Mutational dysphonia, a condition in which a pre-adolescent voice persists into adulthood, can significantly impact personal and professional life but is treatable with voice therapy. A patient with mutational dysphonia usually has a voice that is weak, breathy, or diplophonic, often classified as a “falsetto” voice. In this case report, we present a 20-year-old male who had a typical voice of a boy before adolescence, making it difficult to diagnose as mutational dysphonia. After voice therapy, he successfully gained his post-adolescent voice, highlighting the importance of thorough diagnosis and personalized treatment for mutational dysphonia.

Mutational dysphonia, a condition in which a pre-adolescent voice persists into adulthood, can significantly impact personal and professional life but is treatable with voice therapy. A patient with mutational dysphonia usually has a voice that is weak, breathy, or diplophonic, often classified as a “falsetto” voice. In this case report, we present a 20-year-old male who had a typical voice of a boy before adolescence, making it difficult to diagnose as mutational dysphonia. After voice therapy, he successfully gained his post-adolescent voice, highlighting the importance of thorough diagnosis and personalized treatment for mutational dysphonia.

Mutational dysphonia, a condition in which a pre-adolescent voice persists into adulthood, can significantly impact personal and professional life but is treatable with voice therapy. A patient with mutational dysphonia usually has a voice that is weak, breathy, or diplophonic, often classified as a “falsetto” voice. In this case report, we present a 20-year-old male who had a typical voice of a boy before adolescence, making it difficult to diagnose as mutational dysphonia. After voice therapy, he successfully gained his post-adolescent voice, highlighting the importance of thorough diagnosis and personalized treatment for mutational dysphonia.

In recent decades,the prevalence of diabetes has been increasing year by year,and a series of complications caused by diabetes include diabetic cardiomyopathy,retinopathy,nephropa-thy,osteoporosis and neuropathy.The pathogenesis of these com-plications is still very unclear,and there is an urgent need for some therapeutic drugs to meet the clinical needs.In this re-view,we summarize the pathogenesis of various diabetic compli-cations in the past five years,the markers that have received more attention and the main therapeutic drugs,in order to pro-vide references for the drug research and development of diabetic complications.

Objective:We aimed to develop a novel visualized model based on nomogram to predict postoperative overall survival.Methods:This was a multicenter, retrospective, observational cohort study, including participants with histologically confirmed gastric and colorectal cancer who underwent radical surgery from 11 medical centers in China from August 1, 2015 to June 30, 2018. Baseline characteristics, histopathological data and nutritional status, as assessed using Nutrition Risk Screening 2002 (NRS 2002) score and the scored Patient-Generated Subjective Global Assessment, were collected. The least absolute shrinkage and selection operator regression and Cox regression were used to identify variables to be included in the predictive model. Internal and external validations were performed.Results:There were 681 and 127 patients in the training and validation cohorts, respectively. A total of 188 deaths were observed over a median follow-up period of 59 (range: 58 to 60) months. Two independent predictors of NRS 2002 and Tumor-Node-Metastasis (TNM) stage were identified and incorporated into the prediction nomogram model together with the factor of age. The model's concordance index for 1-, 3- and 5-year overall survival was 0.696, 0.724, and 0.738 in the training cohort and 0.801, 0.812, and 0.793 in the validation cohort, respectively.Conclusions:In this study, a new nomogram prediction model based on NRS 2002 score was developed and validated for predicting the overall postoperative survival of patients with gastric colorectal cancer. This model has good differentiation, calibration and clinical practicability in predicting the long-term survival rate of patients with gastrointestinal cancer after radical surgery.

Objective:To explore the role of NK cells in allogeneic hematopoietic stem cell micro-transplantation(MST)in the treatment of patients with acute myeloid leukemia(AML).Methods:Data from 93 AML patients treated with MST at our center from 2013-2018 were retrospectively analyzed.The induction regimen was anthracycline and cytarabine combined with peripheral blood stem cells transplantation mobilization by granulocyte colony stimulating factor(GPBSC),followed by 2-4 courses of intensive treatment with medium to high doses of cytarabine combined with GPBSC after achieving complete remission(CR).The therapeutic effects of one and two courses of MST induction therapy on 42 patients who did not reach CR before transplantation were evaluated.Cox proportional hazards regression analysis was used to analyze the impact of donor NK cell dose and KIR genotype,including KIR ligand mismatch,2DS1,haplotype,and HLA-Cw ligands on survival prognosis of patients.Results:Forty-two patients received MST induction therapy,and the CR rate was 57.1％after 1 course and 73.7％after 2 courses.Multivariate analysis showed that,medium and high doses of NK cells was significantly associated with improved disease-free survival(DFS)of patients(HR=0.27,P=0.005;HR=0.21,P=0.001),and high doses of NK cells was significantly associated with improved overall survival(OS)of patients(HR=0.15,P=0.000).Donor 2DS1 positive significantly increases OS of patients(HR=0.25,P=0.011).For high-risk patients under 60 years old,patients of the donor-recipient KIR ligand mismatch group had longer DFS compared to the nonmismatch group(P=0.036);donor 2DS1 positive significantly prolonged OS of patients(P=0.009).Conclusion:NK cell dose,KIR ligand mismatch and 2DS1 influence the therapeutic effect of MST,improve the survival of AML patients.

