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Background The aims of this study were to investigate temporal patterns and potential risk factors for severe hyposalivation (xerostomia) after intensity-modulated radiotherapy (IMRT) for head and neck cancer (HNC), and to test the two QUANTEC (Quantitative Analysis of Normal Tissue Effects in the Clinic) guidelines. Patients and methods Sixty-three patients treated at the Memorial Sloan Kettering Cancer Center between 2006 and 2015, who had a minimum of three stimulated whole mouth saliva flow measurements (WMSFM) at a median follow-up time of 11 (range: 3–24) months were included. Xerostomia was defined as WMSFM ≤25% compared to relative pre-radiotherapy. Patients were stratified into three follow-up groups: 1: <6 months; 2: 6–11 months; and 3: 12–24 months. Potential risk factors were investigated (Mann–Whitney U test), and relative risks (RRs) assessed for the two QUANTEC guidelines. Results The incidence of xerostomia was 27%, 14% and 17% at follow-up time points 1, 2 and 3, respectively. At <6 months, the mean dose to the contralateral and the ipsilateral parotid glands (Dmean contra , Dmean ipsi ) was higher among patients with xerostomia (Dmean contra : 25 Gy vs. 15 Gy; Dmean ipsi : 44 Gy vs. 25 Gy). Patients with xerostomia had higher pre-RT WMSFM (3.5 g vs. 2.4 g), and had been treated more frequently with additional chemotherapy (93% vs. 63%; all 4 variables: p < 0.05). At 6–11 months, Dmean contra among patients with xerostomia was higher compared to patients without (26 Gy vs. 20 Gy). The RR as specified by the one- and two-gland QUANTEC guideline was 2.3 and 1.4 for patients with <6 months follow-up time, and 2.0 and 1.2 for patients with longer follow-up (6–11 + 6–24 months). Conclusion Xerostomia following IMRT peaks within six months post-radiotherapy and fades with time. Limiting the mean dose to both parotid glands (ipsilateral <25 Gy, contralateral <25 Gy) and reducing the use of chemotherapy will likely decrease the rate of xerostomia. Both QUANTEC guidelines are effective in preventing xerostomia. [ABSTRACT FROM AUTHOR]

Abstract: Aims: Paraquat (PQ) is known to induce pulmonary injury via a redox cyclic reaction. The present study was aimed to determine the protective effects of quercetin against PQ-induced pulmonary injury in association with its antioxidant activity. Main methods: Male rats were challenged acutely by PQ (50mg/kg, i.p.) with or without quercetin post-treatment. Pulmonary heme oxygenase-1 (HO-1) expression, malondialdehyde (MDA) level, and the total oxyradical scavenging capacity (TOSC) toward hydroxyl, peroxyl radicals and peroxynitrite were measured 24h after PQ treatment. Different groups of rats were instilled with PQ (0.5mg/kg) directly into the right lung. Quercetin was administered to the rats daily for 14days after PQ instillation. Serum NO, pulmonary glutathione (GSH) and 4-hydroxyproline (4-HP) concentrations were quantified in conjunction with histopathological examination to determine the fibrotic changes in lung. Key findings: Pulmonary MDA level and HO-1 expression were elevated and the TOSC was reduced rapidly by an intraperitoneal dose of PQ. These changes were inhibited by quercetin post-treatment. In rat lungs instilled with PQ 14days before, NO, MDA and 4-HP were elevated, and GSH was reduced, which were all inhibited significantly by daily quercetin treatment. Histopathological examination also revealed that quercetin ameliorated the increase in fibroblast distribution and collagen deposition in the lungs instilled with PQ. Significance: The present results demonstrate that quercetin administration to rats effectively inhibits the development of PQ-induced pulmonary injury most probably via its antioxidant activity. [Copyright &y& Elsevier]

The most common use of radioembolization is in the treatment of primary and secondary liver tumors, and the most common radioisotope used is yttrium-90. This form of therapy has been proven to be successful in achieving tumor reduction and prolonging survival. Adverse events, although uncommon and usually self-limiting, have been reported. The present report describes a case of radiation dermatitis caused by shunting of 90Y microspheres to the anterior abdominal wall via a patent falciform artery. When identified, prophylactic embolization of this patent artery may prevent the potential adverse event of radiation-induced dermatitis after radioembolization. [Copyright &y& Elsevier]

