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This Protocol Extension describes the low-cost production of rapidly customizable optical neural probes for in vivo optogenetics. We detail the use of a 3D printer to fabricate minimally invasive microscale inorganic light-emitting-diode-based neural probes that can control neural circuit activity in freely behaving animals, thus extending the scope of two previously published protocols describing the fabrication and implementation of optoelectronic devices for studying intact neural systems. The 3D-printing fabrication process does not require extensive training and eliminates the need for expensive materials, specialized cleanroom facilities and time-consuming microfabrication techniques typical of conventional manufacturing processes. As a result, the design of the probes can be quickly optimized, on the basis of experimental need, reducing the cost and turnaround for customization. For example, 3D-printed probes can be customized to target multiple brain regions or scaled up for use in large animal models. This protocol comprises three procedures: (1) probe fabrication, (2) wireless module preparation and (3) implantation for in vivo assays. For experienced researchers, neural probe and wireless module fabrication requires ~2 d, while implantation should take 30–60 min per animal. Time required for behavioral assays will vary depending on the experimental design and should include at least 5 d of animal handling before implantation of the probe, to familiarize each animal to their handler, thus reducing handling stress that may influence the result of the behavioral assays. The implementation of customized probes improves the flexibility in optogenetic experimental design and increases access to wireless probes for in vivo optogenetic research. This Protocol Extension describes the fabrication and implantation of 3D-printed neural probes for tethered or wireless optogenetics in freely moving rodents.

Herein, we report the results of patch tests and whether these patients have been infected with hepatitis C virus (HCV). Regarding metal patch tests, the allergens were supplied by Torii Pharmaceutical Co., Ltd. Seventeen types of metal reagents were used, including 2% aluminum (Al) chloride, 2% cobalt (Co) chloride, 1% stannic (Sn) chloride, 2% ferric (Fe) chloride, 0.5% chloroplatinic (Pt) acid, 1% palladium (Pd) chloride, 2% manganese (Mn) chloride, 1% indium (In) trichloride, 1% iridium (Ir) tetrachloride, 2% silver (Ag) bromide, 0.5% potassium bichromate (Cr), 2% chromium sulfate (Cr), 5% nickel (Ni) sulfate, 2% zinc (Zn) butter, 0.2% chloroauric acid (Au), 1% copper (Cu) sulfate, and 0.02% mercuric (Hg) chloride. [...]26 patients (51%) were positive for the metals, and 25 (49%) were negative.

Abnormal liver function test results are often observed in acute decompensated heart failure (ADHF). However, the prognostic value of bilirubin fractionation has not been elucidated. The prognostic value of direct bilirubin (DB), in comparison with total bilirubin (TB), was examined in 556 consecutive patients with ADHF. Patients with elevated DB showed mostly similar patient characteristics including signs of elevated right-sided pressure (frequent hepatomegaly, jugular venous distention, dilated inferior vena cava, and elevated gamma-glutamyltransferase) and decreased cardiac output (cold extremities, decreased pulse pressure, and lower blood pressure) and other parameters of heart failure (HF) severity (increased plasma renin activity, decreased sodium, total cholesterol, and ejection fraction) to elevated TB; however, only patients with elevated DB showed a significant difference in the frequency of HF history and alkaline phosphatase value. Kaplan-Meier analysis showed that patients with elevated DB had a significantly higher rate of the composite end point of all-cause mortality or HF readmission (p = 0.021) compared with those with normal DB, whereas patients with elevated TB did not show a statistically significant difference compared with those with normal TB (NS). A multivariate Cox hazards model showed that DB was an independent predictor of adverse events (adjusted hazard ratio 1.052, 95% confidence interval 1.001 to 1.099, p = 0.034), whereas TB was not (adjusted hazard ratio 1.017, 95% confidence interval 0.985 to 1.046, p = 0.27). Adding DB to existing prognostic variables resulted in higher C-statistics than adding TB (C-statistics: 0.670 to 0.675, 0.670 to 0.674, respectively). In conclusion, elevated DB in ADHF was an independent prognostic predictor that was superior to TB. DB may be useful for further risk stratification in ADHF.

High-sensitive cardiac troponin T (hsTnT) is a sensitive biomarker of myocardial damage and predictor of acute decompensated heart failure (ADHF). However, there is little information on changes over time in hsTnT level during ADHF management. The aim of this prospective study was to evaluate changes in hsTnT levels between admission and at discharge in patients with ADHF, and identify factors that determine such levels and their prognostic significance. We evaluated 404 ADHF patients with abnormal hsTnT levels (≥0.0135 ng/ml) on admission. The median (interquartile ranges) hsTnT levels on admission, at discharge, and percent changes in hsTnT levels were 0.038 (0.026 to 0.065), 0.032 (0.021 to 0.049) ng/ml, and -12.0 (-39.8 to 7.4) % respectively. The numbers of patients with falling (hsTnT decrease > -15%), stable (hsTnT change between -15 and +15%) and rising (hsTnT increase > +15%) hsTnT level at discharge were 190, 146, and 68, respectively. The percent change in B-type natriuretic peptide (BNP) levels was greater in the falling group, compared to the stable (p<0.001) and rising groups (p<0.001). Changes in hsTnT levels correlated significantly with changes in BNP levels (ρ = 0.22, p<0.001). Multivariate Cox regression analysis identified rising or stable hsTnT at discharge as a significant predictor of heart failure-related rehospitalization (hazard ratio: 1.69; 95% confidence interval: 1.06 to 2.70; p = 0.03). Persistent increase in hsTnT levels at discharge correlated with inadequate decrease of BNP levels, and was a predictor of poor clinical outcome, with repeat heart failure hospitalizations.