Bioinformatics-based analysis of mechanistic differences in vascular endothelial injury ischemic stroke induced by atrial fibrillation and atherosclerosis.

Studies of the intracranial vasculature in patients with ischemic stroke caused by atherosclerosis (AS) and cardiac embolism have revealed significantly different degrees of AS, plaque, and vascular stenosis. And the endothelium has a great influence on the vasculature throughout the circulatory system, especially in the brain. This study aimed to investigate the mechanistic differences in endothelial injury between atrial fibrillation (AF)- and AS-induced ischemic stroke. All target genes of AF, AS, and the vascular endothelial cell (VC) were obtained from the GeneCards database; the differential genes of AF and AS separately associated with the VC were established by a Venn diagram. A protein-protein interaction network was created, and Gene Ontology and Kyoto Encyclopedia of Genes and Genomes databases were used to perform genomic enrichment and functional enrichment analysis. Hub genes were selected by Maximal Clique Centrality algorithm ranking and correlation linkage in the STRING database, and then, clinical serum samples were used to verify the quantitative expressions in the AF, AF stroke, AS, and AS stroke groups. Fifty-five AF-VC-related genes and ninety-three AS-VC-related genes were screened, which differed in biological function, cellular composition, and molecular function. The genes correlation between AF and vascular endothelial cells (VCs) was KRAS and PTPN11, and those correlation between AS and VCs was IL-4, IFNG, IL-17A, and CSF-2. IL-4 and CSF-2 may be relevant proteins involved in the differences in stroke mechanisms between AF and AS, and they may act by further influencing the function of their downstream cells. This study provides a preliminary theoretical basis for investigating the differences in mechanisms of endothelial injury between AF- and AS-induced ischemic stroke.

Noncentrosymmetric Weyl phase and topological phase transition in bulk MoTe.

Ideal topological materials are those stable materials with less nontrivial band crossing near the Fermi surface and a long Fermi arc. By means of first-principles calculations, here we present that the 3D monochalcogenide molybdenum telluride (Pm-MoTe) without an inversion center shows a type-II Weyl semimetal (WSM) phase which cannot checked by symmetry index method. A total of eight Weyl points (WPs) are found in different quadrants of the Brillouin zone (BZ) of Pm-MoTe, which guarantee a long Fermi arc. The WSM phase is robust against the spin-orbit coupling (SOC) effect because of mirror symmetry and time reversal symmetry. It is also found that a topological phase transition can be tuned by strain. For different types of strain, the number of WPs can be effectively modulated to a minimum number, and their energies could be closer to Fermi level. These findings propose a promising material candidate that partly satisfies the ideal WSM criteria and extends the potential applications of the tunable topological phase.

Effects of Se substitution and transition metal doping on the electronic and magnetic properties of a MoSxSe2-x/h-BN heterostructure.

The van der Waals heterostructures created by stacking two monolayer semiconductors have been rapidly developed experimentally and exhibit various unique physical properties. In this work, we investigate the effects of Se atom substitution and 3d-TM atom doping on the structural, electronic, and magnetic properties of the MoSe2/h-BN heterostructure, by using first-principles calculations based on density functional theory (DFT). It is found that Se atom substitution could considerably enhance the band gaps of MoSe2/h-BN heterostructures. With an increase in the substitution concentration, the energy band changes from an indirect to a direct band gap when the substitution concentration exceeds a critical value. For 3d-TM atom doping, it is shown that V-, Mn-, Fe-, and Co-doped systems exhibit a half-metallic state and magnetic behavior, while there is no spin polarization in the Ni-doped case. The results provide a theoretical basis for the development of diluted magnetic semiconductors and spin devices based on the MoSxSe2-x/h-BN heterostructure.

Non-centrosymmetric Weyl semimetal state and strain effect in the twisted-brick phase transition metal monochalcogenides.

Weyl semimetals are a class of gapless electronic excitation topological quantum materials upon breaking time-reversal or inversion symmetry. Here, we demonstrate the existence of the Weyl semimetal state in the non-centrosymmetric twisted-brick phase MoTe theoretically. The topological properties and strain effects of MoTe have been systematically studied based on first-principles calculations and the Wannier-based tight-binding method. In the absence of spin-orbit coupling (SOC), MoTe exhibits gapless nodal loop states related to the mirror reflection symmetry. When the SOC is turned on, the two nodal loops split into 22 pairs of Weyl points (WPs) with opposite chirality. When the effect of uniaxial (εz) strain is taken into account, the Weyl semimetal phase of MoTe shows great robustness and striking tunable topological strength. In particular, the total number of WPs changes significantly under strain. MoTe under +4% and +8% uniaxial strains have only four pairs of WPs with a relatively large separation in momentum space. These results show that MoTe under weak strain is a promising partly ideal type I Weyl semimetal candidate, while the isolog structure WTe both opens a direct gap with and without SOC, showing a compensated semimetal state.

