Functional Analysis of Membrane-Associated Scaffolding Tight Junction (TJ) Proteins in Tumorigenic Characteristics of B16-F10 Mouse Melanoma Cells.

Tight junction (TJ) proteins (Tjps), Tjp1 and Tjp2, are tight junction-associated scaffold proteins that bind to the transmembrane proteins of tight junctions and the underlying cytoskeleton. In this study, we first analyzed the tumorigenic characteristics of B16-F10 melanoma cells, including cell proliferation, migration, invasion, metastatic potential, and the expression patterns of related proteins, after the CRISPR-Cas9-mediated knockout (KO) of Tjp genes. The proliferation of Tjp1 and Tjp2 KO cells significantly increased in vitro. Other tumorigenic characteristics, including migration and invasion, were significantly enhanced in Tjp1 and Tjp2 KO cells. Zonula occludens (ZO)-associated protein Claudin-1 (CLDN-1), which is a major component of tight junctions and functions in controlling cell-to-cell adhesion, was decreased in Tjp KO cells. Additionally, Tjp KO significantly stimulated tumor growth and metastasis in an in vivo mouse model. We performed a transcriptome analysis using next-generation sequencing (NGS) to elucidate the key genes involved in the mechanisms of action of Tjp1 and Tjp2. Among the various genes affected by Tjp KO-, cell cycle-, cell migration-, angiogenesis-, and cell-cell adhesion-related genes were significantly altered. In particular, we found that the Ninjurin-1 (Ninj1) and Catenin alpha-1 (Ctnna1) genes, which are known to play fundamental roles in Tjps, were significantly downregulated in Tjp KO cells. In summary, tumorigenic characteristics, including cell proliferation, migration, invasion, tumor growth, and metastatic potential, were significantly increased in Tjp1 and Tjp2 KO cells, and the knockout of Tjp genes significantly affected the expression of related proteins.

Glycoconjugate-Specific Developmental Changes in the Horse Vomeronasal Organ.

The vomeronasal organ (VNO) is a tubular pheromone-sensing organ in which the lumen is covered with sensory and non-sensory epithelia. This study used immunohistochemistry and lectin histochemistry techniques to evaluate developmental changes, specifically of the glycoconjugate profile, in the horse VNO epithelium. Immunostaining analysis revealed PGP9.5 expression in some vomeronasal non-sensory epithelium (VNSE) cells and in the vomeronasal receptor cells of the vomeronasal sensory epithelium (VSE) in fetuses, young foals, and adult horses. Olfactory marker protein expression was exclusively localized in receptor cells of the VSE in fetuses, young foals, and adult horses and absent in VNSE. To identify the glycoconjugate type, lectin histochemistry was performed using 21 lectins. Semi-quantitative analysis revealed that the intensities of glycoconjugates labeled with WGA, DSL, LEL, and RCA120 were significantly higher in adult horse VSE than those in foal VSE, whereas the intensities of glycoconjugates labeled with LCA and PSA were significantly lower in adult horse VSE. The intensities of glycoconjugates labeled with s-WGA, WGA, BSL-II, DSL, LEL, STL, ConA, LCA, PSA, DBA, SBA, SJA, RCA120, jacalin, and ECL were significantly higher in adult horse VNSE than those in foal VNSE, whereas the intensity of glycoconjugates labeled with UEA-I was lower in adult horse VNSE. Histochemical analysis of each lectin revealed that various glycoconjugates in the VSE were present in the receptor, supporting, and basal cells of foals and adult horses. A similar pattern of lectin histochemistry was also observed in the VNSE of foals and adult horses. In conclusion, these results suggest that there is an increase in the level of N-acetylglucosamine (labeled by WGA, DSL, LEL) and galactose (labeled by RCA120) in horse VSE during postnatal development, implying that they may influence the function of VNO in adult horses.

PDZ Peptide of the ZO-1 Protein Significantly Increases UTP-Induced MUC8 Anti-Inflammatory Mucin Overproduction in Human Airway Epithelial Cells.

