Search PubMed⌕ Search

Biomedical subjects

J D Gardner

Publications and source records attributed to J D Gardner.

At least 37 records · Page 2Linked to original sources
PubMed1999

Adolescence and breast carcinoma risk.

BACKGROUND: Breast carcinoma risk may be modified by early life factors, including physical growth and development, diet, and life-style factors of preadolescence and adolescence, as well as genetic factors. METHODS: The authors tested their hypothesis that adolescent growth and development are related to breast carcinoma incidence by evaluating 65,140 women who participated in the Nurses' Health Study. During 16 years of follow-up, 806 women were diagnosed with breast carcinoma prior to menopause, and another 1485 were diagnosed after menopause. Because adolescent growth was not directly observed in this cohort, the peak height growth velocity for each participant was estimated by using a model from another longitudinal study. Finally, Cox proportional hazards regression models were used to study associations between breast carcinoma incidence and adolescent factors in the Nurses' Health Study. RESULTS: Later menarche (relative risk [RR] = 0.52 for > or =15 vs. < or =11 years) and more body fatness at age 10 years (RR = 0.60 for fattest vs. leanest) were associated with a decreased risk of premenopausal breast carcinoma. The risk of postmenopausal breast carcinoma was lower for girls with later menarche (RR = 0.80), more body fat at age 10 years (RR = 0.72), and shorter adult height (RR = 1.29 for > or =67 vs. < or =62 inches). Higher peak height growth velocity, derived from these 3 variables, was associated with increased risk of both premenopausal (RR = 1.31 for highest vs. lowest quintile) and postmenopausal (RR = 1.40) breast carcinoma. These analyses controlled for birth cohort, other possible risk factors from the adolescent period, and family history. These associations persisted after controlling for age at the birth of a first child, parity, adult adiposity, and age at menopause. Post-hoc analyses suggested that, although childhood body fatness was associated with lower risk, increasing body fatness between ages 10 and 20 years was not protective against either premenopausal or postmenopausal breast carcinoma. CONCLUSIONS: Earlier menarche, extremely lean body mass at age 10 years, and taller adult height were predictive of elevated breast carcinoma risk. The same three factors were also predictive of higher peak growth velocities during adolescence, lending credence to the hypothesis that more rapid adolescent growth may increase the risk of breast carcinoma development.

Adolescent↗
PubMed1999

Validation of a food frequency questionnaire in Native American and Caucasian children 1 to 5 years of age.

OBJECTIVE: To assess the validity of the Harvard Service Food Frequency Questionnaire (HFFQ) in the diet assessment of Native American and Caucasian children 1 to 5 years of age participating in the North Dakota WIC program. METHODS: The 84-item HFFQ was administered twice to the parent or guardian of 131 Native American and 102 Caucasian children ages 1 to 5 years (total n = 233), first at the child's routine WIC visit and then following the completion of three 24-hr dietary recalls taken over approximately 1 month. Average nutrient intakes from the three 24-hr dietary recalls were compared to average nutrient intakes from the HFFQs by calculating Pearson correlation coefficients and adjusting for energy intake and within person variation. RESULTS: Correlation coefficients ranged from 0.26 for dietary fiber to 0.63 for magnesium. The average correlation was 0.52, similar to that found in validation studies among adolescents and adults. The following nutrients had correlations of 0.50 or greater: carbohydrate, sucrose, total fat, vitamin C, vitamin E, vitamin B1, vitamin B2, niacin, folate, vitamin B6, calcium, magnesium, and iron. CONCLUSIONS: The HFFQ is a simple self-administered questionnaire completed by the child's parent or guardian and is useful in assessing the diets of Native American and Caucasian children. It may also provide important nutritional information about this age group for future program planning, research, education, and intervention purposes.

Child, Preschool↗
PubMed1999

Effects of IBMX on norepinephrine-induced vasoconstriction in small mesenteric arteries.

