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Aim Anastomotic leakage (AL) is one of the most feared postoperative complications after anterior resection (AR) of rectal cancer. An adequate blood supply at the anastomotic site is regarded as a prerequisite for healing. We hypothesize that the Aortic Calcification Index (ACI) might reflect the severity of atherosclerosis in patients, and thereby be a risk factor for AL. Method AL was investigated retrospectively according to the definition of the International Study Group of Rectal Cancer in 423 rectal cancer patients who underwent anterior rectal resection. The ACI was measured by preoperative abdominal CT scan. The cross-section of the aorta was evenly divided into 12 sectors, the number of calcified sectors was counted as the calcification score of each slice. Lasso logistic regression and multivariate regression analysis were used to identify risk factors for AL. Results The percentage of AL after AR was 7.8% (33/423); the mortality of patients who sustained a leak was 3.0% (1/33). Patients with a high ACI had a significantly higher percentage of AL than patients with low ACI (11.2% vs 5.6%, P = 0.04). Among patients with AL, a higher ACI was associated with greater severity of AL (the ACI of patients with grade A leakage, grade B leakage and grade C leakage was 0.5% ± 0.2%, 11.5% ± 9.2% and 24.2% ± 21.7%, respectively; P = 0.008). After risk adjustment, multivariate regression analysis showed that a higher ACI was an independent risk factor for AL (OR 2.391, P = 0.04). Conclusion A high ACI might be an important prognostic factor for AL after AR for rectal cancer. Confirmatory studies are required.

Background The use of extra-levator abdominoperineal resection (ELAPE) procedure for lower rectal cancer is controversial. It is unclear whether the ELAPE procedure could improve surgical safety and lead to better oncological outcomes. Methods Sixty-nine lower rectal cancer patients who underwent ELAPE (36 cases) or conventional abdominoperineal resection (APE; 33 cases) between June 2011 and February 2013 were prospectively investigated. Clinicopathological variables including blood loss, intraoperative perforation (IOP) rate, circumferential resection margin (CRM) involvement, lymph node harvest, the postoperative complications, urinary and sexual function, quality of life (QOL), local recurrence rate and survival were recorded and compared. Results Blood loss (P = 0.021), perineal wound complication (P = 0.039), IOP rate (P = 0.028), local recurrence (P = 0.034) were significantly less frequent in the ELAPE group. There was greater CRM involvement in the conventional APE group but no statistical difference between the two groups. Urinary function, sexual function and QOL were not significantly different between the two groups. Overall survival and progression-free survival were not significantly different between two groups, even when survival was analyzed according to TNM stage, T stage, N stage, and with or without neoadjuvant chemoradiotherapy. In patients who underwent ELAPE there was no statistical difference in postoperative complications between younger and elderly patients (age ≥60). Conclusions ELAPE procedure with definitive anatomic landmarks demonstrated surgical safety and decreased local recurrence for lower rectal cancer patients including the elderly, but there were no survival improvements in compared to conventional APE procedure.

Treatment of human colorectal cancer cells HT29 with interleukin 1beta (IL-1beta) induces expression of the multidrug resistance protein (MRP1) gene encoding the ATP-dependent glutathione S-conjugate export (GS-X) pump and the gamma-glutamylcysteine synthetase (gamma-GCSh) gene encoding heavy (catalytic) subunit of gamma-glutamylcysteine synthetase, the rate-limiting enzyme for the biosynthesis of glutathione (GSH). The induction can be suppressed by N(G)-methyl-L-arginine, a specific inhibitor of nitric oxide synthase (NOS). These results suggest that IL-1beta-mediated MRP1 and gamma-GCSh induction involve nitric oxide (NO) -related signaling. Further supports to the involvement of NO in the induction of MRP1 and gamma-GCSh expression are made by the following observations. (i) Expression of MRP1 and gamma-GCSh genes were induced by treating the cells with NO donors, i.e., S-nitro-N-acetyl-D,L-penicillamide (SNAP) and S-nitroso-L-glutathione, in a concentration-dependent manner. (ii) Ectopic expression of inducible NOS (iNOS) activity by transfecting expressible recombinant iNOS cDNA encoding functional iNOS but not the nonfunctional version resulted in elevated expression of MRP1 and gamma-GCSh. We also demonstrated that HT-29 cells treated with either 1L-1beta or SNAP induced ceramide production, and addition of C2 or C6 ceramides into cultured HT-29 cells resulted in induction of gamma-GCSh but not MRP1 expression. Collectively, our results demonstrate that induction of MRP1 and gamma-GCSh by IL-1beta is regulated, at least in part, by an NO-related signaling, and induction of gamma-GCSh is by NO-related ceramide signaling.

