A missense mutation in Lama3 causes androgen alopecia.

Hair loss disorders such as androgenetic alopecia have caused serious disturbances to normal human life. Animal models play an important role in exploring pathogenesis of disease and evaluating new therapies. NIH hairless mice are a spontaneous hairless mouse discovered and bred in our laboratory. In this study, we resequenced the genomes of NIH normal mice and NIH hairless mice and obtained 3,575,560 high-quality, plausible SNP loci and 995,475 InDels. The Euclidean distance algorithm was used to assess the association of SNP loci with the hairless phenotype, at a threshold of 0.62. Two regions of chromosome 18 having the highest association with the phenotype contained 345 genes with a total length of 13.98 Mb. The same algorithm was used to assess the association of InDels with the hairless phenotype at a threshold of 0.54 and revealed a region of 25.45 Mb in length, containing 518 genes. The mutation candidate gene Lama3 (NM_010680.2: c.652C>T; NP_034810.1: p. Arg217Cys) was selected based on the results of functional gene analysis and mutation prediction screening. Lama3 (R217C) mutant mice were further constructed using CRISPR/Cas9 technology, and the relationship between Lama3 point mutations and the hairless phenotype were clarified by phenotypic observation. The results showed that male Lama3 point mutation mice started to lose hair on the 80th day after birth, and the hair loss area gradually expanded over time. H&E staining of skin sections showed that the point mutation mice had increased sebaceous glands in the dermis and missing hair follicle structure (i.e., typical symptoms of androgenetic alopecia). This study is a good extension of the current body of knowledge about the function of Lama3, and the constructed Lama3 (R217C) mutant mice may be a good animal model for studying androgenetic alopecia.

High expression level of CXCL1/GROα is linked to advanced stage and worse survival in uterine cervical cancer and facilitates tumor cell malignant processes.

BACKGROUND: CXCL1 belongs to a member of the ELR + CXC chemokine subgroups that also known as GRO-alpha. It has been recognized that several types of human cancers constitutively express CXCL1, which may serve as a crucial mediator involved in cancer development and metastasis via an autocrine and/or paracrine fashion. However, the expression pattern and clinical significance of CXCL1 in human uterine cervix cancer (UCC), as well as its roles and mechanisms in UCC tumor biology remains entirely unclear. METHODS: The expression and clinical significance of CXCL1 in UCC tissues was explored using immunohistochemistry and bioinformatics analyses. The expression and effects of CXCL1 in HeLa UCC cells were assessed using ELISA, CCK-8 and transwell assays. Western blotting experiments were performed to evaluate the potential mechanism of CXCL1 on malignant behaviors of HeLa UCC cells. RESULTS: The current study demonstrated that CXCL1 was expressed in HeLa UCC cells, PHM1-41 human immortalized cervical stromal cells, as well as cervical tissues, with UCC tissues having an evidently high level of CXCL1. This high level of CXCL1 in cancer tissues was notably related to poor clinical stages and worse survival probability, rather than tumor infiltration and patient age. In addition, CXCL1 expression was extremely correlated with CCL20, CXCL8 and CXCL3 cancer-associated chemokines expression. In vitro, the growth and migration abilities of HeLa cells were significantly enhanced in the presence of exogenous CXCL1. Gain-function assay revealed that CXCL1 overexpression significantly promoted growth and migration response in HeLa cells in both autocrine and paracrine manners. Finally, we found that CXCL1 overexpression in HeLa cells influenced the expression of ERK signal-related genes, and HeLa cell malignant behaviors derived from CXCL1 overexpression were further interrupted in the presence of the ERK1/2 blocker. CONCLUSION: Our findings demonstrate the potential roles of CXCL1 as a promoter and a novel understanding of the functional relationship between CXCL1 and the ERK signaling pathway in UCC.

Trigger finger at the wrist caused by an intramuscular lipoma within the carpal tunnel: A case report.

