Objective:To explore the mechanism of lncRNA FOXD2-AS1 regulating the expression of LATS1 via EZH2 to affect the proliferation and migration of clear cell renal cell carcinoma(ccRCC)cells.Methods:The GEPIA 2 online tool was used to analyze the expression levels of FOXD2-AS1 in ccRCC tissues from the Cancer Genome Atlas(TCGA)database,and their correlation with patients'overall survival rates was evaluated.Quantitative PCR(qPCR)was performed to analyze the expressions of FOXD2-AS1 in renal cancer cells and 26 clinically collected ccRCC tissue samples.CCK-8 cell proliferation assay and transwell chamber migration assay were employed to observe the effects of FOXD2-AS1 knockdown on the proliferation and migration of renal cancer cells.qPCR and Western blot analysis were utilized to assess the impact of FOXD2-AS1 knockdown on the expression of LATS1.RNA immunoprecipitation(RIP)and chromatin immunoprecipitation(ChIP)assays were performed to analyze the interaction between FOXD2-AS1,EZH2,and LATS1.Results:The GEPIA 2 software analysis revealed that FOXD2-AS1 was significantly upregulated in ccRCC tissues(P<0.01)and patients with high FOXD2-AS1 expression exhibited lower overall survival rates(P<0.05).The qPCR analysis results showed that FOXD2-AS1 was significantly upregulated in 26 samples of ccRCC tissues compared with adjacent normal kidney tissues(P<0.01).Compared with immortalized renal tubular epithelial cell line HK-2,the expression of FOXD2-AS1was significantly elevated in three types of renal cancer cell lines(786-O,ACHN and SN12-PM6)(P<0.01).Knockdown of FOXD2-AS1 expression significantly decreased the proliferation and migration abilities of renal cancer cells(P<0.05),and markedly increased the mRNA and protein expression levels of LATS1(all P<0.01).RIP and ChIP assays confirmed that FOXD2-AS1 can bind and recruit EZH2 to the promoter region of LATS1 to exert its effect.Salvage experiments demonstrated that knocking down LATS1 or overexpressing EZH2 partially reversed the inhibitory effect of FOXD2-AS1 knockdown on the proliferation and migration of renal cancer cells.Conclusion:FOXD2-AS1 is highly expressed in ccRCC,and it negatively regulates the expression of LATS1 by recruiting EZH2 to the promoter region of the LATS1 gene,thereby facilitating the proliferation and migration of renal cancer cells.

Case 1,a 69-year-old male patient,was admitted to our hospital due to"dizziness,fatigue,nausea,diarrhea,and oral bleeding for 10 d",with a recent history of field farming work.The patient exhibited leukopenia,thrombocytopenia,and clinical manifestations of multi-organ dysfunction,including coagulation dysfunction,liver function abnormalities,gastrointestinal disorders,myocardial injury,and respiratory failure.Bone marrow aspiration smear revealed hemophagocytosis,and out-of-hospital testing for the severe fever with thrombocytopenia syndrome bunyavirus was positive.The patient was diagnosed with severe fever with thrombocytopenia syndrome(SFTS)complicated by hemophagocytic lymphohistiocytosis(HLH).After diagnosis,glucocorticoid combined with ribavirin treatment was initiated.However,the patient still died,which may be related to factors such as delayed medical consultation,advanced age,and poor control of viral replication.Case 2,a 73-year-old male patient,was admitted to our hospital due to"fatigue for 1 week",with a recent history of field farming work.The patient also presented with leukopenia and thrombocytopenia,combined with liver and coagulation function abnormalities.Bone marrow aspiration smear showed hemophagocytosis,and the patient was highly suspected of SFTS with HLH.We empirically initiated preemptive treatment with favipiravir for antiviral therapy,combined with glucocorticoid for anti-inflammation,to early inhibit novel bunyavirus replication and cytokine storm.Subsequent testing reported the severe fever with thrombocytopenia syndrome bunyavirus nucleic acid quantification as 2.69×103 50%tissue culture infective dose(TCID50)/mL,confirming the diagnosis of SFTS with HLH.The patient's clinical symptoms and various indicators generally improved.Review of these two similar cases suggests that early empirical preemptive use of favipiravir to control viral replication in clinical practice may improve the treatment and prognosis of patients with SFTS complicated by HLH.

