HMG20A was identified as a key enhancer driver associated with DNA damage repair in oral squamous cell carcinomas.

BACKGROUND: Oral squamous cell carcinoma (OSCC) is the main type of oral cancer. Disturbing DNA repair is an invaluable way to improve the effectiveness of tumor treatment. Here, we aimed to explore the key enhancer drivers associated with DNA damage repair in OSCC cells. METHODS: Gene Set Enrichment Analysis (GSEA), Gene Set Variation Analysis (GSVA) and Kaplan-Meier analysis were applied to explore the relationship among DNA repair-related genes expression and clinical phenotypes based on The Cancer Genome Atlas (TCGA) database. HOMER software and Integrative Genomics Viewer were applied to identify and visualize enhancers using GSE120634. Toolkit for Cistrome Data Browser was applied to predict transcription factors. Human Protein Atlas Database was used to analyze the protein levels of transcription factors in OSCC and control tissues. Seventy-two OSCC patients were included in this study. qRT-PCR was used to detect transcription factor expression in OSCC and adjacent control tissues collected in this study. qRT-PCR and ChIP-qPCR were used to verify the binding of transcription factors to enhancers, and regulation of target genes transcription. Transcription factor knockdown and control cells were treated with cisplatin. CCK8 was used to detect cell viability and proliferation. Western blotting was implemented to detect the levels of DNA repair-related proteins. Transwell assay was used to detect cell invasion. RESULTS: DNA repair was positively associated with the OSCC metastatic phenotype. Patients in the cluster with high expression of DNA repair-related genes had a worse prognosis and a higher proportion of advanced stage, low-differentiation, alcohol consumption and smoking compared to the cluster with low DNA repair-related gene expression. Seventeen metastasis-specific enhancer-controlled upregulated DNA repair-related genes, with the top two upregulated genes being ADRM1 26 S proteasome ubiquitin receptor (ADRM1) and solute carrier family 12 member 7 (SLC12A7) were screened. High mobility group 20 A (HMG20A) was the key prognostic enhancer driver regulating metastasis-specific DNA repair-related genes, with higher expression in OSCC tissues than normal control tissues, and higher expression in metastatic OSCC tissues than non-metastatic OSCC tissues. HMG20A bound to the metastasis-specific enhancers of ADRM1 and SLC12A7, thereby promoting ADRM1 and SLC12A7 expression. Knockdown of HMG20A enhanced cisplatin sensitivity of cells, and inhibited OSCC cells from repairing DNA damage caused by cisplatin, as well as proliferation and invasion of OSCC cells. CONCLUSION: HMG20A was identified as the key prognostic enhancer driver regulating DNA repair in OSCC cells, providing a new therapeutic target for OSCC.

Low bone turnover and reduced angiogenesis in streptozotocin-induced osteoporotic mice.

It is known that type 1 diabetes (T1D) reduces bone mass and increases the risk for fragility fractures, an effect that has been largely ascribed to decreased bone formation. However, the potential role of decreased angiogenesis as a factor in osteogenesis reduction has not been extensively studied. Furthermore, there is controversy surrounding the effect of T1D on bone resorption. This study characterized bone microstructure, bone strength, and bone turnover of streptozotocin (STZ)-induced diabetic mice (T1D mice) and explored the role of angiogenesis in the pathogenesis of T1D-induced osteoporosis. Results demonstrate that T1D deteriorated trabecular microarchitecture and led to reduced bone strength. Furthermore, T1D mice showed reduced osteoblast number/bone surface (N.Ob/BS), mineral apposition rate, mineral surface/BS, and bone formation rate/BS, suggesting attenuated bone formation. Decreased angiogenesis was shown by a reduced number of blood vessels in the femur and decreased expression of platelet endothelial cell adhesion molecule (CD31), nerve growth factor, hypoxia-inducible factor-1α, and vascular endothelial growth factor was observed. On the other hand, reduced bone resorption, an effect that could lead to impaired osteogenesis, was demonstrated by lower osteoclast number/BS and decreased tartrate-resistant acid phosphatase and cathepsin K mRNA levels. Reduced number of osteoblasts and decreased expression of receptor activator for nuclear factor-κB ligand could be responsible for compromised bone resorption in T1D mice. In conclusion, T1D mice display reduced bone formation and bone resorption, suggesting decreased bone turnover. Furthermore, this study points to impairments in angiogenesis as a pivotal cause of decreased bone formation.

