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Biomedical subjects

M Koono

Publications and source records attributed to M Koono.

At least 37 records · Page 2Linked to original sources
PubMed2000

Primary vaginal adenocarcinoma arising from the metanephric duct remnant.

Primary vaginal adenocarcinoma unrelated to in utero exposure to diethylstilbestrol (DES) is very uncommon. We report a case of 65-year-old Japanese woman who presented with primary adenocarcinoma in the anterior wall of the vagina, where the left ureter-like metanephric duct remnant abnormally terminated. Histological examination in serial sections revealed the direct connection between the carcinoma and the metanephric duct remnant. Moreover, the remnant epithelium showed varying degrees of dysplastic changes, including carcinoma in situ in close proximity to the carcinoma. This patient also had a bicornate uterus and left renal aplasia. To our knowledge, this is the first reported case of a primary vaginal adenocarcinoma arising from the metanephric duct remnant. Although the precise mechanism involved in carcinogenesis in this clinicopathological setting remains unknown, adenocarcinoma should be included in the differential diagnosis of vaginal tumors in patients with renal aplasia and/or an ectopic termination of the ureter or metanephric duct remnant, especially when the tumor is in the anterior wall.

Adenocarcinoma↗
PubMed2000

Histologic and biochemical study of the brain, heart, kidney, and liver in asphyxia caused by occlusion of the umbilical cord in near-term fetal lambs.

OBJECTIVE: We sought to determine the relationship between the degree of histologic changes in the brain, heart, kidney, and liver in fetal lambs after severe asphyxia and to analyze the role of oxidative stress in the pathogenesis of fetal multiple organ failure. STUDY DESIGN: Eight chronically instrumented near-term fetal lambs were asphyxiated by partial umbilical cord occlusion for approximately 60 minutes until the fetal arterial pH reached <6.9 and the base excess reached <-20 mEq/L. An additional 6 fetuses were used as sham-asphyxiated controls. Fetal heart rates, blood pressure, fetal breathing movements, and arterial blood gases and acid-base states were serially monitored. The brain, heart, kidney, and liver were collected 72 hours after asphyxia, processed, and histologically examined after hematoxylin and eosin staining. Fetal brain histologic features were classified into 5 grades, with 5 being the most severe damage. The other organs were examined histologically by pathologists who were blinded to the treatment. Each organ was assayed for tissue concentrations of thiobarbituric acid-reactive substances, superoxide dismutase, glutathione, lactate, and glucose. RESULTS: Myocardial changes of necrosis, phagocytosis, and contraction bands occurred in only 2 of the most severely (grade 5) brain-damaged fetuses. The same 2 cases showed fatty changes and congestion in the liver. In the kidney all asphyxiated cases showed tubular necrosis, but glomeruli were generally spared. Of the measures of oxidative stress, only liver tissue levels of thiobarbituric acid-reactive substances and superoxide dismutase were significantly higher in the asphyxiated group than in the control group, but there was no correlation with the degree of damage. Lactate level was higher only in the heart in the asphyxiated fetuses. CONCLUSION: Renal tubular damage was seen with all degrees of asphyxia, despite variable brain damage. Histologic changes in the myocardium and liver were seen only with the most severe brain damage. Oxidative stress appears to play a role in the pathogenesis of liver damage.

Animals↗
PubMed2000

Overexpression of intestinal trefoil factor in human colon carcinoma cells reduces cellular growth in vitro and in vivo.

