Synergistic Activation of LEPR and ADRB2 Induced by Leptin Enhances ROS Generation in TNBC Cells.

Purpose: Leptin interacts not only with leptin receptor (LEPR) but also engages with other receptors. While the pro-oncogenic effects of the adrenergic receptor ß2 (ADRB2) are well-established, the role of leptin in activating ADRB2 in triple-negative breast cancer (TNBC) remains unclear. Materials and Methods: The pro-carcinogenic effects of LEPR were investigated using murine TNBC cell lines, 4T1 and EMT6, and a tumor-bearing mouse model. Expression levels of LEPR, NOX4, and ADRB2 in TNBC cells and tumor tissues were analyzed via Western blot and qPCR. Changes in reactive oxygen species (ROS) levels were assessed using flow cytometry and MitoSox staining, while immunofluorescence double-staining confirmed the co-localization of LEPR and ADRB2. Results: LEPR activation promoted NOX4-derived ROS and mitochondrial ROS production, facilitating TNBC cell proliferation and migration, effects which were mitigated by the LEPR inhibitor Allo-aca. Co-expression of LEPR and ADRB2 was observed on cell membranes, and bioinformatics data revealed a positive correlation between the two receptors. Leptin activated both LEPR and ADRB2, enhancing intracellular ROS generation and promoting tumor progression, which was effectively countered by a specific ADRB2 inhibitor ICI118551. In vivo, leptin injection accelerated tumor growth and lung metastases without affecting appetite, while treatments with Allo-aca or ICI118551 mitigated these effects. Conclusion: This study demonstrates that leptin stimulates the growth and metastasis of TNBC through the activation of both LEPR and ADRB2, resulting in increased ROS production. These findings highlight LEPR and ADRB2 as potential biomarkers and therapeutic targets in TNBC.

Complement factor I knockdown inhibits colon cancer development by affecting Wnt/ß-catenin/c-Myc signaling pathway and glycolysis.

BACKGROUND: Colon cancer (CC) occurrence and progression are considerably influenced by the tumor microenvironment. However, the exact underlying regulatory mechanisms remain unclear. AIM: To investigate immune infiltration-related differentially expressed genes (DEGs) in CC and specifically explored the role and potential molecular mechanisms of complement factor I (CFI). METHODS: Immune infiltration-associated DEGs were screened for CC using bioinformatics. Quantitative reverse transcription polymerase chain reaction was used to examine hub DEGs expression in the CC cell lines. Stable CFI-knockdown HT29 and HCT116 cell lines were constructed, and the diverse roles of CFI in vitro were assessed using CCK-8, 5-ethynyl-2'-deoxyuridine, wound healing, and transwell assays. Hematoxylin and eosin staining and immunohistochemistry staining were employed to evaluate the influence of CFI on the tumorigenesis of CC xenograft models constructed using BALB/c male nude mice. Key proteins associated with glycolysis and the Wnt pathway were measured using western blotting. RESULTS: Six key immune infiltration-related DEGs were screened, among which the expression of CFI, complement factor B, lymphoid enhancer binding factor 1, and SRY-related high-mobility-group box 4 was upregulated, whereas that of fatty acid-binding protein 1, and bone morphogenic protein-2 was downregulated. Furthermore, CFI could be used as a diagnostic biomarker for CC. Functionally, CFI silencing inhibited CC cell proliferation, migration, invasion, and tumor growth. Mechanistically, CFI knockdown downregulated the expression of key glycolysis-related proteins (glucose transporter type 1, hexokinase 2, lactate dehydrogenase A, and pyruvate kinase M2) and the Wnt pathway-related proteins (ß-catenin and c-Myc). Further investigation indicated that CFI knockdown inhibited glycolysis in CC by blocking the Wnt/ß-catenin/c-Myc pathway. CONCLUSION: The findings of the present study demonstrate that CFI plays a crucial role in CC development by influencing glycolysis and the Wnt/ß-catenin/c-Myc pathway, indicating that it could serve as a promising target for therapeutic intervention in CC.

Low GPR81 in ER+ breast cancer cells drives tamoxifen resistance through inducing PPARα-mediated fatty acid oxidation.

