Successful Treatment of Herpes Esophagitis With Ganciclovir in a Liver Transplant Patient

The presence of Herpes Simplex Virüs-1 (HSV-1) esophagitis in patients with liver transplantation has been reported rarely. Among the reports that are accessible in the literature, none could have shown tissue positivity for Herpes virus-1 DNA via Polymerase Chain Reaction (PCR) in patients with liver transplantation. This case is presented as the patient was diagnosed with herpes esophagitis based on the histopathological findings and HSV-1 DNA positivity (detected by PCR) in the biopsy material and was treated with Ganciclovir. Due to the specific action of Ganciclovir against CMV infections, it is natural that the drug cannot use in the treatment of HSV infections. However it is reported that ganciclovir has been reduced the incidence of symptomatic HSV infections after liver transplantation. We report on a patient after liver transplantation with HSV-1 esophagitis, who was successfully treated with Ganciclovir. We assume that most transplant centers according to their protocols use ganciclovir for CMV prophylaxis, which may contribute to avoid HSV infection

Differential expression of Caveolin-1 in hepatocellular carcinoma: correlation with differentiation state, motility and invasion

WOS: 000264914000001PubMed ID: 19239691Turkish Scientific and Technological Research Council (TUBITAK)Turkiye Bilimsel ve Teknolojik Arastirma Kurumu (TUBITAK) [SBAG-107S026]; Dokuz Eylul University Research FoundationDokuz Eylul University [05.KB.SAG.071]We thank Prof. Mehmet Ozturk for providing us HCC cell lines and for his critical reading of the manuscript; and Prof. Aykut Uren for his helpful discussions on the manuscript. We also thank to Evin Ozen for her technical assistance. This work was supported by grants to Nese ATABEY from the Turkish Scientific and Technological Research Council (TUBITAK, SBAG-107S026) and Dokuz Eylul University Research Foundation (05.KB.SAG.071)

Evaluation of GLP-2 receptor expression in gastrointestinal neuroendocrine tumors

Evaluation of GLP-2 receptor expression in gastrointestinal neuroendocrine tumors Background and Aims: Neuroendocrine tumors arise from cells of the neuroendocrine system. These cells show both nerve and endocrine cell characteristics and can be found in many organs in the body. GLP-1 and GLP-2 are released from intestinal L cells in a 1:1 ratio following food intake. GLP-2 receptor recognizes GLP-2. GLP-2 receptor mRNA transcripts have been detected in the stomach, small and large intestine, brain, and lung. The proliferative effect of GLP-2 has been demonstrated in mice, rats, pigs, and humans by administering exogenous GLP-2. The objective is to evalaute the relation between gastroenteropancreatic neuroendocrine tumors and glukagon like peptid-2 and GLP-2 receptor. Materials and Methods: The patients, who were pathologically diagnosed with gastroenteropancreatic neuroendocrine tumor between 2006-2009 were included in the study. There were 47 patients (27 females, 20 males, avarage age: 54 ± 15.5) in the study. There were also 46 control group patients (25 females, 21 males, avarage age: 57.5 ± 14.8). Pathological tissue blocks prepared on poly-L-lysine microscope slides were stained by GLP-2 receptor antibody (1:100 - 1:200, 1 mg/ml) immunohistochemical stain. Results: GLP-2 receptor positivity of colon neuroendocrine tumor group was 30% (4/13) and colon control group was %100. GLP-2 receptor positivity of pancreas neuroendocrine tumor group was 25% (3/12) while it was 100% in pancreas control group. The comparison of colon neuroendocrine tumor and control group showed significant difference (p: 0.003). The comparison of pancreas neuroendocrine tumor and control group also showed statistically significant difference (p < 0.001). The comparison of gastric neuroendocrine tumor with the control yielded comparable results (p: 0.22). Conclusions: We concluded that GLP-2 receptor cannot be as useful as somatostatin receptors in diagnosis and treatment of these tumors. More studies are needed on this subject with different methods

Plexiform neurofibroma of the tongue: a case report of a child

A three-year-old girl with a lingual plexiform neurofibroma treated by total excision is presented. Despite their occurrence in the head and neck region, neural sheath tumors are rarely encountered in the oral cavity. It is reported that 4-7% of patients affected by neurofibromatosis display oral manifestations. Neurofibromatosis is characterized by cafe-au-lait spots and cutaneous neurofibromas. Plexiform neurofibroma is said to be indicative of von Recklinghausen's disease (VRD) even though it may be the only manifestation of the disease. Generally, surgical resection represents the treatment of choice and the diagnosis can only be confirmed after histological examination. Affected patients need regular follow-up to detect malignant degeneration, an early recurrence or appearance of other manifestations of VRD

Active form of AKT controls cell proliferation and response to apoptosis in hepatocellular carcinoma

WOS: 000332694400007PubMed ID: 24337632Hepatocellular carcinoma (HCC) is the third most common cause of cancer-related mortality worldwide. Deregulation of the AKT signaling pathway has been found in HCC. However, the effect of AKT activation on the proliferation and apoptosis in HCC is not clear. Herein, expression of phosphorylated form of AKT (Ser 473) was investigated in HCC tumor (n=73), cirrhosis (n=17), normal liver (n=22) samples and in HCC cell lines (n=8). The results showed that expression of p-AKT was higher in tumor (53%) than in cirrhotic tissues (12%) while it was absent in normal liver (p<0.0001). p-AKT expression was also associated with number of tumor nodules and differentiation status (p<0.05). LY294002 induced cell cycle arrest at G0/G1 in SNU-449 and Mahlavu cells by decreasing expression of CDK2, CDK4, CycD1, CycD3, CycE, CycA and increasing expression of p21 and p27 as well; it also caused a decrease in the E2F1 transcriptional activity through declining phosphorylated Rb. LY294002 did not affect the basal level of apoptosis; however, it amplified cisplatin-induced apoptosis in SNU-449 cells. When the p-AKT level was decreased specifically after transfection with the DN-AKT plasmid, SNU-449 cells became more sensitive to cisplatin-induced apoptosis. HuH-7 cells with no basal p-AKT, were markedly affected by the treatment of doxorubicin. Thus, Akt signaling controls growth and chemical-induced apoptosis in HCC and p-AKT may be a potential target for therapeutic interventions in HCC patients.Scientific and Technological Research Council of Turkey (TUBITAK)Turkiye Bilimsel ve Teknolojik Arastirma Kurumu (TUBITAK) [SBAG- 105S092]; Dokuz Eylul UniversityDokuz Eylul University [DEU-2005. KB.SAG.08]This study was supported by a grant from the Scientific and Technological Research Council of Turkey (TUBITAK) (SBAG- 105S092) and Dokuz Eylul University, DEU-2005. KB.SAG.08

Problems in grading and staging of nonalcoholic steatohepatitis: A study of 597 cases by Turkish National Working Group of Hepatopancreatobiliary Pathology

WOS: 00024945460081