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PubMed2005

Preventing dyslipidemia by Chlorella pyrenoidosa in rats and hamsters after chronic high fat diet treatment.

The effects of Chlorella pyrenoidosa on serum lipid profiles, after concomitant long-term treatment of high-fat diet (HFD) in rats and hamsters was studied. Wistar rats and Syrian hamsters were fed with or without various concentrations of Chlorella pyrenoidosa contained high-fat diet (CHFD) for 2, 4 and 8 weeks prior to assay of serum lipids. Fasting triglycerides, total cholesterol, and LDL cholesterol as well as HDL cholesterol levels in high-fat diet treated rats and hamster were determined. Results showed that triglycerides, total cholesterol and LDL cholesterol levels in HFD treated rats and hamsters were increased from the normal rodent diet (NRD) treated controls after 2, 4, and 8-week treatments. However, the presence of Chlorella pyrenoidosa in high-fat diets significantly decreased the levels of triglycerides, total cholesterol and LDL cholesterol with comparison to HFD group in rats and hamsters. The total cholesterol/HDL ratios, an indication of occurrence of coronary heart disease, were decreased in all CHFD treated grouped rats and hamsters which suggests administration of Chlorella pyrenoidosa could lower the occurring risk of heart diseases. In conclusion, Chlorella pyrenoidosa has the ability to prevent dyslipidemia in chronic high-fat fed animals and could be potential in use to prevent intestinal absorption of redundant lipid from our daily intake and subsequently to prevent hyperlipidemia as well as atherosclerosis.

Animals↗

PubMed2006

Cholinergic regulation of the central nucleus of the amygdala in rats: effects of local microinjections of cholinomimetics and cholinergic antagonists on arousal and sleep.

The amygdala has emerged as an important forebrain modulator of arousal. Acetylcholine plays a role in the regulation of sleep and wakefulness, particularly rapid eye movement sleep (REM). The major cholinergic input to the amygdala comes from the basal forebrain, a region primarily linked to wakefulness. We examined sleep and the encephalogram for 8 h following bilateral microinjections into the central nucleus of the amygdala (CNA) of the cholinergic agonist, carbachol (CARB(L): 0.3 microg; CARB(H): 3.0 microg), the acetylcholinesterase inhibitor, neostigmine (NEO(L): 0.3 microg; NEO(H): 3.0 microg), the muscarinic antagonist, scopolamine (SCO(L): 0.3 microg; SCO(H): 1.0 microg), the nicotinic antagonist, mecamylamine (MEC(L): 0.3 microg; MEC(H): 1.0 microg) and saline (SAL, 0.2 microl) alone. Both doses of CARB and NEO significantly reduced REM, but did not significantly alter non-rapid eye movement sleep (NREM). Both doses of SCO significantly increased NREM, and SCO(H) also produced an initial increase in REM followed by a significant decrease. CARB(H) and NEO(H) decreased REM electroencephalogram (EEG) power in the 5.5-10 Hz band, and NEO(L) and NEO(H) decreased NREM EEG power in the 0.5-5.0 Hz band. CARB(L) decreased waking EEG power in the 0.5-5.0 Hz band, and NEO(H) decreased waking EEG power in the 5.0-10.0 Hz band. Both doses of SCO significantly increased waking EEG power in the 5.5-10.0 Hz band. Compared with SAL, MEC did not significantly alter sleep or EEG power. The reduction of REM by CARB and NEO and the alteration of sleep by SCO indicate that cholinergic regulation of the amygdala is involved in the control of arousal in rodents. In contrast, CARB microinjections into CNA increase REM in cats, though the reasons for the species difference are not known. The results are discussed in the context of anatomical inputs and species differences in the cholinergic regulation of CNA.

Amygdala↗

PubMed2000

Incorporating observability thresholds of tumors into the two-stage carcinogenesis model.

This paper discusses a general way of incorporating the growth kinetics of malignant tumors with the two-stage carcinogenesis model. The model is presented using time-homogeneous rate parameters. In that case, the differential equations comprising the model are straightforward to solve using standard numerical techniques and software. An extension of the method to time-dependent rate parameters is included in Appendix A. Allowing the rate parameters to be time-dependent does incur computational cost. An expression is given for the expected time without visible tumor, a generalization of the expected time to an observable tumor that includes the possibility of tumor regression. The model is illustrated using incidental liver tumor data in control rats from NTP rodent carcinogenicity studies, using linear birth-death kinetics of tumors combined with a non-absorbing detection limit. The approach is also shown to be potentially useful with tumor observability thresholds having more complicated features.

