ObjectiveTo explore the regulatory effect of Ganluqingwen prescription on inflammation and immunity by observing the clinical efficacy of Ganluqingwen prescription in the treatment of community-acquired pneumonia （CAP）， so as to provide a clinical basis for the treatment of CAP by traditional Chinese medicine （TCM）. MethodsA randomized controlled trial was conducted by selecting patients who were diagnosed with CAP and identified as wind-heat attacking lungs in Xinjiang Uygur Autonomous Region Hospital of TCM from January 2024 to May 2024 and assigning the patients to a control group （treated by western medicine treatment） or an experimental group （treated by Ganluqingwen prescription combined with western medicine）. The data of the enrolled patients before treatment， for three-day treatment， for seven-day treatment， and for 14-day treatment were collected， including basic information， medical history， pneumonia severity index （PSI） classification， and distribution and difference of laboratory and imaging information indexes. The peripheral blood specimens were collected from the patients. and the changes of inflammatory factors in peripheral blood were detected by using enzyme-linked immunosorbent assay （ELISA） reagent kits and flow-type multifactor microarrays to evaluate the clinical safety and efficacy of Ganluqingwen prescription in CAP. ResultsCompared with those in the groups before treatment， the total scores of TCM syndromes significantly decreased in both groups （P<0.05）. Compared with those in the control group after treatment， the total scores of TCM syndromes decreased more significantly in the experimental group （P<0.05）. Compared with the control group after treatment， the experimental group displayed a significantly reduced number of days of fever in patients （P<0.05）. Compared with those in the groups before treatment， the leukocyte， neutrophil counts， C-reactive protein （CRP）， procalcitonin （PCT）， interleukin （IL）-6， alanine aminotransferase （ALT）， aspartate aminotransferase （AST）， creatinine （Cr）， creatine kinase （CK）， and creatine kinase isoenzymes （CK-MB） in both groups decreased （P<0.05） after treatment. Compared with that in the control group after treatment， the decrease of leukocyte， neutrophil counts， CRP， PCT， IL-6， ALT， AST， Cr， CK， and CK-MB was more pronounced in the experimental group （P<0.05）. Compared with those in the group before treatment， the partial pressure of carbon dioxide increased in the experimental group for 3 d of treatment （P<0.05）， and the standard alkali residual， actual alkali residual， standard bicarbonate concentration， and actual bicarbonate concentration increased in the experimental group for 7 d of treatment （P<0.05）. Compared with that in the group before treatment， D-dimer decreased in the control group for 7 d of treatment （P<0.05）. D-dimer and activated partial thromboplastin time （APTT） decreased in the experimental group for 3 d of treatment （P<0.05）， and D-dimer， fibrinogen （FIB）， and APTI significantly decreased in the group for 7 d of treatment （P<0.05）. Compared with the group for 3 d of treatment， the experimental group for 7 d of treatment showed decreased FIB （P<0.05）. Compared with those in the groups before treatment， the levels of inflammatory factors IL-4， IL-10， and IL-13 were elevated in the peripheral blood of the two groups after treatment， and the levels of B lymphocyte chemoattractant （BLC）， interferon gamma-induced protein 10 （IP-10）， tumor necrosis factor-alpha （TNF-α）， interferon-gamma （IFN-γ）， monocyte chemoattractant protein-1 （MCP-1）， CRP， IL-2， IL-6， IL-8， IL-17， IL-22， and IL-23p19 were significantly reduced （P<0.01）. Compared with the control group after treatment， the experimental group exhibited more significant improvement in indexes above （P<0.01）. ConclusionThe group treated by Ganluqingwen prescription combined with western medicine shows more significant effects on reducing total scores of TCM syndromes， lowering the ability of leukocyte and neutrophil counts， decreasing BLC， IP-10， TNF-α， IFN-γ， MCP-1， CRP， IL-2， IL-6， IL-8， IL-17， IL-22， and IL-23p19 in the peripheral blood of the patients， and elevating levels of IL-4， IL-10， and IL-13 than the group treated by western drugs alone.

