Intramedullary Spinal Cord Malakoplakia Mimicking Malignant Neoplasm on 18F-FDG PET/CT.

ABSTRACT: We report a rare case of intramedullary spinal cord malakoplakia mimicking malignancy on 18F-FDG PET/CT. A 61-year-old man underwent a contrast-enhanced spinal cord MRI to evaluate 1 week of progressive left-sided weakness. Spinal cord MRI showed a 1.3-cm enhancing intramedullary cervical spinal cord mass at C5 level with cord edema. Subsequently, 18F-FDG PET/CT was performed for evaluation. The images showed a well-circumscribed hypermetabolic mass in the spinal cord; no lesions were suggestive of malignancy or metastasis. A subtotal tumor excision was performed; histopathological examination revealed malakoplakia. This emphasizes the significance of histopathological evaluation and the importance of diagnostic confirmation.

The immunohistochemical expression of c-MET and RON in lung adenocarcinoma with clinicopathologic correlation.

BACKGROUND: Mesenchymal epidermal transition (MET) and receptor originating from nantes (RON) are transmembrane tyrosine kinase receptors. Both are members of a proto-oncogene family and thus play a role in the pathogenesis of various cancers and acquired resistance to kinase inhibitors in lung cancer. AIMS: The aim of this study was to investigate the immunohistochemical expression of c-MET and RON in lung adenocarcinoma and its clinicopathologic correlation. SETTINGS AND DESIGN: Retrospective study. MATERIALS AND METHODS: The immunohistochemical c-MET and RON expression in specimens obtained from lung adenocarcinoma (n = 175) and associated clinicopathologic parameters were evaluated. STATISTICAL ANALYSIS USED: The correlation between c-MET and RON expression was analyzed by Chi-square test. A Cox proportional hazards model and Kaplan-Meier curve analysis were used to evaluate the risk factors and prognosis. RESULTS: High expression of the c-MET protein showed a strong correlation with that of RON (P = 0.013, kappa = 0.183). Five-year survival and recurrence-free 5-year survival were not associated with high expression of c-MET or RON. High c-MET expression was significantly associated with age older than 60 years (P = 0.000), tumor differentiation (P = 0.009), lymphovascular invasion (P = 0.016), and pleural invasion (P = 0.005). High RON expression was associated with a solid growth pattern (P = 0.001) and pleural invasion (P = 0.002). CONCLUSIONS: The results point to the potential of immunohistochemical expression of c-MET and RON as useful prognostic markers of unfavorable histopathologic features in lung adenocarcinoma.

Therapeutic effect of microcurrent therapy in a rat model of secondary lymphedema.

BACKGROUND: Secondary lymphedema is a clinically incurable disease that commonly occurs following surgical cancer treatment and/or radiation. Microcurrent therapy (MT) has been shown to decrease inflammation and promote wound healing. This study aimed to investigate the therapeutic effect of MT in a rat model for forelimb lymphedema induced by axillary lymph node dissection. METHODS: The model was created by dissecting the right axillary lymph node. Two weeks after surgery, 12 Sprague-Dawley rats were randomly divided into two groups: one that underwent MT in the lymphedematous forelimb (MT, n=6) and a sham MT group (sham MT, n=6). MT was applied daily for 1 h in each session for two weeks. The circumferences of the wrist and 2.5 cm above the wrist were measured 3 days and 14 days after surgery, weekly during MT and 14 days after the last MT. Immunohistochemical staining of pan-endothelial marker (CD31), Masson's trichrome, and western blot analysis of vascular endothelial growth factor C (VEGF-C) and vascular endothelial growth factor receptor-3 (VEGFR3) were performed 14 days after the last MT. Quantification of the area covered by blood vessels (CD31+) and fibrotic tissue area were measured using an image analysis program (ImageJ software). RESULTS: The circumference of the carpal joint in the MT group was significantly decreased 14 days after the last MT compared to that in the sham MT group (P=0.021). The area covered by blood vessels (CD31+) was significantly higher in the MT group than in the sham MT and contralateral control group (P<0.05). The extent of fibrotic tissue was significantly attenuated in the MT group compared to the sham MT group (P<0.05). The expression of VEFGR3 was 2.02-fold higher for MT group, compared for the contralateral control group, which was statistically significant (P=0.035). VEGF-C expression was 2.27-fold higher for MT group than that for contralateral control group; however, the difference between the groups was not significant (P=0.051). CONCLUSIONS: Our findings indicate that MT promotes angiogenesis, and improves fibrosis in secondary lymphedema. Therefore, MT may be a novel and non-invasive treatment modality for secondary lymphedema.

