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<title>Journal of Parenteral and Enteral Nutrition current issue</title>
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<prism:coverDisplayDate>NOVEMBER-DECEMBER 2009</prism:coverDisplayDate>
<prism:publicationName>Journal of Parenteral and Enteral Nutrition</prism:publicationName>
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<title>Journal of Parenteral and Enteral Nutrition</title>
<url>http://pen.sagepub.com:80/icons/banner/title.gif</url>
<link>http://pen.sagepub.com</link>
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<item rdf:about="http://pen.sagepub.com/cgi/reprint/33/6/588?rss=1">
<title><![CDATA[A.S.P.E.N. Clinical Guidelines: Nutrition Support of Children With Human Immunodeficiency Virus Infection]]></title>
<link>http://pen.sagepub.com/cgi/reprint/33/6/588?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Sabery, N., Duggan, C., the American Society for Parenteral and Enteral Nutrition (A.S.P.E.N.) Board of Directors]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 10:07:44 PST</dc:date>
<dc:identifier>info:doi/10.1177/0148607109346276</dc:identifier>
<dc:title><![CDATA[A.S.P.E.N. Clinical Guidelines: Nutrition Support of Children With Human Immunodeficiency Virus Infection]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>606</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>588</prism:startingPage>
<prism:section>Clinical Guidelines</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/6/607?rss=1">
<title><![CDATA[Butyrate Increases GLUT2 mRNA Abundance by Initiating Transcription in Caco2-BBe Cells]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/6/607?rss=1</link>
<description><![CDATA[
<p><I>Background:</I> Glucose transporter 2 (GLUT2) is a high-capacity,
facilitative intestinal monosaccharide transporter, known to be upregulated by
short-chain fatty acids (SCFAs) derived from the intestinal microbiota during
fermentation. Understanding the mechanisms regulating intestinal function is
important to optimize therapies for patients with intestinal failure and
ultimately reduce their dependence on parenteral nutrition.
<I>Objective:</I> The objective was to examine the mechanism regulating the
underlying response of GLUT2 to the SCFA butyrate. <I>Methods:</I> GLUT2
messenger RNA (mRNA) abundance was measured in differentiated Caco2-BBe
monolayers treated for 0.5-24 hours with 0-20 mM butyrate using quantitative
reverse transcription&ndash;polymerase chain reaction. Activation of the human
GLUT2 promoter was measured using luciferase reporting in transiently
transfected Caco2-BBe monolayers. <I>Results:</I> GLUT2 mRNA abundance was
higher (<I>P</I> &lt; .0001) with 1-4 hours of exposure to 2.5, 7.5, and 10
mM butyrate. Butyrate induced (<I>P</I> &lt; .0001) promoter activity in a
dose-dependent fashion. Analysis of the GLUT2 promoter indicated that regions
&ndash;282/+522, &ndash;216/+522, and &ndash;145/+522 had a heightened
(<I>P</I> &lt; .05) response to butyrate compared with 1135/+522 and
564/+522. <I>Conclusions:</I> Butyrate upregulates GLUT2 mRNA abundance in
Caco2-BBe monolayers by activating specific regions within the human GLUT2
promoter. These results identify a cellular mechanism wherein butyrate
upregulates intestinal absorption that may be relevant to patients with
reduced function. Additional work is necessary to understand cellular targets
of butyrate therapy and define clinically appropriate means of providing such
strategies, such as consuming prebiotics and probiotics.</p>
]]></description>
<dc:creator><![CDATA[Mangian, H. F., Tappenden, K. A.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 10:07:44 PST</dc:date>
<dc:identifier>info:doi/10.1177/0148607109336599</dc:identifier>
<dc:title><![CDATA[Butyrate Increases GLUT2 mRNA Abundance by Initiating Transcription in Caco2-BBe Cells]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>617</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>607</prism:startingPage>
<prism:section>2009 Harry M. Vars Research Award</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/6/618?rss=1">
<title><![CDATA[Enteral Refeeding Rapidly Restores PN-Induced Reduction of Hepatic Mononuclear Cell Number Through Recovery of Small Intestine and Portal Vein Blood Flows]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/6/618?rss=1</link>
<description><![CDATA[
<p><I>Background:</I> Absence of enteral nutrition (EN) reduces hepatic
mononuclear cell (MNC) numbers and impairs their functions. However, enteral
refeeding (ER) for as little as 12 hours following parenteral nutrition (PN)
rapidly restores hepatic MNC numbers. We hypothesized that changes in small
intestine and portal vein blood flows related to feeding route might be
responsible for this phenomenon. <I>Methods:</I> In experiment 1, mice (n =
19) were randomized to Chow (n = 5), PN (n = 7) or ER (n = 7) groups. The Chow
group was given chow <I>ad libitum</I> with intravenous (IV) saline for 5
days. The PN group was fed parenterally for 5 days, while the ER group was
re-fed with chow for 12 hours following 5 days of PN. Then, small intestine
and portal vein blood flows were monitored and hepatic MNCs were isolated and
counted. In experiment 2, the effects of intravenous administration of
prostaglandin E<SUB>1</SUB> (PGE<SUB>1</SUB>) on hepatic MNC numbers were
examined in fasted mice for 12 hours. Mice (n = 28) were randomized to Control
(n = 8), PG0 (n = 10), or PG1 (n = 10) groups. The Control group was fed chow
<I>ad libitum</I> with IV saline, while the PG0 and PG1 groups were fasted
for 12 hours with infusions, respectively, of saline and PGE<SUB>1</SUB> at 1
&micro;g/kg/minute. Blood flows and hepatic MNC numbers were examined.