Abstract: To explore the molecular mechanism by which long non-coding RNA Surfactant Associated 1 Pseudogene(SFTA1P) promotes the proliferation and migration of clear cell renal cell carcinoma(ccRCC) cells by regulating the microRNA-182-5p(miR-182-5p)/fibronectin 1(FN1) pathway. Methods: GEPIA2 software was utilized to analyze the expression ofSFTA1Pin ccRCC tissues from the TCGA database. Quantitative real-time PCR(qPCR) was employed to detect the expression ofSFTA1Pin ccRCC tissues, normal kidney tissues and ccRCC cell lines. A subcellular localization experiment was performed to explore the localization ofSFTA1Pwithin the human renal cell adenocarcinoma cell line(ACHN) derived from ccRCC. ACHN cells were then divided into the following groups: si-Con group, si-SFTA1P #2 group, mimic NC group, miR-182-5p mimic group, anti-miR-Con group, anti-miR-182-5p group, anti-miR-182-5p+si-FN1 group, si-Con+anti-miR-Con group, si-SFTA1P #2+anti-miR-Con group, and si-SFTA1P #2+anti-miR-182-5p group. CCK-8 and Transwell chamber experiments were conducted to assess cell proliferation and migration abilities. qPCR, Western blot, and dual-luciferase reporter assays were employed to elucidate the regulatory interactions amongSFTA1P,miR-182-5p, andFN1. Results: Analysis of The Cancer Genome Atlas(TCGA) database indicated thatSFTA1Pwas overexpressed in ccRCC tissues(P<0.05). When compared to normal kidney tissues,SFTA1Pexpression was markedly elevated in ccRCC tissues(P<0.01). Furthermore, the expression levels ofSFTA1Pin ccRCC cell lines 786-O, SN12-PM6, ACHN, and A498 were significantly higher than those in human renal proximal tubule cells(HK-2)(allP<0.01). Subcellular localization experiments revealed thatSFTA1Ppredominantly localized in the cytoplasm of ACHN cells. Compared to the si-Con group, the si-SFTA1P #2 group exhibited a significant reduction in proliferation and migration abilities of ACHN cells, accompanied by a decrease inFN1mRNA and protein expression(P<0.05). Compared to the mimic NC group, the expression ofFN1mRNA and protein in ACHN cells in the miR-182-5p mimic group reduced(P<0.01). In comparison to the anti-miR-Con group, the expression levels ofFN1mRNA and protein in ACHN cells were significantly elevated in the anti-miR-182-5p group. Additionally, there was a significant enhancement in both cell proliferation and migration capabilities(P<0.05). Conversely, the proliferation and migration abilities of ACHN cells in the anti-miR-182-5p+si-FN1 group were significantly reduced compared to the anti-miR-182-5p group(P<0.05). Furthermore, relative to the si-SFTA1P #2+anti-miR-Con group, the ACHN cells in the si-SFTA1P #2+anti-miR-182-5p group demonstrated increased proliferation and migration abilities, along with elevatedFN1mRNA and protein expression levels(P<0.05). Conclusion SFTA1Pexhibits elevated expression levels in ccRCC and facilitates the proliferation and migration of ccRCC cells through the modulation of themiR-182-5p/FN1signaling pathway.