Objective:To investigate the effect of genetic polymorphism of MTHFR C677T (rs1801133) on methotrexate (MTX) related toxicity in pediatric mature B-cell lymphoma patients. Methods:Fifty-eight intermediate and high risk patients under 18 years of age with mature B-cell lymphoma who received 5 g/m2 MTX (24 h intravenous infusion) in Sun Yat-sen University Cancer Center from August 2014 to December 2021 were included,and their toxicity of high-dose MTX (HD-MTX) were monitored and analyzed. Results:Among the 58 pediatric patients,the number of CC,CT,and TT genotypes for MTHFR C677T was 33,19 and 6,respectively. A total of 101 courses of HD-MTX therapy were counted,of which plasma MTX level>0.2 μmol/L at 48 h post-MTX infusion were observed in 35 courses,≤0.2 μmol/L in 66 courses. Inter-group comparison showed that plasma MTX level>0.2 μmol/L at 48 h post-MTX infusion increased the risk of developing oral mucositis (P<0.05). Compared with wild-type (CC genotype),patients in the mutant group (CT+TT genotype) were more likely to develop myelosuppression,manifested as anemia,leucopenia,neutropenia and thrombocytopenia. However,plasma MTX level at 48 h was not associated with MTHFR C677T gene polymorphism. Conclusion:The risk of developing oral mucositis in children with mature B-cell lymphoma is associated with plasma MTX concentration. Polymorphism of MTHFR C677T gene is not related to plasma MTX concentration in children with mature B-cell lymphoma,but is related to grade Ⅲ to Ⅳ hematological toxicity.

Aim To predict the mechanism of Fufang Congrong Yizhi Capsules (FCYC) in the treatment of mild cognitive impairment (MCI) by network pharmacology method, and further validate it in combination with cellular experiments. Methods TCMSP, Gene-Cards, OMIM and TTD databases, Chinese Pharmacopoeia and related literature were used to screen the active ingredients of FCYC and the targets of MCI treatment. The TCM-compound-target-disease network and PPI of intersection targets were constructed, and the GO and KEGG analysis were performed by the Ehamb bioinformation platform. GO and KEGG analysis were performed through Yihanbo biological information platform. Cell model of MCI was established by PC-12 injury induced by Aβ

Objective: To examine the effect of icariin plus curcumol on prostate cancer cells PC3 and elucidate the underlying mechanisms. Methods: We employed the Cell Counting Kit 8 assay and colony formation assay to assess cell viability and proliferation. Autophagy expression was analyzed using monodansylcadaverine staining. Immunofluorescence and Western blot analyses were used to evaluate protein expressions related to autophagy, pyroptosis, and the mTOR pathway. Cellular damage was examined using the lactate dehydrogenase assay. Moreover, cathepsin B and NLRP3 were detected by co-immunoprecipitation. Results: Icariin plus curcumol led to a decrease in PC3 cell proliferation and an enhancement of autophagy. The levels of LC3- Ⅱ/LC3-Ⅰ and beclin-1 were increased, while the levels of p62 and mTOR were decreased after treatment with icariin plus curcumol. These changes were reversed upon overexpression of mTOR. Furthermore, 3-methyladenine resulted in a decrease in inflammatory cytokines, pyroptosis-related protein levels, and lactate dehydrogenase concentration, compared to the icariin plus curcumol group. Inhibiting cathepsin B reversed the regulatory effects of icariin plus curcumol. Conclusions: Icariin plus curcumol demonstrates great potential as a therapeutic agent for castration-resistant prostate cancer by enhancing autophagy via the mTOR pathway and promoting pyroptosis mediated by cathepsin B. These findings provide valuable insights into the molecular mechanisms underlying the therapeutic potential of icariin and curcumol for prostate cancer treatment.

Lactic acid produced by muscles during exercise training is transported to the liver for metabolism through the bloodstream.In this process,the lactate acid level increases with the increase of exercise intensity,and the concentration of lactate acid in interstitial matrix of muscle tissues increases subsequently,leading to muscle fatigue.Transcutaneous electrical nerve stimulation(TENS)is a widely used medical method for muscle relaxation and improving peripheral blood circulation.To monitor the potential of TENS to alleviate muscle fatigue,this study adopted electrical impedance tomography(EIT)method to visualize the alleviating effect of TENS on muscle fatigue by detecting the tissue electrical characteristics response caused by the changes in blood lactate concentration,a biomarker of muscle fatigue.An experimental platform was thus constructed to mimic the changes of blood lactate concentration(Cbl)in the muscle tissue model,and to measure the trend of the spatial-mean conductivity((σ))in the mimic model during the Cbl change.The blood flow velocity was closely related to the metabolic rate of the lactate in the blood.TENS could speed up blood flow and effectively reduced the lactate accumulation in muscle tissue.However,too fast blood flow velocity was prone to cause secondary ventricular fibrillation disease,which threatened the safety of human life.To avoid this threat,a real-time blood flow velocity mimic platform was developed in this study to monitor the(σ)changes caused by the changes in blood flow velocity(vph)in the vicinity of mimic blood vessels.The correlations between Cbl vs(σ),and vph vs(σ)in the mimic muscle tissue were verified by Pearson test.Pearson correlation analysis results showed a positive correlation between Cbl and(σ)(r=0.9113,p<0.05),and betweenvph and(σ)(r=0.9782,p<0.001).The approach presented here quantitatively assessed the potential of TENS stimulation-induced changes in lactate concentration and blood flow velocity for alleviating muscle fatigue through(σ).