<I>Results:</I> Experiment 1: ER restored PN-induced reductions in small
intestine and portal vein blood flows and hepatic MNC number to the levels in
the Chow group. Small intestine and portal vein blood flows correlated
positively with hepatic MNC number. Experiment 2: Fasting decreased small
intestine and portal vein blood flows and hepatic MNC number. However,
PGE<SUB>1</SUB> restored portal vein blood flow to the level of the Control
group, and moderately increased hepatic MNC number. There was a positive
correlation between portal blood flow and hepatic MNC number.
<I>Conclusions:</I> Reduced small intestine and portal vein blood flows may
contribute to impaired hepatic immunity in the absence of EN. ER quickly
restores hepatic MNC number through recovery of blood flow in both the small
intestine and the portal vein.</p>
]]></description>
<dc:creator><![CDATA[Omata, J., Fukatsu, K., Murakoshi, S., Noguchi, M., Miyazaki, H., Moriya, T., Okamoto, K., Fukazawa, S., Akase, T., Saitoh, D., Mochizuki, H., Yamamoto, J., Hase, K.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 10:07:44 PST</dc:date>
<dc:identifier>info:doi/10.1177/0148607109336598</dc:identifier>
<dc:title><![CDATA[Enteral Refeeding Rapidly Restores PN-Induced Reduction of Hepatic Mononuclear Cell Number Through Recovery of Small Intestine and Portal Vein Blood Flows]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>626</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>618</prism:startingPage>
<prism:section>Premier Research Papers</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/6/629?rss=1">
<title><![CDATA[Colonic GLP-2 is not Sufficient to Promote Jejunal Adaptation in a PN-Dependent Rat Model of Human Short Bowel Syndrome]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/6/629?rss=1</link>
<description><![CDATA[
<p><I>Background:</I> Bowel resection may lead to short bowel syndrome
(SBS), which often requires parenteral nutrition (PN) due to inadequate
intestinal adaptation. The objective of this study was to determine the time
course of adaptation and proglucagon system responses after bowel resection in
a PN-dependent rat model of SBS. <I>Methods:</I> Rats underwent jugular
catheter placement and a 60% jejunoileal resection + cecectomy with
jejunoileal anastomosis or transection control surgery. Rats were maintained
exclusively with PN and killed at 4 hours to 12 days. A nonsurgical group
served as baseline. Bowel growth and digestive capacity were assessed by
mucosal mass, protein, DNA, histology, and sucrase activity. Plasma
insulin-like growth factor I (IGF-I) and bioactive glucagon-like peptide 2
(GLP-2) were measured by radioimmunoassay. <I>Results:</I> Jejunum
cellularity changed significantly over time with resection but not
transection, peaking at days 3-4 and declining by day 12. Jejunum
sucrase-specific activity decreased significantly with time after resection
and transection. Colon crypt depth increased over time with resection but not
transection, peaking at days 7-12. Plasma bioactive GLP-2 and colon
proglucagon levels peaked from days 4-7 after resection and then approached
baseline. Plasma IGF-I increased with resection through day 12. Jejunum and
colon GLP-2 receptor RNAs peaked by day 1 and then declined below baseline.