ObjectiveTo explore the regulatory effect of Ganluqingwen prescription on inflammation and immunity by observing the clinical efficacy of Ganluqingwen prescription in the treatment of community-acquired pneumonia （CAP）， so as to provide a clinical basis for the treatment of CAP by traditional Chinese medicine （TCM）. MethodsA randomized controlled trial was conducted by selecting patients who were diagnosed with CAP and identified as wind-heat attacking lungs in Xinjiang Uygur Autonomous Region Hospital of TCM from January 2024 to May 2024 and assigning the patients to a control group （treated by western medicine treatment） or an experimental group （treated by Ganluqingwen prescription combined with western medicine）. The data of the enrolled patients before treatment， for three-day treatment， for seven-day treatment， and for 14-day treatment were collected， including basic information， medical history， pneumonia severity index （PSI） classification， and distribution and difference of laboratory and imaging information indexes. The peripheral blood specimens were collected from the patients. and the changes of inflammatory factors in peripheral blood were detected by using enzyme-linked immunosorbent assay （ELISA） reagent kits and flow-type multifactor microarrays to evaluate the clinical safety and efficacy of Ganluqingwen prescription in CAP. ResultsCompared with those in the groups before treatment， the total scores of TCM syndromes significantly decreased in both groups （P<0.05）. Compared with those in the control group after treatment， the total scores of TCM syndromes decreased more significantly in the experimental group （P<0.05）. Compared with the control group after treatment， the experimental group displayed a significantly reduced number of days of fever in patients （P<0.05）. Compared with those in the groups before treatment， the leukocyte， neutrophil counts， C-reactive protein （CRP）， procalcitonin （PCT）， interleukin （IL）-6， alanine aminotransferase （ALT）， aspartate aminotransferase （AST）， creatinine （Cr）， creatine kinase （CK）， and creatine kinase isoenzymes （CK-MB） in both groups decreased （P<0.05） after treatment. Compared with that in the control group after treatment， the decrease of leukocyte， neutrophil counts， CRP， PCT， IL-6， ALT， AST， Cr， CK， and CK-MB was more pronounced in the experimental group （P<0.05）. Compared with those in the group before treatment， the partial pressure of carbon dioxide increased in the experimental group for 3 d of treatment （P<0.05）， and the standard alkali residual， actual alkali residual， standard bicarbonate concentration， and actual bicarbonate concentration increased in the experimental group for 7 d of treatment （P<0.05）. Compared with that in the group before treatment， D-dimer decreased in the control group for 7 d of treatment （P<0.05）. D-dimer and activated partial thromboplastin time （APTT） decreased in the experimental group for 3 d of treatment （P<0.05）， and D-dimer， fibrinogen （FIB）， and APTI significantly decreased in the group for 7 d of treatment （P<0.05）. Compared with the group for 3 d of treatment， the experimental group for 7 d of treatment showed decreased FIB （P<0.05）. Compared with those in the groups before treatment， the levels of inflammatory factors IL-4， IL-10， and IL-13 were elevated in the peripheral blood of the two groups after treatment， and the levels of B lymphocyte chemoattractant （BLC）， interferon gamma-induced protein 10 （IP-10）， tumor necrosis factor-alpha （TNF-α）， interferon-gamma （IFN-γ）， monocyte chemoattractant protein-1 （MCP-1）， CRP， IL-2， IL-6， IL-8， IL-17， IL-22， and IL-23p19 were significantly reduced （P<0.01）. Compared with the control group after treatment， the experimental group exhibited more significant improvement in indexes above （P<0.01）. ConclusionThe group treated by Ganluqingwen prescription combined with western medicine shows more significant effects on reducing total scores of TCM syndromes， lowering the ability of leukocyte and neutrophil counts， decreasing BLC， IP-10， TNF-α， IFN-γ， MCP-1， CRP， IL-2， IL-6， IL-8， IL-17， IL-22， and IL-23p19 in the peripheral blood of the patients， and elevating levels of IL-4， IL-10， and IL-13 than the group treated by western drugs alone.