Mucus hyperproduction and hypersecretion are observed often in respiratory diseases. MUC8 is a glycoprotein synthesized by epithelial cells and generally expressed in the respiratory track. However, the physiological mechanism by which extracellular nucleotides induce MUC8 gene expression in human airway epithelial cells is unclear. Here, we show that UTP could induce MUC8 gene expression through P2Y2-PLCß3-Ca2+ activation. Because the full-length cDNA sequence of MUC8 has not been identified, a specific siRNA-MUC8 was designed based on the partial cDNA sequence of MUC8. siRNA-MUC8 significantly increased TNF-α production and decreased IL-1Ra production, suggesting that MUC8 may downregulate UTP/P2Y2-induced airway inflammation. Interestingly, the PDZ peptide of ZO-1 protein strongly abolished UTP-induced TNF-α production and increased IL-1Ra production and MUC8 gene expression. In addition, the PDZ peptide dramatically increased the levels of UTP-induced ZO proteins and TEER (trans-epithelial electrical resistance). These results show that the anti-inflammatory mucin MUC8 may contribute to homeostasis, and the PDZ peptide can be a novel therapeutic candidate for UTP-induced airway inflammation.

Esculetin and Fucoidan Attenuate Autophagy and Apoptosis Induced by Zinc Oxide Nanoparticles through Modulating Reactive Astrocyte and Proinflammatory Cytokines in the Rat Brain.

We examined the protective effects of esculetin and fucoidan against the neurotoxicity of ZnO NPs in rats. Ninety rats were divided into nine groups and pre-treated with esculetin or fucoidan 1 h before ZnO NP administration on a daily basis for 2 weeks. Serum and brain homogenates were examined by enzyme-linked immunosorbent assay (ELISA), and neurons, microglia, and astrocytes in the hippocampal region were examined with immunohistochemical analysis. The serum levels of interleukin-1-beta (IL-1ß), 3-nitrotyrosine (3-NT), superoxide dismutase (SOD), and 8-hydroxy-2'-deoxyguanosine (8-OHdG) were altered in the ZnO NP treatment groups. Brain IL-1ß and TNF-α levels were elevated after ZnO NP administration, and these effects were inhibited by esculetin and fucoidan. SOD, 8-OHdG, and acetylcholinesterase (AChE) levels in the brain were decreased after ZnO NP administration. The brain levels of beclin-1 and caspase-3 were elevated after ZnO NP treatment, and these effects were significantly ameliorated by esculetin and fucoidan. The number of reactive astrocytes measured by counting glial fibrillary acidic protein (GFAP)-positive cells, but not microglia, increased following ZnO NP treatment, and esculetin and fucoidan ameliorated the changes. Esculetin and fucoidan may be beneficial for preventing ZnO NP-mediated autophagy and apoptosis by the modulation of reactive astrocyte and proinflammatory cytokines in the rat brain.

Monitoring of Corroded and Loosened Bolts in Steel Structures via Deep Learning and Hough Transforms.

In this study, a regional convolutional neural network (RCNN)-based deep learning and Hough line transform (HLT) algorithm are applied to monitor corroded and loosened bolts in steel structures. The monitoring goals are to detect rusted bolts distinguished from non-corroded ones and also to estimate bolt-loosening angles of the identified bolts. The following approaches are performed to achieve the goals. Firstly, a RCNN-based autonomous bolt detection scheme is designed to identify corroded and clean bolts in a captured image. Secondly, a HLT-based image processing algorithm is designed to estimate rotational angles (i.e., bolt-loosening) of cropped bolts. Finally, the accuracy of the proposed framework is experimentally evaluated under various capture distances, perspective distortions, and light intensities. The lab-scale monitoring results indicate that the suggested method accurately acquires rusted bolts for images captured under perspective distortion angles less than 15° and light intensities larger than 63 lux.

Upregulation of Cathepsins in Olfactory Bulbs Is Associated with Transient Olfactory Dysfunction in Mice with Experimental Autoimmune Encephalomyelitis.