BACKGROUND & AIMS: Intestinal trefoil factor (ITF) has a role in gastrointestinal mucosal integrity and the repair of damaged mucosa. However, little is known about its role in tumors. To analyze the role of ITF in colon carcinomas, overexpression of the ITF gene in colon carcinoma cells was used. METHODS: Human colon carcinoma cell lines LoVo and SW837, expressing no endogenous ITF, and WiDr expressing a low level of ITF were stably transfected with an expression vector harboring human ITF complementary DNA. The effects of ITF overexpression on in vitro growth, morphology in collagen gel, response to epidermal growth factor (EGF), mitogen-activated protein kinase (MAPK) activity, and growth in nude mice were assessed. RESULTS: Overexpression of ITF in LoVo and SW837 resulted in significantly reduced growth in vitro and in vivo. In collagen gels, the ITF-expressing LoVo clones formed smaller, more dispersed colonies. EGF-induced phosphorylation of MAPKs was modestly reduced in the ITF-expressing clones. The growth of WiDr was modestly suppressed only in vivo by ITF overexpression. CONCLUSIONS: Overexpression of ITF suppressed the growth of colon carcinoma cells. ITF may function as an inhibitory factor for the growth of colonic neoplasm.

Animals↗
PubMed2000

Genomic structure and chromosomal localization of the human hepatocyte growth factor activator inhibitor type 1 and 2 genes.

Hepatocyte growth factor activator inhibitor type 1 (HAI-1) and type 2 (HAI-2) are recently discovered Kunitz-type serine protease inhibitors which can be purified and cloned from human stomach cancer cell line MKN45 as specific inhibitors against hepatocyte growth factor activator (HGFA). HAI-2 was identical with the protein originally reported as placental bikunin. Both proteins contain two Kunitz inhibitor domains (KDs), of which the first domain (KD1) is mainly responsible for the inhibitory activity against HGFA, and are expressed ubiquitously in various tissues. In this study, we cloned the genes coding for these two structurally similar proteins by screening of human genomic bacterial artificial chromosome (BAC) library and their genomic structures were compared. HAI-1 and -2 genes consist of 11 and 8 exons spanning 12 kbp and 12.5 kbp, respectively. Three exons were inserted between KD1 and KD2 of each gene, of which the middle one was the low-density lipoprotein (LDL) receptor-like domain (HAI-1) and the testis specific exon (HAI-2). Apparently homologous regions between HAI-1 and -2 were not found in 5'-flanking region and neither TATA nor CAAT box was present. The genes were mapped to chromosome 15q15 (HAI-1) and 19q13.11 (HAI-2). These results suggested that although HAI-1 and -2 genes might be derived from same ancestor gene, they acquired distinctive in vivo roles during their evolution.

Amino Acid Sequence↗
PubMed2000

Solitary fibrous tumor of the vagina.

The solitary fibrous tumor (SFT) is a rare tumor that most commonly arises in the pleura. Recent evidence has indicated that this tumor originates from mesenchymal, probably fibroblastic, cells and is not restricted to the pleura. However, its occurrence in the female genital tract is extremely rare. We report a case of primary SFT that originated from the vagina in a 34-year-old female. It was a pedunculated polypoid tumor and occurred at the site of scar tissue, caused by laceration during her last labor 7 years previously. Histologically, the tumor was predominantly composed of a random proliferation of spindle cells, intimately admixed with collagen. Immunohistochemically, the cells were strongly positive for CD34, vimentin and bcl-2, but were negative for S-100 protein, neuron-specific enolase, smooth muscle actin, desmin, CD68, cytokeratins and epithelial membrane antigen. To the best of our knowledge, this is the first reported case of a primary vaginal SFT in the English literature. Our report suggests to include SFT in the differential diagnosis of a spindle cell neoplasm originating from the vagina.

Adult↗
PubMed2000

Protein kinase C-alpha and -epsilon down-regulate cell surface sodium channels via differential mechanisms in adrenal chromaffin cells.

