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1.
In chronic renal failure, substances that are effectively excreted in healthy subjects accumulate in serum. These substances, uremic toxins, include a variety of organic acids. It has been reported that a decrease in the bilirubin (BR) binding capacity occurs in the serum of renal failure patients. 3-Carboxy-4-methyl-5-propyl-2-furanpropanoic acid (CMPF) has a high affinity for human serum albumin (HSA) and is a potent inhibitor of the serum protein binding of many drugs. We recently reported that CMPF and BR share the binding site for dicarboxylate molecules on the HSA molecule [Pharm Res 1999;16:916-923]. In this study, in order to confirm whether CMPF is involved in the decrease of BR serum binding capacity in chronic renal failure patients, the total concentrations of uremic toxins, CMPF, and indoxyl sulfate (IS) and the free BR concentration in serum from healthy volunteers and renal failure patients were determined. Both total CMPF and IS concentrations correlate with the free BR concentration. However, results from the peroxidase method reveal that IS cannot displace BR under the physiological condition [IS]/[HSA] <1. We, therefore, conclude that CMPF is one of the substances which contribute to the decreased binding capacity of BR in uremic serum. 相似文献
2.
Morikawa Takanori Ishida Masaharu Takadate Tatsuyuki Hata Tatsuo Iseki Masahiro Kawaguchi Kei Ohtsuka Hideo Mizuma Masamichi Hayashi Hiroki Nakagawa Kei Motoi Fuyuhiko Kamei Takashi Naitoh Takeshi Unno Michiaki 《Surgery today》2020,50(2):153-162
Surgery Today - We introduced a superior approach and a unique technique to retract the stomach, called the “stomach roll-up technique”, to standardize laparoscopic distal... 相似文献
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The effect of N-benzyl-D-glucamine dithiocarbamate (BGD) on the renal toxicity produced by subacute exposure to cadmium in rats was studied. Rats were injected sc with CdCl2 (1.5 mg Cd/kg) daily for 26 days and thereafter they received 13 injections of BGD (400 mumol/kg) every other day. Urinary protein concentration and AST activity significantly increased after 20 days of cadmium treatment. The pattern of the increase in the urinary excretion of cadmium after cadmium treatment was consistent with that in the urinary excretion of protein and AST. Urinary excretion of amino acid increased gradually after the cessation of cadmium treatment. BGD treatment significantly decreased the urinary excretion of protein, aspartate aminotransferase (AST), and amino acid. Plasma AST activity was elevated 8 days after the beginning of cadmium treatment, indicating that the hepatic damage occurred prior to the renal damage. In addition, the microscopic examination of renal tissue from cadmium-treated rats revealed the necrosis of the proximal tubular cells. The cadmium concentrations in liver and kidney were significantly decreased by BGD treatment. The results of this study indicate that BGD treatment is effective in decreasing the cadmium concentrations in liver and kidney, resulting in the therapeutic effect on the cadmium-induced renal damage. 相似文献
5.
Maeda S Motoi F Onogawa T Morikawa T Shigeru O Sakata N Takadate T Naitoh T Rikiyama T Katayose Y Egawa S Unno M 《International journal of clinical oncology / Japan Society of Clinical Oncology》2011,16(5):539-545
Background
We evaluated the efficacy and feasibility of paclitaxel in patients with gemcitabine-refractory pancreatic cancer. We also evaluated the correlation between tumor marker decline and response rate.Methods
Thirty patients histologically diagnosed with pancreatic cancer who had undergone paclitaxel treatment as salvage chemotherapy were retrospectively analyzed. Paclitaxel treatment was performed with 80?mg/(m2?week) for 3?weeks followed by 1?week rest, and this was continued until failure. Tumor marker response was evaluated by measuring levels of carbohydrate antigen 19-9, carcinoembryonic antigen, and DUPAN-2 monthly.Results
In total, 272?weekly paclitaxel treatments were performed. The median number of treatments per patient was 8 (range 1??2). The median overall survival from the start of paclitaxel treatment was 6.7?months (range 1.2??8.8). The response rate was 10% (3/30 patients) and the disease control rate was 46.7% (14/30 patients). Although grade 3 and 4 hematological and non-hematological toxicities were seen in 7 and 6 patients, respectively, adverse events were managed by conservative treatment. We found a significant correlation between the disease control rate and tumor marker decline within 2?months of paclitaxel treatment (P?=?0.01). Patients with tumor marker decline tended to survive longer.Conclusion
Weekly administration of paclitaxel in patients with gemcitabine-refractory pancreatic cancer seems to be well tolerated and can be effective. Paclitaxel treatment should be considered as salvage chemotherapy after gemcitabine failure in patients with good performance status. 相似文献6.
Kosuke Okuya Junki Mine Kaori Tokorozaki Isshu Kojima Mana Esaki Kohtaro Miyazawa Ryota Tsunekuni Saki Sakuma Asuka Kumagai Yoshihiro Takadate Yuto Kikutani Tsutomu Matsui Yuko Uchida Makoto Ozawa 《Emerging infectious diseases》2022,28(7):1451
Genetic analyses of highly pathogenic avian influenza H5 subtype viruses isolated from the Izumi Plain, Japan, revealed cocirculation of 2 genetic groups of clade 2.3.4.4b viruses among migratory waterfowl. Our findings demonstrate that both continuous surveillance and timely information sharing of avian influenza viruses are valuable for rapid risk assessment. 相似文献
7.
