It is believed that Shengyang Yiwei Decoction （升阳益胃汤， SYD） is effective in regulating the flow of Qi （气）， and can treat various diseases caused by the disorder of the spleen and stomach Qi. In clinical practice， based on the pathological characteristics of children often having insufficient spleen， and adhering to the principle of treating different diseases with the same method， the focus is placed on the core pathogenesis of spleen and stomach Qi disharmony. We use SYD in various pediatric conditions such as allergic rhinitis， post COVID-19 condition， urethral syndrome， and dysfunctional uterine bleeding in adolescence， and emphasize the treatment is flexibly tailored to the symptoms.

BACKGROUND:Ferroptosis is a programmed cell death caused by iron dependent lipid peroxidation,involving various processes such as iron overload,lipid peroxidation,and endoplasmic reticulum stress.Research has found that ferroptosis is closely related to the occurrence and development of myocardial ischemia-reperfusion injury,and has become a new target and perspective for MIRI treatment.Traditional Chinese medicine has advantages such as multi-target,multi-level,and fewer adverse reactions,and has significant effects in the treatment of myocardial ischemia-reperfusion injury,with a far-reaching impact.OBJECTIVE:Taking ferroptosis as the starting point,to systematically elaborate and summarize the research progress in the modulation of ferroptosis against myocardial ischemia-reperfusion injury by monomers of traditional Chinese medicines such as puerarin,resveratrol,ligustrazine,and astragaloside IV in recent years.METHODS:Using the search terms"iron death,myocardial injury,myocardial ischemia-reperfusion injury,signaling pathways,traditional Chinese medicine monomers,flavonoids,polyphenols,alkaloids,terpenes,quinones"in Chinese and English from January 2013 to June 2024,literature retrieval was performed in the CNKI and PubMed respectively for literature related to ferroptosis,myocardial ischemia-reperfusion injury,and the regulatory mechanism of traditional Chinese medicine monomers.Literature that is not highly correlated,repetitive,or outdated was excluded.A total of 1 524 relevant articles were retrieved,and 76 articles were ultimately included for review.RESULTS AND CONCLUSION:Numerous animal and cell experiments have shown that ferroptosis plays an important role in the occurrence and progression of myocardial ischemia-reperfusion injury.Traditional Chinese medicine monomers such as baicalin,resveratrol,and ligustrazine can regulate iron metabolism,reduce iron deposition,and inhibit ferroptosis in myocardial cells.Pectin,quercetin,and salidroside can improve mitochondrial function,enhance cellular antioxidant capacity,and alleviate myocardial ischemia-reperfusion injury.Traditional Chinese medicine monomers can regulate ferroptosis-related signaling pathways,such as solute carrier family 7 member 11/glutathione peroxidase 4,dihydrolactate dehydrogenase/coenzyme Q10,cyclooxygenase 2/prostaglandin E2,and adenosine monophosphate-activated protein kinase,resist myocardial ischemia-reperfusion injury,and reduce ferroptosis in myocardial cells.

Objective To analyze the health economics of ultra-short wave therapy adjuvant to drug therapy for acute pharyngitis,and to provide a more cost-effective treatment option for clinical management.Methods Seventy patients with acute pharyngitis were randomly divided into a control group(35 cases)and an ultra-short wave group(35 cases).The control group received conventional drug therapy,while the ultra-short wave group received ultra-short wave therapy in addition to conventional drug therapy.The cure rate,treatment duration,direct costs,indirect costs,and total costs were compared between the two groups for clinical efficacy and health economics analysis.Results The cure rate in the ultra-short wave group was significantly higher than that in the control group(P=0.008),while the total treatment cost and treatment duration were significantly re-duced.To achieve the same therapeutic effect,the ultra-short wave group required 129.73 yuan less than the control group.Conclusion Ultra-short wave therapy adjuvant to conventional drug treatment for acute pharyngitis can more rapidly alleviate symptoms,reduce indirect costs due to work absence,without significantly increasing treatment expenses.It is a safe,effective,and economical therapy with higher therapeutic value compared to drug therapy alone,and is worthy of widespread promotion.

