Organ transplantation is a crucial approach for saving patients with end-stage organ failure. However, transplant organs are frequently subjected to various pathological insults, such as ischemia-reperfusion injury and rejection during the processes of procurement, preservation and revascularization, which severely compromise graft survival and function. Endothelial dysfunction represents a core determinant of graft function and transplant outcomes. Factors including ischemia-reperfusion injury, rejection, immunosuppressive drug use and cytomegalovirus infection drive endothelial dysregulation through diverse acute or chronic mechanisms. In the acute phase, endothelial injury contributes to delayed graft function and acute rejection, while in the chronic phase, it manifests as graft vasculopathy, ultimately leading to graft failure. This review summarizes the key pathophysiological mechanisms underlying endothelial injury in organ transplantation, its clinical consequences and preventive and therapeutic strategies, aiming to provide insights for improving endothelial function and transplant outcomes.

Objective To explore the differences in peripheral immunological characteristics between acute rejection (AR) and acute kidney injury (AKI) after kidney transplantation. Methods Single-cell RNA sequencing (scRNA-seq) was performed on peripheral blood mononuclear cells from 3 patients with acute T cell-mediated rejection (TCMR) (AR group) and 4 patients with acute tubular injury (AKI group). The data from 3 patients with stable renal function after transplantation and 5 healthy individuals in the public database were integrated to draw a peripheral immune cell map and conduct functional enrichment analysis. Results TCMR was characterized by significant expansion and activation of T cells and B cells; AKI was dominated by significant expansion of monocytes. Although both had CD8⁺ effector memory T cells and mucosal associated invariant T cells mobilization, the activation intensity of T cell antigen presentation, B cell signaling and rejection pathways in TCMR was higher than that in AKI. Conclusions This study is the first to use scRNA-seq technology to compare the peripheral immunological differences between AR and AKI, revealing the differential characteristics of peripheral immune activation between TCMR and AKI, and providing a basis for developing non-invasive identification methods based on peripheral immune maps.

Based on the concept of "regulating the five zang organs and harmonizing the spleen and stomach"， globus hystericus is believed to originate from dysfunction of the five zang organs and disharmony of the spleen and stomach. Treatment primarily focuses on regulating the spleen and stomach while also considering other affected organs， with a self-prescribed Anpiwei Jingyan Formula （安脾胃经验方） for harmonizing the spleen and stomach as the foundational treatment. Additionally， syndrome-based modifications are applied according to imbalances in the heart， lung， kidney， or liver. For heart-yang deficiency， modified Linggui Zhugan Decoction （苓桂术甘汤） could be combined； for heart-yin deficiency， modified Tianwang Buxin Pill （天王补心丹） could be combined. For lung failing to disperse and descend and fluid retention， modified Sanao Decoction （三拗汤） could be combined； for lung and stomach yin deficiency， modified Shashen Maidong Decoction （沙参麦冬汤） could be combined. For kidney-yang deficiency with ascending counterflow of cold water， modified Jingui Shensi Pill （金匮肾气丸） could be combined； for kidney-yin deficiency， modified Liuwei Dihuang Pill （六味地黄丸） could be combined. For liver constraint and spleen deficiency， modified Sini Powder （四逆散） could be combined； for liver-yin deficiency or liver stagnation transforming into fire and attacking the stomach， modified Yiguan Decoction （一贯煎） could be combined.

Based on the traditional Chinese medicine theory that "all pain， itching， and sores are related to the heart"， this paper proposes treating recurrent aphthous ulcers from the perspective of the heart. It suggests that excessive heart fire and tissue erosion due to flaming fire in the heart meridian constitute the core pathogenesis of this condition. Hyperactive heart fire is identified as the key pathogenic factor， while heart yin deficiency， obstruction of the heart collaterals， and malnourishment of the heart spirit are considered significant contributing factors. Clinically， the treatment follows the principle of clearing heart fire as the main strategy， supplemented by nourishing yin， activating collaterals， and calming the spirit. The self-formulated Qingxin Yuchuang Formulation （清心愈疮方） serves as the base prescription， with flexible modifications incorporating the Yuyin Formulation （育阴方）， Huoxue Formulation （活血方）， and Yu'an Formulation （郁安方） to address specific syndromes involving heart yin deficiency， collateral blockage， and emotional disturbance.

