Minimally invasive repair of acute closed Achilles tendon rupture with two-way needle suture technique / 中华创伤骨科杂志

Objective:To investigate the efficacy of two-way needle suture technique (TNST) in the minimally invasive repair of acute closed Achilles tendon rupture.Methods:From June 2019 to June 2021, 26 patients with acute closed Achilles tendon rupture were treated at Zhengzhou Orthopedic Hospital. They were 20 males and 6 females, with a mean age of 28 (23, 31) years. The rupture end was (4.2±1.3) cm away from the calcaneal insertion, and the interval from injury to operation 4.3 (2.0, 5.0) d. Preoperative MRI examinations revealed in all the patients closed Achilles tendon rupture which was to be repaired by TNST. The operation time, incision length, incidence of complications, ankle dorsiflexion and plantar flexion were recorded. The Arner-Lindholm scoring was used to evaluate the clinical efficacy.Results:The operation time was (20.0±5.0) min and the incision length (2.5±0.4) cm. Postoperatively, all incisions healed by the first stage, with no complications like incision infection, skin edge necrosis, deep vein thrombosis at lower limbs, injury to the sural nerve, or re-rupture of the Achilles tendon. All patients were followed up for (12.0±6.0) months. At the last follow-up, the patients walked normally, their incisions healed well, the continuity of the Achilles tendon was good by palpation, their heel lift was strong, and all their activities were restored to the levels before rupture of the Achilles tendon. The ankle dorsiflexion was 22.6°±3.7° and the plantar flexion 25.3°±3.7°, According to the Arner-Lindholm evaluation, the clinical efficacy was rated as excellent in 25 cases and as good in 1 case, giving an excellent and good rate of 100% (26/26).Conclusion:In the minimally invasive repair of acute closed Achilles tendon rupture, TNST shows the advantages of limited surgical invasion, a low incidence of postoperative complications, and reliable curative effects.

Inducible knockout of syncytin-a leads to poor placental glucose transport in mice.

INTRODUCTION: Cell-cell fusion of cytotrophoblasts into the syncytiotrophoblast layer is a key process in placental development. Syncytin, an endogenous retroviral envelope protein, is expressed in placental trophoblasts and specifically mediates syncytiotrophoblast layer formation. Syncytin deficiency has been observed in fetal growth-restricted placentas. Abnormal fetal growth, especially fetal growth restriction, is associated with the decreased expression of glucose transporters. Here, we aimed to determine the role of syncytin in fetal growth restriction in placental glucose transport capacity. METHODS: To better explore the function of syncytin in fetal growth-restricted placenta, we generated an inducible knockout mouse model of syncytin-a gene. The expression levels of glucose transporters in BeWo cells were measured before and after HERV-W knockdown. RESULTS: Syncytin-A disruption was associated with significant abnormalities in placental and fetal development in mice. Syncytin-A destruction causes extensive abnormalities in the maternal-fetal exchange structures in the labyrinth, including an extremely reduced number and dramatically irregular distribution of fetal vessels. Moreover, glucose transporter 1, glucose transporters 3, and connexin 26 expression levels decreased after E14.5. Consistently, low glucose transporter 1, glucose transporter 3, and connexin 26 levels were observed in HERV-W-silenced BeWo cells. DISCUSSION: Syncytin-A is crucial for both syncytiotrophoblast layer development and morphogenesis, suggesting that syncytin-A disruption leads to fetal growth restriction associated with abnormalities in the maternal-fetal exchange barrier and decreased glucose transport.

The treatment process of an extremely rare giant borderline phyllodes tumor of breast: case report and literature review.