[Diagnosis and management of sleep-related painful erections:A report of 9 cases].

Objective: To investigate the pathogenesis and management of sleep-related painful erections(SRPE). Methods: This study included 9 SRPE patients aged 39- 59( mean 47. 8) years and with a mean disease course of 13. 5 ± 1. 2 months. We conducted blood urine routine examinations, collected four blood coagulation indexes, obtained IIEF-5 scores and sexual hormone levels, and recorded the nocturnal penile tumescence( NPT) and results of polysomnographic sleep monitoring of the patients. After 1,4,8,12,and 24 weeks of individualized treatment for each patient, we performed telephone follow-up for therapeutic effects and adverse drug reactions. Results: All the 9 patients were diagnosed with primary SRPE after excluding other diseases,6 of them treated with chlorimipramine or chlorimipramine combined with other medicine and the other 3 by antiandrogen therapy. Complete pain remission was achieved by 77. 78% at 4 weeks and 66. 67% at 24 weeks. The 3 patients treated by antiandrogen therapy experienced recurrence at 24 weeks but relieved after 1 week of adjusted treatment. Conclusion: Chlorimipramine, combination of chlorimipramine with medicine, and antiandrogen therapy are all evidently effective for the treatment of primary SRPE.

The first dog-origin porcine circovirus type 4 complete genomic sequence have high homology with that of pig-derived strains.

Introduction: Porcine circovirus 4 (PCV4) was discovered in 2019 and then proved to be pathogenic to piglets. Nevertheless, few studies were currently available about PCV4 infection in species other than pigs and there is no information about the prevalence of PCV4 in dogs. Methods: To fill this gap, 264 dog samples were collected from animal hospitals in the Southwest of China from 2021 to 2022 and screened for PCV4. Moreover, the complete genome of one PCV4 strain (SCABTC-Dog2022) were obtained successfully and shared a high identity (97.9-99.0%) with other PCV4 strains derived from pigs, dairy cows, raccoon dogs and foxes. The SCABTC-Dog2022 were analyzed together with 51 reference sequences. Results and Discussion: The detected results showed a low percentage of PCV-4 DNA (1.14%, 3/264), indicating that PCV4 could be identified in dogs in southwest China. Phylogenetic tree showed that SCABTC-Dog2022 strain derived from dog were clustered in a closed relative and geographically coherent branch with other PCV4 strains collected from four provinces (Sichuan, Fujian, Hunan and Inner Mongolia) of China. To our knowledge, it is the first detection of PCV4 in dogs globally. The association between PCV4 status and clinical syndromes in dogs deserves additional investigations.

Methodological framework for identifying sustainability intervention priority areas on coastal landscapes and its application in China.

In regional sustainability evaluation and policy analysis, the paradigm of safe operating spaces (SOS) has been widely applied. Yet, SOS is not readily useful for informing policy interventions toward sustainability transition. This study reports on a methodological framework that operationalizes SOS at the regional scale for designing spatially targeted sustainability interventions. In particular, this framework accounts for teleology by integrating policy orientations of the place-variant "major function" of development, and provides early-warnings by integrating long-term social-environmental trends. The framework we proposed has been applied by the Chinese government in a coastal province (Liaoning) for a landscape sustainability project, which is introduced here step-by-step. The four main steps include: (1) Quantifying SOS status across multiple "what to sustain" dimensions, e.g., land scarcity, water scarcity, pollutant discharge, and ecosystem health for the inland, and coastal exploitation intensity, marine environmental quality, and marine ecosystem biodiversity for the sea. (2) Quantifying SOS status in terms of the place-variant "what to develop" dimensions, e.g., urbanization-oriented, agriculture-stock-oriented, versus conservation-oriented development. (3) Integrating the two as a composite indicator of three ordinal levels to classify the current SOS status. (4) Developing a multi-level sustainability early-warning system by cross-analysis of the SOS status and social-environmental interaction trends (e.g., changes in, e.g., resource utilization efficiency, pollutant discharge, and eco-environmental quality). The potential use of the framework is demonstrated through the case of Liaoning Province, China, which helps policy-makers to identify priority areas for sustainability interventions. Methodological robustness and future directions of applying this multi-level sustainability early-warning system are further discussed.

