Objective To compare the clinical efficacy of different sized incisions for phacoemulsification combined with vitrectomy in the treatment of age-related cataract associated with maculopathy. Methods From January 2016 to October 2016, a total of 60 eyes of 60 senile cataract patients with maculopathy were prospectively divided into the micro incision group and the standard incision group according the random number table,with 30 cases in each group.The micro incision group received a 1.8 mm micro incision for phacoemulsification combined with 23G vitrectomy and the standard incision group underwent a 2.8 mm incision for phacoemulsification combined with 23G vitrectomy.The intraoperative conditions and the postoperative complications of the two groups at 1 d, 1 and 6 months after surgery were compared. The intraocular pressure (IOP), best corrected visual acuity (BCVA), surgically induced astigmatism (SIA), dry eye symptoms (Sx), break-up time (tBUT), schirmer test (ST)-Ⅱwere respectively measured at 1 and 6 months after surgery.Results The operation procedures were similar in two groups,and there were no significant differences in the operative time and the incidence of intraoperative complications(P>0.05).There were no significant differences in IOP and the incidence of postoperative complications between two groups at 1 d, 1 and 6 months after surgery (P>0.05). At the time point of 1 month after operation,there was no significant difference in BCVA between two groups,but the level of SIA in micro incision group was lower:0.4 ± 0.2 vs.0.6 ± 0.3,t=3.038,P=0.004;the level of Sx micro incision group was lower: (1.2 ± 0.8)score vs. (1.8 ± 1.1) scores, t = 2.416, P = 0.019; the level of tBUT was higher:(5.2 ± 1.6)s vs.(3.8 ± 1.3)s, t = 3.454,P = 0.001;the level of ST-Ⅱwas higher: (4.7 ± 2.1) mm vs. (3.5 ± 1.8), t = 2.376, P = 0.021; there were significant differences. At 6 months after operation,there were no significant differences in the indexes of BCVA,SIA,Sx,tBUT and ST-Ⅱbetween two groups(P>0.05).Conclusions The different sized incisions for phacoemulsification combined with vitrectomy in the treatment of senile cataract associated with maculopathy are similarly safe and effective. However, the micro incision surgery can improve the surgically-induced astigmatism and dry eye in the early stage,with a shorter postoperative recovery time.

Objective To study the effects of rituximab combined with CHOP chemotherapy on serum Thymidine kinase 1 (TK-1) and vascular endothelial growth factor (VEGF) in patients with non-Hodgkin lymphoma,and to provide guidance for clinical research.Methods A total of 24 patients with non-Hodgkin's lymphoma treated in our hospital from January 2013 to March 2016 were randomly divided into the control group and the observation group,and each with 12 cases.All patients were examined before and after treatment,the control group was only treated with CHOP chemotherapy,and the observation group was treated with rituximab combined with CHOP chemotherapy.The patients were followed up within 1-2 years after treatment.The therapeutic effects of all patients were observed,the TK-1 and VEGF levels were measured and the incidence rate of adverse reactions was recorded.Results The efficiency rates of patients in the observation group and the control group were 66.67％ and 50.00％,respectively after treatment,and the observation group was significantly better than the control group,the difference was statistically significant (P＜0.05);the TK-1 and VEGF levels of the two groups were significantly decreased after treatment (P＜0.05),there was a statistically significant difference.But the two indexes of observation group was significantly lower than the control group,the difference was significant (P＜0.05);the control group showed 1 case of liver dysfunc tion after treatment,4 cases of gastrointestinal dysfunction,1 case of decreased white blood cells,while the observation group were 1,3 and 1 case,respectively.There were no significant differences between two groups (P＞0.05).Conclusion With the treatment of rituximab combined with CHOP chemotherapy,serum TK-1 and VEGF levels of patients with non-Hodgkin lymphoma decreased significantly,the poor prognosis has been significantly improved,and this treatment is worth popularizing in clinical application.

Neuromyelitis optica spectrum disorders (NMOSD) are a severe autoimmune inflammatory demyelinating disease of the central nervous system. NMOSD complicated with immune thrombocytopenia (ITP) is rare. This paper reports a case of NMOSD who was misdiagnosed as multiple sclerosis for many years, and then developed thrombocytopenia. ITP was diagnosed by perfect examination. After immunosuppression and thrombopoiesis therapy, the platelets returned to normal. The review of the case and literatures can help to improve the understanding of this kind of disease, timely diagnose and treat patients, and avoid serious complications.