In cultured bovine adrenal chromaffin cells, our [3H]saxitoxin ([3H]STX) binding, immunoblot, and northern blot analyses specified protein kinase C (PKC) isoform-specific posttranscriptional and posttranslational mechanisms that direct down-regulation of cell surface Na channels. Immunoblot analysis showed that among 11 PKC isoforms, adrenal chromaffin cells contained only conventional (c)PKC-alpha, novel (n)PKC-epsilon, and atypical (a)PKC-zeta. Treatment of adrenal chromaffin cells with 100 nM 12-O-tetradecanoylphorbol 13-acetate (TPA) or 100 nM phorbol 12,13-dibutyrate (PDBu) caused a rapid (<15 min) and sustained (>15 h) translocation of PKC-alpha and -epsilon (but not -zeta) from cytosol to membranes, whereas a biologically inactive 4alpha-TPA had no effect. Thymeleatoxin (TMX), an activator of cPKC, produced similar membrane association of only PKC-alpha at 100 nM, with the potency of TMX being comparable with those of TPA and PDBu. Treatment with either 100 nM TPA or 100 nM TMX reduced cell surface [3H]STX binding to a comparable extent at 3, 6, and 12 h, whereas TPA lowered the binding to a greater extent than TMX at 15, 18, and 24 h; at 15 h, Gö6976, a specific inhibitor of cPKC, completely blocked TMX-induced decrease of [3H]STX binding while preventing by merely 57% TPA-induced decrease of [3H]STX binding. Treatment with 100 nM TPA lowered the Na channel alpha-subunit mRNA level between 3 and 12 h, with its maximum 52% fall at 6 h, and it was accompanied by a subsequent 61 % rise of the beta1-subunit mRNA level at 24 h. Gö6976 failed to prevent TPA-induced reduction of the alpha-subunit mRNA level; TMX did not change the alpha- and beta1-subunit mRNA levels throughout the 24-h treatment. Brefeldin A, an inhibitor of vesicular exit from the trans-Golgi network, augmented TPA- and TMX-induced decrease of [3H]STX binding at 1 and 3 h. Our previous and present studies suggest that PKC down-regulates cell surface Na channels without altering the allosteric gating of Na channels via PKC isoform-specific mechanisms; cPKC-alpha promotes Na channel internalization, whereas nPKC-epsilon decreases the alpha-subunit mRNA level by shortening the half-life of alpha-subunit mRNA without changing its gene transcription.

Adrenal Glands↗
PubMed2000

Pena-shokeir type I syndrome with thymic and systemic lymphoid hyperplasia: report of an autopsy case.

We report a case of Pena-Shokeir type I syndrome in a female neonate who died of respiratory failure shortly after the birth at 32 weeks of gestation. In general appearance, she had apparent ocural hypertelorism, a depressed tip of the nose, low-set malformed ears, and microglossia in the head. There were severe contractures at the ankle, hand, fingers, and toes, and moderate contractures at the hip, shoulder, knee, and elbow. An autopsy analysis showed severe pulmonary hypoplasia and group atrophy of the skeletal muscle tissues. In addition to these findings which are well known characteristics of the infant with this syndrome, the thymus was markedly hyperplastic and lymph nodes were systemically swollen, especially the mesenteric ones which were visible and measured 2-5 mm in diameter. Histologically, the lymph nodes showed massive paracortical hyperplasia without apparent follicular structures, although no atypical lymphocytes were observed in both the thymus and lymph nodes. Immunohistochemically, proliferating lymphocytes seemed to be immature CD4+/CD8+ T cells, suggesting the insufficiency of T-cell negative selection in the thymus. This report is the first case of Pena-Shokeir type I syndrome with T-lymphocytic disorder.

Abnormalities, Multiple↗
PubMed2000

Upregulation of HGF activator inhibitor type 1 but not type 2 along with regeneration of intestinal mucosa.

