[Objective]To study and summarize the experience of traditional Chinese medicine Master ZHOU Zhongying in treating systemic sclerosis from the pathogenesis of phlegm-stasis-heat junction,providing references for clinical practice.[Methods]Through the clinical learning,collation and analysis of Professor ZHOU's medical cases in the treatment of systemic sclerosis,the paper elaborated his clinical thinking and experience in the treatment of systemic sclerosis,which included etiology,pathogenesis,therapy and characteristic clinical medication,and verified it with medical records.[Results]Professor ZHOU thinks the key pathogenesis is phlegm-stasis-heat junction,pathological factors of systemic sclerosis mainly include phlegm,blood stasis and heat,which can depend on each other mutually throughout the course of disease.According to the progression of the disease and the evolution of pathological factors,treatment is primarily focused on phlegm-stasis-heat junction.Phlegm and blood stasis are interrelated,obstructing the circulation of Qi-blood so as to lead to pain and swelling,the treatment should be resolving phlegm,removing blood stasis and activating meridians;phlegm and heat are lingered each other,exacerbating the progression of the condition,it is appropriate to clear away phlegm and heat so that symptoms of skin redness and swelling can be relieved;blood and heat are interweaved together,which invade the skin and joints seriously,it is advisable to expel pathogenic factors by clearing away heat and resolving blood stagnation;Yin is damaged and Qi is consumed terribly,subsequently deficiency-heat is gradually emerging,the way to solve it is to supplement Qi,nourish Yin and strengthen the body resistance to eliminate pathogenic factors.The case was diagnosed as accumulation of phlegm stasis heat,blockage of wind-dampness and deficiency of Qi and Yin by Professor ZHOU,and treated with dissipating phlegm and removing blood stasis,clearing heat and unblocking collaterals,supplementing Qi and nourishing Yin,and the recipe Baiwei Decoction combined with Qinjiao Biejia Powder modified was used.[Conclusion]ZHOU Zhongying,the traditional Chinese medicine Master,who advocates attaching importance to the pathogenesis firstly in the process of syndrome differentiation,treating systemic sclerosis from the pathogenesis of phlegm-stasis-heat junction,which plays a unique role in relief of clinical symptoms,and his experiences are worthy of inheritance and promotion.

Objective:To investigate the efficacy of total laparoscopic radical gastrectomy for locally advanced esophagogastric junction carcinoma and its effect on patient's immune function and levels of tumor markers.Methods:A total of 106 patients who underwent total laparoscopic radical gastrectomy (total endoscopic group) in the Affiliated Cancer Hospital of Shanxi Medical University from January 2016 to April 2020 were collected, and 98 patients who underwent open radical gastrectomy (open group) in the same period were selected. The short-term efficacy, preoperative and postoperative immune function and tumor markers were compared between the two groups.Results:The operative time of the total endoscopic group was longer than that of the open group [(214±49) min vs. (165±32) min, t = 8.87, P < 0.01], the intraoperative blood loss was less than that of the open group [(86±50) ml vs. (113±53) ml, t = 3.59, P < 0.01], the postoperative first exhaust time was shorter than that of the open group [3.0 d (3.0 d, 4.0 d) vs. 3.5 d (3.0 d, 4.5 d), Z = 2.89, P < 0.01], and the incision length was shorter than that of the open group [(4.6±0.6) cm vs. (17.6±2.0) cm, t = 68.63, P < 0.01]. The postoperative proportion of CD4 + T cells, CD4 +/CD8 + and proportion of NK cells in the total endoscopic group were higher than those in the open group [(41±8)% vs.(36±8)%, t = 4.710, P < 0.01; 1.63 (1.19, 2.30) vs. 1.15 (0.87, 1.63), Z = 4.165, P < 0.01; 24.60 % (17.77 %, 32.50 %) vs. 19.25 % (13.35 %, 25.80 %), Z = 3.440, P < 0.01], while the postoperative proportions of CD8 + T cells and regulatory T cells in the total endoscopic group were lower than those in the open group [(26±11)% vs. (30±10)%, t = 2.375, P = 0.018; 3.37% (5.00%, 6.70%) vs. 4.48% (5.70%, 7.20%), Z = 3.057, P = 0.002]. Postoperative carcinoembryonic antigen (CEA) and carbohydrate antigen 199 (CA199) in the total endoscopy were lower than those in the open group group [0.96 μg/L (0.54 μg/L, 1.50 μg/L) vs. 1.27 μg/L (0.70 μg/L, 2.98 μg/L), Z = 2.745, P = 0.036; 8.07 U/ml (5.48 U/ml, 13.07 U/ml) vs. 10.80 U/ml (6.54 U/ml, 19.93 U/ml), Z = 2.690, P = 0.043]. Conclusion:Compared with open surgery, total laparoscopic radical gastrectomy has less trauma and stress response, and has less impact on the gastrointestinal and immune function of patients, and the levels of tumor markers CEA and CA199 are low.

