Objective To analyze the effect of serum lactate dehydrogenase(LDH)and β2-microglobulin(β2-MG)on therapeutic efficacy of the first-line chemotherapy regimen for Waldenstr?m Macroglobulinemia(WM).Methods Data were collected from 113 WM patients admitted from March 2019 to February 2024.All patients completed the established first-line chemotherapy regimen and were divided into the response group(n=85)and the non-response group(n=28).The general data between the two groups were compared,with a focus on analyzing the risk factors for non-response to first-line chemotherapy in WM patients and evaluating the predictive value of serum LDH and β2-MG for the efficacy of first-line chemotherapy.Result The non-responsive group had a higher risk of prognosis based on International Prognostic Scoring System(IPSS),a higher rate of MYD88 L265P mutation,higher TP53 deletion/mutation ratio,and higher proportion of bone marrow lymphoplasmacytic cells,as well as higher serum LDH and β2-MG expression than the response group(P＜0.01).Multivariate logistic regression analysis revealed that risk factors for non-response to first-line chemotherapy in WM patients included a high-risk prognosis based on IPSS,an increased proportion of bone marrow lymphoplasmacytic cells,and higher rate of MYD88 L265P mutation and TP53 deletion/mutation,as well as elevated serum LDH and β2-MG levels(P＜0.05).The area under the curve of serum LDH and β2-MG for predicting the risk of non-response to first-line chemotherapy in WM patients was 0.796 and 0.783 respectively.Through interaction analysis,serum LDH and β2-MG had a positive interaction effect on non-response to chemotherapy in WM patients.Conclusion The non-response to first-line chemotherapy in WM patients is related to abnormal increase in serum LDH and β2-MG.Pre-chemotherapy detection of LDH and β2-MG level has certain predictive value for the risk of non-response to chemotherapy,and the simultaneous increase of both may lead to a higher risk of non-response to chemotherapy.

Objective To analyze the effect of serum lactate dehydrogenase(LDH)and β2-microglobulin(β2-MG)on therapeutic efficacy of the first-line chemotherapy regimen for Waldenstr?m Macroglobulinemia(WM).Methods Data were collected from 113 WM patients admitted from March 2019 to February 2024.All patients completed the established first-line chemotherapy regimen and were divided into the response group(n=85)and the non-response group(n=28).The general data between the two groups were compared,with a focus on analyzing the risk factors for non-response to first-line chemotherapy in WM patients and evaluating the predictive value of serum LDH and β2-MG for the efficacy of first-line chemotherapy.Result The non-responsive group had a higher risk of prognosis based on International Prognostic Scoring System(IPSS),a higher rate of MYD88 L265P mutation,higher TP53 deletion/mutation ratio,and higher proportion of bone marrow lymphoplasmacytic cells,as well as higher serum LDH and β2-MG expression than the response group(P＜0.01).Multivariate logistic regression analysis revealed that risk factors for non-response to first-line chemotherapy in WM patients included a high-risk prognosis based on IPSS,an increased proportion of bone marrow lymphoplasmacytic cells,and higher rate of MYD88 L265P mutation and TP53 deletion/mutation,as well as elevated serum LDH and β2-MG levels(P＜0.05).The area under the curve of serum LDH and β2-MG for predicting the risk of non-response to first-line chemotherapy in WM patients was 0.796 and 0.783 respectively.Through interaction analysis,serum LDH and β2-MG had a positive interaction effect on non-response to chemotherapy in WM patients.Conclusion The non-response to first-line chemotherapy in WM patients is related to abnormal increase in serum LDH and β2-MG.Pre-chemotherapy detection of LDH and β2-MG level has certain predictive value for the risk of non-response to chemotherapy,and the simultaneous increase of both may lead to a higher risk of non-response to chemotherapy.