Objective To explore the action mechanism of Bruton's tyrosine kinase (BTK) inhibitor zanubrutinib on renal fibrosis after renal ischemia-reperfusion injury (RIRI). Methods C57BL/6 mice were randomly divided into sham operation group, modeling group and modeling + zanubrutinib treatment group (zanubrutinib group), with 5 mice in each group. The groups underwent sham operation, RIRI modeling and RIRI modeling + zanubrutinib (5 mg/kg) treatment, respectively. Tissues were collected after 21 days. The morphological changes of the kidneys, histopathological changes, levels of M1 macrophages in the kidneys, inflammatory responses in the kidneys, and the expression of related inflammatory signaling pathways of macrophages induced by lipopolysaccharide(LPS) + interferon(IFN)-γ in vitro after lentivirus transfection were observed. Results Compared with the sham operation group, the kidneys of the modeling group mice shrank, the ratio of unilateral kidney weight to mouse body weight decreased, renal tubular interstitial fibrosis worsened, and the expression of α-smooth muscle actin (α-SMA) and type I collagen in the kidneys increased. The expression of F4/80 and CD86 in the kidneys increased, the lumen of the renal proximal convoluted tubules was significantly dilated, cellular debris accumulated in the lumen and inflammatory cell infiltration occurred, and the messenger RNA (mRNA) levels of CD86, tumor necrosis factor (TNF)-α, interleukin (IL)-6, inducible nitric oxide synthase (iNOS) and IL-1β in the kidneys increased. Compared with the modeling group, the kidneys of the zanubrutinib group mice enlarged after RIRI, the ratio of unilateral kidney weight to mouse body weight increased, renal tubular interstitial fibrosis was alleviated, and the expression of α-SMA and type I collagen in the kidneys decreased. The expression of F4/80 and CD86 in the kidneys decreased, the number of CD45⁺ lymphocytes and CD11b⁺ F4/80⁺ macrophages in the kidneys decreased, the infiltration of CD11b⁺ F4/80⁺ and CD86⁺ macrophages in the damaged tissue decreased, the degree of renal inflammatory pathological changes was milder, and the mRNA levels of CD86, TNF-α, IL-6, iNOS and IL-1β in the kidneys decreased. In vitro experiments using LPS+IFN-γ to induce M1-type macrophages found that the phosphorylation levels of phosphatidylinositol-3-kinase (PI3K), protein kinase B (Akt), and nuclear factor (NF)-κB increased, while the phosphorylation levels decreased after BTK knockdown, indicating that BTK knockdown may inhibit the PI3K/Akt and NF-κB related inflammatory signaling pathways, thereby reducing the pro-inflammatory effects of LPS+IFN-γ induced M1-type macrophages. Conclusions Zanubrutinib may alleviate renal fibrosis after RIRI by inhibiting the PI3K/Akt and NF-κB related inflammatory signaling pathways, reducing the infiltration of M1 macrophages and the expression of related inflammatory factors, providing potential evidence for its clinical application.

This article summarized Professor Liu Qiquan's clinical experience in the treatment of acne from the perspective of"internal retention and stagnation of heat pathogen".Professor Liu believes that the core pathogenesis of acne lies in the internal retention and stagnation of heat pathogen,which manifests as external skin inflammation,with the primary focus being on the heat pathogen.With the pathogen inside the body,the progress of disease and syndrome is related to"toxin,depression,blood stasis and deficiency".At the same time,the disease is also closely related to the dysfunction of the five-zang organs.Professor Liu points out that"to resist the outside,one must first settle the inside",and treats acne from the five internal organs.Based on the idea of"internal retention and stagnation of heat pathogen",according to the symptoms of the patients,the comprehensive use of methods to guide the treatment,such as penetrating turbidity,removing pathogenic factors and detoxifying heat,promoting qi and dispersing stagnant heat,cooling collaterals to control blood and breaking stasis heat,and restraining qi,softening yin and supporting deficiency heat,has been proved to have a good clinical effect.One medical case was attached as evidence.