HMGA1 induces FGF19 to drive pancreatic carcinogenesis and stroma formation.

High mobility group A1 (HMGA1) chromatin regulators are upregulated in diverse tumors where they portend adverse outcomes, although how they function in cancer remains unclear. Pancreatic ductal adenocarcinomas (PDACs) are highly lethal tumors characterized by dense desmoplastic stroma composed predominantly of cancer-associated fibroblasts and fibrotic tissue. Here, we uncover an epigenetic program whereby HMGA1 upregulates FGF19 during tumor progression and stroma formation. HMGA1 deficiency disrupts oncogenic properties in vitro while impairing tumor inception and progression in KPC mice and subcutaneous or orthotopic models of PDAC. RNA sequencing revealed HMGA1 transcriptional networks governing proliferation and tumor-stroma interactions, including the FGF19 gene. HMGA1 directly induces FGF19 expression and increases its protein secretion by recruiting active histone marks (H3K4me3, H3K27Ac). Surprisingly, disrupting FGF19 via gene silencing or the FGFR4 inhibitor BLU9931 recapitulates most phenotypes observed with HMGA1 deficiency, decreasing tumor growth and formation of a desmoplastic stroma in mouse models of PDAC. In human PDAC, overexpression of HMGA1 and FGF19 defines a subset of tumors with extremely poor outcomes. Our results reveal what we believe is a new paradigm whereby HMGA1 and FGF19 drive tumor progression and stroma formation, thus illuminating FGF19 as a rational therapeutic target for a molecularly defined PDAC subtype.

The lysosome as a novel therapeutic target of EGFR-mediated tumor inflammation.

EGFR-mediated tumors have been targeted to overcome several different malignant cancers. EGFR overexpression and mutations are directly related to the malignancy, which makes the therapy more complicated. One reason for the malignancy is the induction of AP1 followed by inflammation via IL-6 secretion. Current therapeutic strategies to overcome EGFR-mediated tumors are tyrosine kinase inhibitors (TKIs), anti-EGFR monoclonal antibodies, and the combination of these two agents with classic chemotherapy or immune checkpoint inhibitors (ICIs). Although the strategies are straightforward and have shown promising efficacy in several studies, there are still hurdles to overcoming the adverse effects and limited efficacy. This study reviews the current therapeutic strategies to target EGFR family members, how they work, and their effects and limitations. We also suggest developing novel strategies to target EGFR-mediated tumors in a novel approach. A lysosome is the main custodial staff to discard unwanted amounts of EGFR and other receptor tyrosine kinase molecules. Targeting this organelle may be a new approach to overcoming EGFR-mediated cancers.

Herpes Simplex Virus Type 1 with Concomitant Pneumonia and Urinary Tract Infection in an Older Patient: A Case Report.

A 76-year-old female patient was unable to ambulate due to sequelae of cerebrovascular disease and had been living in a healthcare facility. On admission, the patient was diagnosed with sepsis and a urinary tract infection caused by Candida tropicalis. Chest radiography showed right lung atelectasis, while bronchoscopy showed bronchial stenosis with anthracotic pigmentation in both bronchi. Bronchial washing cytology revealed herpes simplex virus (HSV) type 1-infected cells with intranuclear inclusions and multinucleation on the 7th day. Moreover, the patient showed microscopic hematuria. Urine cytology also revealed HSV type 1-infected cells. The patient was treated with antiviral (acyclovir), antifungal, and antibiotic agents. One week later, follow-up urine cytology revealed the absence of HSV infection, and her condition was stabilized. However, her clinical condition deteriorated due to an infection caused by multidrug-resistant bacterial pathogens, and she eventually died 4 weeks after admission. We describe a case of HSV type 1 pneumonia and urinary tract infection in an older adult patient.