AIMS: The intricate molecular mechanisms underlying estrogen receptor-positive (ER+) breast carcinogenesis and resistance to endocrine therapy remain elusive. In this study, we elucidate the pivotal role of GPR81, a G protein-coupled receptor, in ER+ breast cancer (BC) by demonstrating low expression of GPR81 in tamoxifen (TAM)-resistant ER+ BC cell lines and tumor samples, along with the underlying molecular mechanisms. MAIN METHODS: Fatty acid oxidation (FAO) levels and lipid accumulation were explored using MDA and FAßO assay, BODIPY 493/503 staining, and Lipid TOX staining. Autophagy levels were assayed using CYTO-ID detection and Western blotting. The impact of GPR81 on TAM resistance in BC was investigated through CCK8 assay, colony formation assay and a xenograft mice model. RESULTS: Aberrantly low GPR81 expression in TAM-resistant BC cells disrupts the Rap1 pathway, leading to the upregulation of PPARα and CPT1. This elevation in PPARα/CPT1 enhances FAO, impedes lipid accumulation and lipid droplet (LD) formation, and subsequently inhibits cell autophagy, ultimately promoting TAM-resistant BC cell growth. Moreover, targeting GPR81 and FAO emerges as a promising therapeutic strategy, as the GPR81 agonist and the CPT1 inhibitor etomoxir effectively inhibit ER+ BC cell and tumor growth in vivo, re-sensitizing TAM-resistant ER+ cells to TAM treatment. CONCLUSION: Our data highlight the critical and functionally significant role of GPR81 in promoting ER+ breast tumorigenesis and resistance to endocrine therapy. GPR81 and FAO levels show potential as diagnostic biomarkers and therapeutic targets in clinical settings for TAM-resistant ER+ BC.

LINC00173 silence and estrone supply suppress ER+ breast cancer by estrogen receptor α degradation and LITAF activation.

Persistent activation of estrogen receptor alpha (ERα)-mediated estrogen signaling plays a pivotal role in driving the progression of estrogen receptor positive (ER+) breast cancer (BC). In the current study, LINC00173, a long non-coding RNA, was found to bind both ERα and lipopolysaccharide (LPS)-induced tumor necrosis factor alpha (TNFα) factor (LITAF), then cooperatively to inhibit ERα protein degradation by impeding the nuclear export of ERα. Concurrently, LITAF was found to attenuate TNFα transcription after binding to LINC00173, and this attenuating transcriptional effect was quite significant under lipopolysaccharide stimulation. Distinct functional disparities between estrogen subtypes emerge, with estradiol synergistically promoting ER+ BC cell growth with LINC00173, while estrone (E1) facilitated LITAF-transcriptional activation. In terms of therapeutic significance, silencing LINC00173 alongside moderate addition of E1 heightened TNFα and induced apoptosis, effectively inhibiting ER+ BC progression.

Mir-142-5p inhibits the osteogenic differentiation of bone marrow mesenchymal stem cells by targeting Lhx8.

Osteoporosis (OP), a common systemic bone metabolism disease with a high incidence rate, is a serious health risk factor. Osteogenic differentiation balance is regulated by bone marrow mesenchymal stem cells (BMSCs) and plays a key role in OP occurrence and progression. Although, LIM homeobox 8 (Lhx8) has been identified to affect BMSCs osteogenic differentiation, its roles in OP and the associated mechanism remains unclear. Here, we aimed to elucidate the role and mechanism of Lhx8 in the osteogenic differentiation of BMSCs. BMSCs isolated from wild type and OP Sprague-Dawley rats were cultured and confirmed via flow cytometry and microscopy. Based on dual-luciferase reporter assay, BMSCs were transfected with miR-142-5p mimics and miR-NC (negative control). Real-time quantitative reverse transcription polymerase chain reaction and Western blot analyses were performed to determine the role of Lhx8 in BMSCs osteogenic differentiation. Lhx8 expression was significantly reduced in OP, whereas that of miR-142-5p, a possible Lhx8 regulator, was significantly upregulated. Dual-luciferase reporter assay demonstrated that miR-142-5p exerted a direct targeted regulatory effect on Lhx8. Moreover, miR-142-5p mimics significantly inhibited BMSCs osteogenic differentiation as well as Lhx8 expression in vitro, indicating that miR-142-5p may be involved in BMSCs osteogenic differentiation via Lhx8 expression regulation and may serve as a potential diagnostic target for OP. Overall, these findings indicated that miR-142-5p inhibits BMSCs osteogenic differentiation by suppressing Lhx8. These may serve as a foundation for further studies on OP treatment based on miR-142-5p targeting.