This article summarized Professor Liu Qiquan's clinical experience in the treatment of acne from the perspective of"internal retention and stagnation of heat pathogen".Professor Liu believes that the core pathogenesis of acne lies in the internal retention and stagnation of heat pathogen,which manifests as external skin inflammation,with the primary focus being on the heat pathogen.With the pathogen inside the body,the progress of disease and syndrome is related to"toxin,depression,blood stasis and deficiency".At the same time,the disease is also closely related to the dysfunction of the five-zang organs.Professor Liu points out that"to resist the outside,one must first settle the inside",and treats acne from the five internal organs.Based on the idea of"internal retention and stagnation of heat pathogen",according to the symptoms of the patients,the comprehensive use of methods to guide the treatment,such as penetrating turbidity,removing pathogenic factors and detoxifying heat,promoting qi and dispersing stagnant heat,cooling collaterals to control blood and breaking stasis heat,and restraining qi,softening yin and supporting deficiency heat,has been proved to have a good clinical effect.One medical case was attached as evidence.

Objective To explore the correlation between helicobacter pylori(Hp)infection and inflam-matory factors,as well as its association with the progression of liver fibrosis in patients with metabolically associ-ated fatty liver disease(MAFLD)and type 2 diabetes mellitus(T2DM).Methods A total of 300 patients diag-nosed with MAFLD and T2DM who were admitted to the Hepatology Department of Hebei Hospital of Traditional Chinese Medicine between April 2023 and March 2024 were recruited.Based on Hp infection status,these patients were classified into an Hp-positive group and an Hp-negative group.Subsequently,the clinical data,inflammatory factors,and liver fibrosis indices of the two groups were comprehensively compared.Furthermore,the patients in the Hp-positive group were randomly assigned to an intervention group and a control group.The intervention group received standard Hp eradication therapy,whereas the control group was administered placebo therapy.Pearson correlation analysis was employed to investigate the associations among Hp infection,inflammatory factors,and liver fibrosis indices.Binary logistic regression analysis was utilized to identify the independent risk factors influencing the progression of liver fibrosis.Results In both the Hp-positive and Hp-negative groups,parameters including age,fasting blood glucose(FPG),glycosylated hemoglobin(HbA1c),total bilirubin(TBIL),direct bilirubin(DBIL),indirect bilirubin(IBIL),tumor necrosis factor-α(TNF-α),and interleukin-6(IL-6),along with C-reactive protein(CRP)and liver stiffness measurement(LSM),were meticulously measured.Statistical analysis revealed that the differences in these parameters between the two groups were significant(P<0.05).Specifically,within the experimental setup,the levels of TNF-α,IL-6,CRP,and LSM in the intervention group were notably lower than those in the control group(P<0.05).Pearson correlation analysis was employed to explore the relation-ships among variables,and the results indicated a positive correlation between the Hp detection value(DPM)and the levels of TNF-α,IL-6,CRP,and LSM(P<0.05).Furthermore,binary logistic regression analysis was con-ducted to identify independent risk factors.The findings demonstrated that positive Hp infection,elevated TNF-α,elevated IL-6,and elevated CRP were independent risk factors for the progression of liver fibrosis(P<0.05).To evaluate the diagnostic performance,the receiver operating characteristic(ROC)curve analysis was carried out.The areas under the curve(AUC)for HP infection,TNF-α,IL-6,and CRP were 0.800,0.786,0.769,and 0.783,respectively.These values were significantly lower than the AUC of 0.896 obtained from the combined detection(P<0.05).Conclusions In MAFLD patients with T2DM,DPM is closely associated with inflammatory factors(such as TNF-α,IL-6,and CRP)and the advancement of liver fibrosis.The combined detection of these factors holds significant value in predicting the progression of liver fibrosis.It can offer a reliable foundation for the clinical assessment of the risk of liver fibrosis progression.