Hepatocyte growth factor (HGF) activator inhibitor type 1 (HAI-1) and type 2 (HAI-2) are new Kunitz-type serine protease inhibitors that were recently purified and cloned from the human stomach cancer cell line MKN45 as specific inhibitors against HGF activator. Both proteins contain two Kunitz inhibitor domains and are expressed abundantly throughout the gastrointestinal tract, in addition to the placenta, pancreas, and kidney. In this study, to assess the possible roles of HAI-1 and HAI-2 in the intestinal mucosa, we examined the expression of HAI-1 and HAI-2 during regeneration of the intestinal mucosa. Immunohistochemical studies revealed that HAI-1 but not HAI-2 was detected more strongly in regenerative epithelium than in normal epithelium, although both proteins were detected throughout the human gastrointestinal tract. During the course of acetic acid-induced experimental colitis in an in vivo mouse model, HAI-1 but not HAI-2 was upregulated in the recovery phase, suggesting that HAI-1 but not HAI-2 is associated with the regeneration of damaged colonic mucosa. Upregulation of HAI-1 may serve to downregulate the proliferative response after initial activation of MET receptor by HGF/scatter factor after an injury.

Acetic Acid↗
PubMed1999

Role of fibroblasts in HGF/SF-induced cohort migration of human colorectal carcinoma cells: fibroblasts stimulate migration associated with increased fibronectin production via upregulated TGF-beta1.

Carcinoma cells frequently invade the surrounding tissue as coherent clusters or nests of cells. We have called this type of movement "cohort migration." We have previously presented an in vitro two-dimensional cohort migration model, in which highly metastatic variant L-10 cells of human rectal adenocarcinoma cell line RCM-1 moved as coherent cell sheets when stimulated with 12-O-tetradecanoylphorbol-13-acetate (TPA) or hepatocyte growth factor/scatter factor (HGF/SF). Pericellular deposition of EDA-containing fibronectin (EDA+FN) was essential for TPA-induced cohort migration. In this study, we investigated how colon-derived fibroblasts could affect the induction of cohort migration of colorectal carcinoma cells by HGF/SF, since carcinoma cell-fibroblast interactions frequently regulate biological events during cancer cell invasion. Fibroblasts co-cultured with L-10 carcinoma cells stimulated HGF/SF-induced cohort migration of L-10 cells up to 2 to 3-fold. Conditioned medium (CM) from fibroblasts that were cultured alone was not effective but CM from fibroblasts cocultured with carcinoma cells enhanced HGF/SF-induced cohort migration, and this effect in CM was found to be mediated by TGF-beta1 upregulated in co-cultured conditions. Among the motogenic growth factors examined, only TGF-beta1 synergistically stimulated HGF/SF-induced L-10 cell cohort migration, although TGF-beta1 alone did not induce cohort migration. TGF-beta1 also exhibited synergistic effect in several other human colorectal carcinoma cell lines. The synergistic stimulation of L-10 cell cohort migration by HGF/SF and TGF-beta1 was associated with increased production of motility-enhancing EDA+FN by L-10 cells, and blocking FN with a specific antibody effectively inhibited the synergistic effect.

Adenocarcinoma↗
PubMed1999

Regulation of matrix metalloproteinase-2 (MMP-2) by hepatocyte growth factor/scatter factor (HGF/SF) in human glioma cells: HGF/SF enhances MMP-2 expression and activation accompanying up-regulation of membrane type-1 MMP.

Hepatocyte growth factor/scatter factor (HGF/SF) contributes to the malignant progression of human gliomas. We investigated the effect of HGF/SF on matrix metalloproteinase-2 (MMP-2), membrane type 1 matrix metalloproteinase (MT1-MMP) and tissue inhibitors of metalloproteinases (TIMPs), expressions of c-Met/HGF receptor-positive human glioblastoma cells. Treatment of U251 human glioblastoma cells with HGF/SF resulted in enhanced secretion of MMP-2 with an increased level of the active form. This was accompanied by enhanced expression (2.5-fold) of mRNA specific for MMP-2. The stimulatory effect of HGF/SF on MMP-2 expression did not occur in the presence of herbimycin A, a protein tyrosine kinase inhibitor. MT1 -MMP, a cell-surface activator of proMMP-2, was also up-regulated by HGF/SF in a dose-dependent manner. By contrast, the level of TIMP- 1 mRNAs was not altered significantly and that of TIMP-2 was reduced mildly by the HGF/SF treatment, suggesting that HGF/SF may eventually modulate a balance between MMP-2 and TIMPs in favor of the proteinase activity in the glioma cell microenvironment. HGF/SF also stimulated MMP-2 expression of other glioblastoma cell lines. Since glioblastomas frequently co-express HGF/SF and its receptor, our results suggest that HGF/SF might contribute to the invasiveness of glioblastoma cells through autocrine induction of MMP-2 expression and activation.