Objective:To investigate the clinical efficacy of lenalidomide combined with bortezomib and dexamethasone (RVd) regimen in treatment of newly diagnosed multiple myeloma (NDMM) patients and its effect on the levels of regulatory T cells (Treg cells) and natural killer (NK) cells.Methods:Thirty-eight NDMM patients who were admitted to the Second Affiliated Hospital of Bengbu Medical College from September 2019 to May 2022 were selected for a prospective study, and were divided into control group (18 cases) and observation group (20 cases) according to random number table method. The control group was treated with bortezomib+epirubicin+dexamethasone (VAd) regimen, and the observation group was treated with RVd regimen. The efficacy and safety were compared between the two groups. The levels of Treg cells (CD4 + CD25 + FOXP3 +) and NK cells (CD3 - CD56 + CD16 +) before and after treatment in the two groups were detected by flow cytometry, and the results were compared. Results:After 4 courses of treatment, the objective response rate (ORR) of the observation group was 95.0% (19/20), which was higher than that of the control group [77.8% (14/18)], and the difference was statistically significant ( P = 0.016). Before treatment, there was no statistical difference in the levels of Treg cells and NK cells between the two groups ( P values were 0.381 and 0.650). After treatment, the level of Treg cells in the control group increased from (1.5±0.5)% before treatment to (4.7±1.3)% ( P = 0.008), while the level of Treg cells in the observation group increased from (1.4±0.5)% before treatment to (6.8±1.5)% ( P = 0.001), and the level in the observation group was higher than that in the control group ( P = 0.027); the level of NK cells in the control group increased from (16±6)% before treatment to (20±5)% ( P = 0.004), while the level of NK cells in the observation group increased from (16±6)% before treatment to (24±6)% ( P = 0.006), and the level in the observation group was higher than that in the control group ( P = 0.032). The incidence rates of thrombocytopenia and neutropenia in the observation group were higher than those in the control group, and the differences were statistically significant ( P values were 0.012 and 0.027), which was reversible after active treatment. There was no statistical difference in the incidence rates of other adverse reactions (all P>0.05). Conclusions:RVd regimen for NDMM is clinically effective, safe and reliable, and the patients' levels of Treg cells and NK cells elevate after treatment.

Background/Aims: Ubiquitination is widely involved in the progression of hepatocellular carcinoma (HCC) by regulating various cellular processes. However, systematic strategies for screening core ubiquitin-related genes, clarifying their functions and mechanisms, and ultimately developing potential therapeutics for patients with HCC are still lacking. Methods: Cox and LASSO regression analyses were performed to construct a ubiquitin-related gene prediction model for HCC. Loss- and gain-of-function studies, transcriptomic and metabolomics analysis were used to explore the function and mechanism of UBE2S on HCC cell glycolysis and growth. Results: Based on 1,423 ubiquitin-related genes, a four-gene signature was successfully constructed to evaluate the prognosis of patients with HCC. UBE2S was identified in this signature with the potential to predict the survival of patients with HCC. E2F2 transcriptionally upregulated UBE2S expression by directly binding to its promoter. UBE2S positively regulated glycolysis in a HIF-1α-dependent manner, thus promoting the proliferation of HCC cells. Mechanistically, UBE2S enhanced K11-linkage polyubiquitination at lysine residues 171 and 196 of VHL independent of E3 ligase, thereby indirectly stabilizing HIF-1α protein levels by mediating the degradation of VHL by the proteasome. In particular, the combination of cephalomannine, a small molecule compound that inhibits the expression of UBE2S, and PX-478, an inhibitor of HIF-1α, significantly improved the anti-tumor efficacy. Conclusions UBE2S is identified as a key biomarker in HCC among the thousands of ubiquitin-related genes and promotes glycolysis by E3 enzyme-independent ubiquitination, thus serving as a therapeutic target for the treatment of HCC.

