Objective Sleep is an important physiological process for maintaining normal cognitive functions,but with the accelerated pace and increased work pressure in modern society,sleep deprivation has become a common phenomenon.It has been shown that sleep deprivation interferes with higher cognitive functions such as working memory,but the specific mechanism of its effect is still not completely clear.The present study aimed to systematically investigate the effects of 36 hours of sleep deprivation on the stages of the working memory processing chain and its neural mechanisms through behavioral and event-related potential(ERP)techniques.Methods Using a randomized controlled experimental design,48 healthy adult subjects were recruited and randomly assigned to sleep deprivation and control groups.All subjects completed a 2-back phonological working memory task,and behavioral data(response time and correctness)and ERP data(P2,N2,and P3 component wave amplitudes)were collected at 0 and 36 hours,respectively.The effects of sleep deprivation on working memory behavioral performance and neurophysiological indices were assessed by ANOVA.Results Behavioral results showed that the sleep deprivation group had a significantly longer response time after 36 hours,but no significant decrease in correctness,indicating a decrease in response efficiency but stable accuracy.ERP results showed that P2 amplitude did not change significantly before and after sleep deprivation,indicating that the early perception and categorization stages were limitedly affected by sleep deprivation;whereas,N2 and P3 amplitudes decreased significantly after sleep deprivation,reflecting that later cognitive processing such as conflict monitoring and resource allocation and other late cognitive processing were significantly disturbed.Conclusion Through ERP technology,this study uncovers the phased impact of 36-hour sleep deprivation on the working memory processing chain.The study found that early perceptual and categorization stages may be less susceptible to the effects of sleep deprivation,likely due to their relatively automatic processing and lower demand for cognitive resources.In contrast,during later stages of cognitive processing,particularly in higher-order functions such as conflict monitoring and resource allocation,sleep deprivation significantly impaired task performance efficiency by disrupting prefrontal cortex function.This finding deepens the understanding of the mechanisms underlying the effects of sleep deprivation and provides a scientific basis for cognitive intervention and management strategies in high-stress occupational groups.Future studies can further explore the long-term effects of sleep deprivation and its neural mechanisms by combining multimodal techniques.

Objective:To explore how benzydamine (BA) improves brain edema in mice after cerebral ischemia-reperfusion.Methods:(1) One hundred and twenty 8 week-old male C57BL/6 mice were randomly divided into a sham-operated group, a middle cerebral artery occlusion (MCAO) group, a MCAO+low-dose BA group (L-BA group), and a MCAO+high-dose BA group (H-BA group), with 30 mice in each group. MCAO models in mice of the later 3 groups were established by suture method, while mice in the sham-operated group underwent the same surgical procedure without MCAO. At 6 hours after modeling, mice in the L-BA group and H-BA group were intraperitoneally injected with 5 mg/kg or 10 mg/kg BA, respectively, once daily for 3 days, while mice in the shamoperated group and MCAO group were intraperitoneally injected with same volume of normal saline instead. Dynamics of cerebral perfusion were monitored by laser speckle imaging in MCAO model mice at baseline, during occlusion, and following reperfusion. Three days after modeling, neurological deficits were assessed by modified neurological severity score (mNSS), neurological function was evaluated by forelimb grip strength and rotarod tests; cerebral infarct size was detected by 2,3,5-triphenyltetrazolium chloride (TTC) staining, and neuronal death was assessed by Fluoro-Jade B staining; cerebral edema was quantified by dry-wet weight method, blood-brain barrier (BBB) permeability was assessed by Evans blue dye extravasation, and expressions of tight junction proteins (Claudin-5, zonula occludens-1 [ZO-1]) were detected by immunofluorescent staining; expressions of neutrophil extracellular traps (NETs)-related proteins (citrullinated histone H3 [citH3], myeloperoxidase [MPO] and matrix metalloproteinase 9 [MMP-9]) were determined by Western blotting. (2) Bone marrow neutrophils were extracted from male C57BL/6 mice and randomly divided into a control group, a phorbol 12-myristate 13-acetate (PMA) group, and a PMA+BA group; neutrophils in the PMA group were stimulated with PMA (50 nmol/L), while neutrophils in the PMA+BA group were co-treated with 50 nmol/L PMA and 50 μmol/L BA; and those in the control group were given an equal amount of dimethyl sulfoxide. Sytox Green staining was used to detect the NETs proportion in neutrophils.Results:(1) Baseline cerebral perfusion was robust (1 237.75±98.16 PU), which was markedly reduced during occlusion (297.36±77.63 PU) in the ipsilateral middle cerebral artery territory, and improved following reperfusion (939.21±73.63 PU). Compared with the MCAO group, mice in the L-BA group and H-BA group had lower mNSS score, increased paw grip strength, prolonged rotarod retention time, reduced infarct size, fewer neuronal death, lower brain tissue water content, reduced blood-brain barrier permeability, increased fluorescent intensities of Claudin-5 (0.51±0.11, 0.71±0.04, and 0.83±0.05) and ZO-1 (0.43±0.09, 0.65±0.05, and 0.81±0.03), and decreased protein expressions of citH3 (2.33±0.15, 1.92±0.03, and 1.42±0.04), MPO (2.14±0.08, 1.71±0.06, and 1.37±0.03) and MMP-9 (2.62±0.09, 1.83±0.06, and 1.41±0.05), with significant differences ( P<0.05). All the above changes in the H-BA group were more significant than those in the L-BA group ( P<0.05). (2) Compared with that in the control group (10.00%±8.00%), the proportion of NETs formation per field in both PMA group (85.33%±2.08%) and PMA+BA group (58.46%±5.29%) was significantly increased ( P<0.05); the PMA+BA group showed a significant reduction in NETs formation compared with the PMA group ( P<0.05). Conclusion:BA can alleviate cerebral edema in mice after cerebral ischemia-reperfusion, and its mechanism may be involved in inhibiting NETs formation.

Objective:To investigate the effect of nefazodone on excessive activation of microglia and its regulatory mechanism, as well as its effect on neurological injury in mice subjected to middle cerebral artery occlusion (MCAO).Methods:(1) BV2 cell line was routinely cultured in vitro, and primary microglia from the cortex of neonatal C57BL/6J mice were cultured. Cell counting kit-8 (CCK-8) assay was employed to assess the effects of nefazodone (0, 10, 20, 30, 50 μmol/L) on viability of BV2 cells and primary microglia to determine the working concentration. BV2 cells and primary microglia were divided into a normal control group, a lipopolysaccharide (LPS) group, and a nefazodone group; cells in the nefazodone group were pretreated with 20 μmol/L nefazodone for 2 h; cells in the LPS group and nefazodone group were stimulated with LPS (0.5 μg/mL for BV2 cells and 0.1 μg/mL for primary microglia) for 24 h; cells in the normal control group received an equivalent volume of solvent. Immunofluorescent staining was used to detect the expressions of ionized calcium-binding adapter molecule 1 (Iba1) and CD68. Reverse transcription quantitative PCR (RT-qPCR) was performed to measure interleukin ( IL) -1β, IL-6, tumor necrosis factor-α ( TNF-α), nitric oxide synthase 2 ( Nos2), C-C motif chemokine ligand 2 ( CCL2), and β-hexosaminidase subunit β ( Hexb) mRNA expressions. ELISA was used to quantify the concentrations of supernatant IL-1β, IL-6, and TNF-α in BV2 cells. Western blotting was applied to detect the protein expressions of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in BV2 cells. Griess reagent assay was used to measure supernatant nitric oxide (NO) level in BV2 cells. Western blotting was also used to assess the protein expressions of extracellular signal-regulated kinase (ERK), phosphorylated (p)-ERK, c-Jun N-terminal kinase (JNK), p-JNK, p38, p-p38, nuclear