Growth factors contribute to the mediation of angiogenic capacity of glioma-associated mesenchymal stem cells.

Mesenchymal stem cells (MSCs) are important components of stromal cell populations and serve a crucial role in tumor growth and progression. Previously, our laboratory successfully isolated and cultured MSCs from human glioma issues and demonstrated that glioma-associated mesenchymal stem cells (gb-MSCs) participate in and maintain tumor angiogenesis. Furthermore, growth factors, such as fibroblast growth factor and vascular endothelial cell growth factor, were demonstrated to be associated with endothelial cell tube formation. However, the effect of transforming growth factor ß1 (TGF-ß1) and platelet-derived growth factor-BB (PDGF-BB) on the angiogenic activity of gb-MSCs remains unknown. The present study aimed therefore to explore their effects in gb-MSCs angiogenesis. In the present study, gb-MSCs were isolated from patients with glioma and were characterized using flow cytometry and differentiation experiments. Furthermore, the results from tube formation assay revealed that TGF-ß1 and PDGF-BB could mediate the angiogenic capacity of gb-MSCs in vitro. In addition, results from immunofluorescence demonstrated that gb-MSCs expressed TGF-ß1R and PDGFR, which are the receptors for TGF-ß1 and PDGF-BB, respectively. Taken together, these findings indicated that TGF-ß1 and PDGF-BB may serve a crucial role in mediating gb-MSC angiogenesis, which might provide a therapeutic strategy for targeting the angiogenic capacity of gb-MSCs in patients with glioma.

Cell fusion in cancer hallmarks: Current research status and future indications.

Cell fusion is involved in several physiological processes, such as reproduction, development and immunity. Although cell fusion in tumors was reported 130 years ago, it has recently attracted great interest, with recent progress in tumorigenesis research. However, the role of cell fusion in tumor progression remains unclear. The pattern of cell fusion and its role under physiological conditions are the basis for our understanding of the pathological role of cell fusion. However, the role of cell fusion in tumors and its functions are complicated. Cell fusion can directly increase tumor heterogeneity by forming polyploids or aneuploidies. Several studies have reported that cell fusion is associated with tumorigenesis, metastasis, recurrence, drug resistance and the formation of cancer stem cells. Given the diverse roles cell fusion plays in different tumor phenotypes, methods based on targeted cell fusion have been designed to treat tumors. Research on cell fusion in tumors may provide novel ideas for further treatment.

CD90low glioma-associated mesenchymal stromal/stem cells promote temozolomide resistance by activating FOXS1-mediated epithelial-mesenchymal transition in glioma cells.

