Objective To investigate the value of serum long noncoding RNA small nucleolar RNA host gene 7(lncRNA SNHG7)and microRNA(miR)-34a-5p expression in the diagnosis and prognostic evaluation of bloodstream infection(BSI).Methods A total of 193 suspected BSI patients admitted to the emergency department of Guangxi Wuzhou Red Cross Hospital from March 2022 to March 2023 were collected as the study subjects.After diagnosis,BSI patients were included as the infection group(n=100),and non BSI patients were included as the non infection group(n=93).After 28 days of treatment,BSI patients were separated into a death group(n=32)and a survival group(n=68)based on their prognosis.The real time fluorgenic quantitative PCR(qRT-PCR)method was applied to detect the expression levels of serum lncRNA SNHG7 and miR-34a-5p.The Target Scan Human website was applied to predict the targeting relationship between miR-34a-5p and lncRNA SNHG7.Pearson method was applied to analyze the correlation between serum lncRNA SNHG7 level and miR-34a-5p level.Multivariate Logistic regression was applied to analyze the influencing factors of prognosis in patients with BSI.Receiver operating characteristic(ROC)curve was applied to analyze the prognostic value of serum lncRNA SNHG7 and miR-34a-5p.Results The serum lncRNA SNHG7 level(1.47±0.35)in the infection group was obviously higher than that in the non infection group(1.03±0.15),and the miR-34a-5p level(0.85±0.21)was obviously lower than that in the non infection group(1.02±0.13),and the differences were statistically significant(t=11.203,6.703,all P<0.05).Compared with survival group,the serum lncRNA SNHG(1.68±0.21 vs 1.37±0.19),C-reactive protein(CRP)(85.74±9.16mg/L vs 63.18±7.68mg/L),procalcitonin(PCT)levels(56.37±8.72ng/ml vs 34.69±5.54ng/ml),albumin(92.51±10.18g/L vs 65.27±7.24g/L),Acute Physiological and Chronic Health Evaluation(APACHE II)scores(28.15±5.12scores vs 16.35±4.31scores)of the death group were obviously higher,and serum miR-34a-5p level(0.67±0.14 vs 0.93±0.16)was obviously lower,the differences were statistically significant.(t=7.357～15.340,all P<0.05).LncRNA SNHG7 had a targeted binding site with miR-34a-5p,and lncRNA SNHG7 was negatively correlated with miR-34a-5p(r=-0.568,P<0.05).Serum lncRNA SNHG7 and miR-34a-5p were prognostic factors for BSI patients(all P<0.05).The area under the curve(AUC)of serum lncRNA SNHG7,miR-34a-5p,and their combined evaluation of prognosis in BSI patients was better than that of serum lncRNA SNHG7 and miR-34a-5p detected sepatately(Z=0.001,2.304,all P<0.05),with sensitivity and specificity of 78.12%and 97.06%,respectively.Conclusion The serum lncRNA SNHG7 level in BSI patients is obviously elevated,while the serum miR-34a-5p level is obviously reduced.The two are closely related to the prognosis of BSI patients,and the combination of the two has good evaluation value for the prognosis of BSI patients.

Objective This study examines the factors influencing oral frailty in the elderly community,develops a risk prediction model,and validates its efficacy,so as to provide references for identifying and preventing oral weakness in the elderly.Methods 556 elderly individuals from 4 communities were selected by convenience sampling from June to August 2024 in Zigong City Sichuan Province.They were randomly divided into a training group(383 cases)and a validation group(165 cases).Data were collected by a general information questionnaire,Social Frailty Scale,Geriatric Depression Scale,and the Oral Frailty Index-8 screening tool.Logistic regression was used to determine the influencing factors,and R software was used to establish a nomogram model for predicting the risk of oral frailty.Bootstrap method and the validation group were used for internally validation of the model.Calibration curve was used to evaluate the prediction performance of the model.Results 548 valid questionnaires were collected.The final model variables included whether the age ≥80 years,wearing removable dentures,reduced frequency of going out,brushing teeth less than twice a day,frequent dry mouth,increased difficulty in eating hard foods,and choking.The area under the receiver operating characteristic curve of the training group was 0.95(95％CI:0.93～0.97),and the best cutoff value was 0.687.The model achieved an accuracy of 87％,sensitivity of 91％,specificity of 85％,positive predictive value of 0.75,and negative predictive value of 0.95.The Hosmer-Lemeshow fitting test show that x2=3.036,P=0.932,indicating a good model fit.Conclusion The oral frailty prediction model demonstrated a good discrimination,calibration,and clinical utility,which can provide a scientific basis for the prevention and early screening of oral frailty in the elderly.