factor kappa B p65 and p-p65 in BV2 cells. (2) Thirty male C57BL/6J mice were randomly divided into a normal control group, a MCAO group, and a nefazodone group, with 10 mice in each group. MCAO model in the MCAO group and nefazodone group was established using suture method; the nefazodone group received an intraperitoneal injection of nefazodone (15 mg/kg) 30 min after modeling, while the normal control group received an equivalent volume of solvent. Three days after modeling, neurological deficits were evaluated using modified neurological severity score (mNSS), and behavioral changes were evaluated by paw grip strength test and foot-fault test. Cerebral infarction volume was assessed by 2,3,5-triphenyltetrazolium chloride (TTC) staining. Iba1 protein expression in the ischemic penumbra was detected by Western blotting. Results:(1) CCK-8 assay showed no significant difference in viability of BV2 cells between the normal control group and 10 or 20 μmol/L nefazodone groups ( P>0.05), and viability of BV2 cells in 30 and 50 μmol/L nefazodone groups was statistically lower than that of normal control group ( P<0.05). Immunofluorescent staining revealed that compared with the normal control group, the LPS group had significantly increased fluorescent intensities of CD68 and Iba1; compared with the LPS group, the nefazodone group had significantly decreased fluorescent intensities of CD68 and Iba1 ( P<0.05). RT-qPCR results indicated that compared with those in the normal control group, the Nos2, CCL2, IL-1β, IL-6, and TNF-α mRNA expressions in both BV2 cells and primary microglia of the LPS group were significantly increased; compared with the LPS group, the nefazodone group had significantly decreased CCL2, IL-1β, and IL-6 mRNA expressions in BV2 cells, and significantly decreased Nos2, CCL2, IL-1β, IL-6, and TNF-α mRNA expressions in primary microglia ( P<0.05). ELISA showed that compared with those in the normal control group, the supernatant IL-1β, IL-6, and TNF-α levels significantly increased in the BV2 cells of LPS group; compared with those in the LPS group, supernatant IL-1β, IL-6 and TNF-α levels statistically decreased in the nefazodone group ( P< 0.05). Western blotting demonstrated that compared with those in the normal control group, the iNOS and COX-2 protein expressions significantly increased in BV2 cells of the LPS group ( P<0.05); compared with those in the LPS group, the iNOS and COX-2 protein expressions in BV2 cells of the nefazodone group statistically decreased ( P<0.05). Griess assay showed that compared with the normal control group, BV2 cells in the LPS group had significantly increased supernatant NO concentration ( P <0.05); compared with the LPS group, BV2 cells in the nefazodone group had significantly decreased supernatant NO concentration ( P<0.05). Western blotting revealed that compared with those in the normal control group, the p-ERK/ERK and p-JNK/JNK ratios significantly increased in BV2 cells of the LPS group ( P<0.05); compared with the LPS group, the p-p65/p65, p-ERK/ERK and p-JNK/JNK ratios significantly decreased in BV2 cells of the nefazodone group ( P<0.05). (2) Behavioral tests showed that compared with the normal control group, the MCAO group had significantly decreased forelimb grip strength and increased foot-fault rate ( P<0.05); compared with the MCAO group, the nefazodone group had significantly decreased mNSS score, increased forelimb grip strength and decreased foot-fault rate ( P<0.05). The percentage of cerebral infarction volume in the nefazodone group was significantly lower than that in the MCAO group ([9.56±1.81]% vs. [21.71±12.26]%, P< 0.05). The MCAO group had statistically higher Iba1 protein expression in ischemic penumbra (7.27±2.88) than the normal control group (1.00±0.64), and the nefazodone group had significantly lower Iba1 protein expression in ischemic penumbra (1.75±0.86) than the MCAO group ( P<0.05). Conclusion:Nefazodone can improve neurological function impairment in MCAO mice by inhibiting the excessive activation of microglia; cytological experiments suggest that its mechanism may be related to the negative regulation of ERK/JNK/NF-κB p65 signaling axis.

