ObjectiveTo construct a scale for the diagnosis of chronic atrophic gastritis （CAG） with turbid toxin accumulating in the stomach. MethodsFirst， a research group was established to construct the scale framework. Relevant literature of CAG with syndrome of turbid toxin accumulating in the stomach was searched in CNKI， Wanfang Database （WF）， and VIP Database （CQVIP） from April 1， 2003 to April 1， 2023， and items were preliminarily selected after standardization of terms. Through clinical investigation， the discrete trend method， correlation coefficient method， Cronbach's coefficient method， and factor analysis method were used to screen symptom items， and the frequency method was used to screen signs， tongue coating， and pulse conditions. Three rounds of Delphi expert consultation were conducted to determine the items of the scale. The weight of each item was obtained by the analytic hierarchy process. ResultsA total of 49 articles were included， and 45 items were obtained after primary screening， including 28 symptoms， 2 signs， 10 tongue coatings， and 5 pulse conditions. After clinical investigation， 15 symptoms were retained， and 8 signs and pulse conditions of tongue coating were retained. The positive coefficients of experts in three rounds of Delphi expert consultation were 100%， 96.67%， and 100%， respectively. The expert authority coefficients were 0.86， 0.87， and 0.87， respectively， and the coordination coefficients were 0.18， 0.25， and 0.30. After core group discussion， Delphi method investigation， and AHP weight assignment， the diagnostic scale items of CAG with turbid toxin accumulating in stomach syndrome were finally established， namely， dark red or purplish tongue proper with yellow greasy （or dry） coating （30 points）， epigastric stuffiness and fullness or pain （15 points）， sticky and unsmooth defecation （10 points）， taste disturbance （sticky mouth， fetid breath， bitter taste， 7 points）， heartburn or acid regurgitation （6 points）， dizziness and clouding （5 points）， general heaviness and fatigue （5 points）， slippery， string‑slippery， or slippery‑rapid pulse （5 points）， dysuria （or yellow or deep yellow urine， 4 points）， poor appetite （4 points）， dull complexion （3 points）， sticky， greasy， and fetid secretions （3 points）， and poor sleep （3 points）. ConclusionBased on the establishment， screening， confirmation， and weighting of an item pool， combined with subjective and objective approaches as well as qualitative and quantitative methods， a diagnostic scale for CAG with the syndrome of turbid toxin accumulating in the stomach was successfully constructed.

This paper summarizes professor LI Guolie's clinical experience in treating orthostatic hypotension （OH） based on the theory of "raising the clear and directing the turbid downward". It is considered that the core pathogenesis of OH lies in the body's transition from a supine to an upright position， during which dysfunction of the middle jiao （焦） transformation and transportation， along with impaired pivot function， hinders the ascending of clear yang and the descending of turbid yin. Treatment should follow the general principle of "ascending the clear and directing the turbid downward"， placing emphasis on distinguishing the primary and secondary aspects. For cases where the clear yang fails to ascend， the self-formulated Li's Shengqing Jiangzhuo Decoction （李氏升清降浊汤）is used to supplement qi， raise the clear， and strengthen the middle jiao. For cases where the turbid yin fails to descend， the self-formulated Wuxiang Qingzhuo Beverage（五香清浊饮）with modifications is applied to resolve phlegm， eliminate stasis， harmonize the middle， and descend the turbid.

This paper summarizes professor LI Guolie's clinical experience in treating orthostatic hypotension （OH） based on the theory of "raising the clear and directing the turbid downward". It is considered that the core pathogenesis of OH lies in the body's transition from a supine to an upright position， during which dysfunction of the middle jiao （焦） transformation and transportation， along with impaired pivot function， hinders the ascending of clear yang and the descending of turbid yin. Treatment should follow the general principle of "ascending the clear and directing the turbid downward"， placing emphasis on distinguishing the primary and secondary aspects. For cases where the clear yang fails to ascend， the self-formulated Li's Shengqing Jiangzhuo Decoction （李氏升清降浊汤）is used to supplement qi， raise the clear， and strengthen the middle jiao. For cases where the turbid yin fails to descend， the self-formulated Wuxiang Qingzhuo Beverage（五香清浊饮）with modifications is applied to resolve phlegm， eliminate stasis， harmonize the middle， and descend the turbid.

