ObjectiveTo explore the application and effectiveness of three-pedicle reduction mammoplasty in breast cancer patients with moderate or greater breast hypertrophy and/or moderate-to-severe breast ptosis. Methods The clinical data of 15 breast cancer female patients with hypertrophy and/or moderate-to-severe breast ptosis treated by three-pedicle reduction mammaplasty with inverted T incision between January 2019 and March 2021 were retrospectively analysed. The patients were aged 31-58 years, with a median age of 39 years. The disease duration ranged from 10 days to 9 months (median, 3.4 months). All patients had unifocal tumor, with a maximum diameter of primary tumor of 0.5-3.9 cm (mean, 2.0 cm), of which 12 were diagnosed with invasive carcinoma and 3 carcinoma in situ. Tumor stage: TisN0M0 in 3 cases, T1N0M0 in 4 cases, T1N2M0 in 2 cases, T2N0M0 in 4 cases, and T2N1M0 in 2 cases. The preoperative cup sizes of patients were D cup in 3 cases, DD cup in 1 case, E cup in 2 cases, EE cup in 2 cases, F cup in 2 cases, FF cup in 1 case, and ≥G cup in 4 cases. The distance from nipple to inframammary fold was 8-18 cm (mean, 12.2 cm) before operation. The patients were followed up regularly after operation to evaluate the breast reduction effect and complications; Breast cancer reporting outcome scale (BREAST-Q) was used to assess patients’ satisfaction and quality of life; and ultrasound, chest and abdominal CT, whole-body bone scan were performed to assess local tumor recurrence or distant metastasis. Results The postoperative nipple position was slightly higher than inframammary fold in all patients. Postoperative cup sizes were A cup in 3 cases, B cup in 6, C cup in 4, D cup in 1, and DD cup in 1, which showing significant difference when compared with preoperative cup sizes (Z=3.420, P=0.001). The median follow-up time was 9 months (range, 6-33 months). Postoperatively, 2 cases (13.3%) had wound-site cellulitis, 1 (6.7%) had mild fat liquefaction, 2 (13.3%) had nipple and areola hypoesthesia but recovered after 3 months. No complication such as fat necrosis, papillary areola complex, or flap necrosis occurred. All patients had undergone adjuvant radiotherapy, of which 1 (6.7%) showed mild skin color change after radiotherapy, but no radiotherapy-related complication occurred in all patients. No patient was readmitted, received reoperation, or delayed to adjuvant therapy due to complications. In the BREAST-Q score, breast satisfaction and quality of life scores at 3 and 6 months after operation were significantly better than those before operation and at 1 month after operation (P<0.05); no significant difference was found between at 1 month after operation and before operation (P>0.05). Nipple satisfaction scores at 1, 3, and 6 months after operation were 15.6±2.2, 18.5±1.4, 19.3±0.7, respectively. At discharge after operation, the patient’s satisfaction with the outcome of the operation was scored 84.7±11.4. The score of adverse events of radiotherapy at 6 months after operation was 6.5±0.8. During the follow-up, patient had no local recurrence, distant metastasis, or breast cancer related death. Conclusion For breast cancer patients with moderate or greater breast hypertrophy and/or moderate-to-severe breast ptosis, three-pedicle reduction mammoplasty can not only remove the lesions, but also reduce hypertrophic breasts, accomplish the mammoplasty, reduce the radiotherapy complications, and improve the satisfaction and quality of life of patients.
Objective To investigate the effect of myoblast transplantation on duchenne muscular dystrophy (DMD) and to explore the method and feasibil ity of applying gene therapy to DMD. Methods Myoblast of C57/BL10 mice were cultured using multiple-step enzyme digestion method and differential velocity adherent technique. The morphology of the cells was observed with inverted phase contrast microscope. The cells at passage 4 were labeled with 5-BrdU. Twenty-four DMDmodel mice (mdx mice: aged 4-6 weeks, male, 13.8-24.6 g) were randomly divided into two groups (n=12 per group): group A, 1 × 106/mL labeled myoblast were injected via ven caudal is twice at an interval of 2 weeks; group B: 1 mL DMEM/F12 was injected in the same manner serving as a control group. The mice were killed 4 weeks after operation and the motor abil ity of the mice was detected by one-time exhaustive swimming before their death. HE staining and immunohistochemistry staining observation for 5-BrdU, desmin, and dystrophin (Dys) were preformed, and the imaging analysis was conducted. Results The primary myoblast could be sub-cultured 5-7 days after culture, providing stable passage and sufficient cells. The time of onetime exhaustive swimming was (60.72 ± 5.76) minutes in group A and (47.77 ± 5.40) minutes in group B, there was significant significance between two groups (P lt; 0.01). At 4 weeks after injection, HE staining showed that in group A, there were round and transparent-stained myocytes and the percentage of centrally nucleated fibers (CNF) was 67%; while in group B, there were uneven muscle fiber with such pathological changes as hypertrophia, atrophia, degeneration, and necrosis, and the percentage of CNF was above 80%. Immunohistochemistry staining revealed that the expression of 5-BrdU, desmin, and Dys was positive in group A; while in group B, those expressions were l ittle or negative. Image analysis result displayed that integral absorbency (IA) value of desmin was 489.70 ± 451.83 in group A and 71.15 ± 61.14 in group B (P lt; 0.05) and the ratio of positive area to thetotal vision area was 0.314 3 ± 0.197 3 in group A and 0.102 8 ± 0.062 8 in group B (P lt; 0.05); the Dys IA value was 5 424.64 ± 2 658.01 in group A and 902.12 ± 593.51 in group B (P gt; 0.05) and the ratio of positive area to the total vision area was 0.323 7 ± 0.117 7 in group A and 0.035 2 ± 0.032 9 in group B (P lt; 0.05). Conclusion Myoblast transplantation has certain therapeutic effect on DMD of mice.