A 66-year-old female patient with lung adenocarcinoma was treated with crizotinib [the first-generation anaplastic lymphoma kinase (ALK) inhibitors] 250 mg twice daily. Prior to treatment, the patient's liver and kidney functions were normal. One month after treatment, her serum creatinine (Scr) was 85 μmol/L, and alanine aminotransferase (ALT) was 115 U/L. After discontinuing crizotinib for 10 days, both Scr and ALT returned to normal. One month later, the patient underwent a right lower lobectomy. Crizotinib was restarted postoperatively, and she developed symptoms of lower limb edema and poor appetite. After more than 3 months of treatment, her Scr increased to 129 μmol/L, ALT was 96 U/L, and aspartate aminotransferase (AST) was 83 U/L. Crizotinib was then switched to alectinib (the second-generation ALK inhibitors) 600 mg orally twice daily, and the patient's gastrointestinal symptoms and liver function were rapidly improved. However, her Scr continued to increase gradually (140-150 μmol/L). Renal biopsy pathology indicated IgA nephropathy and acute tubular injury. After 4 months of alectinib treatment, Scr was 174 μmol/L, and the drug was promptly discontinued. One month after discontinuation, Scr decreased to 125 μmol/L. Due to tumor progression, the patient restarted alectinib at a reduced dose (300 mg twice daily). Three months later, Scr increased to 177 μmol/L. Subsequently, alectinib was replaced with lorlatinib (the third-generation ALK inhibitors) 100 mg once daily due to tumor progression. After 6 months of treatment, the tumor condition was controlled, and Scr decreased to 124 μmol/L.

Anticipatory anxiety is a negative emotion that arises when individuals encounter potential threats or uncertainties in the future. It is the core symptom of a variety of anxiety disorders, and is closely associated with the occurrence, severity, treatment outcome, and prognosis of anxiety disorders, which has garnered a growing amount of focus in clinical practice. Nevertheless, scientific research on anticipatory anxiety continues to face obstacles such as unclear pathological mechanisms, the absence of simple and consistent self-assessment tools, and effective interventions. To improve understanding of the role of anticipatory anxiety in the diagnosis and treatment of anxiety disorders, this study reviews pertinent domestic and international literature, and briefly introduces the concept, assessment and measurement, activation paradigm, pathological mechanisms, and interventions of anticipatory anxiety.

Objective:To explore the role of glutathione peroxidase 4 (GPX4)-dependent ferroptosis in diclofenac-induced kidney injury.Methods:Human kidney tubular epithelial cells (HK-2 cells) were cultured and then divided into 3 groups: control group, diclofenac group, and iron death inhibitor ferrostatin-1 (Fer-1) group. The same amount of 1% Fer-1 (final concentration 10 μmol/L) and phosphate buffered saline was respectively added to cells in the Fer-1 group and the other 2 groups. After 48 hours of culture, diclofenac 200 μmol/L was added to cells in the diclofenac group and the Fer-1 group. The cell viability of each group was detected by cell counting kit-8 (CCK-8). The cell cycle, apoptosis and intracellular reactive oxygen species (ROS) levels were detected by flow cytometry. The levels of intracellular iron ion, lactate dehydrogenase (LDH), malondialdehyde (MDA) and GPX4 were detected by enzyme-linked immunosorbent assay. The expression level of GPX4 was detected by Western blotting method.Results:Compared with the control group, the cell viability and G1 phase cell percentage of the diclofenac group were significantly lower, and compared with the diclofenac group, those were significantly higher (all P<0.05). The apoptosis rate of diclofenac group was significantly higher than that of the control group ( P<0.05), but there was no significant difference in apoptosis rate between Fer-1 group and diclofenac group ( P>0.05). Compared with the control group, the intracellular ROS, iron content, LDH, and MDA levels were significantly higherin the diclofenac group, while the expression level of GPX4 was lower (all P<0.05). However, the ROS, iron content, LDH, and MDA levels in the Fer-1 group were lower than those in the diclofenac group, while GPX4 expression was higher than that in the diclofenac group (all P<0.05). Conclusion:Diclofenac can induce ferroptosis in HK-2 cells and inhibiting the ferroptosis can alleviate cell injury, suggesting that GPX4-dependent ferroptosis may be involved in kidney injury induced by diclofenac.