Kyohei?AriakeEmail author Fuyuhiko?Motoi Hideo?Ohtsuka Koji?Fukase Kunihiro?Masuda Masamichi?Mizuma Hiroki?Hayashi Kei?Nakagawa Takanori?Morikawa Shimpei?Maeda Tatsuyuki?Takadate Takeshi?Naitoh Shinichi?Egawa Michiaki?Unno 《Surgery today》2017,47(12):1434-1442
Purpose
To evaluate the risk factors for peritoneal recurrence (PR) of pancreatic adenocarcinoma and to discuss the appropriate management strategies.Methods
We reviewed the medical records of 236 patients who underwent pancreatectomy for pancreatic adenocarcinoma. We then compared the clinicopathological characteristics of patients with vs. those without PR. The independent risk factors for PR were defined using the Cox proportional hazards regression model.Results
The median survival of patients with PR was 13.3 months after surgical treatment. The PR group had a significantly higher incidence of portal vein resection, longer operative time (≥648 min), greater blood loss (≥2179 mL), blood transfusion, tumor size, portal vein invasion, artery invasion, pancreatic nerve plexus invasion, and histological grade. Multivariate analysis revealed that excessive blood loss (≥2179 mL; P = 0.010), artery invasion (P = 0.025), pancreatic nerve plexus invasion (P = 0.001), and histological grade 3 (P = 0.011) were independent risk factors for PR. Excessive blood loss was also strongly related to tumor size (P = 0.018).Conclusions
Local invasion and tumor size-related factors suggested the possibility of intraoperative dissemination at the time of tumor resection. Preoperative treatment and an operative procedure to prevent tumor exposure may help prevent PR.8.
Filoviruses, including marburgviruses and ebolaviruses, have a single transmembrane glycoprotein (GP) that facilitates their entry into cells. During entry, GP needs to be cleaved by host proteases to expose the receptor-binding site that binds to the endosomal receptor Niemann-Pick C1 (NPC1) protein. The crystal structure analysis of the cleaved GP (GPcl) of Ebola virus (EBOV) in complex with human NPC1 has demonstrated that NPC1 has two protruding loops (loops 1 and 2), which engage a hydrophobic pocket on the head of EBOV GPcl. However, the molecular interactions between NPC1 and the GPcl of other filoviruses remain unexplored. In the present study, we performed molecular modeling and molecular dynamics simulations of NPC1 complexed with GPcls of two ebolaviruses, EBOV and Sudan virus (SUDV), and one marburgvirus, Ravn virus (RAVV). Similar binding structures were observed in the GPcl–NPC1 complexes of EBOV and SUDV, which differed from that of RAVV. Specifically, in the RAVV GPcl–NPC1 complex, the tip of loop 2 was closer to the pocket edge comprising residues at positions 79–88 of GPcl; the root of loop 1 was predicted to interact with P116 and Q144 of GPcl. Furthermore, in the SUDV GPcl–NPC1 complex, the tip of loop 2 was slightly closer to the residue at position 141 than those in the EBOV and RAVV GPcl–NPC1 complexes. These structural differences may affect the size and/or shape of the receptor-binding pocket of GPcl. Our structural models could provide useful information for improving our understanding the differences in host preference among filoviruses as well as contributing to structure-based drug design. 相似文献
9.
No HeadingPurpose. Evidence suggests that uremic toxins such as hippurate (HA), indoleacetate (IA), indoxyl sulfate (IS), and 3-carboxy-4-methyl-5-propyl-2-furanpropionate (CMPF) promote the progression of renal failure by damaging tubular cells via rat organic anion transporter 1 (rOat1) and rOat3 on the basolateral membrane of the proximal tubules. The purpose of the current study is to evaluate the in vivo transport mechanism responsible for their renal uptake.Methods. We investigated the uremic toxins transport mechanism using the abdominal aorta injection technique [i.e., kidney uptake index (KUI) method], assuming minimal mixing of the bolus with serum protein from circulating serum.Results. Maximum mixing was estimated to be 5.8% of rat serum by measuring estrone sulfate extraction after addition of 0–90% rat serum to the arterial injection solution. Saturable renal uptake of p-aminohippurate (PAH, Km = 408 M) and benzylpenicillin (PCG, Km = 346 M) was observed, respectively. The uptake of PAH and PCG was inhibited in a dose-dependent manner by unlabeled PCG (IC50 = 47.3 mM) and PAH (IC50 = 512 M), respectively, suggesting that different transporters are responsible for their uptake. A number of uremic toxins inhibited the renal uptake of PAH and PCG. Excess PAH, which could inhibit rOat1 and rOat3, completely inhibited the saturable uptake of IA, IS, and CMPF by the kidney, and by 85% for HA uptake. PCG inhibited the total saturable uptake of HA, IA, IS, and CMPF by 10%, 10%, 45%, and 65%, respectively, at the concentration selective for rOat3.Conclusions. rOat1 could be the primary mediator of the renal uptake of HA and IA, accounting for approximately 75% and 90% of their transport, respectively. rOat1 and rOat3 contributed equally to the renal uptake of IS. rOat3 could account for about 65% of the uptake of CMPF under in vivo physiologic conditions. These results suggest that rOat1 and rOat3 play an important role in the renal uptake of uremic toxins and the induction of their nephrotoxicity. 相似文献
10.