BACKGROUND: The tumour microenvironment contributes to chemotherapy resistance in gliomas, and glioma-associated mesenchymal stromal/stem cells (gaMSCs) are important stromal cell components that play multiple roles in tumour progression. However, whether gaMSCs affect chemotherapy resistance to the first-line agent temozolomide (TMZ) remains unclear. Herein, we explored the effect and mechanism of gaMSCs on resistance to TMZ in glioma cells. METHODS: Human glioma cells (cell line U87MG and primary glioblastoma cell line GBM-1) were cultured in conditioned media of gaMSCs and further treated with TMZ. The proliferation, apoptosis and migration of glioma cells were detected by Cell Counting Kit-8 (CCK-8), flow cytometry and wound-healing assays. The expression of FOXS1 in glioma cells was analysed by gene microarray, PCR and Western blotting. Then, FOXS1 expression in glioma cells was up- and downregulated by lentivirus transfection, and markers of the epithelial-mesenchymal transformation (EMT) process were detected. Tumour-bearing nude mice were established with different glioma cells and treated with TMZ to measure tumour size, survival time and Ki-67 expression. Finally, the expression of IL-6 in gaMSC subpopulations and its effects on FOXS1 expression in glioma cells were also investigated. RESULTS: Conditioned media of gaMSCs promoted the proliferation, migration and chemotherapy resistance of glioma cells. The increased expression of FOXS1 and activation of the EMT process in glioma cells under gaMSC-conditioned media were detected. The relationship of FOXS1, EMT and chemotherapy resistance in glioma cells was demonstrated through the regulation of FOXS1 expression in vitro and in vivo. Moreover, FOXS1 expression in glioma cells was increased by secretion of IL-6 mainly from the CD90low gaMSC subpopulation. CONCLUSIONS: CD90low gaMSCs could increase FOXS1 expression in glioma cells by IL-6 secretion, thereby activating epithelial-mesenchymal transition and resistance to TMZ in glioma cells. These results indicate a new role of gaMSCs in chemotherapy resistance and provide novel therapeutic targets.

Roles of long non-coding RNAs in the hallmarks of glioma.

Glioma is one of the most common types of tumor of the central nervous system. Due to the aggressiveness and invasiveness of high-level gliomas, the survival time of patients with these tumors is short, at ~15 months, even after combined treatment with surgery, radiotherapy and/or chemotherapy. Recently, a number of studies have demonstrated that long non-coding RNA (lncRNAs) serve crucial roles in the multistep development of human gliomas. Gliomas acquire numerous biological abilities during multistep development that collectively constitute the hallmarks of glioma. Thus, in this review, the roles of lncRNAs associated with glioma hallmarks and the current and future prospects for their development are summarized.

Donor Lung Sequence Number and Survival after Lung Transplantation in the United States.

RATIONALE: In the United States, an algorithm known as the "match-run" creates an ordered ranking of potential recipients for available lung allografts. A potential recipient's match-run position, or "sequence number," is available to the transplant center when contacted with a lung offer. Lung offers with higher sequence numbers may be interpreted as a crowd-sourced evaluation of poor organ quality, though the association between the sequence number at which a lung is accepted and its recipient's post-transplant outcomes is unclear. OBJECTIVES: We sought to evaluate the primary reasons provided when a lung offer was refused by a transplant center, transplant center and donor/organ factors associated with a higher sequence number at acceptance, and the association of the sequence number at acceptance with post-transplant mortality and graft failure. METHODS: Match-run outcomes for lung offers that occurred in the United States from May 2007 through June 2014 were merged with recipient follow-up data through December 2017. Associations between the sequence number at the time of acceptance and selected transplant center and donor characteristics were estimated using multivariable logistic and multinomial regression models. The associations between the final sequence number and recipient survival and graft survival were estimated using multivariable time-to-event models. RESULTS: Of 10,981 lung offer acceptances, nearly 70% were accepted by one of the top 10 ranked candidates. Higher median annual center volume and potential indicators of organ quality (e.g., abnormal chest radiograph or bronchoscopy) were associated with a higher sequence number at acceptance. There was weak evidence for a small positive relationship between the sequence number at acceptance and both mortality and graft failure. For example, the unadjusted and adjusted hazard ratios for death associated with the log-sequence number at acceptance were 1.019 (95% confidence interval, 1.001-1.038) and 1.011 (95% confidence interval, 0.989-1.033), respectively. On the absolute scale, using the multivariable model, a 10-fold increase in the sequence number translated into a 0.8% absolute decline in the predicted 5-year survival. CONCLUSIONS: Acceptance of a donor lung offer at a later point in the match-run was associated with measurable indicators of organ quality, but not with clinically meaningful differences in post-transplant mortality or graft failure.

Endoscopic anatomic characterization of the frontal recess and its implications in frontal sinus surgery.