High-Grade Endometrial Stromal Sarcoma: Molecular Alterations and Potential Immunotherapeutic Strategies.

Endometrial stromal tumor (EST) is an uncommon and unusual mesenchymal tumor of the uterus characterized by multicolored histopathological, immunohistochemical, and molecular features. The morphology of ESTs is similar to normal endometrial stromal cells during the proliferative phase of the menstrual cycle. ESTs were first classified into benign and malignant based on the number of mitotic cells. However, recently WHO has divided ESTs into four categories: endometrial stromal nodules (ESN), undifferentiated uterine sarcoma (UUS), low-grade endometrial stromal sarcoma (LG-ESS), and high-grade endometrial stromal sarcoma (HG-ESS). HG-ESS is the most malignant of these categories, with poor clinical outcomes compared to other types. With advances in molecular biology, ESTs have been further classified with morphological identification. ESTs, including HG-ESS, is a relatively rare type of cancer, and the therapeutics are not being developed compared to other cancers. However, considering the tumor microenvironment of usual stromal cancers, the advance of immunotherapy shows auspicious outcomes reported in many different stromal tumors and non-identified uterine cancers. These studies show the high possibility of successful immunotherapy in HG-ESS patients in the future. In this review, we are discussing the background of ESTs and the BCOR and the development of HG-ESS by mutations of BCOR or other related genes. Among the gene mutations of HG-ESSs, BCOR shows the most common mutations in different ways. In current tumor therapies, immunotherapy is one of the most effective therapeutic approaches. In order to connect immunotherapy with HG-ESS, the understanding of tumor microenvironment (TME) is required. The TME of HG-ESS shows the mixture of tumor cells, vessels, immune cells and non-malignant stromal cells. Macrophages, neutrophils, dendritic cells and natural killer cells lose their expected functions, but rather show pro-tumoral functions by the matricellular proteins, extracellular matrix and other complicated environment in TME. In order to overcome the current therapeutic limitations of HG-ESS, immunotherapies should be considered in addition to the current surgical strategies. Checkpoint inhibitors, cytokine-based immunotherapies, immune cell therapies are good candidates to be considered as they show promising results in other stromal cancers and uterine cancers, while less studied because of the rarity of ESTs. Based on the advance of knowledge of immune therapies in HG-ESS, the new strategies can also be applied to the current therapies and also in other ESTs.

Targeting lncRNAs of colorectal cancers with natural products.

Non-coding RNA (ncRNA) is one of the functional classes of RNA that has a regulatory role in various cellular processes, such as modulation of disease onset, progression, and prognosis. ncRNAs, such as microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs), have been actively studied in recent years. The change in ncRNA levels is being actively studied in numerous human diseases, especially auto-immune disorders and cancers; however, targeting and regulating ncRNA with natural products to cure cancer has not been fully established. Recently many groups reported the relationship between ncRNA and natural products showing promising effects to serve as additional therapeutic approaches to cure cancers. This mini-review summarizes the aspects of lncRNAs related to cancer biology focusing on colorectal cancers that natural products can target.

Two methods of extracorporeal shock-wave therapy in a rat model of secondary lymphedema: a pilot study.