Repair of a finger pulp or fingertip defect using a palmar rotatory flap pedicled with the perforating branch of the proper palmar digital artery: a retrospective study.

BACKGROUND: Soft tissue defects in the hand may result from trauma, oncological procedures, or severe infections. This study aimed to introduce an innovative method for repairing soft tissue defects on the palmar side of the distal segment of the affected finger or fingertip. We explored this surgical method and its curative effect on the volar rotation pedicled flap base on a perforator of the palmar digital artery (VRPF-PPDA) for repairing ventral or fingertip soft tissue defects of the distal segment of the affected finger without impairing its main blood vessels. METHODS: Between June 2019 and January 2021, 13 patients with finger pulp or fingertip soft tissue defects were treated with VRPF-PPDA. Flap survival rate, complication rate, two-point discrimination (2PD), and patient satisfaction were used to evaluate the efficacy of this method. The function of the affected finger was evaluated using the upper limb function evaluation method issued by the Trial Standards for Evaluation of Partial Function of the Upper Extremity of the Chinese Society for Surgery of the Hand of the Chinese Medical Association (CMA) and the Disabilities of the Arm, Shoulder, and Head (DASH) score, 6-12 months after the flap-based operation. RESULTS: Thirteen patients (18 fingers) achieved complete flap survival. The finger pulp flap was full, and no complications occurred. 2PD checks of the flaps revealed that all of them were 4-10 mm in length. According to the Trial Standards for Evaluation of Partial Function of the Upper Extremity of the Chinese Society for Surgery of the Hand of the CMA, hand function was excellent in 12 patients (17 fingers) and good in one patient, with a mean DASH score of 26.05 ± 0.45. Eleven patients selected "excellent" on the subjective satisfaction survey, while the other two selected "good." CONCLUSION: VRPF-PPDA surgery is a simple, effective, minimally invasive, and reliable method for repairing soft tissue defects in the distal finger pulp or fingertips. Optimal esthetic reconstruction and anatomical and functional repair can be achieved in fingers repaired using the VRPF-PPDA surgical approach.

3D bioprinted mesenchymal stromal cells in skin wound repair.

Skin tissue regeneration and repair is a complex process involving multiple cell types, and current therapies are limited to promoting skin wound healing. Mesenchymal stromal cells (MSCs) have been proven to enhance skin tissue repair through their multidifferentiation and paracrine effects. However, there are still difficulties, such as the limited proliferative potential and the biological processes that need to be strengthened for MSCs in wound healing. Recently, three-dimensional (3D) bioprinting has been applied as a promising technology for tissue regeneration. 3D-bioprinted MSCs could maintain a better cell ability for proliferation and expression of biological factors to promote skin wound healing. It has been reported that 3D-bioprinted MSCs could enhance skin tissue repair through anti-inflammatory, cell proliferation and migration, angiogenesis, and extracellular matrix remodeling. In this review, we will discuss the progress on the effect of MSCs and 3D bioprinting on the treatment of skin tissue regeneration, as well as the perspective and limitations of current research.

Single-cell RNA-seq reveals interferon-induced guanylate-binding proteins are linked with sarcopenia.

BACKGROUND: Sarcopenia is defined as an age-related progressive loss of muscle mass and/or strength. Although different factors can contribute to this disease, the underlying mechanisms remain unclear. We assessed transcriptional heterogeneity in skeletal muscles from sarcopenic and control mice at single-cell resolution. METHODS: A mouse model was established to study sarcopenic skeletal muscles. Single-cell RNA-seq was performed on tibialis anterior (TA) muscle cells collected from sarcopenic and control mice. A series of bioinformatic analyses were carried out to identify and compare different cell types under different conditions. Immunofluorescence staining and western blotting were used to validate the findings from single-cell experiments. Tube formation assays were conducted to further evaluate the effects of Gbp2 on endothelial cells during angiogenesis. RESULTS: A murine sarcopenia model was successfully established using a senescence-accelerated mouse strain (SAMP6, n = 5). Sarcopenia phenotype was induced by administration of dexamethasone (20 mg/kg) and reduced physical activity. Senescence-resistant mice strain (SAMR1) and SAMP6 strain with similar activity but injected with PBS were recruited as two control groups. As signs of sarcopenia, body weight, muscle cell counts and cross-sectional fibre area were all significantly decreased in sarcopenic mice (P value = 0.004, 0.03 and 0.035, respectively). After quality control, 13 612 TA muscle single-cell transcriptomes were retained for analysis. Fourteen cell clusters were identified from the profiled cells. Among them, two distinct endothelial subtypes were found to be dominant in the sarcopenia group (42.2% cells) and in the two control groups (59.1% and 47.9% cells), respectively. 191 differentially expressed genes were detected between the two endothelial subtypes. Sarcopenia-specific endothelial cell subtype exhibited a dramatic increase in the interferon family genes and the interferon-inducible guanylate-binding protein (GBP) family gene expressions. For example, Igtp and Gbp2 in sarcopenic endothelial cells were 5.4 and 13.3 times higher than those in the control groups, respectively. We further validated our findings in muscle specimens of sarcopenia patients and observed that GBP2 levels were increased in endothelial cells of a subset of patients (11 of 40 patients, 27.5%), and we identified significantly higher CD31 and GBP2 co-localization (P value = 0.001128). Finally, we overexpressed Gbp2 in human umbilical vein endothelial cells in vitro. The endothelial cells with elevated Gbp2 expression displayed compromised tube formation. CONCLUSIONS: Our single-cell-based results suggested that endothelial cells may play critical roles in sarcopenia development through interferon-GBP signalling pathways, highlighting new therapeutic directions to slow down or even reverse age-related sarcopenia.