The present study assesses the effects of the phosphodiesterase inhibitor IBMX on norepinephrine (NE)-induced constriction of small mesenteric arteries. Arteries ( approximately 150 micrometer) were dissected from rats and mounted on a wire myograph for isometric force measurement. NE concentration effect curves were generated after exposure to 500 microM IBMX for 60 min. IBMX significantly reduced NE-induced tension development. Studies were also conducted following sarcoplasmic reticulum (SR) depletion (ryanodine, 10 microM) or L-type Ca2+ channel blockade [(+)-BAY K 8644, 10 microM] in the presence and absence of IBMX. Both SR depletion and L-channel blockade reduced NE-induced tension generation, consistent with incomplete Ca2+ mobilization. IBMX significantly attenuated NE responses in ryanodine and (+)-BAY K 8644-treated vessels. Finally, treatment of NE-stimulated vessels with IBMX (500 microM) caused a reduction in vascular tension that was greater than the concomitant reduction in cytosolic Ca2+ concentration ([Ca2+]i), indicating that a portion of the IBMX-mediated relaxation is Ca2+-independent. These data suggest that IBMX attenuation of NE responsiveness not only involves a reduction in [Ca2+]i but also a significant decrease in Ca2+ sensitivity.

1-Methyl-3-isobutylxanthine↗
PubMed1998

Myoglobin function evaluated in working heart tissue.

Previous modeling efforts suggest that myoglobin-facilitated diffusion contributes very little to oxygen transport in a Krebs-Henseleit perfused isolated heart when literature-derived values for the diffusion coefficient of myoglobin (DMb) were used. Simulations have strongly suggested that the contractile mechanisms of muscle may augment diffusion in working preparations. Myoglobin-facilitated oxygen diffusion may be augmented by the same mechanism. In this study, parameters of an oxygen transport to tissue model are optimized to investigate the possibility of elevated diffusion coefficients for oxygen and myoglobin in working heart tissue. The Radially-Averaged, Axially-Distributed (RAAD) model considers axial diffusion of oxygen in tissue, myoglobin facilitation of oxygen transport, and pO2-dependent oxygen consumption (Michaelis-Menten kinetics). Models are solved numerically using a variable-mesh finite-difference scheme. Parameters are optimized using a Nelder-Mead simplex routine and are chosen to minimize the sum-of-squares error (SSE) between model oxygen partial pressure (pO2) predictions and experimental pO2 data. Models are solved both with and without myoglobin facilitation. Myoglobin was found to have little effect on the oxygen distribution predicted by the models. Optimized values for the oxygen diffusion coefficient remained elevated. However, optimized values for myoglobin diffusion coefficient were found to be less than measured values. The RAAD model optimization results suggest that myoglobin does not significantly facilitate oxygen diffusion to tissue in the steady state and that myoglobin diffusion is not elevated in working heart.

Animals↗
PubMed1998

Dynamic displacement changes of the bladder neck with the patient supine and standing.

PURPOSE: With the patient standing and supine we determine the differences in dynamic changes of the bladder neck and directions of dynamic bladder neck displacement. MATERIALS AND METHODS: To evaluate the dynamic movement of the bladder neck we recruited into the study 78 consecutive women 27 to 69 years old with various urogynecological complaints. The anatomical changes of the bladder neck from rest to maximal straining and from rest to holding were evaluated and compared with the patients supine and standing. RESULTS: Except for bladder neck rotational angle with the patient standing, all parameters were significantly different from corresponding measurements with the patient supine. Mean rotational angle of rest to maximal straining plus or minus standard deviation was 39.4 +/- 18.9 degrees when standing versus 39.8 +/- 23.4 degrees when supine (p > 0.05). The distances between the bladder neck and symphysis pubis at rest, and during maximal straining and holding the bladder neck in the supine position were significantly longer than those in the standing position. The direction of bladder neck displacement from rest to maximal straining was more caudad and ventral when standing. The bladder neck moved cephalad and ventral when the patient was standing, and cephalad and dorsal with the patient supine and holding the bladder neck. CONCLUSIONS: The anatomical locations and dynamic displacements of the bladder neck at rest, and during maximal straining and holding were significantly different in the supine and standing positions. While evaluating the dynamic motion of the bladder neck to determine bladder neck mobility, patient position must be considered and specified in accordance with diagnostic standards.

Adult↗
PubMed1997

Evaluation of myoglobin function in the presence of axial diffusion.

