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As has been widely observed, the volatility of GDP has declined since the mid-1980s compared to the prior years. One leading explanation of this decline is that monetary policy significantly improved in the later period. We utilize a cross-section of 2-digit manufacturing and trade industries to further investigate this explanation. Since a major channel through which monetary policy operates is through variation in the federal funds rate, we hypothesized that more interest sensitive industries should have experienced larger declines in the variance of their outputs in the post-1983 period. We estimate interest sensitivity measures for each industry from a variety of VAR models and then run cross-sectional regressions explaining industry volatility ratios as a function of their interest sensitivity measures. These regressions reveal little evidence of a statistically significant relationship between industry volatility reductions and our measures of the industry interest sensitivity. This result poses challenges for the hypothesis that improved monetary policy explains the decline in GDP volatility. Keywords: GDP volatility; Monetary policy; Great moderation

A number of explanations for the observed decline in GDP volatility since the mid-1980s have been offered. Valerie Ramey and Daniel Vine (2003a. 2003b) in a couple of recent papers offer the hypothesis that a decline in the persistence of sales is an explanation for the decline in GDP volatility [Ramey, V.A., Vine, D.J., 2003a. The Effects of Sales Persistence on Volatility in a Production Smoothing Model. Draft dated November 18; Ramey, V.A., Vine, D.J., 2003b. Tracking the source of the decline in GDP volatility: an analysis of the automobile industry. Unpublished Working Paper, presented on the ASSA program, San Diego, January 2004]. Their models show that a decrease in sales persistence leads to a decline in the variance of production relative to the variance of sales. They provide econometric evidence that the persistence of unit automobile sales has declined at both the aggregate and model level. This paper explores reasons why sales persistence may have declined and then tests the Ramey--Vine hypothesis with monthly chain-weighted sales data from 2- and 3-digit manufacturing and trade industries. The estimates confirm the Ramey Vine findings for motor vehicle retailers, wholesalers, and manufacturers. For a number of industries outside of motor vehicles, especially those in wholesaling and nondurable manufacturing, considerable evidence is found of declines in sales persistence. These declines seem to be consistent with changes in supply and distribution chains that have occurred as the result of the introduction of new information, inventory, and production control systems. However, in equations estimated for aggregate manufacturing, wholesaling, and retail sector sales, declines in sales persistence are not found. Keywords: GDP volatility: Sales persistence; Great moderation; Inventory: Production

This paper reports the results of a detailed examination of the hypothesis that improved inventory management and production techniques are responsible for the decline in the volatility of U.S. GDP growth. Our innovations are to look at the data at a finer level of disaggregation than previous studies, to exploit cross-sectional heterogeneity to obtain clearer identification of this hypothesis, and to provide a complete decomposition of the change in GDP volatility. At the aggregate level, changes in inventory behavior can account directly for almost half of the total reduction in GDP volatility. However, reduced volatility of sales and lower covariance among the output of major sectors in the economy each account for more than one-fourth of the reduction in GDP volatility. Improved inventory management appears to be associated loosely with lower volatility at the industry level. Keywords: Inventory investment; Output; GDP volatility; Covariance; Business cycles; Stability

This paper documents econometrically that US Inventory to Sales Ratios have time trends and that there have been significant breaks in these time trends at both the aggregate and industry level. Using techniques developed by Bai (Rev. Econ. Stat. (1997) 551) and by Bai and Perron (Econometrica 66 (1) (1998) 47), we simultaneously estimate the time trend parameters and the dates of statistically significant breaks in those trends. Using data from 1967 through 2001, it is estimated that aggregate Manufacturing and Trade Inventory to Sales ratio trended upwards at a 0.76%/year rate before 1985 Q3 and has trended downwards at a 1.29%/year rate since then. Downtrends are estimated to have begun in Manufacturing ratios in 1983, Wholesalers in 1985, and Retailers in 1990. Before the mid-1990s nearly all the reductions in ratios occurred in industries carrying durable goods. Examination of the timing and possible explanations of trend breaks for the 20 two-digit manufacturing industries suggests that breaks are much more likely to have occurred in recessions and may be related to changes in the variance of the industry's sales growth rate. Keywords: Inventory to Sales Ratios; Inventory; Trend breaks