Novel CD19-specific γ/δ TCR-T cells in relapsed or refractory diffuse large B-cell lymphoma.

BACKGROUND: T cell receptor (TCR)-T cells possess similar effector function, but milder and more durable signal activation compared with chimeric antigen receptor-T cells. TCR-T cell therapy is another active field of cellular immunotherapy for cancer. METHODS: We previously developed a human anti-CD19 antibody (ET190L1) and generated novel CD19-specific γ/δ TCR-T cells, ET019003, by fusing the Fab fragment of ET190L1 with γ/δ TCR constant chain plus adding an ET190L1-scFv/CD28 co-stimulatory molecule. ET019003 cells were tested in preclinical studies followed by a phase 1 clinical trial. RESULTS: ET019003 cells produced less cytokines but retained comparable antitumor potency than ET190L1-CAR-T cells in vivo and in vitro. In the first-in-human trial, eight patients with relapsed or refractory DLBCL were treated. CRS of grade 1 was observed in three (37.5%) patients; ICANS of grade 3 was noted in one (12.5%) patient. Elevation of serum cytokines after ET019003 infusion was almost modest. With a median follow-up of 34 (range 6-38) months, seven (87.5%) patients attained clinical responses and six (75%) achieved complete responses (CR). OS, PFS and DOR at 3 years were 75.0%, 62.5%, and 71.4%, respectively. Notably, patient 1 with primary CNS lymphoma did not experience CRS or ICANS and got an ongoing CR for over 3 years after infusion, with detectable ET019003 cells in CSF. ET019003 showed striking in vivo expansion and persisted in 50% of patients at 12 months. Three patients received a second infusion, one for consolidation therapy after CR and two for salvage therapy after disease progression, but no response was observed. ET019003 expansion was striking in the first infusion, but poor in the second infusion. CONCLUSIONS: CD19-specific γ/δ TCR-T cells, ET019003, had a good safety profile and could induce rapid responses and durable CR in patients with relapsed or refractory DLBCL, even primary CNS lymphoma, presenting a novel and potent therapeutic option for these patients. TRIAL REGISTRATION: NCT04014894.

Derkash's Classification and Vas Visual Analog Scale to Access the Long-Term Outcome of Neurothoracic Outlet Syndrome: A Meta-Analysis and Systematic Review.

Objective: Many publications report outcomes of surgical treatment for neurothoracic outlet syndrome (NTOS); however, high-quality meta-analyses regarding objective evaluation system accessing the long-term outcome of NTOS are lacking. This meta-analysis summarizes and compares the outcomes of Derkosh's classification and vas visual analog scale of the supraclavicular neuroplastic of brachial plexus (SNBP) and trams auxiliary first rib resection (TFRR). Methods: The Cochrane Library, PubMed, EMBASE, Allied and Complementary Medicine (AMED) were searched for papers published between January 1980 and February 2021, using the keywords "thoracic outlet syndrome," "treatment, surgical." Articles were eligible for inclusion if the following criteria were met studies describing outcomes of surgery for NTOS, published in English, human studies, and available in full text. The exclusion criteria were case reports (n < 10), reviews, abstracts, and studies lacking a control group or without evaluation for two types of surgery. Results: We included 10 studies with 1,255 cases, out of which 622 were in the SNBP group; and 633 were in the TFRR group. After surgery (≥12 months), Derkash's classification was improved in 425 cases with SNBP and 364 cases with TFRR. OR = 1.34 (95% CI: 0.94, 1.92), P = 0.03; vas visual analog scale was improved in 282 cases in the SNBP group and 214 cases in the TFRR group. OR = 1.08 (95% CI: 0.63, 1.85), P = 0.78. Conclusion: This meta-analysis shows that both SNBP and TFRR are effective for NTOS, but that SNBP is better than TFRR in improving Derkash's classification in the long term. Although patients treated with SNBP are more satisfactory, there is no significant difference in vas visual analog scale from TFRR. Systematic Review Registration: https://www.crd.york.ac.uk/PROSPERO/display_record.asp?ID=CRD42021254203, PROSPERO CRD42021254203.