Cathepsins are a family of lysosomal/endosomal proteolytic enzymes that include serine, aspartate, and cysteine proteases. The role of cathepsin in neurodegenerative diseases, including Alzheimer's disease and Parkinson's disease, remains elusive. We evaluated the expression level and localization of different cathepsins in the olfactory bulbs of mice with experimental autoimmune encephalomyelitis (EAE), a model of human multiple sclerosis. Quantitative real-time PCR results and Western blotting analyses revealed that serine, aspartate, and cysteine cathepsins are expressed at significantly higher levels in the olfactory bulbs of mice with EAE in the paralytic stage compared with those of control mice. Immunohistochemical analyses indicated that cathepsin A, D, and S were expressed in the glomerulus layer, external plexiform layer, and mitral cell layer. Furthermore, cathepsins were detected in astrocytes, microglia, inflammatory cells, and vascular cells in the olfactory bulb of EAE mice at the paralytic stage. Collectively, these results suggest that the upregulation of cathepsins in the olfactory bulb of mice with EAE is associated with transient olfactory dysfunction in autoimmune encephalomyelitis.

Alendronate alleviates the symptoms of experimental autoimmune encephalomyelitis.

Nitrogen-containing bisphosphonates, such as alendronate, have been widely used to treat osteoporosis because they may target multiple signals in the mevalonate cascade. The present study evaluated the therapeutic effects of alendronate on experimental autoimmune encephalomyelitis (EAE), which is a prototypical autoimmune disease model. EAE was induced in C57BL/6 mice by immunization with myelin oligodendrocyte glycoprotein (MOG)35-55 peptide. The mice were checked daily for clinical symptoms, such as paralysis, and the levels of inflammatory cytokines were analyzed using ELISA, western blot analyses, and immunohistochemistry. The daily oral administration of alendronate to EAE-induced mice significantly reduced the severity of paralysis and lowered T cell proliferation. Additionally, histopathological examinations confirmed that alendronate mitigated inflammation in the spinal cord after EAE induction, suppressed the infiltration of CD68-positive inflammatory cells, and reduced the production of various pro-inflammatory cytokines, including interleukin (IL)-1ß, IL-6, tumor necrosis factor (TNF)-α, and interferon (IFN)-γ, as well as inducible nitric oxide synthase (iNOS). Furthermore, the alendronate-treated group exhibited a decrease in the number of iNOS-positive inflammatory cells compared to the vehicle-treated group. Taken together, the present results suggest that alendronate alleviated neuro-inflammation in the spinal cords of EAE-induced mice, which is an animal model of multiple sclerosis, possibly by inhibiting the downstream effects of the mevalonate cascade.

Hesperidin improves motor disability in rat spinal cord injury through anti-inflammatory and antioxidant mechanism via Nrf-2/HO-1 pathway.

Spinal cord injury (SCI) is associated with inflammation with concurrent oxidative stress and glial activation. The aim of this study was to evaluate whether hesperidin, a representative flavonoid in citrus fruits, ameliorates SCI-induced motor dysfunction and neuro-pathologic degeneration in rat model. Rats received hesperidin (100 mg/kg body weight/daily, oral administration) from 7 days prior to SCI to 7 days post SCI. Behavioral test was done on rats with SCI until 6 weeks. For the study of inflammatory molecules in SCI rats with hesperidin treatment, rats were sacrificed at day 4 post SCI, and spinal cords were collected and studied histopathologically. Behavioral tests on hind-limbs of rats with SCI revealed that treatment of hesperidin in rats with SCI significantly ameliorate the hind-limb paralysis beginning at day 21 post SCI. Hesperidin treatment in rats with SCI reduced the neuropathological changes (e.g., hemorrhage, inflammatory cell infiltration, and tissue loss) and pro-inflammatory cytokines including tumor necrotic factor-α and interleukin-1ß. In addition, oxidative stress related molecules including superoxide dismutase, catalase, nuclear factor erythroid 2-related factor-2 and heme oxygenase-1 were also increased by hesperidin treatment. Furthermore, Fe2+, bilirubin and p38 mitogen activated protein kinase, these by-product of heme catabolism in serum and spinal cord of rats with hesperidin-treatment groups were significantly increased compared with those of vehicle-treatment group. Collectively, this study implies that hesperidin accelerates recovery of locomotor function and tissue repair of damaged spinal cord, with concurrent upregulation of heme oxygenase-1 as far as rat SCI model is concerned.

Benefits of hesperidin in central nervous system disorders: a review.