BACKGROUND: Trigger finger at the wrist, which occurs with finger movement, is an uncommon presentation. Few reports describing cases of trigger finger at the wrist have been published. Thus, we present a case of an intramuscular lipoma arising from an anomalous flexor digitorum muscle belly in a 48-year-old female patient causing painful finger triggering at the wrist and carpal tunnel syndrome (CTS). CASE SUMMARY: A 48-year-old woman with complaints of a catching sensation during wrist motion and a progressive tingling sensation on the palmar aspect of the right hand for approximately 2 years was referred to our hospital. Triggering of the index to middle finger was evident with a palpable and audible clunk over the carpal tunnel during passive motion. Tinel's sign was positive over the carpal tunnel of the right wrist with a positive Phalen's test. Nerve conduction studies of the median nerve demonstrated a right CTS. Ultrasound examination revealed a 2.5 cm × 2.0 cm subcutaneous hyperechoic mass with no obvious blood flow at the wrist of the right arm. Surgical excision of the tumor and muscle mass led to a resolution of the patient's symptoms, and any triggering or discomfort disappeared. The patient has had no evidence of recurrence at more than 1 year of follow-up. CONCLUSION: Triggering of the fingers at the wrist is rare. It must be noted that there are many possible causes and types of triggering or clicking around the wrist. Accurate diagnosis is mandatory to avoid inaccurate treatment of patients with trigger wrist. During the diagnosis and treatment of CTS, attention should be paid to the variation of tendon tissue in the carpal tunnel, to avoid only focusing on the release of transverse carpal ligament and ignoring the removal of anomalous muscle belly.

NCK1-AS1 promotes the progression of melanoma by accelerating cell proliferation and migration via targeting miR-526b-5p/ADAM15 axis.

BACKGROUND: Long non-coding RNAs (lncRNAs) are vital regulators of gene expression and cellular processes in multiple cancers, including melanoma. Nevertheless, the function of lncRNA NCK1-antisense 1 (NCK1-AS1) in melanoma remains unknown. METHODS: RT-qPCR was used to analyze the expression of NCK1-AS1, microRNA-526b-5p (miR-526b-5p) and ADAM metallopeptidase domain 15 (ADAM15). Cell proliferation was determined by CCK-8, colony formation and EdU assays. Cell migration was assessed by transwell migration and wound healing assays. Mechanism experiments including luciferase reporter, RIP and RNA pull down assays were conducted to demonstrate the interactions between RNAs. Xenograft model was established to verify the function of NCK1-AS1 and miR-526b-5p in melanoma in vivo. RESULTS: NCK1-AS1 was overexpressed in melanoma cell lines and NCK1-AS1 knockdown hampers the proliferation and migration of melanoma cells. Besides, miR-526b-5p binds to NCK1-AS1 in melanoma and ADAM15 was validated as its downstream target. Further, the inhibitory effects of NCK1-AS1 knockdown on cell proliferation and migration in melanoma were reversed by the depletion of miR-526b-5p and further counteracted by ADAM15 knockdown. The growth of melanoma tumors was hindered by the down-regulation of NCK1-AS1 or up-regulation of miR-526b-5p. CONCLUSION: NCK1-AS1 facilitates cell proliferation and migration in melanoma via targeting miR-526b-5p/ADAM15 axis.

MicroRNA-101 inhibits growth and metastasis of human ovarian cancer cells by targeting PI3K/AKT.

INTRODUCTION: Ovarian cancer is the most frequent cause of gynecological cancer related mortality in woman. This study was designed to investigate the role and therapeutic potential of miRNA-101 in ovarian cancer. MATERIAL AND METHODS: Expression analysis was carried out by real-time quantitative polymerase chain reaction. Transfections were performed with the help of Lipofectamine 2000 reagent. AO/EB and annexin V/PI staining was used to detect apoptosis and flow cytometry was used for cell cycle analysis. Western blotting was employed for cell cycle analysis. RESULTS: It was found that miRNA-101 was significantly down-regulated in ovarian cancer cells. The over-expression of miRNA-101 causes a significant decrease in the viability of ovarian cancer cells via the initiation of apoptosis and sub-G1 arrest of OVACAR-3 cells. It was indicated that PTEN was the potential target of miRNA-101 in OVACAR-3 cells. There was 4.5-fold up-regulation of PTEN expression in ovarian cancer cell lines and the over-expression of miRNA-101 in OVACAR-3 cells resulted in the down-regulation of PTEN expression. The inhibition of PTEN in the OVACAR-3 cells arrested the proliferation of these cells. The over-expression of miRNA-101 causes significant down-regulation in PI3K and AKT expression of OVACAR-3 cells. CONCLUSIONS: It can be concluded that miRNA-101 acts as a tumor suppressor which may be beneficial in the treatment of ovarian cancer.

