PubMed Health⌕ Search

Biomedical subjects

C Dubé

Publications and source records attributed to C Dubé.

At least 19 recordsLinked to original sources
PubMed2004

Quantitative polygraphic controlled study on efficacy and safety of oral splint devices in tooth-grinding subjects.

The efficacy of occlusal splints in diminishing muscle activity and tooth-grinding damage remains controversial. The objective of this study was to compare the efficacy and safety of an occlusal splint (OS) vs. a palatal control device (PCD). Nine subjects with sleep bruxism (SB) participated in this randomized study. Sleep laboratory recordings were made on the second night to establish baseline data. Patients then wore each of the splints in the sleep laboratory for recording nights three and four, two weeks apart, according to a crossover design. A statistically significant reduction in the number of SB episodes per hour (decrease of 41%, p = 0.05) and SB bursts per hour (decrease of 40%, p < 0.05) was observed with the two devices. Both oral devices also showed 50% fewer episodes with grinding noise (p = 0.06). No difference was observed between the devices. Moreover, no changes in respiratory variables were observed. Both devices reduced muscle activity associated with SB.

Adult↗
PubMed2004

Celiac disease.

Explore the source record for details and available documents.

Adult↗
PubMed2003

Transfer of protein from milk to cheese.

This report concerns measurement of paracasein in milk and transfer of protein from milk to cheese. In the main experiment, two vats of Cheddar cheese were made from each of 11 lots of milk from one large herd over a period of 7 mo. Exclusion of solutes from moisture in paracasein micelles in milk and cheese was central to estimation of paracasein and to the transfer of protein from milk to cheese and whey. Solute-exclusion by paracasein and its changes during cheesemaking could be visualized by considering paracasein micelles to be a very fine sponge. The sponge excludes solutes, especially the large solutes like whey proteins. The sponge shrinks during cheesemaking and expels solute-free liquid, thereby slightly diluting the whey surrounding the micelles inside the curd. Paracasein N in milk was calculated as the difference between total milk N and rennet whey N, the latter adjusted to its level in milk. Adjustment used appropriate solute-exclusion factors (h) of the protein fractions of whey and 1.08 for paracasein and associated salts. They were combined to give a factor Fpc, which adjusted the level of rennet whey N to its level in milk: 1.001 x (1 - 1.01 x FM/100 - Fpc x pc/100), where FM = fat in milk, pc = estimated paracasein, and 1.001 = dilution of milk by chymosin and CaCl2. The mean Fpc was 3.03. Differences in values were small among different procedures for calculating paracasein, but they are considered to be important because they represent biases, which, in turn, are important in analyses commercially. We conclude that solute exclusion by moisture in paracasein must have decreased during cheesemaking because the ratio of moisture to paracasein in the final cheese was 1.5, much less than the h of 2.6 for serum proteins by paracasein. Release of solute-excluding moisture from paracasein during cooking was likely the reason for lower total N in cheese whey than in the rennet whey in the paracasein analysis. Paracasein, estimated to be in cheese, curd fines, salted whey, and whey during cheddaring, was 98.21, 0.20, 0.25 and 0.19%, respectively, of the paracasein in milk for a total of 98.85% (SD of 22 vats = 0.46); the location of the missing paracasein is not known. On the other hand, recovery of milk N in cheese and wheys was 99.92% (SD = 0.37%). Nitrogen in paracasein and its hydrolysis products in cheese was estimated to be 98.51% of total cheese N. Proteose-peptone from milk appeared not to be included with the paracasein in appreciable amounts. Some was apparently included with denatured serum proteins during Rowland fractionation of whey, perhaps as a coprecipitate. Measured paracasein would include fat globule membrane proteins in milk containing fat, and denatured whey proteins in heated milks. It was concluded that the method of measurement and the associated calculations are integral parts of the definition and quantification of paracasein in milk.

Animals↗
PubMed2001

Relationship between neuronal loss and interictal glucose metabolism during the chronic phase of the lithium-pilocarpine model of epilepsy in the immature and adult rat.