Citrus species contain significant amounts of flavonoids that possess antioxidant activities; furthermore, dietary citrus is not associated with adverse effects or cytotoxicity in healthy individuals. Hesperidin, which is an abundant flavanone glycoside in the peel of citrus fruits, possesses a variety of biological capabilities that include antioxidant and anti-inflammatory actions. Over the last few decades, many studies have been investigated the biological actions of hesperidin and its aglycone, hesperetin, as well as their underlying mechanisms. Due to the antioxidant effects of hesperidin and its derivatives, the cardioprotective and anti-cancer effects of these compounds have been widely reviewed. Although the biological activities of hesperidin in neurodegenerative diseases have been evaluated, its potential involvement in a variety of central nervous system (CNS) disorders, including autoimmune demyelinating disease, requires further investigation in terms of the underlying mechanisms. Thus, the present review will focus on the potential role of hesperidin in diverse models of CNS neuroinflammation, including experimental autoimmune encephalomyelitis, with special consideration given to its antioxidant and anti-inflammatory effects in neurodegenerative disease models. Additionally, current evidence provides information regarding the nutraceutical use of hesperidin to prevent various CNS disorders.

Black Radish (Raphanus sativus L. var. niger) Extract Mediates Its Hepatoprotective Effect on Carbon Tetrachloride-Induced Hepatic Injury by Attenuating Oxidative Stress.

Nonalcoholic fatty liver disease is a serious liver disorder associated with oxidative stress. Black radish (Raphanus sativus L. var. niger) extract (BRE) can lower the risk of this disease. The hepatoprotective effect of BRE containing 3-(E)-(methylthio)methylene-2-pyrrolidinethione was evaluated in human hepatocyte carcinoma (HepG2) cells and in rat livers with carbon tetrachloride (CCl4)-induced hepatic injury. BRE was administered at 125, 250, 500, and 1000 µg/mL to the oleic acid-induced HepG2 cells. Male Sprague-Dawley rats were randomly divided into seven groups: the control group, BRE group, CCl4 group, and BRE + CCl4 group. BRE was administered orally at 125, 250, 500, and 1000 mg/kg/day once daily for 7 consecutive days, followed by a single oral treatment of 1.5 mL/kg CCl4. Inhibition of lipid accumulation, serum markers of liver injury, histological evaluations, levels of oxidative stress related enzymatic and nonenzymatic antioxidants in HepG2 cells and liver tissue were investigated. The protein expression of main liver P450 isoenzymes such as cytochrome p450(CYP)2E1, the expression of nuclear factor erythroid 2-related factor-2(Nrf-2) and heme oxygenase-1(HO-1) were also studied. BRE has an inhibitory effect on lipid accumulation and caused acute hepatotoxicity manifested by increased levels of lipid peroxidation, serum alanine aminotransferase, and aspartate aminotransferase with corresponding histopathological changes and high levels of oxidative stress. BRE treatment significantly increased the level of CYP2E1, Nrf-2, and HO-1 in a dose-dependent manner. Besides, 3-(E)-(methylthio)methylene-2-pyrrolidinethione significantly increased radical-scavenging effects and the expression of Nrf-2 in oleic acid-treated HepG2 cells. These results suggest that BRE treatment reduces lipid accumulation in oleic acid-induced steatosis of HepG2 cells, and has a hepatoprotective effect against CCl4-induced liver injury in rats, possibly through Nrf-2/HO-1-mediated antioxidant effects.

Amelioration of experimental autoimmune encephalomyelitis by Ishige okamurae.

Experimental autoimmune encephalomyelitis (EAE) is a T-cell-mediated autoimmune central nervous system disease characterized by inflammation with oxidative stress. The aim of this study was to evaluate an anti-inflammatory effect of Ishige okamurae on EAE-induced paralysis in rats. An ethanolic extract of I. okamurae significantly delayed the first onset and reduced the duration and severity of hind-limb paralysis. The neuropathological and immunohistochemical findings in the spinal cord were in agreement with these clinical results. T-cell proliferation assay revealed that the ethyl-acetate fraction of I. okamurae suppressed the proliferation of myelin basic protein reactive T cells from EAE affected rats. Flow cytometric analysis showed TCRαß+ T cells was significantly reduced in the spleen of EAE rats with I. okamurae treatment with concurrent decrease of inflammatory mediators including tumor necrosis factor-α and cyclooxygenase-2. Collectively, it is postulated that I. okamurae ameliorates EAE paralysis with suppression of T-cell proliferation as well as decrease of pro-inflammatory mediators as far as rat EAE is concerned.

