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Biomedical subjects

R R Rogers

Publications and source records attributed to R R Rogers.

At least 19 recordsLinked to original sources
PubMed2001

Iron absorption during recovery from malnutrition.

OBJECTIVE: In infants and children recovering from severe malnutrition, iron deficiency is common, and the ability to absorb iron during such recovery is uncertain. The objective of this study was to determine iron absorption during recovery from malnutrition. METHODS: During the later stages of recovery from malnutrition, erythrocyte incorporation of orally administered 58Fe was determined as a surrogate for iron absorption. Based on four indices, subjects were classified as iron-sufficient, iron-deficient or indeterminate. RESULTS: Of the 25 subjects, 9 were classified as iron sufficient, 5 as indeterminate and 11 as iron deficient; all but 5 had evidence of inflammation or infection. Geometric mean erythrocyte incorporation of 58Fe was 32.0% of the dose in the iron-deficient subjects, which was not significantly different (p = 0.073) than the 13.1% in the iron-sufficient subjects. Incorporation of 58Fe by the iron-sufficient subjects did not differ significantly from that by normal subjects in the same age range. Surprisingly, we found no correlation of erythrocyte incorporation of 58Fe and reticulocyte count. CONCLUSIONS: Even in the presence of infection or inflammation, iron absorption by children during a late stage of recovery from malnutrition is not impaired.

Absorption↗
PubMed2000

Less than 80% of absorbed iron is promptly incorporated into erythrocytes of infants.

Erythrocyte incorporation of an administered iron isotope has been used as a surrogate for iron retention on the assumption (validated in normal and iron-deficient adults) that 80-100% of the retained isotope is promptly incorporated into circulating erythrocytes. This assumption has not been validated in infants or children. The purpose of our study was to determine concurrently in normal infants absorption and erythrocyte incorporation of the stable isotope, (58)Fe. In a preliminary study (Study 1), we demonstrated that fecal excretion of ingested isotope occurs predominantly during the first 4 d after administration but continues beyond 7 d after ingestion, that is, beyond the point at which isotope in feces can be explained either by excretion of isotope that failed to enter enterocytes or by exfoliation of isotope-enriched enterocytes. In Study 2, we administered (58)Fe to nine younger (age 20-69 d) and nine older (age 165-215 d) term infants and collected feces for 11 d. Geometric mean retention of (58)Fe by the younger infants was 31.2% of intake at 4 d and 26.9% at 11 d, and by the older infants, 35.0% at 4 d and 32.5% at 11 d. Erythrocyte incorporation of (58)Fe 14 d after ingestion was 5.2% of the dose by the younger infants and 12.5% by the older infants. Utilization of retained (11 d) isotope thus was 19.8% by the younger infants and 38.3% by the older infants. We conclude that far less than 80% of retained isotope is promptly incorporated into erythrocytes (utilized) by infants.

Absorption↗
PubMed2000

Time course of and effect of dietary iron level on iron incorporation into erythrocytes by infants.

As a part of our effort to explore various aspects of ferrokinetics in infancy, the present study was designed to determine the timing of entry of an orally ingested iron isotope into circulating erythrocytes, and the effect of the level of dietary iron [0.3 mg/100 kcal (418.4 kJ) vs. 1.8 mg/100 kcal] after isotope administration on erythrocyte incorporation of the isotope. We administered the stable isotope, (58)Fe, orally to 56-d-old and 168-d-old infants. All infants were fed a low-iron formula (LF) before and until 5 h after isotope administration. Thereafter, half the infants were fed a formula high in iron (HF group) while the remaining infants continued to receive the LF (LF group) for an additional 28 d. The quantity of (58)Fe in circulating erythrocytes increased from 14 to 28 d after isotope administration was nearly constant from 28 through 84 d of age (plateau value) and decreased between 84 and 112 d. Erythrocyte incorporation of (58)Fe was greater by the 168-d-old infants than by the 56-d-old infants, presumably because of the lesser iron stores of the older infants. In the 56-d-old infants, erythrocyte incorporation of (58)Fe was greater by the LF than by the HF group, but this difference was not significant in the 168-d-old infants. Thus, at least in younger infants, the level of iron intake after administration of an iron isotope affects erythrocyte incorporation of the isotope. The fact that less isotope was present in erythrocytes 112 d than 84 d after administration indicates that the life span of erythrocytes of infants, even beyond the immediate newborn period, is less than the 120-d life span of erythrocytes in the adult.

