BIA-ALCL often occurs 7-10 years after breast reconstruction surgery with breast implants and its incidence is about 23-33 per million. The most common symptoms include breast swelling with seroma, breast mass and lymphadenopathy. It’s assumed that BIA-ALCL is associated with immune response induced by textured breast implants with clonal expansion of local CD30 + T cell, some gene mutations such as JAK1 and STAT3 mutations as well as pathogen infections. Currently, ultrasonography, cytological and immunological tests of exudate as well as biopsy of breast mass are commonly applied for diagnosis. From the perspective of oncology, we propose the following suggestions: (1) We should be alert to the risk of missed diagnosis in the current medical environment, and clinical information is suggested to be collected especially for Asian patients. (2) Due to the low incidence and good prognosis of BIA-ALCL, those who have used textured implants don’t need to be over-worried. (3) It is suggested that researches about manufacturing technology of textured breast implants, JAK-STAT mutations and pathogen infections should be carried out to explore the pathogenic mechanisms of BIA-ALCL, and multi-disciplinary cooperation should be advocated to cope with the diagnosis and treatment of this disease.

BIA-ALCL often occurs 7-10 years after breast reconstruction surgery with breast implants and its incidence is about 23-33 per million. The most common symptoms include breast swelling with seroma, breast mass and lymphadenopathy. It’s assumed that BIA-ALCL is associated with immune response induced by textured breast implants with clonal expansion of local CD30 + T cell, some gene mutations such as JAK1 and STAT3 mutations as well as pathogen infections. Currently, ultrasonography, cytological and immunological tests of exudate as well as biopsy of breast mass are commonly applied for diagnosis. From the perspective of oncology, we propose the following suggestions: (1) We should be alert to the risk of missed diagnosis in the current medical environment, and clinical information is suggested to be collected especially for Asian patients. (2) Due to the low incidence and good prognosis of BIA-ALCL, those who have used textured implants don’t need to be over-worried. (3) It is suggested that researches about manufacturing technology of textured breast implants, JAK-STAT mutations and pathogen infections should be carried out to explore the pathogenic mechanisms of BIA-ALCL, and multi-disciplinary cooperation should be advocated to cope with the diagnosis and treatment of this disease.

Objective:To investigate the expression of microRNA-296 (miR-296) in rabbit hypertrophic scars and its role in human fibroblasts (HFbs).Methods:The experimental method was used. Twelve healthy adult New Zealand long-eared rabbits regardless gender were randomly divided into normal control group and scar group, with 6 rabbits in each group. The rabbit ear hypertrophic scar model was created in scar group according to the literature, and the rabbits in normal control group did not receive any treatment. On 60 days after setting up the models in scar group, hematoxylin-eosin staining was performed to observe the growth and arrangement of fibroblasts (Fbs) in the ear scars and skin tissue of rabbits in the two groups. The mRNA expressions of miR-296 and transforming growth factor-β 1 (TGF-β 1) in ear scars and skin tissue of rabbits in the two groups were detected by real-time fluorescent quantitative reverse transcription polymerase chain reaction, and the correlation of mRNA between miR-296 and TGF-β 1 was performed with Pearson regression analysis. Two batches of HFbs were used and transfected respectively with corresponding sequences, with the 1st batch being divided into TGF-β 1 wild type+miR-296 negative control group and TGF-β 1 wild type+miR-296 mimic group and the 2nd batch being divided into TGF-β 1 mutant type+miR-296 negative control group and TGF-β 1 mutant type+miR-296 mimic group. At 48 h after transfection, luciferase reporter gene detection kit was used to detect the luciferase and renal luciferase expression of TGF-β 1 in the cells of each group, with their ratio being used to reflect the gene expression level. Two batches of HFbs were used, and each batch of cells were divided into miR-296 negative control group and miR-296 mimic group, being transfected with the corresponding sequences. At 0 (immediately), 12, 24, 36, and 48 h after transfecting the first batch of cells, the cell proliferation was detected by thiazolyl blue method. At 24 h after transfecting the second batch of cells, the expression of TGF-β 1 and collagen type Ⅰ was detected by Western blotting. The number of samples in cell experiments was 3. Data were statistically analyzed with analysis of variance for factorial design, independent sample t test. Results:On 60 days after setting up the models in scar group, the Fbs of rabbit ear scar tissue in scar group proliferated and arranged disorderly, while the growth and arrangement of Fbs in rabbit ear skin tissue in normal control group were normal. The mRNA expression of miR-296 of rabbit scar tissue in scar group (0.65±0.11) was significantly lower than 1.19±0.12 of rabbit ear skin tissue in normal control group ( t=5.175, P<0.01). The mRNA expression of TGF-β 1 of rabbit ear scar tissue in scar group (1.47±0.06) was significantly higher than 1.10±0.03 of rabbit ear skin tissue in normal control group ( t=12.410, P<0.01). Pearson regression analysis showed that there was a negative correlation between the mRNA expression of miR-296 and TGF-β 1 in the ear scars and skin tissue of 12 rabbits ( F=7.278, P<0.05). At 48 h after transfection, the gene expression of TGF-β 1 of cells in TGF-β 1 wild type+miR-296 mimic group was significantly lower than that in TGF-β 1 wild type+miR-296 negative control group ( t=35.190, P<0.01), while the gene expression of TGF-β 1 of cells in the two TGF-β 1 mutant type groups were close ( P>0.05). The HFbs proliferation ability in miR-296 mimic group was significantly lower than that in miR-296 negative control group at 12, 24, 36, and 48 h after transfection( t=3.275, 11.980, 10.460, 17.260, P<0.05 or P<0.01). At 24 h after transfection, the protein expressions of TGF-β 1 and type Ⅰ collagen of cells in miR-296 negative control group were significantly higher than those in miR-296 mimic group ( t=3.758, 29.390, P<0.05 or P<0.01). Conclusions:The miR-296 expression in rabbit hypertrophic scars is down-regulated; miR-296 can inhibit the proliferation of HFbs and the expression of type Ⅰ collagen by down regulating the expression of TGF-β 1.