CPEB3 regulates neuron-specific alternative splicing and involves neurogenesis gene expression.

In the mammalian brain, alternative pre-mRNA splicing is a fundamental mechanism that modifies neuronal function dynamically where secretion of different splice variants regulates neurogenesis, development, pathfinding, maintenance, migration, and synaptogenesis. Sequence-specific RNA-Binding Protein CPEB3 has distinctive isoform-distinct biochemical interactions and neuronal development assembly roles. Nonetheless, the mechanisms moderating splice isoform options remain unclear. To establish the modulatory trend of CPEB3, we cloned and excessively expressed CPEB3 in HT22 cells. We used RNA-seq to analyze CPEB3-regulated alternative splicing on control and CPEB3-overexpressing cells. Consequently, we used iRIP-seq to identify CPEB-binding targets. We additionally validated CPEB3-modulated genes using RT-qPCR. CPEB3 overexpression had insignificant effects on gene expression in HT22 cells. Notably, CPEB3 partially modulated differential gene splicing enhanced in the modulation of neural development, neuron cycle, neurotrophin, synapse, and specific development pathway, implying an alternative splicing regulatory mechanism associated with neurogenesis. Moreover, qRT-PCR verified the CPEB3-modulated transcription of neurogenesis genes LCN2 and NAV2, synaptogenesis gene CYLD, as well as neural development gene JADE1. Herein, we established that CPEB3 is a critical modulator of alternative splicing in neurogenesis, which remarkably enhances the current understanding of the CPEB3 mediated alternative pre-mRNA splicing.

Silencing circRNA_001937 may inhibit cutaneous squamous cell carcinoma proliferation and induce apoptosis by preventing the sponging of the miRNA­597­3p/FOSL2 pathway.

Circular RNAs (circRNAs) are reported to be aberrantly expressed and perform different functions in numerous types of tumor; however, their expression levels in cutaneous squamous cell carcinoma (CSCC) remain largely unclear. Thus, the purpose of the present study was to investigate the function of circRNA_001937 in CSCC. Differential circRNA expression profiles of CSCC were analyzed using the Arraystar Human circRNAs chip and reverse transcription­quantitative PCR (RT­qPCR); and the effects of circRNA_001937 on cell behavior, in particular its regulation over the microRNA (miRNA)­597­3p/Fos­related antigen 2 (FOSL2) pathway, was investigated using a dual­luciferase reporter assay, and verified using RT­qPCR and western blotting. circRNA_001937 expression levels were significantly increased in CSCC tissues and cell lines compared with the corresponding adjacent tissues and control cells (P<0.05). The genetic silencing of circRNA_001937 with small interfering RNA significantly inhibited cell proliferation, and induced cell apoptosis (P<0.05). circRNA_001937 was observed to directly bind to miRNA­597­3p and serve as a sponge, which indirectly increased the expression levels of FOSL2, a miRNA­597­3p target gene. In conclusion, circRNA_001937 expression was increased in CSCC and silencing circRNA_001937 gene expression may inhibit CSCC progression by sponging the miRNA­597­3p/FOSL2 pathway.

DDX46 silencing inhibits cell proliferation by activating apoptosis and autophagy in cutaneous squamous cell carcinoma.

DEAD­Box Helicase 46 (DDX46) is an ATP­dependent RNA helicase that plays a central role in transcription splicing and ribosome assembly. However, the role of DDX46 in cutaneous squamous cell carcinoma (CSCC) remains to be elucidated. The aim of the present study was to investigate the role of DDX46 in CSCC by assessing DDX46 expression levels in CSCC tissues and cell lines. The effect of DDX46 silencing on CSCC cell proliferation, apoptosis and autophagy were also analyzed. It was demonstrated that DDX46 was significantly overexpressed in CSCC tissues and cells (P<0.05). Furthermore, it was found that DDX46 silencing could dramatically inhibit cell proliferation (P<0.05). Moreover, cell apoptosis and autophagy were activated in DDX46 silencing groups (P<0.05). Therefore, the present results suggested that DDX46 was overexpressed in CSCC and that DDX46 silencing can inhibit cell proliferation by inducing apoptosis and activating autophagy. Thus, DDX46 may serve as a novel potential therapeutic target for CSCC.