Masquelet technique combined with modified Sauve­Kapandji, negative pressure drainage and flap transplantation for the treatment of a Gustilo­Anderson III type C open fracture of the forearm: A case report.

Gustilo-Anderson III Type C open fracture is a high-energy injury with severe bone defects and extensive soft-tissue and vascular damage. Successful limb salvage remains challenging for surgeons due to the inherent risks of vascular damage, infection, nonunion and even amputation. The present case study reports on a 55-year-old male who presented with a Gustilo-Anderson III type C open fracture, which was successfully salvaged by a combined Masquelet and microsurgical approach. The modified Sauve-Kapandji technique was used to improve wrist mobility. Sufficient preoperative evaluation, a detailed surgical plan, positive revascularization, thorough debridement and prevention of complications are key to successful limb salvage. The range of motion test was excellent one year after surgery. The patient was able to take care of their daily life, return to performing a light-labor job and is satisfied with the function of the limb. Therefore, the Masquelet technique combined with modified Sauve-Kapandji technique, negative pressure drainage and skin-flap transplantation may be a reasonable and effective treatment for Gustilo-Anderson III type C open forearm fracture.

Prolonged postoperative urine leakage due to a calyceal diverticulum mimicking a renal cyst: A case report and literature review.

Background: The calyceal diverticulum is a rare cystic cavity that communicates with the collecting system via a narrow neck or infundibulum. In clinical practice, part of the calyceal diverticula is difficult to differentiate from simple renal cysts even after contrast-enhanced CT. To date, there have been few kinds of literature works on the diagnosis and treatment of calyceal diverticulum combined with renal pelvis dilatation, especially concerning the treatment of prolonged postoperative urine leakage. Case description: A 53-year-old woman with calyceal diverticulum and renal pelvis dilatation mimicking a simple renal cyst suffered urine leakage after receiving laparoscopic unroofing of the renal cyst. A persistent urine leakage was observed immediately after surgery, with about 200 ml of drainage fluid per day. We first attempted to place a double-J ureteral stent and indwell a catheter. After failing that, conservative treatment was performed. The core idea of the conservative treatment is retaining the drainage tube for more than 1 month, then clamping the drainage tube for 1 week, and finally removing the drainage tube. By 3 weeks of follow-up, the urine leakage disappeared, and the CT scan showed hydronephrosis of the right kidney without perirenal exudation and the lower pole cyst of the right kidney shrank significantly. Conclusion: This case, we reported here, is to attract the attention of clinicians. Renal cysts should exclude the possibility of the calyceal diverticulum. If urine leakage is inevitable after surgical treatment, our conservative treatment strategy is also an alternative method.

Circular RNA hsa_circ_0013958 Functions as an Oncogenic Gene Through Modulating miR-532-3p/WEE1 Axis in Hepatocellular Carcinoma.