Giant phyllodes tumors are rare fibroepithelial neoplasms, usually defined as >10 cm. It is often difficult for pathologists to distinguish fibroadenomas from phyllodes tumors and determine the malignant potential level. The current treatment principle is to ensure the extended resection of tumors with a margin of 1 cm or more. For patients with multiple local recurrences or large tumors after surgery, simple mastectomy is recommended. Axillary management should be considered when breast cancer is diagnosed at the same time. We now present a rare case: a female patient found a right breast mass in 2014, and the mass had continued to grow for more than 7 months, and she was ultimately diagnosed with a giant phyllodes tumor with a diameter of 30 cm. Extensive resection is a suitable method to treat smaller phyllodes tumors, but giant phyllodes tumors require mastectomy, so the patient in this case underwent a total mastectomy. We removed the mass completely without destroying the normal tissue and structure. The treatment effect was obvious, and no related adverse events occurred during or after the operation, the postoperative recovery was good, and the patient was discharged once she was verified to be in a stable condition. This case is the first reported case of a patient who had a giant borderline phyllodes tumor with a diameter of 30 cm, underwent total mastectomy, and was followed up for 6 months without recurrence. The long-term effect of the treatment will be further evaluated after 5 years.

Deep brain stimulation of subthalamic nucleus combined with drugs in two patients with Parkinson's disease related neuroleptic malignant syndrome / 中华神经医学杂志

Objective To explore the role of deep brain stimulation of subthalamic nucleus (STN-DBS) in treatment of Parkinson's disease (PD) related neuroleptic malignant syndrome (NMS).Methods The medical history,clinical features,STN-DBS programmed treatment process and treatment results of two patients admitted to our hospital in December 2014 and November 2018 were retrospectively analyzed.Results Two patients with post-operative STN-DBS were evoked by dose-reduced treatment of anti-parkinsonian drugs,and presented with high fever,disorder of consciousness,aggravation of the original parkinsonism,and increase of creatine phosphokinase,which were not correlated with outcomes of infection.After admission,anti-parkinsonian drugs and other supportive therapies were supplemented;STN-DBS modulation were given to improve the symptoms;the final parameters of patient one were the left (C+,2-,1-),pulse width 110 μs,frequency 200 Hz,and strength 3.8 V;the right side (C+,6-,5-),pulse width 110 μs,frequency 200 Hz,strength 4.4 V;and those of patient two were the left (C+,3-),pulse width 60 μs,frequency 130 Hz,strength 2.0 V;right side (C+,6-),pulse width 80 μs,frequency 160 Hz,and strength 2.8 V.Both patients were cured,but their motor function and self-care ability were severely impaired.Conclusion STN-DBS may play an important role in the treatment of PD related NMS.

Defective expression of TGFBR3 gene and its molecular mechanisms in non-small cell lung cancer cell lines / 中国肺癌杂志

<p><b>BACKGROUND AND OBJECTIVE</b>It has been reported that defective expression of TGFBR3 was found in non-small cell lung cancer (NSCLC). However, its molecular mechanisms remain unclear. The aim of this study is to investigate expression of TGFBR3 in NSCLC cell lines and normal human bronchial epithelial cell (HBEpiC), and to explore potential molecular mechanisms underlying inactivation of TGFBR3 gene.</p><p><b>METHODS</b>Western blot was performed to determine the expression of TGFBR3 in HBEpiC and NSCLC cell lines. Automatic image analysis was carried out to estimate relative expression of TGFBR3 protein. We screened for mutation of the promoter region of TGFBR3 gene using DNA direct sequencing. Bisulfite-sodium modification sequencing was used to detect the methylation status of TGFBR3 promoter.</p><p><b>RESULTS</b>TGFBR3 protein level was abnormally reduced in NSCLC cell lines as compared with HBEpiC. There was significant difference in TGFBR3 expression between the highly metastatic cell line 95D and non-metastatic cell lines, including LTEP-alpha-2, A549 and NCI-H460. No mutation and methylation was found in upstream sites -165 to -75 of the proximal promoter of TGFBR3 in HBEpiC and NSCLC cell lines. Hypermethylation was shown in upstream sites -314 to -199 of the distal promoter of TGFBR3 in HBEpiC and NSCLC cell lines.</p><p><b>CONCLUSION</b>Reduced expression of TGFBR3 was observed in NSCLC cell lines, especially in 95D, suggesting that TGFBR3 might play an important role in development and progression of NSCLC and correlate with NSCLC invasion and migration. The methylation event occurring at TGFBR3 promoter is not a major cause for reduction of TGFBR3 expression.</p>