Animals↗

PubMed2003

Effects of caloric restriction on cognition and behavior in developing mice.

The effects of caloric restriction (CR) on cognition and behavior in developing mice were investigated in this study. Male and female Kunmin mice were fed a standard rodent diet ad libitum (Control); 80% of control (20% CR) or 65% of control (35% CR) for 6 months. Body weight gain was significant reduced in CR mice relative to control. Learning and memory retention test in a Y maze demonstrated that CR increased learning but not retention in male mice, whereas CR did not affect learning or retention in females. Open field test revealed no difference in exploratory activity between CR and control mice. These findings suggest that CR produce sex-dependent effect on cognition, but not exploratory activity, in developing animals.

Aging↗

PubMed2000

Higher ketogenic diet ratios confer protection from seizures without neurotoxicity.

The present study was designed to establish a dose-response relationship for the efficacy of the ketogenic diet (KD). Sprague-Dawley rats were fed ketogenic diets containing varying ratios of fats; (carbohydrates + proteins) whereas control animals were fed rodent chow. Unless otherwise indicated, all animals were fed calorie-restricted, isocaloric diets beginning at P37 and ketonemia, seizure threshold and neurotoxic effects were determined. Despite being provided isocaloric quantities, animals fed lower ketogenic ratios gained weight relative to those fed diets having greater proportions of fats. A significantly increased metabolic rate was noted for animals fed a high-fat diet, suggesting a basis for the weight differences. Results also showed that the animals fed calorie-restricted high-fat diets exhibited significant ketonemia and protection from pentylenetetrazole (PTZ)-induced seizures. There were no detectable neurotoxic effects for any diet group. For animals of the same age, there was no correlation between beta-hydroxybutyrate (beta-OHB) and seizure threshold. These findings suggest that beta-OHB is not directly involved in the anticonvulsant mechanism of the diet. Also, data presented here show that the conventional 4:1 ketogenic diet does not confer the greatest level of seizure protection. We conclude that a 6:1 ketogenic diet, which shows no evidence of neurotoxicity, may be maximally efficacious in rats.

3-Hydroxybutyric Acid↗

PubMed2003

Sucrose feeding effects inhibition of gamma-glutamyltranspeptidase in the liver of the rat: possible mediation by thyroid hormone.

The effect of sucrose on Fischer 344 rat liver gamma-glutamyltranspeptidase (gammaGT) was studied: in adults fed sucrose for 3 weeks; and rats exposed to sucrose from the 18th day of gestation to the 40th day after birth. Rats fed regular rodent chow served as controls. Sucrose caused mild lipemia; and in the liver an increase in size and fat build-up without damage. In adult sucrose-fed rats, compared to controls, plasma glucose levels were increased: 1.12-, 1.40- and 1.13-fold after 24, 48h and 3 week consumption of sucrose, respectively. Insulin levels were unaltered for the first week of sucrose consumption but increased from control levels: 16% at 1 week, and 2.0-fold at 3 weeks. The T3 levels were comparable to control levels 24h after the sucrose was started and were increased: 1.22-, 1.13- and 1.12-fold at 48h, 1 and 3 weeks, respectively. The T4 levels were comparable at all time points between sucrose-fed and control rats. Liver gammaGT activity exhibited a steady decrease from control levels: after 24, 48h, 1 and 3 weeks of sucrose feeding the decrease was 5, 8, 21 and 37%, respectively in homogenates; and 10, 17, 24 and 41%, respectively in plasma membranes. Perinatal sucrose exposure effected in 40-day-old rats, compared controls: a 1.09-fold increase in plasma glucose; no change in plasma insulin; an increase of 1.15- and 1.39-fold in plasma levels of total and free T3, respectively; a decrease of 20 and 14% in plasma levels of total and free T4, respectively. gammaGT activity was decreased in liver plasma membranes isolated from sucrose-exposed rats relative to those of control: 80% in the male; 82% in the female. Relative specific activities of gammaGT were the same in both males: 15.4 and 16.1 in control and sucrose-exposed male rats, respectively; and females: 14.1 and 15.4 in control and sucrose-exposed female rats, respectively. gammaGT was 2-fold higher in the livers of female relative to male rats in sucrose-exposed and control groups. Kidney gammaGT activities were the same in control and sucrose-exposed rats. The involvement of T3 in the sucrose-induced decrease in liver gammaGT is discussed.