<I>Conclusions:</I> After bowel resection resulting in SBS in the rat, peak
proglucagon, plasma GLP-2, and GLP-2 receptor levels are insufficient to
promote jejunal adaptation. The colon adapts with resection, expresses
proglucagon, and should be preserved when possible in massive intestinal
resection.</p>
]]></description>
<dc:creator><![CDATA[Koopmann, M. C., Liu, X., Boehler, C. J., Murali, S. G., Holst, J. J., Ney, D. M.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 10:07:44 PST</dc:date>
<dc:identifier>info:doi/10.1177/0148607109336597</dc:identifier>
<dc:title><![CDATA[Colonic GLP-2 is not Sufficient to Promote Jejunal Adaptation in a PN-Dependent Rat Model of Human Short Bowel Syndrome]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>639</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>629</prism:startingPage>
<prism:section>Premier Research Papers</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/6/640?rss=1">
<title><![CDATA[Measurement of Resting Energy Expenditure in Healthy Children]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/6/640?rss=1</link>
<description><![CDATA[
<p><I>Background:</I> The role that the components of energy expenditure
play in the etiology of childhood obesity has highlighted the need for greater
accuracy and standardized protocols for the measurement of resting energy
expenditure (REE). However, protocols used to assess REE in children are
varied, and consensus on a suitable method for measuring REE in children has
not been reached. This study was undertaken to determine the effect of
measurement time and measurement device (mask or mouthpiece) on REE in healthy
children. <I>Design:</I> Following a 12-hour fast and abstinence from
exercise, 23 children (age, 7&ndash;12 years) completed two 35-minute
protocols: one with a face mask and the other with a mouthpiece/noseclip.
Energy expenditure was measured continuously via indirect calorimetry, while
device acceptability was assessed using a 6-point comfort rating scale.
<I>Results:</I> Repeated measures ANOVA indicated that there was no
significant difference in REE when measured after 10, 15, 20, or 25 minutes of
rest compared to 30 minutes for either the mask or mouthpiece/noseclip (REE
range, 1371&ndash;1460 kcal/d). Examination of the percentage coefficient of
varia tion (CV) in energy expenditure for each time period by device showed
that the least variation existed after 20 minutes of measurement using the
mask (CV 6%). Paired <I>t</I> test analysis indicated significantly less
discomfort when wearing the mask compared to the mouthpiece/noseclip.
<I>Conclusion:</I> It would appear that a 20-minute protocol using a mask
may increase compliance and prove to be a more practical protocol for
measuring REE in children.</p>
]]></description>
<dc:creator><![CDATA[Mellecker, R. R., McManus, A. M.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 10:07:44 PST</dc:date>
<dc:identifier>info:doi/10.1177/0148607109336603</dc:identifier>
<dc:title><![CDATA[Measurement of Resting Energy Expenditure in Healthy Children]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>645</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>640</prism:startingPage>
<prism:section>Techniques, Materials, and Devices</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/6/646?rss=1">
<title><![CDATA[Disparate Response to Metoclopramide Therapy for Gastric Feeding Intolerance in Trauma Patients With and Without Traumatic Brain Injury]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/6/646?rss=1</link>
<description><![CDATA[
<p>Patients with traumatic brain injury (TBI) have delayed gastric emptying
and often require prokinetic drug therapy to improve enteral feeding
tolerance. The authors hypothesized that metoclopramide was less efficacious
for improving gastric feeding tolerance for trauma patients with TBI compared
to trauma patients without TBI. A retrospective analysis was conducted of
patients admitted to the trauma or neurosurgical intensive care unit who
received gastric feeding from January 2006 to April 2008. Gastric feeding
intolerance was defined by a gastric residual volume &gt;200 mL or emesis with
abdominal distension or discomfort. Patients with gastric feeding intolerance
were given metoclopramide 10 mg intravenously every 6 hours, followed by a
dose escalation to 20 mg, and then combination therapy with metoclopramide and
erythromycin 250 mg intravenously every 6 hours if intolerance persisted. In
total, 882 trauma patients (49% with TBI) were evaluated. TBI patients had a
higher incidence of gastric feeding intolerance than those without TBI (18.6%
vs 10.4%, <I>P</I> &le; .001). Efficacy rates for metoclopramide 10 mg,
metoclopramide 20 mg, and metoclopramide-erythromycin were 55%, 62%, and 79%,
respectively (<I>P</I> &le; .03). Metoclopramide failure occurred in 54% of
patients with TBI compared to 35% of patients without TBI, respectively
(<I>P</I> &le; .02), due to a greater prevalence of tachyphylaxis.