Administration, Oral↗
PubMed2000

Identity revisited in the new technological culture.

Cultural changes permeate incrementally our individual and collective identities in subtle, barely perceptible ways. The recent rapid advances in technology impacted, skewed, and changed pre-existing pillars of individual and collective identities. The paper focuses on the changes in roles and relationships between generations. Acceptance and ability to absorb the benefits of globalization demands adjustment, including some tolerance of the pitfalls of globalization. Special concern is voiced about the developing trend, demand, and interest in speed of communication that leads to a decrease in depth of evaluation. There is an increased focus on talking rather than on thinking, and a decrease in human relationship, while technology and finance are enthroned as the overriding determinants of human interaction. These profound changes demand psychosocial flexibility. In order to benefit from the overwhelming benefits of new technology, personal, social, professional, and cultural views need to undergo profound re-examination and re-evaluation.

Communication↗
PubMed1999

Infant formula with protein-energy ratio of 1.7 g/100 kcal is adequate but may not be safe.

BACKGROUND: An adequate protein-energy ratio of infant formulas has been defined as one that permits growth similar to that of infants fed relatively generous protein-energy ratios, and serum concentrations of albumin and urea nitrogen no less than those observed in breast-fed infants. A safe ratio has been defined as one with no detectable adverse effects. The hypothesis was that a protein-energy ratio of 1.7 g/100 kcal is adequate and safe. METHODS: Healthy male infants were fed Formula 1.7, a milk-based formula, as the sole source of energy from the 8th to the 112th day of life. Weight, length, and energy intake were measured; serum albumin and urea nitrogen were determined; and the results were compared with data from appropriate reference groups of infants. RESULTS: Energy intake from 8 through 55 days was significantly higher than that of infants in the formula-fed reference group. Gain in weight was significantly more than that of the formula-fed reference group or of a breast-fed reference group, whereas gain in length was similar to that of the formula-fed reference group. Body mass index was significantly higher than that of either reference group, suggesting more fat accumulation in infants fed Formula 1.7. Plasma concentrations of albumin and urea nitrogen were similar to those of the breast-fed reference group. CONCLUSION: Infants fed Formula 1.7 received adequate intakes of protein. Because of the possibility that ad libitum feeding of diets with moderately inadequate protein-energy ratios is associated with increased food intake leading to excess weight gain, it is not possible to conclude that a protein-energy ratio of 1.7 g/100 kcal is safe.

Blood Urea Nitrogen↗
PubMed1996

Palm olein in infant formula: absorption of fat and minerals by normal infants.

Palm olein, a low-melting fraction of palm oil, and soy oil can be combined to obtain fat blends with proportions of palmitic and oleic acids similar to those of human milk. We compared the absorption of fat and calcium by infants fed a formula containing a blend of palm olein (53%) and soy oil (47%) (Formula PO/S) with that by infants fed a formula containing a blend of soy oil (60%) and coconut oil (40%) (Formula S/C). In a randomized crossover design, one study was performed with each formula in each of 11 normal infants ranging in age from 27 to 161 d. Six of the infants were admitted for 72-h metabolic balance studies. In the other five infants, feces (with some admixture of urine) were collected at home for 96 h by using acid-washed cloth diapers. Mean (+/- SD) absorption of fat was 90.6 +/- 1.6% of intake when Formula PO/S was fed and 95.2 +/- 1.1% of intake when Formula S/C was fed; the difference was significant (P < 0.001). The difference in excretion of fat by infants fed the two formulas was explained by the difference in excretion of palmitic acid. Absorption of calcium averaged 39.0 +/- 8.3% of intake with Formula PO/S and 48.4 +/- 10.3% with Formula S/C; the difference was significant (P < 0.01). We conclude that fat is less well absorbed from a mixture of 53% palm olein and 47% soy oil than from a mixture of 60% soy oil and 40% coconut oil, and that absorption of calcium is less from a formula containing palm olein, presumably because of the formation of insoluble calcium soaps of unabsorbed palmitic acid.

Absorption↗
PubMed1993

Listening to what the patient does not tell us.