Case 1,a 69-year-old male patient,was admitted to our hospital due to"dizziness,fatigue,nausea,diarrhea,and oral bleeding for 10 d",with a recent history of field farming work.The patient exhibited leukopenia,thrombocytopenia,and clinical manifestations of multi-organ dysfunction,including coagulation dysfunction,liver function abnormalities,gastrointestinal disorders,myocardial injury,and respiratory failure.Bone marrow aspiration smear revealed hemophagocytosis,and out-of-hospital testing for the severe fever with thrombocytopenia syndrome bunyavirus was positive.The patient was diagnosed with severe fever with thrombocytopenia syndrome(SFTS)complicated by hemophagocytic lymphohistiocytosis(HLH).After diagnosis,glucocorticoid combined with ribavirin treatment was initiated.However,the patient still died,which may be related to factors such as delayed medical consultation,advanced age,and poor control of viral replication.Case 2,a 73-year-old male patient,was admitted to our hospital due to"fatigue for 1 week",with a recent history of field farming work.The patient also presented with leukopenia and thrombocytopenia,combined with liver and coagulation function abnormalities.Bone marrow aspiration smear showed hemophagocytosis,and the patient was highly suspected of SFTS with HLH.We empirically initiated preemptive treatment with favipiravir for antiviral therapy,combined with glucocorticoid for anti-inflammation,to early inhibit novel bunyavirus replication and cytokine storm.Subsequent testing reported the severe fever with thrombocytopenia syndrome bunyavirus nucleic acid quantification as 2.69×103 50%tissue culture infective dose(TCID50)/mL,confirming the diagnosis of SFTS with HLH.The patient's clinical symptoms and various indicators generally improved.Review of these two similar cases suggests that early empirical preemptive use of favipiravir to control viral replication in clinical practice may improve the treatment and prognosis of patients with SFTS complicated by HLH.

Objective To analyze the expression of long non-coding RNA(lncRNA)ABHD11-AS1 in clear cell renal cell carcinoma(ccRCC)and renal cancer cell lines,and explore its potential functions and mechanisms of action.Methods The bioinformatics tool GEPIA2 software was used to analyze The Cancer Genome Atlas(TCGA)database and compare the expression levels of ABHD11-AS1 in ccRCC and normal kidney tissues.Real-time quantitative PCR was performed to assess ABHD11-AS1 expression in ccRCC tissues,normal kidney tissues,and renal cancer cell lines.Subcellular localization experiments were performed to determine the subcellular locali-zation of ABHD11-AS1 in renal cancer cells.The MTT assay,Transwell assay,real-time quantitative PCR,and Western blotting were used to detect the effects of ABHD11-AS1 and miR-133a-3p on the proliferation,invasion,and expression of SLC6A1 in renal cancer cells.A dual-luciferase reporter gene experiments was performed to validate the binding effect of ABHD11-AS1 to miR-133a-3p and the effect of miR-133a-3p on SLC6A1.Results GEPIA2 software and real-time quantitative PCR analyses indicated that ABHD11-AS1 was highly expressed in ccRCC tissues compared to normal kidney tissues(P＜0.05).Compared to the immortalized renal tubular epithelial cell line HK-2 cells,the expression of ABHD11-AS1 was significantly upregulated in the ACHN,786-O,and SN12-PM6 cells,with the highest expression observed in 786-O cells.The results of the subcellular localization experiments indicated that ABHD11-AS1 was primarily distributed in the cytoplasm of 786-O cells.ABHD11-AS1 knockdown reduced the proliferative and invasive abilities of 786-O cells and decreased SLC6A1 mRNA and protein expression(P＜0.05).Dual-luciferase reporter gene experiments demonstrated that ABHD11-AS1 targets and binds to miR-133a-3p,which in turn binds to SLC6A1.Overexpression of miR-133a-3p reduced the mRNA and protein levels of SLC6A1 in 786-O cells,whereas downregulation of miR-133a-3p had the opposite effect.Downregulation of miR-133a-3p enhanced the proliferation and invasion of 786-O cells,while knockdown of SLC6A1 partially reversed the promoting effect of miR-133a-3p downreg-ulation on the proliferation and invasion of 786-O cells(P＜0.05).Simultaneously,downregulation of miR-133a-3p could also partially reverse the inhibitory effects of ABHD11-AS1 knockdown on 786-O cell proliferation,invasion,and SLC6A1 expression(P＜0.05).Con-clusion ABHD11-AS1 exerts a pro-cancer effect on ccRCC by regulating the miR-133a-3p/SLC6A1 axis,which influences the prolifera-tion and invasion of renal cancer cells.

