Objective To discuss the potential mechanisms by which programmed cell death(PCD)might contribute to the pathogenesis of diabetic kidney disease(DKD).Methods Retrieve the datasets GSE30529 and GSE30122 from the Gene Expression Omnibus database and analyze them to obtain differentially expressed genes(DEGs)associated with DKD.Utilize the Gene Set Enrichment Analysis website,the ferroptosis database,and the autophagy database,along with relevant literature,to identify genes associated with apoptosis,necroptosis,pyroptosis,autophagy,and ferroptosis.Cross-reference these genes with the DKD DEGs to identify PCD-related genes that are differentially expressed in DKD.Perform Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathway enrichment analyses to explore the biological functions and potential pathways of the core genes.Conduct a protein-protein interaction network analysis to examine the interaction relationships of the target genes,and use the CytoHubba plugin in Cytoscape to screen for Hub genes.Results In the GSE30529 dataset,a total of 460 DEGs were identified,while the GSE30122 dataset yielded 992 DEGs.After merging and removing duplicates,932 DEGs were obtained.By intersecting these DEGs with PCD-related genes,61 apoptosis-related genes,7 necroptosis-related genes,39 pyroptosis-related genes,18 autophagy-related genes,and 16 ferroptosis-related genes associated with DKD were identified.The KEGG analysis results indicated that the DEGs related to apoptosis,necroptosis,pyroptosis,and autophagy in PCD were primarily enriched in pathways associated with diabetic complications,including the AGE-RAGE,IL-17,NF-κB,and TNF signaling pathways.In contrast,DEGs related to ferroptosis were mainly enriched in the fatty acid degradation pathway.GO enrichment analysis revealed that the biological processes of the differentially expressed PCD related genes in DKD were primarily involved in the regulation of signals such as NF-κB-inducing kinase/NF-κB,IL-1,and IL-17.Conclusions Differentially expressed PCD-related genes in DKD are mainly enriched in related signal pathways such as AGE-RAGE,IL-17,NF-κB and TNF,suggesting a critical role of PCD in the pathogenesis of DKD.

Preeclampsia(PE)is a severe pregnancy complication that poses significant risks to maternal and fetal health,and its pathogenesis remains unclear.Recent studies have shown that lactate dehydrogenase(LDH),a key enzyme in glycolysis,plays a piv-otal role in the development and progression of PE.This article reviews the abnormal changes in the levels of LDH and its isozymes in serum and placental tissue and their impact on the pathogenesis of PE and analyzes the molecular mechanisms by which LDH subunits contribute to placental dysfunction through multiple pathways including hypoxia,inflammation,autophagy dysregulation,and cellular damage.In addition,this article discusses the role of lactate,a metabolic product of LDH activity,in the pathogenesis of PE.LDH can be used as a potential biomarker for PE,and the regulation of non-metabolic functions and metabolic reprogramming mediated by LDH provide new targets for the prevention and treatment of PE.