LncRNA BLACAT1 Promotes Proliferation, Migration and Invasion of Prostate Cancer Cells via Regulating miR-29a-3p/DVL3 Axis.

BACKGROUND: Long non-coding RNA bladder cancer associated transcript 1 (BLACAT1) is oncogenic in several types of cancers. However, little is known concerning its expression and function in prostate cancer. METHODS: Paired prostate cancer samples were collected, and the expression levels of BLACAT1, miR-29a-3p and disheveled segment polarity protein 3 (DVL3) were examined by quantitative real-time polymerase chain reaction (qRT-PCR); BLACAT1 shRNAs were transfected into PC-3 and LNCaP cell lines, and proliferative ability was detected by cell counting kit-8 (CCK-8) assay; qRT-PCR and Western blot were used to analyze the changes of miR-29a-3p and DVL3; dual-luciferase reporter gene assay was used to determine the regulatory relationships between miR-29a-3p and BLACAT1, and miR-29a-3p and DVL3. RESULTS: BLACAT1 expression was significantly up-regulated in cancerous tissues of prostate cancer samples and positively correlated with the expression of DVL3, while negatively associated with miR-29a-3p. After the transfection of BLACAT1 shRNAs into prostate cancer cells, the proliferative ability and metastatic ability of cancer cells were significantly inhibited; BLACAT1 shRNAs could reduce the expression of DVL3 on both mRNA and protein expressions levels, the luciferase activity of BLACAT1 reporter was inhibited by miR-29a-3p, and DVL3 was validated as a target gene of miR-29a-3p. CONCLUSION: BLACAT1 expression is abnormally up-regulated in prostate cancer tissues. BLACAT1 can modulate the proliferative and metastatic ability of prostate cancer cells and have the potential to be the "ceRNA" to regulate the expression of DVL3 by sponging miR-29a-3p.

A bispecific CAR-T cell therapy targeting BCMA and CD38 in relapsed or refractory multiple myeloma.

BACKGROUND: BCMA-specific chimeric antigen receptor-T cells (CAR-Ts) have exhibited remarkable efficacy in refractory or relapsed multiple myeloma (RRMM); however, primary resistance and relapse exist with single-target immunotherapy. Bispecific CARs are proposed to mitigate these limitations. METHODS: We constructed a humanized bispecific BM38 CAR targeting BCMA and CD38 and tested the antimyeloma activity of BM38 CAR-Ts in vitro and in vivo. Twenty-three patients with RRMM received infusions of BM38 CAR-Ts in a phase I trial. RESULTS: BM38 CAR-Ts showed stronger in vitro cytotoxicity to heterogeneous MM cells than did T cells expressing an individual BCMA or CD38 CAR. BM38 CAR-Ts also exhibited potent antimyeloma activity in xenograft mouse models. In the phase I trial, cytokine release syndrome occurred in 20 patients (87%) and was mostly grade 1-2 (65%). Neurotoxicity was not observed. Hematologic toxicities were common, including neutropenia in 96% of the patients, leukopenia in 87%, anemia in 43% and thrombocytopenia in 61%. At a median follow-up of 9.0 months (range 0.5 to 18.5), 20 patients (87%) attained a clinical response and minimal residual disease-negativity (≤ 10-4 nucleated cells), with 12 (52%) achieving a stringent complete response. Extramedullary plasmacytoma was eliminated completely in 56% and partially in 33% and of 9 patients. The median progression-free survival was 17.2 months. Two relapsed patients maintained BCMA and CD38 expression on MM cells. Notably, BM38 CAR-Ts cells were detectable in 77.8% of evaluable patients at 9 months and 62.2% at 12 months. CONCLUSION: Bispecific BM38 CAR-Ts were feasible, safe and significantly effective in patient with RRMM. TRIAL REGISTRATION: Chictr.org.cn ChiCTR1800018143.

miR-21-5p promotes cell proliferation and G1/S transition in melanoma by targeting CDKN2C.