We have synthesized more than 80 novel triterpenoids, all derivatives of oleanolic and ursolic acid, as potential anti-inflammatory and chemopreventive agents. These triterpenoids have been tested for their ability to suppress the de novo formation of two enzymes, inducible nitric oxide synthase (iNOS) and inducible cyclooxygenase (COX-2), using IFN-gamma-stimulated primary mouse macrophages or lipopolysaccharide (LPS)-activated RAW 264.7 macrophages as assay systems. Two synthetic oleananes, 3,12-dioxoolean-1-en-28-oic acid (TP-69) and 3,11-dioxoolean-1,12-dien-28-oic acid (TP-72), were highly active inhibitors of de novo formation of both iNOS and COX-2. Both TP-69 and TP-72 blocked the increase in iNOS or COX-2 mRNA induced by IFN-gamma or LPS. In addition, TP-72 suppressed NF-KB activation in primary macrophages treated with the combination of IFN-gamma and LPS or IFN-gamma and tumor necrosis factor. The 3-alpha(axial)-epimer of ursolic acid suppressed de novo formation of COX-2, in contrast to naturally occurring 3-beta(equatorial)-ursolic acid. Inhibitory effects of TP-69 or TP-72 on iNOS formation were not blocked by the glucocorticoid receptor antagonist RU-486, indicating that these triterpenoids do not act through the glucocorticoid receptor, nor does TP-72 act as an iNOS or COX-2 enzyme inhibitor when added to RAW cells in which synthesis of these two enzymes in response to LPS has already been induced. It may be possible to develop triterpenoids as useful agents for chemoprevention of cancer or other chronic diseases with an inflammatory component.

We demonstrate a frequency-tunable superconducting coplanar waveguide resonator, with a tuning range of half a gigahertz and a switching time of 1 ns. The resonator is made tunable by inserting a superconducting quantum interference device in the center strip of the resonator. Quantum measurements are made by probing the resonator with a superconducting qubit, allowing us to use microwave photon Fock states to benchmark the resonator performance. Using the resonator, we shuttle energy quanta between the qubit and a microscopic two-level state. The tunable resonator can, therefore, serve as a communication bus or memory element in a prototype quantum processor.

The promoter of the murine gene encoding inducible nitric oxide synthase (iNOS) contains an NF-kappa B site beginning 55 base pairs upstream of the TATA box, designated NF-kappa Bd. Reporter constructs containing truncated promoter regions, when transfected into macrophages, revealed that NF-kappa Bd is necessary to confer inducibility by bacterial lipopolysaccharide (LPS). Oligonucleotide probes containing NF-kappa Bd plus the downstream 9 or 47 base pairs bound proteins that rapidly appeared in the nuclei of LPS-treated macrophages. The nuclear proteins bound to both probes in an NF-kappa Bd-dependent manner, but binding was resistant to cycloheximide only for the shorter probe. The proteins binding both probes reacted with antibodies against p50 and c-rel but not RelB; those binding the shorter probe also reacted with anti-RelA (p65). Pyrrolidine dithiocarbamate, which acts as a specific inhibitor of NF-kappa B, blocked both the activation of the NF-kappa Bd-binding proteins and the production of NO in LPS-treated macrophages. Thus, activation of NF-kappa B/Rel is critical in the induction of iNOS by LPS. However, additional, newly synthesized proteins contribute to the NF-kappa Bd-dependent transcription factor complex on the iNOS promoter in LPS-treated mouse macrophages.

We have proved that iNOS is regulated by induction of transcription. The induction of iNOS mRNA requires synthesis of an intermediary protein(s) and probably involves action of a protein kinase or kinases. We have cloned and sequenced a 1.7-kilobase pair fragment from the 5'-flanking region of the iNOS gene and proved that this region contains a promoter which confers inducibility of iNOS by LPS and IFN-gamma.

The effect of fluorosis on lactation, lactotroph function and ultrastructure were studied in lactating rats. The results were as follows: 1) Inhibition of lactation in lactating rats with chronic fluorosis was assessed by stunting growth of pups and decrease in the amount of milk suckled by pups in 30 min. Metoclopramide, a blocker of dopamine receptor, could improve lactation in these rats. 2) During chronic fluorosis serum PRL level was decreased, however, PRL content in pituitary was increased. Electronmicroscopic examination showed accumulation of large mature secretory granules and appearance of extremely large abnormal secretory granules in lactotroph cytoplasma. These findings indicate that hormone release of pituitary lactotrophs is obstructed in lactating rats with fluorosis, and the toxic effect of fluoride is mediated by an enhanced function of dopaminergic system in hypothalamus.

This laboratory had reported that acupuncture at "Tan-Zhong" acupoint could stimulate pituitary prolactin (PRL) secretion in both lactating and non-lactating (male, female, ovariectomized estrogen-supplemented) rats. Hu et al had discovered that acupuncture could increase plasma PRL level in women of lactation deficiency. As was known, pituitary PRL secretion was under the control of prolactin inhibitory factor (PIF) and prolactin releasing factor (PRF) released from hypothalamic neurons as well as several central neurotransmitters. In the past decade, many studies in neuroendocrinology revealed that Tubero-infundibular dopamine (TIDA) neurons of hypothalamus play a major modulating role in PRL secretion. It is generally agreed that dopamine was the major PIF. The central noradrenaline (NE) is also a modulator. It was reported that NE could inhibit PRL secretion, but others obtained opposite result. The GABA has dual actions on PRL secretion: central action is stimulatory, but inhibitory on pituitary directly Using agonist or antagonist of central neurotransmitter as well as its biosynthesis blocker etc., this paper mainly observed the possible role of catecholamine and r-aminobutyric acid in prolactin-elevating effect of acupuncture. This will help further studying on and provide possible central mechanism for the effect of promoting milk yield and elevating PRL secretion by acupuncture.