The lithium-pilocarpine (Li-Pilo) model of epilepsy reproduces most of the features of human temporal lobe epilepsy. After having studied the metabolic changes occurring during the silent phase, in the present study, we explored the relationship between interictal metabolic changes and neuronal loss during the chronic phase following status epilepticus (SE) induced by Li-Pilo in 10-day-old (P10), 21-day-old (P21), and adult rats. Rats were observed and their EEG was recorded to detect the occurrence of spontaneous recurrent seizures (SRS). Local cerebral glucose utilization was measured during the interictal period of the chronic phase, between 2 and 7 months after SE, by the [(14)C]2-deoxyglucose method in rats subjected to SE at P10, P21, or as adults. Neuronal damage was assessed by cell counting on adjacent cresyl violet stained sections. When SE was induced at P10, rats did not become epileptic, did not develop lesions and cerebral glucose utilization was in the normal range 7 months later. When SE was induced in adult rats, they all became epileptic after a mean duration of 25 days and developed lesions in the forebrain limbic areas, which were hypometabolic during the interictal period of the chronic phase, 2 months after SE. When SE was induced in P21 rats, 24% developed SRS, and in 43% seizures could be triggered (TS) by handling, after a mean delay of 74 days in both cases. The remaining 33% did not become epileptic (NS). The three groups of P21 rats developed quite comparable lesions mainly in the hilus of the dentate gyrus, lateral thalamus, and entorhinal cortex; at 6 months after SE, the forebrain was hypometabolic in NS and TS rats while it was normo- to slightly hypermetabolic in SRS rats. These data show that interictal metabolic changes are age-dependent. Moreover, there is no obvious correlation, in this model, between interictal hypometabolism and neuronal loss, as reported previously in human temporal lobe epilepsy.

Action Potentials↗
PubMed2001

A coelectroporation method for the isolation of cryptic plasmids from Lactococcus lactis.

AIMS: A coelectroporation method using a marker plasmid for indirect selection of lactococcal plasmids with unassigned functions was evaluated. METHODS AND RESULTS: Cryptic plasmids were mixed with an erythromycin resistance (Eryr) marker plasmid and introduced into a recipient strain by electroporation, followed by plasmid extraction of erythromycin-resistant transformants. By optimizing the ratio between the marker plasmid and the cryptic plasmids, an average of 20% cotransformants was obtained, including combinations of more than one cryptic plasmid. The marker plasmid pSA3 was easily eliminated from the cotransformed cells by subculture without selective pressure. CONCLUSION: This cotransformation approach reduces the number of colonies that must be screened to find transformants harbouring cryptic plasmids. SIGNIFICANCE AND IMPACT OF THE STUDY: The method facilitates the isolation of cryptic plasmids, helps in assigning functions to unknown plasmids and allows construction of food-grade lactococcal strains with new combinations of wild-type plasmids.

Anti-Bacterial Agents↗
PubMed2001

Capacitation is associated with tyrosine phosphorylation and tyrosine kinase-like activity of pig sperm proteins.

Capacitation represents the final maturational steps that render mammalian sperm competent to fertilize, either in vivo or in vitro. Capacitation is defined as a series of events that enables sperm to bind the oocyte and undergo the acrosome reaction in response to the zona pellucida. Although the molecular mechanisms involved are not fully understood, sperm protein phosphorylation is associated with capacitation. The hypothesis of this study is that protein tyrosine phosphorylation and kinase activity mediate capacitation of porcine sperm. Fresh sperm were incubated in noncapacitating or capacitating media for various times. Proteins were extracted with SDS, subjected to SDS-PAGE, and immunoblotted with an antiphosphotyrosine antibody. An M(r) 32 000 tyrosine-phosphorylated protein (designated as p32) appeared only when the sperm were incubated in capacitating medium and concomitant with capacitation as assessed by the ionophore-induced acrosome reaction. The p32 was soluble in Triton X-100. Fractionation of sperm proteins with Triton X-114 demonstrated that after capacitation, this tyrosine phosphoprotein is located in both the cytosol and the membrane. Enzyme renaturation of sperm proteins was conducted in gels with or without either poly glu:tyr (a tyrosine kinase substrate) or kemptide (a protein kinase A substrate). An M(r) 32 000 enzyme with kinase behavior was observed in all gels but was preferentially phosphorylated on tyrosine, as assessed by phosphorimagery and by thin layer chromotography to identify the phosphoamino acids. Indirect immunolocalization showed that the phosphotyrosine residues redistribute to the acrosome during capacitation, which is an appropriate location for a protein involved in the acquisition of fertility.