Repair of soft tissue and extensor tendon defects on the dorsum of the hand by transfer of dorsal foot flap and extensor digitorum brevis tendon in a 3-year-old child: A case report.

RATIONALE: Repair of soft tissue defects on the dorsum of the hand with accompanying tendon defects is a challenging problem in clinical practice. PATIENT CONCERNS: Here, we describe the case of a 3-year-old boy with a 1-week old soft tissue injury with infection due to a soft tissue defect on the dorsum of his right hand, and further describe its treatment. DIAGNOSIS: A diagnosis of a soft tissue defect of the dorsum with extensor tendon defects in the fore, middle, ring, and little fingers of the right hand was made. INTERVENTIONS: The defects were repaired using a dorsal foot flap combined with the extensor digitorum brevis tendon, under spinal anesthesia, and a small dose of the sedative phenobarbital (Lumina) was administered via pump injection after the surgery. OUTCOMES: The patient was followed-up for 6 months. The shape of the dorsal hand flap recovered satisfactorily and the skin color was almost normal. Protective sensation was restored and the tendon graft functioned well in vivo. Satisfactory outcomes were achieved in the flexion and extension of each finger. LESSONS: This case study provides evidence that for soft tissue defects on the dorsum of the hand with tendon defects, 1-stage transfer of a dorsal foot flap with the extensor digitorum brevis tendon can be effective for recovery of appearance and extensor function. In case of infant patients, postoperative use of low-dose sedation can effectively reduce the risk of vascular crisis, thus promoting survival of the flap graft, and ensuring the success of the operation.

Discrimination of Chinese Baijiu grades based on colorimetric sensor arrays.

In this study, a novel colorimetric sensor array based on chemo dyes including porphyrins and pH indicators were developed to analyse the volatile organic compounds of Chinese Baijiu with different grades. Ethyl acetate, ethyl butyrate and ethyl caproate appeared by significantly different concentration in different Baijiu grades measuring by gas chromatography and mass spectrometry and they were chosen as characteristic volatile organic components. The olfactory visualization system based on colorimetric sensor arrays was used to identify different Baijiu grades. The data were processed by building the principle components analysis, linear discriminant analysis and K-nearest neighbor classification models with the results of sensory evaluation and olfactory visualization system. This work presents a new-style colorimetric sensor using sensitive chemo dyes which has significant potential in quantitative analysis of volatile organic compounds, afterwards identifying different grades of Baijiu.

Acute compartment syndrome secondary to anterolateral thigh flap harvesting in a pediatric patient: A case report.

INTRODUCTION: The anterolateral thigh (ALT) flap is the most popularly used flap for major soft tissue reconstruction. Although it is widely used, acute compartment syndrome (ACS) in pediatric patients has rarely been reported in the literature. We herein reported a case of ACS in a 6-year-old girl after ALT flap harvest with direct closure of the donor site. PATIENT CONCERNS: A 6-year-old girl was admitted to the Second Hospital of Jilin University with crush injury on the palmar aspect of the right hand and wrist. DIAGNOSIS: Examination showed soft tissue defect of the hand and wrist, damage on the thenar muscles, lightly crushed flexor tendons, crushed median nerve, and ulnar artery thrombosis. INTERVENTIONS: The defect was closed with an ipsilateral ALT flap measuring 9 cm in length by 6 cm in width. OUTCOMES: After debridement was performed 3 times, the majority of the rectus femoris and lateral femoris were removed. Secondary closure by skin grafting was performed 2 weeks later. Three days after the procedure, necrotic tissues were noted on the edges of the wound. The diagnosis of ACS of the right was made. A second exploration was decided, and an extensive anterior compartment fasciotomy was performed. After 6 weeks of vacuum sealing drainage therapy, the defect was closed with a free latissimus dorsi musculocutaneous flap. At 4 months of follow-up, the right thigh wound had healed. At 6 months of follow-up, quadriceps muscle weakness remained. At 1 year of follow-up, the patient's mobility had been significantly improved, but diminished sensation remained on the lateral aspect of the thigh. CONCLUSION: ACS can occur after ALT flap harvesting in pediatric patients and should be recognized as early as possible to avoid devastating complications.