Changes in the expression and localization of signaling molecules in mouse facial motor neurons during regeneration of facial nerves.

After injury, peripheral axons usually re-extend toward their target, and neuronal functions recover. Previous studies have reported that expression of various molecules are transiently altered in motor neurons after nerve injury, but the time course of these changes and their relationship with functional recovery have not been clearly demonstrated. We used the mouse facial nerve transection and suturing model, and examined the changes in expression of five molecules, choline acetyl transferase (ChAT), galanin, calcitonin gene-related protein (CGRP), gephyrin, and potassium chloride co-transporter 2 (KCC2) in the facial motor neurons after surgery until recovery. Number of ChAT-positive neurons was markedly decreased at days 3 and 7, and recovered to the normal level by day 60, when facial motor functions recovered. Localization of two neuropeptides, CGRP and galanin, was increased in the perikarya and axons during regeneration, and returned to the normal levels by days 60 and 28, respectively. Expression of two postsynaptic elements of γ-amino butyric acid synapses, gephyrin and KCC2, was decreased at days 3 and 7, and recovered by day 60. These results suggest that ChAT, CGRP, and KCC2 may be objective indicators of regeneration, and altering their expression may be related to the functional recovery and axonal re-extension.

Glycan diversity in the vomeronasal organ of the Korean roe deer, Capreolus pygargus: A lectin histochemical study.

Glycans in the epithelium play an important role in cell-to-cell communication and adhesion. No detailed evaluation of glycoconjugates in the vomeronasal organs (VNO) of the roe deer has been published previously. The aim of this study was to characterize glycan epitopes in the vomeronasal sensory epithelium (VSE) and non-sensory epithelium (VNSE) using lectin histochemistry. Glycan epitopes identified by lectin histochemistry were grouped as follows: N-acetylglucosamine (s-WGA, WGA, BSL-II, DSL, LEL, STL), mannose (Con A, LCA, PSA), galactose (RCA120, BSL-I, Jacalin, PNA, ECL), N-acetylgalactosamine (VVA, DBA, SBA, and SJA), fucose (UEA-I) and complex type N-glycan (PHA-E and PHA-L) groups. The free border of the VSE was positive for all 21 lectins, and 18 of the lectins (excluding DBA, SJA, and PHA-L) showed weak and/or moderate staining in the receptor cells. The supporting cells were weakly positive for 19 lectins (excluding PNA and SJA). Moreover, 17 lectins (excluding BSL-II, Jacalin, PNA, and SJA) were expressed in the basal cells. In the VNSE of roe deer, the free border showed staining for all 21 lectins examined. The ciliated cells were positive for 16 lectins (excluding BSL-II, DSL, PNA, VVA, and SJA). Furthermore, 15 lectins (excluding DSL, LEL, ECL, UEA-I, PHA-E, and PHA-L) were expressed in goblet cells. Twenty lectins (excluding SJA) were expressed in the acini of the vomeronasal glands. Collectively, both VSE and VNSE were rich in N-acetylglucosamine, mannose, galactose, N-acetylgalactosamine, fucose, and complex-type N-glycans, although the different cell types of the VSE and VNSE expressed different glycoconjugates of varying intensities, suggesting that these carbohydrate residues may be involved in odor perception as well as cell-to-cell communication in the VNO.

Potential involvement of glycogen synthase kinase (GSK)-3ß in a rat model of multiple sclerosis: evidenced by lithium treatment.

Glycogen synthase kinase (GSK)-3ß has been known as a pro-inflammatory molecule in neuroinflammation. The involvement of GSK-3ß remains unsolved in acute monophasic rat experimental autoimmune encephalomyelitis (EAE). The aim of this study was to evaluate a potential role of GSK-3ß in central nervous system (CNS) autoimmunity through its inhibition by lithium. Lithium treatment significantly delayed the onset of EAE paralysis and ameliorated its severity. Lithium treatment reduced the serum level of pro-inflammatory tumor necrosis factor a but not that of interleukin 10. Western blot analysis showed that the phosphorylation of GSK-3ß (p-GSK-3ß) and its upstream factor Akt was significantly increased in the lithium-treated group. Immunohistochemical examination revealed that lithium treatment also suppressed the activation of ionized calcium binding protein-1-positive microglial cells and vascular cell adhesion molecule-1 expression in the spinal cords of lithium-treated EAE rats. These results demonstrate that lithium ameliorates clinical symptom of acute monophasic rat EAE, and GSK-3 is a target for the suppression of acute neuroinflammation as far as rat model of human CNS disease is involved.

