obvious changed.When baPWV or CIMT were set as the dependent variables,multiple linear regression analysis showed that systolic blood pressure(β =0.226,P =0.007),fasting blood glucose(β =0.209,P =0.018),and age(β =0.279,P =0.002) were risk factors of baPWV;systolic blood pressure(β =0.118,P =0.015),body mass index(β =0.109,P =0.001),and age(β =0.396,P =0.001) were risk factors of CIMT.Conclusions Body mass index,triglycerides,and fasting blood sugar were the independent risk factors of prehypertension.The early subclinical damage of hardening of the arteries was occurred in the prehypertension cases,and systolic blood pressure was closely related with baPWV or CIMT.

Objective:To standardize the naming of organ at risk (OAR) and target area during cervical cancer radiotherapy based on AAPM TG-263.Methods:After self-programming of Matlab software to implement the reading and resolution of radiotherapy structure files, the naming of each substructure was automatically output, recorded and restored. After naming all substructures, the structure names were classified by keywords. According to TG-263, a standard naming conversion table of OAR and target area was developed, and the classified structure names were standardized through procedures. Finally, the standardized named radiotherapy structure files were output and imported into the treatment planning system (TPS).Results:The radiation structure of 144 patients with cervical cancer was successfully transformed and displayed correctly in TPS. Before the transformation, the naming of OAR and target area lacked of uniform norms and standards, and the naming of the same structure significantly differed. After the transformation, 43 naming methods of OAR and 74 naming methods of the target area were unified into 20 and 8 naming methods, which were more convenient for staff understanding and communication.Conclusion:The standardization of cervical cancer radiotherapy structure naming can reduce the inconsistency of naming and provide reference for the standardized naming of pelvic tumors.

Objective To investigate the changes in the percentages of CD4+T lymphocyte subsets and the homeostasis of T lymphocytes among MSM ( men who have sex with men) population with different stages of HIV-1 infection. Methods A total of 166 untreated MSM with HIV infection were enrolled and di-vided into three groups including early HIV infection (EHI, n=38) , HIV (n=94) and AIDS (n=34) groups. Sixty-two MSM negative for anti-HIV antibody were selected as healthy controls. Blood samples were collected into EDTA tubes and detected to analyze the changes in the distribution of CD4+ T cells and CD8+T lymphocyte subsets ( CD4+ CD45RA+, CD8+ CD28+, CD4+ CD25+ CD127-) and the percentages of activated (CD38, HLA-DR) and apoptotic cells (CD95) with disease progression by flow cytometry. Re-sults The expression of CD4+CD45RA+ T lymphocytes gradually decreased with the progression of AIDS. The percentage of CD4+CD45RA+ T lymphocytes in HIV group was lower than that of the control group, but higher than that of the AIDS group (P=0. 015, P=0. 000). No significant difference was found between the EHI and the control groups (P>0. 05). CD8+CD28+T cells were significantly reduced in the EHI group and remained at a low level with disease progression. No significant difference in the proportion of CD4+CD25+CD127- T cells was observed among all groups (P>0. 05). The percentage of CD4+CD38+HLA-DR+T cells increased gradually and the highest level was detected in the AIDS group, followed by those in the HIV, EHI and control groups (P<0. 01). The percentages of CD8+CD38+, CD8+HLA-DR+, CD8+ CD38+HLA-DR+and CD8+CD95+T cells in the EHI, HIV and AIDS groups were significantly higher than those in the control group (P<0. 01), but there was no significant difference among the former three groups (P>0. 05). Con-clusion HIV infection caused the changes in the numbers and functions of T lymphocyte subsets and accel-erated the activation and apoptosis of T lymphocytes, which aggravated the T lymphocyte immune dysfunction even further. A comprehensive analysis of the alterations in different T cell subsets would be conducive to re-flect the immune deficiency and the severity of disease. CD4+ and CD8+ T cells were activated in the early stage of HIV infection, which indicated that studying the immune response during that stage might help to understand their roles in disease progression.