Objective To explore the correlation between helicobacter pylori(Hp)infection and inflam-matory factors,as well as its association with the progression of liver fibrosis in patients with metabolically associ-ated fatty liver disease(MAFLD)and type 2 diabetes mellitus(T2DM).Methods A total of 300 patients diag-nosed with MAFLD and T2DM who were admitted to the Hepatology Department of Hebei Hospital of Traditional Chinese Medicine between April 2023 and March 2024 were recruited.Based on Hp infection status,these patients were classified into an Hp-positive group and an Hp-negative group.Subsequently,the clinical data,inflammatory factors,and liver fibrosis indices of the two groups were comprehensively compared.Furthermore,the patients in the Hp-positive group were randomly assigned to an intervention group and a control group.The intervention group received standard Hp eradication therapy,whereas the control group was administered placebo therapy.Pearson correlation analysis was employed to investigate the associations among Hp infection,inflammatory factors,and liver fibrosis indices.Binary logistic regression analysis was utilized to identify the independent risk factors influencing the progression of liver fibrosis.Results In both the Hp-positive and Hp-negative groups,parameters including age,fasting blood glucose(FPG),glycosylated hemoglobin(HbA1c),total bilirubin(TBIL),direct bilirubin(DBIL),indirect bilirubin(IBIL),tumor necrosis factor-α(TNF-α),and interleukin-6(IL-6),along with C-reactive protein(CRP)and liver stiffness measurement(LSM),were meticulously measured.Statistical analysis revealed that the differences in these parameters between the two groups were significant(P<0.05).Specifically,within the experimental setup,the levels of TNF-α,IL-6,CRP,and LSM in the intervention group were notably lower than those in the control group(P<0.05).Pearson correlation analysis was employed to explore the relation-ships among variables,and the results indicated a positive correlation between the Hp detection value(DPM)and the levels of TNF-α,IL-6,CRP,and LSM(P<0.05).Furthermore,binary logistic regression analysis was con-ducted to identify independent risk factors.The findings demonstrated that positive Hp infection,elevated TNF-α,elevated IL-6,and elevated CRP were independent risk factors for the progression of liver fibrosis(P<0.05).To evaluate the diagnostic performance,the receiver operating characteristic(ROC)curve analysis was carried out.The areas under the curve(AUC)for HP infection,TNF-α,IL-6,and CRP were 0.800,0.786,0.769,and 0.783,respectively.These values were significantly lower than the AUC of 0.896 obtained from the combined detection(P<0.05).Conclusions In MAFLD patients with T2DM,DPM is closely associated with inflammatory factors(such as TNF-α,IL-6,and CRP)and the advancement of liver fibrosis.The combined detection of these factors holds significant value in predicting the progression of liver fibrosis.It can offer a reliable foundation for the clinical assessment of the risk of liver fibrosis progression.

In recent years,the infection of nontuberculous mycobacterium(NTM)has been increasing rapidly,which captivates widespread attention.The infection rate of NTM in kidney transplant recipients is more significantly elevated due to the impact of immunosuppressive drugs and other factors.However,due to the lack of sufficient research evidence,relevant guidelines for the diagnosis and treatment of NTM after kidney transplantation are still lacking.To further standardize the diagnosis and treatment of NTM disease in kidney transplant recipients,and deepen medical practitioners'understanding and diagnosis and treatment of NTM disease in organ transplantation in China,Branch of Organ Transplantation of Chinese Medical Association organized relevant experts to formulate this guideline by referring to the latest edition of"An official ATS/IDSA statement:diagnosis,treatment,and prevention of nontuberculous mycobacterial diseases","Expert Consensus on the Diagnosis and Treatment of Nontuberculous Mycobacterial Disease",and"Technical Specification for Clinical Diagnosis and Treatment of Nontuberculous Mycobacteria in Organ Transplant Recipients(2019 Edition)",and considering the characteristics of kidney transplant recipients.