OBJECTIVE: This study was designed to describe the anatomic features of the frontal recess by transnasal endoscopy (nasoscope), to analyze its implications in endoscopic frontal sinus surgery and to discuss the issues that may be experienced during such operations. MATERIALS AND METHODS: The patients included in this analysis were adults with chronic sinusitis or nasal polyp (n = 301, 562 sides) hospitalized in our hospital from August 1998 to April 2001. Chronic frontal sinusitis was confirmed in 280 cases (479 sides) by coronal and axial CT scan. Patients with a previous surgical history were excluded from the analysis. The surgical outcomes of these patients and CT imaging data were retrospectively reviewed and analyzed. The drainage pattern of the frontal sinus was identified based on CT scans preoperatively. Endoscopic frontal sinus surgery was performed in 250 cases (421 sides). The anatomic features of the frontal recess under nasoscope were classified into 2 types. RESULTS: The coronal CT results confirmed the position of the frontal sinus ostium between the uncinate process and the middle turbinate in 203 sides (48.2%) of all operated patients and the ostium was found to be located between the uncinate process and the lamina papyracea in 218 sides (51.8%). According to the location of the frontal sinus ostium, we grouped the anatomic features of the frontal recess into 2 types. Type I was documented in 203 sides (48.2%) and type II was seen in 218 sides (51.8%). CONCLUSIONS: The anatomic features of the frontal recess under nasoscope and their classification are very important and helpful for endoscopic frontal sinsus surgery. The upper part of the uncinate process is a dependable anatomic landmark for the localization of the frontal sinus ostium in CT scan and endoscopic frontal sinus surgery.

Current status and potential challenges of mesenchymal stem cell-based therapy for malignant gliomas.

Glioma, which accounts for more than 30% of primary central nervous system tumours, is characterised by symptoms such as headaches, epilepsy, and blurred vision. Glioblastoma multiforme is the most aggressive, malignant, and lethal brain tumour in adults. Even with progressive combination treatment with surgery, radiotherapy, and chemotherapy, the prognosis for glioma patients is still extremely poor. Compared with the poor outcome and slowly developing technologies for surgery and radiotherapy, the application of targeted chemotherapy with a new mechanism has become a research focus in this field.Moreover, targeted therapy is promising for most solid tumours. The tumour-tropic ability of stem cells, including neural stem cells and mesenchymal stem cells, provides an alternative therapeutic approach. Thus, mesenchymal stem cell-based therapy is based on a tumour-selective capacity and has been thought to be an effective anti-tumour option over the past decades. An increasing number of basic studies on mesenchymal stem cell-based therapy for gliomas has yielded complex outcomes.In this review, we summarise the biological characteristics of human mesenchymal stem cells, and the current status and potential challenges of mesenchymal stem cell-based therapy in patients with malignant gliomas.

CD90 determined two subpopulations of glioma-associated mesenchymal stem cells with different roles in tumour progression.

Human glioma-associated mesenchymal stem cells (gbMSCs) are the stromal cell components that contribute to the tumourigenesis of malignant gliomas. Recent studies have shown that gbMSCs consist of two distinct subpopulations (CD90+ and CD90- gbMSCs). However, the different roles in glioma progression have not been expounded. In this study, we found that the different roles of gbMSCs in glioma progression were associated with CD90 expression. CD90high gbMSCs significantly drove glioma progression mainly by increasing proliferation, migration and adhesion, where as CD90low gbMSCs contributed to glioma progression chiefly through the transition to pericytes and stimulation of vascular formation via vascular endothelial cells. Furthermore, discrepancies in long non-coding RNAs and mRNAs expression were verified in these two gbMSC subpopulations, and the potential underlying molecular mechanism was discussed. Our data confirm for the first time that CD90high and CD90low gbMSCs play different roles in human glioma progression. These results provide new insights into the possible future use of strategies targeting gbMSC subpopulations in glioma patients.

Reciprocal regulation of DGCR5 and miR-320a affects the cellular malignant phenotype and 5-FU response in pancreatic ductal adenocarcinoma.

Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive and lethal malignancies. Long non-coding microRNAs (lncRNAs) are a newly discovered type of regulatory molecule with both diagnostic and prognostic value, but the role of lncRNA in PDAC has not been well investigated until now. Here, we present evidence that shows that the lncRNA DGCR5 is significantly reduced in PDAC tissues as well as in PDAC cell lines and that the downregulation of DGCR5 predicts poor prognosis. Ectopic expression of DGCR5 inhibits the proliferation and migration, and promotes 5-FU resistances of PDAC cells. Further experiments demonstrated that DGCR5 and miR-320a regulate each other in a reciprocal manner and that DGCR5 reverses the inhibition of PDCD4 by miR-320a, which is involved in the regulation of the PDAC cell phenotype and response to 5-FU. Our findings provide novel information about the functions of lncRNAs in PDAC, some of which might be beneficial to the precise diagnosis, prognosis and individualized therapy of patients with PDAC in the future.

Preoperative TN staging of esophageal cancer: comparison of miniprobe ultrasonography, spiral CT and MRI.

AIM: To evaluate the value of miniprobe sonography (MPS), spiral CT and MR imaging (MRI) in the tumor and regional lymph node staging of esophageal cancer. METHODS: Eight-six patients (56 men and 30 women; age range of 39-73 years, mean 62 years) with esophageal carcinoma were staged preoperatively with imaging modalities. Of them, 81 (94 %) had squamous cell carcinoma, 4(5 %) adenocarcinoma, and 1(1 %) adenoacanthoma. Eleven patients (12 %) had malignancy of the upper one third, 41 (48 %) of the mid-esophagus and 34 (40 %) of the distal one third. Forty-one were examined by spiral CT in whom 13 were co-examined by MPS, and forty-five by MRI in whom 18 were also co-examined by MPS. These imaging results were compared with the findings of the histopathologic examination for resected specimens. RESULTS: In staging the depth of tumor growth, MPS was significantly more accurate (84 %) than spiral CT and MRI (68 % and 60 %, respectively, P<0.05). The specificity and sensitivity were 82 % and 85 % for MPS; 60 % and 69 % for spiral CT; and 40 % and 63 % for MRI, respectively. In staging regional lymph nodes, spiral CT was more accurate (78 %) than MPS and MRI (71 % and 64 %, respectively), but the difference was not statistically significant. The specificity and sensitivity were 79 % and 77 % for spiral CT; 75 % and 68 % for MPS; and 68 % and 62 % for MRI, respectively. CONCLUSION: MPS is superior to spiral CT or MRI for T staging, especially in early esophageal cancer. However, the three modalities have the similar accuracy in N staging. Spiral CT or MRI is helpful for the detection of far-distance metastasis in esophageal cancer.

Dimethyloxalylglycine prevents bone loss in ovariectomized C57BL/6J mice through enhanced angiogenesis and osteogenesis.