Single-drug therapy with metoclopramide was less effective for TBI trauma
patients compared to trauma patients without TBI. Combination therapy with
erythromycin as first-line therapy for TBI trauma patients with gastric
feeding intolerance is indicated if there are no contraindications or
significant drug interactions.</p>
]]></description>
<dc:creator><![CDATA[Dickerson, R. N., Mitchell, J. N., Morgan, L. M., Maish, G. O., Croce, M. A., Minard, G., Brown, R. O.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 10:07:44 PST</dc:date>
<dc:identifier>info:doi/10.1177/0148607109335307</dc:identifier>
<dc:title><![CDATA[Disparate Response to Metoclopramide Therapy for Gastric Feeding Intolerance in Trauma Patients With and Without Traumatic Brain Injury]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>655</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>646</prism:startingPage>
<prism:section>Original Communications</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/6/656?rss=1">
<title><![CDATA[Riboflavin Status in Acutely Ill Patients and Response to Dietary Supplements]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/6/656?rss=1</link>
<description><![CDATA[
<p><I>Background:</I> Although a number of studies have reported riboflavin
deficiency in free-living older people, no data are available on riboflavin
intake and status in older people during acute illness. <I>Methods:</I> To
determine the riboflavin response to dietary supplements during acute illness,
297 hospitalized, acutely ill older patients are randomly assigned to receive
a daily oral nutritional supplement containing 1.3 mg of riboflavin or a
placebo for 6 weeks. Outcome measures are riboflavin intake and riboflavin
biochemical status at baseline, 6 weeks, and 6 months using the erythrocyte
glutathione reductase activation coefficient (EGRAC), a measure of riboflavin
tissue saturation. EGRAC values are inversely proportional to riboflavin
status. <I>Results:</I> Fifty-six percent of patients (167/297) have
suboptimal riboflavin status (EGRAC &gt; 1.30). No significant correlation is
found between EGRAC and either total energy or riboflavin intakes. Significant
correlations are found between total energy intake and riboflavin intakes both
in hospital and at home (<I>r</I> = 0.67, <I>P</I> &lt; .0001 and
<I>r</I> = 0.57, <I>P</I> &lt; .0001, respectively). Smokers and patients
with chronic obstructive pulmonary disease (COPD) have lower riboflavin status
(high EGRAC values) compared with nonsmokers and those without COPD.
Riboflavin status improves significantly in the supplement group at 6 weeks
compared with the placebo group, but status declines between 6 weeks and 6
months, after patients stop taking the supplements. <I>Conclusions:</I> A
high proportion of acutely ill patients have suboptimal riboflavin status.
Supplementation with a physiological amount of riboflavin in a mixed-nutrient
supplement significantly improves riboflavin status, but the effect is
transient and status deteriorates again after patients stop taking the
supplements.</p>
]]></description>
<dc:creator><![CDATA[Gariballa, S., Forster, S., Powers, H.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 10:07:44 PST</dc:date>
<dc:identifier>info:doi/10.1177/0148607109336602</dc:identifier>
<dc:title><![CDATA[Riboflavin Status in Acutely Ill Patients and Response to Dietary Supplements]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>661</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>656</prism:startingPage>
<prism:section>Original Communications</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/6/662?rss=1">
<title><![CDATA[Intestinal Redox Status of Major Intracellular Thiols in a Rat Model of Chronic Alcohol Consumption]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/6/662?rss=1</link>
<description><![CDATA[
<p><I>Background:</I> Alcohol consumption is associated with oxidative
stress in multiple tissues in vivo, yet the effect of chronic alcohol intake
on intestinal redox state has received little attention. In this study, we
investigated the redox status of 2 major intracellular redox regulating
couples: glutathione (GSH)/glutathione disulfide (GSSG) and cysteine
(Cys)/cystine (CySS) in a rat model of chronic alcohol ingestion.
