Acute Pancreatitis: A Rare Post-Colonoscopy Sequela

Sujit P. Nair,Prasanta Debnath,Suhas Udgirkar,Parmeshwar Junare,Sanjay Chandnani,Shubham Jain,Vinay B. Pawar,Pravin M. Rathi 대한소화기내시경학회 2020 Clinical Endoscopy Vol.53 No.5

Abdominal pain is a common but benign symptom after colonoscopy. We report a case of acute pancreatitis that occurred just after anelective screening colonoscopy; this is a rare event with very few reported cases. A healthy, asymptomatic male underwent screeningcolonoscopy at our center and developed abdominal pain and emesis after the procedure. An abdominal X-ray ruled out perforation but laboratory tests revealed elevated levels of amylase and lipase. The patient had no etiological risk factors for pancreatitis. Thepresumed mechanism of pancreatitis in this case is mechanical and pressure trauma from excessive insuffation, external abdominal pressure, and repeated withdrawal of the colonoscope due to tight angulation of the splenic flexure, a structure that is in close proximityto the pancreatic tail. Acute pancreatitis should be considered in the differential diagnosis of patients who present with abdominal painafter colonoscopy once more common etiologies have been excluded.

Modulation of Activator Protein-1 (AP-1) and MAPK Pathway by Flavonoids in Human Prostate Cancer PC3 Cells

Gopalakrishnan, Avanthika,Xu, Chang-Jiang,Nair, Sujit S.,Chen, Chi,Hebbar, Vidya,Kong, Ah-Ng Tony The Pharmaceutical Society of Korea 2006 Archives of Pharmacal Research Vol.29 No.8

In last couple of decades the use of natural compounds like flavonoids as chemopreventive agents has gained much attention. Our current study focuses on identifying chemopreventive flavonoids and their mechanism of action on human prostate cancer cells. Human prostate cancer cells (PC3), stably transfected with activator protein 1 (AP-1) luciferase reporter gene were treated with four main classes of flavonoids namely flavonols, flavones, flavonones, and isoflavones. The maximum AP-1 luciferase induction of about 3 fold over control was observed with $20\;{\mu}M$ concentrations of quercetin, chrysin and genistein and $50\;{\mu}M$ concentration of kaempferol. At higher concentrations, most of the flavonoids demonstrated inhibition of AP-1 activity. The MTS assay for cell viability at 24 h showed that even at a very high concentration $(500\;{\mu}M)$, cell death was minimal for most of the flavonoids. To determine the role of MAPK pathway in the induction of AP-1 by flavonoids, Western blot of phospho MAPK proteins was performed. Four out of the eight flavonoids namely kaempferol, apigenin, genistein and naringenin were used for the Western Blot analysis. Induction of phospho-JNK and phospho-ERK activity was observed after two hour incubation of PC3-AP1 cells with flavonoids. However no induction of phospho-p38 activity was observed. Furthermore, pretreating the cells with specific inhibitors of JNK reduced the AP-1 luciferase activity that was induced by genistein while pretreatment with MEK inhibitor reduced the AP-1 luciferase activity induced by kaempferol. The pharmacological inhibitors did not affect the AP-1 luciferase activity induced by apigenin and naringenin. These results suggest the possible involvement of JNK pathway in genistein induced AP-1 activity while the ERK pathway seems to play an important role in kaempferol induced AP-1 activity.

Modulation of Activator Protein-1 (AP-1) and MAPK Pathway by Flavonoids in Human Prostate Cancer PC3 Cells

Avanthika Gopalakrishnan,Chang-Jiang Xu,Sujit S Nair,Chi Chen,Vidya Hebbar,Ah-Ng Tony Kong 대한약학회 2006 Archives of Pharmacal Research Vol.29 No.8

In last couple of decades the use of natural compounds like flavonoids as chemopreventive agents has gained much attention. Our current study focuses on identifying chemopreventive flavonoids and their mechanism of action on human prostate cancer cells. Human prostate cancer cells (PC3), stably transfected with activator protein 1 (AP-1) luciferase reporter gene were treated with four main classes of flavonoids namely flavonols, flavones, flavonones, and isoflavones. The maximum AP-1 luciferase induction of about 3 fold over control was observed with 20 μM concentrations of quercetin, chrysin and genistein and 50 μM concentration of kaempferol. At higher concentrations, most of the flavonoids demonstrated inhibition of AP-1 activity. The MTS assay for cell viability at 24 h showed that even at a very high concentration (500 μM), cell death was minimal for most of the flavonoids. To determine the role of MAPK pathway in the induction of AP-1 by flavonoids, Western blot of phospho MAPK proteins was performed. Four out of the eight flavonoids namely kaempferol, apigenin, genistein and naringenin were used for the Western Blot analysis. Induction of phospho-JNK and phospho-ERK activity was observed after two hour incubation of PC3-AP1 cells with flavonoids. However no induction of phospho-p38 activity was observed. Furthermore, pretreating the cells with specific inhibitors of JNK reduced the AP-1 luciferase activity that was induced by genistein while pretreatment with MEK inhibitor reduced the AP-1 luciferase activity induced by kaempferol. The pharmacological inhibitors did not affect the AP-1 luciferase activity induced by apigenin and naringenin. These results suggest the possible involvement of JNK pathway in genistein induced AP-1 activity while the ERK pathway seems to play an important role in kaempferol induced AP-1 activity.

