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Biomedical subjects

R M Gilbert

Publications and source records attributed to R M Gilbert.

At least 19 recordsLinked to original sources
PubMed1984

Caffeine consumption.

This chapter provides details about the production, trade, and consumption of caffeine, which is probably the world's most widely used drug. The focus is on caffeine derived from coffee, which accounts for about 54% of all caffeine use, because other chapters in the volume give details of tea and cocoa consumption. Tea accounts for about 43% of all caffeine consumption. Total world caffeine consumption in 1981 was estimated to be approximately 120,000 tonnes, equivalent to 70 mg a day for each inhabitant. The per capita rate of caffeine use in Canada and the United States is approximately three times that for the world as a whole, but only half that of a heavy coffee-consuming country such as Sweden or a heavy tea-consuming country such as the United Kingdom.

Beverages↗
PubMed1982

Early effects of quitting smoking.

Heart rate, hand tremor, skin temperature, eating, and craving for cigarettes were examined in 19 smokers who quit for 1 day. Measures of heart rate and hand tremor were lower during abstinence; craving seemed greater, skin temperature was higher, and there was more eating, particularly snacking, but no shift in preference towards sweet foods. Quitting brings about profound changes in a smoker's physiology and behaviour, even during the first day. Anticipation of these changes could help would-be quitters, and those who advise them.

Adult↗
PubMed1981

Temporary threshold shifts produced by wideband noise.

Groups of human subjects were exposed in a sound field to a wideband noise for 24 or for 8 h on consecutive days. The wideband noise was composed of octave bands centered at 0.5, 1, 2, and 4 kHz. For the 24-h exposure, temporary threshold shift (TSS) increased for about 8 h and then reached a plateau or asymptote. TTS's at asymptote (ATS) increased about 1.7 dB/dB increase in noise level above about 78 dBA. TTS produced by single-octave band exposures were used to predict the TTS produced by the wideband exposures. Predictions were based on the "Intensity Rule" [W. D. Ward, A. Glorig, and D. L. Sklar, "Temporary threshold shift from octave-band noise: Applications to DRC's," J. Acoust. Soc. Am. 31, 522-528 (1959)]. Predictions were acceptably accurate and the validity of the "Intensity Rule" for 24-h exposures or 8-h exposures is supported. There is a remarkable coincidence between the relation which describes ATS and noise level, and the relation which describes noise-induced permanent threshold shift (in industrial workers) and noise level. This coincidence and animal data are used to support the hypothesis that TTS grows to an asymptote rather than a plateau, and that TTS at asymptote (ATS) produced by a given sound is an upper bound on any permanent threshold shift that can be produced by that sound.

Acoustic Stimulation↗
PubMed1979

Temporary threshold shifts in humans exposed to octave bands of noise for 16 to 24 hours.

Groups of human subjects were exposed in a diffuse sound field for 16--24 h to an octave-band noise centered at 4, 2, 1, or 0.5 kHz. Sound-pressure levels were varied on different exposure occasions. At specified times during an exposure, the subject was removed from the noise, auditory sensitivity was measured, and the subject was returned to the noise. Temporary threshold shifts (TTS) increased for about 8 h and then reached a plateau or asymptote. The relation between TTS and exposure duration can be described by a simple exponential function with a time constant of 2.1 h. In the frequency region of greatest loss, threshold shifts at asymptote increased about 1.7 dB for every 1 dB increase in the level of the noise above a critical level. Critical levels were empirically estimated to be 74.0 dB SPL at 4 kHz. 78 dB at 2 kHz, and 82 dB at 1 and 0.5 kHz. Except for the noise centered at 4.0 kHz, threshold shifts were maximal about 1/2 octave above the center frequency of the noise. A smaller second maximum was observed also at 7.0 kHz for the noise centered at 2.0 kHz, at 6.0 kHz for the noise centered at 1.0 kHz, and at 5.5 kHz for the noise centered at 0.5 kHz. After termination of the exposure, recovery to within 5 dB of pre-exposure thresholds was achieved within 24 h or less. Recovery can be described by a simple exponential function with a time constant of 7.1 h. The frequency contour defined by critical levels matches almost exactly the frequency contour defined by the E-weighting network.

Adult↗
PubMed1979

Augmentation of alcohol consumption by caffeine in malnourished rats.

The alcohol consumption of malnourished rats increased substantially when caffeine, but not isohedonic quinine, was added to their available fluids. The effect was not observed in rats receiving an adequate diet. Conversely, food restriction raised alcohol consumption substantially in adequately fed but not in malnourished rats.

Alcohol Drinking↗
PubMed1978

Schedule induction and sweetness as factors in ethanol consumption and preference by rats.