<I>Methods:</I> Sprague-Dawley rats were fed the liquid Lieber-DeCarli diet
consisting of 36% ethanol of total calories for 6 weeks. Control rats were
pair-fed with an isocaloric, ethanol-free liquid diet. Defined mucosal samples
from the jejunum, ileum, and colon were obtained and analyzed by
high-performance liquid chromatography (HPLC) for GSH and Cys pool redox
status. Mucosal free malondialdehyde (MDA) was measured as an indicator of
lipid peroxidation. <I>Results:</I> In the ethanol-fed rats, Cys and mixed
disulfide (GSH-Cys) were significantly decreased in all 3 segments of
intestinal mucosa. Free MDA was increased in jejunal but not in ileal or
colonic mucosa. Chronic ethanol ingestion significantly increased mucosal GSH
concentration in association with a more reducing GSH/GSSG redox potential in
the jejunum, but these indices were unchanged in the ileum. In the colon,
chronic ethanol ingestion increased oxidant stress as suggested by decreased
GSH and oxidized GSH/GSSG redox potential. <I>Conclusions:</I> Chronic
alcohol intake differentially alters the mucosal redox status in proximal to
distal intestinal segments in rats. Such changes may reflect different
adaptability of these intestinal segments to the oxidative stress challenge
induced by chronic ethanol ingestion.</p>
]]></description>
<dc:creator><![CDATA[Tian, J., Brown, L. A. S., Jones, D. P., Levin, M. S., Wang, L., Rubin, D. C., Ziegler, T. R.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 10:07:44 PST</dc:date>
<dc:identifier>info:doi/10.1177/0148607109336600</dc:identifier>
<dc:title><![CDATA[Intestinal Redox Status of Major Intracellular Thiols in a Rat Model of Chronic Alcohol Consumption]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>668</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>662</prism:startingPage>
<prism:section>Original Communications</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/6/669?rss=1">
<title><![CDATA[Clinical Application of Magnetic Resonance Spectroscopy of the Liver in Patients Receiving Long-Term Parenteral Nutrition]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/6/669?rss=1</link>
<description><![CDATA[
<p><I>Background:</I> Intestinal failure&ndash;associated liver disease
(IFALD) may have progressed to an advanced stage by the time it becomes
evident via laboratory or physical signs. A safe, noninvasive technique for
assessing the liver could significantly aid in monitoring the effects of
therapeutic intervention, improve the timing of liver and small intestinal
transplantation, and increase our understanding of the causes of IFALD.
<I>Methods:</I> Six female patients fed intravenously for &gt;1 year and 6
controls matched for body mass index (BMI) underwent liver magnetic resonance
scanning with acquisition of <sup>1</sup>H and <sup>31</sup>P resonance
spectra. Areas under the curve for lipid (the sum of CH, CH<SUB>2</SUB>, and
CH<SUB>3</SUB>), water, and choline peaks were calculated and expressed
semi-quantitatively as ratios of lipid:water and choline:lipid.
Phosphomonoester (PME) and phosphodiester (PDE) peak areas were similarly
expressed as a ratio. Controls and cases were compared using Mann-Whitney
<I>U</I> test; least squares regression analysis was used to compare the
effect of measured variables on the lipid:water peak area ratio.
<I>Results:</I> Patients and controls were well matched for BMI. Parenteral
feeding was associated with a highly significant increase in lipid:water peak
ratio (<I>P</I> &lt; .005). Choline:lipid (<I>P</I> &lt; .05) and
choline:water (not significant) ratios were reduced in patients compared with
controls. The increase in lipid:water ratios in patients was independent of
BMI and choline:water ratios. A ratio of PME:PDE of &gt;0.3 (and &gt;3 SD from
the control mean) predicted the 2 patients at most risk of advanced liver
disease. <I>Conclusions:</I> This pilot study confirms the potential of
magnetic resonance spectroscopic techniques in evaluating IFALD and could
contribute significantly to our understanding and management of this
condition.</p>
]]></description>
<dc:creator><![CDATA[Woodward, J. M., Priest, A. N., Hollingsworth, K. G., Lomas, D. J.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 10:07:44 PST</dc:date>
<dc:identifier>info:doi/10.1177/0148607109332908</dc:identifier>
<dc:title><![CDATA[Clinical Application of Magnetic Resonance Spectroscopy of the Liver in Patients Receiving Long-Term Parenteral Nutrition]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>676</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>669</prism:startingPage>
<prism:section>Original Communications</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/6/677?rss=1">
<title><![CDATA[Intravascular Embolization of Venous Catheter--Causes, Clinical Signs, and Management: A Systematic Review]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/6/677?rss=1</link>
<description><![CDATA[
<p><I>Background:</I> Intravascular embolization of device fragments is a
rare but potentially serious complication. <I>Method:</I> A systematic
search of the PubMed and MEDLINE databases for all articles pertaining to
central catheter related embolization published in English between 1985 and
2007 was made. <I>Results:</I> A total of 215 cases of intravenous catheter
embolization were identified. There were 143 totally implanted venous devices
(TIVD) or port catheters and 72 percutaneous venous catheters (PVC). Sites of
catheter fragments following embolization were the superior vena cava or
peripheral veins (15.4%), the right atrium (27.6%), right ventricle (22%), and
pulmonary arteries (35%). Clinical signs of catheter embolization included
