Inhibition of hydroxyapatite growth by casein,a potential salivary phosphoprotein homologue

Salivary phosphoproteins are essential in tooth mineral regulation but are often overlooked in vitro. This study aimed to evaluate the effect of casein, as a salivary phosphoprotein homologue, on the deposition and growth of hydroxyapatite (HA) on tooth surfaces. Hydroxyapatite growth was quantified using seeded crystal systems. Artificial saliva (AS) containing HA powder and 0, 10, 20, 50, or 100 μg ml^?1 of casein, or 100 μg ml^?1 of dephosphorylated casein (Dcasein), was incubated for 0–8 h at 37°C, pH 7.2. Calcium concentrations were measured using atomic absorption spectroscopy (AAS). Surface precipitation of HA on bovine enamel and dentine blocks, incubated in similar conditions for 7 d, was examined using field emission scanning electron microscopy (FE‐SEM) and transmission electron microscopy (TEM) with selected area electron diffraction (SAED). Casein adsorption was assessed using modified Lowry assays and zeta‐potential measurements. The AAS results revealed a concentration‐dependent inhibition of calcium consumption. Hydroxyapatite precipitation occurred when no casein was present, whereas precipitation of HA was apparently completely inhibited in casein‐containing groups. Adsorption data demonstrated increasingly negative zeta‐potential with increased casein concentration and an affinity constant similar to proline‐rich proteins with Langmuir modelling. Casein inhibited the deposition and growth of HA primarily through the binding of esterized phosphate to HA active sites, indicating its potential as a mineral‐regulating salivary phosphoprotein homologue in vitro.     

Decline in eGFR over time and incidence of cardiovascular events: Shinken database analysis

BackgroundIt has been reported that a large decline in estimated glomerular filtration rate (eGFR) over time is associated with increased incidence of cardiovascular disease. We investigated whether this association differs according to the baseline eGFR.MethodsA total of 4666 patients (male 71%) with measurements of eGFR at both baseline and 1 year and that had no cardiovascular events at 1-year follow-up were retrieved from the Shinken Database between June 2004 and March 2015. The study population was divided into three groups by baseline eGFR (mL/min/1.73 m²): high (≥60, n = 1650), intermediate (45–59, n = 1947), and low (<45, n = 1069) eGFR groups. Each eGFR group was further divided into two groups by eGFR slope (change at 1 year, <-10 and ≥-10 mL/min/1.73 m²). The patient characteristics and the incidences of cardiovascular events within 3 years (after 1-year follow-up) were compared between the negatively large eGFR slope (<-10) and others (≥-10) in each eGFR group.ResultsA total of 187 cardiovascular events occurred during the mean follow-up of 2.8 ± 0.6 years. The adjusted hazard ratios of eGFR slope (<-10 with reference to ≥-10) were 2.37 (95% CI, 1.28–4.40), 3.10 (95% CI, 1.78–5.40), and 2.66 (95% CI, 1.15–6.13) in the high, middle, and low eGFR groups, respectively. Similar results were found in patients with structural heart disease, but not in those without.ConclusionsDecline in eGFR was associated with an increase in cardiovascular events, and this effect was consistent regardless of the baseline eGFR.     

Effects of a small dose of triazolam on P300

Ten healthy men (mean age, 33.9 years) participated in two experimental sessions cross-overed randomly in a double-blind manner: one with the placebo and another with 0.125 mg of triazolam (TRZ). Resting electroencephalography and event-related potential under oddball paradigm were recorded before the drug administration, and 1, 2, 4, 6 and 8 h after that. P300 waveforms were analyzed by peak amplitudes and 30-ms bin data. Triazolam may cause cognitive dysfunction without general sedation or apparent sleepiness, and this effect appeared 2 h, 4 h and 6 h, most prominently 6 h, after TRZ administration.     

Assessment of Underlying Blood Vessels in Gastric Ulcers with Bleeding Episode by Endoscopic Color Doppler Ultrasonography

We used endoscopic color Doppler ultrasonography to detect hemorrhagic gastric ulcer, and to determine whether this modality could show blood vessels present deep to ulcers and whether these vessels influenced clinical course. Subjects were 20 patients with hemorrhagic gastric ulcers which had visible vessels on the ulcer base endoscopically. In 11 of 20 patients (group P) color signals indicating blood flow were observed, in which a weak pulsatile wave was detected in five cases. In two operated cases the signals were confirmed as blood vessels histologically. The diameters of these vessels were over 0.35 mm. It was thought that in cases undetectable on endoscopic color Doppler ultrasonography (group N) the diameter of vessels was too narrow or the velocity of blood too slow. There were no differences in the clinical background of group P and group N. However, ulcer bleeding was more severe in group P cases (P<0.05). Many patients in whom blood flow was detected experienced repeated ulcer bleeding as well as ulcer recurrences. Patients with hemorrhagic ulcers and in whom ultrasonic imaging demonstrates blood flow should be managed with great care. (Dig Endosc 1999; 11: 231–235)     

Nuclear accumulation and activation of nuclear factor kappaB after split-dose irradiation in LS174T cells

Although radiation-induced gene expression has been extensively studied, most of the studies to date have focused on that after single-dose irradiation. As split-dose irradiation, rather than single-dose irradiation, is usual in clinical situations, we investigated the effects of split-dose irradiation on nuclear factor kappaB (NF-kappaB) in the human rectum carcinoma cell line, LS174T. After either single- or split-dose irradiation with a different interval, nuclear localization of NF-kappaB was examined by Western blot and immunofluorescence and its DNA-binding activity was measured by ELISA-based assay. Irradiation-induced NF-kappaB nuclear accumulation and DNA binding activity increased in a dose-dependent manner. The peak of NF-kappaB nuclear accumulation and DNA binding activity was seen 2 to 6 hours after a single dose of 4 Gy irradiation and returned to control levels after 12 hours. In split-dose irradiation, NF-kappaB activity was similar after the first and second doses of 4 Gy irradiation separated by 12 hours. In addition, NF-kappaB activity was decreased by lengthening the interval between irradiation. The cell survival, which was assessed by colony formation assay, showed inverse correlation to this: the surviving fraction was higher after split-dose irradiation than after single-dose irradiation of the same total dose and it increased as the interval between irradiation was lengthened. Thus the present results showed a correlation between NF-kappaB activation and the repair of sublethal damage in split-dose irradiation.