Age Factors↗

PubMed1989

Models to assess the potential of Capillaria hepatica to control population outbreaks of house mice.

Population outbreaks of house mice (Mus domesticus) occur periodically in the wheatlands of southeastern Australia. This paper uses mathematical models to assist in the evaluation of the potential of a nematode, Capillaria hepatica, as a biological control agent to reduce the severity of these 'plagues'. C. hepatica is unique amongst helminths of mammals in that its eggs are released only upon the death of an infected host. The major goal of the modelling in this paper is to determine the impact of this feature on the population dynamics of the host-parasite interaction. Simple differential equation models are used to examine the general properties of the system and determine which population parameters are most crucial to the outcome of the interaction. These models are supplemented by age-structured models which investigate the initial behaviour of the system after introduction of the parasite. The necessity of host death for transmission is a strongly destabilizing factor, suggesting that C. hepatica cannot regulate most populations stably in the absence of strong resource limitation, although it has the potential to depress mouse populations below infection-free levels. Although C. hepatica influences mouse fecundity at lower burdens than it affects mortality, the age-structured models show that parasite-induced host death cannot be neglected. Because transmission requires host death, the parasite life-cycle operates on a time-scale similar to that of the hosts, and introduction of the parasite as early as possible in the development period of an outbreak will therefore be necessary to achieve substantial reductions in plague intensity.

Animals↗

PubMed1999

Control of milk secretion and apoptosis during mammary involution.

Lactation depends on regular suckling or milking of the mammary gland. Without this stimulus, milk secretion stops and mammary involution is induced. Involution caused by abrupt cessation of milk removal is characterized by de-differentiation and apoptosis of mammary epithelial cells, the extent and time course of the latter varying between species. Apoptosis is inhibited and milk secretion is restored by re-suckling, if milk stasis is of short duration. Mammary involution and apoptosis also occur during weaning, even in concurrently-pregnant animals when the interval between lactations is restricted, suggesting that tissue remodeling is essential for subsequent lactation. Declining milk production in ruminants after peak lactation is also associated with, and probably results from, net cell loss by apoptosis. Involution and apoptosis are controlled by changes in systemic galactopoietic hormone levels, and by intra-mammary mechanisms responsive to milk removal. Milk stasis precipitated by litter removal or cessation of milking may involve intra-mammary control related to physical distension of the epithelium. Local control of apoptosis in rodents during weaning, and after peak lactation in dairy animals, may be due to the actions of milk-borne survival factors or their inhibitors, and can be manipulated by frequency of milk removal.

Animals↗

PubMed1999

Creation of human tumour cells with defined genetic elements.

During malignant transformation, cancer cells acquire genetic mutations that override the normal mechanisms controlling cellular proliferation. Primary rodent cells are efficiently converted into tumorigenic cells by the coexpression of cooperating oncogenes. However, similar experiments with human cells have consistently failed to yield tumorigenic transformants, indicating a fundamental difference in the biology of human and rodent cells. The few reported successes in the creation of human tumour cells have depended on the use of chemical or physical agents to achieve immortalization, the selection of rare, spontaneously arising immortalized cells, or the use of an entire viral genome. We show here that the ectopic expression of the telomerase catalytic subunit (hTERT) in combination with two oncogenes (the simian virus 40 large-T oncoprotein and an oncogenic allele of H-ras) results in direct tumorigenic conversion of normal human epithelial and fibroblast cells. These results demonstrate that disruption of the intracellular pathways regulated by large-T, oncogenic ras and telomerase suffices to create a human tumor cell.

Animals↗

PubMed1997

Influence of dietary selenium on the disposition of arsenate in the female B6C3F1 mouse.