Objective:To explore the role and mechanism of serum response factor (SRF) and lncRNA FGD5-AS1 in lung adenocarcinoma (LUAD).Methods:The plasma and tissue wax of LUAD patients treated in Tangshan People's Hospital from 2020 to 2022 and the plasma of healthy people were collected. The expression of SRF in LUAD tissues and cells, and the expression of lncRNA FGD5-AS1 in LUAD tissues, plasma and cells were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The expression levels of SRF and lncRNA FGD5-AS1 in LUAD tissue microarray were detected by immunohistochemistry and in situ hybridization. LUAD cells A549, H1299 and H1975 were cultured in vitro and divided into si-NC and si-SRF groups, si-NC and si-lncRNA FGD5-AS1 groups, pcDNA3.1 and lncRNA FGD5-AS1 groups, si-NC+pcDNA3.1/si-SRF+pcDNA3.1/si-SRF+lncRNA FGD5-AS1 groups. The effects of the above groups on the proliferation, invasion and migration of LUAD cells were detected by CCK-8, cloning formation, EdU, Transwell and scratch test. The JASPAR database was used to predict the downstream lncRNA FGD5-AS1 that can be regulated by SRF; double luciferase experiment, chromatin Immunoprecipitation (CHIP) and electrophoretic mobility shift assay (EMSA) experiment were used to verify the regulatory effect between SRF and lncRNA FGD5-AS1, and the subcutaneous tumorigenesis experiment in nude mice was used to detect the effects of cells that stably knock down SRF and stably overexpress lncRNA FGD5-AS1 on the growth of transplanted tumors. Results:The results of immunohistochemistry showed that the mean optical density of SRF in LUAD tissues (1.49±0.33) was higher than that in adjacent tissues (1.00±0.00, P＜0.001). The expression level of SRF in paraffin tissues of LUAD patients was higher than that in normal tissues adjacent to cancer ( P=0.037). CCK-8, cloning, scratch and Transwell experiments showed that knockdown SRF could inhibit the proliferation, migration and invasion of A549 and H1299 cells, respectively. [For A549 cells: The clone formation count, migration count, invasion count, and 48-h migration distance ratio were (233.70±18.50), (808.70±6.11), (489.70±53.00), and 1.00±0.03, respectively, in the si-NC group; and (131.30±22.50), (403.00±9.54), (372.70±26.27), and 2.14±0.09, respectively, in the si-SRF group. For H1299 cells: The clone formation count, migration count, invasion count, and 48-h migration distance ratio were (194.30±20.98), (988.70±64.52), (907.70±67.02), and 1.00±0.05, respectively, in the si-NC group; and (137.70±7.77), (665.70±157.10), (565.70±67.01), and 1.52±0.03, respectively, in the si-SRF group. All comparisons showed statistically significant differences ( P＜0.05)] JASPAR database prediction shows that SRF and lncRNA FGD5-AS1 have binding site. The double luciferase experiment, CHIP and EMSA experiments showed that SRF could regulate lncRNA FGD5-AS1. In situ hybridization showed that the mean optical density of lncRNA FGD5-AS1 in tissue microarray of LUAD patients (1.28±0.31) was higher than that in adjacent tissues (1.00±0.00, P＜0.001). The results of qRT-PCR experiment showed that the expression level of lncRNA FGD5-AS1 in wax tissues of LUAD patients was higher than that in normal tissues adjacent to cancer ( P=0.017). The expression level of lncRNA FGD5-AS1 in plasma of LUAD patients (3.48±2.62) was higher than that of healthy people (1.02±0.03, P＜0.001). CCK-8, cloning, EDU, scratch and Transwell experiments showed that overexpression of lncRNA FGD5-AS1 could promote cell proliferation [For A549 cells: The clone formation count, EdU-positive cell count, invasion count, and 48-h migration distance ratio were (22.67±5.86), (1.00±0.09), (135.70±13.20), and 0.35±0.02, respectively, in the pcDNA3.1 group; and (46.33±9.07), (1.65±0.10), (205.00±13.23), and 0.20±0.01, respectively, in the FGD5-AS1-overexpressing group. All comparisons showed statistically significant differences ( P＜0.05)], migration and invasion and vice versa [For H1975 cells: The clone formation count, EdU-positive cell count, invasion count, and 48-h migration distance ratio were (75.33±4.16), (1.00±0.02), (258.70±45.79), and 0.18±0.01, respectively, in the NC group; and (37.00±4.00), (0.52±0.07), (130.70±9.07), and 0.53±0.04, respectively, in the lncRNA FGD5-AS1 knockdown group (si-lncRNA FGD5-AS1 group). All comparisons showed statistically significant differences ( P＜0.05)]. Overexpression of lncRNA FGD5-AS1 could rescue the effect of knockdown SRF on the proliferation, migration and invasion of A549 and H1299 cells. The results of subcutaneous tumorigenesis experiment in nude mice indicated that the tumorigenicity of LUAD cells stably knockdown SRF was weakened and vice versa. Conclusion:SRF can promote the progress of LUAD by regulating lncRNA FGD5-AS1.

