Guinea pig, pigeon and toad are the vertebrates on different evolution level. The acid phosphatase content in the hepatocytes of centrilobular area and periportal area of hepatic lobules were quantitatively measured by microspectrophotometer and image analyser. The results showed that the content of acid phosphatase of hepatocytes was highest in guinea pig, lowest in pigeon, and toad in between the both. The average density of acid phosphatase distribution in the hepatocytes increases according to the evolution order. The significance of this phenomenon was discussed.

Objective To investigate the relationship between the efficacy of autologous epidermal grafting and the levels of epidermal cytokines in vitiligo. Methods A total of 57 patients with stable vitiligo receiving autologous epidermal grafting were included in this study. Before grafting, 17 patients were irradiated with narrow-band UVB on vitiliginous sites. Suction blister fluid was collected from the recipient site (vitiligous lesions) and donor site (normal skin) in these patients (including the 17 patients irradiated with NB-UVB). ELISA was used to detect the levels of endothelin-1 (ET-1 ) and stem cell factors (SCF) in suction blister fluid. Clinical efficacy was evaluated through a 3-month follow-up. Resttlts Among these 57 patients, 45 successfully responded to autologous epidermal grafting. In these 45 patients, the levels of ET-1 and SCF in vitiligous lesions were 728.97±286.12 ng/L and 329.97±114.13 ng/L respectively, significantly higher than those in nomal skin (503.16±251.44 ng/L, 224.73±107.91 ng/L, t = 5.443, 5.897, respectively, both P < 0.05 ). In those who responded poorly, significant difference was also observed in the level of SCF between the normal skin and vitiligous lesions (309.00±163.89 ng/L vs 204.22±83.25 ng/L, t = 3.03, P < 0.05), but not in the level of ET-1. Increased level of ET-1 was observed in both vitiligous lesions and normal skin of patients who responded well compared to those who responded poorly, while no difference was noticed in the level of SCF between these two groups of patients. The level of ET-1 was statistically higher in vitiligous lesions in patients exposed to NB-UVB than in those without exposure (t = 1.44, P > 0.05). In those patients who responded successfully, the level of ET-1 was lower in the 15 patients exposed to NB-UVB compared to the other 30 patients without exposure (548.48±230.22 ng/L vs 794.60±278.72 ng/L, P<0.05); no significant difference in the level of SCF was noted. Conclusions ET-1 and SCF may both play important roles in the repigmentation of vitiligo, with ET-1 exerting a more important role.

Objective To observe the curative effect of narrow-band ultraviolet(NB-UVB)on stable vitiligo with autologous epidermis grafting.Methods A total of 82 patients with stable vitiligo were recruited and randomly divided into a control group and a treatment group.The patients in the treatment group were pretreated with NB-UVB before autologous epidermis grafting,while those in the control group were not.The pretreatment with NB-UVB was implemented twice a week for at least 4 weeks before the autologous epidermis grafting. A 3-month follow-up observation was conducted with regard to the effectiveness. Results Pretreatment with NB-UVB could significantly increase the survival rate of skin grafts and rate of repigment of leukoplakia,when compared with autologous epidermises transplantation alone.The rate of complete repigment raised significantly(P＜0.05),and so did the curative effect for vulgaris generalized vitiligo(P＜0.029).It was found that the curative effect on vitiligo was closely related to the frequency of NB-UVB radiation,location of leukoplakia,color of skin,and the time of repigment appearance. ConclusiOn Pretreatment with NB-UVB can significantly improve curative effect of autologous epidermis grafting on vitiligo.

Esophageal squamous cell carcinoma (ESCC) is one of the most aggressive cancers in China, but the underlying molecular mechanism of ESCC is still unclear. Involvement of micro-RNAs has been demonstrated in cancer initiation and progression. Despite the reported function of miR-503 in several human cancers, its detailed anti-oncogenic role and clinical significance in ESCC remain undefined. In this study, we examined miR-503 expression by qPCR and found the downregulation of miR-503 expression in ESCC tissue relative to adjacent normal tissues. Fur-ther investigation in the effect of miR-503 on ESCC cell proliferation, migration, and invasion showed that enhanced expression of miR-503 inhibited ESCC aggressive phenotype and overexpres-sion of CCND1 reversed the effect of miR-503-mediated ESCC cell aggressive phenotype. Our study further identified CCND1 as the target gene of miR-503. Thus, miR-503 functions as a tumor suppressor and has an important role in ESCC by targeting CCND1.