Diabetic nephropathy(DN)ranks as a frequent and serious complication in diabetes mellitus,and it's a key factor in chronic kidney disease and end-stage renal disease(ESRD),greatly diminishing the life quality of patients.Presently,the conventional treatment approaches for DN mainly involve strict regulation of blood sugar and pressure,in conjunction with the application of renin-angiotensin-aldosterone system inhibitors.While these therapies can slow down the advancement of DN,they are ineffective in stopping its final development into ESRD.Lately,the involvement of the gut-kidney axis in the development and advancement of DN has attracted growing interest.Individuals suffering from DN show changes in the variety of gut microbiota,which are crucial in the development and management of DN due to metabolic interactions with the host.The goal of this analysis is to explore the fundamental processes of gut microbiota's role in DN and explore treatment approaches focusing on gut microbiota,aiming to offer new perspectives for the clinical handling of DN.

Objective To analyze the health economics of ultra-short wave therapy adjuvant to drug therapy for acute pharyngitis,and to provide a more cost-effective treatment option for clinical management.Methods Seventy patients with acute pharyngitis were randomly divided into a control group(35 cases)and an ultra-short wave group(35 cases).The control group received conventional drug therapy,while the ultra-short wave group received ultra-short wave therapy in addition to conventional drug therapy.The cure rate,treatment duration,direct costs,indirect costs,and total costs were compared between the two groups for clinical efficacy and health economics analysis.Results The cure rate in the ultra-short wave group was significantly higher than that in the control group(P=0.008),while the total treatment cost and treatment duration were significantly re-duced.To achieve the same therapeutic effect,the ultra-short wave group required 129.73 yuan less than the control group.Conclusion Ultra-short wave therapy adjuvant to conventional drug treatment for acute pharyngitis can more rapidly alleviate symptoms,reduce indirect costs due to work absence,without significantly increasing treatment expenses.It is a safe,effective,and economical therapy with higher therapeutic value compared to drug therapy alone,and is worthy of widespread promotion.

Lung adenocarcinoma (LUAD) is a global malignancy with significant chemoresistance impacting patient prognosis. The pro-tumorigenic role of hyaluronan-mediated motility receptor (HMMR) in LUAD is recognized. This study was designed to investigate the underlying mechanisms by which HMMR affects chemoresistance in LUAD. Bioinformatics presented the expression patterns of HMMR in LUAD patients and the association between HMMR levels and patient survival, followed by qRT-PCR to verify HMMR expression in LUAD tissues and cells. Further, bioinformatics was leveraged to identify the signaling pathways enriched by HMMR and its relevance to glycolytic genes, we also analyzed changes in the glycolytic activity of LUAD cells by manipulating HMMR expression. Stemness was evaluated through cell aggregation assays and Western blot, and drug responsiveness was gauged using CCK-8 assays, alongside flow cytometry for apoptosis analysis. HMMR was highly expressed in LUAD tissues and cells, and this overexpression correlated with poorer prognoses in patients. GSEA showed that HMMR was notably enriched in the glycolysis and gluconeogenesis pathways, correlating positively with the expression of key glycolytic genes. Cellular experiments confirmed that HMMR knockdown notably suppressed aerobic glycolysis in LUAD cells. Moreover, overexpression of HMMR could further enhance the stemness and cisplatin resistance of LUAD cells by stimulating glycolysis. In brief, this study has validated that high levels of HMMR in LUAD are predictive of poor patient prognosis, and that overexpression of HMMR can catalyze aerobic glycolysis, thus promoting stemness and chemoresistance in LUAD cells. Thus, HMMR could be a target for improving chemosensitivity in LUAD.

Lung adenocarcinoma (LUAD) is a global malignancy with significant chemoresistance impacting patient prognosis. The pro-tumorigenic role of hyaluronan-mediated motility receptor (HMMR) in LUAD is recognized. This study was designed to investigate the underlying mechanisms by which HMMR affects chemoresistance in LUAD. Bioinformatics presented the expression patterns of HMMR in LUAD patients and the association between HMMR levels and patient survival, followed by qRT-PCR to verify HMMR expression in LUAD tissues and cells. Further, bioinformatics was leveraged to identify the signaling pathways enriched by HMMR and its relevance to glycolytic genes, we also analyzed changes in the glycolytic activity of LUAD cells by manipulating HMMR expression. Stemness was evaluated through cell aggregation assays and Western blot, and drug responsiveness was gauged using CCK-8 assays, alongside flow cytometry for apoptosis analysis. HMMR was highly expressed in LUAD tissues and cells, and this overexpression correlated with poorer prognoses in patients. GSEA showed that HMMR was notably enriched in the glycolysis and gluconeogenesis pathways, correlating positively with the expression of key glycolytic genes. Cellular experiments confirmed that HMMR knockdown notably suppressed aerobic glycolysis in LUAD cells. Moreover, overexpression of HMMR could further enhance the stemness and cisplatin resistance of LUAD cells by stimulating glycolysis. In brief, this study has validated that high levels of HMMR in LUAD are predictive of poor patient prognosis, and that overexpression of HMMR can catalyze aerobic glycolysis, thus promoting stemness and chemoresistance in LUAD cells. Thus, HMMR could be a target for improving chemosensitivity in LUAD.