Objective This study examines the factors influencing oral frailty in the elderly community,develops a risk prediction model,and validates its efficacy,so as to provide references for identifying and preventing oral weakness in the elderly.Methods 556 elderly individuals from 4 communities were selected by convenience sampling from June to August 2024 in Zigong City Sichuan Province.They were randomly divided into a training group(383 cases)and a validation group(165 cases).Data were collected by a general information questionnaire,Social Frailty Scale,Geriatric Depression Scale,and the Oral Frailty Index-8 screening tool.Logistic regression was used to determine the influencing factors,and R software was used to establish a nomogram model for predicting the risk of oral frailty.Bootstrap method and the validation group were used for internally validation of the model.Calibration curve was used to evaluate the prediction performance of the model.Results 548 valid questionnaires were collected.The final model variables included whether the age ≥80 years,wearing removable dentures,reduced frequency of going out,brushing teeth less than twice a day,frequent dry mouth,increased difficulty in eating hard foods,and choking.The area under the receiver operating characteristic curve of the training group was 0.95(95％CI:0.93～0.97),and the best cutoff value was 0.687.The model achieved an accuracy of 87％,sensitivity of 91％,specificity of 85％,positive predictive value of 0.75,and negative predictive value of 0.95.The Hosmer-Lemeshow fitting test show that x2=3.036,P=0.932,indicating a good model fit.Conclusion The oral frailty prediction model demonstrated a good discrimination,calibration,and clinical utility,which can provide a scientific basis for the prevention and early screening of oral frailty in the elderly.

Objective To investigate the value of serum long noncoding RNA small nucleolar RNA host gene 7(lncRNA SNHG7)and microRNA(miR)-34a-5p expression in the diagnosis and prognostic evaluation of bloodstream infection(BSI).Methods A total of 193 suspected BSI patients admitted to the emergency department of Guangxi Wuzhou Red Cross Hospital from March 2022 to March 2023 were collected as the study subjects.After diagnosis,BSI patients were included as the infection group(n=100),and non BSI patients were included as the non infection group(n=93).After 28 days of treatment,BSI patients were separated into a death group(n=32)and a survival group(n=68)based on their prognosis.The real time fluorgenic quantitative PCR(qRT-PCR)method was applied to detect the expression levels of serum lncRNA SNHG7 and miR-34a-5p.The Target Scan Human website was applied to predict the targeting relationship between miR-34a-5p and lncRNA SNHG7.Pearson method was applied to analyze the correlation between serum lncRNA SNHG7 level and miR-34a-5p level.Multivariate Logistic regression was applied to analyze the influencing factors of prognosis in patients with BSI.Receiver operating characteristic(ROC)curve was applied to analyze the prognostic value of serum lncRNA SNHG7 and miR-34a-5p.Results The serum lncRNA SNHG7 level(1.47±0.35)in the infection group was obviously higher than that in the non infection group(1.03±0.15),and the miR-34a-5p level(0.85±0.21)was obviously lower than that in the non infection group(1.02±0.13),and the differences were statistically significant(t=11.203,6.703,all P<0.05).Compared with survival group,the serum lncRNA SNHG(1.68±0.21 vs 1.37±0.19),C-reactive protein(CRP)(85.74±9.16mg/L vs 63.18±7.68mg/L),procalcitonin(PCT)levels(56.37±8.72ng/ml vs 34.69±5.54ng/ml),albumin(92.51±10.18g/L vs 65.27±7.24g/L),Acute Physiological and Chronic Health Evaluation(APACHE II)scores(28.15±5.12scores vs 16.35±4.31scores)of the death group were obviously higher,and serum miR-34a-5p level(0.67±0.14 vs 0.93±0.16)was obviously lower,the differences were statistically significant.(t=7.357～15.340,all P<0.05).LncRNA SNHG7 had a targeted binding site with miR-34a-5p,and lncRNA SNHG7 was negatively correlated with miR-34a-5p(r=-0.568,P<0.05).Serum lncRNA SNHG7 and miR-34a-5p were prognostic factors for BSI patients(all P<0.05).The area under the curve(AUC)of serum lncRNA SNHG7,miR-34a-5p,and their combined evaluation of prognosis in BSI patients was better than that of serum lncRNA SNHG7 and miR-34a-5p detected sepatately(Z=0.001,2.304,all P<0.05),with sensitivity and specificity of 78.12%and 97.06%,respectively.Conclusion The serum lncRNA SNHG7 level in BSI patients is obviously elevated,while the serum miR-34a-5p level is obviously reduced.The two are closely related to the prognosis of BSI patients,and the combination of the two has good evaluation value for the prognosis of BSI patients.