BACKGROUND: circ0013958 was identified as a biomarker, which can be used for the diagnosis and screening of lung cancer. However, the role of circ0013958 in hepatocellular carcinoma (HCC) remains unclear. METHODS: In our study, quantitative real-time polymerase chain reaction was performed to determine the levels of circ0013958 in HCC tissues and cell lines. EdU, CCK-8, transwell, flow cytometry and tumorigenesis assays were applied to assess the functions of circ0013958 in HCC in vitro and in vivo. Western blot assay was to detect the expression of WEE1. Luciferase reporter assay, bioinformatics analysis and rescue experiments were used to examine the interaction among circ0013958, miR-532-3p and WEE1. RESULTS: It revealed that circ0013958 was significantly up-regulated in HCC, which was positively correlated with poor prognosis of HCC patients. Circ0013958 promoted HCC cell proliferation and invasion, inhibited cell apoptosis in vitro, and promoted tumorigenesis in vivo. Circ0013958 acted as a miR-532-3p sponge to regulate WEE1 expression, thus promoting the progression of HCC. CONCLUSIONS: Circ0013958 promotes HCC progression through miR-532-3p/WEE1 axis. Circ0013958 may serve as a potential diagnostic biomarker and therapeutic target of HCC.

TASP1 Promotes Proliferation and Migration in Gastric Cancer via EMT and AKT/P-AKT Pathway.

Threonine aspartase 1 (TASP1) was reported to function in the development of cancer. However, the regulatory mechanism of TASP1 in gastric cancer (GC) remains unclear. In this study, we determined the expression of TASP1 in tissues of GC patients, GC cells by qRT-PCR, and western blot and assessed the relationship between TASP1 and GC cell proliferation and migration via CCK-8 and transwell assay. It was found that the expression of TASP1 in GC tissues or GC cell lines was significantly higher than that in normal adjacent tissues or normal cells. The proliferation and migration of GC cells were inhibited upon TASP1 knockdown. Mechanism investigation revealed that TASP1 promoted GC cell proliferation and migration through upregulating the p-AKT/AKT expression. TASP1 induced GC cell migration via the epithelial -mesenchymal transition (EMT) pathway. In conclusion, TASP1 promotes GC progression through the EMT and AKT/p-AKT pathway, and it may serve as a new potential biomarker and therapeutic target for GC.

Management of haemorrhoids: protocol of an umbrella review of systematic reviews and meta-analyses.

INTRODUCTION: The prevalence of haemorrhoidal diseases was high in general population, and many treatments are proposed for the management of haemorrhoids. The treatments include conservative and surgical interventions; the credibility and strength of current evidence of their effectiveness are not comprehensively evaluated. We aim to evaluate the credibility of systematic reviews and meta-analyses that assess the effectiveness of the treatments for haemorrhoidal diseases through an umbrella review. METHODS AND ANALYSIS: We will search Ovid Medline, Embase, Cochrane library and Web of Science from inception to March 2020 without any language restriction. We will include meta-analyses that examine the effectiveness of treatments in the management of haemorrhoids. Two reviewers will independently screen the titles and abstracts of retrieved articles, and they will extract data from the included meta-analyses. For each meta-analysis, we will estimate the effect size of a treatment through the random-effect model and the fixed-effect model, and we will evaluate between-study heterogeneity (Cochrane's Q and I2 statistics) and small-study effect (Egger's test); we will also estimate the evidence of excess significance bias. Evidence of each treatment will be graded according to prespecified criteria. Methodological quality of each meta-analysis will be evaluated by using Assessment of Multiple Systematic Reviews 2. The corrected cover area method will be used to assess the impact of overlap in reviews on the findings of the umbrella review. ETHICS AND DISSEMINATION: We will present the results of the umbrella review at conferences and publish the final report in a peer-reviewed journal. The umbrella review does not require ethical approval. PROSPERO REGISTRATION NUMBER: CRD42019140702.

Long Non-Coding RNA ELFN1-AS1 Promoted Colon Cancer Cell Growth and Migration via the miR-191-5p/Special AT-Rich Sequence-Binding Protein 1 Axis.