Objective:To investigate the effects of highly active anti-retroviral therapy (HAART) on the activation of T lymphocytes and expression of CD4 + CD45RA + T cell subsets in HIV/AIDS patients. Methods:This study prospectively analyzed 105 HIV/AIDS patients undergoing HAART and 35 HIV-1-negative cases (healthy controls). Flow cytometry was used to detect the activation of T lymphocytes and the percentages of CD4 + CD45RA + T cell subsets in whole blood samples taken from healthy controls and HIV/AIDS patients before and after therapy. Results:The activation of T lymphocytes was significantly enhanced in the 105 HIV/AIDS patients than in the healthy controls before treatment ( P<0.01). The activated T lymphocytes gradually decreased after HAART. Firstly, CD4 + CD38 + HLA-DR + , CD8 + CD38 + and CD8 + HLA-DR + T lymphocytes decreased one month after therapy ( P<0.05). Then, four indicators of T lymphocyte activation including the expression of CD8 + CD38 + HLA-DR + T lymphocytes decreased significantly six months after therapy ( P<0.01). The percentage of CD8 + CD38 + HLA-DR + T lymphocytes detected 12 months after therapy was significantly lower than that analyzed six months after therapy ( P<0.01). No significant difference was found in the expression of the other three indicators for activation ( P>0.05). Twelve months after therapy, the four indicators for T lymphocyte activation in HIV/AIDS patients were still significantly higher than those of the control group ( P<0.01). The percentages of CD4 + CD45RA + T lymphocytes in HIV/AIDS patients were significantly lower than those in healthy controls before and 12 months after treatment ( P>0.05). Conclusions:HAART could reduce immune activation after six months of treatment, but could not reverse the activation nor restore the expression of CD4 + CD45RA + T lymphocytes in HIV/AIDS patients.

Objective:To explore the abundance, diversity, and structural changes of early postoperative pulmonary bacterial microbiota in lung transplant recipients.Methods:Recruiting 40 recipients who underwent lung transplantation surgery at the First Affiliated Hospital of Guangzhou Medical University from October 2020 to May 2022 for the study.All recipients did not receive antibiotic treatment within 4 weeks prior to surgery, and all recipients received a unified immunosuppressive and anti infection regimen after surgery.The bronchoalveolar lavage fluid(BALF) was collected from the amputated lung in vitro before the transplantation for 16S ribosomal RNA sequencing and flora analysis.BALF was also collected at the scheduled time from the transplanted lung on the 7th, 14th and 30th days post transplantaion for analysis.Results:The study included a total of 40 recipients who did not receive antibiotic treatment within 4 weeks before surgery, including 35 males.Among the study participants, there were 14 cases of primary obstructive pulmonary disease, 19 cases of interstitial lung disease, 3 cases of occupational lung disease, and 4 others.Microbiome in BALF of transplanted and detached autologous lungs at the first week after surgery α( P<0.05) and β diversity is statistically significant( R2=0.08, P=0.001), and the bacterial community in the transplanted lungs α Diversity is lower than that of explant lungs.Starting from the second week after surgery, the richness and species diversity of the transplanted lung microbiota gradually increase.The bacterial structure was also changed with postoperative time, and the relative abundance of the same bacterial species were varied at different time points.The bacterial community in BALF was mainly dominated by Proteobacteria both explant lungs and transplant lungs.The relative abundance of Staphylococcus and Acinetobacter genera at the BALF in transplanted lungs was higher than that in explant lung samples, but their relative abundance decreased over time after surgery. Conclusions:The α diversity of the early postoperative pulmonary microbiota after lung transplantation was lower than that of the amputated autologous lung, and the bacterial richness and species diversity in the microbiota of the transplanted lung gradually increased at the second week after the transplantation.The bacterial microbiota of the transplanted lung is changed complicatedly with time.

Objective: To analyze the clinical phenotype and genomic abnormality of an adult featuring congenital heart defect and multiple developmental disorders. Methods: The patient was subjected to conventional G-banding chromosomal karyotyping and single nucleotide polymorphism microarray (SNP-array) analysis. Results: The patient showed a normal karyotype, while SNP-array revealed a 42.7 Mb mosaic uniparental disomy (UPD) in the 11p15.5p12 region ([hg19] chr11: 491 333 - 43 189 376). Conclusion The mosaicism of UPD of 11p15.5p12 region probably underlies the congenital heart defect and developmental disorders in the patient.

