نتایج جستجو برای: acinar cells

تعداد نتایج: 1385250  

2011
Parini Mankad Andrew James Ajith K. Siriwardena Austin C. Elliott Jason I. E. Bruce

Background: Impaired metabolism and cytosolic Ca overload in pancreatic acinar cells can trigger pancreatitis. Results: Insulin protected cells from oxidantinduced Ca overload, inhibition of the plasma membrane calcium pump (PMCA) and ATP depletion. Conclusion: Insulin switches metabolism towards glycolysis and fuels the PMCA even when mitochondria are impaired. Significance: This mechanism may...

Journal: :American journal of physiology. Gastrointestinal and liver physiology 2006
Taiichi Otani Akira Matsukura Takeshi Takamoto Yasuji Seyama Yasuhito Shimizu Michiyo Shinomiya Hiroshi Usui Fred S Gorelick Masatoshi Makuuchi

To examine mechanisms that might be related to biliary pancreatitis, we examined the effects of pancreatic duct ligation (PDL) with pancreatic stimulation in vivo. PDL alone caused no increase in pancreatic levels of trypsinogen activation peptide (TAP), trypsin, or chymotrypsin and did not initiate pancreatitis. Although bombesin caused zymogen activation within the pancreas, the increases wer...

2016
Tatiana M. F. Mattioli Luciana R. A. Alanis Silvana da Silva Sapelli Antonio A. S. de Lima Lucia de Noronha Edvaldo A. R. Rosa Yusuf S. Althobaiti Atiah H. Almalki Youssef Sari Sergio A. Ignacio Aline C. B. R. Johann Ana M. T. Gregio

BACKGROUND Benzodiazepines (BZDs), the most commonly prescribed psychotropic drugs with anxiolytic action, may cause hyposalivation. It has been previously shown that BZDs can cause hypertrophy and decrease the acini cell number. In this study, we investigated the effects of BZDs and pilocarpine on rat parotid glands, specifically on acinar, ductal, and myoepithelial cells. METHODS Ninety mal...

Journal: :Arthritis and rheumatism 1997
Y T Konttinen L A Platts S Tuominen K K Eklund N Santavirta J Törnwall T Sorsa M Hukkanen J M Polak

OBJECTIVE To measure levels of salivary nitrite (NO2-) and to localize nitric oxide synthases (NOS) in the labial salivary glands (LSGs) of patients with Sjögren's syndrome (SS). METHODS NO2- was measured by the Griess reaction. LSGs were analyzed using NADPH-diaphorase histochemical and immunohistochemical studies to determine the constitutive NOS (neuronal [ncNOS] and endothelial [ecNOS]) a...

2017
Hong Xiang Xufeng Tao Shilin Xia Jialin Qu Huiyi Song Jianjun Liu Dong Shang

Pancreatitis is an inflammatory disease that is responsible for substantial morbidity and mortality, and it can induce pancreatic necrosis that starts within pancreatic acinar cells in severe cases. Emodin, a pleiotropic natural product isolated from the Chinese herb Rheum palmatum L., has effective anti-inflammatory activities. In this paper, we investigated the protective effects and molecula...

2016
Ralph Gruber Richard Panayiotou Emma Nye Bradley Spencer-Dene Gordon Stamp Axel Behrens

BACKGROUND & AIMS Pancreatitis is the most important risk factor for pancreatic ductal adenocarcinoma (PDAC). Pancreatitis predisposes to PDAC because it induces a process of acinar cell reprogramming known as acinar-to-ductal metaplasia (ADM)-a precursor of pancreatic intraepithelial neoplasia lesions that can progress to PDAC. Mutations in KRAS are found at the earliest stages of pancreatic t...

2013
Fumihiko Furuya Hiroki Shimura Keiichi Asami Sayaka Ichijo Kazuya Takahashi Masahiro Kaneshige Yoichi Oikawa Kaoru Aida Toyoshi Endo Tetsuro Kobayashi

Background: One goal of diabetic regenerative medicine is to convert mature pancreatic acinar cells into insulin-producing cells. Results: Ligand-bound thyroid hormone receptor α (TRα), which interacts with p85α, induces Phosphatidylinositol 3-Kinase (PI3K) signaling and insulin expression. Conclusion: PI3K signaling must be activated for TRα-induced reprogramming of pancreatic acinar cells. Si...

2012
Yung-Hua Koh Shabbir Moochhala Madhav Bhatia

Acute pancreatitis (AP) has been associated with an up-regulation of substance P (SP) and neurokinin-1 receptor (NK1R) in the pancreas. Increased SP-NK1R interaction was suggested to be pro-inflammatory during AP. Previously, we showed that caerulein treatment increased SP/NK1R expression in mouse pancreatic acinar cells, but the effect of SP treatment was not evaluated. Pancreatic acinar cells...

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