ObjectiveTo investigate the effect and therapeutic role of quercetin on ferroptosis in lipopolysaccharide （LPS）-induced acute kidney injury （AKI） rats based on the Kelch-like epichlorohydrin-related protein-1 （Keap1）/nuclear factor erythroid-2-related factor 2 （Nrf2）/antioxidant response element （ARE） pathway. MethodsSixty male SD rats were randomly divided into normal group， model group， quercetin high-dose （100 mg·kg^-1） and low-dose （10 mg·kg^-1） groups， ferroptosis inhibitor Ferrostatin 1 （FER1） group （5 mg·kg^-1）， and quercetin high-dose + Nrf2 inhibitor group （ML385， 30 mg·kg^-1）. Except for the normal group， the AKI rat model was established in each group by intraperitoneal injection of LPS （10 mg·kg^-1）. Following successful modeling， each treatment group received the corresponding dose of drug intervention， while the normal and model groups were administered an equal volume of normal saline. The intervention lasted for 3 weeks. Serum creatinine （SCr） and blood urea nitrogen （BUN） levels were measured biochemically to assess renal function. Serum tumor necrosis factor-α （TNF-α） and interleukin （IL）-1β and IL-6 levels were detected by enzyme-linked immunosorbent assay （ELISA）. The levels of Fe²⁺， malondialdehyde （MDA）， superoxide dismutase （SOD）， and glutathione （GSH） in renal tissue were detected. Hematoxylin-eosin （HE）， Masson， and periodic acid-Schiff （PAS） staining were employed to observe pathological morphological changes in renal tissue. Mitochondrial morphological changes were observed using transmission electron microscopy. Reactive oxygen species （ROS） levels in renal tissue were detected by immunofluorescence （IF）. The protein and mRNA expression levels of Keap1， Nrf2， heme oxygenase-1 （HO-1）， glutathione peroxidase 4 （GPX4）， transferrin receptor （TFR1）， and kidney injury molecule-1 （KIM-1） were assessed by immunohistochemistry （IHC） and real-time fluorescence quantitative polymerase chain reaction （Real-time PCR）. ResultsCompared with the normal group， the model group exhibited significantly elevated serum levels of SCr， BUN， TNF-α， IL-1β， IL-6， Fe²⁺ and MDA in renal tissue， and significantly reduced SOD and GSH levels （P<0.01）. Pathological injury in renal tissue was severe， with evident mitochondrial damage characteristic of ferroptosis and a reduced mitochondrial count. ROS levels in renal tissue were significantly increased. The protein and mRNA expression levels of Keap1， TFR1， and KIM-1 in renal tissue were significantly elevated， while those of Nrf2， HO-1， and GPX4 were significantly decreased （P<0.01）. Compared with the model group， serum levels of SCr， BUN， TNF-α， IL-1β， IL-6， Fe²⁺ and MDA in renal tissue in the quercetin dosage groups and FER1 group showed varying degrees of reduction， while SOD and GSH levels were significantly increased （P<0.05）. Pathological injury in renal tissue was markedly alleviated， mitochondrial damage improved， and mitochondrial counts increased. ROS levels in renal tissue were significantly reduced. The protein and mRNA levels of Keap1， TFR1， and KIM-1 in renal tissue were significantly decreased， while those of Nrf2， HO-1， and GPX4 were significantly increased， with the most notable improvement in the high-dose quercetin group （P<0.05）. In comparison to the high-dose quercetin group， the ML385 group significantly weakened the protective effect of quercetin on AKI rats （P<0.05）. ConclusionQuercetin effectively inhibits ferroptosis， improves renal tissue injury， and repairs renal function in AKI rats， and its mechanism may be related to the activation of the Keap1/Nrf2/ARE pathway.