Purpose To evaluate the feasibility of cardiac magnetic resonance fractal analysis in evaluating left ventricular trabecular complexity in hypertrophic cardiomyopathy(HCM),and to study the degree of left ventricular trabecular complexity in HCM and the relationship between excessive trabecular complexity and cardiac function.Materials and Methods From August 2020 to December 2022,a total of 80 patients with HCM from the Second Affiliated Hospital of Nanchang University were retrospectively analyzed.Additionally,80 healthy volunteers were recruited as the control group.Left ventricular functional parameters and fractal dimension(FD)of left ventricular trabecular myocardium were measured.The differences of mean global FD,max basal FD and max apical FD were compared between the HCM group and the control group,the correlation between FDs and cardiac function parameters was evaluated.The diagnostic efficiency of mean global FD,max apical FD and max basal FD was analyzed via receiver operating characteristic curve.Results The mean global FD of HCM group was significantly higher than that of normal group,and the difference was statistically significant(1.303±0.047 vs.1.229±0.026;t=-12.387,P<0.001).Mean global FD showed the best performance in differentiating HCM from normal control group.The optimal cut-off value for the diagnosis of HCM was 1.251,with the area under curve of 0.933(95%CI 0.896-0.969).Mean global FD was positively correlated with maximum wall thickness and left ventricular mass index(r=0.686,0.687,P<0.001),and max apical FD was positively correlated with left ventricular ejection fraction(r=0.520,P<0.001).Conclusion The FD obtained by cardiac magnetic resonance fractal analysis technique is reproducible and has definite value in the diagnosis of HCM,with association with the structure and function of left heart.

Alport syndrome (AS), also known as "eye-ear-kidney syndrome or hereditary nephritis", is a common hereditary disorder. AS is caused by pathogenic mutations of type Ⅳ collagen genes ( COL4α3, COL4α4 and COL4α5), leading to defects in the basement membrane of glomeruli, cochlea, and ocular lens. Patients present with hematuria, proteinuria, and progressive renal failure. With the redefinition of AS and the clinical application of high-throughput sequencing technology, the prevalence of AS may be much higher than the previously recognized. The specific pathogenic mechanism of AS is unknown. Recent studies have showed that type Ⅳ collagen gene mutation may lead to kidney injury by causing abnormal basement membrane components, lipid deposition, energy metabolism disorders, endoplasmic reticulum stress, inflammation and fibrosis. Renin-angiotensin system inhibitor is the main therapy of AS, but the effect is not satisfactory. The new therapeutic strategies mainly include inhibition of abnormal collagen signal transduction, reduction of endoplasmic reticulum stress in podocytes, regulation of energy metabolism, antioxidant stress, anti-inflammation and fibrosis, gene and stem cell therapy. The paper reviewed the research progress on pathogenesis and new therapies of AS.

Pancreatic cancer induced by mutation KRAS exhibited a higher risk of incidence, recurrence and mortality. C-Myc is downstream of KRAS and can be involved in the regulation of multiple oncogenic pathways and signaling pathways in pancreatic cancer. Over expressing of C-Myc promotes glycolysis and glutamine uptake in pancreatic cancer cells, promotes cell metabolism and proliferation, is an important factor driving the progress and maintenance of pancreatic cancer, and is related to chemotherapy and immunotherapy drug resistance. C-Myc also interacts with cell cyclin-dependent kinase(CDK) and non-coding RNA to regulate the proliferation, development and metastasis of pancreatic cancer. Therefore, targeting C-Myc was regarded as an effective strategy for the treatment of pancreatic cancer. The activation of C-Myc depends on heterodimerization with its partner MAX and thereby paly a role through binding to the canonical E-Box sequence 5’-CACGTG-3’. Researches showed direct targeting of C-Myc can inhibit the growth of pancreatic carcinoma,such as promoting the degradation of C-Myc, inhibiting the binding of C-Myc/MAX and blocking the binding of C-Myc/MAX to E-box. However, direct targeting has been proved challenging because of its special protein structure. Indirect targeting of C-Myc provided a new strategy for the treatment of pancreatic cancer. C-Myc can be indirected targeting through inhibiting transcription and translation of C-Myc, C-Myc-MAX heterodimerization and promote the ubiquitination and degradation of C-Myc, thus affects the occurrence, development and metastasis of pancreatic cancer.