Involvement of orbit in maxillofacial fractures: "Evaluation of its spectrum, characteristics, and treatment in 200 patients"-Prospective study.

BACKGROUND: To evaluate the orbital involvement epidemiology in facial fractures, the clinical distribution and effects of orbital involvement in these patients, the frequency and nature of treatment procedures performed for these involvements, and the immediate- and intermediate-term effects of these treatment procedures. METHODS: Two hundred patients with hard tissue maxillofacial injuries were included in this study. Clinical examination was performed in-depth. Images were taken to determine and confirm clinical observations and to finalize treatment modality. Orbital involvement in patients was noted as present or absent. The clinical effects and features in postoperative imaging studies were noted until 3 months after trauma in each patient. RESULTS: Out of 200 patients, about one-third patients (58;29%) had orbital involvement and out of which 49 were males. Regarding clinical-radiological signs in orbit involved fractures, the incidences were variable, that is, periorbital ecchymosis (77.6%), periorbital edema (74.1%), subconjunctival hemorrhage (67.2%), palpable step/crepitus in orbital rim (62.1%), infraorbital nerve paresthesia (46.6%), restricted globe movement (5.2%), orbital rim discontinuity/step (72.4%), maxillary sinuses (51.7%), orbital wall/floor/roof rupture (55.2%), and infraorbital foramen involvement (36.2%). Palpable step/crepitus in orbital rim was recovered remarkably earlier in patients of open reduction internal fixation (ORIF) group, and features of restricted globe movements, orbital rim discontinuity/step, orbital wall/floor/roof rupture, and infraorbital foramen involvement in patients were recovered immediately after open reduction and internal fixation treatment. CONCLUSION: Early repair of the maxillofacial injuries with orbital involvement has better functional and esthetic outcome.

Biosynthesis of size-controlled gold nanoparticles using M. lucida leaf extract and their penetration studies on human skin for plastic surgery applications.

Recently, majority of the studies were focusing on the nanoparticles (NPs) and their abilities of penetrating Stratum Corneum (SC), as they can be prominently utilized in the plastic surgeries. In the current work, we demonstrated the penetrating abilities of gold NPs (AuNPs) through anthropological skin with diameters of 10 and 15 nm, varying in sizes, with the help of Multiphoton Microscopy. In addition, we also demonstrated a rapid facile environment friendly process of synthesizing AuNPs of adjustable sizes with the help of aqueous M. lucida leaf extract. Surface plasmon resonance was performed to confirm the synthesis of AuNPs at 530 nm with the help of UV-vis spectrophotometer. By differentiating the quantities of M. lucida leaf aqueous extracts, we studied the reduction time, morphological differences and size of the AuNPs. By performing Fourier Transformation Infrared Spectroscopy (FTIR), UV-vis spectroscopy, Transmission Electron Microscopy (TEM), Powder X-ray Diffraction (XRD), Energy Dispersive X-ray Spectroscopy (EDAX) and Selected Area Electron Diffraction (SAED), we characterized the fabricated AuNPs. The further aggregation and growth of AuNPs was protected by the polyphenols in the oxidised form by having a coordination with the surface of AuNPs. Moreover, the experiments of skin penetration showed an effort to deeply examine the factors leading to the penetration of particles into the human skin. These responses indicate that NPs at the determined size ranges penetrate the SC in the same pattern of the drug molecules, mostly by the intercellular paths. These responses attained were essential for developing a unique transdermal transporter as well as for understanding the basic interaction of skin-NPs for the application of plastic surgeries.

Thiophenol-formaldehyde triazole causes apoptosis induction in ovary cancer cells and prevents tumor growth formation in mice model.

