Prophylactic Pancreatic Stents: Does Size Matter? A Comparison of 4-Fr and 5-Fr Stents in Reference to Post-ERCP Pancreatitis and Migration Rate

Background and Aims  

The ideal pancreatic stent to prevent post-ERCP pancreatitis (PEP) has yet to be determined. The aim of our study was to assess the relative benefit of 4-Fr versus 5-Fr stents in a population at high risk for post-ERCP pancreatitis, and the relative frequency of spontaneous migration.     

Type 1 Phototherapeutic Agents,Part I: Preparation and Cancer Cell Viability Studies of Novel Photolabile Sulfenamides

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Hydrophilic pyrazine dyes as exogenous fluorescent tracer agents for real-time point-of-care measurement of glomerular filtration rate

Various hydrophilic pyrazine-bis(carboxamides) derived from 3,5-diamino-pyrazine-2,5-dicarboxylic acid bearing neutral and anionic groups were prepared and evaluated for use as fluorescent glomerular filtration rate (GFR) tracer agents. Among these, the dianionic d-serine pyrazine derivatives 2d and 2j, and the neutral dihydroxypropyl 2h, exhibited favorable physicochemical and clearance properties. In vitro studies show that 2d, 2h, and 2j have low plasma protein binding, a necessary condition for renal excretion. In vivo animal model results show that these three compounds exhibit a plasma clearance equivalent to iothalamate (a commonly considered gold standard GFR agent). In addition, these compounds have a higher urine recovery compared to iothalamate. Finally, the plasma clearance of 2d, 2h, and 2j remained unchanged upon blockage of the tubular secretion pathway with probenecid, a necessary condition for establishment of clearance via glomerular filtration only. Hence, 2d, 2h, and 2j are promising candidates for translation to the clinic as exogenous fluorescent tracer agents in real-time point-of-care monitoring of GFR.     

Type 1 Phototherapeutic Agents. 2. Cancer Cell Viability and ESR Studies of Tricyclic Diarylamines

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Carbon Monoxide (CO) Protects Renal Tubular Epithelial Cells against Cold-Rewarm Apoptosis

Recent studies have suggested that carbon monoxide (CO) inhalation can reduce ischemia-reperfusion injury of kidneys. The purpose of the present study was to determine whether the direct application of CO using tricarbonylchloro (glycinato) ruthenium II (CORM3) would reduce cold-rewarm-associated apoptosis in renal tubular epithelial (RPTE) cells. RPTE cells were subjected to 48 hours of cold followed by 24 hours of rewarming with increasing concentrations (0–500 μM) of CORM3. CORM3 (100 μM) reduced apoptosis as determined by the TUNEL method from 21.6 ± 5.2 to 5.8 ± 1.1 % (untreated vs. treated, n?=?5; p < 0.001). We subsequently observed that the incubation of RPTE cells with CORM3 induced heme oxygenase (HO)-1 gene expression. As HO-1 itself can confer protection against cold rewarm injury, we investigated the role of HO-1 in the protective actions of CORM3 using siRNA oligonucleotides directed against HO-1. CORM3 treatment of RPTE cells caused a 4.9- fold increase in HO-1 gene expression as determined by real time PCR. Prior treatment of RPTE cells with siRNAs against HO-1 was able to completely abolish the CORM3 mediated induction of HO-1 mRNA and protein. The abolition of HO-induction with siRNAs did reduce CORM3-mediated protection against cold rewarm-induced apoptosis; however, CORM3 was able to significantly protect RPTE cells against cold-rewarm injury: apoptosis was 33.7 ± 0.9% vs. 15.4 ± 0.5% vs. 62.8 ± 1.5% vs. 23.5 ± 3.4 in control cold-rewarm vs. cold-rewarm + CORM3 (100 μM) vs. cold-rewarm + HO-1 siRNA vs. cold-rewarm + CORM3 (100 μM) + HO-1 siRNA (n?=?4). These results suggest that increased levels of CO alone can protect against cold-rewarm-induced apoptosis.     

Hepatic circulatory diseases associated with chronic myeloid disorders

These liver diseases are diseases of the hepatic circulation. Myeloproliferative disorders are among the most common prothrombotic disorders that lead to Budd-Chiari syndrome and PVT. SOS, previously known as hepatic veno-occlusive disease, is mainly seen in North America and Western Europe as a complication of the conditioning regimen for hematopoietic stem cell transplantation. SOS is caused by damage to SECs, and the initiating circulatory blockage occurs because of the embolism of sinusoidal lining cells. Myeloproliferative disorders are an uncommon cause of NRH, which is believed to be caused by uneven perfusion of the liver at the venous or sinusoidal level. Peliosis hepatis is believed to result from damage to SECs and is seen mainly in immunosuppressed patients, patients with a wasting illness, or patients with a drug toxicity.     

Renal vascular responses to CORM-A1 in the mouse.

CORM-A1 is a newly described water-soluble carbon monoxide (CO) releasing molecule (CORM) that can deliver CO to various vascular beds in the absence of dramatic changes in blood carboxy-hemoglobin (COHb) levels. We tested the in vivo and in vitro renal vascular effects of CORM-A1 administration using anesthetized mice instrumented with a renal flow probe as well as in isolated, pressurized renal interlobar arteries. Administration of CORM-A1 (0.96 micromol) resulted in a significant increase in renal blood flow (RBF) of 33 +/- 6% as compared to control. Administration of acetylcholine (50 pmol) caused a similar increase in RBF (25 +/- 4%). In order to determine if the vasodilatory effect of CORM-A1 in vivo was mediated through activation of soluble guanylate cyclase (sGC), mice were pretreated with the sGC inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ, 1 nmolkg(-1)min(-1)) for 30min. Pretreatment with ODQ significantly reduced the CORM-A1 mediated increase in RBF to 9 +/- 5% of control. In isolated pressurized renal interlobar arteries, CORM-A1 caused dose dependent vasodilatation of phenylephrine constricted arteries. The CORM-A1 mediated vasodilatation was significantly attenuated by ODQ to similar levels as observed in vivo. Inhibition of calcium activated potassium channels (Kca) with iberiotoxin resulted in a complete blockade of the CORM-A1 mediated vasodilatation in pressurized renal interlobar arteries. We conclude that CO released from CORM-A1 causes an increase in RBF and a decrease in vascular resistance through activation of sGC and opening of Kca channels in the kidney of the mouse.