Interactions between arsenic (As) and selenium (Se) at the metabolic level are multifaceted and complex. These interactions are of practical significance because populations in various parts of the world are simultaneously exposed to inorganic As in drinking water and Se mainly in the diet at varying levels. The primary goal of this study was to investigate whether differing dietary Se status would alter the profile of urinary metabolites or their time course for elimination after exposure to arsenate [As(V)]. Weanling female B6C3F1 mice were maintained for 28 d on either a control diet of powdered rodent meal sufficient in Se (A, 0.2 ppm) or Torula yeast-based (TYB) diets deficient (B, 0.02 ppm Se), sufficient (C, 0.2 ppm Se), or excessive (D, 2.0 ppm Se) in Se; mice then received by oral gavage 5 mg (As)/kg as sodium [73As] arsenate. The time course for elimination of total arsenic and metabolites in urine was measured over a 48-h period, and total arsenic was determined in feces and tissues at 48 h. Mice on the Se excess diet excreted a significantly higher percentage of urinary As as inorganic As, with a significantly decreased ratio of organic to inorganic As compared to Se-sufficient mice, suggesting that As methylation was decreased. Mice on the Se-deficient diet appeared to eliminate As(V), arsenite, and dimethylarsinic acid (DMA) in urine more slowly than Se-sufficient mice; however, further studies are required to confirm this finding. Mice on the Se-sufficient meal diet (A) excreted significantly less (by percent) arsenate-derived radioactivity in urine and more in feces compared to mice on the Se-sufficient TYB diet (C), with total elimination being similar for both groups. This indicates that mice on the meal diet absorbed significantly less As(V) than mice on the TYB diet, and this may be due to more fiber or "bulk" in the meal diet. This finding emphasizes the importance of considering dietary composition when interpreting and comparing As disposition studies. Overall this study provides suggestive evidence that dietary Se status alters As metabolism and disposition. This indicates that dietary Se status may be an issue that should be considered in the design and interpretation of epidemiologic studies.

Analysis of Variance↗

PubMed2005

Rapid discovery of putative protein biomarkers of traumatic brain injury by SDS-PAGE-capillary liquid chromatography-tandem mass spectrometry.

We report the rapid discovery of putative protein biomarkers of traumatic brain injury (TBI) by SDS-PAGE-capillary liquid chromatography-tandem mass spectrometry (SDS-PAGE-Capillary LC-MS(2)). Ipsilateral hippocampus (IH) samples were collected from naive rats and rats subjected to controlled cortical impact (a rodent model of TBI). Protein database searching with 15,558 uninterpreted MS(2) spectra, collected in 3 days via data-dependent capillary LC-MS(2) of pooled cyanine dye-labeled samples separated by SDS-PAGE, identified more than 306 unique proteins. Differential proteomic analysis revealed differences in protein sequence coverage for 170 mammalian proteins (57 in naive only, 74 in injured only, and 39 of 64 in both), suggesting these are putative biomarkers of TBI. Confidence in our results was obtained by the presence of several known biomarkers of TBI (including alphaII-spectrin, brain creatine kinase, and neuron-specific enolase) in our data set. These results show that SDS-PAGE prior to in vitro proteolysis and capillary LC-MS(2) is a promising strategy for the rapid discovery of putative protein biomarkers associated with a specific physiological state (i.e., TBI) without a priori knowledge of the molecules involved.

Amino Acid Sequence↗

PubMed1997

Leptin receptor gene variation and obesity: lack of association in a white British male population.

Leptin, a hormone secreted by adipocytes, plays a pivotal role in the control of body weight. Rodents with mutations in the leptin receptor gene develop morbid obesity. It is possible, therefore, that leptin receptor gene mutations contribute to human obesity. To test this possibility, we determined the entire coding sequence of the human leptin receptor cDNA from peripheral blood lymphocytes of 22 morbidly obese patients with body-mass index (BMI) between 35.1 and 60.9 kg/m2. We identified five common DNA sequence variants distributed throughout the coding sequence at codons 109, 223, 343, 656 and 1019, one rare silent mutation at codon 986 and one novel alternatively spliced form of transcript. None of the five common variants, including the three that predict amino acid changes, are null mutations causing morbid obesity, because homozygotes for the variant sequences were also found in lean subjects. Furthermore, the frequency of each variant allele and the distribution of genotypes and haplotypes were similar in 190 obese (BMI >28 kg/m2) and 132 lean (BMI <22 kg/m2) white British males selected from a population-based epidemiological survey. In these subjects, there was no evidence for a significant effect of the common variants on obesity or obesity-related phenotypes. These results suggest that mutations in the leptin receptor gene are not a common cause of human obesity.

Adult↗

PubMed2002

Effects of dietary restriction on growth, neurobehavior, and reproduction in developing Kunmin mice.

