Publications by authors named "Puapairoj A"

Background: IgA nephropathy in children has various clinical manifestations. Kidney biopsy is a gold standard for diagnosis by using Oxford classification 2016 with few studies about the correlation between clinical and pathology manifestations. This study aims to find these correlations at the time of diagnosis and during short-term follow-up.

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A combination of Opisthorchis viverrini infection and high fat/high fructose diets (HFa/HFr) intake is likely to enhance fatty liver and kidney pathologies. Here we investigated the combined effects of chronic O. viverrini infection and HFa/HFr intake on liver and kidney pathologies, metabolism, and gut microbiome in hamsters.

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Introduction: Opisthorchis viverrini (OV) is a major cause of infection in Southeast Asia. Previous studies in mouse models have shown that OV infection can contribute to immune-complex glomerulonephritis (GN). However, OV infection in human kidney tissue has never been demonstrated.

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(Ov) infection causes hepatobiliary diseases and is a major risk factor for cholangiocarcinoma. While several omics approaches have been employed to understand the pathogenesis of opisthorchiasis, effects of Ov infection on the host systemic metabolism and fecal microbiota have not been fully explored. Here, we used a H NMR spectroscopy-based metabolic phenotyping approach to investigate Ov infection-induced metabolic disturbances at both the acute (1 month postinfection, 1 mpi) and chronic (4 mpi) stages in hamsters.

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Background: The information guiding the treatment decision(s) for renal diseases in systemic sclerosis (SSc) is the renal pathological finding. This study aimed to evaluate the renal pathological diagnosis and its clinical feature among SSc.

Method: A historical cohort study was performed on adult Thai SSc patients who underwent renal biopsy during January 2005-December 2016.

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Background: Cholangiocarcinoma (CCA) is a fatal liver cancer arising from bile duct epithelium. Polycomb repressive complex 2 (PRC2) is a histone methyltransferase enzyme that catalyzes trimethylation of histone H3 on lysine 27, resulting transcriptional gene silencing. The key components of PRC2 are EZH2, SUZ12 and EED, which EZH2 is a catalytic subunit.

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Background: Renal involvement in type 2 diabetes is mainly due to diabetic nephropathy (DN). Nevertheless, a sizable proportion of diabetic patients could actually have nondiabetic renal diseases (NDRDs) or DN plus NDRDs. This study aimed to explore the pathological features of NDRD in diabetic patients and to assess the predictability of diagnosing NDRD (±DN) versus isolated DN on the basis of clinical parameters.

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The adaptive response of the genome protection mechanism occurs in cells when exposed to genotoxic stress due to the overproduction of free radicals via inflammation and infection. In such circumstances, cells attempt to maintain health via several genome protection mechanisms. However, evidence is increasing that this adaptive response may have deleterious effect; a reduction of antioxidant enzymes and/or imbalance in the DNA repair system generates microsatellite instability (MSI), which has procarcinogenic implications.

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Background: Experimental studies have linked peritubular capillary (PTC) loss with progression of chronic kidney disease. Minimal information on PTC in lupus nephritis (LN) has been reported. We therefore evaluated the PTC area in different classes of LN and determined if specific clinical characteristics correlated with PTC changes.

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Objective: Haem oxygenase-1 (HO-1) plays important roles in cytoprotection and tumour growth. Cholangiocarcinoma (CCA) is a deadly malignancy with very poor prognosis. The role of HO-1 in tumour progression in CCA up to now has been relatively unexplored, thus, its possible therapeutic implications in CCA have been investigated here.

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L-type amino acid transporter 1 (LAT1) is highly expressed in various human cancers, including cholangiocarcinoma (CCA), the most common cancer in Northeast Thailand. Chronic inflammation and oxidative stress induced by liver fluke, Opisthorchis viverrini, infection has been recognized as the major cause of CCA in this area. We show here that an increased expression of LAT1 and its co-functional protein CD98 are found during carcinogenesis induced by Ov in hamster CCA tissues.

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Background And Aim: Trophoblast cell surface antigen 2 (TROP2) or tumor-associated calcium signal transducer 2 (TACSTD2) is a 36-kDa type I transmembrane glycoprotein and exerts dual functions as an oncogene and tumor suppressor in cancer cells. In this study, we investigated the expression and functions of TROP2 in liver fluke-associated cholangiocarcinoma (CCA).

Material And Methods: TROP2 expression in 85 CCA tissues was detected by using immunohistochemistry.

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Opisthorchis viverrini (Ov) infection is the major etiological factor for cholangiocarcinoma (CCA), especially in northeast Thailand. We have previously reported significant involvement of PI3K/AKT/PTEN and Wnt/β- catenin in human CCA tissues. The present study, therefore, examined the expression and activation of PI3K/ AKT/PTEN and Wnt/β-catenin signaling components during Ov-induced cholangiocarcinogenesis in a hamster animal model.

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Background: Up-regulation and association of nuclear factor kappa B (NF-κB) with carcinogenesis and tumor progression has been reported in several malignancies. In the current study, expression of NF-κB in cholangiocarcinoma (CCA) patient tissues and its clinical significance were determined. The possibility of using NF-κB as the therapeutic target of CCA was demonstrated.