Benzoquinones↗
PubMed1999

Hepatocyte growth Factor/Scatter factor (HGF/SF) is a regulator of fibronectin splicing in MDCK cells: comparison between the effects of HGF/SF and TGF-beta1 on fibronectin splicing at the EDA region.

EDA-containing fibronectin (EDA + FN) is selectively produced under several physiological and pathological conditions requiring tissue remodeling, where cells actively proliferate and migrate. Only a few growth factors, such as transforming growth factor (TGF)-beta1, have been reported to regulate FN splicing at the EDA region. In the present study, we showed for the first time that hepatocyte growth factor/scatter factor (HGF/SF), which is mainly produced by mesenchymal cells and functions as a motogenic and mitogenic factor for epithelial cells, modulates FN splicing at the EDA region in MDCK epithelial cells. HGF/SF treatment increased the ratio of EDA + FN mRNA to mRNA of FN that lacks EDA (EDA - FN) (EDA+/EDA- ratio) more than TGF-beta1 treatment did: at a range from 0.02 to 20 ng/ml, HGF/SF increased the ratio in a dose-dependent manner by up to 2. 1-fold compared with nontreated control, while TGF-beta1 stimulated the EDA+/EDA- ratio by 1.5-fold at the optimum dose of 10 ng/ml. However, TGF-beta1 increased total FN mRNA levels by 3-fold at 10 ng/ml, but HGF/SF did not. We previously demonstrated that fibroblasts cultured at low cell density expressed more EDA + FN than those at high cell density. The same effect of cell density was also observed in MDCK cells. Furthermore, at low cell density, HGF/SF stimulated EDA inclusion into FN mRNA more effectively than did TGF-beta1, whereas at high cell density, TGF-beta1 was more potent than HGF/SF. Simultaneous treatment of cells with HGF/SF and TGF-beta1 synergistically stimulated EDA inclusion into FN mRNA. This stimulation of EDA inclusion into FN mRNA by HGF/SF led to increased EDA + FN protein production and secretion by cells, which was demonstrated by immunoblotting. Thus, our studies have shown that HGF/SF is an enhancer of EDA inclusion into FN mRNA as is TGF-beta1. However, these two factors were different in their effects at low and high cell densities and also in their effects on total FN mRNA levels.

Animals↗
PubMed1999

Hepatocyte growth factor activator inhibitor type 2 lacking the first Kunitz-type serine proteinase inhibitor domain is a predominant product in mouse but not in human.

Hepatocyte growth factor activator inhibitor type 2 (HAI-2) is a new Kunitz-type serine protease inhibitor, which is purified and cloned from human stomach cancer cell line MKN45. The mature HAI-2 protein contains two Kunitz domains and the first domain is mainly responsible for the inhibitory activity against hepatocyte growth factor activator (HGFA). In this study, we identified the mouse homolog of HAI-2 (mHAI-2) by screening the data base of public expressed sequence tag (dbEST). In addition to a full-length cDNA corresponding to human HAI-2, a shorter size of mHAI-2 cDNA was obtained from mouse kidney by reverse-transcription polymerase chain reaction (RT-PCR). Sequence analysis of this shorter cDNA revealed that the region encoding the first Kunitz domain was completely deleted. Analysis of mouse genomic DNA showed that the deleted cDNA was generated by an alternative splicing mechanism. Surprisingly, the spliced form lacking the first Kunitz domain was a predominant transcript in all tissues of mice tested but not in those of human as assessed by RT-PCR analysis. This phenomenon is also confirmed by Western blot analysis using the specific antiserum against human HAI-2 protein. These results suggest that most of HAI-2 expressed in various tissues of mice may be unable to inhibit HGFA efficiently.