Objective To discuss the potential mechanisms by which programmed cell death(PCD)might contribute to the pathogenesis of diabetic kidney disease(DKD).Methods Retrieve the datasets GSE30529 and GSE30122 from the Gene Expression Omnibus database and analyze them to obtain differentially expressed genes(DEGs)associated with DKD.Utilize the Gene Set Enrichment Analysis website,the ferroptosis database,and the autophagy database,along with relevant literature,to identify genes associated with apoptosis,necroptosis,pyroptosis,autophagy,and ferroptosis.Cross-reference these genes with the DKD DEGs to identify PCD-related genes that are differentially expressed in DKD.Perform Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathway enrichment analyses to explore the biological functions and potential pathways of the core genes.Conduct a protein-protein interaction network analysis to examine the interaction relationships of the target genes,and use the CytoHubba plugin in Cytoscape to screen for Hub genes.Results In the GSE30529 dataset,a total of 460 DEGs were identified,while the GSE30122 dataset yielded 992 DEGs.After merging and removing duplicates,932 DEGs were obtained.By intersecting these DEGs with PCD-related genes,61 apoptosis-related genes,7 necroptosis-related genes,39 pyroptosis-related genes,18 autophagy-related genes,and 16 ferroptosis-related genes associated with DKD were identified.The KEGG analysis results indicated that the DEGs related to apoptosis,necroptosis,pyroptosis,and autophagy in PCD were primarily enriched in pathways associated with diabetic complications,including the AGE-RAGE,IL-17,NF-κB,and TNF signaling pathways.In contrast,DEGs related to ferroptosis were mainly enriched in the fatty acid degradation pathway.GO enrichment analysis revealed that the biological processes of the differentially expressed PCD related genes in DKD were primarily involved in the regulation of signals such as NF-κB-inducing kinase/NF-κB,IL-1,and IL-17.Conclusions Differentially expressed PCD-related genes in DKD are mainly enriched in related signal pathways such as AGE-RAGE,IL-17,NF-κB and TNF,suggesting a critical role of PCD in the pathogenesis of DKD.

Objective:To investigate the effect of a breathing pattern intervention (RPI) on the oral feeding of pre-term infants with suck-swallow-breath (SSwB) coordination disorder.Methods:Sixty pre-term infants with SSwB coordination disorder were divided into an observation group ( n=30) and a control group ( n=30) using a random number table. Both groups were given routine feeding training, including oral exercise intervention, non-nutritive sucking training, and swallowing induction training during nursing, while the observation group was additionally provided with 15 minutes of breathing pattern training once a day, including breathing pattern observation, resistive breathing training prior to eating and passive breathing pattern intervention during eating. Before and after the 7-day intervention, the Pre-term Infant Oral Feeding Readiness Assessment (PIOFRA) was used to evaluate each subject′s oral feeding ability. Rate of transfer (RT), proficiency (PRO), minimum oxygen partial pressure (SaO 2) and SaO 2 fluctuations were also recorded during the feeding process. Results:After 1 week of the intervention, significant improvement was observed in both groups. In the observation group the average RT (2.76±0.36ml/min), PRO, minimum SaO 2, the number of SaO 2 fluctuations, and PIOFRA score (33.28±0.58) were all significantly better than the control group′s averages. Conclusion:Breathing pattern intervention based on routine feeding training can enhance breathing coordination during swallowing and ultimately improve the oral feeding of pre-term infants with SSwB coordination disorders in a relatively short period of time.

OBJECTIVE To discuss the correlation between effectual time and the curative effect in patients with all frequency descending sudden deafness. METHODS According to effectual time,the subjects were divided into first week effectual group and second week effectual group and the curative effect of each group was compared. RESULTS In patients with flat descent sudden deafness, the curative rate of the first week effectual group was higher than that of the second week effectual group, but there was no significant difference between the two groups(χ2=1.599, P =0.206). Meanwhile, the total significant effective rate of the first week effectual group was higher than that of the second week effectual group, without obvious difference between the two groups(χ2=0.124, P =0.725). Furthermore, in patients with total deafness type of sudden deafness, the curative rate of the first week effectual group was higher than that of the second week effectual group, showing no remarkable difference between the two groups(χ2=2.493, P =0.114). Besides, there was no remarkable difference in the comparison of the total significant effective rate (χ2=2.308, P =0.129), which was higher in the first week effectual group than that in the second week effectual group. CONCLUSION The course of treatment should be at least 2 weeks in patients with all frequency descending sudden deafness after onset.