Human melanoma is a highly malignant tumor originating from cutaneous melanocytes. The noncoding RNA microRNA (miR)-21-5p has been reported to be expressed at high levels in malignant melanocytic skin tissues, but its potential functional role in melanoma remains poorly understood. Here, we explored the cellular effects of miR-21-5p on melanoma in vitro and the underlying mechanisms. Quantitative real-time PCR was used to show that miR-21-5p is significantly up-regulated in clinical samples from patients with melanoma as compared with adjacent noncancerous tissues. Overexpression of miR-21-5p significantly enhanced, whereas knockdown attenuated, cell proliferation and G1/S transition in melanoma cell lines (A375 and M14). Luciferase reporter assays were used to show that the cyclin-dependent kinase inhibitor 2C (CDKN2C) is a downstream target of miR-21-5p. Furthermore, miR-21-5p mimics resulted in a decrease in CDKN2C expression, and CDKN2C expression was observed to be inversely correlated with miR-21-5p expression in melanoma tissues. Rescue experiments were performed to show that overexpression of CDKN2C partially reversed the effects of miR-21-5p up-regulation on A375 cells. Consistently, knockdown of CDKN2C abolished the effects of miR-21-5p down-regulation on A375 cells. Overall, our studies demonstrate that miR-21-5p can promote the growth of melanoma cells by targeting CDKN2C, which may induce G0/G1 phase arrest of melanoma cells.

MicroRNA-151 regulates the growth, chemosensitivity and metastasis of human prostate cancer cells by targeting PI3K/AKT.

PURPOSE: Prostate cancer causes significant mortality and microRNAs (miRs) have been shown to regulate the growth and metastasis of different cancers. In this context, the present study was designed to investigate the potential of miR-151 in the treatment of prostate cancer. METHODS: The normal and the prostate cancer cell lines (LNCaP, PC-3 and Du-145) were used in this study. The expression of miR-151 was determined by qRT-PCR. The DAPI and annexin V/propidium iodide (PI) staining were used for the detection of apoptosis. Transwell assay was used for the estimation of cell migration and invasion. Western blot analysis was used for the determination of the protein expression. RESULTS: miR-151 was downregulated in prostate cancer cells and showed inhibitory effect on cell growth which was manifested as decline in cell survival and loss of viability of cancer cells. Additionally, the chemosensitivity of prostate cancer cells to 5-FU was enhanced under miR-151 overexpression. Furthermore, miR-151 also inhibited the migration and invasion of cancer cells. The results of western blot analysis showed that miR-151 overexpression blocks the Pi3K/AKT signalling pathway in prostate cancer cells. CONCLUSION: Taken together, miR-151 has growth inhibitory effect against prostate cancer and negatively regulates the cell migration and invasion along with enhancement of chemosensitivity of cancer cells.

Long non-coding RNA CASC2 targeting miR-18a suppresses glioblastoma cell growth, metastasis and EMT in vitro and in vivo.

Long non-coding RNAs (lncRNAs) cancer susceptibility candidate 2 (CASC2) has been characterized as a tumor suppressor in glioma. Although CASC2 may predict the prognosis of glioma patients, the role and mechanism of CASC2 in human glioblastoma remain to be fully illuminated. Expression of CASC2 and miR- 18a was detected using RT-qPCR. Cell growth was evaluated by MTT assay, colony formation assay, and flow cytometry; metastasis and epithelial-mesenchymal transition (EMT) were determined with transwell assay and Western blot, respectively. The target binding between CASC2 and miR-18a was predicted on Starbase software, and confirmed by luciferase reporter assay and RNA immunoprecipitation. Xenograft experiment measured tumor growth. As a result, CASC2 was downregulated and miR-18a was upregulated in glioblastoma tumor tissues and cells (T98 and A172). Overexpression of CASC2 promoted apoptosis rate and E-cadherin expression, but suppressed cell viability, colony-forming ability, migration, invasion, and expression of N-cadherin and Vimentin in T98 and A172 cells, accompanied with tumor growth inhibition in vivo; whereas, silencing of CASC2 exerted the opposite effect on cell growth, metastasis and EMT of T98 and A172 cells in vitro. However, reintroduction of miR-18a could reverse CASC2 upregulation-mediated suppression on above cell behaviors in vitro. More importantly, miR-18a was a downstream target for CASC2, and was negatively regulated by CASC2. Collectively, this study demonstrated that CASC2 served as tumor suppressor in glioblastoma by inhibiting cell growth, metastasis and EMT both in vitro and in vivo partially via CASC2- miR-18a axis.