AIM:To investigate the effect of gastro-din on the expression of brain-derived neurotroph-ic factor(BDNF)and interleukin-6(IL-6)in the stria-tum of cerebral ischemia rats,and to explore the potential mechanism of gastrodin in treating cere-bral ischemia.METHODS:The rats were randomly divided into four groups:normal,sham,model,and gastrodin groups,each consisting of 10 rats.After successful modeling using middle cerebral artery occlusion(MCAO),the gastrodin group received in-traperitoneal injection of gastrodin injection at a dose of 10 mg/kg once a day for 14 consecutive days.Pathological changes in striatal neurons were observed using Nissl staining.Immunohistochemis-try was utilized to detect positive expression of BDNF and IL-6 proteins in the striatum.Additional-ly,immunoblot analysis was performed to deter-mine the expression levels of BDNF and IL-6 pro-teins in the striatum.RESULTS:Nissl staining re-vealed clear and intact structures of striatal neu-rons in the normal and sham groups,with tightly arranged cells.In the model group,the number of cells was significantly reduced compared to the sham group(P＜0.01),and there was a noticeable cytosolic atrophy and loose cell arrangement.The gastrodin group showed a significant increase in the number of Nissl-positive neurons compared to the model group(P＜0.01),and there was also a sig-nificant improvement in cell morphology.The re-sults of immunohistochemistry and immunoblot were consistent,and there was no statistically sig-nificant difference in BDNF and IL-6 protein expres-sion between the normal group and the sham group(P＞0.05).Compared to the sham group,the model group showed a decrease in the protein ex-pression level of BDNF in the striatum on the isch-emic side(P＜0.01)and an increase in the protein expression level of IL-6(P＜0.05,P＜0.01).In con-trast,the gastrodin group showed an increase in the protein expression level of BDNF in the stria-tum on the ischemic side(P＜0.05,P＜0.01)and a decrease in the protein expression level of IL-6(P＜0.05,P＜0.01)compared to the model group.CON-CLUSION:Gastrodin has a significant protective ef-fect on striatal injury caused by cerebral ischemia,and its mechanism may be related to the up-regula-tion of the anti-inflammatory factor BDNF and the down-regulation of the pro-inflammatory factor IL-6.

AIM:To investigate the effect of gastro-din on the expression of brain-derived neurotroph-ic factor(BDNF)and interleukin-6(IL-6)in the stria-tum of cerebral ischemia rats,and to explore the potential mechanism of gastrodin in treating cere-bral ischemia.METHODS:The rats were randomly divided into four groups:normal,sham,model,and gastrodin groups,each consisting of 10 rats.After successful modeling using middle cerebral artery occlusion(MCAO),the gastrodin group received in-traperitoneal injection of gastrodin injection at a dose of 10 mg/kg once a day for 14 consecutive days.Pathological changes in striatal neurons were observed using Nissl staining.Immunohistochemis-try was utilized to detect positive expression of BDNF and IL-6 proteins in the striatum.Additional-ly,immunoblot analysis was performed to deter-mine the expression levels of BDNF and IL-6 pro-teins in the striatum.RESULTS:Nissl staining re-vealed clear and intact structures of striatal neu-rons in the normal and sham groups,with tightly arranged cells.In the model group,the number of cells was significantly reduced compared to the sham group(P＜0.01),and there was a noticeable cytosolic atrophy and loose cell arrangement.The gastrodin group showed a significant increase in the number of Nissl-positive neurons compared to the model group(P＜0.01),and there was also a sig-nificant improvement in cell morphology.The re-sults of immunohistochemistry and immunoblot were consistent,and there was no statistically sig-nificant difference in BDNF and IL-6 protein expres-sion between the normal group and the sham group(P＞0.05).Compared to the sham group,the model group showed a decrease in the protein ex-pression level of BDNF in the striatum on the isch-emic side(P＜0.01)and an increase in the protein expression level of IL-6(P＜0.05,P＜0.01).In con-trast,the gastrodin group showed an increase in the protein expression level of BDNF in the stria-tum on the ischemic side(P＜0.05,P＜0.01)and a decrease in the protein expression level of IL-6(P＜0.05,P＜0.01)compared to the model group.CON-CLUSION:Gastrodin has a significant protective ef-fect on striatal injury caused by cerebral ischemia,and its mechanism may be related to the up-regula-tion of the anti-inflammatory factor BDNF and the down-regulation of the pro-inflammatory factor IL-6.