Objective:To explore how benzydamine (BA) improves brain edema in mice after cerebral ischemia-reperfusion.Methods:(1) One hundred and twenty 8 week-old male C57BL/6 mice were randomly divided into a sham-operated group, a middle cerebral artery occlusion (MCAO) group, a MCAO+low-dose BA group (L-BA group), and a MCAO+high-dose BA group (H-BA group), with 30 mice in each group. MCAO models in mice of the later 3 groups were established by suture method, while mice in the sham-operated group underwent the same surgical procedure without MCAO. At 6 hours after modeling, mice in the L-BA group and H-BA group were intraperitoneally injected with 5 mg/kg or 10 mg/kg BA, respectively, once daily for 3 days, while mice in the shamoperated group and MCAO group were intraperitoneally injected with same volume of normal saline instead. Dynamics of cerebral perfusion were monitored by laser speckle imaging in MCAO model mice at baseline, during occlusion, and following reperfusion. Three days after modeling, neurological deficits were assessed by modified neurological severity score (mNSS), neurological function was evaluated by forelimb grip strength and rotarod tests; cerebral infarct size was detected by 2,3,5-triphenyltetrazolium chloride (TTC) staining, and neuronal death was assessed by Fluoro-Jade B staining; cerebral edema was quantified by dry-wet weight method, blood-brain barrier (BBB) permeability was assessed by Evans blue dye extravasation, and expressions of tight junction proteins (Claudin-5, zonula occludens-1 [ZO-1]) were detected by immunofluorescent staining; expressions of neutrophil extracellular traps (NETs)-related proteins (citrullinated histone H3 [citH3], myeloperoxidase [MPO] and matrix metalloproteinase 9 [MMP-9]) were determined by Western blotting. (2) Bone marrow neutrophils were extracted from male C57BL/6 mice and randomly divided into a control group, a phorbol 12-myristate 13-acetate (PMA) group, and a PMA+BA group; neutrophils in the PMA group were stimulated with PMA (50 nmol/L), while neutrophils in the PMA+BA group were co-treated with 50 nmol/L PMA and 50 μmol/L BA; and those in the control group were given an equal amount of dimethyl sulfoxide. Sytox Green staining was used to detect the NETs proportion in neutrophils.Results:(1) Baseline cerebral perfusion was robust (1 237.75±98.16 PU), which was markedly reduced during occlusion (297.36±77.63 PU) in the ipsilateral middle cerebral artery territory, and improved following reperfusion (939.21±73.63 PU). Compared with the MCAO group, mice in the L-BA group and H-BA group had lower mNSS score, increased paw grip strength, prolonged rotarod retention time, reduced infarct size, fewer neuronal death, lower brain tissue water content, reduced blood-brain barrier permeability, increased fluorescent intensities of Claudin-5 (0.51±0.11, 0.71±0.04, and 0.83±0.05) and ZO-1 (0.43±0.09, 0.65±0.05, and 0.81±0.03), and decreased protein expressions of citH3 (2.33±0.15, 1.92±0.03, and 1.42±0.04), MPO (2.14±0.08, 1.71±0.06, and 1.37±0.03) and MMP-9 (2.62±0.09, 1.83±0.06, and 1.41±0.05), with significant differences ( P<0.05). All the above changes in the H-BA group were more significant than those in the L-BA group ( P<0.05). (2) Compared with that in the control group (10.00%±8.00%), the proportion of NETs formation per field in both PMA group (85.33%±2.08%) and PMA+BA group (58.46%±5.29%) was significantly increased ( P<0.05); the PMA+BA group showed a significant reduction in NETs formation compared with the PMA group ( P<0.05). Conclusion:BA can alleviate cerebral edema in mice after cerebral ischemia-reperfusion, and its mechanism may be involved in inhibiting NETs formation.

