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PubMed2004

The effects of NMDA and GABAA pharmacological manipulations on acute and rapid tolerance to ethanol during ontogeny.

BACKGROUND: Sensitivity to several ethanol effects increases during ontogeny, perhaps in part because of a notable decline in acute tolerance. In contrast, rapid tolerance to ethanol-induced sedation emerges slowly during ontogeny. This study tested the hypothesis that ontogenetic differences in glutamate and/or gamma-aminobutyric acid systems influence tolerance expression. METHODS: Sprague-Dawley rats at postnatal day (P)26 or P70 received (+)MK-801, muscimol, or saline before ethanol (3.5 or 4.5 g/kg) or saline on day 1 and ethanol only on day 2. Loss of and time to regain the righting reflex and blood alcohol levels at recovery were recorded. The presence of acute tolerance was indicated as a positive slope of the linear regression of blood alcohol levels at recovery versus ethanol dose. Rapid tolerance was estimated on day 2 by comparing animals given ethanol only on day 2 with those given ethanol on both days. RESULTS: Acute tolerance on day 1 only was observed at P26; this was disrupted by (+)MK-801 but not muscimol. Evidence for acute tolerance also emerged in adults on day 2. Whereas both drugs increased ethanol sedation at both ages, they did not facilitate ontogenetic expression of rapid tolerance: rapid tolerance was not evident at P26 regardless of pretreatment when indexed in terms of recovery time. CONCLUSIONS: These data provide further evidence for an ontogenetic dissociation in the expression of acute and rapid tolerance to ethanol-induced sedation. Pharmacological attenuation of the expression of acute tolerance was sufficient but not necessary to delay recovery of righting after ethanol. The greater propensity of young animals to develop acute tolerance, seemingly modulated in part by NMDA receptors, may contribute to their relative resistance to ethanol, although other factors, including pharmacokinetic factors, also contribute to their more rapid recovery from ethanol sedation.

Aging↗

PubMed1987

The influence of gravity on horizontal and vertical vestibulo-ocular and optokinetic reflexes in the rabbit.

The influence of the linear acceleration of gravity on the vertical and horizontal vestibulo-ocular reflexes (VVOR, HVOR) as well as the vertical and horizontal optokinetic reflexes (VOKR, HOKR) has been examined in rabbits. Rabbits were mounted in a biaxial rate table in front of a rear projection tangent screen. Eye movements were measured with a light projection technique. The HVOR, VVOR, HOKR and VOKR were measured in rabbits which were maintained both prone and supine. The gain of the HVOR for the supine orientation was reduced at all frequencies tested (0.01-0.80 Hz). Similarly there was a reduction in the gain of the HOKR. By contrast, the gain of the VVOR in the supine orientation was enhanced over a lower range of frequencies (0.02-0.04 Hz) and reduced at higher frequencies (0.10-0.80 Hz). The gain of the VOKR was not reduced in the supine orientation. The range of eye positions over which compensatory eye movements occurred was restricted in the supine orientation. The altered orientation of the medio-laterally polarized hair cells of the utricular maculae with respect to gravity in the supine orientation may cause postural instability and facilitate 'righting reflexes'. A reduction in the gains of the HVOR, VVOR and HOKR caused by linear accelerations in the sagittal plane during locomotion may decrease automatic postural responses during certain movements in which these automatic postural adjustments would not necessarily be adaptive.

Animals↗

PubMed2001

Ethanol enhances GABAA receptor function in short sleep and long sleep mouse brain membranes.

BACKGROUND: SS and LS mice have been used to explore the genetic and neurochemical bases for differences in sensitivity to ethanol. The present study investigated the effects of ethanol on GABAA receptor function in microsacs from these genotypes. The purpose was to test a key element of the hypothesis that differences between these lines in sensitivity to ethanol-induced enhancement of GABAA receptor function underlie their selected differences in sensitivity to ethanol-induced loss of righting reflex (LORR). METHODS: The effects of ethanol on GABA-activated 36Cl- uptake in brain membranes (microsacs) isolated from male SS and LS mice were tested using a chloride flux filtration assay. RESULTS: Ethanol significantly enhanced GABA-activated 36Cl- uptake in SS microsacs at concentrations of 100-300 mM. Ethanol did not significantly affect GABA-activated chloride uptake in this preparation at concentrations of 25 and 50 mM. Ethanol significantly enhanced GABA-activated 36Cl- uptake in LS microsacs at concentrations of 25-100 mM, but not at 200 mM. CONCLUSION: The present studies are the first to show a statistically significant effect of ethanol on GABA-activated chloride uptake in both SS and LS mice with a clear difference between the genotypes in threshold. The relative threshold differences between SS and LS microsacs in sensitivity to ethanol indicate that selection for resistance to ethanol-induced LORR in SS mice has shifted the ethanol-GABAA receptor concentration-response curve to the right. The findings add key evidence that supports a cause-effect relationship between sensitivity to ethanol-induced potentiation of GABAA receptor function and genetically determined sensitivity to ethanol's behavioral effects.