Objective:To evaluate the accuracy of diffusion weighted magnetic resonance imaging (DWI-MRI) combined with high resolution temporal bone CT (HRCT) in the location diagnosis of middle ear cholesteatoma and its value in the postoperative follow-up.Methods:134 patients with inital cholesteatoma and 22 patients with suspected recurrent cholesteatoma were selected for HRCT, conventional MRI and DWI examination. Based on the intraoperative and pathological diagnosis, DWI and HRCT images were combined to evaluate the consistency between the lesion location and invasion area of the initial cholesteatoma and intraoperative lesions. The results of HRCT and DWI in the diagnosis of recurrent middle ear cholesteatoma were statistically analyzed to evaluate their diagnostic efficacy.Results:The accuracy rate of DWI combined with HRCT was 90.3%.The sensitivity, specificity, positive predictive value and negative predictive value of HRCT and DWI in the diagnosis of recurrent middle ear cholesteatoma were 27.8%, 75.0%, 83.3%, 18.8% and 100%, 75.0%, 94.7% and 100%, respectively, and the Kappa values consistent with the pathological results were 0.024 and 0.843, respectively. Chi-square test confirmed that there were differences in the diagnosis between groups ( P<0.001). Conclusions:Combined with the high sensitivity of DWI and the high resolution of HRCT, the accuracy of preoperative positioning of the newly diagnosed cholesteatoma can be improved and surgery strategy can be guided. DWI is also of high diagnostic value for recurrent cholesteatoma in the middle ear.

Objective:To explore the effect of chronic intermittent hypoxia(CIH)on learning and memory dysfunc-tion in rats,as well as the expression of high mobility group box-1(HMGB1)and nuclear transcription factor-KB(NF-κB)in the hippocampus region.Methods:The CIH rat model was established,and forty SD rats were randomly divid-ed into four groups:normoxia group,hypoxia for 4 weeks group(CIH4 group),hypoxia for 8 weeks group(CIH8 group),and hypoxia for 12 weeks group(CIH12 group).Morris water maze was used to assess the learning memory ability of rats,and immunohistochemistry and ELISA were used to detect the expression of HMGB1 and NF-κB in the hippocampus of rats.Results:Compared with the normoxia group,the CIH12 and CIH8 groups had longer escape la-tency,the number of crossing the platform and the residence time in the quadrant of the platform were significantly shortened,but there was no significant difference in the CIH4 group.Additionally,there was no significant expression of HMGB1 and NF-κB in the hippocampal region of the normoxia group,but little expression was observed in CIH4 group,and significantly expressed in CIH8 group and CIH12 group,and the expression of CIH12 group was significantly higher than that of CIH8 group.Conclusion:CIH can lead to a decline in learning and memory function in rats,and the longer time of intermittent hypoxia led to the more significant effect on their learning and memory function.In addi-tion,CIH also leads to increased expression levels of HMGB1 and NF-κB in the hippocampus region,and the expres-sion increased more significantly after hypoxia for 12 weeks,comparing to hypoxia for 8 weeks.