Background/Aims: Ubiquitination is widely involved in the progression of hepatocellular carcinoma (HCC) by regulating various cellular processes. However, systematic strategies for screening core ubiquitin-related genes, clarifying their functions and mechanisms, and ultimately developing potential therapeutics for patients with HCC are still lacking. Methods: Cox and LASSO regression analyses were performed to construct a ubiquitin-related gene prediction model for HCC. Loss- and gain-of-function studies, transcriptomic and metabolomics analysis were used to explore the function and mechanism of UBE2S on HCC cell glycolysis and growth. Results: Based on 1,423 ubiquitin-related genes, a four-gene signature was successfully constructed to evaluate the prognosis of patients with HCC. UBE2S was identified in this signature with the potential to predict the survival of patients with HCC. E2F2 transcriptionally upregulated UBE2S expression by directly binding to its promoter. UBE2S positively regulated glycolysis in a HIF-1α-dependent manner, thus promoting the proliferation of HCC cells. Mechanistically, UBE2S enhanced K11-linkage polyubiquitination at lysine residues 171 and 196 of VHL independent of E3 ligase, thereby indirectly stabilizing HIF-1α protein levels by mediating the degradation of VHL by the proteasome. In particular, the combination of cephalomannine, a small molecule compound that inhibits the expression of UBE2S, and PX-478, an inhibitor of HIF-1α, significantly improved the anti-tumor efficacy. Conclusions UBE2S is identified as a key biomarker in HCC among the thousands of ubiquitin-related genes and promotes glycolysis by E3 enzyme-independent ubiquitination, thus serving as a therapeutic target for the treatment of HCC.

Background/Aims: Ubiquitination is widely involved in the progression of hepatocellular carcinoma (HCC) by regulating various cellular processes. However, systematic strategies for screening core ubiquitin-related genes, clarifying their functions and mechanisms, and ultimately developing potential therapeutics for patients with HCC are still lacking. Methods: Cox and LASSO regression analyses were performed to construct a ubiquitin-related gene prediction model for HCC. Loss- and gain-of-function studies, transcriptomic and metabolomics analysis were used to explore the function and mechanism of UBE2S on HCC cell glycolysis and growth. Results: Based on 1,423 ubiquitin-related genes, a four-gene signature was successfully constructed to evaluate the prognosis of patients with HCC. UBE2S was identified in this signature with the potential to predict the survival of patients with HCC. E2F2 transcriptionally upregulated UBE2S expression by directly binding to its promoter. UBE2S positively regulated glycolysis in a HIF-1α-dependent manner, thus promoting the proliferation of HCC cells. Mechanistically, UBE2S enhanced K11-linkage polyubiquitination at lysine residues 171 and 196 of VHL independent of E3 ligase, thereby indirectly stabilizing HIF-1α protein levels by mediating the degradation of VHL by the proteasome. In particular, the combination of cephalomannine, a small molecule compound that inhibits the expression of UBE2S, and PX-478, an inhibitor of HIF-1α, significantly improved the anti-tumor efficacy. Conclusions UBE2S is identified as a key biomarker in HCC among the thousands of ubiquitin-related genes and promotes glycolysis by E3 enzyme-independent ubiquitination, thus serving as a therapeutic target for the treatment of HCC.

Background/Aims: Ubiquitination is widely involved in the progression of hepatocellular carcinoma (HCC) by regulating various cellular processes. However, systematic strategies for screening core ubiquitin-related genes, clarifying their functions and mechanisms, and ultimately developing potential therapeutics for patients with HCC are still lacking. Methods: Cox and LASSO regression analyses were performed to construct a ubiquitin-related gene prediction model for HCC. Loss- and gain-of-function studies, transcriptomic and metabolomics analysis were used to explore the function and mechanism of UBE2S on HCC cell glycolysis and growth. Results: Based on 1,423 ubiquitin-related genes, a four-gene signature was successfully constructed to evaluate the prognosis of patients with HCC. UBE2S was identified in this signature with the potential to predict the survival of patients with HCC. E2F2 transcriptionally upregulated UBE2S expression by directly binding to its promoter. UBE2S positively regulated glycolysis in a HIF-1α-dependent manner, thus promoting the proliferation of HCC cells. Mechanistically, UBE2S enhanced K11-linkage polyubiquitination at lysine residues 171 and 196 of VHL independent of E3 ligase, thereby indirectly stabilizing HIF-1α protein levels by mediating the degradation of VHL by the proteasome. In particular, the combination of cephalomannine, a small molecule compound that inhibits the expression of UBE2S, and PX-478, an inhibitor of HIF-1α, significantly improved the anti-tumor efficacy. Conclusions UBE2S is identified as a key biomarker in HCC among the thousands of ubiquitin-related genes and promotes glycolysis by E3 enzyme-independent ubiquitination, thus serving as a therapeutic target for the treatment of HCC.