Animals↗

PubMed2002

Pathology of cultured paua Haliotis iris infected with a novel haplosporidian parasite, with some observations on the course of disease.

Mortalities among juvenile paua Haliotis iris Martyn 1784 in a commercial culture facility were reported in April 2000. Histology of moribund paua showed heavy systemic infections of a uni- to multi-nucleate stage of a novel organism later confirmed by transmission electron microscopy (TEM) and molecular studies to be a haplosporidian. Multinucleate plasmodia up to 25 microm diameter with up to 17 nuclei were detectable in wet preparations of hemolymph from heavily infected paua. The presence of the haplosporidian in the affected facility was associated with mortalities of slow growing 'runt' paua during the summer months. Total mortalities in affected raceways 6 mo after mortalities began were between 82.5 and 90%. Heavily infected paua exhibited behavioural abnormalities including lethargy, loss of righting reflex, and were easily detached from surfaces. Some heavily infected paua exhibited oedema and pale lesions in the foot and mantle, but no reliable gross signs of disease were noted. Light infections of the haplosporidian were also found in apparently healthy paua from the facility. Histology indicated that the early stages of infection were characterised by small numbers of plasmodia in the connective tissue surrounding the gut, amongst glial cells adjacent to nerves in the mantle and foot and within gill lamellae. In heavy infections, large numbers of small plasmodia (mean size 5.5 x 7 microm in histological sections) were present in the hemolymph, gills, heart, kidneys, mantle, foot, epipodium and connective tissue of the digestive gland. Infections were not transferred horizontally at 14 and 19 degrees C after cohabiting heavily infected paua with uninfected paua for 3 mo in aquaria, or 3 mo after injecting healthy paua with hemolymph containing haplosporidian plasmodia. This may indicate that the prepatent period for disease is longer than 3 mo, that disease is not expressed below 20 degrees C, or that an intermediate host is required for transmission. Spore formation was not observed in juvenile paua but sporocyst-like bodies containing putative spores were observed amongst haplosporidian plasmodia in the right kidney of poorly performing adult paua collected from the wild.

Animals↗

PubMed1993

Sex-dependent relations of grasp-reflex strengths from right and left hands to serum gonadotropin (FSH and LH) levels in human neonates with regard to cerebral lateralization.

The relation of grasp-reflex strength to serum FSH and LH levels were studied in human neonates. The grasp-reflex strengths from the right and left hands were found to be negatively linearly correlated with serum FSH level in males without familial sinistrality (-FS), but there was no significant correlations between these parameters in females. Serum LH levels were not correlated with grasp reflex in -FS neonates. The grasp-reflex strength from the right hand showed a significant negative linear correlation with LH only in +FS males. The right minus left (R-L) grasp-reflex strength decreased linearly with serum LH levels only in +FS males. These results did not support the testosterone hypothesis of cerebral lateralization. It was suggested that FSH and LH may indirectly influence the brain development according to sex and genetically pre-determined cerebral organization.

Female↗

PubMed2000

Chlorpyrifos exposure during a critical neonatal period elicits gender-selective deficits in the development of coordination skills and locomotor activity.