Objective:To investigate the effect of nefazodone on excessive activation of microglia and its regulatory mechanism, as well as its effect on neurological injury in mice subjected to middle cerebral artery occlusion (MCAO).Methods:(1) BV2 cell line was routinely cultured in vitro, and primary microglia from the cortex of neonatal C57BL/6J mice were cultured. Cell counting kit-8 (CCK-8) assay was employed to assess the effects of nefazodone (0, 10, 20, 30, 50 μmol/L) on viability of BV2 cells and primary microglia to determine the working concentration. BV2 cells and primary microglia were divided into a normal control group, a lipopolysaccharide (LPS) group, and a nefazodone group; cells in the nefazodone group were pretreated with 20 μmol/L nefazodone for 2 h; cells in the LPS group and nefazodone group were stimulated with LPS (0.5 μg/mL for BV2 cells and 0.1 μg/mL for primary microglia) for 24 h; cells in the normal control group received an equivalent volume of solvent. Immunofluorescent staining was used to detect the expressions of ionized calcium-binding adapter molecule 1 (Iba1) and CD68. Reverse transcription quantitative PCR (RT-qPCR) was performed to measure interleukin ( IL) -1β, IL-6, tumor necrosis factor-α ( TNF-α), nitric oxide synthase 2 ( Nos2), C-C motif chemokine ligand 2 ( CCL2), and β-hexosaminidase subunit β ( Hexb) mRNA expressions. ELISA was used to quantify the concentrations of supernatant IL-1β, IL-6, and TNF-α in BV2 cells. Western blotting was applied to detect the protein expressions of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in BV2 cells. Griess reagent assay was used to measure supernatant nitric oxide (NO) level in BV2 cells. Western blotting was also used to assess the protein expressions of extracellular signal-regulated kinase (ERK), phosphorylated (p)-ERK, c-Jun N-terminal kinase (JNK), p-JNK, p38, p-p38, nuclear factor kappa B p65 and p-p65 in BV2 cells. (2) Thirty male C57BL/6J mice were randomly divided into a normal control group, a MCAO group, and a nefazodone group, with 10 mice in each group. MCAO model in the MCAO group and nefazodone group was established using suture method; the nefazodone group received an intraperitoneal injection of nefazodone (15 mg/kg) 30 min after modeling, while the normal control group received an equivalent volume of solvent. Three days after modeling, neurological deficits were evaluated using modified neurological severity score (mNSS), and behavioral changes were evaluated by paw grip strength test and foot-fault test. Cerebral infarction volume was assessed by 2,3,5-triphenyltetrazolium chloride (TTC) staining. Iba1 protein expression in the ischemic penumbra was detected by Western blotting. Results:(1) CCK-8 assay showed no significant difference in viability of BV2 cells between the normal control group and 10 or 20 μmol/L nefazodone groups ( P>0.05), and viability of BV2 cells in 30 and 50 μmol/L nefazodone groups was statistically lower than that of normal control group ( P<0.05). Immunofluorescent staining revealed that compared with the normal control group, the LPS group had significantly increased fluorescent intensities of CD68 and Iba1; compared with the LPS group, the nefazodone group had significantly decreased fluorescent intensities of CD68 and Iba1 ( P<0.05). RT-qPCR results indicated that compared with those in the normal control group, the Nos2, CCL2, IL-1β, IL-6, and TNF-α mRNA expressions in both BV2 cells and primary microglia of the LPS group were significantly increased; compared with the LPS group, the nefazodone group had significantly decreased CCL2, IL-1β, and IL-6 mRNA expressions in BV2 cells, and significantly decreased Nos2, CCL2, IL-1β, IL-6, and TNF-α mRNA expressions in primary microglia ( P<0.05). ELISA showed that compared with those in the normal control group, the supernatant IL-1β, IL-6, and TNF-α levels significantly increased in the BV2 cells of LPS group; compared with those in the LPS group, supernatant IL-1β, IL-6 and TNF-α levels statistically decreased in the nefazodone group ( P< 0.05). Western blotting demonstrated that compared with those in the normal control group, the iNOS and COX-2 protein expressions significantly increased in BV2 cells of the LPS group ( P<0.05); compared with those in the LPS group, the iNOS and COX-2 protein expressions in BV2 cells of the nefazodone group statistically decreased ( P<0.05). Griess assay showed that compared with the normal control group, BV2 cells in the LPS group had significantly increased supernatant NO concentration ( P <0.05); compared with the LPS group, BV2 cells in the nefazodone group had significantly decreased supernatant NO concentration ( P<0.05). Western blotting revealed that compared with those in the normal control group, the p-ERK/ERK and p-JNK/JNK ratios significantly increased in BV2 cells of the LPS group ( P<0.05); compared with the LPS group, the p-p65/p65, p-ERK/ERK and p-JNK/JNK ratios significantly decreased in BV2 cells of the nefazodone group ( P<0.05). (2) Behavioral tests showed that compared with the normal control group, the MCAO group had significantly decreased forelimb grip strength and increased foot-fault rate ( P<0.05); compared with the MCAO group, the nefazodone group had significantly decreased mNSS score, increased forelimb grip strength and decreased foot-fault rate ( P<0.05). The percentage of cerebral infarction volume in the nefazodone group was significantly lower than that in the MCAO group ([9.56±1.81]% vs. [21.71±12.26]%, P< 0.05). The MCAO group had statistically higher Iba1 protein expression in ischemic penumbra (7.27±2.88) than the normal control group (1.00±0.64), and the nefazodone group had significantly lower Iba1 protein expression in ischemic penumbra (1.75±0.86) than the MCAO group ( P<0.05). Conclusion:Nefazodone can improve neurological function impairment in MCAO mice by inhibiting the excessive activation of microglia; cytological experiments suggest that its mechanism may be related to the negative regulation of ERK/JNK/NF-κB p65 signaling axis.