Animals↗
PubMed2001

Age-dependent consequences of seizures and the development of temporal lobe epilepsy in the rat.

The age-related functional changes underlying epileptogenesis remain to be clarified. In the present study, we explored the correlation between metabolic changes, neuronal damage and epileptogenesis during the acute, silent and chronic phases following status epilepticus (SE) induced by lithium-pilocarpine (Li-Pilo) in 10- (P10), 21-day-old (P21) and adult rats. Local cerebral metabolic rates for glucose (LCMRglcs) were measured by the [14C]2-deoxyglucose method during SE, the silent period and the interictal phase of the chronic period. Neurodegeneration was assessed by cresyl violet staining. During SE, LCMRglcs dramatically increased at all ages mainly in forebrain vulnerable regions. During the silent phase, in P21 and adult rats, metabolic decreases were recorded in damaged forebrain regions involved in the genesis and propagation of seizures 14 days after SE. At the end of the silent phase, P21 and adult rats exhibited metabolic increases in intact brainstem areas involved in the remote control of epilepsy. During the interictal phase of the chronic period, LCMRglcs decreased in damaged forebrain areas of adult and P21 rats that were not spontaneously epileptic, while LCMRglcs were similar to control levels in epileptic P21 rats. In P10 rats, there was no damage and no metabolic consequences at any time after SE. In conclusion, the process of epileptogenesis and its functional consequences differ in P21 and adult rats. The factors underlying these age-related differences remain to be explored.

Age Factors↗
PubMed2000

Progressive metabolic changes underlying the chronic reorganization of brain circuits during the silent phase of the lithium-pilocarpine model of epilepsy in the immature and adult Rat.

The lithium-pilocarpine (Li-Pilo) model of epilepsy reproduces most of the features of human temporal lobe epilepsy. In the present study, we explored the correlation between metabolic changes, neuronal damage, and epileptogenesis during the silent phase following status epilepticus (SE) induced by Li-Pilo in 10- (P10) and 21-day-old (P21) and adult rats. Cerebral metabolic rates for glucose (CMR(glcs)) were measured at 14 and 60 days after SE by the 2-[(14)C]deoxyglucose method and neurodegeneration was assessed by the silver staining and cresyl violet techniques. In P10 rats, there was no damage and no metabolic consequences at any time after SE. In P21 rats, metabolic decreases were recorded at 14 days after SE, mainly in damaged forebrain regions. Conversely at 60 days after SE, P21 rats exhibited metabolic increases in both forebrain-damaged and brain-stem-intact areas. Finally, in adult rats studied at 14 days after SE, CMR(glcs) decreased in damaged forebrain areas involved in the circuitry of spontaneous seizures and increased in nondamaged brain-stem areas involved in the remote control of epilepsy. The increase in CMR(glcs) in damaged forebrain areas of P21 rats at 60 days after SE may reflect the genesis of a new circuitry underlying the occurrence of spontaneous seizures. The metabolic increase recorded in nondamaged brain-stem areas of P21 and adult rats occurs in regions involved in the remote control of seizures and might underlie a process of protection against the occurrence of seizures.

Age Factors↗
PubMed2000

Synergistic action of endothelin (ET)-1 on the activation of bronchial fibroblast isolated from normal and asthmatic subjects.