The separate and joint effects of spaced feeding of small portions of the daily food ration (schedule induction) and sweetening of one or the other fluid by 0.2% sodium saccharin on the consumption and selection of water and a 5% ethanol solution were examined in three groups of four male, hooded rats. Fluids were available simultaneously throughout 50-min sessions during which 50 Noyes 45-mg pellets were available either altogether at the beginning of each session or singly at 60-sec intervals. Water was available in home cages. Each group experienced a different sequence of procedures that provided alternation and replication of critical conditions. Sweetening increased consumption of the sweetened fluid and suppressed consumption of the unsweetened fluid. Spaced feeding raised consumption of the preferred fluid. Exceptionally high levels of consumption were recorded when one or the other fluid was sweetened and food presentation was intermittent.

Alcohol Drinking↗
PubMed1978

Functional profile of the isolated uremic nephron. Impaired water permeability and adenylate cyclase responsiveness of the cortical collecting tubule to vasopressin.

Resistance of the chronically diseased kidney to vasopressin has been proposed as a possible explanation for the urinary concentrating defect of uremia. The present studies examined the water permeability and adenylate cyclase responsiveness of isolated cortical collecting tubules (CCT) from remnant kidneys of uremic rabbits to vasopressin. In the absence of vasopressin the CCTs of both normal and uremic rabbits were impermeable to water. At the same osmotic gradient, addition of a supramaximal concentration of vasopressin to the peritubular bathing medium led to a significantly lower net water flux per unit length (and per unit luminal surface area) in uremic CCTs than in normal CCTs. Transepithelial osmotic water permeability coefficient, P(f), was 0.0232 +/-0.0043 cm/s in normal CCTs and 0.0059+/-0.001 cm/s in uremic CCTs (P < 0.001). The impaired vasopressin responsiveness of the uremic CCTs was observed whether normal or uremic serum was present in the bath. Basal adenylate cyclase activity per microgram protein was comparable in normal and uremic CCTs. Stimulation by NaF led to equivalent levels of activity in both, whereas vasopressin-stimulated activity was 50% lower in the uremic than in the normal CCTs (P < 0.025). The cyclic AMP analogue, 8-bromo cyclic AMP, produced an increase in the P(f) of normal CCTs closely comparable to that observed with vasopressin. In contrast, the P(f) of uremic CCTs was only minimally increased by this analogue and was not further stimulated by theophylline. These studies demonstrate an impaired responsiveness of the uremic CCT to vasopressin. This functional defect appears to be a result, at least in part, of a blunted responsiveness of adenylate cyclase to vasopressin. The data further suggest that an additional defect in the cellular response to vasopressin may exist, involving a step (or steps) subsequent to the formation of cyclic AMP.A unifying concept of the urinary concentrating defect of uremia is proposed which incorporates a number of hitherto unexplained observations on the concentrating and diluting functions of the diseased kidney.

Adenylyl Cyclases↗
PubMed1977

Chronic alcohol drinking and subsequent withdrawal in rats exposed to different diurnal distributions of schedule-induction sessions.

Eight rats drank large amounts of 6.25% alcohol as a consequence of daily exposure to 6 hours of schedule-induction sessions in which a small food pellet was delivered every 90 sec. Rats having a 1-hr session every 4 hr showed slightly more withdrawal distress than rats having a 6-hr session every 24 hr. More significant may have been two different kinds of indication of possible loss of control over drinking by the inducing schedule. Rats experiencing six sessions a day did not drink water excessively when it replaced the alcohol solution. Rats experiencing one session a day drank half their total alcohol intake between sessions. If the schedule-induction procedure loses control over alcohol drinking, its chronic application to animals fails as a model of the factors that maintain excessive alcohol use in humans.

Alcoholism↗
PubMed1976

Caffeine content of beverages as consumed.

Quantitative analysis of beverages prepared at home by staff of the Addiction Research Foundation revealed a lower and much more variable caffeine content of both tea and coffee than had been reported in earlier studies, most of which were based on analysis of laboratory-prepared beverages. Median caffeine concentration of 37 home-prepared samples of tea was 27 mg per cup (range, 8 to 91 mg); for 46 coffee samples the median concentration was 74 mg per cup (range, 29 to 176 mg). If tea and coffee as drunk contain less caffeine than generally supposed, the potency of caffeine may be greater than commonly realized, as may the relative caffeine content of certain commercial preparations, including chocolate and colas. The substantial variation in caffeine content emphasizes the need to establish actual caffeine intake in clinical, epidemiologic and experimental investigations of caffeine effects.

Beverages↗
PubMed1976

A study of the intrarenal recycling of urea in the rat with chronic experimental pyelonephritis.