OBJECTIVES: To compare the effectiveness of two methods of extracorporeal shock-wave therapy (ESWT) in a rat model of forelimb lymphedema, induced by axillary lymph node dissection. METHODS: Sprague-Dawley rats were randomly allocated to a group that received 500 ESWT shocks only in the lymphedematous forelimb (Forelimb/ESWT) and a group that received 300 ESWT shocks in the axilla and 200 shocks in the lymphedematous forelimb (Axilla+Forelimb/ESWT). The circumferences of each limb were then measured. Immunohistochemistry for a pan-endothelial marker (cluster of differentiation [CD]31) and lymphatic vessel endothelial hyaluronan receptor-1, and western blot analysis for vascular endothelial growth factor receptor-3 (VEGFR3) and VEGF-C were performed. RESULTS: The circumferences of the limbs showed significant effects of group and time following surgery. The circumferences at the carpal joint and 2.5 cm above were smallest in the naïve limbs, larger in the Axilla+Forelimb/ESWT group, and the largest in the control group. VEGFR3 tended to be expressed at a higher level in the Axilla+Forelimb/ESWT group (1.96-fold) than in the Forelimb/ESWT group (1.20-fold) versus the opposite non-edematous forelimbs, although this difference was not statistically significant. CONCLUSIONS: These data suggest that ESWT protocols have differential effects on angiogenesis and lymphangiogenesis in lymphedematous limbs.

Effects of intra-articular pulsed radiofrequency current administration on a rabbit model of rheumatoid arthritis.

Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by synovial proliferation and inflammation. Intra-articular corticosteroid injections are commonly used for the treatment of arthritis affecting one or two joints. Although corticosteroid injections are fast-acting, repeated usage can result in severe adverse events. Recently, intra-articular pulsed radiofrequency (PRF) stimulation has been proposed to treat arthritis. The aim of the present study was to compare the effectiveness of intra-articular PRF with corticosteroid injection based on histopathological and motion analysis of an ovalbumin (OVA)-induced RA rabbit model. RA was induced in the right knee joint of 18 rabbits via OVA injection. The rabbits were randomly allocated into a PRF, an intra-articular corticosteroid injection or a sham PRF stimulation group. Movement was assessed in the rabbits before treatment, then at 2, 4 and 8 weeks after treatment using walking distance, fast walking time and mean walking speed. Histopathological evaluation of the distal femur and synovium was conducted 2, 4 and 8 weeks after treatment. Motion analysis demonstrated that changes in all movement variables showed significant group and time interaction as well as group effect among the three groups. The semiquantitative score based on the histopathological findings for the distal femoral condyle decreased 2 and 4 weeks after both the PRF and steroid groups, compared with the sham PRF group. Moreover, in the synovium, the semiquantitative histological score in the PRF and steroid groups tended to be lower compared with the sham PRF group, although this result was not statistically significant. Thus, intra-articular PRF stimulation may delay cartilage destruction and improve functional motion in RA.

Cilostazol protects hepatocytes against alcohol-induced apoptosis via activation of AMPK pathway.

Alcoholic liver disease (ALD) is a worldwide health problem and hepatocyte apoptosis has been associated with the development/progression of ALD. However, no definite effective pharmacotherapy for ALD is currently available. Cilostazol, a selective type III phosphodiesterase inhibitor has been shown to protect hepatocytes from ethanol-induced apoptosis. In the present study, the underlying mechanisms for the protective effects of cilostazol were examined. Primary rat hepatocytes were treated with ethanol in the presence or absence of cilostazol. Cell viability and intracellular cAMP were measured. Apoptosis was detected by Hoechst staining, TUNEL assay, and caspase-3 activity assay. The roles of cAMP and AMP-activated protein kinase (AMPK) pathways in the action of CTZ were explored using pharmacological inhibitors and siRNAs. Liver from mice received ethanol (5 g/kg body weight) by oral gavage following cilostazol treatment intraperitoneally was obtained for measurement of apoptosis and activation of AMPK pathway. Cilostazol inhibited ethanol-induced hepatocyte apoptosis and potentiated the increases in cAMP level induced by forskolin. However, the anti-apoptotic effect of cilostazol was not reversed by an inhibitor of adenylyl cyclase. Interestingly, cilostazol activated AMPK and increased the level of LC3-II, a marker of autophagy. The inhibition of AMPK abolished the effects of cilostazol on LC3-II expression and apoptosis. Moreover, the inhibition of LKB1 and CaMKK2, upstream kinases of AMPK, dampened cilostazol-inhibited apoptosis as well as AMPK activation. In conclusion, cilostazol protected hepatocytes from apoptosis induced by ethanol mainly via AMPK pathway which is regulated by both LKB1 and CaMKK2. Our results suggest that cilostazol may have potential as a promising therapeutic drug for treatment of ALD.