Leakage of Majorana bound states in an inhomogeneous topological nanowire.

We present an exact solution of the continuum Bogolyubov-de-Gennes Hamiltonian for Majorana bound states (MBSs) generated in a superconductor-semiconductor hybrid topological nanowire. The full energy spectra that include the band states and in-gap states could be obtained. We show that for relatively short wire length, the zero energy mode could be induced even in the topological trivial regime, which also indicates oscillatory dependence on the chemical potential. With the increase of the Zeeman field, the MBSs are almost fully spin-polarized and do not localize at the wire ends gradually. We also extend our discussion to the property of Majorana modes in an inhomogeneous nanowire, in which a local gate voltage is applied to one end of the nanowire. It is found that the local potential barrier or well could modulate the Majorana energy splitting periodically. The leakage of MBSs to the potential region is exponentially suppressed for the barrier case. A potential well could induce near-zero-energy bound states and these states merge with MBSs, leading to the delocalization of MBSs. In the potential well region, both the spin-up and spin-down components of the trivial states account for a significant proportion, which can be detected experimentally.

Long Noncoding RNA NEAT1 Aggravates Aß-Induced Neuronal Damage by Targeting miR-107 in Alzheimer's Disease.

PURPOSE: Alzheimer's disease (AD) is the most common neurodegenerative disease, with a rising prevalence worldwide. Long noncoding RNAs (lncRNAs) have been found to play important roles in the development and treatment of AD. However, the exact role of lncRNA nuclear enriched abundant transcript 1 (NEAT1) in neuronal damage in AD is largely unknown. MATERIALS AND METHODS: The AD model was established in SH-SY5Y and SK-N-SH cells via treatment with amyloid ß1-42 (Aß). The expression of NEAT1 and microRNA-107 (miR-107) was measured by quantitative real-time polymerase chain reaction. Cell viability and apoptosis were detected by MTT assay, immunocytochemistry, and flow cytometry. The expression of phosphorylated tau protein (p-Tau) was measured by Western blot. The interaction between NEAT1 and miR-107 was explored by bioinformatics analysis, luciferase activity, and RNA immunoprecipitation assays. RESULTS: NEAT1 expression was enhanced in Aß-treated SH-SY5Y and SK-N-SH cells, and its knockdown attenuated Aß-induced inhibition of viability and promotion of apoptosis and p-Tau levels. NEAT1 was indicated as a decoy of miR-107. miR-107 abundance was reduced in Aß-treated cells, and its overexpression reversed Aß-induced injury. Moreover, interference of miR-107 abated silencing of NEAT1-mediated inhibition of neuronal damage in Aß-treated SH-SY5Y and SK-N-SH cells. CONCLUSION: LncRNA NEAT1 aggravated Aß-induced neuronal damage by sponging miR-107, indicating a novel avenue for treatment of AD.

Regulation of capillary tubules and lipid formation in vascular endothelial cells and macrophages via extracellular vesicle-mediated microRNA-4306 transfer.

OBJECTIVE: This study aimed to examine regulation of capillary tubules and lipid formation in vascular endothelial cells and macrophages via extracellular vesicle-mediated microRNA (miRNA)-4306 transfer. METHODS: Whole blood samples (12 mL) were collected from 53 patients, and miR-4306 levels in extracellular vesicles (EVs) were analyzed by reverse transcription-polymerase chain reaction. Human coronary artery vascular endothelial cells (HCAECs) and human monocyte-derived macrophages (HMDMs) were transfected with a scrambled oligonucleotide, an miR-4306 mimic, or an anti-miR-4306 inhibitor. The direct effect of miR-4306 on the target gene was analyzed by a dual-luciferase reporter assay. RESULTS: EV-contained miR-4306 released from HMDMs was significantly upregulated in coronary artery disease. Oxidized low-density lipoprotein (ox-LDL)-stimulated HMDM-derived EVs inhibited proliferation, migration, and angiogenesis abilities of HCAECs in vitro. However, ox-LDL-stimulated HCAEC-derived EVs enhanced lipid formation of HMDMs. The possible mechanism of these findings was partly due to EV-mediated miR-4306 upregulation of the Akt/nuclear factor kappa B signaling pathway. CONCLUSIONS: Paracrine cellular crosstalk between HCAECs and HMDMs probably supports the pro-atherosclerotic effects of EVs under ox-LDL stress.

Disorder-induced suppression of the zero-bias conductance peak splitting in topological superconducting nanowires.