Bone marrow microenvironment is a highly complex environment surrounding tumor, which plays an important role in the survival, proliferation, drug resistance and migration of multiple myeloma (MM) cells. As an important cellular component in tumor microenvironment, tumor-associated macrophages(TAM) has attracted attention due to its key role in tumor progression and drug resistance. Targeting TAM has shown potential therapeutic value in cancer treatment. In order to clarify the role of macrophages in MM progression, it is necessary to understand the differentiation of TAM and its characteristics of promoting MM. This paper reviews the research progress on how TAM is programmed in MM and the mechanism of TAM promoting tumor development and drug resistance.
Humans ; Multiple Myeloma/pathology* ; Tumor-Associated Macrophages ; Macrophages/pathology* ; Cell Differentiation ; Tumor Microenvironment

ObjectiveTo investigate the dietary preference and nutritional knowledge needs of the elderly people who dined at meal service sites. MethodsUsing the form of stratified and convenience sampling method with self-designed questionnaire was used， in November 2021， to select 700 elderly people who dine at meal service sites in 7 jurisdictions in Shanghai were selected， and a self-designed questionnaire was used to investigate the basic information. Results91.64% of the elderly surveyed would eat at relatively fixed meal service sites， and the total Dietary Diversity Score （DDS9） was 3.56±1.46. 41.45% of the elderly with diseases preferred unhealthy cooking methods. Only 8.03% of the surveyed seniors said they were unwilling to accept targeted and personalized nutrition tips and reminders. Multivariate logistic regression analysis showed that the probability reaching the “understanding” level of “Food Guide Pagoda for Chinese Residents” and “Four Principles Recommended by the Core Dietary Guidelines for the Elderly” was different in the elderly with different education levels. The willingness of the elderly to expect to receive different nutrition tips and reminders was related to whether they cared about the corresponding contents. There was a statistically significant difference （P<0.05） among the elderly who were concerned about different health problems in terms of the willingness to receive different nutritional tips. There were significant differences in the proportion of elderly people with different health status for intervention （χ²=5.402， P<0.05）. ConclusionThe elderly who dine at meal service sites are highly dependent on the sites， have a low level of dietary diversification， and do not have a high degree of understanding of nutrition-related knowledge， and have a high demand for targeted nutritional interventions. Nutritional interventions for the sick elderly should be piloted through multiple channels.