Cytopathologic Features of Secretory Carcinoma of Salivary Gland: Report of Two Cases.

Secretory carcinoma of the salivary gland (SC) is a newly introduced rare salivary gland tumor that shares histological, immunohistochemical, and genetic characteristics with secretory carcinoma of the breast. Here, we report the cytologic features of two cases of SC confirmed by surgical resection. In these two cases, SC was incidentally detected in a 64-year-old female and a 56-yearold male. Fine needle aspiration cytology revealed nests of tumor cells with a papillary or glandular structure floating in mucinous secretions. The tumor cells demonstrated uniform, round, smooth nuclear contours and distinct nucleoli. Multiple characteristic cytoplasmic vacuoles were revealed. Singly scattered tumor cells frequently showed variable sized cytoplasmic vacuoles. The cytopathologic diagnosis of SC should be considered when characteristic cytological findings are revealed. Further immunohistochemistry and gene analyses are helpful to diagnose SC.

Beneficial effects of melittin on ovalbumin-induced atopic dermatitis in mouse.

Atopic dermatitis (AD) is an inflammatory skin disease characterized by intense pruritus and relapsable eczematous lesions. The hallmarks of AD are defects in the epidermal barrier and immunoglobulin E (IgE)-mediated sensitization to several environmental allergens, as well as an immune disorder mediated by an imbalance toward T-helper-2 response. Melittin, a major component of bee venom, has been studied in various inflammatory diseases. However, the beneficial effects of melittin on mouse with AD-like symptoms have not been explored. Therefore, we investigated the anti-allergic effects of melittin. AD was induced by ovalbumin (OVA) patch. After agent treatment, skin tissues and sera were extracted from the sacrificed mice were used to demonstrate the effects of melittin through various molecular biological methods. The results showed that OVA-induced skin thickening and inflammatory infiltration were decreased in the melittin-treated group. Melittin prevented OVA-induced filaggrin deficiency and imbalanced inflammatory mediators. Furthermore, melittin inhibited IL-4/IL-13-induced filaggrin downregulation through the blockade of STAT3 activation in human keratinocytes. In summary, this study has shown that melittin ameliorated OVA-induced AD-like symptoms from various perspectives. The findings of this study may be the first evidence of the anti-inflammatory effects of melittin on OVA-induced AD.

A Case of Engorged Female Hard Tick in the External Auditory Canal of an Infant.

An oval-shaped mass with a smooth surface was found in the ear canal of a 22-month-old male infant. Although the mass appeared to be almost entirely blocking the ear canal, it was successfully removed under a surgical microscope without general anesthesia at the outpatient department. Under an optical microscope with hematoxylin and eosin staining, the specimen was observed to have a cuticle with a serrated surface and a pore canal, as well as parts of the capitulum, salivary glands, muscles, midgut, and the legs. The specimen was identified as a hard tick of the family Ixodidae, based on gross and histological findings. This paper is the first report in Korea on the diagnosis and treatment of a tick bite in the ear canal.

Bee Venom Inhibits Porphyromonas gingivalis Lipopolysaccharides-Induced Pro-Inflammatory Cytokines through Suppression of NF-κB and AP-1 Signaling Pathways.