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The activation of Ephrin (Eph) receptors, the largest tyrosine kinase families of cell surface receptor, has recently been addressed in human cholangiocarcinoma (CCA). Therefore, the present study aimed to investigate the role of Eph receptors and its ligands in CCA. Of all 50 cases of human CCA tested, immunohistochemical staining demonstrated that EphB2, EphB4, ephrinB1, and ephrinB2 were 100 % positive in CCA tissues with overexpressions of the above proteins as 56, 56, 70, and 48 % of cases, respectively.

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Background: The epithelial-mesenchymal transition (EMT) process strongly contributes to cancer metastasis. This study was to investigate the alteration of EMT-related proteins (ZEB1, ZEB2 and S100A4) in cholangiocarcinoma (CCA) tissues. The effect of tumor necrosis factor-α (TNF-α) on the expression of those molecules in CCA cells was investigated.

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Tumor progression is characterized by loss of cell adhesion and increase of invasion and metastasis. E-cadherin, a cell adhesion molecule, is frequently downregulated and has been proposed as an important mediator in epithelial-mesenchymal transition (EMT) in tumors. In this study, we investigated the expression of E-cadherin and its association with cancer invasion and prognosis in cholangiocarcinoma (CCA).

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Prostaglandin E2 (PGE2) involves in progression of various chronic inflammation-related cancers including cholangiocarcinoma (CCA). This study aimed to determine the role of PGE2 signaling, its biosynthesis-related enzymes in a clinical prognosis, and their targeted inhibition in CCA progression. The immunohistochemical staining of cyclooxygenase (COX)-1, COX-2, mPGES-1, EP1, and EP4 was examined in CCA tissues, and their expressions were compared with clinicopathological parameters.

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De novo lupus nephritis (LN) is a rare complication in renal transplantation recipients. We present the clinical manifestations of de novo LN in a 12-year-old boy who received a cadaveric renal transplant. The cause of end-stage renal disease was prune belly syndrome with renal dysplasia.

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The Wnt/β-catenin signaling pathway is pathologically activated in cholangiocarcinoma (CCA). Here, we determined the expression profile as well as biological role of activated Wnt/β-catenin signaling in CCA. The quantitative reverse transcription polymerase chain reaction demonstrated that Wnt3a, Wnt5a, and Wnt7b mRNA were significantly higher in CCA tissues than adjacent non-tumor tissues and normal liver tissues.

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Cholangiocarcinoma (CCA), a malignancy of biliary duct with a very poor prognosis, is the leading cause of cancer death in countries of the Mekong subregion. Liver fluke infection is the main etiological factor, but genetic variation has been recognized as also important in conferring susceptibility to CCA risk. Nuclear factor (erythroid derived 2)-like 2 (NRF2) is a key transcription factor in detoxification and antioxidant defense.

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Phosphatidylinositol 3-kinase (PI3K) signaling plays a critical role in cholangiocarcinoma (CCA), as well as anti-cancer drug resistance and autophagy, the type II program cell death regulation. In this work, we aimed to: (1) determine the expression levels of several key components of PI3K signaling and (2) evaluate whether NVP-BEZ235, a novel dual PI3K/mTOR inhibitor, could inhibit CCA cell growth. Immunohistochemistry for p85α, p110α, AKT, p-AKT (T308), mTOR, p-mTOR (S2448), GSK-3β, p-GSK-3β (S9), PTEN, and p-PTEN (S380, T382/383) was performed in 30 CCA patients.

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Background: To evaluate outcomes using a Thai herbal medicine, Vilac Plus (G716/45) with standard radiotherapy in comparison with historic controls from literature reports of the results of treatment in stage IIIB cervical cancer.

Materials And Methods: Between March 2003 and June 2005, thirty patients with advanced cervical cancer stage IIIB-IV who had a poor performance status were treated by palliative radiotherapy along with an adjuvant daily dose of 15-30 ml of Thai herbal tonic solution (Vilac Plus G716/45) administered orally three times after meals as an additional supportive therapy. The results were analyzed from the aspect of the overall survival rates with curves estimated by the Kaplan-Meier method.

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Cholangiocarcinoma (CCA) associated with Opisthorchis viverrini (Ov) chronic infection is the most frequent primary liver cancer in Thailand, and current approaches to early diagnosis and curative treatments are largely disappointing. We hypothesize a role for protein kinase A (PKA) in Ov-induced CCA. First, we studied the PKA isozyme switching in the liver from the hamster CCA model using quantitative (q) PCR, in situ hybridization, and immunohistochemical and western blot analysis.

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Epithelial-mesenchymal transition (EMT) is a series of events during which epithelial cells lose many of their epithelial characteristics and take on properties that are typical of mesenchymal cells that lack cell-cell adhesion properties. EMT may be activated by various types of growth factors or inflammatory cytokines. In many types of epithelial cancers, the EMT-derived tumor cells are susceptible to metastasis.

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