In the intimacy of outpatient psychotherapy, the psychiatrist's ethical responsibility (burdensome at times) is always to place the emotional priorities of the patient ahead of the therapist's external and internal agendas. For example, the therapist's schedule (anticipated vacation), the therapist's interest in the patient for the sake of a publication, presentation, teaching, have to be subordinated to the emotional and somatic vulnerabilities and needs of the patient. The only sensor for this interaction is the professional conscience of the therapist. Excerpts from psychotherapy with six patients will highlight the dilemmas which each patient had which forced them to camouflage their hurts from themselves. An attempt will also be made to highlight ethical and professional dilemmas of the therapist.

Adult↗
PubMed1991

Immunotoxicity of 2-methoxyethanol following oral administration in Fischer 344 rats.

The immunotoxicity of the glycol ether 2-methoxyethanol (ME) was evaluated in adult Fischer 344 rats using a variety of in vitro and in vivo immune function assays. In the first phase of this study, male rats were dosed by oral gavage with ME in water, at dosages ranging from 50 to 200 mg/kg/day, for 10 consecutive days. Decreases in thymus weights were observed at dosages of 50-200 mg/kg/day in the absence of decreased body weights. Lymphoproliferative (LP) responses to concanavalin A and phytohemagglutinin were reduced at 50-200 mg/kg/day while pokeweed mitogen and Salmonella typhimurium mitogen responses were reduced at 200 mg/kg/day. No alterations were observed in natural killer cell activity, mixed lymphocyte reaction, or cytotoxic T lymphocyte responses. The frequency of W3/25-positive splenocytes was reduced in rats dosed at 200 mg/kg/day. Interleukin-2 production was reduced in splenocytes from rats exposed to all dosages of ME. The plaque-forming cell (PFC) response to sheep red blood cells was enhanced in rats dosed at 50 mg/kg/day. However, the PFC response to trinitrophenyl-lipopolysaccharide (TNP-LPS) was suppressed at all dosages. Similarly, the PFC response to TNP-LPS was suppressed in adult female rats dosed with ME. A reduction in the expulsion of adult worms was observed in rats dosed at 200 mg/kg/day that were infected with Trichinella spiralis. A number of male reproductive parameters were also evaluated in rats dosed with ME over 10 days. A significant reduction in testicular weight was observed in rats dosed at 200 mg/kg/day. In the second phase of this study, the PFC response to TNP-LPS was employed to assess the role that metabolism of ME to 2-methoxyacetic acid (MAA) plays in the immunotoxicity of this glycol ether. Ten-day oral dosing with MAA resulted in the inhibition of the PFC response to TNP-LPS at dosages of 50-200 mg/kg/day. Concomitant exposure of rats to ME and the alcohol dehydrogenase inhibitor 4-methylpyrazole blocked ME-induced suppression of this PFC response. Attempts to ameliorate ME-induced suppression of the PFC response with serine, which has been shown to reverse ME-induced developmental and reproductive toxicity, were unsuccessful. These results suggest that the immune system may be more sensitive than the reproductive system to the toxic effects of ME. Furthermore, it appears that MAA is the proximate toxicant for ME-induced alterations in the immune system, as has been demonstrated for ME-induced reproductive and developmental toxicity.

Administration, Oral↗
PubMed1991

Host resistance to murine malaria in mice exposed to the adenosine deaminase inhibitor, 2'-deoxycoformycin.

Resistance to infection with the nonlethal rodent malaria parasite Plasmodium yoelii 17XNL (Py 17XNL) is mediated by humoral, T-cell and accessory cell activity. The purpose this study was to profile host resistance to infection with this organism in mice exposed to 2'-deoxycoformycin (2dCF), a potent adenosine deaminase (ADA) inhibitor. Inhibition of ADA activity by 2dFC results in defective T-cell function and either suppression or augmentation of the humoral response, depending on whether 2dCF exposure precedes (suppression) or follows (augmentation) immunization. In this study, mice injected with 2dCF during the first five days of infection cleared the infection at the same time as controls, but had lower peak parasitemia than controls. Mice infected with the lethal variant of P. yoelii were more susceptible to infection when injected with 2dCF after infection, suggesting that 2dCF injection did not directly affect the parasite. Rather, suppression of parasitemia in 2dCF-treated mice may have been mediated by augmented humoral immunity, since 2dCF injection increases antibody responses when 2dCF injection follows antigen (in this case, parasite) injection. Conversely, in mice given 2dCF prior to infection, parasitemia peaked 2 days later and was eliminated more gradually than in control mice. Exposure to 2dCF did not deplete reticulocytes and thus temporarily limit parasitemia. Similarly, enrichment of NK cells or augmentation of macrophage phagocytic activity prior to infection were not sufficient to alter the pattern of infection. In contrast, the pattern of infection in mice treated with tilorone (a macrophage activator which also causes suppressed T-cell function) prior to infection was similar to that observed in 2dCF-exposed animals. These results indicate that 2dCF, given before or after infection, alters the host response to infection with Py17XNL. It appears that a combination of increased macrophage activity and altered T-cell activity contributed to the delay in peak parasitemia and clearance of infection in mice exposed to 2dCF before infection with Py17XNL.