Periodontitis is a chronic inflammatory disease that leads to destruction of tooth supporting tissues. Porphyromonas gingivalis (P. gingivalis), especially its lipopolysaccharides (LPS), is one of major pathogens that cause periodontitis. Bee venom (BV) has been widely used as a traditional medicine for various diseases. Previous studies have demonstrated the anti-inflammatory, anti-bacterial effects of BV. However, a direct role and cellular mechanism of BV on periodontitis-like human keratinocytes have not been explored. Therefore, we investigated the anti-inflammatory mechanism of BV against P. gingivalis LPS (PgLPS)-induced HaCaT human keratinocyte cell line. The anti-inflammatory effect of BV was demonstrated by various molecular biological methods. The results showed that PgLPS increased the expression of Toll-like receptor (TLR)-4 and pro-inflammatory cytokines, such as tumor necrosis factor (TNF)-α, interleukin (IL)-1ß, IL-6, IL-8, and interferon (IFN)-γ. In addition, PgLPS induced activation of the signaling pathways of inflammatory cytokines-related transcription factors, nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and activator protein 1 (AP-1). BV effectively inhibited those pro-inflammatory cytokines through suppression of NF-κB and AP-1 signaling pathways. These results suggest that administration of BV attenuates PgLPS-induced inflammatory responses. Furthermore, BV may be a useful treatment to anti-inflammatory therapy for periodontitis.

The biological role of epithelial-mesenchymal transition in lung cancer (Review).

Epithelial-mesenchymal transition (EMT) is a process whereby epithelial cells gradually transform into mesenchymal-like cells losing their epithelial functionality and characteristics. EMT is thought to be involved in the pathogenesis of numerous lung diseases ranging from developmental disorders and fibrotic tissue remodeling to lung cancer. Lung cancer is the most lethal form of cancer worldwide, and despite significant therapeutic improvements, the patient survival rate still remains low. Activation of EMT endows invasive and metastatic properties upon cancer cells that favor successful colonization of distal target organs. The present review provides a brief insight into the mechanism and biological assessment methods of EMT in lung cancer and summarizes the recent literature highlighting the controversial experimental data and conclusions.

Epithelial-mesenchymal transition in patients of pulmonary adenocarcinoma: correlation with cancer stem cell markers and prognosis.

Adenocarcinoma is the most common histologic type of non-small cell lung carcinomas. The existence of lung cancer stem cells (CSCs) and epithelial-mesenchymal transition (EMT) in human tissue is controversy. The aim of this study is to investigate the expression and clinical significance of CSCs and EMT markers and evaluate the correlation between the two in lung adenocarcinoma. A total of 97 cases comprise the tissue microarray from surgical resection for primary lung adenocarcinoma. Immunohistochemistry for ALDH1 and CD44 as CSC markers and E-cadherin, vimentin, fibronectin, SMA as EMT markers was performed. High ALDH1A1 expression was statistically associated with female gender (P=0.001), smoker (P=0.012), and high pT stages (P=0.046). High CD44 expression was statistically associated with female gender (P=0.008), non-smoker (P=0.000), and no pleural invasion (P=0.039). High expression of ALDH1 was associated with good overall survival (P=0.021). High expression of CD44 was correlated with both good overall survival (P=0.024) and disease-free survival (P=0.000). Vimentin expression was associated with pT stage (P=0.001) and pleural invasion (P=0.028). E-cadherin, fibronectin and SMA were not associated with clinicopathologic correlation and all EMT markers were not correlated with survival of lung adenocarcinoma. CSC markers expression was not related to EMT. Our results showed that the expression of CSCs was associated with a good prognosis in lung adenocarcinoma. The prognostic significance of EMT markers was skeptical in this study. There is a need for more research about CSC, EMT, and the relation between these two in human lung adenocarcinoma.

Transcription factors related to epithelial mesenchymal transition in tumor center and margin in invasive lung adenocarcinoma.