Objective:To construct a frailty prediction model for elderly diabetic inpatients based on machine learning algorithms and evaluate the predictive performance of the model, providing a basis for the early identification and prevention of frailty in elderly diabetic patients.Methods:A convenience sampling method was used to select 380 elderly diabetic inpatients from the Endocrinology Department and Geriatrics Department of two ClassⅢ Grade A hospitals in Jingzhou, admitted from March to October 2023. Binary Logistic regression analysis was used to identify the factors influencing frailty in elderly diabetic patients. The prediction models, including random forest, support vector machine, and K-nearest neighbors algorithms, were constructed using Python 3.8.2 and sklearn library functions. The accuracy, precision, recall, F1 score, and area under the receiver operating characteristic curve ( AUC) for each model were evaluated. Results:Factors such as comorbidity, polypharmacy, self-management ability of diabetes, nutritional status, 25-hydroxyvitamin D 3, duration of diabetes, and activities of daily living were identified as risk factors for frailty in elderly diabetic patients ( P<0.05). The AUC for the random forest, support vector machine, and K-nearest neighbors prediction models were 0.85, 0.83, and 0.79, respectively. Conclusions:The constructed random forest model is the optimal model, capable of effectively predicting the risk of frailty in elderly diabetic inpatients, which is beneficial for healthcare professionals to early screen high-risk populations for frailty.

Kidney disease constitutes a significant global public health issue,with its associated healthcare burden escalating annually.Lipid metabolism disorders play a crucial role in the onset and progression of various kidney diseases.Given the diversity of lipid species and the complexity of metabolic pathways,traditional research methods often fall short in fully elucidating the intricate roles of lipids in kidney diseases.In this context,lipido-mics,the systematic analysis of lipid molecules and their metabolic alterations in biological samples,emerges as a powerful tool with unique research value and clinical potential.This review summarizes the latest findings in lipido-mics across various kidney diseases and discusses the challenges encountered in clinical application and future research directions.

To investigate the association between neutrophil to lymphocyte ratio (NLR) andestimated glomerular filtration rate (eGFR) in patients with diabetes using large-scale data.

Kidney disease constitutes a significant global public health issue,with its associated healthcare burden escalating annually.Lipid metabolism disorders play a crucial role in the onset and progression of various kidney diseases.Given the diversity of lipid species and the complexity of metabolic pathways,traditional research methods often fall short in fully elucidating the intricate roles of lipids in kidney diseases.In this context,lipido-mics,the systematic analysis of lipid molecules and their metabolic alterations in biological samples,emerges as a powerful tool with unique research value and clinical potential.This review summarizes the latest findings in lipido-mics across various kidney diseases and discusses the challenges encountered in clinical application and future research directions.