Bronchial subepithelial fibrosis is an histological characteristic of asthma. Cytokines and other mediators, such as PDGF-BB, TGF-beta1 and ET-1 found in the asthmatic submucosa can potentially activate a repair process that leads to fibroblast proliferation and collagen synthesis. The mechanisms of modulation of the repair process leading to extracellular matrix deposition are still to be documented. In this study, we assessed the in vitro proliferation and collagen synthesis of bronchial fibroblasts isolated from normal and asthmatic subjects in response to ET-1, platelet-derived growth factor (PDGF)-BB and transforming growth factor (TGF)-beta1 alone or in combination, in the presence or absence of dexamethasone. The combination of ET-1 with one of the other two growth factors, or the triple combination, significantly increased DNA synthesis and collagen production of bronchial fibroblasts isolated from both normal and asthmatic subjects, but the same growth factors used separately had no significant effect on the same parameters. These results suggest that the simultaneous presence of ET-1, PDGF-BB and TGF-beta1 in both normal and asthmatic subjects is necessary to activate bronchial fibroblast proliferation and collagen synthesis. As these mediators are present in the submucosa of the asthmatic bronchi, they could be responsible, at least in part, for the accumulation of collagen in the mucosa.

Analysis of Variance↗
PubMed2000

A metabolic and neuropathological approach to the understanding of plastic changes that occur in the immature and adult rat brain during lithium-pilocarpine-induced epileptogenesis.

PURPOSE: The age-related functional changes that underlie epileptogenesis remain to be clarified. In the present study, we explored the correlation between metabolic changes, neuronal damage, and epileptogenesis during the silent and chronic phases after status epilepticus (SE) induced by lithium-pilocarpine in 10-day-old (P10), 21-day-old (P21), and adult rats. METHODS: Local cerebral metabolic rates for glucose (LCMRglcs) were measured by the [14C]2-deoxyglucose method during the silent period (14 and 60 days after SE in P10 and P21 rats and only at 14 days after SE in adult rats because the silent phase lasts for about 14 days in adults and 60 days in P21 rats) and the interictal phase of the chronic period (2 months after spontaneous seizures or 6 to 7 months after SE in P10 and P21 rats that do not become epileptic). Neurodegeneration was assessed by the silver staining and cresyl violet techniques. RESULTS: In P10 rats, there was no damage and no metabolic consequences at any time after SE. During the silent phase in P21 rats, metabolic decreases were recorded at 14 days after SE, mainly in damaged forebrain regions. At 60 days after SE, P21 rats exhibited metabolic increases in both damaged forebrain and intact brainstem areas. In adult rats studied at 14 days after SE, LCMRglcs decreased in damaged forebrain areas involved in the genesis and propagation of seizures and increased in brainstem areas involved in the remote control of epilepsy. During the interictal phase of the chronic period, LCMRglcs decreased in damaged forebrain areas of adult epileptic rats and P21 rats that were not spontaneously epileptic, whereas it was similar to control levels in epileptic P21 rats. CONCLUSIONS: The process of epileptogenesis and its effects differ in duration and functional consequences in P21 and adult rats. The factors that underlie these age-related differences remain to be explored.

Age Factors↗
PubMed2000

The prevention of chronic NSAID induced upper gastrointestinal toxicity: a Cochrane collaboration metaanalysis of randomized controlled trials.