Long non-coding RNAs (lncRNAs) are reported to participate in tumor development. It has been manifested in previous researches that lncRNA ELFN1-AS1 is involved in early-stage colon adenocarcinoma with potential diagnostic value. However, no studies have revealed the specific mechanism of ELFN1-AS1 in colon cancer, and there are no other studies on whether ELFN1-AS1 is associated with tumorigenesis. In our study, ELFN1-AS1 with high expression in colon cancer was selected by TCGA analysis, and the survival analysis was carried out to verify it. Subsequently, qRT-PCR was adopted for validating the results in tissues and cell lines. Cell counting kit-8 (CCK8), 5-ethynyl-2'-deoxyuridine (EdU), cell colon, cell apoptosis, cell cycle, cell migration, and invasion assays were utilized to assess the role of ELFN1-AS1 in colon cancer. Results uncovered that ELFN1-AS1 expression was prominently raised in colon cancer cells and tissues. ELFN1-AS1 decrement restrained cells to grow through interfering with distribution of cell cycle and promoting apoptosis. Meanwhile, ELFN1-AS1 decrement weakened the capacity of cells to migrate and invade. What's more, ELFN1-AS1 was uncovered to act as a competing endogenous RNA (ceRNA) to decrease miR-191-5p expression, thus raising special AT-rich sequence-binding protein 1 (SATB1), a downstream target of ceRNA. To sum up, ELFN1-AS1 drives colon cancer cells to proliferate and invade through adjusting the miR-191-5p/SATB1 axis. The above results disclose that lncRNA ELFN1-AS1 is possibly a novel treatment target for colon cancer cases.

No association between HMGB1 polymorphisms and cancer risk: evidence from a meta-analysis.

The aim of the present study was to determine whether High mobility group box 1 (HMGB1) polymorphism was associated with cancer susceptibility. PubMed, Embase, and ISI Web of Science were extensively searched without language restriction. Data were extracted using a standardized data collection sheet after two reviewers scanned studies independently. The association between HMGB1 polymorphism and cancer risks was indicated as odds ratio (OR) along with its related 95% confidence interval (95%CI). Meta-analysis was conducted via RevMan 5.3 software. A total of ten studies comprising 4530 cases and 5167 controls were included in our study. Meta-analysis revealed no statistical association between rs1045411, rs1360485, rs1412125, or rs2249825 polymorphisms in HMGB1 gene and risk of cancer, either did subgroup analysis of rs1045411 stratified by cancer types and ethnic groups. Our results revealed no statistical association between current four polymorphism loci and cancer risks, suggesting that the attempt of applying HMGB1 variants as a therapeutic target or a prognosis predictor might still require a second thought. However, HMGB1 is deemed to play pleiotropic roles in cancers, we strongly call for large-scale studies with high evidence level to uncover the exact relationship between HMGB1 gene variants and cancer progression.

Clinical characteristics and therapeutic analysis of 51 patients with Marjolin's ulcers.

Marjolin's ulcers, which are epidermoid carcinomas arising on non-healing scar tissue, may be of various pathological types, including squamous cell carcinoma. The pathogenesis of squamous cell carcinoma arising in an ulcer differs from that of the primary cutaneous squamous cell carcinoma. This squamous cell carcinoma is aggressive in nature, and has a high rate of metastasis. Between January 2001 and September 2013, 51 patients with Marjolin's ulcers were admitted to the Departments of Plastic Surgery of the Affiliated Foshan Hospital and the Second Affiliated Hospital of Sun Yat-sen University. The ulcers included 43 cases of squamous cell carcinoma, six of melanoma, one of basal cell carcinoma and one of epithelioid sarcoma. The clinical data of these patients were retrospectively analyzed. Patients were followed until mortality. Among the patients with squamous cell carcinoma, 30.23% exhibited sentinel lymph node metastasis and 11.63% had distant metastasis. Among the patients with melanoma, 66.67% had sentinel lymph node metastasis and 33.33% had distant metastasis. Sentinel lymph node metastasis was successfully detected in 11 patients with Marjolin's ulcer using 18F-fluorodeoxyglucose positron emission tomography-computed tomography and B-mode ultrasound guided biopsy. Squamous cell carcinoma was often treated by extended resection and skin grafting or skin flap repair. Patients with deep, aggressive squamous cell carcinoma of an extremity and sentinel lymph node metastasis underwent amputation and lymph node dissection. This treatment was also used for melanoma type Marjolin's ulcers.

Transcriptome and expression profiling analysis link patterns of gene expression to antennal responses in Spodoptera litura.