Facilitation of oxygen transport by myoglobin has been assessed by many researchers. Yet, the models used in these studies often assume that radial diffusion is the primary transport mechanism in tissue. Axial diffusion is typically neglected. In this study, oxygen transport by myoglobin facilitation is added to a proven cardiac tissue model which contains axial diffusion in the tissue and capillary regions, the Radially-Averaged, Axially-Distributed (RAAD) model. Previous research has shown that the axial diffusion in the capillary and tissue regions becomes coupled, causing a reduction in the pO2 at the capillary inlet. The objective is to determine if this coupling effect increases the facilitation of oxygen transport by myoglobin. The RAAD model consists of non-interacting cylinders of tissue (Krogh cylinders), with each perfused by a central capillary. Derivation of the equations describing the RAAD model yields a stiff, fourth-order, non-linear, ODE, BVP. The equation set is solved numerically. Parameters for myoglobin concentration and diffusion coefficient are chosen to maximize myoglobin facilitation. The effect of myoglobin is assessed by observing changes in the pO2 profiles for the model with and without myoglobin. Also, the RAAD model is compared to experimental pO2 data to determine if the inclusion of myoglobin improves the model prediction. The computer simulations show that myoglobin does facilitate diffusion, but only to a small extent. The changes in the capillary pO2 profiles for the model with and without myoglobin are not significant, pO2 reductions are 0.8% at the inlet and 2% at the outlet. The model prediction is not substantially improved with the addition of myoglobin. The sum of squared error is reduced by 0.1%, from 5.6834 without myoglobin, to 5.6779 with myoglobin. The steady state solution of the RAAD model with myoglobin suggests that, in the presence of axial diffusion, facilitation of oxygen diffusion to tissue is not myoglobin's primary function. No conclusion can be made about the transient function of myoglobin.

Animals↗
PubMed1997

The results of laparoscopic adhesiolysis for intractable urinary frequency.

PURPOSE: We evaluated urinary frequency related to pelvic adhesions around the bladder serosa and the result of laparoscopic adhesiolysis on intractable urinary frequency caused by adhesions that did not respond to conservative treatment. MATERIALS AND METHODS: Laparoscopic adhesiolysis was performed for the diagnosis and treatment of 10 referred patients with a history of pelvic surgery in whom conservative treatment had failed. Urinary symptoms and signs, a urinary diary and cystometry were followed before and after surgery. RESULTS: In all cases there were various degrees of pelvic adhesion, mainly around the bladder. Frequency and urgency were improved in 9 of 10 patients. Urinary diary and cystometry parameters showed improvement at followup. CONCLUSIONS: Adhesions involving the bladder wall may restrict bladder distension in most of these patients. Laparoscopic adhesiolysis is beneficial in the diagnosis and treatment of this subgroup of patients.

Adult↗
PubMed1995

Cellular distribution of isoforms of protein kinase C (PKC) in pancreatic acini.

As in a previous study (Biochim, Biophys. Acta 1224 (1994) 127-138), we used quantitative immunoblot analysis and found that rat pancreatic acini possess four different isoforms of PKC-alpha, delta, epsilon and zeta. The phorbol ester 12-O-tetradecanoyl phorbol 13-acetate (TPA) caused translocation of each isoform from the cytosol to the membrane fraction. CCK-8 increased diacylglycerol (DAG) and caused translocation of PKC-sigma and PKC-epsilon but not that of PKC-alpha or PKC-zeta. L-364,718, a CCK receptor antagonist, prevented as well as reversed the effects of CCK-8 on DAG and on translocation of PKC-sigma and PKC-epsilon. To explore the possibility that different isoforms of PKC might have different distributions in rat pancreas, we used immunocytochemistry to determine the cellular distribution of different isoforms of PKC in intact pancreas as well as pancreatic acini. In intact pancreas, PKC-alpha and PKC-sigma were detected in islet cells but not in duct or acinar cells. PKC-epsilon was detected in the apical region of acinar cells and PKC-zeta was detected over the luminal surfaces of acinar cells and the ductules that extend from the acinus. Neither PKC-epsilon nor PKC-zeta was detected in islets. In pancreatic acini PKC-alpha and PKC-sigma were detected in islets or fragments of islets that contaminated the preparation but were not detected in acinar cells. PKC-epsilon was detected in the apical region of acinar cells and adding 1 microM TPA or 1 microM CCK-8 accentuated the immunostaining but did not alter its cellular distribution. L-364,718 reversed the changes in immunostaining caused by CCK-8. PKC-zeta was detected over the luminal surface of the acinar cells. TPA, but not CCK-8 or CCK-8 followed by L-364,718, increased the number of acini that showed staining of the luminal surfaces of acinar cells. Thus, the present results demonstrate that different isoforms of PKC are distributed differently in rat pancreas and that the different patterns of distribution can explain, at least in part, the different responses to CCK-8.

Animals↗
PubMed1995

Modulation of cholecystokinin activity by albumin.

