The optical losses in both platforms are measured and used to predict their performance for different lengths. The results show that for an optimal waveguide length, two orders of magnitude

enhancement in the Selleck RG 7112 Raman signal can be achieved for aqueous solutions using HCPCFs. This length, however, cannot be achieved using normal capillary effects. By integrating the interface of the fluidic pump and the HCPCF into a microfluidic chip, we are able to control fluid transport and fill longer lengths of HCPCFs regardless of the viscosity of the sample. The long-term stability and reproducibility of Raman spectra attained through this platform are demonstrated for naphthalenethiol, which is a well-studied organic compound. Using the HCPCF platform, the detection limit of normal Raman scattering in the range of micro-molars has been achieved. In addition to the higher

signal-to-noise ratio of the Raman signal from the HCPCF-platform, selleck kinase inhibitor more Raman modes of naphthalenethiol are revealed using this platform. (C) 2011 American Institute of Physics. [doi:10.1063/1.3592961]“
“Background: Citrate is one of the most important inhibitors in urolithiasis. Hypocitraturia is a common risk factor in stone formers. Citrate excretion is regulated – amongst others – by acidosis and protein intake. A considerable number of stone formers, however, show hypocitraturia in the presence of normal urine pH levels. This is potentially due to defects in the renal tubular citrate carriers

(NaDC 1 and 3) which may be genetically determined. Patients and Methods: 350 consecutive stone formers were examined. Exclusion Fedratinib criteria were urinary tract infection, hypokalemia, and steatorrhea. The following parameters were measured: serum: creatinine, calcium, potassium, and uric acid; urine: pH profiles, citrate, calcium, uric acid, ammonia, urea, and creatinine. Results: 83/350 patients were hypocitraturic (48 males, 35 females). 14/83 had low urine pH (<= 6), 69/83 showed normal levels (1 6). In the latter group there was a significantly higher recurrence rate (23 vs. 9%). The two groups were not different in serum parameters apart from uric acid. In urine, only pH and calcium (males) were significantly lower in the first group. Citrate did not correlate with urine pH and creatinine in the hypocitraturia-normal pH group, only with calcium in both sexes and urea and ammonia in females. In the hypocitraturia-low pH patients, there was no significant correlation between citrate and any other parameter tested. Conclusions: Hypocitraturia with normal urine pH is an entity indicating a high risk for recurrence. Since there was no correlation between citrate and pH, urea and ammonia, respectively, citrate excretion is not regulated in these patients as usual. There may be a link to calcium excretion. Potentially, these patients have defects in the renal tubular citrate carriers which may be genetically determined.