Objective:To study the amino acid site variation of HIV-1 Tat protein from different parts of AIDS patients with HAD and non HAD and its effect on oxidative stress of U87 cells.Methods:HIV-1 Tat amino acid sequences were analyzed by BLAST and MEGA6 software to study the variation of amino acid sites in four parts of central nervous tissue basal ganglia(BG) and peripheral spleen (SPL) of an HIV-associated dementia (HAD) patient(H) and a non-HAD patient(N), The HIV-1 tat genes were transfected into U87 cell. The green fluorescent protein was observed under microscope to determine the Tat protein expression. The expression of Tat protein in U87 cells was detected by Western blotting. CK-8 method , Western blotting and malondialdehyde (MDA) detection kit were used to study the effect of Tat protein on cell activity, oxidative stress index glutathione peroxidase (GPX), MDA level. Results:Amino acid sequence analysis showed that the key amino acid sites of HIV-1 Tat protein from N-BG, N-SPL, H-BG and H-SPL were different; Tat protein could inhibit the activity of U87 cells, which could be reversed by antioxidant N-acetyl-L-cysteine (NAC). Compared with the control group, the levels of MDA were increased and the expression of GPX protein was decreased in the four experimental groups ( P<0.05). And different sources of Tat protein had different ability to induce oxidative stress, the level of MDA in H-BG group was higher than that in N-BG group( P<0.05). The expression of GPX protein in BG group of both HAD and non-HAD patients was lower than that of SPL group( P<0.05). Conclusions:There are differences in the key amino acid sites of Tat protein in peripheral and central nervous system between HAD and non-HAD patients, and their effects on oxidative stress were also different.

Objective: To study the clinical reference pulpal blood flow(PBF) values detected by laser doppler flowmetry(LDF) in healthy young population and to analyze their possible affected factors. Methods: Undergraduate students at the age of 17-23 years were enrolled. PBF of 12-22 were detected by LDF based on the standard procedure. Difference of the test results between different sex was analyzed by T test and variance homogeneity test, and the correlation with age was analyzed by the chi-square test, and the difference between the different teeth was analyzed by the random group analysis. Results: 400 students(250 males and 150 females with the average age of 19. 83 years) met the inclusion criteria. The clinical reference values of PBF of different anterior teeth were obtained by the detection of LDF. For the same tooth, PBF values of females were higher than that of males (P＜ 0. 05). PBF values of different ages shared no statistical significance(P＞ 0. 05). For the same gender, PBF values of middle incisor were higher than that of lateral incisors(P＜ 0. 05). Conclusion: The determination of the clinical reference values of PBF detected by LDF may promote the clinical use of this technology.

Objective: To investigate the toxic effect of HIV-1 Vpr protein on neurons. Methods: HIV-1 vpr gene was amplified by nested PCR in four parts of peripheral spleen (SPL) and central nervous tissue meninges (MG) of HIV-associated dementia (HAD) patients and non-HAD patients. Eukaryotic expression vector pEGFP-N1-vpr was constructed. The gene sequence and key amino acid sites were analyzed by BLAST and MEGA6. The expression of Vpr protein in N2a cells was detected by Western-blotting. The effects of Vpr proteins from different sources on the activity and cell cycle of N2a cells were studied by flow cytometry. Results: HIV-1 vpr gene was successfully amplified by PCR. Sequence analysis showed that the vpr gene sequence belonged to HIV-1B subtype. There were amino acid mutations at C-terminal 84, 86 and 87 sites of central Vpr protein from HAD and non-HAD patients. Vpr protein could inhibit the activity of nerve cells, leading to G2 phase arrest. Different sources of Vpr had different intensity of action. Compared with other groups, Vpr protein from the meninges of HAD patients showed stronger inhibition of cell activity and G2 phase arrest ability. Conclusions Variations in key amino acid sites of Vpr protein could cause significant changes in its biological functions, and its significance in the pathogenesis of HAD remains to be further studied.