Hepatoprotective effects of allyl isothiocyanate against carbon tetrachloride-induced hepatotoxicity in rat.

We evaluated the hepatoprotective activity of allyl isothiocyanate (AITC) against carbon tetrachloride (CCl4)-induced liver injury in rats. Sprague Dawley rats were orally administered AITC at doses of 5 (AITC 5) and 50 (AITC 50) mg/kg body weight once daily for 3 days, with or without intraperitoneal injection of CCl4. Serum chemistry was assessed for changes in alanine aminotransferase (ALT) and aspartate aminotransferase (AST). The enzyme activities of superoxide dismutase (SOD), catalase (CAT), and malondialdehyde (MDA) were examined in liver tissues, while pro-inflammatory cytokines including tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1ß) mRNA expression were analyzed using real-time polymerase chain reaction. And heme oxygenase-1 (HO-1) and ionized calcium binding protein-1 (Iba-1) immunoreactivities were evaluated by Western blot analysis and immunohistochemistry, respectively. In serum chemistry, the oral administration of AITC itself did not affect the serum levels of ALT or AST, furthermore pretreatment with AITC 5 and AITC 50 significantly reduced the ALT and AST activity levels that were elevated in CCl4-intoxicated rats. In addition, AITC significantly suppressed the reduction of SOD and CAT, and the elevation of MDA, TNF-α mRNA expression, on the other hands, induced the expression of HO-1 compared with those of the vehicle-treated CCl4 group. The histopathological evaluation and Iba-1 immunoreactivity also supported the hepatoprotective effects of AITC against CCl4-induced liver injury. These results suggest that AITC ameliorates oxidative liver injury, possibly through reducing lipid peroxidation, enhancing antioxidant enzymes, and suppressing Kupffer cells and macrophages.

Histological and lectin histochemical studies of the vomeronasal organ of horses.

The morphological characteristics and glycoconjugate composition of the vomeronasal organ (VNO) of the horse was investigated using histological, immunohistochemical, and lectin histochemical methods. The VNO is bilaterally located at the base of the nasal septum, has a tubular structure surrounded by cartilage, and consists of sensory and non-sensory epithelia. Immunohistochemical examination showed that the vomeronasal sensory epithelium (VSE) consisted of receptor cells positive for both olfactory marker protein (OMP) and protein gene product 9.5 (PGP 9.5), supporting cells, and basal cells. VNO receptor cells were positive for G protein Gαi2 (vomeronasal receptor type 1 marker), but not Gαo (vomeronasal receptor type 2 marker). Lectin histochemical studies using 21 biotinylated lectins showed that the free border of the VSE was positive for 20 lectins. The receptor and supporting cells reacted with 16 lectins while the basal cells reacted with 15 lectins, with varying intensities. In the vomeronasal non-sensory epithelium, the free border was positive for 19 lectins. The cilated cells were positive for 17 lectins and the basal cells were positive for 15 lectins. The vomeronasal glands, positioned in the lamina propria, were stained with both periodic acid Schiff (PAS) and alcian blue (pH 2.5). Eighteen lectins stained the acinar cells of the vomeronasal glands with various binding patterns. These findings suggest that horse VNO receptor cells express vomeronasal receptor type 1, and the VNO glands have mucous to seromucous characteristics. Moreover, each lectin differentially binds each cell type in both the VNO sensory and non-sensory epithelia.

Comparison of Surgical Outcomes according to Suturing Methods in Single Port Access Laparoscopic Myomectomy.