Symmetric peripheral gangrene (SPG) is a rare and disabling severe complication, often associated with critical conditions like septic shock. However, the occurrence of SPG in the context of stone-related urosepsis is extremely uncommon. This article reports a patient who developed SPG as a complication of urosepsis induced by urinary stone. The patient was admitted with sepsis secondary to a right ureteral stone, and the condition rapidly progressed to septic shock. After receiving anti-shock treatment and relief of the ureteral obstruction, the patient developed ischemic signs in the extremities. Despite appropriate treatment, the patient's fingers returned to normal, while both toes progressed to SPG. After two months, both feet remained swollen, with necrosis and detachment of the right toes. The patient also experienced a loss of pain, temperature, and tactile sensation, along with marked limitations in both flexion and extension of the right toes.

Objective To analyze the expression of long non-coding RNA(lncRNA)ABHD11-AS1 in clear cell renal cell carcinoma(ccRCC)and renal cancer cell lines,and explore its potential functions and mechanisms of action.Methods The bioinformatics tool GEPIA2 software was used to analyze The Cancer Genome Atlas(TCGA)database and compare the expression levels of ABHD11-AS1 in ccRCC and normal kidney tissues.Real-time quantitative PCR was performed to assess ABHD11-AS1 expression in ccRCC tissues,normal kidney tissues,and renal cancer cell lines.Subcellular localization experiments were performed to determine the subcellular locali-zation of ABHD11-AS1 in renal cancer cells.The MTT assay,Transwell assay,real-time quantitative PCR,and Western blotting were used to detect the effects of ABHD11-AS1 and miR-133a-3p on the proliferation,invasion,and expression of SLC6A1 in renal cancer cells.A dual-luciferase reporter gene experiments was performed to validate the binding effect of ABHD11-AS1 to miR-133a-3p and the effect of miR-133a-3p on SLC6A1.Results GEPIA2 software and real-time quantitative PCR analyses indicated that ABHD11-AS1 was highly expressed in ccRCC tissues compared to normal kidney tissues(P＜0.05).Compared to the immortalized renal tubular epithelial cell line HK-2 cells,the expression of ABHD11-AS1 was significantly upregulated in the ACHN,786-O,and SN12-PM6 cells,with the highest expression observed in 786-O cells.The results of the subcellular localization experiments indicated that ABHD11-AS1 was primarily distributed in the cytoplasm of 786-O cells.ABHD11-AS1 knockdown reduced the proliferative and invasive abilities of 786-O cells and decreased SLC6A1 mRNA and protein expression(P＜0.05).Dual-luciferase reporter gene experiments demonstrated that ABHD11-AS1 targets and binds to miR-133a-3p,which in turn binds to SLC6A1.Overexpression of miR-133a-3p reduced the mRNA and protein levels of SLC6A1 in 786-O cells,whereas downregulation of miR-133a-3p had the opposite effect.Downregulation of miR-133a-3p enhanced the proliferation and invasion of 786-O cells,while knockdown of SLC6A1 partially reversed the promoting effect of miR-133a-3p downreg-ulation on the proliferation and invasion of 786-O cells(P＜0.05).Simultaneously,downregulation of miR-133a-3p could also partially reverse the inhibitory effects of ABHD11-AS1 knockdown on 786-O cell proliferation,invasion,and SLC6A1 expression(P＜0.05).Con-clusion ABHD11-AS1 exerts a pro-cancer effect on ccRCC by regulating the miR-133a-3p/SLC6A1 axis,which influences the prolifera-tion and invasion of renal cancer cells.