catheter malfunction (56.3%), arrhythmia (13%), pulmonary symptoms (4.7%), and
septic syndromes (1.8%), but 24.2% of cases were asymptomatic. The causes of
intravascular catheter embolization were pinch-off syndrome (40.9%), catheter
injury during explantation (17.7%), catheter disconnection (10.7%), and
catheter rupture (11.6%). In 19.1% of cases, the cause of catheter
embolization could not be identified. Most embolized catheter fragments
(93.5%) were removed percutaneously. In 4.2% of cases, fragments were retained
in the vascular bed; in 2.3%, embolized fragments were removed surgically via
thoracotomy. <I>Conclusion:</I> Intravascular catheter embolization can go
undiagnosed for prolonged periods. Patients might be asymptomatic or may
develop severe systemic clinical signs. The mortality rate is 1.8%. There were
no significant differences in clinical features of embolization between TIVD
and PVC groups.</p>
]]></description>
<dc:creator><![CDATA[Surov, A., Wienke, A., Carter, J. M., Stoevesandt, D., Behrmann, C., Spielmann, R.-P., Werdan, K., Buerke, M.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 10:07:44 PST</dc:date>
<dc:identifier>info:doi/10.1177/0148607109335121</dc:identifier>
<dc:title><![CDATA[Intravascular Embolization of Venous Catheter--Causes, Clinical Signs, and Management: A Systematic Review]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>685</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>677</prism:startingPage>
<prism:section>Original Communications</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/6/686?rss=1">
<title><![CDATA[Laparoscopic Surgery Improves Blood Glucose Homeostasis and Insulin Resistance Following Distal Gastrectomy for Cancer]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/6/686?rss=1</link>
<description><![CDATA[
<p><I>Background</I>: Prevention of blood glucose elevation and insulin
resistance could be more pronounced in patients undergoing laparoscopic rather
than open gastrectomy. <I>Methods</I>: Fifty-seven patients underwent distal
gastrectomy by either laparoscopy (n = 36) or an open approach (n = 21). Blood
glucose, serum insulin, and the daily insulin secretion rate (urinary
C-peptide) were measured. Insulin resistance was evaluated using an adapted
homeostasis model assessment of insulin resistance (HOMA-R). <I>Results</I>:
Blood glucose levels were lower in the laparoscopy group than in the open
group on the operative day and on postoperative days (POD) 1 and 3 (<I>P</I>
&lt; .001, <I>P</I> = .001, and <I>P</I> = .024, respectively). Serum
insulin levels were lower in the laparoscopy group than in the open group on
POD 1 and 3 (<I>P</I> = .045 and <I>P</I> = .027, respectively). HOMA-R
was lower in the laparoscopy group than in the open group on POD 1 and 3
(<I>P</I> = .024 and <I>P</I> = .009, respectively). Daily insulin
secretion rates were lower in the laparoscopy group than in the open group on
POD 1 (<I>P</I> = .023). <I>Conclusions</I>: Laparoscopic surgery prevents
blood glucose elevation and improves insulin resistance compared with open
surgery.</p>
]]></description>
<dc:creator><![CDATA[Kanno, H., Kiyama, T., Fujita, I., Tani, A., Kato, S., Tajiri, T., Barbul, A.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 10:07:44 PST</dc:date>
<dc:identifier>info:doi/10.1177/0148607109333003</dc:identifier>
<dc:title><![CDATA[Laparoscopic Surgery Improves Blood Glucose Homeostasis and Insulin Resistance Following Distal Gastrectomy for Cancer]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>690</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>686</prism:startingPage>
<prism:section>Original Communications</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/6/691?rss=1">
<title><![CDATA[Neonatal Parenteral Nutrition Hypersensitivity: A Case Report Implicating Bisulfite Sensitivity in a Newborn Infant]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/6/691?rss=1</link>
<description><![CDATA[
<p>This report describes a case of parenteral nutrition hypersensitivity in a
37 weeks' gestation infant with congenital diaphragmatic hernia complicated by
bowel necrosis and functional short bowel syndrome. The patient developed a
rash with subsequent urticaria beginning on the 50th day of life. The
reactions were confirmed with a positive rechallenge. After the amino acid
solution was replaced with a non&ndash;bisulfite-containing product, the
infant was able to continue to receive nutrition support through parenteral
nutrition without recurrence of symptoms. It is speculated that the bisulfite
additive in the amino acid solution may have interacted with the lipid
emulsion to sensitize the patient.</p>
]]></description>
<dc:creator><![CDATA[Huston, R. K., Baxter, L. M., Larrabee, P. B.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 10:07:44 PST</dc:date>
<dc:identifier>info:doi/10.1177/0148607109347643</dc:identifier>
<dc:title><![CDATA[Neonatal Parenteral Nutrition Hypersensitivity: A Case Report Implicating Bisulfite Sensitivity in a Newborn Infant]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>693</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>691</prism:startingPage>
<prism:section>Original Communications</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/6/694?rss=1">
<title><![CDATA[Low Availability of Aluminum in Formulations for Parenteral Nutrition Containing Silicate]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/6/694?rss=1</link>
<description><![CDATA[
<p><I>Background</I>: Silicate (Si) and aluminum (Al) may be concomitant
impurities in solutions for parenteral nutrition (PN). Silicate can bind to Al
to form stable hydroxyaluminosilicates (HAS), thus reducing Al availability.