Adenosine Deaminase Inhibitors↗
PubMed1991

Evaluation of the immunotoxicity of orally administered 2-methoxyacetic acid in Fischer 344 rats.

We previously demonstrated that the glycol ether 2-methoxyethanol (ME) is immunotoxic in the rat. In this study, the immunotoxicity of 2-methoxyacetic acid (MAA), the principal metabolite of ME, was evaluated in adult male Fischer 344 rats. Rats were dosed by gavage with MAA on 10 consecutive days at dosages ranging from 50 to 200 mg/kg/day. Thymic involution, in the absence of body weight loss, was observed at 100 and 200 mg/kg/day MAA. Lymphoproliferative responses to the mitogens concanavalin A, phytohemagglutinin, and pokeweed mitogen were also reduced at these dosages. The in vitro generated cytotoxic T lymphocyte response was reduced at 200 mg/kg/day MAA. The mixed lymphocyte reaction and natural killer cell activity were unaffected by exposure to MAA. Enumeration of splenic lymphocyte populations revealed a reduction in the percentage of W3/25-positive cells at 100 and 150 mg/kg/day and an increase in the percentage of OX39-positive cells at 200 mg/kg/day; however, no changes in the absolute number of either of these subsets were observed. The plaque forming cell (PFC) response to trinitrophenyl-lipopolysaccharide (TNP-LPS) was suppressed at 50-200 mg/kg/day MAA, while the PFC response to sheep red blood cells (SRBC) was elevated at 50 mg/kg/day. Immunization of rats with TNP-LPS or SRBC followed by oral exposure to MAA at 4 and 28 hr postimmunization resulted in the suppression of the PFC response to TNP-LPS and SRBC at dosages of 100 and 200 mg/kg and 200 and 400 mg/kg, respectively. Equal suppression of the PFC response to TNP-LPS was achieved at equimolar concentrations of ME and MAA. The effects of MAA on the immune system of the rat presented here are very similar to results reported from this lab for ME-induced immune alterations. These results, along with results of experiments in which ME-induced suppression of the PFC response to TNP-LPS was reversed by 4-methylpyrazole, an inhibitor of the oxidation of ME to MAA by alcohol dehydrogenase, indicate that MAA is the proximate immunotoxicant following exposure to the glycol ether 2-methoxyethanol.

Acetates↗
PubMed1991

Reference data on gains in weight and length during the first two years of life.

Serial data from studies of infants at the University of Iowa and from the Fels Longitudinal Study were used to develop sex-specific percentiles for increments in weight and recumbent length for selected intervals during the first 24 months of life. Weight increments are presented for 1-month intervals from birth to 6 months, 2-month intervals from birth to 12 months, and 3-month intervals from birth to 24 months. Length increments are presented for 2-month intervals from birth to 6 months, and for 3-month intervals from birth to 24 months of age. Weights and lengths at the target ages were obtained for the Iowa data by simple interpolation, and for the Fels data by fitting families of three-parameter mathematical functions to the serial data from ages 1 to 24 months. The tabular presentations are based on the Iowa data from birth to 3 months of age, on the combined Iowa and Fels data from 3 to 6 months of age, and on the Fels data from 6 to 24 months of age. We believe that these reference data will be useful in screening for deviations from normal growth and may aid in early detection of failure to thrive or excessive weight gain during early life.

Age Factors↗
PubMed1990

Immune alterations in rats following subacute exposure to tributyltin oxide.