We found that a variety of cholecystokinin (CCK) receptor ligands bind to bovine serum albumin (BSA). This binding was rapid, fully reversible, temperature independent, of low affinity, and specific for BSA; it depended on the concentration of BSA, the chemical structure of the ligand, and the chemical composition of the incubation medium. BSA also decreased the binding of 125I-labeled CCK octapeptide (125I-CCK-8) to CCK receptors on pancreatic acini and membranes but increased the potency with which CCK-8 inhibited binding of 125I-CCK-8. These counterintuitive findings appeared to result from BSA altering the affinities of CCK-8 for different affinity states of the pancreatic CCK receptor. An alternate hypothesis is that BSA increased the efficacy of CCK-8 such that it bound to receptors and also caused biochemical changes in other receptors that reduced their ability to bind 125I-CCK-8. BSA enhanced the ability of CCK-8 to stimulate amylase secretion from pancreatic acini and to cause contraction of dispersed gastric smooth muscle cells. Thus, CCK can bind to BSA, and the BSA-CCK complex has substantially different activities from the free, uncomplexed hormone.

Animals↗
PubMed1994

Multiple affinity states of different cholecystokinin receptors.

We transfected COS cells with cDNA for rat cholecystokinin-A (CCK-A) and different CCK-B receptors and measured binding of 125I-CCK-8, [3H]L-364,718 and [3H]L-365,260 to characterize the different affinity states for each type of CCK receptor. Rat CCK-A and CCK-B receptors, canine CCK-B receptors and canine mutant CCK-B (M-CCK-B) receptors in which the leucine in position 355 was replaced by valine each existed in three different affinity states for CCK-8, high affinity, low affinity, and very low affinity. In rat CCK-A and probably CCK-B receptors, most were in the very low affinity state, whereas with canine CCK-B and M-CCK-B receptors, most were in the low affinity state. Studies with CCK receptor agonists, CCK-8, gastrin, and CCK-JMV-180, in conjunction with CCK receptor antagonists, L-364,718 and L-365,260, showed a different pattern of affinities for these ligands at the different CCK receptors. Thus, each transfected CCK receptor can exist in three different affinity states for CCK-8 and has a characteristic pattern of interaction with different ligands. This ability to exist in multiple affinity states is an intrinsic property of the CCK receptor molecule itself.

Animals↗
PubMed1994

Characterization of the three different states of the cholecystokinin (CCK) receptor in pancreatic acini.

By measuring binding of [125I]CCK-8 and [3H]L-364,718 to rat pancreatic acini we demonstrated directly that the pancreatic CCK receptor can exist in three different affinity states with respect to CCK--high affinity, low affinity and very low affinity. Binding of [125I]CCK-8 reflects interaction of the tracer with the high and low affinity states, whereas binding of [3H]L-364,718 reflects interaction of the tracer with the low and very low affinity states. Treating acini with carbachol abolished the high affinity state of the CCK receptor and converted approximately 25% of the low affinity receptors to the very low affinity state. Carbachol treatment was particularly useful in establishing the values of Kd for the high and low affinity states for different CCK receptor agonists and antagonists. Of the various CCK receptor agonists tested, CCK-8 had the highest affinity for the high affinity state (Kd approximately 1 nM), whereas CCK-JMV-180 had the highest affinity for the low (Kd 7 nM) and very low affinity (Kd 200 nM) states. Gastrin and de(SO4)CCK-8 had affinities for the high and low affinity states of the receptor that were 100- to 400-fold less than those of CCK-8 but had affinities for the very low affinity state that were only 3- to 10-fold less than that of CCK-8. CCK receptor antagonists showed several patterns in interacting with the different states of the CCK receptor. L-364,718 had the same affinity for each state of the CCK receptor. CR1409 and Bt2cGMP each had similar affinities for the high and low affinity states and lower affinity for the very low affinity state. L-365,260 and CCK-JMV-179 had the highest affinity for the low affinity state and lower affinities for the high and very low affinity states. Different CCK receptor agonists caused the same maximal stimulation of amylase secretion but showed different degrees of amplification in terms of the relationship between their abilities to stimulate amylase secretion and their abilities to occupy the low affinity state of the CCK receptor. When amplification was expressed quantitatively as the value of Kd for the low affinity state divided by the corresponding EC50 for stimulating amylase secretion the values were CCK-8 (1000), de(SO)CCK-8 (1500), gastrin (100) and CCK-JMV-180 (Menozzi, D., Vinayek, R., Jensen, R.T. and Gardner, J.D. (1991) J. Biol. Chem. 266, 10385-1091).(ABSTRACT TRUNCATED AT 400 WORDS)

Amylases↗
PubMed1994

Biochemical regulation of the three different states of the cholecystokinin (CCK) receptor in pancreatic acini.