Objective:To investigate the necessity of adaptive re-planning during radiotherapy for nasopharyngeal carcinoma (NPC) and its impact on dose improvement.Methods:Clinical data of 89 NPC patients admitted to Sun Yat-sen University Cancer Center from July 2014 to December 2017 were retrospectively analyzed. All patients received 25+7 rounds of adaptive re-planning during radiotherapy. Plan-A was defined as the initial CT scan-based 25-fraction radiotherapy plan, while plan-B was defined as the re-planned 7-fraction radiotherapy plan based on a subsequent CT scan. The changes in the target and parotid gland volumes were compared between plan-A and plan-B. Plan-I was a one-time simulation of plan-A extended to 32 fraction radiotherapy plan, and plan-II was generated through registration and fusion of the plan-A and plan-B for adaptive re-planning. The differences in dose metrics, homogeneity index (HI), conformity index (CI), and dose to organs at risk (OAR) were compared between plan-I and plan-II. Statistical analysis was performed by using paired t-test. Results:Compared with plan-A, the gross tumor volume of massive bleeding lesions (GTV nx) and parotid gland volume of plan-B were decreased by 13.14% and 11.12%, respectively (both P<0.001). While planning clinical target volume of metastatic lymph nodes (PCTV nd) of plan-B was increased by 7.75%( P<0.001). There were significant changes in the lymph nodes of plan-A and plan-B. The D mean, D 5%, D 95% of massive bleeding lesions planning target volume (PTV nx) and D 5% of high risk planning target volume (PTV1) in plan-II were all significantly higher than those in plan-I (all P<0.05). The CI of PTV nx and PTV1 in plan-II was closer to 1 than that in plan-I. In all assessed OAR, the D mean, D 50%, and D max of plan-II were significantly lower than those of plan-I (all P<0.05). Conclusions:During radiotherapy, NPC patients may experience varying degrees of primary tumor shrinkage, parotid gland atrophy, and lymph node changes. It is necessary to deliver re-planning and significantly improve the dose of target areas and OAR.

Autophagy is mediated by multiple molecules and pathways. In cardiovascular diseases， autophagy can play a role through key signaling pathways such as phosphoinositide 3-kinase （PI3K）/protein kinase B （Akt）/mammalian target of rapamycin （mTOR）， adenosine monophosphate-activated protein kinase （AMPK）/mTOR， mitogen-activated protein kinases （MAPK）， p53， Wnt/β-catenin， etc. Traditional Chinese medicine （TCM） monomers for promoting blood circulation and removing blood stasis such as hydroxysafflor yellow A， ginsenoside Rb1， salidroside， ligustrin， curcumin， etc.， and TCM prescription and preparations such as Huangqi baoxin decoction， Taohong siwu decoction， Tongxinluo capsule， Shuangshen ningxin capsule， Suxiao jiuxin pills， etc. can regulate autophagy through the above-mentioned key signaling pathways， thereby alleviating the progression of cardiovascular diseases.

ObjectiveTo investigate the effects of the volatile oil of Linderae Radix on the apoptosis and autophagy of human gastric cancer cell line AGS， and to explore the regulatory role of adenosine monophosphate-activated protein kinase （AMPK）/mammalian target of rapamycin （mTOR） signaling pathway in this process. MethodThe volatile oil of Linderae Radix was extracted by steam distillation， and the effect of the volatile oil on the viability of AGS cells was detected by thiazolyl tetrazolium （MTT） colorimetry. The optimal intervention dose and time were determined according to the half maximal inhibitory concentration （IC₅₀） for subsequent research. The blank， low， medium， and high-dose volatile oil （0， 15， 30， 60 mg·L^-1） groups and the positive drug cyclophosphamide （CTX， 350 mg·L^-1） group were designed. AGS cells were treated with different doses of volatile oil for 48 h. The changes in cell proliferation， cycle， and migration were measured by colony formation assay， flow cytometry， and cell scratch test， respectively. Hematoxylin-eosin （HE） staining was employed to observe the changes of cell morphology， Annexin-V/propidium iodide （PI） double staining to measure the apoptosis， and acridine orange （AO） staining to measure the autophagy level of the cells. Western blotting was employed to determine the expression of the autophagy effectors Beclin-1， p62， microtubule-associated protein 1-light chain 3 （LC3）， B-cell lymphoma-2 （Bcl-2）， Bcl-2-associated X protein （Bax）， cleaved Caspase-3， cleaved poly ADP-ribose polymerase （PARP）， adenosine monophosphate-activated protein kinase （AMPK）， phosphorylated AMPK （p-AMPK）， mTOR， and phosphorylated mTOR （p-mTOR）. ResultCompared with the blank group， 24 h and 48 h of intervention with the volatile oil of Linderae Radix inhibited the viability of AGS cells in a concentration- and time-dependent manner （P<0.05， P<0.01）. Compared with the blank group， the volatile oil decreased the cell proliferation and migration （P<0.05， P<0.01） and blocked the AGS cell cycle in G₂/M phase （P<0.05， P<0.01） in a concentration-dependent manner. The cells treated with the volatile oil became spherical and smaller， with the formation of apoptotic bodies and increased apoptosis rate （P<0.05， P<0.01）. As the dose of the volatile oil increased， the number of autophagosomes increased and the red fluorescence gradually enhanced， indicating the elevated level of autophagy. Compared with the blank group， different doses of volatile oil up-regulated the protein levels of Beclin-1， LC3 Ⅱ/LC3 Ⅰ， cleaved Caspase-3， cleaved PARP， Bax/Bcl-2， and AMPK （P<0.05， P<0.01） and down-regulated the protein levels of p62 and p-mTOR （P<0.05， P<0.01）. ConclusionThe volatile oil of Linderae Radix induces the apoptosis and exerts the autophagy-mediated growth inhibition of AGS cells by regulating the AMPK/mTOR signaling pathway.