Adult male Fischer 344 rats were dosed by oral gavage with bis(tri-n-butyltin)oxide (TBTO) in peanut oil for 10 consecutive days, at dosages ranging from 1.25 to 15 mg/kg/day. Other groups of rats were dosed daily for 10 days by oral gavage with cyclophosphamide (CY) at dosages ranging from 0.75 to 6 mg/kg/day. These rats served as positive controls for the immune assays employed. The immune function parameters examined included the following: delayed-type hypersensitivity (DTH) and antibody responses to bovine serum albumin (BSA), primary antibody responses to sheep red blood cells (SRBC) and trinitrophenyl lipopolysaccharide (TNP-LPS) and enumeration of splenic lymphocyte populations. The DTH and antibody responses to BSA were not affected by TBTO exposure; however these responses were suppressed in rats dosed with CY at 6 mg/kg/day. The plaque forming cell (PFC) response to the T cell-dependent antigen SRBC was enhanced in rats dosed with TBTO at from 5 to 15 mg/kg/day. On the other hand, the PFC response to the T cell-independent antigen TNP-LPS was unaffected by TBTO exposure. Rats dosed with CY had suppressed PFC responses to SRBC and TNP-LPS at dosages of 3 and 6 mg/kg/day, respectively. Enumeration of splenic lymphocyte populations from TBTO-exposed rats revealed a reduction in OX8- but not W3/25- or IgG-positive cells. These results, as well as results from an earlier study from this lab, suggest that T lymphocytes are a primary target for TBTO-induced immune alterations and that the enhancement of the PFC response to SRBC in TBTO-exposed rats may be mediated by alterations in the suppressor (OX8-positive) T lymphocyte population.

Animals↗
PubMed1990

Cow milk feeding in infancy: further observations on blood loss from the gastrointestinal tract.

Because feeding of cow milk causes normal infants to lose increased amounts of occult blood from the gastrointestinal tract, we conducted a prospective trial to measure intestinal blood loss quantitatively and to monitor iron nutritional status. Fifty-two infants entered the trial at 168 days of age and were assigned at random to receive either cow milk or a milk-based formula. Initially, 31 infants had been breast-fed and 21 had been fed formulas. With the feeding of cow milk, the proportion of guaiac-positive stools increased from 3.0% at baseline to 30.3% during the first 28 days of the trial (p less than 0.01), whereas the proportion of positive stools remained low (5.0%) with the feeding of formula. The proportion of guaiac-positive stools among cow milk-fed infants declined later, but for the entire trial it remained significantly (p less than 0.01) elevated. Stool hemoglobin concentration increased markedly with the introduction of cow milk, rising from a mean (+/- SD) of 622 +/- 527 micrograms/gm dry stool at baseline to 3598 +/- 10,479 micrograms/gm dry stool during the first 28 days of ingestion of cow milk. Among infants fed formula, stool hemoglobin did not increase and was significantly (p less than 0.01) less than in the cow milk group. Among infants fed cow milk, the increase in hemoglobin concentration tended to be greater for those who had initially been fed human milk than for those who had initially been fed formulas. Iron nutritional status was not significantly different between the two feeding groups. However, one infant became iron deficient after 4 weeks of ingesting cow milk. We conclude that cow milk feeding leads to increased intestinal tract blood loss in a large proportion of normal infants and that the amount of iron lost is nutritionally important.

Animals↗
PubMed1989

Immunotoxicity of tributyltin oxide in rats exposed as adults or pre-weanlings.