This possibility is investigated by heating solutions containing constituents
of PN in glass containers to promote the release of Si and Al.
<I>Methods</I>: The total amount of Si and Al in solution is measured by
atomic absorption spectrometry, and the Al not bound to Si is evaluated by
reaction with morin. <I>Results:</I> When the Si:Al molar ratio is &gt;5, no
free Al is found in solution. For ratios &lt;5, it is found that the lower the
ratio, the higher the free Al fraction. However, in solutions of some amino
acids, even with a low Si:Al ratio (&lt;2), the amount of free Al is lower
than that found in other solutions. The same tendency is observed among
commercial formulations. Although in salt solutions the free fraction of Al
reaches almost 100% when the Si concentration is low, in amino acid
formulations the free fraction of Al does not surpass 50%. Moreover, even for
Si:Al ratios &gt;5, there is a "residual" fraction of free Al in
amino acid formulations. <I>Conclusions</I>: The concomitant presence of Al
and Si in solutions for PN reduces the amount of Al available attributable to
the formation of HAS. In amino acid formulations this effect may be slightly
reduced given the affinity of certain amino acids for Al. Therefore, amino
acids may behave in the same fashion as silicate.</p>
]]></description>
<dc:creator><![CDATA[Bohrer, D., Bortoluzzi, F., Nascimento, P. C. d., de Carvalho, L. M., de Oliveira, S. R.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 10:07:44 PST</dc:date>
<dc:identifier>info:doi/10.1177/0148607109333004</dc:identifier>
<dc:title><![CDATA[Low Availability of Aluminum in Formulations for Parenteral Nutrition Containing Silicate]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>701</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>694</prism:startingPage>
<prism:section>Original Communications</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/6/702?rss=1">
<title><![CDATA[Enteral Nutrition and Cardiovascular Failure: From Myths to Clinical Practice]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/6/702?rss=1</link>
<description><![CDATA[
<p>Cardiovascular failure and low flow states may arise in very different
conditions from both cardiac and noncardiac causes. Systemic hemodynamic
failure inevitably alters splanchnic blood flow but in an unpredictable way.
Prolonged low splanchnic blood flow causes intestinal ischemia, increased
mucosal permeability, endotoxemia, and distant organ failure. Mortality
associated with intestinal ischemia is high. Why would enteral nutrition (EN)
be desirable in these complex patients when parenteral nutrition could easily
cover energy and substrate requirements? Metabolic, immune, and practical
reasons justify the use of EN. In addition, continuous enteral feeding
minimizes systemic and myocardial oxygen consumption in patients with
congestive heart failure. Further, early feeding in critically ill
mechanically ventilated patients has been shown to reduce mortality,
particularly in the sickest patients. In a series of cardiac surgery patients
with compromised hemodynamics, absorption has been maintained, and 1000-1200
kcal/d could be delivered by enteral feeding. Therefore, early EN in
stabilized patients should be attempted, and can be carried out safely under
close clinical monitoring, looking for signs of incipient intestinal ischemia.
