OBJECTIVETo observe the clinical effects of free musculo-cutaneous flap bridging with contralateral posterior tibial vessel on repair of lower extremity soft tissue defect.

METHODSFrom February 2006 to June 2013, 10 patients with soft tissue defect on lower shank and foot were included. The posterior tibial vessel on healthy lower extremity was chosen as recipient vessel and anastomosed with free latissimus dorsi musculo-cutaneous flap, or free latissimus dorsi musculo-cutaneous flap combined with thoracic-umbilical skin flap or anterolateral femoral musculo-cutaneous flap. The retrograde bridged flap was transposed to repair defect on contralateral lower shank and foot. The wound area ranged from 40 cm x 21 cm to 22 cm x 15 cm, with flap size from 48 cm x 26 cm to 25 cm x 18 cm. Meanwhile the defects on donor sites were covered with skin graft and both lower extremities were fixed with kirschner wires at middle tibia and calcaneus. The kirschner wires were removed at 4 weeks and pedicles were cut off 5-8 weeks postoperatively. Six patients received posterior tibial vessel reanastomosis at the same time of pedicle cutting.

RESULTSAll the 10 flaps survived and 3 patients received thinning of flaps due to excessive thickness. During the follow-up period of 3 months to 2 years follow up, the ambulatory function of injured legs recovered gradually with satisfactory appearance. The reanastomosed posterior tibial vessel on the healthy side was recovered.

CONCLUSIONSAppropriate bridged musculo-cutaneous flaps is suitable for extensive soft tissue defect of lower shank and foot. It is a safe and effective method for limb salvage.

Foot ; Free Tissue Flaps ; transplantation ; Humans ; Lower Extremity ; Skin Transplantation ; Soft Tissue Injuries ; surgery ; Wound Healing

Cholangiocarcinoma is a primary malignant tumor derived from the epithelium of the intrahepatic and extrahepatic bile ducts, and vasculogenic mimicry induced by hypoxia and lack of nutrition is a key factor for malignant proliferation, recurrence, and metastasis of cholangiocarcinoma. Previous studies have shown that autophagy maintains cell nutrition metabolism under the condition of a lack of nutrition, and preliminary experiments have confirmed that autophagy was associated with VM in cholangiocarcinoma and there was high expression of PAT4 in cholangiocarcinoma cells; on the basis of these studies, it is pointed out that in cholangiocarcinoma, protective autophagy regulates VM formation by maintaining intracellular metabolic balance and cellular homeostasis. As a nutrient sensor in tumor microenvironment, PAT4 mediates protective autophagy via the PI3K-Akt-mTORC1 signaling pathway to regulate VM formation. Histological, cellular molecular, and in vivo experiments have confirmed that autophagy regulates VM formation by maintaining cell metabolism, stem cell features, and extracellular matrix remodeling, which helps to investigate the signal mechanism for PAT4 mediating autophagy to regulate VM. It is suggested that autophagy is the source of energy and nutrition in cholangiocarcinoma cells under the condition of a lack of nutrition, and PAT4 is the trigger point for autophagy in regulating VM formation. These findings provide new thoughts for the metabolism of cholangiocarcinoma cells and lay a theoretical foundation for antiangiogenic drugs combined with autophagy inhibitors in the treatment of highly aggressive tumors.

Compared with conventional radiotherapy, FLASH radiotherapy has advantages in protecting normal tissues, while the dose rate is increased by more than 100 times. If the shielding design of the treatment room is carried out according to the existing standard, the thickness and cost of the shielding wall will be significantly increased, or even hardly to meet the requirement of the standards, resultsing in the failure of the application of FLASH radiotherapy. By investigating the domestic and foreign standards and literature, this paper analyzes the challenges brought by FLASH radiotherapy technology to the shielding design of radiotherapy treatment room in China. Dose rate control standards adopted by different countries in the shielding design are emphatically compared as well. In several countries, the average dose rate under the actual treatment conditions was considered in the shielding design. In China, the method of instantaneous dose rate taking acount of occupancy factor is adopted. However, if FLASH radiotherapy technology is applied, the requirement of instantaneous dose rate will be difficult to meet. In order to improve the high dose rate radiotherapy technology such as FLASH radiotherapy, the revision of the existing standards is advised if the authorized limits are not changed. To use the average dose rate limit within a certain period of time for control, or to raise the control standard in the case of flash radiotherapy, are also avaliable.

Objective:To introduce the clinical dosimetry commissioning methods and results of the 1.5 T MR-linac.Methods:In May, 2019, an Elekta Unity 1.5 T MR-linac was installed in Cancer Hospital, Chinese Academy of Medical Sciences and dosimetry commissioning was performed with magnetic field compatible measuring instruments. Commissioning items include absolute dose calibration, data acquisition and planning system model verification.Results:Absolute dose calibration in magnetic field should be corrected by magnetic field correction factor. The standard output dose of Unity was 87 cGy. Gamma analysis (3%/2 mm) was performed on the beam collection data and the planning system calculation data. The average pass rate of dose verification of standard field test cases was 96.41%, and the TG119 test case was 98.24%. The IROC end to end test case was 97.5%(7%/4 mm).Conclusions:The planning system model and the beam collection data have good consistency. The dose verification results of the standard field and TG119 test cases meet the general tolerance limit requirements of the AAPM TG218 report, and the verification results of the IROC end-to-end test cases meet the IROC center standards.

Metabolic reprogramming is a hallmark of cancer, including lung cancer. However, the exact underlying mechanism and therapeutic potential are largely unknown. Here we report that protein arginine methyltransferase 6 (PRMT6) is highly expressed in lung cancer and is required for cell metabolism, tumorigenicity, and cisplatin response of lung cancer. PRMT6 regulated the oxidative pentose phosphate pathway (PPP) flux and glycolysis pathway in human lung cancer by increasing the activity of 6-phospho-gluconate dehydrogenase (6PGD) and α-enolase (ENO1). Furthermore, PRMT6 methylated R324 of 6PGD to enhancing its activity; while methylation at R9 and R372 of ENO1 promotes formation of active ENO1 dimers and 2-phosphoglycerate (2-PG) binding to ENO1, respectively. Lastly, targeting PRMT6 blocked the oxidative PPP flux, glycolysis pathway, and tumor growth, as well as enhanced the anti-tumor effects of cisplatin in lung cancer. Together, this study demonstrates that PRMT6 acts as a post-translational modification (PTM) regulator of glucose metabolism, which leads to the pathogenesis of lung cancer. It was proven that the PRMT6-6PGD/ENO1 regulatory axis is an important determinant of carcinogenesis and may become a promising cancer therapeutic strategy.