ObjectiveTo observe the influence and therapeutic effect of quercetin on cuproptosis in rheumatoid arthritis rats and to explore its possible mechanism based on the solute carrier family 31 member 1 （SLC31A1）/ferredoxin 1 （FDX1） pathway. MethodsSixty male SD rats were divided into six groups： A control group， a model group， high- and low-dose quercetin groups （150 and 50 mg·kg^-1）， a cuproptosis inhibitor （tetrathiomolybdate， TTM） group （10 mg·kg^-1）， and a methotrexate group （2 mg·kg^-1）， 10 rats in each group. Except for the control group， the model of rheumatoid arthritis （CIA） rats was established by type Ⅱ collagen induction method. After successful modeling， each drug group was intervened according to the corresponding dose of drugs， and the control group and the model group were given the same amount of normal saline by gavage， once a day， which lasted for 4 weeks. The swelling degree of rats' feet was observed， and the clinical arthritis scores were determined. The levels of serum rheumatoid factor （RF）， matrix metalloproteinase-3 （MMP-3）， tumor necrosis factor-α （TNF-α）， interleukin-1β （IL-1β）， interleukin-10 （IL-10）， and ceruloplasmin （Cp） were detected by enzyme-linked immunosorbent assay （ELISA）. The content of copper ion （Cu）， malondialdehyde （MDA）， superoxide dismutase （SOD）， and glutathione （GSH） in joint tissue was detected. Hematoxylin-eosin （HE） staining was used to observe the pathological changes of joint tissue. The levels of reactive oxygen species （ROS） and dihydrolipoic acid transacetylase （DLAT） were detected by immunofluorescence （IF）. The protein and mRNA expression of SLC31A1， FDX1， lipoic acid synthase （LIAS）， heat shock protein 70 （HSP70）， pyruvate dehydrogenase E1 subunit β （PDHB）， and copper transporting P-type ATPase β （ATP7B） was detected by immunohistochemistry （IHC） and real-time fluorescence quantitative polymerase chain reaction （Real-time PCR）. ResultsCompared to the control group， the model group exhibited joint swelling and deformity， significantly increased clinical arthritis scores， obvious bone destruction， synovial hyperplasia， and inflammatory cell infiltration in joint tissue. In addition， the serum levels of RF， MMP-3， TNF-α， IL-1β， and Cp showed significant elevation， while the level of IL-10 was significantly reduced. The levels of Cu， MDA， ROS， and DLAT in joint tissue were markedly increased， whereas SOD and GSH content was significantly decreased. The protein and mRNA expression of SLC31A1 and HSP70 was significantly up-regulated， while the protein and mRNA expression of FDX1， LIAS， PDHB， and ATP7B was significantly down-regulated （P<0.01）. Compared to the model group， each treatment group exhibited varying degrees of improvement in joint swelling and deformation as well as clinical arthritis scores in rats. Additionally， there was a reduction in joint bone destruction， inflammatory cell infiltration， and synovial hyperplasia in rats. Furthermore， the serum levels of RF， MMP-3， TNF-α， IL-1β， and Cp significantly decreased， while the level of IL-10 increased significantly. In joint tissue， the levels of Cu， MDA， ROS， and DLAT showed significant decreases， while SOD and GSH content exhibited significant increases. The protein and mRNA expression of SLC31A1 and HSP70 was down-regulated， while the protein and mRNA expression of FDX1， LIAS， PDHB， and ATP7B was up-regulated （P<0.05）. ConclusionQuercetin effectively reduces synovial hyperplasia and inflammatory infiltration in rats with rheumatoid arthritis， thereby alleviating pathological damage to joint tissue. This effect may be attributed to the blockade of the SLC31A1/FDX1 signaling pathway activation and inhibition of excessive cuproptosis.