Changes in traditionally constructed aggregate inventory to sales ratios are shown to not necessarily measure changes in underlying subsector inventory behavior. This is because while traditionally constructed aggregate inventory to sales ratios can be viewed as the weighted average of the underlying subsector inventory to sales ratios, the aggregation weights vary over time reflecting shifts in the composition of sales across the subsectors. For example, aggregate ratios can increase when most of the underlying subsectors are reducing inventory to sales ratios; this is shown to have been the case for the US Retail Sector. As a solution to this measurement problem, the use of fixed weight aggregate inventory sales ratios is proposed. These should help business cycle analysts and researchers better gauge the condition of inventories. Keywords: Aggregate inventory to sales ratios; Measurement problems; Macroeconomics

In contrast to earlier studies, we find that inventory holding in the US has become much more efficient since the mid-1980s. This result is found by examining trends in fixed weight aggregate inventory to sales ratios rather than traditional inventory to sales ratios, whose trends are shown to have been distorted by shifts in the composition of sales towards sectors carrying heavier stocks. Nearly all of the reductions in inventory holdings relative to sales are found to have occurred in sectors carrying durable goods. The adoption of just-in-time (JIT) and other inventory control systems by Durable Manufacturers is shown to have greatly reduced their inventory holdings. Keywords: Trends in inventory to sales ratios; Inventory; Macroeconomics; JIT

US financial deregulation was theoretically supposed to help consumers by making it possible for a larger number of households to earn a market (unregulated) rate of interest on their savings. [...]

PtdIns(4,5)P2 production by the enzyme PtdIns4P 5-kinase C (PIPkin C) was examined in thrombin-stimulated human platelets. Thrombin caused a rapid, transient 2-3-fold increase in PIPkin activity and a transient net dephosphorylation of the enzyme. PIPkin C was phosphorylated on serine and threonine residues in unstimulated platelets; no evidence for tyrosine phosphorylation was found. The phosphatase inhibitor okadaic acid promoted PIPkin C hyperphosphorylation and a concomitant marked inhibition of its activity in immunoprecipitates. Activity was restored by treatment with alkaline phosphatase, suggesting the existence of an inhibitory phosphorylation site. In support of this idea, alkaline phosphatase treatment of PIPkin C immunoprecipitated from unstimulated platelets caused a modest (1.6-fold) but significant activation of the enzyme. However, alkaline phosphatase treatment of PIPkin C immunoprecipitated from thrombin-stimulated platelets caused a decrease in activity to approximately the same levels, suggesting that the phosphorylation of PIPkin C also contributes to the observed stimulation. Two-dimensional phosphopeptide mapping of immunoprecipitated PIPkin C revealed that the enzyme is multiply phosphorylated and that, whereas some phosphopeptides are indeed lost on stimulation, consistent with the net dephosphorylation of the enzyme, at least two novel sites become phosphorylated. This suggests that thrombin causes complex changes in the phosphorylation state of PIPkin C, one consequence of which is its activation.

Treatment of intact hepatocytes with cholera toxin at 37 degrees C caused a stable activation of adenylate cyclase activity after a lag period of around 10 min. The presence of either insulin (10 nM) or glucagon (10 nM) in the incubation medium had little effect on this lag period; however, these hormones markedly attenuated the maximal activation of adenylate cyclase activity that could be achieved by treatment with cholera toxin. Such actions of insulin and glucagon were dose-dependent, with EC50 values (concn. giving 50% inhibition) of 0.20 nM for insulin and 0.49 nM for glucagon, and were not additive. Treatment of intact hepatocytes with either glucagon or insulin did not affect the ability of cholera toxin to cause the ADP-ribosylation of the 45 kDa alpha-subunit of the stimulatory guanine nucleotide regulatory protein, Gs, in intact hepatocytes. It is suggested that treatment of intact hepatocytes with either insulin or glucagon attenuates the stimulatory action of ADP-ribosylated Gs on adenylate cyclase.