Guided by the theory of spleen-stomach ascending and descending， it is believed that the core pathogenesis of childhood simple obesity lies in the disorder of spleen-stomach ascending and descending， which leads to dysregulation of lipid metabolism. This pathogenesis is also closely associated with other pathological factors， such as deficiency， dampness， phlegm， heat， and blood stasis. Based on this， the basic therapeutic principles of regulating ascending and descending functions and resolving turbidity and lipids are proposed. In clinical practice， childhood simple obesity is divided into three stages for syndrome differentiation and treatment. For overweight stage， it is often attributed to spleen deficiency with failure to ascend clear qi and liver wood overacting on earth， so the treatment focuses on strengthening the spleen， soothing the liver， dispelling dampness， and resolving turbidity， with modified Xiaoyao Powder （逍遥散） combined with Erchen Decoction （二陈汤） as the recommended formula. For obesity stage， it is commonly caused by failure to transportation due to spleen deficiency， hyperactive stomach failing to descend， and phlegm-heat congestion， then the therapeutic strategy involves clearing stomach heat， descending turbidity， eliminating phlegm， and unblocking fu organs， while also regulating the spleen， with self-formulated Qingshen Xiaozhi Decoction （轻身消脂饮）. For severe obesity stage， it is typically linked to spleen deficiency affecting the kidney and interming-ling of phlegm and blood stasis， and the treatment emphasizes warming and tonifying the spleen and kidney， resolving phlegm， and dissipating blood stasis， using modified Fuzi Lizhong Pill （附子理中丸） combined with Guizhi Fuling Pill （桂枝茯苓丸）.

Cell death is a fundamental phenomenon for organisms to maintain their basic morphology.When a pathogen infects a cell,the process of programmed cell death is activated,the lysed cells carrying the pathogen ac-tivate the immune response of the organism in the process of removing infected cells,thus exerting immune de-fense.The molecular mechanisms of the 4 types of cell death modes apoptosis,pyroptosis,necroptosis and pan-apoptosis as well as their effects on innate immune defense against microbial infections were mainly elaborated in the article,the interactions among the different programmed cell death pathways were briefly interpreted so as to provide new ideas for further study of pathogenic mechanisms of infectious diseases.

Radiotherapy-induced late effects(RILE)or delayed reactions have significant impacts on patients'long-term quality of life.However,current understanding of their developmental mechanisms remains limited,with a lack of effective risk prediction models and preventive interventions.Radiobiological studies and radiation-induced senescence models have revealed that radiotherapy can alter the epigenetic characteristics in late-responding tissue cells,leading to derepression of retrotransposable elements(particularly endogenous retroviral elements),subsequent activation of cytoplasmic nucleic acid sensor systems(cGAS-STING,MDA5/RIG-I-MAVS)and type Ⅰ interferon-mediated immune-inflammatory responses.This review summarized relevant research findings,proposing that the autoimmune-like inflammatory response induced by the'radiotherapy-epigenetic alteration-retrotransposable element activation'cascade is an underinvestigated mechanistic basis in the development of RILE.Constructing risk prediction models for late effects based on epigenetic signatures,cell type,and radiation dose,along with developing strategies to epigenetically suppress retrotransposable element expression,holds promise for preventing or mitigating RILE.

Cell death is a fundamental phenomenon for organisms to maintain their basic morphology.When a pathogen infects a cell,the process of programmed cell death is activated,the lysed cells carrying the pathogen ac-tivate the immune response of the organism in the process of removing infected cells,thus exerting immune de-fense.The molecular mechanisms of the 4 types of cell death modes apoptosis,pyroptosis,necroptosis and pan-apoptosis as well as their effects on innate immune defense against microbial infections were mainly elaborated in the article,the interactions among the different programmed cell death pathways were briefly interpreted so as to provide new ideas for further study of pathogenic mechanisms of infectious diseases.

Radiotherapy-induced late effects(RILE)or delayed reactions have significant impacts on patients'long-term quality of life.However,current understanding of their developmental mechanisms remains limited,with a lack of effective risk prediction models and preventive interventions.Radiobiological studies and radiation-induced senescence models have revealed that radiotherapy can alter the epigenetic characteristics in late-responding tissue cells,leading to derepression of retrotransposable elements(particularly endogenous retroviral elements),subsequent activation of cytoplasmic nucleic acid sensor systems(cGAS-STING,MDA5/RIG-I-MAVS)and type Ⅰ interferon-mediated immune-inflammatory responses.This review summarized relevant research findings,proposing that the autoimmune-like inflammatory response induced by the'radiotherapy-epigenetic alteration-retrotransposable element activation'cascade is an underinvestigated mechanistic basis in the development of RILE.Constructing risk prediction models for late effects based on epigenetic signatures,cell type,and radiation dose,along with developing strategies to epigenetically suppress retrotransposable element expression,holds promise for preventing or mitigating RILE.