Alternative Splicing↗
PubMed1999

Enhanced tumor growth and invasiveness in vivo by a carboxyl-terminal fragment of alpha1-proteinase inhibitor generated by matrix metalloproteinases: a possible modulatory role in natural killer cytotoxicity.

Matrix metalloproteinases (MMPs) are believed to contribute to the complex process of cancer progression. They also exhibit an alpha1-proteinase inhibitor (alphaPI)-degrading activity generating a carboxyl-terminal fragment of approximately 5 kd (alphaPI-C). This study reports that overexpression of alphaPI-C in S2-020, a cloned subline derived from the human pancreas adenocarcinoma cell line SUIT-2, potentiates the growth capability of the cells in nude mice. After stable transfection of a vector containing a chimeric cDNA encoding a signal peptide sequence of tissue inhibitor of metalloproteinase-1 followed by cDNA for alphaPI-C into S2-020 cells, three clones that stably secrete alphaPI-C were obtained. The ectopic expression of alphaPI-C did not alter in vitro cellular growth. However, subcutaneous injection of the alphaPI-C-secreting clones resulted in tumors that were 1.5 to 3-fold larger than those of control clones with an increased tendency to invasiveness and lymph node metastasis. These effects could be a result of modulation of natural killer (NK) cell-mediated control of tumor growth in nude mice, as the growth advantage of alphaPI-C-secreting clones was not observed in NK-depleted mice, and alphaPI-C-secreting clones showed decreased NK sensitivity in vitro. In addition, production of alphaPI and generation of the cleaved form of alphaPI by MMP were observed in various human tumor cell lines and in a highly metastatic subline of SUIT-2 in vitro. These results provide experimental evidence that the alphaPI-degrading activity of MMPs may play a role in tumor progression not only via the inactivation of alphaPI but also via the generation of alphaPI-C.

Adenocarcinoma↗
PubMed1999

TPA-enhanced motility and invasion in a highly metastatic variant (L-10) of human rectal adenocarcinoma cell line RCM-1: selective role of PKC-alpha and its inhibition by a combination of PDBu-induced PKC downregulation and antisense oligonucleotides treatment.

We previously found that 12-O-tetradecanoylphorbol-13-acetate (TPA)-enhanced invasiveness was associated with augmentation of cell motility but not that of metalloproteinase activity in a highly metastatic variant (L-10) of the human colon adenocarcinoma cell line RCM-1 and that this enhancement was possibly mediated by protein kinase C (PKC). In this study, we first intended to determine the specific isoforms of PKC involved in this TPA-enhanced L-10 cell motility that leads to invasion, and then investigated the way to inhibit the enhanced motility and invasion by using antisense oligodeoxynucleotides (ODN) targeting the isoform. An activator of conventional PKC isoforms (cPKC), thymeleatoxin, enhanced L-10 cell motility and invasion like TPA, and an inhibitor of cPKC, Go-6976, efficiently inhibited TPA-enhanced motility and invasion. TPA treatment induced a shift of PKC-alpha, but not other isoforms, from the cytosol to the membrane fraction, indicating the activation of the isoform. During the assay period, only activation but not downregulation of PKC-alpha occurred with the low concentration of TPA used in our assays. Antisense ODNs specific for PKC-alpha efficiently reduced its expression at the protein levels and inhibited L-10 cell motility in the absence of TPA. With TPA treatment, however, the remaining PKC-alpha was sufficient for activation leading to enhanced invasion. Only a combination of depletion of PKC by prolonged stimulation with a high concentration of phorbol 12,13 dibutyrate (PDBu) and treatment with antisense ODNs effectively inhibited L-10 cell invasion even in the presence of TPA. These results suggested that downregulation of PKC isoforms by treatment with antisense ODNs alone is insufficient to suppress the isoform-mediated cellular events in the presence of PKC activators, and thus that some additional treatments are necessary for the successful downregulation of them.