In the present study a library of thiophenol-formaldehyde-triazole (TFT) derivatives was synthesized and screened against CAOV3, CAOV4 and ES-2 ovary cancer cell lines. Initial screening revealed that five-compounds 5a, 5b, 5j, 5h and 5i inhibited the viability of tested cell lines. Analysis of apoptosis revealed that increase in compound 5a (most active) concentration from 0.25 to 2.0 µM enhanced apoptotic cell proportion. Transwell assay showed reduction in invasive potential of CAOV3 cells on treatment with compound 5a. In wound healing assay increasing the concentration of compound 5a from 0.5 to 2.0 µM caused a significant (P < 0.05) decrease in the migration potential. Western blotting showed that compound 5a treatment markedly decreased the level of matrix metalloproteinase (MMP)-2 and -9 in CAOV3 cells. Treatment of CAOV3 cells with compound 5a caused a marked decrease in Focal Adhesion Kinase (FAK) activation. Tumor growth was inhibited in the compound 5a treated mice markedly than those of untreated group. The tumor metastasis to liver, intestine, spleen and peritoneal cavity was markedly decreased in mice treated with 10 mg/kg dose of compound 5a. Examination of Von Willebrand factor (vWF) expression in liver, intestinal and pulmonary lesions showed a marked decrease in the compound 5a-treated mice. The infiltration of macrophages in the metastatic lesions showed a significant decrease in compound 5a-treated mice. In conclusion, the compound 5a inhibited ovary cancer cell viability and induced apoptosis through decrease in expression of vWF and metalloproteinase, suppression of FAK activation and decrease in infiltration of macrophages. The compound 5a therefore can be investigated further for the treatment of ovary cancer.

MicroRNA-34 suppresses proliferation of human ovarian cancer cells by triggering autophagy and apoptosis and inhibits cell invasion by targeting Notch 1.

Ovarian cancer is one the prevalent cancers in women and is responsible for 5% of all the cancer related mortalities in women. Owing to late diagnosis, frequent relapses, side effects of chemotherapy, development of drug resistance, there is pressing need to screen out novel and effective treatment options. Accumulating evidences suggest that miRNAs may prove essential therapeutic targets for the treatment of cancer. This study was designed to investigate the role and therapeutic potential of miR-34 in ovarian cancer. It was found that miR-34 is significantly downregulated in ovarian cancer cell lines. Overexpression of miR-34 causes significant decrease in the proliferation of OVACAR-3 ovarian cancer cells via activation of apoptosis and autophagy. The miR-34 overexpression was concomitant with upsurge of apoptosis related proteins (Bax) and the autophagy associated protein (LC3 II and p62). TargetScan analysis showed Notch 1 to be the main target of miR-34 in OVACAR-3 cells which was further validated by luciferase reporter assay. The qRT-PCR results showed Notch 1 to be 3.2-4.1 fold higher in the ovarian cancer cell lines relative to the non-cancerous cells. Nonetheless, miR-34 overexpression in OVACAR-3 cells resulted in the post-transcriptional suppression of Notch 1 expression. Silencing of Notch 1 also caused inhibition of OVACAR-3 cell proliferation via induction of apoptosis and autophagy. Overexpression of Notch 1 could partially rescue the effects of miR-34 overexpression on the proliferation of OVACAR-3 cells. Moreover, overexpression of miR-34 causes significant inhibition of the invasion of the OVACAR-3 cells. The findings of the present study indicate the tumor suppressive role of miR-34 in ovarian cancer and may therefore prove to be a potential therapeutic target.

Levels of circulating soluble receptor activator of NF-κB and interleukins-1 predicting outcome of locally advanced basal cell carcinoma.

Decreasing levels of cytokines are associated with better responses to therapies, while increasing levels are related to progression or recurrence and decreased survival. NF-κB's role in the cell cycle and its ubiquity are only stressed out by the evidence for the importance of activation (aberrant activation in the majority of cancers) of both canonical and non-canonical pathways in advanced basal cell carcinomas (aBCCs), a subset of basal cell carcinoma (BCC). NF-κB acts through its canonical, or classical, form activated by interleukin-1 (IL-1), regulates cytoprotective, innate, and adaptive immune responses. However, NF-κB2 often acts through its non-canonical or alternate pathway. During the two-year study period, we selected 21 patients presenting with aBCCs due to delay in accessing medical attention with an advanced form of BCCs (n = 19) and infiltrative BCCs (n = 2). Initial diagnosis of BCCs of head and neck was made clinically and verified by skin biopsy. Venous blood was drawn and serum was obtained. Samples were collected at baseline and every three days thereafter (days 3, 6, 9, etc. until surgery). Antigenes' quantities (cytokines) were determined by ELISA kits. Initially, the mean value of all cytokine subjects was significantly different related to the control group (P <0.05). Changes in serum levels of circulating soluble receptor activator of NF-κB and interleukins-1 (α and ß) were observed following the surgery. Changes in serum levels of circulating soluble receptor activator of NF-κB and interleukins-1 (α and ß) are evident throughout our study period and a certain regularity in its dynamics is evident as the follow-up period moves away. It was therefore concluded that measurement of these factors might be useful in predicting the overall outcome of patients with aBCCs. This study highlights the systemic effects of aBCCs, but further studies are required on this topic.