Diabetic nephropathy(DN)ranks as a frequent and serious complication in diabetes mellitus,and it's a key factor in chronic kidney disease and end-stage renal disease(ESRD),greatly diminishing the life quality of patients.Presently,the conventional treatment approaches for DN mainly involve strict regulation of blood sugar and pressure,in conjunction with the application of renin-angiotensin-aldosterone system inhibitors.While these therapies can slow down the advancement of DN,they are ineffective in stopping its final development into ESRD.Lately,the involvement of the gut-kidney axis in the development and advancement of DN has attracted growing interest.Individuals suffering from DN show changes in the variety of gut microbiota,which are crucial in the development and management of DN due to metabolic interactions with the host.The goal of this analysis is to explore the fundamental processes of gut microbiota's role in DN and explore treatment approaches focusing on gut microbiota,aiming to offer new perspectives for the clinical handling of DN.

Lung adenocarcinoma (LUAD) is a global malignancy with significant chemoresistance impacting patient prognosis. The pro-tumorigenic role of hyaluronan-mediated motility receptor (HMMR) in LUAD is recognized. This study was designed to investigate the underlying mechanisms by which HMMR affects chemoresistance in LUAD. Bioinformatics presented the expression patterns of HMMR in LUAD patients and the association between HMMR levels and patient survival, followed by qRT-PCR to verify HMMR expression in LUAD tissues and cells. Further, bioinformatics was leveraged to identify the signaling pathways enriched by HMMR and its relevance to glycolytic genes, we also analyzed changes in the glycolytic activity of LUAD cells by manipulating HMMR expression. Stemness was evaluated through cell aggregation assays and Western blot, and drug responsiveness was gauged using CCK-8 assays, alongside flow cytometry for apoptosis analysis. HMMR was highly expressed in LUAD tissues and cells, and this overexpression correlated with poorer prognoses in patients. GSEA showed that HMMR was notably enriched in the glycolysis and gluconeogenesis pathways, correlating positively with the expression of key glycolytic genes. Cellular experiments confirmed that HMMR knockdown notably suppressed aerobic glycolysis in LUAD cells. Moreover, overexpression of HMMR could further enhance the stemness and cisplatin resistance of LUAD cells by stimulating glycolysis. In brief, this study has validated that high levels of HMMR in LUAD are predictive of poor patient prognosis, and that overexpression of HMMR can catalyze aerobic glycolysis, thus promoting stemness and chemoresistance in LUAD cells. Thus, HMMR could be a target for improving chemosensitivity in LUAD.

Lung adenocarcinoma (LUAD) is a global malignancy with significant chemoresistance impacting patient prognosis. The pro-tumorigenic role of hyaluronan-mediated motility receptor (HMMR) in LUAD is recognized. This study was designed to investigate the underlying mechanisms by which HMMR affects chemoresistance in LUAD. Bioinformatics presented the expression patterns of HMMR in LUAD patients and the association between HMMR levels and patient survival, followed by qRT-PCR to verify HMMR expression in LUAD tissues and cells. Further, bioinformatics was leveraged to identify the signaling pathways enriched by HMMR and its relevance to glycolytic genes, we also analyzed changes in the glycolytic activity of LUAD cells by manipulating HMMR expression. Stemness was evaluated through cell aggregation assays and Western blot, and drug responsiveness was gauged using CCK-8 assays, alongside flow cytometry for apoptosis analysis. HMMR was highly expressed in LUAD tissues and cells, and this overexpression correlated with poorer prognoses in patients. GSEA showed that HMMR was notably enriched in the glycolysis and gluconeogenesis pathways, correlating positively with the expression of key glycolytic genes. Cellular experiments confirmed that HMMR knockdown notably suppressed aerobic glycolysis in LUAD cells. Moreover, overexpression of HMMR could further enhance the stemness and cisplatin resistance of LUAD cells by stimulating glycolysis. In brief, this study has validated that high levels of HMMR in LUAD are predictive of poor patient prognosis, and that overexpression of HMMR can catalyze aerobic glycolysis, thus promoting stemness and chemoresistance in LUAD cells. Thus, HMMR could be a target for improving chemosensitivity in LUAD.