The widespread use of chlorpyrifos has raised concern about the potential consequences of fetal and childhood exposure. Previous studies have shown that apparently subtoxic doses of chlorpyrifos are nevertheless capable of affecting brain development by inhibiting mitosis, eliciting apoptosis, and altering neuronal activity and reactivity. To determine whether these biochemical changes elicit behavioral abnormalities, we evaluated coordination skills and open field behaviors in developing rats. Administration of 1 mg/kg s.c. of chlorpyrifos on postnatal (PN) days 1-4 elicited deficits in reflex righting on PN3-4 and in geotaxic responses on PN5-8, an effect that was specific to females. However, the ontogeny of more complex behaviors indicated a subsequent selectivity toward males. In the periweaning period, open-field locomotor activity and rearing were markedly reduced in male rats that had been exposed to chlorpyrifos on PN1-4, whereas no effect was detected in females. The gender-selective behavioral effects were associated with greater sensitivity of males to inhibition of cholinesterase in the first few hours after chlorpyrifos treatment. In contrast to the effects seen after administration on PN1-4, shifting the period of chlorpyrifos exposure to PN11-14 had a much less notable effect, even when higher doses were used: no decreases in locomotor activity and overall increases in rearing and grooming that were not significantly gender-selective. Administration on PN11-14 did not produce differential effects on cholinesterase in males and females. These studies indicate that chlorpyrifos given during a critical neonatal period, even at levels below the threshold for overt toxicity, can elicit both immediate and delayed gender-selective behavioral abnormalities. The ultimate evaluation of the developmental neurotoxicity of chlorpyrifos will thus require long-term assessments of neurobehavioral consequences of exposure during discrete developmental periods.

Animals↗

PubMed1998

Increased neuronal cell survival after L-deprenyl treatment in experimental thiamine deficiency.

Experimental thiamine deficiency results in a reproducible pattern of selective neuronal cell death. Events such as blood-brain barrier breakdown, N-methyl-D-aspartic acid (NMDA) receptor-mediated excitotoxicity, and increased reactive oxygen species have been implicated in thiamine deficiency-induced neural loss. L-deprenyl protects dopaminergic, noradrenergic, and acetylcholinergic neurons from neurotoxic, mechanical, and excitotoxic damage. In the present study, the effects of l-deprenyl on neuronal cell survival were examined in rats made thiamine deficient by daily administration of the central thiamine antagonist pyrithiamine (0.5 mg/kg s.c.). Rats assigned to thiamine deficient or control groups received daily injections of l-deprenyl (0.25, 0.5, or 1.0 mg/kg/day i.p.) or vehicle until they reached a state of severe thiamine deficiency (loss of righting reflex). At this stage, thiamine status was restored by daily injections of thiamine (10 mg/kg s.c.) for 3 days, after which the animals were killed, and their brains were processed for neuronal cell counts (cresyl violet staining), astrocytic proliferation [glial fibrillary acidic protein (GFAP) immunohistochemistry], and monoamine oxidase B (MAO-B) activity. All rats receiving l-deprenyl (all doses) had significantly decreased neuronal cell loss in thalamic nuclei, in the inferior colliculus, and in the inferior olive and had a concomitant decrease in reactive astrocytic proliferation compared with the thiamine-deficient, vehicle-treated rats. The neuroprotective effects of l-deprenyl in thiamine deficiency induced brain damage most likely result from its properties other than its effects as an MAO-B inhibitor.

Animals↗

PubMed1998

Regional activation of L-type voltage-sensitive calcium channels in experimental thiamine deficiency.

During pyrithiamine-induced thiamine deficiency (PTD), specific regions of the brain develop histological damage. The basis of this selective vulnerability is unknown but the mechanism may involve a glutamate-mediated excitotoxic process in affected structures, leading to alterations in membrane potential and disturbances in calcium homeostasis. In this study, we have examined the volume of distribution of [3H]nimodipine, an L-type voltage-sensitive calcium channel (VSCC) antagonist, in the brain of the PTD rat. An increase in specific binding of [3H]nimodipine was detected only in the posterior thalamus at the symptomatic stage, immediately following the loss of righting reflexes (P < 0.0001). There was also an increase in nonspecific binding in the medial geniculate and inferior colliculi. Replenishment with thiamine at the symptomatic stage returned [3H]nimodipine binding to normal levels. These findings provide evidence that depolarization and activation of L-type VSCCs occur in the posterior thalamus and may contribute to the appearance of histological lesions in this structure during experimental thiamine deficiency.

Animals↗

PubMed1999

Early microglial response in experimental thiamine deficiency: an immunohistochemical analysis.