OBJECTIVE: To review the effectiveness of common interventions for the prevention of nonsteroidal antiinflammatory drug (NSAID) induced upper gastrointestinal (GI) toxicity. METHODS: Randomized controlled clinical trials (RCT) of prostaglandin analogs, H2-receptor antagonists (H2RA), or proton pump inhibitors (PPI) for the prevention of chronic NSAID induced upper GI toxicity were identified through electronic databases, the Cochrane control trials register, conference proceedings, and by contacting content experts and companies. Outcome measures investigated were endoscopic ulcers, ulcer complications, symptoms, overall dropouts, dropouts due to symptoms, and study quality. RESULTS: Thirty-four RCT met the inclusion criteria. All doses of misoprostol significantly reduced the risk of endoscopic ulcers. Misoprostol 800 microg/day was superior to 400 microg/day for the prevention of endoscopic gastric ulcers (RR 0.18, RR 0.38, respectively; p = 0.0055). A dose-response relationship was not seen with duodenal ulcers. Misoprostol caused diarrhea at all doses, although significantly more at 800 than 400 microg/day (p = 0.0012). Misoprostol was the only prophylactic agent documented to reduce ulcer complications. Standard doses of H2RA were effective at reducing the risk of endoscopic duodenal (RR 0.24, 95% CI 0.10-0.57) but not gastric ulcers (RR 0.73, 95% CI 0.50-1.09). Both double dose H2RA and PPI were effective at reducing the risk of endoscopic duodenal and gastric ulcers (RR 0.44, 95% CI 0.26-0.74 and RR 0.37, 95% CI 0.27-0.51, respectively, for gastric ulcer) and were better tolerated than misoprostol. CONCLUSION: Misoprostol, PPI, and double dose H2RA are effective in preventing chronic NSAID related endoscopic gastric and duodenal ulcers. Lower doses of misoprostol are less effective and are still associated with diarrhea. Only misoprostol 800 microg/day has been directly shown to reduce the risk of ulcer complications.

Adult↗
PubMed1999

Correlation between hypermetabolism and neuronal damage during status epilepticus induced by lithium and pilocarpine in immature and adult rats.

The correlation between seizure-induced hypermetabolism and subsequent neuronal damage was studied in 10-day-old (P10), 21-day-old (P21), and adult rats subjected to lithium-pilocarpine status epilepticus (SE). Local CMRglc (LCMRglc) values were measured by the [14C]2-deoxyglucose method for a duration of 45 minutes starting at 60 minutes after the onset of SE, and neuronal damage was assessed by cresyl violet staining at 6 days after SE. In P21 and adult rats, LCMRglc values were increased by 275 to 875% in all thalamic, cortical, forebrain, and hypothalamic regions plus the substantia nigra. In addition, at P21 there were also large increases in LCMRglc in brainstem regions. In P10 rats, metabolic increases were mostly located in cortical and forebrain regions plus the substantia nigra but did not affect hypothalamic, thalamic, or brainstem areas. In adult rats, there was an anatomical correlation between hypermetabolism and neuronal damage. At P21, although hypermetabolism occurred in regions with damage, the extent of damage varied considerably with the animals and ranged from an almost negligible to a very extended degree. Finally, in P10 rats, although quite pronounced hypermetabolism occurred, there was no neuronal damage induced by the seizures. Thus, in the present model of epilepsy, the correlation between marked hypermetabolism and neuronal damage can be shown in adult rats. Conversely, immature rats can sustain major metabolic activations that lead either to a variable extent of damage, as seen at P21, or no damage, as recorded at P10.

Aging↗
PubMed1998

C-Fos, Jun D and HSP72 immunoreactivity, and neuronal injury following lithium-pilocarpine induced status epilepticus in immature and adult rats.

In order to follow the maturation-related evolution of neuronal damage, cellular activation and stress response subsequent to Li-Pilo seizures in the 10- (P10), 21-day-old (P21) and adult rat, we analyzed the expression of the c-Fos protein as a marker of cellular activation, HSP72 immunoreactivity as the stress response and silver staining for the assessment of neuronal damage in 20 selected brain regions. The early wave of c-Fos measured at 2 h after the onset of seizures was present in most structures of the animals at the three ages studied and particularly strong in the cerebral cortex, hippocampus and amygdala. The late wave of c-Fos measured at 24 h after the onset of seizures and that was shown to correlate to neuronal damage was absent from the P10 rat brain, and present mainly in the cerebral cortex and hippocampus of P21 and adult rats. The expression of the stress response, assessed by the immunoreactivity of HSP72 at 24 h after the seizures was absent from the P10 rat brain and present in the entorhinal cortex, amygdala, hippocampus and thalamus of P21 and adult rats. The expression of Jun D at 24 h after the seizures was discrete and present in most brain regions at all ages. Neuronal injury assessed by silver staining at 6 h after the onset of seizures was very discrete in the brain of the P10 rat and limited to a few neurons in the piriform and entorhinal cortices. In older animals, marked neuronal degeneration occurred in the cerebral cortex, amygdala, hippocampus, lateral septum and thalamus. Thus the immediate cell activation induced by lithium-pilocarpine seizures which is present at all ages translates only into a late wave of c-Fos and the expression of HSP72 in P21 and adult animals in which there will be extensive cell damage.