OBJECTIVES: This study was performed to consider the clinical experience of surgical outcome of single port access (SPA) laparoscopic myomectomy according to suturing methods. METHODS: The authors operated with 2 suturing method in SPA laparoscopic myomectomy for 246 patients and compared the surgical outcomes. RESULTS: The some significant difference of surgical outcome according to two suturing methods was demonstrated. Operating time was 100.50 minutes (± 42.09 minutes) in interrupted suture method group than 121.04 minutes (± 61.56 minutes) in continuous interlocking suture method group (P = 0.021). Estimated blood loss was less 222.59 mL (± 144.94 mL) in interrupted suture group than 340.11 mL (± 380.62 mL) in continuous interlocking suture method group (P = 0.042). CONCLUSION: This experience suggests that interrupted suture method was effective for operating time and estimated blood loss than continuous interlocking method in SPA laparoscopic myomectomy.

Transient activation of an adaptor protein, disabled-2, in rat spinal cord injury.

We previously reported that disabled-2 (Dab-2), a cytosolic adaptor protein, was expressed in inflammatory and glial cells in the central nervous system (CNS) in experimental autoimmune encephalomyelitis and cerebral cryoinjury. Here, to determine the pattern of Dab-2 expression in a clip compression-induced rat spinal cord injury (SCI) model, the protein level and localization of Dab-2 in the spinal cord were investigated in rats with SCI using Western blotting and immunohistochemistry. Western blotting revealed that the expression of both the 75- and 100-kDa isoforms of Dab-2 peaked significantly in the spinal cord after clip compression injury 7 days post-injury compared to sham controls, and declined slightly thereafter. Immunohistochemistry revealed weak Dab-2 immunostaining in some neurons, glial cells, and ependymal cells in the spinal cords of the control animals, compared to staining in the macrophages and reactive astrocytes in lesions of the SCI animals. Overall, these findings suggest that both isoforms of Dab-2 are transiently upregulated in response to SCI and that the increased expression of Dab-2 is associated with the early activation of macrophages and astrogliosis in the course of CNS inflammation.

Eosinophilic pleuritis due to sparganum: a case report.

Sparganosis is a rare parasitic disease caused by migrating plerocercoid tapeworm larva of the genus Spirometra. Infection in humans is mainly caused by the ingestion of raw or inadequately cooked flesh of infected frogs, snakes, and chickens. Here, we report a rare case of a 45-year-old man who was admitted to our hospital with left lower chest pain. The chest radiograph and computed tomography (CT) scan revealed localized pleural effusion in the left lower lobe; further, peripheral blood eosinophilia and eosinophilic pleural effusion were present. Percutaneous catheter drainage was performed, which revealed long worm-shaped material that was identified as a sparganum by DNA sequencing. The patient showed clinical improvement after drainage of the sparganum. This study demonstrates the importance of considering parasitic diseases in the differential diagnosis of eosinophilic pleural effusion.

Application of various compositions of thoracodorsal perforator flap for craniofacial contour deformities.

BACKGROUND: Craniofacial contour defects are challenging to restore because they may involve multiple tissues and span several aesthetic subunits in a non-contiguous manner. Some of these deformities may be associated with significant dead space in the region of sinus and orbit. The numerous subtle contours of the craniofacial regions must be preserved or restored to achieve a pleasing outcome. PATIENT AND RESULTS: We managed six patients with various craniofacial contour deformities as a result of hemifacial microsomia, infection, post excision of venous malformation, lipodystrophy, craniectomy for chronic frontal sinusitis and infected pneumocephalus. They were reconstructed with thoracodorsal perforator flaps bearing various components, that is, adiposal, adipofascial, dermoadiposal, adipomyofascial and osteomuscular elements. Half of the flaps were in chimaeric form. The largest flap size was 11 × 17 cm. All flaps survived and no patient required secondary contouring procedure, except for cranioplasty in one patient. CONCLUSION: The thoracodorsal perforator flap is very suitable for restoration of craniofacial contour deformities. Its advantages include: (1) ease of customisation of size and thickness, (2) several choices of donor tissue from the lateral thoracic region yielding multiple tissue components, for example, adiposal, adipofascial, dermoadiposal, adipomyofascial and osteomuscular flaps, (3) presence of adjacent perforators in the thoracodorsal system, allowing chimaeric flap configuration, thereby improving adaptation to non-contiguous contour defects, (4) ability to tailor the donor and recipient vessel size match by varying how proximal to harvest along the thoracodorsal vessels, (5) primary closure of donor site and (6) flap harvesting in supine position allowing a two-team approach.