The effects of dietary restriction (DR) on growth, neurobehavior, and reproduction in developing Kunmin mice were investigated in this study. Male and female mice were fed a standard rodent diet ad libitum (control), 80% of control (20% DR), or 65% of control (35% DR) for 3 months. Body weight of DR mice was reduced relative to control except that of females in the 20% DR group (no difference as compared with control group). Learning and memory retention test in a Y maze demonstrated that DR increased learning, but not retention, in male mice, whereas neither learning nor retention was affected in females. The open-field test revealed no difference in exploratory activity in all groups. Reproductive assessment showed that 35% DR retarded the maturation of reproductive function and reduced fertility compared with other groups. Furthermore, both 20% and 35% DR led to a lower level of sperm motility and a higher level of abnormal sperm relative to control mice. These findings indicate that DR does not cause damaging effects on growth and neurobehavior, but imposes a risk to reproductive development events.

Animals↗

PubMed1991

Hormonal manipulation of the prenatal environment alters reproductive morphology and increases longevity in autoimmune NZB/W mice.

Steroid hormones, which affect development of reproductive traits, alter immune responses in rodents and appear to control severity of disease in F1 hybrid NZB/W mice, an animal model of systemic lupus erythematosus. We tested the hypothesis that exposure of NZB/W fetuses to altered hormonal environments would influence subsequent expression of autoimmune renal disease and affect longevity. NZB females, pregnant with NZB/W fetuses, were treated from Days 13-18 of gestation with testosterone or the antiandrogen, flutamide. Similar treatments were carried out in C57BL/6 dams mated to DBA/2 males to permit comparison with nonautoimmune hybrid mice. Serum concentrations of testosterone were greater in testosterone-implanted dams of both strains, but concentrations of estradiol were greater only in C57BL/6 dams treated with flutamide. Alpha fetoprotein (AFP), which binds estrogen and modulates immune responsiveness, was greater in serum from both groups of testosterone-treated dams, while flutamide treatment increased serum AFP only in NZB dams. We conclude that factors governing circulating estradiol and AFP differed in pregnant NZB and C57BL/6 females. Morphological analyses confirmed effects of hormonal manipulation on the developing fetuses. Testosterone implants resulted in female offspring with greater anogenital spaces, and treatment of dams with flutamide eliminated the expected difference between anogenital spaces in females and males. Effects of altered prenatal hormonal environments on immune-mediated disease in NZB/W offspring were examined in a longevity study. Early deaths were delayed in NZB/W females produced by flutamide-treated dams. An unexpected result was observed in NZB/W males. Male offspring from both testosterone- and flutamide-treated mothers lived longer than males from control dams. This paradox suggested that a characteristic shared by both groups of treated NZB dams had similar effects on the developing fetuses. It is proposed that elevated concentrations of AFP modulated the course of autoimmune disease and contributed to increased longevity in NZB/W offspring of treated dams.

Animals↗

PubMed1990

Effect of mechanical ventilation on systemic oxygen extraction and lactic acidosis during early septic shock in rats.

We studied the effect of mechanical ventilation on systemic oxygen extraction and lactic acidosis in peritonitis and shock in rats. Sepsis was induced by cecal ligation and perforation. After tracheostomy, rats were randomized to spontaneous breathing (S) or mechanical ventilation with paralysis (V). Five animals were studied in each group. The V animals were paralyzed with pancuronium bromide to eliminate respiratory effort. Mechanical ventilation consisted of controlled ventilation using a rodent respirator with periodic adjustment of minute ventilation to maintain PaCO2 and pH within normal range. Arterial and central venous blood gases and thermodilution cardiac output were measured at baseline before abdominal surgery, and sequentially at 0.5, 3.5, and 6 h after surgery. At 6 h, cardiac output was 193 +/- 30 ml/kg.min in S animals and 199 +/- 32 ml/kg.min in V animals (NS). The central venous oxygen saturation was 27.4 +/- 4.7% in S animals and 30.0 +/- 6.4% in V animals (NS). Systemic oxygen extraction was 70 +/- 5% in S animals and 67 +/- 6% in V animals (NS). Arterial lactate was 2.4 +/- 0.4 mmol/L in S animals and 2.2 +/- 0.5 mmol/L in V animals (NS). The S animals developed lethal hypotension at 6.6 +/- 0.4 h compared to 6.8 +/- 0.4 h in V animals (NS). These data suggest that mechanical ventilation does not decrease systemic oxygen extraction or ameliorate the development of lactic acidosis during septic shock.