Objective:To explore the mechanism of lncRNA FOXD2-AS1 regulating the expression of LATS1 via EZH2 to affect the proliferation and migration of clear cell renal cell carcinoma(ccRCC)cells.Methods:The GEPIA 2 online tool was used to analyze the expression levels of FOXD2-AS1 in ccRCC tissues from the Cancer Genome Atlas(TCGA)database,and their correlation with patients'overall survival rates was evaluated.Quantitative PCR(qPCR)was performed to analyze the expressions of FOXD2-AS1 in renal cancer cells and 26 clinically collected ccRCC tissue samples.CCK-8 cell proliferation assay and transwell chamber migration assay were employed to observe the effects of FOXD2-AS1 knockdown on the proliferation and migration of renal cancer cells.qPCR and Western blot analysis were utilized to assess the impact of FOXD2-AS1 knockdown on the expression of LATS1.RNA immunoprecipitation(RIP)and chromatin immunoprecipitation(ChIP)assays were performed to analyze the interaction between FOXD2-AS1,EZH2,and LATS1.Results:The GEPIA 2 software analysis revealed that FOXD2-AS1 was significantly upregulated in ccRCC tissues(P<0.01)and patients with high FOXD2-AS1 expression exhibited lower overall survival rates(P<0.05).The qPCR analysis results showed that FOXD2-AS1 was significantly upregulated in 26 samples of ccRCC tissues compared with adjacent normal kidney tissues(P<0.01).Compared with immortalized renal tubular epithelial cell line HK-2,the expression of FOXD2-AS1was significantly elevated in three types of renal cancer cell lines(786-O,ACHN and SN12-PM6)(P<0.01).Knockdown of FOXD2-AS1 expression significantly decreased the proliferation and migration abilities of renal cancer cells(P<0.05),and markedly increased the mRNA and protein expression levels of LATS1(all P<0.01).RIP and ChIP assays confirmed that FOXD2-AS1 can bind and recruit EZH2 to the promoter region of LATS1 to exert its effect.Salvage experiments demonstrated that knocking down LATS1 or overexpressing EZH2 partially reversed the inhibitory effect of FOXD2-AS1 knockdown on the proliferation and migration of renal cancer cells.Conclusion:FOXD2-AS1 is highly expressed in ccRCC,and it negatively regulates the expression of LATS1 by recruiting EZH2 to the promoter region of the LATS1 gene,thereby facilitating the proliferation and migration of renal cancer cells.

Symmetric peripheral gangrene (SPG) is a rare and disabling severe complication, often associated with critical conditions like septic shock. However, the occurrence of SPG in the context of stone-related urosepsis is extremely uncommon. This article reports a patient who developed SPG as a complication of urosepsis induced by urinary stone. The patient was admitted with sepsis secondary to a right ureteral stone, and the condition rapidly progressed to septic shock. After receiving anti-shock treatment and relief of the ureteral obstruction, the patient developed ischemic signs in the extremities. Despite appropriate treatment, the patient's fingers returned to normal, while both toes progressed to SPG. After two months, both feet remained swollen, with necrosis and detachment of the right toes. The patient also experienced a loss of pain, temperature, and tactile sensation, along with marked limitations in both flexion and extension of the right toes.

Objective To investigate the impact of LncRNA FOXP4-AS1 regulating the EZH2/LATS2 axis on the proliferation and migration of bladder urothelial carcinoma(BUC)cells.Methods The Cancer Genome Atlas(TCGA)database and real-time quantitative PCR were utilized to analyze the expression of FOXP4-AS1 and LATS2 mRNA in BUC tissues.Cell proliferation was observed using MTT experiments,and migration was checked using Transwell assays.Western blot assays were performed to determine the expression of LATS2 and H3K27me3 proteins.RNA immunoprecipitation(RIP)and chromatin immunoprecipitation(ChIP)assays were employed to verify the relationship between FOXP4-AS1,EZH2 and LATS2.Results Compared with normal bladder tissues,FOXP4-AS1 expression was increased in tumor tissues,while LATS2 mRNA expression was decreased(P<0.01).Moreover,FOXP4-AS1 expression was elevated in EJ,T24,BIU-87,and 5637 cell lines compared to SV-HUC-1(P<0.01).The inhibition of FOXP4-AS1 resulted in a significant decrease in the proliferation,migration,and expression of H3K27me3 protein in BUC cells,while concurrently upregulating the expression of LATS2 mRNA and protein.Conversely,the overexpression of FOXP4-AS1 yielded contrasting effects(P<0.05).RIP and ChIP assays revealed that FOXP4-AS1 could recruit EZH2 to the promoter region of LATS2,leading to an enrich-ment of H3K27me3 in this region.Interference with LATS2 or EZH2 expression partially reversed the effects of FOXP4-AS1 silencing or overexpression on the proliferation and migration of BUC cells,with concomitant effects on LATS2 expression.Conclusion FOXP4-AS1 demonstrates a notable increase in expression in BUC,leading to a suppression of LATS2 expression through the recruitment of EZH2 to the promoter region of LATS2.This regula-tory process ultimately influences the proliferation and migration of BUC cells.