AIM:To investigate the effect of gastro-din on the expression of brain-derived neurotroph-ic factor(BDNF)and interleukin-6(IL-6)in the stria-tum of cerebral ischemia rats,and to explore the potential mechanism of gastrodin in treating cere-bral ischemia.METHODS:The rats were randomly divided into four groups:normal,sham,model,and gastrodin groups,each consisting of 10 rats.After successful modeling using middle cerebral artery occlusion(MCAO),the gastrodin group received in-traperitoneal injection of gastrodin injection at a dose of 10 mg/kg once a day for 14 consecutive days.Pathological changes in striatal neurons were observed using Nissl staining.Immunohistochemis-try was utilized to detect positive expression of BDNF and IL-6 proteins in the striatum.Additional-ly,immunoblot analysis was performed to deter-mine the expression levels of BDNF and IL-6 pro-teins in the striatum.RESULTS:Nissl staining re-vealed clear and intact structures of striatal neu-rons in the normal and sham groups,with tightly arranged cells.In the model group,the number of cells was significantly reduced compared to the sham group(P＜0.01),and there was a noticeable cytosolic atrophy and loose cell arrangement.The gastrodin group showed a significant increase in the number of Nissl-positive neurons compared to the model group(P＜0.01),and there was also a sig-nificant improvement in cell morphology.The re-sults of immunohistochemistry and immunoblot were consistent,and there was no statistically sig-nificant difference in BDNF and IL-6 protein expres-sion between the normal group and the sham group(P＞0.05).Compared to the sham group,the model group showed a decrease in the protein ex-pression level of BDNF in the striatum on the isch-emic side(P＜0.01)and an increase in the protein expression level of IL-6(P＜0.05,P＜0.01).In con-trast,the gastrodin group showed an increase in the protein expression level of BDNF in the stria-tum on the ischemic side(P＜0.05,P＜0.01)and a decrease in the protein expression level of IL-6(P＜0.05,P＜0.01)compared to the model group.CON-CLUSION:Gastrodin has a significant protective ef-fect on striatal injury caused by cerebral ischemia,and its mechanism may be related to the up-regula-tion of the anti-inflammatory factor BDNF and the down-regulation of the pro-inflammatory factor IL-6.

AIM: To investigate the effect of gastrodin on the expression of brain-derived neurotrophic factor (BDNF) and interleukin-6 (IL-6) in the striatum of cerebral ischemia rats, and to explore the potential mechanism of gastrodin in treating cerebral ischemia. METHODS: The rats were randomly divided into four groups: normal, sham, model, and gastrodin groups, each consisting of 10 rats. After successful modeling using middle cerebral artery occlusion (MCAO), the gastrodin group received intraperitoneal injection of gastrodin injection at a dose of 10 mg/kg once a day for 14 consecutive days. Pathological changes in striatal neurons were observed using Nissl staining. Immunohistochemistry was utilized to detect positive expression of BDNF and IL-6 proteins in the striatum. Additionally, immunoblot analysis was performed to determine the expression levels of BDNF and IL-6 proteins in the striatum. RESULTS: Nissl staining revealed clear and intact structures of striatal neurons in the normal and sham groups, with tightly arranged cells. In the model group, the number of cells was significantly reduced compared to the sham group (P<0.01), and there was a noticeable cytosolic atrophy and loose cell arrangement. The gastrodin group showed a significant increase in the number of Nissl-positive neurons compared to the model group (P<0.01), and there was also a significant improvement in cell morphology. The results of immunohistochemistry and immunoblot were consistent, and there was no statistically significant difference in BDNF and IL-6 protein expression between the normal group and the sham group (P>0.05). Compared to the sham group, the model group showed a decrease in the protein expression level of BDNF in the striatum on the ischemic side (P<0.01) and an increase in the protein expression level of IL-6 (P<0.05, P<0.01). In contrast, the gastrodin group showed an increase in the protein expression level of BDNF in the striatum on the ischemic side (P<0.05, P<0.01) and a decrease in the protein expression level of IL-6 (P< 0.05, P<0.01) compared to the model group. CONCLUSION: Gastrodin has a significant protective effect on striatal injury caused by cerebral ischemia, and its mechanism may be related to the up-regulation of the anti-inflammatory factor BDNF and the down-regulation of the pro-inflammatory factor IL-6.