Objective To investigate the establishment of focal cerebral ischemia model in rabbits with the improved suture method.Methods A total of 45 healthy and clean adult New Zealand rabbits were divided into either a sham operation group (n =5) or a model group (n =40) using random number table method before modeling,and the sex was not limited.The self-made head ends of 2-0 fishing lines dipped in paraffin were used as the sutures.The external carotid artery was cut and inserted into a intracranial artery through the internal carotid artery and blocked the origin of middle cerebral artery.The neurological function score was performed after 6 h.The neurological deficit scores ≥2 was successful modeling.The rabbits were killed by anesthesia.The brain slices were stained with 2％ 2,3,5-triphenyl tetrazolium chloride solution.The infarct foci were observed.The diameters of suture head and the depth of suture insertion were compared in the model rabbits with successful modeling,failure,and death in the model group.Results There were 40 rabbits in the model group,six of them died,including 4 died of subarachnoid hemorrhage within 4 h after operation,and 2 died from anesthetic accident.The mortality rate was 15.0％.Seven rabbits failed,mainly because of cerebral vasospasm and the insertion depth of suture was insufficient.Twenty-seven had successful modeling,and the success rate was 67.5％.All the rabbits in the sham operation group survived.The diameter of the suture head and insertion depth in the successful modeling rabbits were compared with the death and failure outcome in rabbits.The difference was statistically significant (diameter:0.52 ± 0.14 mm vs.0.45 ±0.40 mm and 0.58 ±0.17 mm;depth:5.49 ±0.17 cm vs.6.04 ± 0.11 cm and 4.26 ±0.30 cm;all P ＜ 0.05).Conclusions The improved suture method can successfully prepare the focal cerebral ischemia model of middle cerebral artery in rabbits.The method is simple.Its repeatability and practicability are better.

Objective To evaluate the effect of epigallocatechin-3-gallate (EGCG) treatment on the proliferation and osteogenic differentiation of human periodontal ligament cell (hPDLC) and to explore the potential role of EGCG in promoting periodontal hard tissue regeneration.Methods The hPDLC was isolated from periodontal ligament tissue obtained from freshly extracted human teeth.The effect of treatments with various concentrations of EGCG (0 μmol/L,2 μmol/L,4 μmo]/L,6 μmol/L,8 μmol/L and 10 μmol/L) on cell proliferations were determined by cell counting kits (CCK) after 24-,48-and 72-hour-incubations,respectively.Osteogenic differentiation abilities of hPDLCs were assessed by using alkaline phosphatase (ALP) activity tests after 7-and 14-day-incubations,respectively.The mineralized nodules were quantitatively examined and analyzed by using alizarin red staining after 21-day-incubation.The real-time PCR (RT-PCR) assays were conducted fordetecting the expressions of Runt related transcription factor-2 (Runx2),ALP and collagen type Ⅰ (COL Ⅰ) after 7-day-incubation.Results Treatment with 4 μ mol/L EGCG increased hDPLC proliferation at 24 h,while 8 μmol/L or 10 μ mol/L EGCG treatment groups showed inhibiting effects at 24 h and 72 h,respectively.Findings of alizarin redstaining showed orange to red colored extracellular mineralized nodules in all groups.The the A values of 2,4,6,8,10 μ mol/L EGCG groups were 0.119±0.001,0.167±0.003,0.173±0.003,0.110±0.001 and 0.083±0.003,respectively.A values of 2-8 μmol/L EGCG groups were significantly higher than that of the control group,however there was no significant difference of the A values betweenl0 μmol/L EGCG group and the control group (0.077±.0.001).Treatments with 2-10 μmol/L EGCG could significantly increase the mRNA expressions of COL Ⅰ and ALP with the highest values in 4-6 μ mol/L EGCG treatment groups.Although treatments with 4 and 6 μmol/L EGCG both could increase the mRNA expressions of Runx2,the result in 4 μmol/L group was much better than that of 6 μmol/L group.Conclusions Treatment of 4 μmol/L EGCG could promote hPDLC proliferation at early stageand treatments with 4-6 μ mol/L EGCG could significantly promote the osteogenesis of hPDLCs which might play a promising role in periodontal hard tissue regeneration.