ObjectiveTo identify and validate the optimal compatibility dosage of astragaloside Ⅰ （ASⅠ） and calycosin （CY） in the treatment of cholestatic liver fibrosis. MethodsA 3，5-diethoxycarbonyl-1，4-dihydrocollidine （DDC） diet was used to establish a mouse model of liver fibrosis， and the uniform design method was used to identify the optimal combination ratio of the saponin component ASⅠ and the flavonoid component CY in Astragalus membranaceus. In the uniform design experiment， 80 male C57/BL6J mice were divided into normal group， model group， total astragalosides （TAS） group， groups A — F with a uniform design， and obeticholic acid （OCA） group using a random number table， with 8 mice in each group. The multiple regression analysis was used to establish the optimal regression equation and obtain the potential optimal combination ratio. The in vivo efficacy of the empirically optimal combination identified in the uniform design and the optimal dose combination predicted by the regression equation were compared for validation. A one-way analysis of variance was used for comparison of continuous data between multiple groups； the Levene test was used to determine the homogeneity of variance， and the least significant difference t-test was used for comparison of data with homogeneity of variance between two groups， while the Dunnett T3 test was used for comparison of data with heterogeneity of variance. ResultsIn the uniform design regimen， the JYB combination （3.125 mg/kg ASI+50 mg/kg CY） significantly reduced the serum levels of alanine aminotransferase （ALT）， aspartate transaminase （AST）， alkaline phosphatase （ALP）， total bile acid （TBA）， total bilirubin （TBil）， and indirect bilirubin （IBil） in mice with DDC-induced cholestatic liver fibrosis （all P<0.05）， and it also reduced hepatic Hyp content （P<0.01）， semi-quantified collagen deposition area （P<0.001）， and the mRNA expression levels of Acta2， Col1a1， Ck7， Ck19， Adgre1， TLR4， TNF-α， and CCL5 in liver tissue （all P<0.05）. The regression equation showed that 50 mg/kg ASⅠ+50 mg/kg CY was the potential optimal combination， which was named as P1 combination. However， subsequent validation experiments showed that P1 combination only significantly improved the serum levels of AST and IBil and hepatic Hyp content in DDC mice （all P<0.05）， with no significant impact on hepatic collagen deposition and the mRNA expression levels of Acta2， Ck7， Ck19， Adgre1， and CCL5 （all P>0.05）. In contrast， the JYB combination significantly improved the serum levels of ALP， ALT， AST， TBA， TBil， and IBil， hepatic collagen deposition， hepatic Hyp content， and the mRNA expression levels of Acta2， Col1a1， Ck7， Ck19， Adgre1， TLR4， TNF-α， and CCL5 （all P<0.05）. ConclusionThis study shows that the JYB combination （3.125 mg/kg ASⅠ+50 mg/kg CY） can significantly alleviate DDC-induced liver fibrosis， with comparable efficacy to total saponins from Astragalus membranaceus， and compared with ASⅠ or CY administered alone， the JYB combination has a significantly better regulatory effect on the serum levels of ALP and TBA.

Objective To investigate the effect and mechanism of miR-155-5p targeting suppressor of cytokine signaling 1(SOCS1)in regulating the Janus kinase 2(JAK2)/signal transducer and activator of transcrip-tion 3(STAT3)signaling pathway in renal injury associated with lupus nephritis(LN).Methods Thirty female MRL-faslpr lupus model mice were randomly divided into five groups(n=6 per group):the model group,the antagomir NC group,the miR-155-5p antagomir group,the miR-155-5p antagomir+shRNA control group,and the miR-155-5p antagomir+SOCS1 shRNA group.The mice were treated with adeno-associated virus vectors carrying miR-155-5p antagomir,antagomir NC,SOCS1 shRNA,or shRNA control.Additionally,six age-matched C57BL/6 mice served as a control group and received an equivalent volume of saline.Serum blood urea nitrogen(BUN)and creatinine(Scr)levels,renal histopathological changes,and the expression levels of miR-155-5p,SOCS1,phosphorylated JAK2(p-JAK2),and phosphorylated STAT3(p-STAT3)in renal tissues were evaluated.Results Compared with the normal group,the model group exhibited significantly elevated levels of BUN,Scr,miR-155-5p,p-JAK2,and p-STAT3 proteins in the kidneys(P<0.01),while the expression level of SOCS1 was markedly reduced(P<0.01).Compared with both the model group and the antagomir NC group,the miR-155-5p antagomir group showed decreased levels of BUN,Scr,miR-155-5p,p-JAK2,and p-STAT3 proteins(P<0.01),along with a significant increase in SOCS1 expression(P<0.01).Similarly,compared with the miR-155-5p antagomir group and the miR-155-5p antagomir+shRNA control group,the miR-155-5p antagomir+SOCS1 shRNA group demon-strated significantly higher levels of BUN,Scr,miR-155-5p,p-JAK2,and p-STAT3 proteins(P<0.01),while SOCS1 expression was notably decreased(P<0.01).Renal pathology analysis revealed that,compared to the normal group,the model group exhibited glomerular atrophy,extensive infiltration of inflammatory cells in the renal tubulointerstitial region,and partial renal tubular necrosis.In contrast,the miR-155-5p antagomir group showed marked improvements in glomerular atrophy,tubular necrosis,and inflammatory cell infiltration compared with the model group and antagomir NC group.Furthermore,compared with the miR-155-5p antagomir group and the miR-155-5p antagomir+shRNA control group,the miR-155-5p antagomir+SOCS1 shRNA group exhibited more severe glomerular atrophy,tubular necrosis,and inflammatory cell infiltration.Conclusion MiR-155-5p exacerbates renal damage in MRL-faslpr lupus model mice by targeting SOCS1,potentially through the activation of the JAK2/STAT3 signaling pathway.