A comparison was made between adult and pre-weanling rats of the immunotoxic effects of subacute dosing with bis(tri-n-butyltin) oxide (TBTO). Adult (9 weeks old) male Fischer rats were dosed by oral gavage with TBTO for 10 consecutive days at 1.25-10 mg/kg per dose or 3 times/week for a total of 10 doses at 5-20 mg/kg per dose. Adult rats similarly dosed by oral gavage with 6 mg/kg per dose cyclophosphamide (CY) served as positive controls. Pre-weanling rats (3-24 days old) were dosed 3 times/week for a total of 10 doses at 2.5, 5 or 10 mg/kg per dose. At various times after dosing rats were evaluated for alterations in body and lymphoid organ weights, mitogen and mixed lymphocyte reaction (MLR) lymphoproliferative (LP) responses, natural killer (NK) cell activity, cytotoxic T lymphocyte (CTL) responses and primary antibody plaque-forming cell (PFC) responses. In adult rats given 10 daily doses of TBTO, thymic involution was observed at a dosage of 2.5 mg/kg and mitogen responses to Con A and PHA were suppressed at 5 mg/kg. The PFC response was enhanced in adult rats dosed daily at 2.5 mg/kg. A dosage of 5 mg/kg given intermittently (3 times/week) to adults or pre-weanlings resulted in thymic involution. Reductions in mitogen responses were observed in adults dosed intermittently at 10 and 20 mg/kg and in pre-weanlings at 5 and 10 mg/kg. The MLR response was suppressed in adult rats dosed intermittently at 20 mg/kg and in pre-weanling rats at 10 mg/kg. NK cell activity was suppressed only in pups dosed intermittently at 10 mg/kg. CTL responses were not affected in either age group. Within 3 weeks following the last exposure of adult rats to TBTO all parameters returned to normal. On the other hand, LP responses to mitogens were suppressed in 10-week-old rats that were dosed with 10 mg/kg TBTO as pre-weanlings. However, this exposure regimen in reductions in body weight that persisted for up to 13 weeks of age, which suggests that TBTO may be a developmental toxicant. These data indicate that while exposure of young rats to TBTO resulted in immune alterations at doses lower than those required to suppress responses in adults, the observed effects may also be influenced by the developmental toxicity of this compound.

Age Factors↗
PubMed1989

Suppression of lymphocyte proliferation by hexamethylene diamine.

The antiproliferative potential of hexamethylene diamine (HMDA) for mitogen-stimulated splenic lymphocytes was evaluated in vitro at final concentrations of 0.1-16 mM. Addition at the start of culture or after 24 or 48 h of culture decreased the proliferative response to T and B cell mitogens. However, the concentration of HMDA required to cause suppression increased with incubation time. Removal of diamine after 24 h allowed cells to proliferate normally upon reculture with mitogen. Mitogenic responses of cultures containing the potent ornithine decarboxylase (ODC) inhibitor alpha-difluoromethylornithine (DFMO) were also inhibited in a time and dose dependent fashion. ODC activity, which was much greater in cultures stimulated with Con A than LPS, was markedly decreased by inclusion of diamine or DFMO in the culture medium. Addition of putrescine to cultures did not reverse the suppressive effects of diamine on proliferation but did restore DFMO-containing cultures to control levels of activity. These results indicate that HMDA does suppress lymphocyte proliferation in vitro by alteration of ODC and polyamine activity. However, comparison of results obtained with DFMO and HMDA suggests that HMDA may act via multiple pathways, only one of which involves inhibition of ODC activity.

Animals↗
PubMed1989

Evaluation of the immunotoxicity of low level PCB exposure in the rat.

Weanling male Fischer 344 rats were exposed daily by gastric intubation for up to 15 weeks to the polychlorinated biphenyl (PCB) Aroclor 1254 at 0.1, 1, 10, or 25 mg/kg body weight. At 5, 10 and 15 weeks groups of rats were killed and immune functions were evaluated. The immune parameters examined included the following: body and lymphoid organ weights, mitogen-stimulated lymphoproliferative (LP) responses, natural killer (NK) cell activity, mixed lymphocyte reaction (MLR), and cytotoxic T lymphocyte (CTL) response. After 15 weeks of dosing body weights were reduced in rats receiving 25 mg/kg PCB while thymus weights were decreased in rats receiving 10 and 25 mg/kg. NK cell activity was reduced in rats dosed for 15 weeks at 10 and 25 mg/kg. The LP response to phytohemagglutinin was enhanced in rats dosed for 15 weeks at 25 mg/kg PCB. Exposure of rats to PCB did not affect the MLR or CTL responses. Other groups of rats were exposed to cyclophosphamide (CY) and served as positive controls for the immune assays employed. CY induced alterations in all of the immune parameters measured, indicating that this is an appropriate battery of immune function tests which is capable of detecting immune alterations in the rat. Alterations in immune function induced by daily gastric intubation with PCB were accompanied by reductions in body weight and/or hepatomegaly. These results suggest that the observed immune alterations may be related to the overt toxicity of this PCB in the rat.

Animals↗