In vivo Pharmacokinetics, Activation of MAPK Signaling and Induction of Phase II/III Drug Metabolizing Enzymes/Transporters by Cancer Chemopreventive Compound BHA in the Mice

Hu, Rong,Shen, Guoxiang,Yerramilli, Usha Rao,Lin, Wen,Xu, Changjiang,Nair, Sujit,Kong, Ah-Ng Tony The Pharmaceutical Society of Korea 2006 Archives of Pharmacal Research Vol.29 No.10

Phenolic antioxidant butylated hydroxyanisole (BHA) is a commonly used food preservative with broad biological activities, including protection against chemical-induced carcinogenesis, acute toxicity of chemicals, modulation of macromolecule synthesis and immune response, induction of phase II detoxifying enzymes, as well as its undesirable potential tumor-promoting activities. Understanding the molecular basis underlying these diverse biological actions of BHA is thus of great importance. Here we studied the pharmacokinetics, activation of signaling kinases and induction of phase II/III drug metabolizing enzymes/transporter gene expression by BHA in the mice. The peak plasma concentration of BHA achieved in our current study after oral administration of 200 mg/kg BHA was around $10\;{\mu}M$. This in vivo concentration might offer some insights for the many in vitro cell culture studies on signal transduction and induction of phase II genes using similar concentrations. The oral bioavailability (F) of BHA was about 43% in the mice. In the mouse liver, BHA induced the expression of phase II genes including NQO-1, HO-1, ${\gamma}-GCS$, GST-pi and UGT 1A6, as well as some of the phase III transporter genes, such as MRP1 and Slco1b2. In addition, BHA activated distinct mitogen-activated protein kinases (MAPKs), c-Jun N-terminal kinase (JNK), extracellular signal-regulated protein kinase (ERK), as well as p38, suggesting that the MAPK pathways may play an important role in early signaling events leading to the regulation of gene expression including phase II drug metabolizing and some phase III drug transporter genes. This is the first study to demonstrate the in vivo pharmacokinetics of BHA, the in vivo activation of MAPK signaling proteins, as well as the in vivo induction of Phase II/III drug metabolizing enzymes/transporters in the mouse livers.

In vivo Pharmacokinetics, Activation of MAPK Signaling and Induction of Phase II/III 911Drug Metabolizing Enzymes/Transporters by Cancer Chemopreventive CompoundBHA in the Mice

Rong Hu,Guoxiang Shen,Usha Rao Yerramilli,Wen Lin,Changjiang Xu,Sujit Nair,Ah-Ng Tony Kong 대한약학회 2006 Archives of Pharmacal Research Vol.29 No.10

Phenolic antioxidant butylated hydroxyanisole (BHA) is a commonly used food preservative with broad biological activities, including protection against chemical-induced carcinogenesis, acute toxicity of chemicals, modulation of macromolecule synthesis and immune response, induction of phase II detoxifying enzymes, as well as its undesirable potential tumor-promoting activities. Understanding the molecular basis underlying these diverse biological actions of BHA is thus of great importance. Here we studied the pharmacokinetics, activation of signaling kinases and induction of phase II/III drug metabolizing enzymes/transporter gene expression by BHA in the mice. The peak plasma concentration of BHA achieved in our current study after oral administration of 200 mg/kg BHA was around 10 μM. This in vivo concentration might offer some insights for the many in vitro cell culture studies on signal transduction and induction of phase II genes using similar concentrations. The oral bioavailability (F) of BHA was about 43% in the mice. In the mouse liver, BHA induced the expression of phase II genes including NQO-1, HO-1, γ-GCS, GST-pi and UGT 1A6, as well as some of the phase III transporter genes, such as MRP1 and Slco1b2. In addition, BHA activated distinct mitogen-activated protein kinases (MAPKs), c-Jun N-terminal kinase (JNK), extracellular signal-regulated protein kinase (ERK), as well as p38, suggesting that the MAPK pathways may play an important role in early signaling events leading to the regulation of gene expression including phase II drug metabolizing and some phase III drug transporter genes. This is the first study to demonstrate the in vivo pharmacokinetics of BHA, the in vivo activation of MAPK signaling proteins, as well as the in vivo induction of Phase II/III drug metabolizing enzymes/transporters in the mouse livers.

Herd Protection by a Bivalent Killed Whole-Cell Oral Cholera Vaccine in the Slums of Kolkata, India

Ali, Mohammad,Sur, Dipika,You, Young Ae,Kanungo, Suman,Sah, Binod,Manna, Byomkesh,Puri, Mahesh,Wierzba, Thomas F.,Donner, Allan,Nair, G. Balakrish,Bhattacharya, Sujit K.,Dhingra, Mandeep Singh,Deen, J Oxford University Press 2013 Clinical infectious diseases Vol.56 No.8

<P>We evaluated the herd protection conferred by the bivalent killed oral cholera vaccine. The vaccine conferred significant herd protection, suggesting that significant public health impact in cholera control may be achieved even with modest vaccination coverage.</P>