Urinary Recovery of Salicylamide as Its Glucuronide in Liver Disease

An attempt was made to establish the method for the estimation of glucuronide formation in vivo using salicylamide and further to study the alteration in the glucuronide formation in liver disease. The results were as follows: 1. The method for the determination of free salicylamide separately from other conjugates of salicylamide in urine, without involving any hydrolysis of the other conjugates, was presented. When 1 g. of salicylamide was administered to the subjects with or without liver injuries, no free salicylamide was detected by the present method in the urine following the salicylamide administration. 2. The analytical method for the determination of salicylamide glucuronide was also devised by employing a hydrolysis with &#946;-glucuronidase. The ratio of the salicylamide liberated by the enzymatic hydrolysis of the 10-hour urine following the administration of 1 g. of salicylamide to the total salicylamide excreted in the same urine was neither affected by the total recovery of the salicylamide nor by the urine volume. This ratio was thus used as a means of estimating the capacity of the glucuronide formation in vivo, although it was considered that the ratio might be affected to some extent by the competition between the glucuronide and other conjugate formations in vivo. 3. As a result of this salicylamide glucuronide excretion test, it was indicated that the in vivo formation of salicylamide glucuronide in the patients with postnecrotic cirrhosis was slightly decreased compared with that in normal controls.</p

A Large Speculator in Contagious Currency Crises

This paper studies the implications of the presence of a large speculator like George Soros during a contagious currency crisis. The model proposes a new contagion channel and shows how a currency crisis can spread from one country to another even when these countries are totally unrelated in terms of economic fundamentals. This model enables us to distinguish between whether a crisis is a coincidence or due to contagion when it happens in two countries. It finds that the better the economic fundamentals in the originating crisis country, the more severe the contagion under certain conditions. The large speculator is more aggressive in attacking the currency peg than he would be if his size were small. Furthermore, the mere presence of the large speculator makes other small speculators more aggressive in attacking the currency peg, which in turn makes countries more vulnerable to currency crises. But surprisingly, the presence of the large speculator mitigates contagion of crises across countries. The model presents policy implications as to financial disclosure and size regulation of speculators such as hedge funds, which recently have been hot topics among policy makers. First, financial disclosure by speculators eliminates contagion, but may make countries more vulnerable to crises. Second, regulating the size of speculators (e.g., prohibiting hedge funds from high-leverage and thereby limiting the amount of short-selling) makes countries less vulnerable to crises, but makes contagion more severeContagion; Currency Crises; George Soros; Global Game

Contagion of Currency Crises across Unrelated Countries without Common Lender

I construct a micro-model to show that a currency crisis can spread from one country to another even when these countries are unrelated in terms of economic fundamentals and there is no capital linkage across countries through a common lender or an interbank market. The key to explaining contagious currency crises in the model lies in each speculator's private information and learning behavior about other speculators' type. Since the payoff of each speculator depends on other speculators' behavior determined by their types, each speculator's behavior depends on her belief about other speculators' types. If a currency crisis in one country reveals the speculators' types to some degree, it leads to an updating of each speculator's belief about other speculators' types and therefore a change in her optimal behavior, which in turn can cause a currency crisis even in another unrelated country without capital linkage. Although the presence of contagion itself is not new in the literature, there is an important implication difference between the literature and this paper. The model shows that the crisis with better economic fundamentals can be more contagious than that with worse economic fundamentals; this has not been shown in the literature. This is because the former conveys information about types of speculators while the latter does not. Even if country B does not suffer from a contagious crisis due to bad economic fundamentals from country A, it does not necessarily mean that it will never suffer contagion from some other country with better economic fundamentals than country AContagion; Currency Crises; Global Game

Lending Channels and Financial Shocks: The Case of Small and Medium-Sized Enterprise Trade Credit and the Japanese Banking Crisis

We offer a new paradigm for understanding the impact of financial shocks on the flow of credit to small and medium-sized enterprises (SMEs). Drawing from research on the lending view of monetary policy and research on SME financial contracting, we introduce the concept of glending channels.h A lending channel is a two-dimensional conduit through which SMEs obtain financing. In particular, a lending channel consists of a specific lending technology provided by a specific type of institution. We hypothesize that during financial shocks some lending channels may close and other channels may expand to absorb the slack. We empirically test a possible implication of this hypothesis by examining whether one lending channel, trade credit, played a significant role as a substitute for other lending channels in offsetting a contraction in SME lending of other lending channels during the Japanese financial crisis. We find little evidence that trade credit played such a role. To the contrary, we find some evidence that trade credit and financial institution lending are complements, rather than substitutes, during the Japanese financial crisis periods. This does not preclude the possibility that other lending channels may have behaved in a manner consistent with this hypothesis.Trade credit; Credit crunch

Enzymatic studies of glucuronide formation in impaired liver. II. Activating effect of boiled liver extract on liver glucuronide formation

The effect of the boiled liver extract on the velocity of 4-methyl umbelliferone lucuronide formation by mouse liver homogenate was studied. The results were as follows: 1. Addition of mouse or rat liver boiled extract to the complete system for the glucuronide formation produced an increase in the velocity of the glucuronide formation. 2. The boiled liver extract produced the increase in the velocity of the glucuronide formation not as a substrate but as an activator. 3, The activator in the boiled liver extract was relatively heat stable, acid labile, and precipitated as a fairly ethanol-soluble barium salt. The solution of the activator partially purified by ethanol fractionation of the barium salt indicated its absorption maximum at 262 m&#956;. These results suggested that the most possible substance in the boiled liver extract responsible for the activation of 4methyl umbelliferone glucuronide formation might be a sugar nucleotide.</p

Enzymatic Studies of Glucuronide Formation in Impaired Liver III. Effects of Carbon Tetrachloride and Ectromelia Virus Infection on Liver Glucuronide Formation in Mouse

Glucuronide formations by mouse liver homogenate in several liver impairments were studied by using 4-methyl umbelliferone as a glucuronide receptor. The results were as follows : 1. Subcutaneous or intraperitoneal administration of carbon tetrachloride to the mouse produced a significant increase in the liver glucuronyl transferase activity 12 or 24 hours after the treatment regardless of histological and enzymatic evidences of liver-cell necrosis. This increase was not attributed to the increase in the 'activator' of glucuronide formation but to the increase in the enzyme activity itself. 2. In Ectromelia virus mouse hepatitis, the glucuronyl transferase activity of the liver tissue was markedly reduced in severe cases. In moderate or milder cases, a slight increase in the activity was observed in a few of them in the early stage of the disease, and the activity was significantly decreased on the recovery in all of the cases which survived. 3. In the early stage of carbon tetrachloride injury when the glucuronyl transferase activity of whole mouse liver was increased and the decomposition of uridine diphosphate glucuronic acid by the liver tissue was also enhanced, the glucuronide formation in vivo was rather increased. It was thus considered that the whole liver glucuronyl transferase activity rather than the uridine diphosphate glucuronic acid content was responsible for the glucuronide formation in vivo as a rate-limiting factor.</p

Isolation of Endogenous Activator of Glucuronide For­mation in Liver

A purified compound of the activator of glucuronide formation was isolated from a boiled extract of rat liver by charcoal adsorption, ethanol fractionation of barium salts, and finally paper and Dowex-l column chromatographies. The analytical data and the chemical properties of the compound sugggested that the endogenous activator of glucuronide formation in rat liver might be uridine diphosphate N-acetylglucosamine.</p