We investigate the effect of three types of intrinsic disorder, including that in pairing energy, chemical potential, and hopping amplitude, on the transport properties through the superconducting nanowires with Majorana bound states (MBSs). The conductance and the noise Fano factor are calculated based on a tight-binding model by adopting a non-equilibrium Green's function method. It is found that the disorder can effectively lead to a reduction in the conductance peak spacings and significantly suppress the peak height. Remarkably, for a longer nanowire, the zero-bias peak could be reproduced by weak disorder for a finite Majorana energy splitting. It is interesting that the shot noise provides a signature to discriminate whether the zero-bias peak is induced by Majorana zero mode or disorder. For Majorana zero mode, the noise Fano factor approaches zero in the low bias voltage limit due to the resonant Andreev tunneling. However, the Fano factor is finite in the case of a disorder-induced zero-bias peak.

Magnetic impurity in topological nodal loop semimetals.

We investigate the Kondo effect of a spin-1/2 magnetic impurity in a topological nodal loop semimetal, in which band touchings form a nodal loop. The Fermi surface of a nodal loop semimetal is a torus or a drum-like structure, which is determined by chemical potential. When the chemical potential µ lies at the nodal loop ([Formula: see text]), the magnetic impurity and the conduction electrons form bound states only if their coupling exceeds a critical value. As the chemical potential is tuned away from the nodal loop, the Fermi surface becomes a torus or drum-like structure and the impurity and the host material always favor a bound state due to the finite density of state. Due to the anisotropic dispersion relationship in the energy band, the spatial spin-spin correlations [Formula: see text]([Formula: see text]) are of power-law decay with the decay rates proportional to [Formula: see text] and [Formula: see text] in different directions, respectively. The product [Formula: see text] and [Formula: see text] oscillates in coordinate space and the period is enhanced gradually as the Fermi surface evolves from a torus surface into a drum-like structure.

Clinical application of free groin flap in repairing soft tissue defect in extremities / 中华显微外科杂志

Objective:To observe and summarise the clinical effect of free groin flap in repairing of soft tissue defects in extremities, and to explore the selection of main vessel in a flap.Methods:From January 2018 to January 2021, 146 patients with soft tissue defects in extremities were treated with free groin flaps in the Department of Hand and Microsurgery, Guangxi Guilin Xing'an Jieshou Orthopaedic Hospital. There were 126 patients with traumatic wound and 20 with chronic ulcer. In addition, 86 of the patients with bone fracture and exposure of internal fixator, 18 with tendon, nerve or artery injuries or defects. There were 6 patients with severe infection and other 3 with deep dead space. The sizes of wound ranged from 2.0 cm×3.0 cm to 25.0 cm×6.0 cm. The flap was the same size as the wound and not enlarged. Firstly, the superficial branch of superficial iliac circumflex artery was explored as the axial artery for all the flaps, then the blood supply vessels of the flap were selected according to the availability of the axial artery. The size, course, adjacent and possible length to be freed of the axial artery and the accompanying veins of a flap were recorded. The donor sites were directly sutured and closed. All patients were included in the postoperative follow-up at outpatient clinic.Results:Free groin flap were used to repair the wounds in all patients. However, the main blood supply vessel of the flap was not constant, and it was often required to adjust the way of flap harvesting. Superficial circumflex iliac artery was taken as the axial vessels in 141 patients (96.6%), among them, 133 cases(94.3%) had the superficial branch as the axis and 5 cases (3.6%) had deep branch as the axis. Three patients (2.1%) had the bone and soft tissue defects reconstructed with vascularised iliac mosaic osteocutaneous flap with superficial circumflex iliac artery as axial vessel and 5 cases(3.4%) had the superficial epigastric artery as axial vessel. The axial arteries were measured as follow: the superficial branch of the superficial circumflex iliac artery was 0.5-0.9 mm in diameter and 7.0-9.0 cm in length, the outer diameter of the deep branch was 1.2-1.4 mm and 9.0-11.0 cm in length, and the outer diameter of superficial epigastric artery was 1.0-1.6 mm and 8.0-11.3 cm in length. All the flaps survived smoothly after surgery and the follow-up period ranged 6-40 (mean 26) months. The texture of the flaps was soft with good function.Conclusion:Free groin flap can be used to repair soft tissue defects in extremities. The main axial vessel is the superficial branch of the superficial circumflex iliac artery, followed by the deep branch or the trunk. The superficial abdominal artery can also be used as an axial vessel. Under the circumstances, the flap design needs to be adjusted without changing the supply area