Humans ; Leukemia, Lymphocytic, Chronic, B-Cell/drug therapy* ; Immune Checkpoint Inhibitors/therapeutic use* ; Lymphoma, Large B-Cell, Diffuse ; Disease Progression ; T-Lymphocytes ; Cell Transformation, Neoplastic

Objective:To compare the efficacy and safety of insulin degludec and insulin glargine U100 in patients with type 2 diabetes mellitus.Methods:This study was a retrospective cohort study. The subjects were patients with type 2 diabetes mellitus who were hospitalized in 13 3A-level general hospitals in Shandong Province from September 2018 to December 2021. According to the type of basal insulin used, the patients were divided into insulin degludec group and insulin glargine U100 group. The basic information and laboratory test results in patients in the 2 groups were collected, the differences of fasting blood glucose level and incidence of hypoglycemia between the 2 groups were compared. The patients with complete blood glucose monitoring data in the 2 groups were selected and their blood glucose fluctuations were compared.Results:A total of 1 152 patients were entered in the study, including 552 patients in the insulin degludec group and 600 patients in the insulin glargine U100 group. The difference in the basic conditions in patients in the 2 groups was not statistically significant (all P>0.05). After treatment, the fasting blood glucose levels in patients in the 2 groups were lower than those before treatment, with statistically significant differences [10.2 (8.8, 12.5) mmol/L vs. 7.5 (6.6, 8.7) mmol/L, Z=-19.443, P<0.001; 10.0 (8.6, 11.7) mmol/L vs. 7.8 (6.6, 9.0) mmol/L, Z=-15.449, P<0.001], but the difference in fasting blood glucose levels between the 2 groups after treatment was not statistically significant ( Z=-1.427, P>0.05). The incidence of hypoglycemia in the insulin degludec group was lower than that in the insulin glargine U100 group [1.09% (6/552) vs. 2.83% (17/600), Z=4.481, P=0.032]. The intraday blood glucose standard deviation, maximum blood glucose fluctuation range, postprandial blood glucose fluctuation range, and average blood glucose fluctuation range in patients with complete blood glucose monitoring data in the insulin degludec group were significantly lower than those in the insulin glargine U100 group [(1.7±0.6) mmol/L vs. (2.4±1.0) mmol/L, (4.5±1.6) mmol/L vs. (6.7±2.9) mmol/L, (1.8±1.0) mmol/L vs. (3.3±1.2) mmol/L, (2.9±1.3) mmol/L vs. (4.6±2.1) mmol/L; all P<0.001]. Conclusion:The efficacy of insulin degludec in the treatment of type 2 diabetes mellitus is equivalent to that of insulin glargine U100, but the risk of hypoglycemia and blood glucose fluctuation is lower.

Objective:To compare the efficacy and safety of insulin degludec and insulin glargine U100 in patients with type 2 diabetes mellitus.Methods:This study was a retrospective cohort study. The subjects were patients with type 2 diabetes mellitus who were hospitalized in 13 3A-level general hospitals in Shandong Province from September 2018 to December 2021. According to the type of basal insulin used, the patients were divided into insulin degludec group and insulin glargine U100 group. The basic information and laboratory test results in patients in the 2 groups were collected, the differences of fasting blood glucose level and incidence of hypoglycemia between the 2 groups were compared. The patients with complete blood glucose monitoring data in the 2 groups were selected and their blood glucose fluctuations were compared.Results:A total of 1 152 patients were entered in the study, including 552 patients in the insulin degludec group and 600 patients in the insulin glargine U100 group. The difference in the basic conditions in patients in the 2 groups was not statistically significant (all P>0.05). After treatment, the fasting blood glucose levels in patients in the 2 groups were lower than those before treatment, with statistically significant differences [10.2 (8.8, 12.5) mmol/L vs. 7.5 (6.6, 8.7) mmol/L, Z=-19.443, P<0.001; 10.0 (8.6, 11.7) mmol/L vs. 7.8 (6.6, 9.0) mmol/L, Z=-15.449, P<0.001], but the difference in fasting blood glucose levels between the 2 groups after treatment was not statistically significant ( Z=-1.427, P>0.05). The incidence of hypoglycemia in the insulin degludec group was lower than that in the insulin glargine U100 group [1.09% (6/552) vs. 2.83% (17/600), Z=4.481, P=0.032]. The intraday blood glucose standard deviation, maximum blood glucose fluctuation range, postprandial blood glucose fluctuation range, and average blood glucose fluctuation range in patients with complete blood glucose monitoring data in the insulin degludec group were significantly lower than those in the insulin glargine U100 group [(1.7±0.6) mmol/L vs. (2.4±1.0) mmol/L, (4.5±1.6) mmol/L vs. (6.7±2.9) mmol/L, (1.8±1.0) mmol/L vs. (3.3±1.2) mmol/L, (2.9±1.3) mmol/L vs. (4.6±2.1) mmol/L; all P<0.001]. Conclusion:The efficacy of insulin degludec in the treatment of type 2 diabetes mellitus is equivalent to that of insulin glargine U100, but the risk of hypoglycemia and blood glucose fluctuation is lower.