Acidosis, Lactic↗

PubMed1998

Repair of nasal defects using collagen gels containing insulin-like growth factor 1.

OBJECTIVE: Facial osseous defects are a common and challenging problem for the otolaryngologist-head and neck surgeon. Current methods of repair including synthetic grafts, cadaveric material, and autologous tissue have drawbacks of foreign body reactions, infectious agent transmission, and the morbidity of a second surgical site. In the effort to develop an ideal technique for osseous reconstruction, a critical-size facial defect has previously been developed in the Sprague-Dawley rat. This model exhibits less than 10% healing by surface area over 6 months. A novel approach to osseous reconstruction is attempted using this model with type I collagen gel augmented with insulin-like growth factor 1 (IGF-1). STUDY DESIGN: Randomized controlled trial using a rodent model. METHODS: Twelve adult male Sprague-Dawley rats underwent a surgical procedure to produce a critical-size nasal defect by removing the nasal bones with a cutting burr. Six animals were repaired with 300 microg of type I collagen gel. Six animals were repaired with 300 microg of type I collagen gel augmented with 3.0 microg of IGF-1. Thirty days later, the animals were examined after necropsy. Precise planimetry, radiodensitometric analysis, and histologic sectioning were performed. RESULTS: All animals had complete coverage of this defect with a thin layer of bone. Radiodensitometric analysis indicated that there was a statistically significant (P < .037) increase in bone density in the collagen plus IGF-1 group compared with that of collagen only. In addition, histologic evaluation revealed increased bone density and thickness in the IGF-1 group. CONCLUSION: Type I collagen gel augmented with IGF-1 results in a significant increase in healing of a nasal critical-size defect in a rodent model.

Absorptiometry, Photon↗

PubMed2000

Effect of photodynamic therapy on revascularization of fasciocutaneous flaps.

OBJECTIVE: Photodynamic therapy (PDT) may be used as an adjuvant intraoperative treatment to improve locoregional control. PDT has been shown both to delay wound healing and to have a deleterious effect on flap survival after a primary ischemic insult. This delay in wound healing may make the flap dependent on its pedicled blood supply for a prolonged period. Long-term flap loss may be experienced. The effect of PDT on flap revascularization, with subsequent dependence on its vascular pedicle, is evaluated. STUDY DESIGN: Randomized controlled trial using a rodent model. METHODS: A rat fasciocutaneous flap was used. Study groups were as follows: group I received no treatment; group II received treatment with 630-nm light; groups IH and IV were given Photofrin (in group III, loupes without a fiberoptic light source were used for flap elevation, and in group IV, light source was employed); and group V was given Photofrin and 630-nm light. Primary ischemic times of 2 or 4 hours were used. Vascular pedicles were ligated on postoperative day (POD) 5, 6, or 7, and percentage of flap survival was evaluated 7 days later. RESULTS: With 2 hours of ischemia, revascularization was decreased in the PDT group on POD 6 (P < .05) and on day 7 (P < .005) when compared with the other groups. With 4 hours of ischemia, revascularization was decreased in the PDT group on PODs 5 (P < .001), 6 (P < .01), and 7 (P < .005). CONCLUSION: Intraoperative PDT decreases revascularization of a rat fasciocutaneous flap.

Animals↗

PubMed1988

Review: the enterochromaffin-like cell, intragastric acidity and the trophic effect of plasma gastrin.

Although enterochromaffin-like (ECL) cells form the major endocrine cell population of the non-antral stomach, they have been largely overlooked in the study of gastric disease. In the human, their product and functions are unknown, but they are associated with histamine secretion in rodents. The cells are controlled by neural and hormonal factors, the most significant of the latter being gastrin. Interest in ECL cells has been stimulated by the observation that hyperplasia of these cells, sometimes leading to formation of gastric carcinoid tumours, occurs in conditions of persistent hypergastrinaemia - for example, in response to the achlorhydria of individuals with pernicious anaemia. The advent of new highly potent inhibitors of gastric acid secretion is allowing more information to be obtained on the physiology and functions of the ECL cell. However, there is clearly a great deal more to be discovered about this enigmatic endocrine cell type.

Animals↗