Early glial changes have consistently been reported in experimental thiamine deficiency (TD) (Tellez and Terry, Am. J. Pathol. 52:777-794, 1968.) and in Wernicke Encephalopathy in humans (Victor et al., F.A. Davis Co., Philadelphia, 1989.). However, the precise nature of these changes and their relationship to the phenomenon of selective neuronal cell loss in TD has not been elucidated. In the present studies, antibodies against GFAP and ED1 were used to evaluate astrocytic and microglial/macrophagic changes respectively in adjacent sections of the brains of thiamine-deficient rats at various stages (n = 6 per stage) during the progression of encephalopathy. Additionally, the integrity of the blood-brain barrier at the same stages was assessed using IgG immunohistochemistry. Counts of immuno-positive cells revealed significant increases of ED1-immunostaining in the inferior olive, medial geniculate nucleus, and medial thalamic nuclei on day 8 of the treatment paradigm, prior to any evidence of increased IgG immunostaining or significant neuronal cell loss. ED1 immunostaining increased over time, resulting in intense staining by the loss of righting reflex stage (day 13-15). Focal increases of IgG-immunoreactivity in inferior olive, medial dorsal thalamus, and medial geniculate nucleus were observed on day 10, followed by increased GFAP-immunostaining consistent with reactive gliosis. Early microglial activation leading to the release of cytotoxic substances including reactive oxygen species, glutamate and cytokines appears to be the initial cellular response to TD and could be responsible for the focal neuronal loss characteristic of this disorder.

Animals↗

PubMed2005

Behavioral effects of prenatal folate deficiency in mice.

BACKGROUND: Folate supplementation decreases the incidence of birth defects such as neural tube defects (NTDs). We and others have shown that gestational dietary folate deficiency that does not produce overt NTDs can alter fetal neural histology. Accordingly, murine offspring were examined for the possible functional consequences of prenatal folate deficiency. METHODS: CD-1 mice were fed a diet of chow containing 400, 600, or 1200 nmol of folic acid/kg of chow for eight weeks prior to breeding and until GD18, at which time all dams were placed on folate-replete chow. Behavioral tests of male and female offspring included righting reflex, negative geotaxis, forelimb hanging, motor coordination, open field activity, and elevated plus maze activity. RESULTS: Of greatest significance, the adult offspring that were prenatally folate-deficient exhibited more anxiety-related behavior in the elevated plus maze. Offspring of the 400 nmol of folic acid/kg of chow diet group exhibited significantly shorter durations in the open arms and longer durations in the closed arms. Further, these two behaviors were dose-related. There was also a trend for the prenatally folate-deficient adult mice to exhibit more thigmotaxis (wall-hugging) behavior in the open field, entering the central area less frequently than controls. There were few other differences in tested behaviors between folate-deficient and folate-replete mice. CONCLUSIONS: Prenatal folate deficiency that is repleted at birth can manifest later with increased anxiety 9-12 weeks after birth.

Animals↗

PubMed1984

Studies on prenatal and postnatal development in rats exposed to 60-Hz electric fields.

A series of three experiments was performed to determine the effects of 30-day exposures to uniform 60-Hz electric fields (100 kV/m) on reproduction and on growth and development in the fetuses and offspring of rats. In the first experiment, exposure of females for 6 days prior to and during the mating period did not affect their reproductive performance, and continued exposure through 20 days of gestation (dg) did not affect the viability, size, or morphology of their fetuses. In the second experiment, exposure of the pregnant rat was begun on 0 dg and continued until the resulting offspring reached 8 days of age. In the third experiment, exposure began at 17 dg and continued through 25 days of postnatal life. In the second and third experiments, no statistically significant differences suggesting impairment of the growth or survival of exposed offspring were detected. In the second experiment, a significantly greater percentage of the exposed offspring showed movement, standing, and grooming at 14 days of age than among-sham-exposed offspring. There was a significant decrease at 14 days in the percentage of exposed offspring displaying the righting reflex in the second experiment and negative geotropism in the third experiment. These differences were all transient and were not found when the animals were tested again at 21 days of age. Evaluation of the reproductive integrity of the offspring of the second experiment did not disclose any deficits.

Age Factors↗

PubMedDate not supplied

The effects of dietary flaxseed on the Fischer 344 rat: I. Development, behaviour, toxicity and the activity of liver gamma-glutamyltranspeptidase.