Nonalcoholic fatty liver is involved in the development of nonalcoholic steatohepatitis and chronic liver injury. Impairment of hepatic transsulfuration reactions is suggested to be critically linked with alcoholic liver injury, but its role in nonalcoholic fatty liver remains unknown. We examined the early changes in sulfur-amino acid metabolism and their implication in nonalcoholic fatty liver disease (NAFLD). Male rats were provided with a standard liquid diet or a high-fat liquid diet (HFI for 3 wk. An additional group of rats received the HF diet supplemented with betaine (1%). HF diet intake elevated hepatic triglyceride and serum tumor necrosis factor-a (TNFa) concentrations. Antioxidant capacity of liver cytosol against hydroxyl and peroxyl radicals was reduced significantly. Hepatic S-adenosylmethionine (SAM) and glutathione IGSH) decreased, but hypotaurine and taurine concentrations increased. Methionine adenosyltransferase (MAT) activity, not its concentration, was depressed, whereas both activity and concentration of cysteine dioxygenase and GSH S-transferase were elevated. Betaine supplementation of the HF diet inhibited hepatic fat accumulation and serum TNFa elevation. The decrease in cytosolic antioxidant capacity was also prevented. MAT activity and its concentration were induced significantly. Hepatic SAM and GSH increased and elevation of hypotaurine and taurine was depressed. The results indicate that the metabolism of S-containing substances is significantly disturbed by the HF diet, suggesting a causal role of impairment of hepatic transsulfuration reactions in NAFLD. Betaine supplementation protects the liver from nonalcoholic steatosis and oxidative stress most probably via its effects on the transsulfuration reactions. J. Nutr. 139: 63-68, 2009. [ABSTRACT FROM AUTHOR]

Circular RNAs (circRNAs) are a class of endogenous noncoding RNAs that form covalently closed circles. Although circRNAs influence many biological processes, little is known about their role in intestinal epithelium homeostasis. We surveyed circRNAs required to maintain intestinal epithelial integrity and identified circular homeodomain-interacting protein kinase 3 (circHIPK3) as a major regulator of intestinal epithelial repair after acute injury. Intestinal mucosal tissues were collected from mice exposed to cecal ligation and puncture for 48 hours and patients with inflammatory bowel diseases and sepsis. We isolated primary enterocytes from the small intestine of mice and derived intestinal organoids. The levels of circHIPK3 were silenced in intestinal epithelial cells (IECs) by transfection with small interfering RNAs targeting the circularization junction of circHIPK3 or elevated using a plasmid vector that overexpressed circHIPK3. Intestinal epithelial repair was examined in an in vitro injury model by removing part of the monolayer. The association of circHIPK3 with microRNA 29b (miR-29b) was determined by biotinylated RNA pull-down assays. Genome-wide profile analyses identified ∼300 circRNAs, including circHIPK3 , differentially expressed in the intestinal mucosa of mice after cecal ligation and puncture relative to sham mice. Intestinal mucosa from patients with inflammatory bowel diseases and sepsis had reduced levels of circHIPK3. Increasing the levels of circHIPK3 enhanced intestinal epithelium repair after wounding, whereas circHIPK3 silencing repressed epithelial recovery. CircHIPK3 silencing also inhibited growth of IECs and intestinal organoids, and circHIPK3 overexpression promoted intestinal epithelium renewal in mice. Mechanistic studies revealed that c ircHIPK3 directly bound to miR-29b and inhibited miR-29 activity, thus increasing expression of Rac1, Cdc42, and cyclin B1 in IECs after wounding. In studies of mice, IECs, and human tissues, our results indicate that circHIPK3 improves repair of the intestinal epithelium at least in part by reducing miR-29b availability. [Display omitted] Circular RNA circHIPK3 enhances intestinal epithelial repair and promotes mucosal growth by reducing microRNA 29b activity, but its levels decrease in patients with inflammatory bowel disease. [ABSTRACT FROM AUTHOR]