To establish a simple,convenient,sensitive,and specific method for rapid detection of Zi-ka virus(ZIKV),the whole genome sequences of ZIKV isolated from different times and regions were analyzed.The specific primers and probes were designed based on the screened target se-quences located in the conserved region of the ZIKV NS5 gene.By combining RT-LAMP isother-mal amplification technology and immunochromatography technology,a reverse transcription loop mediated isothermal amplification nucleic acid and flow visualization strip(RT-LAMP-VF)detec-tion method for ZIKV was established.The results showed that the method had good specificity and sensitivity.When the ratio of inner,outer,and ring primers(FIP∶LF∶F3)was 4∶2∶1,the detection method can specifically detect 102 copies/pL RNA transcripts or 2.15 pfu ZIKV at 61 ℃for 45 minutes,with no cross reaction with other flaviviruses such as Japanese encephalitis virus and classical swine fever virus.Other RNAs in blood tissue samples did not affect the sensitivity and specificity of RT-LAMP-VF,indicating that the method can be applied to clinical practice.The ZIKV RT-LAMP-VF detection method established in this study is easy to perform and does not require special instruments and equipment.It is particularly suitable for the rapid detection of ZIKV in grassroots units,providing technical support and material support for the establishment of on-site rapid detection and early warning and prediction systems for ZIKV disease.

AIM:To investigate the effect of gastro-din on the expression of brain-derived neurotroph-ic factor(BDNF)and interleukin-6(IL-6)in the stria-tum of cerebral ischemia rats,and to explore the potential mechanism of gastrodin in treating cere-bral ischemia.METHODS:The rats were randomly divided into four groups:normal,sham,model,and gastrodin groups,each consisting of 10 rats.After successful modeling using middle cerebral artery occlusion(MCAO),the gastrodin group received in-traperitoneal injection of gastrodin injection at a dose of 10 mg/kg once a day for 14 consecutive days.Pathological changes in striatal neurons were observed using Nissl staining.Immunohistochemis-try was utilized to detect positive expression of BDNF and IL-6 proteins in the striatum.Additional-ly,immunoblot analysis was performed to deter-mine the expression levels of BDNF and IL-6 pro-teins in the striatum.RESULTS:Nissl staining re-vealed clear and intact structures of striatal neu-rons in the normal and sham groups,with tightly arranged cells.In the model group,the number of cells was significantly reduced compared to the sham group(P＜0.01),and there was a noticeable cytosolic atrophy and loose cell arrangement.The gastrodin group showed a significant increase in the number of Nissl-positive neurons compared to the model group(P＜0.01),and there was also a sig-nificant improvement in cell morphology.The re-sults of immunohistochemistry and immunoblot were consistent,and there was no statistically sig-nificant difference in BDNF and IL-6 protein expres-sion between the normal group and the sham group(P＞0.05).Compared to the sham group,the model group showed a decrease in the protein ex-pression level of BDNF in the striatum on the isch-emic side(P＜0.01)and an increase in the protein expression level of IL-6(P＜0.05,P＜0.01).In con-trast,the gastrodin group showed an increase in the protein expression level of BDNF in the stria-tum on the ischemic side(P＜0.05,P＜0.01)and a decrease in the protein expression level of IL-6(P＜0.05,P＜0.01)compared to the model group.CON-CLUSION:Gastrodin has a significant protective ef-fect on striatal injury caused by cerebral ischemia,and its mechanism may be related to the up-regula-tion of the anti-inflammatory factor BDNF and the down-regulation of the pro-inflammatory factor IL-6.