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The aim of this study was to establish an experimental rat model of temporomandibular joint (TMJ) anterior disc displacement (ADD). A pilot study was conducted to determine the most appropriate surgical protocol. In the main experiment, 40 rats were used. Twenty-four rats were subjected to ADD in the right TMJ, and subsequently thereafter six, nine, and nine rats were sacrificed at 1, 4, and 8 weeks, respectively, for gross evaluation. Twelve rats that underwent a sham operation were equally divided and sacrificed at each of the above time points. Four nontreated control rats were sacrificed at the beginning of the study. TMJ blocks were harvested for radiological and histological assessment. Gross examination showed that 14 rats in the ADD group (58.3%) had anterior displacement of the TMJ disc. In the ADD joints, posterior condylar cartilage thickness decreased during the follow-up period; however, there was no significant difference between the sham-treated and ADD joints, or among the follow-up time points (P > 0.05). The anterior condylar cartilage exhibited obvious qualitative alterations. Radiologic signs of osteoarthrosis appeared after ADD surgery, but this became attenuated with time. The model investigated in this study successfully induced ADD in rats, and should be useful for assessment of progressive changes in the TMJ following ADD. [ABSTRACT FROM AUTHOR]

The article studies the synthesis of tetrahydroisoquinolines by enzymatic Pictet-Spengler reaction. The stydy uses an N-terminally truncated (S)-norcoclaurine synthase (NCS) from Coptis japonica expressed in Escherichia coli, where NCS catalyzes stereoselective Pictet-Spengler reaction for benzylisoquinoline alkaloid synthesis in plants. The study reflects versatility of the enzyme in synthesizing high yields of 6,7-dihydroxy-l-phenethyl-l,2,3,4-tetrahydroisoquinoline.

Inappropriate activation of the intrarenal renin--angiotensin system induces generation of reactive oxygen species and tubulointerstitial inflammation, which contribute to salt-sensitive hypertension (SSHT). Liver-type fatty acid-binding protein is expressed in proximal tubules in humans, but not in rodents, and may play an endogenous antioxidative role. The objective of the present study was to examine the antioxidative effect of liver-type fatty acid-binding protein on post-angiotensin II SSHT model in transgenic mice with selective overexpression of human liver-type fatty acid-binding protein in the proximal tubules. The transgenic mice showed marked protection against angiotensin II-induced SSHT. Overexpression of tubular liver-type fatty acid-binding protein prevented intrarenal T-cell infiltration and also reduced reactive oxygen species generation, intrarenal renin-angiotensin system activation, and monocyte chemotactic protein-1 expression. We also performed an in vitro study using the murine proximal tubular cell lines with or without recombinant liver-type fatty acid-binding protein and murine proximal tubular cell lines transfected with human liver-type fatty acid-binding protein, and found that gene transfection of liver-type fatty acid-binding protein and, in part, recombinant liver-type fatty acid-binding protein administration had significantly attenuated angiotensin II-induced reactive oxygen species generation and the expression of angiotensinogen and monocyte chemotactic protein-1 in murine proximal tubular cell lines. These findings indicated that liver-type fatty acid-binding protein in the proximal tubules may protect against angiotensin II-induced SSHT by attenuating activation of the intrarenal renin-angiotensin system and reducing oxidative stress and tubulointerstitial inflammation. Present data suggest that liver-type fatty acid--binding protein in the proximal tubules may be a novel therapeutic target for SSHT. [ABSTRACT FROM AUTHOR]

Intrarenal renin-angiotensin system (RAS) plays an important role for the pathogenesis of renal injuries. Experimental studies have demonstrated that angiotensinogen levels in renal tissues reflect the activity of intrarenal RAS. However, dynamics of urinary angiotensinogen have not been investigated in detail. Therefore, we examined the preservation conditions of the measured values of urinary angiotensinogen concentrations and an ultradian rhythm of urinary angiotensinogen excretion in humans. Urine samples were collected from 24 healthy volunteers. The urinary concentrations of angiotensinogen were measured by using ELISA. Two different urine preservation conditions were examined. One cycle of freeze-and-thaw did not change the measured values of urinary angiotensinogen concentrations. Moreover, to keep urine samples at room temperature for 12 hours did not change the measured values of urinary angiotensinogen concentrations. Thus, preservation conditions do not change the measured values of urinary angiotensinogen concentrations. Regarding an ultradian rhythm, blood pressure and the urinary concentrations of angiotensinogen were measured at 09:00, 13:00, and 16:00. The averaged levels of blood pressure were similar over the time. The average of urinary angiotensinogen/creatinine (Cr) ratios was 8.73 ±1.15 ng/mg Cr at 09:00, 9.53 ± 1.58 ng/mg Cr at 13:00, and 8.58 ± 1.26 ng/mg Cr at 16:00. The urinary angiotensinogen excretion in healthy volunteers does not have an ultradian change during the daytime (P = 0.482). This may be another indication that the intrarenal RAS is independent of the systemic RAS. We have to pay attention to these findings in handling urine samples for measurements of angiotensinogen. [ABSTRACT FROM AUTHOR]