We used rat pancreatic acini and measured binding of [125I]CCK-8 and [3H]L-364,718 to the three different states of the CCK receptor to examine potential biochemical regulation of ligand binding for each receptor state. Binding of [125I]CCK-8 to the high affinity state of the receptor was measured as carbachol-inhibitable binding of [125I]CCK-8, whereas binding of [125I]CCK-8 to the low affinity state was measured as carbachol-resistant binding of [125I]CCK-8. Interaction of CCK-8 with the very low affinity state of the CCK receptor was measured as CCK-8-inhibitable binding of [3H]L-364,718. [125I]CCK-8 that was bound to the high affinity state dissociated slowly at a rate of 0.20%/min and this dissociation was not altered by 30 mM NaF. Dissociation of [125I]CCK-8 bound to the low affinity state was biphasic--22% of the bound radioactivity dissociated completely within 3 min and the remaining 78% dissociated slowly at a rate of 0.19%/min. Dissociation of [125I]CCK-8 from the low affinity state was not altered by 30 mM NaF. The pattern of dissociation of bound [125I]CCK-8 from the pancreatic CCK receptor expressed in COS cells was also biphasic and closely resembled that observed in pancreatic acini. CCK-8 that was bound to the very low affinity state dissociated completely during a 20-min period of washing and resuspension of acini that had been first incubated with CCK-8. We found extensive biochemical regulation of the different states of the CCK receptor in pancreatic acini. Bombesin, TPA, NaF, CCCP and trifluoperazine each altered binding of [125I]CCK-8 to the high affinity state and to the low affinity state, and except for bombesin each agent was more potent in affecting the high affinity state than the low affinity state. No agent tested affected the low affinity state but not the high affinity state. In contrast, a number of agents affected the high affinity state but not the low affinity state. These included receptor-mediated agonists (carbachol, secretin, VIP), 8Br-cAMP, NEM, agents that affect microtubules or microfilaments (cytochalasin B, vinblastine), calmodulin inhibitors (W-7, chlorpromazine) and genistein. Experiments with EGTA, A23187 and thapsigargin indicated that none of the three receptor states was influenced by intracellular or extracellular calcium. No agent tested altered the interaction of CCK-8 with the very low affinity state of the CCK receptor.(ABSTRACT TRUNCATED AT 400 WORDS)

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1994

Effects of cholecystokinin (CCK) and other secretagogues on isoforms of protein kinase C (PKC) in pancreatic acini.

We used rat pancreatic acini and measured the effects of various agents on digestive enzyme secretion, diacylglycerol (DAG) and the cellular distribution of protein kinase C (PKC) enzyme activity as well as isoforms of PKC determined by quantitative immunoblot analysis. TPA, but not CCK-8, caused translocation of PKC enzyme activity from the cytosol fraction to the membrane fraction. Immunoblot analysis detected PKC-alpha, PKC-delta, PKC-epsilon and PKC-zeta. PKC-beta, PKC-gamma and PKC-eta were not detected. TPA caused translocation of all isoforms from cytosol to membrane, whereas CCK-8 caused translocation of PKC-delta and PKC-epsilon, carbachol caused translocation of PKC-epsilon, and bombesin and secretin caused no detectable translocation of any isoform. Specific receptor antagonists could prevent, as well as reverse completely, the translocation of PKC isoforms caused by CCK-8 or carbachol. Agonists added in sequence with an interposed addition of a specific receptor antagonist caused cycling of PKC-epsilon between cytosol and membrane fractions. Each receptor-mediated agonist that caused translocation of PKC also increased DAG, and with CCK-8 and carbachol cycling of PKC-epsilon between cytosol and membrane was accompanied by corresponding cyclic changes in cellular DAG. CCK-JMV-180, bombesin and secretin increased DAG but did not cause translocation of any PKC isoform. Translocation of a PKC isoform could be accounted for by whether the increased DAG originated from PIP2 (accompanied by translocation) or from phosphatidylcholine (no accompanying translocation). Thus it appeared that DAG, in pancreatic acini, is functionally compartmentalized depending on the source of the lipid. Studies using CCK-8 and CCK-JMV-180 indicated that occupation of the low affinity state of the CCK receptor by either peptide increased DAG from phosphatidylcholine, whereas occupation of the very low affinity state by CCK-8 increased DAG from PIP2 and caused translocation of PKC-delta and PKC-epsilon. TPA stimulated amylase secretion, indicating that activation of PKC can stimulate enzyme secretion; however, with the various receptor-mediated secretagogues there was no consistent, unequivocal correlation between translocation of an isoform of PKC and accompanying changes in enzyme secretion.