BACKGROUND: The study of olfaction is key to understanding the interaction of insects with their environment and provides opportunities to develop novel tactics for control of pest species. Recent developments in transcriptomic approaches enable the molecular basis of olfaction to be studied even in species with limited genomic information. Here we use transcriptome and expression profiling analysis to characterize the antennal transcriptome of the noctuid moth and polyphagous pest Spodoptera litura. RESULTS: We identify 74 candidate genes involved in odor detection and recognition, encoding 26 ORs, 21 OBPs, 18 CSPs and 9 IRs. We examine their expression levels in both sexes and seek evidence for their function by relating their expression with levels of EAG response in male and female antennae to 58 host and non-host plant volatiles and sex pheromone components. The majority of olfactory genes showed sex-biased expression, usually male-biased in ORs. A link between OR gene expression and antennal responses to odors was evident, a third of the compounds tested evoking a sex-biased response, in every case also male-biased. Two candidate pheromone receptors, OR14 and OR23 were especially strongly expressed and male-biased and we suggest that these may respond to the two female sex pheromone components of S. litura, Z9E11-14:OAc and Z9E12-14:OAc, which evoked strongly male-biased EAG responses. CONCLUSIONS: Our results provide the molecular basis for elucidating the olfactory profile of moths and the sexual divergence of their behavior and could enable the targeting of particular genes, and behaviors for pest management.

[The application of fluorescence in situ hybridization and automated image cytometry in the diagnosis of urothelial carcinoma of bladder].

OBJECTIVE: To discuss the application of automated DNA image cytometry (ICM) and fluorescence in situ hybridization (FISH) in the diagnosis of urothelial carcinoma of bladder. METHODS: From August 2008 to March 2009, 60 volunteers with informed consent were divided into two groups, 40 patients proven as urothelial carcinoma of bladder by pathology and 20 healthy individuals as control. Urine was collected and tested by cytology, ICM and FISH. RESULTS: Overall sensitivity of FISH was significantly higher in detection of malignancy than that of ICM (82.5% vs 62.5%, P < 0.05) and that of urine cytology (82.5% vs 25.0%, P < 0.05), while ICM was more sensitive to diagnose urothelial carcinoma of bladder than urine cytology (62.5% vs 25.0%, P < 0.05). Specificities of urine cytology, ICM and FISH were 100% in diagnosis of urothelial carcinoma of bladder (P > 0.05). Sensitivities of urine cytology, ICM and FISH have no correlation with pathological stage (P > 0.05), but have significant correlation with grade (P < 0.05). CONCLUSIONS: ICM and FISH have the same specificity as urine cytology in diagnosis of urothelial carcinoma of bladder, but they have significantly higher sensitivity than urine cytology. FISH has the highest sensitivity among three diagnostic methods. Therefore, FISH may become a newly non-invasive technique for the diagnosis and surveillance of urothelial carcinoma of bladder.

[Treatment of deep partial thickness burns by a single dressing of porcine acellular dermal matrix].

OBJECTIVE: To explore the effect of one dressing of porcine acellular dermal matrix on deep partial thickness burns. METHODS: From January 1997 to January 2004, sixty-seven cases of deep partial thickness total burned surface area (TBSA) from 50% to 90% burn wound were treated by a single dressing of porcine acellular dermal matrix (the porcine acellular dermal matrix group). Ten cases of deep partial thickness burned patients with the same TBSA treated by exposure method served as the exposure method group. The healing time of the wound was observed. The patients were followed up for 3 months to 2 years, and the scar proliferation was observed. RESULTS: The deep partial-thickness wound would be healed without dressing change in the porcine acellular dermal matrix group, and the average healing time was (12.2 +/- 2.6) days. The average healing time of the exposure method group was (27.4 +/- 3.5) days. Follow up of the patients within 3 months to 2 years showed that scar proliferation in the porcine acellular dermal matrix group was much less than that in the exposure method group, even no scar proliferation was observed in some patients. CONCLUSION: Without tangential excision, autografting and dressing change, a single dressing of porcine acellular dermal matrix on deep partial thickness burn wound could shorten the healing time and inhibit scar proliferation.

[Use of lower trapezius musculocutaneous pedicle flap in repairing of maxillofacial region penetrating defect].

OBJECTIVE: To investigate an safe and effective new technology (treatment) to repair maxillofacial region penetrating defect. METHODS: The lower trapezius musculocutaneous flap is parallel just like as two leaves which is connected to each other, and was folded to provide the liner of oral cavity and external cover. RESULTS: Totally twelve folding lower trapezius musculocutaneous pedicle flap survived. Postoperative follow-up for 1 approximately 3 years, the patients restored the function as well as the shape of maxillofacial region. CONCLUSIONS: The lower trapezius musculocutaneous pedicle flap is a suitable material for maxillofacial region reconstruction, further more, the successful rate is perfect.