[Reconstruction of large nasal defects with lateral nasal artery pedicled nasolabial flap].

OBJECTIVE: To evaluate the curative effect of the lateral nasal artery pedicled nasolabial flap for reconstruction of nasal defects. METHODS: From August 2005 to March 2009, 12 cases of large nasal tip and alar defects were repaired with the lateral nasal artery pedicled nasolabial flap. There were 5 male patients and 7 female patients with a mean age of 48.6 years (range, 35-60 years). Five cases of nasal defects were caused by trauma and other defects were caused by excision of carcinoma or hemangioma; the courses of disease were 1 to 10 years and 3 months to 40 years, respectively. The nasal defect size ranged from 2.0 cm x 1.5 cm to 4.5 cm x 2.5 cm. All defects were reconstructed with lateral nasal artery pedicled nasolabial flap in 9 cases and with island flap in 3 cases. The flap size ranged from 2.5 cm x 2.0 cm to 7.0 cm x 3.0 cm. Five patients required cartilage grafts for alar rim support and the distal end of the nasolabial flap was thinned and folded to repair the nasal lining. The donor sites were sutured directly. RESULTS: The mild venous stasis at the distal end of three island flaps occurred at 5-24 hours postoperatively and alleviated spontaneously. All flaps survived. Incision at donor and accepted sites healed by first intention. Flap revision was performed in 5 cases after 6-15 months because of mild swelling at the pedicles of skin flaps. All patients were followed up 8-24 months, with an average of 13 months. All patients achieved satisfactory results in nasal appearance, flap texture and color, and ventilatory function. No obvious scar was found at donor sites. CONCLUSION: The nasolabial flap is an excellent choice for reconstruction of defects of nasal tip and ala.

Nidus vespae protein inhibiting proliferation of HepG2 hepatoma cells through extracellular signal-regulated kinase signaling pathways and inducing G1 cell cycle arrest.

A protein named NVP(1) was isolated from Nidus vespae. The aim of the present study was to elucidate whether and how NVP(1) modulates the proliferation of HepG2 cells. NVP(1) at a concentration of 6.6 microg/ml could arrest the cell cycle at stage G1 and inhibit the mRNA expression of cyclinB, cyclinD1 and cyclinE. NVP(1) suppressed cdk2 protein expression, but increased p27 and p21 protein expression. However, NVP(1) did not alter p16 protein expression levels. NVP(1) promoted apoptosis in HepG2 cells as indicated by nuclear chromatin condensation, and in addition, the extracellular signal-regulated kinase (ERK) signaling pathway was activated. Moreover, the p-ERK protein expression level was attenuated when the HepG2 cells were pretreated with ERK inhibitor PD98059. These results demonstrate that NVP(1) inhibits proliferation of HepG2 through ERK signaling pathway. NVP(1) could be a potential drug for liver cancer.

K-19 mRNA RT-PCR in detecting micrometastasis in regional lymph nodes of gastric cancer.

AIM: To investigate the value and prospect of RT-PCR in detecting micrometastasis in regional lymph nodes of gastric cancer. METHODS: Histopathology was used and K19 mRNA expression was detected by RT-PCR in tumor tissues and lymph nodes from gastric cancer patients undergoing radical resection of gastric carcinoma. RESULTS: K19 mRNA was expressed in all tumor specimens of 30 cases; of the 126 lymph nodes, 26 were histopathologically positive (20.6%), and 42 positive (33.3%) by RT-PCR. Amplification fragments of 460 and 540 bp were shown in all the tumor tissues and metastatic lymph nodes after K19 and beta-actin RT-PCR, while only a 540 bp fragment appeared in the lymph nodes of non-tumor patients. CONCLUSION: K19 mRNA RT-PCR is sensitive and specific in testing micrometastasis in regional lymph nodes of gastric cancer, and it is superior to routine histopathology.