Amylases↗
PubMed1994

Direct demonstration of three different states of the pancreatic cholecystokinin receptor.

We used rat pancreatic acini as well as COS-7 cells transfected with the cloned pancreatic cholecystokinin (CCK) receptor and measured the abilities of CCK octapeptide (CCK-8) and L-364,718 (a CCK receptor antagonist) to inhibit binding of 125I-labeled CCK-8 (125I-CCK-8) and [3H]L-364,718. With pancreatic acini 125I-CCK-8 bound to two different states of the CCK receptor. The high-affinity state (1% of the receptors) had a Kd for CCK-8 of 985 pM and the low-affinity state (19% of the receptors) had a Kd for CCK-8 of 30 nM. [3H]L-364,718 bound to low-affinity receptors and to a previously unrecognized very-low-affinity state (80% of the receptors) having a Kd for CCK-8 of 13 microM. L-364,718 had the same affinity (Kd 3 nM) for each of the three different states of the CCK receptor. Similar measurements using transfected COS cells also identified three different states of the CCK receptor, with the very-low-affinity state being the most abundant. Thus, the ability of the CCK receptor to exist in three different states is an intrinsic property of the CCK receptor molecule itself.

Animals↗
PubMed1994

Effect of inhibition of microsomal Ca(2+)-ATPase on cytoplasmic calcium and enzyme secretion in pancreatic acini.

We used thapsigargin (TG), 2,5-di-tert-butyl-1,4-benzohydroquinone (BHQ) and cyclopiazonic acid (CPA), each of which inhibits microsomal Ca(2+)-ATPase, to evaluate the effects of this inhibition on cytoplasmic free calcium ([Ca2+]i) and secretagogue-stimulated enzyme secretion in rat pancreatic acini. Using single-cell microspectrofluorimetry of fura-2-loaded acini we found that all three agents caused a sustained increase in [Ca2+]i by mobilizing calcium from inositol-(1,4,5)-trisphosphate-sensitive intracellular calcium stores and by promoting influx of extracellular calcium. Concentrations of all three agents that increased [Ca2+]i potentiated the stimulation of enzyme secretion caused by secretagogues that activate adenylate cyclase but inhibited the stimulation of enzyme secretion caused by secretagogues that activate phospholipase C. With BHQ, potentiation of adenylate cyclase-mediated enzyme secretion occurred immediately whereas inhibition of phospholipase C-mediated enzyme secretion occurred only after several min of incubation. In addition, the effects of BHQ and CPA on both [Ca2+]i and secretagogue-stimulated enzyme secretion were reversed completely by washing whereas the actions of TG could not be reversed by washing. Concentrations of BHQ in excess of those that caused maximal changes in [Ca2+]i inhibited all modes of stimulated enzyme secretion by a mechanism that was apparently unrelated to changes in [Ca2+]i. Finally, in contrast to the findings with TG and BHQ, CPA inhibited bombesin-stimulated enzyme secretion over a range of concentrations that was at least 10-fold lower than the range of concentrations over which CPA potentiated VIP-stimulated enzyme secretion.

Amylases↗
PubMed1994

The predictive value of childhood body mass index values for overweight at age 35 y.

Larger body mass index values (BMI in kg/m2) are associated with increased morbidity and mortality in adulthood and there are significant correlations between BMI values in childhood and in adulthood. The present study addresses the predictive value of childhood BMI for overweight at 35 +/- 5 y, defined as BMI > 28 for men and > 26 for women. Analyses of data for 555 white children indicated that overweight at 35 y can be predicted from BMI at younger ages. The prediction is excellent at age 18 y, good at 13 y, but only moderate at ages younger than 13 y. For 18-y-olds with a BMI value exceeding the 60th percentile, the odds of overweight at 35 y are 34% for men and 37% for women. A clinically applicable method is provided to assign an overweight child to a group with a known probability of high BMI values in adulthood.

Adolescent↗