(1) The removal of the nuclear envelope from isolated rat-liver nuclei by washing with Triton X-100 (TX-100) was assessed by electron microscopy. All the envelope was removed by 0.04% (w/v) TX-100. (2) After this removal, phosphorylation of inositol lipids and diacylglycerol (DAG) from [γ-32P]ATP still occurs, despite the near complete absence of detectable (by mass assay) DAG and PtdIns. This suggests that the majority of these two lipids in nuclei are present in the nuclear membrane, but the small amounts remaining after extraction, defined as intranuclear, are available for phosphorylation by lipid kinases (36% for DAG and 24% for PtdIns respectively, when expressed as a percentage of incorporation of intact nuclei). (3) PtdIns(4,5)P2 did not follow the same pattern as PtdIns and DAG; after removal of the nuclear membrane, 40% of the mass of this lipid was left in the nucleus. Moreover, a similar amount of PtdIns(4,5)P2 was also resistant to extraction with even higher concentrations of detergent, suggesting that PtdIns(4,5)P2 has a discrete intranuclear location, probably bound to nuclear proteins. (4) Addition of exogenous substrates, PtdIns, PtdIns(4)P and DAG, to membrane-depleted nuclei resulted in reconstitution of the majority of lipid phosphorylations from [γ-32P]ATP (70%, 90% and 94% of intact nuclei respectively), suggesting a predominantly intranuclear location for the respective kinases. (5) Nuclei also showed phosphomonoesterase and phosphatidic acid hydrolase activity; dephosphorylation of pre-radiolabelled PtdIns(4)P, PtdIns(4,5)P2 and phosphatidic acid was observed when [γ-32P]ATP was removed. However, some of the radioactivity was apparently resistant to these enzymes, suggesting the existence of multiple pools of these lipids. (6) Addition of excess non-radiolabelled ATP to nuclei pre-labelled with [γ-32P]ATP resulted in an initial increase in the label in PtdIns(4,5)P2, implying a precursor-product relationship between the radiolabelled pools of PtdIns(4)P and PtdIns(4,5)P2. This was confirmed by analysis of the incorporation of 32P into the 4ʹ-phosphate group of PtdIns(4)P and the individual 4ʹ- and 5ʹ-phosphate groups of PtdIns(4,5)P2. The data from these experiments also indicated that PtdIns(4,5)P2 can be produced from a pre-existing pool of PtdIns(4)P, as well as de novo from PtdIns. (7) Taken together our data suggest that isolated rat-liver nuclei have an intranuclear inositol lipid metabolism mechanism utilizing enzymes and substrates equivalent to those found in cytosol and plasma membrane, and that there may be some, but not complete, compartmentalization of the components of the nuclear inositol cycle.

Absence of physiological concentrations of extracellular Ca2+ in the Krebs-Henseleit incubation buffer did not affect the ability of 10 nM glucagon (< 5%) to increase hepatocyte intracellular cyclic AMP concentrations, but severely ablated (by approximately 70%) the ability of 10 nM insulin to decrease these elevated concentrations. Cyclic AMP metabolism is determined by production by adenylate cyclase and degradation by cyclic AMP phosphodiesterase (PDE). In the absence of added extracellular Ca2+ (2.5 mM), insulin's ability to activate PDE activity was selectively compromised, showing a failure of insulin to activate two of the three insulin-stimulated activities, namely the ‘dense-vesicle’ and peripheral plasma-membrane (PPM) PDEs. In the absence of added Ca2+, insulin's ability to inhibit adenylate cyclase activity in intact hepatocytes was decreased dramatically. Vasopressin and adrenaline (+ propranolol) failed to elicit the activation of either the ‘dense-vesicle’ or the PPM-PDEs. The presence of physiological concentrations of extracellular Ca2+ in the incubation medium is shown to be important for the appropriate generation of insulin's actions on cyclic AMP metabolism.

The occurrence of famines in various parts of the world, especially in primitive tropical areas, has compelled the inhabitants of those regions to subsist at such times primarily on an enormous variety of wild plants, a few of which are discussed in this article, that otherwise would be relatively little utilized by them.

The writer is an agriculturist who taught botany for many years at Achimota.

8-Phenyl-2-quinolyl nitrene, generated by pyrolysis of 9- phenyltetrazolo[1,5-a]-quinoline at 530/0.2 mm, rearranged to form a single product, 7H-pyrido[2,3,4-gh]-phenanthridine (82%). The formation of this product is consistent with rearrangement by ring expansion of 8-phenyl-2-quinolyl nitrene followed by ring contraction to give 8- phenyl-1-isoquinolyl nitrene.