Objective:To explore the diagnosis and treatment of adolescence-onset methylenetetrahydrofolate reductase (MTHFR) deficiency.Methods:This was a retrospective case study. Nine patients with adolescence-onset MTHFR deficiency were diagnosed at Peking University First Hospital from January 2016 to December 2022, and followed up for more than 1 year. Their general information, clinical manifestations, laboratory tests, cranial images, MTHFR gene variants, diagnosis, treatment, and outcome were analyzed retrospectively.Results:The 9 patients came from 8 families. They had symptoms at age of 8.0 years to 17.0 years and diagnosed at 9.0 years to 17.5 years. Eight were male and 1 was female. Two patients were brothers, the elder brother developed abnormal gait at 17.0 years; and the younger brother was then diagnosed at 15.0 years of age and treated at the asymptomatic stage, who was 18.0 years old with normal condition during this study. The main manifestations of the 8 symptomatic patients included progressive dyskinesia and spastic paralysis of the lower limbs, with or without intellectual decline, cognitive impairment and behavioral abnormalities. Totally, 15 variants of MTHFR gene were identified in the 9 patients, including 8 novel variants. Five patients had brain image abnormalities. Increased plasma total homocysteine level (65-221 μmol/L) was found in all patients, and decreased to 20-70 μmol/L after treatment with betaine and calcium folinate. Besides, the 8 symptomatic patients had their behavior and cognitive problems significantly improved, with a legacy of lower limb motor disorders.Conclusions:Late-onset MTHFR deficiency can occur in adolescence. The diagnosis is usually delayed because of non-specific clinical symptoms. The test of blood total homocysteine could be used as a selective screening test. Eight novel varients of MTHFR gene were identified. Timely treatment can improve clinical condition significantly, and pre-symptomatic treatment may prevent brain damage.

Objective:To investigate the clinical features and outcomes of adolescence-onset methylmalonic acidemia (MMA) and explore preventive strategies.Methods:This was a retrospective case analysis of the phenotypes, genotypes and prognoses of adolescence-onset MMA patients. There were 55 patients diagnosed in Peking University First Hospital from January 2002 to June 2023, the data of symptoms, signs, laboratory results, gene variations, and outcomes was collected. The follow-ups were done through WeChat, telephone, or clinic visits every 3 to 6 months.Results:Among the 55 patients, 31 were males and 24 were females. The age of onset was 12 years old (range 10-18 years old). They visited clinics at Tanner stages 2 to 5 with typical secondary sexual characteristics. Nine cases (16%) were trigged by infection and 5 cases (9%) were triggered by insidious exercises. The period from onset to diagnosis was between 2 months and 6 years. Forty-five cases (82%) had neuropsychiatric symptoms as the main symptoms, followed by cardiovascular symptoms in 12 cases (22%), kidney damage in 7 cases (13%), and eye disease in 12 cases (22%). Fifty-four cases (98%) had the biochemical characteristics of methylmalonic acidemia combined with homocysteinemia, and 1 case (2%) had the isolated methylmalonic acidemia. Genetic diagnosis was obtained in 54 cases, with 20 variants identified in MMACHC gene and 2 in MMUT gene. In 53 children with MMACHC gene mutation,1 case had dual gene variants of PRDX1 and MMACHC, with 105 alleles. The top 5 frequent variants in MMACHC were c.482G>A in 39 alleles (37%), c.609G>A in 17 alleles (16%), c.658_660delAAG in 11 alleles (10%), c.80A>G in 10 alleles (10%), c.567dupT and c.394C>T both are 4 alleles (4%). All patients recovered using cobalamin, L-carnitine, betaine, and symptomatic therapy, and 54 patients (98%) returned to school or work.Conclusions:Patients with adolescence-onset MMA may triggered by fatigue or infection. The diagnosis is often delayed due to non-specific symptoms. Metabolic and genetic tests are crucial for a definite diagnosis. Treatment with cobalamin, L-carnitine, and betaine can effectively reverse the prognosis of MMA in adolescence-onset patients.

Acute respiratory tract infection is the most common infectious disease in children, which seriously threatens children′s health.Rapid and accurate etiological diagnosis is of great significance for the clinical treatment and control of these diseases.Pathogen nucleic acid test was applied and became the main method of respiratory tract infection diagnosis for its high sensitivity and specificity.To regulate the application of pathogen nucleic acid amplification test in respiratory tract infection in children, improve the diagnosis level, expert consensus on nucleic acid amplification test of respiratory pathogens in children was prepared to guide the application and promote pathogens diagnosis ability.