The concentrating ability of the kidney was studied by clearance and micropuncture techniques and tissue slice analyses in normal rats with two intact kidneys (intact controls), normal rats with a solitary kidney (uninephrectomized controls), and uremic rats with a single pyelonephritic kidney. Urinary osmolality after water deprivation for 24 h and administration of antidiuretic hormone was 2,501+/-217 and 2,874+/-392 mosmol/kg H2O in intact and uninephrectomized control rats, respectively, and 929+/-130 mosmol/kg H2O in pyelonephritic rats (P less than 0.001 compared to each control group). Fractional water reabsorption and concentrating ability were significantly decreased in the pyelonephritic group, and, to achieve an equivalent fractional excretion of urea, a greater fractional excretion of water was required in the pyelonephritic rats than in the control rats. Whole animal glomerular filtration rate was 1.57+/-0.19 ml/min and 1.39+/-0.18 ml/min in intact and in uninephrectomized controls, respectively, and 0.30+/-0.07 ml/min in pyelonephritic rats (P less than 0.001 compared to each control group). Single nephron glomerular filtration rate was 35.6+/-3.8 nl/min in intact control rats and was significantly increased (P less than 0.05) in both uninephrectomized (88.0+/-10.8 nl/min) and pyelonephritic rats (71.5+/-14.4 nl/min). In all groups fractional water delivery and fractional sodium delivery were closely comparable at the end of the proximal convoluted tubule and at the beginning of the distal convoluted tubule. In contrast, fractional urea delivery out of the proximal tubule was greater in the intact control group (73+/-8%) than in either the uninephrectomized (52+/-2%) or the pyelonephritic group (53+/-3%) (P less than 0.005). Fractional urea delivery at the early part of the distal tubule increased significantly to 137+/-11% and 93+/-6% of the filtered load in intact control and uninephrectomized control rats, respectively (P less than 0.001 compared to the late proximal values of each group), but failed to increase significantly in pyelonephritic rats (65+/-13%), indicating interruption of the normal recycling of urea in the latter group. Analysis of tissue slices demonstrated a rising corticopapillary gradient for total tissue water solute concentration as well as for tissue water urea concentration in both groups of control rats. In contrast, the pyelonephritic animals exhibited no similar gradients from cortex to papilla. These data indicate that the pyelonephritic kidney fails to recycle urea and accumulate interstitial solute. The latter must inevitably lead to a concentrating defect.

Animals↗
PubMed1976

Dietary caffeine and alcohol consumption by rats.

The alcohol consumption of malnourished rats increased slowly but substantially during a 4-week period in which caffeine was added to their marginally adequate diet. Consumption fell to precaffeine levels as soon as caffeine was withdrawn.

Alcohol Drinking↗
PubMed1975

Involvement of separate pathways in the repair of mutational and lethal lesions induced by a monofunctional sulfur mustard.

The mutagenic and lethal effects of a monofunctional sulfur mustard, 2-chloro-ethylethylsulfide (CEES), have been studied in a number of repair deficient variants of Escherichia coli K12, B/r and B. The results indicate that CEES induces a (pre)mutational lesion which is subject to Uvr+-excision-repair. Extensive CEES-induced mutagenesis can occur in exrA- uvrA- and recA- uvrB- variants suggesting that the majority of the mutations in Uvr-bacteria do not arise from error-prone repair. These findings are similar to results previously reported with a volatile degradation product of captan and with ethyl methanesulfonate (EMS) but differ from those reported with methyl methanesulfonate (MMS). It is hypothesized that CEES alkylates guanine at the O-6 position (R-O-6-G) and that this R-O-6-G which is Uvr+-excisable is directly mutagenic by producing G-C to A-T transitions during replication. Reduced levels of induced mutation frequencies observed in an endonuclease II-deficient variant lead us to postulate that, in constrast to Uvr- bacteria, CEES-induced mutation in wild-type cells arise from error-prone repair of apurinic sites. Analysis of the lethal actions of CEES indicates that the lesion produced is largely unexcisable by the Uvr+ system. Host-cell reactivation of CEES-treated TI bacteriophage shows that the production of the (pre)ethal lesion is dependent on both the initial dose and post-treatment incubation. The efficient repair of the (pre)ethal lesion requires both endonuclease II and polymerase I. Moreover, deficiencies of these two enzymes rendered bacteria more sensitive to the cytotoxic action of CEES. It is postulated that the lethal mechanism of CEES involves: (I) alkylation at the N-3 position of adenine and the N-7 position of guanine; (2) spontaneous depurination of these alkylated bases; and (3) production of apurinic sites which are lethal unless repaired by the endonuclease II-polymerase I excision-repair system.

Adenine↗