The clinical outcome of Narakas II obstetric brachial plexus palsy by neurolysis and never grafting / 中华显微外科杂志

Objective:To explore the efficacy of neurolysis or nerve grafting in the treatment of the conducting neuroma of Narakas II obstetric brachial plexus palsy (OBPP), and provide the reference basis for choosing an optimal method.Methods:From January, 2009 to December, 2014, 32 patients undergoing surgical treatment due to Narakas II OBPP were included in this study. Neurolysis was performed in 15 patients, and the procedure of nerve grafting was performed in 17 patients. The general information included gender, age, birth weight, injury cause, etc. were recorded and compared to each other between 2 groups. A followed-up study had been conducting after surgery, the functional rating systems of Gilbert and Raimondi were used for quantitative comparison between preoperative function and postoperative function of shoulder joint, elbow joint and hand. In addition, the differences of the measurement data were compared with the single factor analysis of variance and paired t-test by using SPSS 22.0 statistical software. When P<0.05, it was considered statistically significant. Results:There was no statistically significant difference in the baseline information between 2 groups ( P>0.05). The average time of follow-up was 58.44 (48-96) months. And the fourth year' average score of shoulder joint, elbow joint, hand of the neurolysis group improved from preoperative (1.07±0.85) , (2.07±0.77) and (3.47±0.62) score to (3.00±0.73), (4.13±0.62) and (4.53±0.72) score ( P<0.05), and the nerve grafting group rose from an average of (0.76±0.73), (1.71±0.46) and (3.71±0.67) score to (3.24±0.55), (4.29±0.46) and (4.65±0.48) score ( P<0.05). But the different score between 2 groups was no statistically significant ( P>0.05), respectively. In addition, the proportion of the patients who needed the secondary operation about functional reconstruction in the neurolysis group and the nerve grafting group was 73.33% and 35.29% respectively, besides the proportion of the shoulder joint and elbow joint in the surgical sites accounted for 82.35%, 17.65% respectively. Conclusion:Nerve grafting is a better choice for the treatment of conducting neuroma of Narakas II OBPP at present.

Clinical analysis of 24 cases of multi-segment injury of brachial plexus / 中华显微外科杂志

Objective:To explore the diagnosis and treatment of the multi-segment injury of brachial plexus and provide reference for diagnosis and treatment in clinical practice.Methods:From October, 2012 to January, 2015, 24 patients (21 males and 3 females, aged 7-46, average at 25.06±13.01 years) who suffered multi segments injury of brachial plexus were treated by surgical operations. Time from injury to surgery was 7 days to 7 months, with (2.43±2.15) months in average. The general data, injuries and surgical procedures of the patients were recorded. Muscle strength grading was used to evaluate and analyse the curative effect.Results:Twenty-four cases were followed-up for 3.1-7.2 years, with 4.3 years in average. Of the patients, 58.3% of the injuries were caused by mechanical traction. Combined injuries were counted for 83.3%, of which 62.5% combined with ipsilateral limb fractures, 20.8% (5/24) involved in the root of brachial plexus, 79.2% (19/24) with upper part of the clavicle, 91.6% (22/24) with lower part of the clavicle, 16.7% (4/24) with branches of the brachial plexus and 91.7% (22/24) with injuries of 2 segments, 8.3% (2/24) with injuries of 3 segments. At the last followed-up, 55.0% of the patients achieved better than M 3 in total muscle strength. The excellent and good rate was 70.8% in neurolysis group and 42.9% in multiple segment injury group. Conclusion:The mechanism of multi segments injury of brachial plexus is special, and the actual injury is difficult to be located. For patients with multi segments injury, surgical operation should be carried out as early as possible, and the correct surgical procedure can only be determined after the exploration of all sections of the brachial plexus.

Research progress on the treatment of exposure keratitis / 国际眼科杂志(Guoji Yanke Zazhi)

@#Exposure keratitis refers to corneal inflammation caused by corneal dryness, epithelial exfoliation and secondary infection when the cornea loses the protection of the eyelid and is exposed to air. It is a potentially vision-threatening disease and is not uncommon in clinical work, so the treatment and prevention of exposure keratitis remain important. This article reviews the treatment and research progress of exposure keratitis.