Objective:To investigate the clinical efficacy of strengthening the spleen to nourish the lung in treating stable chronic obstructive pulmonary disease (COPD) with lung and spleen qi deficiency complicated by sarcopenia. Methods:This study was designed as a prospective study. A total of 65 patients with stable COPD and sarcopenia who received treatment at Kunshan Hospital of Chinese Medicine from January 2021 to December 2021 were included in the study. They were randomly divided into a control group and an observation group using the random number table method. The control group ( n = 34) was treated with conventional therapy, while the observation group ( n = 31) was treated with Shenling Baizhu Powder, a traditional Chinese medication based on the principle of strengthening the spleen to nourish the lung, in addition to the conventional therapy given to the control group. Both groups were treated for 1 month. Traditional Chinese medicine syndrome score, pulmonary function, grip strength, walking speed, albumin and prealbumin levels were compared between the two groups. Results:After treatment, the scores of all traditional Chinese medicine syndromes in the observation group were significantly lower than those in the control group (all P < 0.05). Compared with the control group, the levels of forced expiratory volume in the first second (FEV 1)[(1.51 ± 0.27) L vs. (1.32 ± 0.20) L, t = 3.11, P < 0.001 ] and FEV 1/forced vital capacity (FVC) [(57.20 ± 8.41)% vs. (52.89 ± 5.66)%, t = 2.30, P = 0.025] were significantly higher in the observation group. Compared with before treatment, gait speed [(1.07 ± 0.27) m/s vs. (0.90 ± 0.30) m/s, t = 7.66, P < 0.001], grip strength [(20.62 ± 5.07) kg vs. (19.42 ± 5.78) kg, t = 3.55, P < 0.001], albumin [(231.38 ± 49.40) g/L vs. (200.26 ± 65.87) g/L, t = 3.70, P < 0.001] and prealbumin [(39.53 ± 3.45) g/L vs. (35.81 ± 4.46) g/L, t = 4.08, P < 0.001] levels in the observation group were significantly increased after treatment. There were no significant differences in gait speed, grip strength, albumin, and prealbumin levels in the control group before and after treatment (all P > 0.05). Conclusions:The method of strengthening the spleen to nourish the lung shows good clinical efficacy in treating stable COPD with lung and spleen deficiency complicated by sarcopenia, and it has great potential for broader application.

Olfactory diagnosis refers to the method of diagnosing diseases by smelling the odor emitted from the patient's body,secretions and excreta,and the odor of the sick room.It is one of the important diagnostic methods under the guidance of traditional Chinese medicine(TCM)theory,and is included in the"inquiry and olfaction"of TCM.In recent years,there has been rapid development in medical-engineering integration,artificial intelligence,big data,and other interdisciplinary fields.This has been promoting the TCM gradually to develop towards accurate,efficient and personalized medical treatment,which has opened a new era of"Smart TCM".In this paper,the ancient literature related to olfactory diagnosis was systematically reviewed,the developmental characteristics of olfactory diagnosis theories in various periods was sorted out,and the different views of TCM specialists on the odors emitted by the human body in physiological and pathological states was summarized.The paper is to explore the origin of TCM olfactory diagnosis and its periodization,clarify the diagnosis of abnormal odors,corresponding to the nature,etiology and prognosis of the disease,and clarify the development of TCM olfactory diagnosis.It provides a theoretical source and literature basis for promoting the research of"smart olfactory diagnosis of TCM"and facilitating the development of objectivity,standardization and intelligence of olfactory diagnosis in TCM.