Hypoxia-inducible factor 1-α (HIF-1α) plays a critical role in angiogenesis-osteogenesis coupling during bone development and bone regeneration. Previous studies have shown that 17ß-estradiol activates the HIF-1α signaling pathway and that mice with conditional activation of the HIF-1α signaling pathway in osteoblasts are protected from ovariectomy (OVX)-induced bone loss. In addition, it has been shown that hypoxia facilitates the osteogenic differentiation of mesenchymal stem cells (MSCs) and modulates Wnt/ß-catenin signaling. Therefore, we hypothesized that activation of the HIF-1α signaling pathway by hypoxia-mimicking agents would prevent bone loss due to estrogen deficiency. In this study, we confirmed the effect of dimethyloxalylglycine (DMOG), a hypoxia-mimicking agent, on the HIF-1α signaling pathway and investigated the effect of DMOG on MSC osteogenic differentiation and the Wnt/ß-catenin signaling pathway. We then investigated the effect of DMOG treatment on OVX-induced bone loss. Female C57BL/6J mice were divided into sham, OVX, OVX+L-DMOG (5 mg/kg/day), and OVX+H-DMOG (20 mg/kg/day) groups. At sacrifice, static and dynamic bone histomorphometry were performed with micro computed tomography (micro-CT) and undecalcified sections, respectively. Bone strength was assessed with the three-point bending test, and femur vessels were reconstructed and analyzed by micro-CT. Serum vascular endothelial growth factor (VEGF), osteocalcin, and C-terminal telopeptides of collagen type(CTX) were measured by ELISA. Tartrate-resistant acid phosphatase staining was used to assess osteoclast formation. Alterations in the HIF-1α and Wnt/ß-catenin signaling pathways in the bone were detected by western blot. Our results showed that DMOG activated the HIF-1α signaling pathway, which further activated the Wnt/ß-catenin signaling pathway and enhanced MSC osteogenic differentiation. The micro-CT results showed that DMOG treatment improved trabecular bone density and restored the bone microarchitecture and blood vessels in OVX mice. Bone strength was also partly restored in DMOG-treated OVX mice. Dynamic bone histomorphometric analysis of the femur metaphysic revealed that DMOG increased the mineralizing surface, mineral apposition rate, and bone formation rate. The serum levels of VEGF and osteocalcin were higher in DMOG-treated OVX mice. However, there were no significant differences in serum CTX or in the number of tartrate-resistant acid phosphatase-stained cells between DMOG-treated OVX mice and OVX mice. Western blot results showed that DMOG administration partly rescued the decrease in HIF-1α and ß-catenin expression following ovariectomy. Collectively, these results indicate that DMOG prevents bone loss due to ovariectomy in C57BL/6J mice by enhancing angiogenesis and osteogenesis, which are associated with activated HIF-1α and Wnt/ß-catenin signaling pathways.

Chemical constituents and antioxidant activity of Ficus callosa.

One new megastigmane glycoside, ficalloside (1), and eleven known compounds, were isolated from methanol extract of Ficus callosa leaves by repeated column chromatography. Their structures were established on the basis of spectral and chemical evidence. The antioxidant activities of these compounds were measured using the oxygen radical absorbance capacity (ORAC) assay. Compound 8 exhibited potent antioxidant activity of 10.6 microM trolox equivalents at the concentration of 2 microM. At this concentration, compounds 4-7 and 9-12 showed significant antioxidant activity with ranging of 2.1-6.1 microM trolox equivalents.

[Clinical study on the relationship among the dermis, fat dome and postburn hyperplastic scar formation].

OBJECTIVE: To explore the influence of dermal defect and fat dome structure destruction in burn wounds on the formation of hyperplastic scar. METHODS: Fifty two wounds in 24 burn patients with deep partial thickness burn indicating tangential excision in the extremities were enrolled in the study, and they were divided into three groups according to the extent of exposure of dermal fat granules, i.e. A (without fat exposure), B (with little fat exposure) and C (with much fat exposure) groups. These three groups were subdivided into A1 (without grafting), A2 (grafting with razor thin skin), B1 (without grafting), B2 (with razor thin skin grafting), C1 (without grafting) and C2 (with split-thickness skin grafting) groups, with 9 wounds in each group. The dermal depth and exposure rate of the fat granules in each group were measured and analyzed by KS400 photography analysis apparatus. The follow-up conditions of the scars 6 months after operation were evaluated with Vancouver remark system by Vancouver score assessment. RESULTS: There was obvious difference in the dermal depth and exposure rate of the fat granules among all the groups (P < 0.05 or 0.01). The fat exposure rate was positively correlated with the extent of the dermal defect (gamma = 0.554, P < 0.05). The Vancouver score in group A was lower than that in B and C groups (P < 0.05), while that in B1 group (3.714 +/- 2.498) was evidently higher than that in other groups (P < 0.01). The scar score was lowered when the wounds were grafted with the dermis with its thickness similar to the depth of the defect, The scar score was increased along with the elevation of fat exposure rate (P < 0.05). CONCLUSION: There was a positive correlation between the degree of dermal defect and that of hyperplastic scar after burns. The disruption of fat dome structure might also be an important factor in the scar development.