The tumor microenvironment has many roles involving tumor progression, invasion and metastasis. The tumor cells at the tumor border loose epithelial properties and acquire mesenchymal features. This, epithelial-to-mesenchymal transition (EMT) has been suggested to be an important process for tissue and lymphovascular invasion. Pulmonary tissue samples from 15 patients with primary adenocarcinoma were evaluated with using immunofluorescence multi-staining the EMT-associated markers including E-cadherin and alpha-smooth muscle actin (α-SMA), and transcription factors including E-SNAIL and SLUG, and ZEB1. The data were analyzed in specific area, such as tumor center and tumor border. In this study we show that the invasive adenocarcinoma differentially expressed SNAIL and SLUG, and Zeb1 and it was associated with the loss of epithelial marker (E-cadherin) and gaining of mesenchymal marker (α-SMA) at the invasive border of lung carcinoma. The positive rates of SNAIL and ZEB1 were 26.7% and 0% in the tumor center and 40% and 20% in tumor margin, respectively. In addition, the expression of both SNAIL and ZEB1 at the border of tumor was observed in two cases (2/10). These two cases were associated with lymph node metastasis and advanced stage. The process of EMT has been suggested to be of prime importance for tissue and lymphovascular invasion. The process of EMT may be activated in the tumor border of lung adenocarcinoma. Related transcription factors, such as SNAIL and SLUG, and ZEB1, might be induced by paracrine effects of surrounded inflammatory cells and fibroblasts.

A case of mucosa-associated lymphoid tissue lymphoma of the sigmoid colon presenting as a semipedunculated polyp.

Mucosa-associated lymphoid tissue (MALT) lymphomas are characterized by lymphoepithelial lesions pathologically. Colonic MALT lymphomas are relatively rarer than lymphomas of the stomach or small intestine. Endoscopically, colonic MALT lymphoma frequently appears as a nonpedunculated protruding polypoid mass and/or an ulceration in the cecum and/or rectum. We report a unique case of a colonic MALT lymphoma presenting as a semipedunculated polyp. A 54-year-old man was found to have a 2-cm semipedunculated polyp in the sigmoid colon during screening colonoscopy. The polyp was removed by endoscopic mucosal resection. Histologic examination of the resected polyp revealed diffuse epithelial infiltration by discrete aggregates of lymphoma cells. We diagnosed the tumor as low-grade B-cell MALT lymphoma by immunohistochemical staining.

The possibility of microbial cellulose for dressing and scaffold materials.

In recent years, natural polymers such as cellulose, alginate and chitosan have been used worldwide as biomedical materials and devices, as they offer more advantages over synthetic polymers. The aim of this study was to clarify the usefulness of microbial cellulose (MC) for use as a dressing and scaffold material. For evaluating the biodegradability and toxicity of MC, we divided the rats (n = 12) into two groups (the implanted group and the non-implanted group). In the implanted group, we implanted the film type of MC in the backs of six rats. In the non-implanted group, however, we did not implant the film type of MC in the backs of the six rats. Four weeks later, we compared two groups by the gross, histological and biochemical characteristics by using blood and tissue samples. To evaluate the wound healing effects of MC, three full-thickness skin defects were made on the backs of each rat (n = 20). Three wounds on the backs of the same rats were treated with other dressing materials, namely, Vaseline gauze (group Con), Algisite M(®) (group Alg) and MC (group MC). We analysed the gross, histological and biochemical characteristics by western blotting. MC was found to be biodegradable and non-toxic. On day 3, the MC film was visible under the subcutaneous tissue; however, after 4 weeks, no remnants of the film were visible under the subcutaneous tissue. Furthermore, there was no evidence of MC-induced toxicity. Moreover, group MC showed more rapid wound healing compared with group Con. On day 14 after skin excision, group MC showed greater decrease in wound size compared with group Con (33% versus 7·2%). The wound healing effects were also substantiated by the histological findings (greater reduction in inflammation and rapid collagen deposition as well as neovascularisation) and western blotting (decreased expression of vascular endothelial growth factor and transforming growth factor-ß1 in group MC on day 14 after skin excision, unlike group Con). This study showed that, in addition to having wound healing effects, MC is biodegradable and non-toxic and can, therefore, be used as a dressing and scaffold material.