Age Factors↗
PubMed1997

Physicians counseling smokers. A population-based survey of patients' perceptions of health care provider-delivered smoking cessation interventions.

OBJECTIVE: To examine associations between sociodemographic and psychological characteristics of smokers and delivery of 5 types of smoking cessation counseling interventions by physicians and office staff. METHODS: We used a telephone survey of a population-based sample of adult cigarette smokers (N = 3037) who saw a physician in the last year. Primary outcomes included patients' report of whether a physician or other health care provider (1) talked about smoking, (2) advised them to quit, (3) offered help to quit, (4) arranged a follow-up contact, and (5) prescribed nicotine gum or other medication. RESULTS: Fifty-one percent of smokers were talked to about their smoking; 45.5% were advised to quit; 14.9% were offered help; 3% had a follow-up appointment arranged; and 8.5% were prescribed medication. In multivariate analyses, the most consistent predictors of receipt of almost all counseling behaviors were medical setting (private physician's office only > care in other settings), health status (fair or poor > good, very good, or excellent), more years of education, greater number of cigarettes smoked per day, stage of readiness to quit smoking (preparation > precontemplation), and greater reported benefits of smoking. CONCLUSIONS: Physicians and other health care providers are not meeting the standards of smoking intervention outlined by the National Cancer Institute and the Agency for Health Care Policy and Research. Health care providers who intervene only with those patients who are ready to quit smoking are missing opportunities to provide effective smoking interventions to the majority of their patients. Interventions are also less likely to be provided to healthier and lighter smokers.

Adult↗
PubMed1992

Teaching medical interviewing. A basic course on interviewing and the physician-patient relationship.

Recent advances in educational theory and methodology have made it possible to teach medical interviewing with as much rigor as other clinical skills. We describe a first-semester, first-year medical student course that effectively teaches basic interviewing skills. This course provides faculty development, small group learning, detailed faculty and student coursebooks, and an interview checklist that delineates specific interviewing skills and content areas, serving as a template for teaching, practice, and feedback. Students have many opportunities for practice in role play and with patients, followed by feedback by self, peers, and faculty. Use of audiotape and videotape reviews enhances the learning experience. This article describes our course, suggests educational principles and standards for the teaching of medical interviewing, and presents educational research demonstrating significant gains in students' skills associated with improvement in standardized patient satisfaction.

Education, Medical, Undergraduate↗
PubMed1991

In micronodular cirrhosis, hepatocytes retain a normal C-25 hydroxylation capacity toward vitamin D3: a study using the rat carbon tetrachloride-induced cirrhotic model.