Adenocarcinoma↗
PubMed1999

Simultaneous up-regulation of urokinase-type plasminogen activator (uPA) and uPA receptor by hepatocyte growth factor/scatter factor in human glioma cells.

Several lines of evidence indicate that hepatocyte growth factor/scatter factor (HGF/SF) and its receptor, c-Met, may play an important role in progression of human glioma. In this study, effects of HGF/SF on urokinase- type plasminogen activator (uPA)-mediated proteolysis network were examined in c-Met-positive human glioma cell lines. Treatment of the glioma cells with various concentrations of HGF/SF resulted in an enhanced secretion of uPA proteins accompanying increased transcription of uPA mRNA in a dose dependent fashion. The levels of uPA receptor (uPAR) mRNAs were also elevated simultaneously upon HGF/SF stimulation, and the cell-surface associated uPA activity was also elevated by the treatment. Since concomitant expression of HGF and its receptor c-Met are frequently observed in malignant gliomas, these results suggest that HGF/SF participates in invasive process of malignant glioma cells not only by its motility-stimulating activity but also through enhanced degradation of the extracellular matrix induced by autocrine activation of uPA proteolysis network.

Central Nervous System Neoplasms↗
PubMed1999

Retroperitoneal bronchogenic cyst: report of a case and literature review.

A large cystic mass was found in the subdiaphragmatic region of a 46-year-old woman who had complained of continuous pain in the left flank . The cyst was located in the retroperitoneum just below the diaphragm and was adhered to the diaphragmatic skeletal muscle and abdominal aorta, but was separate from the spleen, pancreas, left adrenal gland and left kidney. The surgically resected cyst measured 8 x 8 x 7 cm and was filled with protein-rich fluid, which contained amylase and embryonal proteins such as carcinoembryonic antigen, CA125 and CA19-9. Histologically, the cyst wall was composed of a fibrovascular connective tissue containing thin smooth muscle layers and mucus-secreting glands and was lined by a ciliated pseudostratified or tall columnar epithelium without dysplastic changes. Thus, a diagnosis of bronchogenic cyst, which is usually discovered in the posterior part of the mediastinum, was made. A rare case of bronchogenic cyst and a literature review is presented.

Biomarkers↗
PubMed1999

Aeromonas sobria infection with severe soft tissue damage and segmental necrotizing gastroenteritis in a patient with alcoholic liver cirrhosis.

A 49-year-old man, who had a 3-year history of liver dysfunction but had not been treated, was admitted to the hospital with a sudden onset of fever and generalized muscle pain. He subsequently developed generalized purpura with scattered hemorrhagic bullae of the skin and massive bloody stools. Aeromonas sobria was proven by culture of both blood and bullous fluid. In spite of the extensive treatment with antibiotics and other medications in the intensive care unit (ICU), the patient went into septic shock and died 2 days after admission. Pathological examination on autopsy revealed segmental necrotizing gastroenteritis with bacterial colonies and alcoholic liver cirrhosis, in addition to extensive severe soft tissue damage involving cellulitis and rhabdomyolysis and epidermolysis. Although the prognosis for Vibrio vulnificus infection with severe soft tissue damage in patients with liver cirrhosis, malignancy, diabetes mellitus or other pre-existing diseases is poor, the unfavorable progression of Aeromonas species, especially A. sobria infection is rare. This is thought to be the first report of an autopsied case.

Aeromonas↗