ObjectiveTo explore the anti-inflammatory effect of Duhuo Jishengtang （DHJST） on collagen-induced arthritis （CIA） model rats and its effect on the Toll-like receptor 2 （TLR2）/p38 mitogen-activated protein kinase （MAPK）/nuclear factor-κB （NF-κB） signaling pathway. MethodForty-eight male SD rats were randomly divided into the following six groups （n=8）： normal group， model group， methotrexate （MTX） group， low-dose DHJST （DHJST-L） group， medium-dose DHJST （DHJST-M） group， and high-dose DHJST （DHJST-H） group. The CIA model was established by injecting bovine type Ⅱ collagen into the rat tail root with the collagen antibody induction method. After model induction， rats were treated with drugs by gavage. The rats in the MTX group received MTX at 2.0 mg·kg^-1， three times a week， and those in the DHJST groups received DHJST at 3.8， 7.6， 15.2 g·kg^-1·d^-1 for 28 days. The rats in the normal group and the model group were given the same dose of normal saline. The weight of the rats was recorded， and the paw swelling degree was observed. The arthritis index and immune organ index were measured， and the changes in the microcirculation indexes of the rats were detected with a microcirculation detector. Hematoxylin-eosin （HE） staining was used to detect the pathological morphologic changes in rat synovial tissues and the apoptosis rate of synovial cells was detected by flow cytometry to determine the therapeutic effect of DHJST on rheumatoid arthritis. Enzyme-linked immunosorbent assay （ELISA） was used to detect the changes in serum levels of tumor necrosis factor-α （TNF-α）， interleukin （IL）-1β， IL-17A， and interferon-γ （IFN-γ）. The protein expression of TLR2， NF-κB p65， phosphorylated NF-κB p65 （p-NF-κB p65）， p38 MAPK， and p-p38 MAPK was detected by Western blot. ResultCompared with the normal group， the model group showed reduced body weight （P<0.01）， increased paw swelling degree， arthritis index， and immune organ index （P<0.01）， increased comprehensive microvascular score and vascular resistance （P<0.01）， significant hyperplasia of synovial tissues and massive infiltration of inflammatory cells as revealed by pathological sections， and up-regulated expression levels of TNF-α， IL-1β， IL-17A， and IFN-γ in serum， and TLR2， p-NF-κB p65/NF-κB p65 and p-p38 MAPK/p38 MAPK in synovial tissues （P<0.01）. Compared with the model group， the DHJST groups showed increased body weight of rats （P<0.01）， decreased paw swelling degree， arthritis index， and immune organ index （P<0.05， P<0.01）， reduced comprehensive microvascular score and vascular resistance （P<0.05， P<0.01）， improved synovial histopathological injury， increased apoptosis rate of synovial cells （P<0.01）， and down-regulated levels of TNF-α， IL-1β， IL-17A， and IFN-γ in serum （P<0.05， P<0.01） and TLR2， p-NF-κB p65/NF-κB p65 and p-p38 MAPK/p38 MAPK in synovial tissues （P<0.05， P<0.01）. ConclusionDHJST may alleviate the inflammatory reaction in CIA rats by regulating the TLR2/p38 MAPK/NF-κB signaling pathway， thus exerting its anti-rheumatoid arthritis effect.