The effect of exposure to, followed by consumption of, 10% flax chow from the 18th day of gestation to the 86th day after birth was examined in male and female Fischer 344 rats. Growth curves of the flax chow-fed rats were identical to those of regular chow-fed rats, as were such developmental milestones as pinna development, growth of hair and eye opening. Acoustical startle and the righting reflexes, developmental behavioural indices, were also the same. Blood glucose levels were comparable in flax chow-fed and regular chow-fed rats at all stages of development, indicating that flax is without effect on glucose balance. There were no signs of toxicity in the flax chow-fed rats since their plasma levels of alanine aminotransferase and gamma-glutamyltranspeptidase (gammaGT) were the same as those of regular chow-fed rats. The activity of gammaGT displayed an increase in the livers of flax chow-fed rats after puberty, more so in the male-four-fold-than in the female-1.38-fold. This is suggestive of an estrogenic effect which implicates an effect of an estrogenic flax lignan. An hepatobeneficial effect of the flax-induced increase in liver gammaGT is discussed. In summary, dietary 10% flax chow is without long-term effect on growth, development and behaviour, is non-toxic and may be hepatoprotective.

Animals↗

PubMed1975

The synthesis and pharmacology of a novel benzodiazepine derivative, 1-(beta-methylsulfonylethyl)-5-(o-fluorophenyl)-7-chloro-1,3-dihydro-2H-1,4-benzodiazepin-2-one (ID-622).

The pharmacological profiles of a new benzodiazepine derivative, 1-(beta-methylsulfonylethyl)-5-(o-fluorophenyl)-7-chloro-1,3-dihydro-2H-1,4-benzodiazepin-2-one (ID-622), were shown. In anti-convulsant test, ID-622 was more potent than diazepam and medazepam when tested with pentylenetetrazol or bemegride, but was less potent than diazepam tested with strychnine or MES in mice. Taming effects of ID-622 were more potent than diazepam in both electroshock- and isolation-induced fighting mice tests, but were less potent in both septal rats and O.B. rats tests. ID-622 had only a weak influence on the spontaneous locomotor activity, and did not cause the righting reflex loss. In EEG, ID-622 increased fast activity and depressed hippocampal I-waves and amygdala after-discharge in cats. Acute toxicity of ID-622 was very low.

Animals↗

PubMed2005

Movement suppression during anesthesia: neural projections from the mesopontine tegmentum to areas involved in motor control.

Microinjection of pentobarbital and GABA(A)-receptor agonists into a brainstem region we have called the mesopontine tegmental anesthesia area (MPTA; Devor and Zalkind [2001] Pain 94:101-112) induces a general anesthesia-like state. As in systemic general anesthesia, rats show loss of the righting reflex, atonia, nonresponsiveness to noxious stimuli, and apparent loss of consciousness. GABA(A) agonist anesthetics acting on the MPTA might suppress movement by engaging endogenous motor regulatory systems previously identified in research on decerebrate rigidity and REM sleep atonia. Anterograde and retrograde tracing revealed that the MPTA has multiple descending projections to pontine and medullary areas known to be associated with motor control and atonia. Prominent among these are the dorsal pontine reticular formation and components of the rostral ventromedial medulla (RVM). The MPTA also has direct projections to the intermediate gray matter and ventral horn of the spinal cord via the lateral and anterior funiculi. These projections show a rostrocaudal topography: neurons in the rostral MPTA project to the RVM, but only minimally to the spinal cord, while those in the caudal MPTA project to both targets. Finally, the MPTA has ascending projections to motor control areas including the substantia nigra, subthalamic nucleus, and the caudate-putamen. Projections are bilateral with an ipsilateral predominance. We propose that GABA(A) agonist anesthetics induce immobility at least in part by acting on these endogenous motor control pathways via the MPTA. Analysis of MPTA connectivity has the potential for furthering our understanding of the neural circuitry responsible for the various functional components of general anesthesia.

Anesthetics↗

PubMed1982

Brood patch function for the ventral scent gland of the female Mongolian gerbil, Meriones unguiculatus.

Infants of gerbil mothers whose ventral scent gland has been excised were compared on a number of developmental indices with pups of mothers who had had an equivalent section of lateral skin removed. The removal of the mother's ventral scent gland retarded the offsprings' pattern of ultrasounding during the 1st 21 days of development. In addition, infants from such mothers showed a retarded righting reflex. Inhibitions in the developmental behavior of gerbil pups might have resulted from less effective heat transfer during mother-pup contact. Indeed, excision of the gland resulted in lower ventral temperatures. The duality of function of the gland as an odor source for communication and as a heat source for offspring development suggests integrated communicative and thermoregulatory processes.