This study aimed to explore the role of miR-130a-3p in cardiomyocyte hypertrophy and its underlying mechanisms. Pressure-overload induced myocardial hypertrophy mice model was constructed by thoracic aortic constriction (TAC). In vitro, norepinephrine (NE) was used to stimulate neonatal rat cardiomyocytes (NRCMs) and H9c2 rat cardiomyocytes to induce hypertrophic phenotypes. The expression of miR-130a-3p was detected in mice hypertrophic myocardium, hypertrophic NRCMs and H9c2 cells. The mimics and inhibitors of miR-130a-3p were transfected into H9c2 cells to observe the role of miR-130a-3p on the hypertrophic phenotype change of cardiomyocytes separately. Furthermore, whether miR-130a-3p regulated hypertrophic related signaling pathways was explored. The results showed that the expression of miR-130a-3p was significantly decreased in hypertrophic myocardium, hypertrophic NRCMs and H9c2 cells. After transfection of miR-130a-3p mimics, the expression of hypertrophic marker genes, atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and β-myosin heavy chain (β-MHC), and the cell surface area were notably down-regulated compared with the control group (mimics N.C. + NE group). But after transfection of miR-130a-3p inhibitor, the expression of ANP, BNP and β-MHC in H9c2 cells increased significantly, and the cell area increased further. By Western blot, it was found that the protein phosphorylation level of Akt and mTOR were down-regulated after over-expression of miR-130a-3p. These results suggest that miR-130a-3p mimics may alleviate the degree of cardiomyocyte hypertrophy, meanwhile its inhibitor can further aggravate cardiomyocyte hypertrophy. Over-expression of miR-130a-3p may attenuate cardiomyocytes hypertrophy by affecting the Akt pathway.
Deep hypothermic circulatory arrest (DHCA) is an important assistant technique for complex cardiac surgery, which creates convenient operating conditions for surgery, and is also one of the measures to protect the brain during operation. However, the complications caused by this technique cannot be ignored, and it should be noticed that the occurrence of intestinal injury is relatively insidious, but brings great pain to patients and significantly reduces the quality of life after operation. Studies have shown that intestinal ischemia-reperfusion injury is induced by DHCA. It causes mast cells to activate and release many inflammatory mediators that destroy the intestinal mucosal epithelium barrier, and eventually lead to intestinal injury. This article reviewed the research progress of mast cells in the mechanism of DHCA-induced intestinal injury.
Objective To investigate the effect of tranilast on wound healing and the mechanism of inhibiting scar hyperplasia in mice, and to study the relationship between the inhibiting ability of tranilast on scar hyperplasia and administration time. Methods Sixty-six Kunming mice were selected to build deep II degree burn model, and were randomly divided into the control group (18 mice), the early intervention group (18 mice), the medium intervention group (18 mice), and the late intervention group (12 mice). The mice in the early intervention group, the medium-term intervention group, and the late intervention group were given tranilast 200 mg/(kg·d) by gastrogavage at immediate, 7 days, and 14 days after burn respectively, and the mice in the control group were managed with same amount of normal saline every day. The wound healing was observed regularly. At 14, 28, and 42 days in the early and medium intervention groups and at 28 and 42 days in the late intervention group, fresh tissues were taken from 6 mice to observe the shape of mast cells by toluidine blue staining, collagen content by Masson staining; the collagen type I and collagen type III content were measured to calculate the I/III collagen content ratio by immunohistochemistry method, the contents of transforming growth factor β1 (TGF-β1) and histamine were detected by ELISA; and the ultrastructure of fibroblasts was observed under transmission electron microscope. Results There was no significant difference in wound healing time between groups (F=1.105,P=0.371). The mast cells number, collagen content, TGF-β1 content, histamine content, and the I/III collagen content ratio in the early intervention group were significantly less than those in the other groups (P<0.05). Significant difference was found in mast cells number, collagen content, and histamine content between control group and medium or late intervention group at the other time points (P<0.05) except between control group and late intervention group at 42 days (P>0.05). Compared with the control group, the activity of fibroblasts in the early intervention group was obviously inhibited, and the arrangement of the fibers was more regular; the fibroblast activity in the medium and late intervention groups was also inhibited obviously. Conclusion Tranilast has no obvious effect on the wound healing time in mice. Tranilast intervention shows the inhibitory effect on the scar hyperplasia which can significantly reduce the number of mast cells, the content of histamine and TGF-β1, inhibit the ability of fibroblasts synthetic collagen and adjust the proportion of collagen synthesis. The immediate tranilast intervention may have the best inhibitory effect on scar hyperplasia.