Background Context: Recent literature has raised some apprehensions with regard to the usage of cervical cages. Purpose: Radiological review of cases performed at our institution with a novel cage made of polyetheretherketone (PEEK). Study Design: Retrospective study. Methods: A retrospective review of the first 15 consecutive cases of single-level anterior cervical interbody fusion using the Solis cage (PEEK material) for cervical spondylotic radiculopathy or myelopathy was performed. The follow-up ranged from 12 to 35 months (average 18 months). Anteroposterior and lateral radiographs were taken immediately after the surgery and at intervals of 3, 6, 12, and 24 months after surgery. Anterior disc height (ADH), posterior disc height (PDH), interbody height ratio (IBHR), distance between the posterior margin of the cage and the posterior wall of the vertebral body (D-CPW), and interbody angle (IBA) were measured on the lateral radiographs and compared. Fusion was assessed by examining for trabecular continuity, bridging of bone across the disc space, and sclerosis at the vertebral end plates on both sides. The parameters assessed were time for fusion, subsidence, segmental sagittal alignment of the operated segment, and presence/absence of migration of the cage. Data were analyzed using the Mann-Whitney nonparametric test. Results: Fusion was evident at 3-6 months postsurgery in all cases except one (93.33% fusion rate at 6 months). At the last follow-up, fusion was maintained in all cases. The immediate postoperative ADH and PDH was significantly greater than the respective preoperative values and was maintained at the last follow-up though there was a significant amount of subsidence when the follow-up radiographs were compared with the immediate postoperative X-rays. The immediate postoperative IBHR was significantly greater than the preoperative IBHR, and was maintained at the last follow-up, but not statistically significant. The immediate postoperative IBA (lordotic angle) was greater than the preoperative IBA but was not statistically significant. The IBA at the last follow-up was lesser than the preoperative value but with no statistical significance. The IBA measured at the last follow-up was less than the value at the immediate postoperative period, but not statistically significant. There was no migration or extrusion of the cage at latest follow-up. Conclusions: The high fusion rate, low subsidence, stability provided by the cage, and facilitation of radiological assessment are the result of the physical properties of the PEEK material as well as the design of the cage. [ABSTRACT FROM AUTHOR]

Background/Aims: Oxidative stress via generation of reactive oxygen species is suggested to be the major mechanism of alcohol-induced liver injury. We investigated the effects of glutathione peroxidase-1 and catalase double deficiency (Gpx-1−/−/Cat−/−) on liver injury and changes in the sulfur amino acid metabolism induced by binge ethanol administration. Methods: Ethanol (5g/kg) was administered orally to the wild-type and the Gpx-1−/−/Cat−/− mice every 12h for a total of three doses. Mice were sacrificed 6h after the final dose. Results: The Gpx-1/Cat deficiency alone increased malondialdehyde levels in liver significantly. Hepatic methionine adenosyltransferase (MAT) activity and S-adenosylmethionine levels were decreased, however, glutathione contents were not changed. Ethanol administration to the Gpx-1−/−/Cat−/− mice increased the elevation of serum alanine aminotransferase activity, plasma homocysteine levels, hepatic fat accumulation and lipid peroxidation compared with the wild-type animals challenged with ethanol. Also the reduction of MAT activity and S-adenosylmethionine levels was enhanced, but MATI/III expression was increased significantly. Conclusions: The results indicate that Gpx-1 and Cat have critical roles in the protection of liver against binge ethanol exposure. Augmentation of ethanol-induced oxidative stress may be responsible for the impairment of the transsulfuration reactions and the aggravation of acute liver injury in the Gpx-1−/−/Cat−/− mice. [Copyright &y& Elsevier]

Abstract: We described a simple route to TiO2 nanoparticles with anatase phase by the acid-catalyzed sol–gel process of titanium(IV) bis(acetylacetonate) diisopropoxide in water, and studied the effect of chelation of the precursor on the crystallite and size of anatase TiO2. The nanocrystalline anatase TiO2 was obtained by controlling pH of aqueous solution containing the precursor at temperatures as low as room temperature. The ligands of the precursor complex were characterized by FT-IR and UV–vis spectroscopy. The sustenance of chelation of the precursor in an acidic solution may be a key factor to determine the crystalline phase of TiO2 at such mild conditions. [Copyright &y& Elsevier]

Summary: Metastatic spine tumour surgery (MSTS) and metastatic musculoskeletal tumour surgery (MMTS) are associated with substantial blood loss. Allogeneic blood transfusion is the present method used to replenish this blood. Intraoperative cell salvage (IOCS) is a viable alternative, but is contraindicated in tumour surgery because of the risk of tumour dissemination. Use of IOCS–leucocyte depletion filter (LDF) allows removal of tumour cells from blood salvaged during oncological surgery. However, no reports exist on use of IOCS in MSTS or MMTS. We systematically reviewed studies on IOCS in oncological surgery to investigate whether sufficient evidence exists to support its use in MSTS or MMTS. [ABSTRACT FROM AUTHOR]