To test further the competence of the cirrhotic liver to metabolize vitamin D3 at C-25, hepatocytes were isolated from controls and from CCl4-induced cirrhotic rat livers, as well as from partially hepatectomized rats. The transformation of D3 into 25-hydroxyvitamin D3 was studied in the presence of 10(7) hepatocytes at D3 concentrations of 20 nmol/L to 15.4 mumol/L. Histologically, micronodular cirrhosis was present in all CCl4-treated rats, whereas controls had normal livers; portal venous pressure (p less than 0.008) and intrahepatic collagen content (p less than 0.0001) were significantly increased in CCl4-treated rats, whereas no difference was found between the two groups in the total and ionized serum calcium, D3 metabolites, ALT, AST and alkaline phosphatase. Cytochrome P-450 was 0.27 +/- 0.02 and 0.25 +/- 0.02 nmol/10(6) hepatocytes in controls and cirrhotic rats (N.S.), and it significantly increased in both groups after phenobarbital or 3-methylcholanthrene administration (p less than 0.0001). 25-Hydroxyvitamin D3 formation was best described by power law equations and varied between 0.02 +/- 0.0004 and 29.57 +/- 2.8 in controls, and 0.024 +/- 0.0004 and 32.0 +/- 7.0 pmol.hr-1.10(6) hepatocytes-1 in cirrhotic rats. No statistically significant difference was found in the slopes of the 25-hydroxyvitamin D3 formation, but the y-axis intercept was found to be lower in cirrhotic rats under basal resting conditions (p less than 0.005). Inducers of the mixed function oxidases significantly increased 25-hydroxyvitamin D3 formation in controls as well as in cirrhotic rats (p less than 0.005). Moreover, both groups were found to respond similarly to the addition of modulators of the enzyme such as the calcium ionophore A23187 and parathyroid hormone. Partial hepatectomy was also without effect on the activation of D3. Furthermore, the cell sequestration of D3 was also found to be unperturbed in hepatocytes obtained from either cirrhotic or partially hepatectomized livers. The data indicate that in well-compensated micronodular cirrhosis, the C-25 hydroxylation of D3 is generally intrinsically normal at the cellular level and that it also remains fully responsive to in vivo and in vitro modulators of its activity.

Animals↗
PubMed1990

Vitamin D depletion retards the normal regeneration process after partial hepatectomy in the rat.

1,25-Dihydroxyvitamin D3 [1,25-(OH)2D3], the hormone of the vitamin D3 (D3) endocrine system, has been shown to influence malignant and normal cell proliferation/differentiation, while insulin (I) is known to be essential for liver growth. To investigate the influence of D3 on liver regeneration, the effect of the D status was studied in D-depleted rats (D-) pretreated with: G1, placebo (D-, hypocalcemic); G2, oral calcium only (D-, normocalcemic); G3, D3; and G4, 1,25-(OH)2D3. Two thirds hepatectomy (HX) or sham operation was performed, and regeneration was studied for 3 weeks. I response to glucose challenge and the hepatic I receptor were also studied. Cell volume, DNA, and RNA were not affected by pretreatment. After HX, the pattern of [3H]thymidine incorporation into DNA (P less than 0.003) and the cell labeling index (P less than 0.0001) were highly influenced by pretreatment and suggestive of an earlier appearance of the S phase of the cell cycle in the 1,25-(OH)2D3-treated compared to the D- hypocalcemic group. Furthermore, the mitotic index revealed a significant effect of pretreatment (P less than 0.01), with peak mitosis 24 h after HX in D3-treated and 1,25-(OH)2D3-treated rats compared to 30-36 h after HX in the D- groups. Liver weight restitution was impaired in D- rats (P less than 0.009) and is illustrated by the estimated time required to achieve 70% recovery of the resected liver mass, which was found to be 186 and 300 h in G1 and G2, and 154 and 107 h in G3 and G4. G1 rats had significantly higher glucose concentrations (fasting as well as after glucose injection) and reduced I secretion when challenged with glucose (P less than 0.001); they also had an upregulation in hepatic I receptor number (P less than 0.005) compared to calcium or D3-treated rats, while 1,25-(OH)2D3 led to a liver I receptor number similar to that found in hypocalcemic D- rats; the affinity of the I receptor was, however, only slightly changed by pretreatment (P less than 0.08). Our data indicate that in D depletion, hypocalcemia retards DNA synthesis and liver mass recovery, while normocalcemia contributes to DNA synthesis, but fails to sustain mitosis and compensatory liver growth to a level comparable to that found after D3 and/or 1,25-(OH)2D3 repletion. The observation that both D3 and 1,25-(OH)2D3 significantly promoted normal liver recovery after partial HX illustrates the role of the D endocrine system in normal cell physiology in vivo.

Animals↗