Animals↗

PubMed1984

The effects of prenatal exposure to predictable or unpredictable stress on early development in the rat.

Pregnant rats were exposed to different schedules of noise and light stress, and the development of their offspring was studied during the first 2 weeks of life. Motor development was measured by different tests: Righting reflex (Days 2-4); cliff avoidance (Days 4-10); turning on an inclined plane (Days 5-10); and swimming behavior (Days 6-10). Development of motivation-involved behavior was measured with a home-seeking test (Days 6-16). Other developmental landmarks such as acoustic response (Days 12-14) and eye-opening (Days 14-17) were also recorded. Thrice-weekly random stress resulted in a delay in the development of all behaviors studied. Daily stress exposure throughout pregnancy resulted in smaller litters with heavier pups, but otherwise normal behavioral and physical development. Rats exposed to daily stress during the last week of pregnancy only produced litters that did not differ in size and body weight, but that displayed accelerated development of all parameters (except for eye-opening) from Day 6 onwards. It is concluded that the unpredictable nature of prenatal stress is responsible for delays in behavior of offspring.

Animals↗

PubMed1990

Effects of prenatal alcohol exposure on rat pups' ability to elicit retrieval behavior from dams.

Research on fetal alcohol syndrome (FAS) has historically held that postnatal deficits result directly from prenatal alcohol exposure. Such exposure may alter infant behavior, and this in turn may affect maternal responsiveness and consequently increase the infant's risk for postnatal deficits. This study examined the effect of prenatal alcohol exposure on postnatal blood ethanol concentrations, pup development, and the ability of pups to elicit retrieval behaviors from the dam. Dams given access to a 15% ethanol solution throughout gestation and lactation showed blood ethanol concentrations of 0.1%, whereas their pups had concentrations below the sensitivity of the test. Prenatal alcohol exposure was shown to have pharmacological effects on the pup's righting reflex and nutritional effects on its rate of weight gain. Control pups were better able to elicit retrieval behavior from control and alcoholic dams than were fetally alcoholic pups. These results indicate that the condition of the pup can influence maternal responsiveness which, in turn, can influence pup development.

Animals↗

PubMed1997

Protective effect of L-carnitine in ammonia-precipitated encephalopathy in the portacaval shunted rat.

L-carnitine administration prevents the neurological symptoms of acute ammonia toxicity. To further evaluate its efficacy in the prevention of hepatic encephalopathy in hyperammonemic conditions, L-carnitine (16 mmol/kg, intraperitoneally [i.p.] was administered 1 hour before ammonium acetate (NH4OAc) (8.5 mmol/kg, subcutaneously) to portacaval shunted (PCS) rats. Cerebrospinal fluid (CSF) ammonia, lactate, and amino acid levels were measured in relation to deteriorating neurological status in these animals. None of 35 L-carnitine-treated animals showed neurological deterioration after NH4OAC administration compared with saline-treated controls; the latter manifested severe encephalopathy progressing through loss of righting reflex to coma. Survival rate was 100% in the L-carnitine-treated group compared with 5% in saline-treated controls. Following NH4OAC administration to PCS rats, CSF ammonia increased to 0.93 +/- 0.15 mmol/L and 1.24 +/- 0.15 mmol/L at precoma and coma stages of encephalopathy (P < .01) respectively. Treatment with L-carnitine reduced CSF ammonia at both precoma and coma stages; the time-course of this protective effect paralleled blood and CSF L-carnitine accumulation. CSF alanine and lactate increases following NH4OAC administration to PCS rats were significantly attenuated following L-carnitine treatment. However, L-carnitine treatment did not lead to significant reductions in plasma ammonia nor CSF or brain glutamine in these animals. These findings show the therapeutic efficacy of L-carnitine in ammonia-precipitated coma in PCS rats and suggest that this protective effect is centrally mediated involving improved mitochondrial respiration. L-carnitine could be of therapeutic benefit in the prevention of hepatic encephalopathy precipitated by ammoniagenic conditions in humans with chronic liver disease.

Amino Acids↗