Skeletal muscle dysfunction is a common extrapulmonary comorbidity of chronic obstructive pulmonary disease (COPD) and is associated with decreased quality-of-life and survival in patients. The autophagy lysosome pathway is one of the proteolytic systems that significantly affect skeletal muscle structure and function. Intriguingly, both promoting and inhibiting autophagy have been observed to improve COPD skeletal muscle dysfunction, yet the mechanism is unclear. This paper first reviewed the effects of macroautophagy and mitophagy on the structure and function of skeletal muscle in COPD, and then explored the mechanism of autophagy mediating the dysfunction of skeletal muscle in COPD. The results showed that macroautophagy- and mitophagy-related proteins were significantly increased in COPD skeletal muscle. Promoting macroautophagy in COPD improves myogenesis and replication capacity of muscle satellite cells, while inhibiting macroautophagy in COPD myotubes increases their diameters. Mitophagy helps to maintain mitochondrial homeostasis by removing impaired mitochondria in COPD. Autophagy is a promising target for improving COPD skeletal muscle dysfunction, and further research should be conducted to elucidate the specific mechanisms by which autophagy mediates COPD skeletal muscle dysfunction, with the aim of enhancing our understanding in this field.
Pulmonary Disease, Chronic Obstructive/physiopathology* ; Autophagy/physiology* ; Humans ; Muscle, Skeletal/pathology* ; Mitophagy ; Animals ; Mitochondria/metabolism* ; Lysosomes

Periodontitis is a common oral disease characterized by progressive alveolar bone resorption and inflammation of the periodontal tissues. Dimethyl fumarate (DMF) has been used in the treatment of various immune-inflammatory diseases due to its excellent anti-inflammatory and antioxidant functions. Here, we investigated for the first time the therapeutic effect of DMF on periodontitis. In vivo studies showed that DMF significantly inhibited periodontal destruction, enhanced mitophagy, and decreased the M1/M2 macrophage ratio. In vitro studies showed that DMF inhibited macrophage polarization toward M1 macrophages and promoted polarization toward M2 macrophages, with improved mitochondrial function, inhibited oxidative stress, and increased mitophagy in RAW 264.7 cells. Furthermore, DMF increased intracellular mitochondrial Tu translation elongation factor (TUFM) levels to maintain mitochondrial homeostasis, promoted mitophagy, and modulated macrophage polarization, whereas TUFM knockdown decreased the protective effect of DMF. Finally, mechanistic studies showed that DMF increased intracellular TUFM levels by protecting TUFM from degradation via the ubiquitin-proteasomal degradation pathway. Our results demonstrate for the first time that DMF protects mitochondrial function and inhibits oxidative stress through TUFM-mediated mitophagy in macrophages, resulting in a shift in the balance of macrophage polarization, thereby attenuating periodontitis. Importantly, this study provides new insights into the prevention of periodontitis.
Dimethyl Fumarate/pharmacology* ; Mitophagy/drug effects* ; Animals ; Mice ; Macrophages/metabolism* ; Periodontitis/prevention & control* ; RAW 264.7 Cells ; Oxidative Stress/drug effects* ; Peptide Elongation Factor Tu/metabolism* ; Mice, Inbred C57BL ; Male ; Mitochondria/drug effects*

Cemental tear is a rare and indetectable condition unless obvious clinical signs present with the involvement of surrounding periodontal and periapical tissues. Due to its clinical manifestations similar to common dental issues, such as vertical root fracture, primary endodontic diseases, and periodontal diseases, as well as the low awareness of cemental tear for clinicians, misdiagnosis often occurs. The critical principle for cemental tear treatment is to remove torn fragments, and overlooking fragments leads to futile therapy, which could deteriorate the conditions of the affected teeth. Therefore, accurate diagnosis and subsequent appropriate interventions are vital for managing cemental tear. Novel diagnostic tools, including cone-beam computed tomography (CBCT), microscopes, and enamel matrix derivatives, have improved early detection and management, enhancing tooth retention. The implementation of standardized diagnostic criteria and treatment protocols, combined with improved clinical awareness among dental professionals, serves to mitigate risks of diagnostic errors and suboptimal therapeutic interventions. This expert consensus reviewed the epidemiology, pathogenesis, potential predisposing factors, clinical manifestations, diagnosis, differential diagnosis, treatment, and prognosis of cemental tear, aiming to provide a clinical guideline and facilitate clinicians to have a better understanding of cemental tear.
Humans ; Dental Cementum/injuries* ; Consensus ; Diagnosis, Differential ; Cone-Beam Computed Tomography ; Tooth Fractures/therapy*