Energy delivery and balance should be monitored, and combined feeding
considered when enteral feeds cannot be advanced to target within 4-6
days.</p>
]]></description>
<dc:creator><![CDATA[Berger, M. M., Chiolero, R. L.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 10:07:44 PST</dc:date>
<dc:identifier>info:doi/10.1177/0148607109341769</dc:identifier>
<dc:title><![CDATA[Enteral Nutrition and Cardiovascular Failure: From Myths to Clinical Practice]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>709</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>702</prism:startingPage>
<prism:section>CNW 2009 Keynote Address</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/6/710?rss=1">
<title><![CDATA[Malnutrition Syndromes: A Conundrum vs Continuum]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/6/710?rss=1</link>
<description><![CDATA[
<p>This provocative commentary critically examines historic definitions for
adult malnutrition syndromes as they apply to developed countries with modern
healthcare. To stimulate further discussion, the authors propose an updated
approach that incorporates current understanding of the systemic inflammatory
response to help guide assessment, diagnosis, and treatment. An appreciation
of a continuum of inflammatory response in relation to malnutrition syndromes
is described. This discussion serves to highlight a research agenda to address
deficiencies in diagnostics, biomarkers, and therapeutics of inflammation in
relation to malnutrition.</p>
]]></description>
<dc:creator><![CDATA[Jensen, G. L., Bistrian, B., Roubenoff, R., Heimburger, D. C.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 10:07:44 PST</dc:date>
<dc:identifier>info:doi/10.1177/0148607109344724</dc:identifier>
<dc:title><![CDATA[Malnutrition Syndromes: A Conundrum vs Continuum]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>716</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>710</prism:startingPage>
<prism:section>Invited Commentary</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/6/717?rss=1">
<title><![CDATA[How Immunocompromised Are Short Bowel Patients Receiving Home Parenteral Nutrition? Apropos a Case of Disseminated Fusarium Oxysporum Sepsis]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/6/717?rss=1</link>
<description><![CDATA[
<p><I>Background:</I> Catheter-related sepsis is the most frequent
complication in patients receiving home parenteral nutrition (HPN) for short
bowel syndrome (SBS). A low-grade systemic inflammatory state and an altered
mucosal immune response, as well as diminished intestinal barrier function
have been characterized in these patients. The possibility of systemic
immunocompromise has only recently been suggested. <I>Case Description:</I>
A 45-year-old female with traumatic SBS was admitted for possible
catheter-related sepsis. She was asplenic and had insulin-dependent diabetes
mellitus as a result of a pancreatic resection. A large skin ulceration was
present on her left calf, which appeared unusual for a disseminated bacterial
infection. Chest x-ray and computed tomography scan revealed multiple
subpleural pulmonary infiltrates consistent with bacterial or fungal
dissemination. Blood cultures from the port system and from the peripheral
blood grew <I>Staphylococcus haemolyticus</I> and <I>Fusarium
oxysporum</I>. The port system was removed, and flucloxacillin and
voriconazole were given for 33 and 35 days, respectively. Clinical signs of
disseminated sepsis resolved slowly. Bone marrow biopsy ruled out primary
hematologic disease. <I>Conclusions:</I> (1) Catheter-related sepsis in
patients on HPN is usually caused by Gram-positive or Gram-negative bacteria
or by <I>Candida</I> species. Identification of molds in blood cultures
strongly suggests <I>Fusarium</I> species, which should be treated
appropriately with voriconazole or amphotericin B. (2) HPN and SBS aggravated
by asplenism and diabetes mellitus can cause severe immunocompromise. (3)
Fusaria have a strong tendency to persist or reappear after bone marrow
transplantation, which is therefore relatively contraindicated in these
patients.</p>
]]></description>
<dc:creator><![CDATA[Muller, C., Schumacher, U., Gregor, M., Lamprecht, G.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 10:07:44 PST</dc:date>
<dc:identifier>info:doi/10.1177/0148607109346321</dc:identifier>
<dc:title><![CDATA[How Immunocompromised Are Short Bowel Patients Receiving Home Parenteral Nutrition? Apropos a Case of Disseminated Fusarium Oxysporum Sepsis]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>720</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>717</prism:startingPage>
<prism:section>Case Reports</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/6/721?rss=1">
<title><![CDATA[Percutaneous Gastrojejunostomy Placement in a Heart Failure Patient With Biventricular Assist Devices]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/6/721?rss=1</link>
<description><![CDATA[
<p>Heart failure patients who require a ventricular assist device often
present a nutrition challenge. A 39-year-old woman suffering from an acute ST
elevated myocardial infarction and severe cardiogenic shock underwent implant
of left and right ventricular assist devices (BiVAD). Neurologic deficits
prevented her from safely resuming oral intake, and long-term feeding access
was required. The decision was made to insert a percutaneous gastrojejunostomy
under fluoroscopic guidance. Patients implanted with ventricular assist
devices may require enteral nutrition support. Placement of feeding access
other than through the nasoenteric route can be rendered more challenging
because of anatomical constraints related to BiVAD positioning; however,
whenever enteral nutrition support is required for extended periods,
percutaneous or ostomy access offers easier delivery of nutrition. Although
technically difficult, successful placement of the enteral feeding tube
allowed for continuous 24-hour feeds to optimize nutrition intake. This is the
first time that a percutaneous enteral feeding access was obtained for a
ventricular assist device patient at the authors' institution, and it has
proven valuable in providing long-term nutrition in a safe and efficient
manner.</p>
]]></description>
<dc:creator><![CDATA[Page, S., Cecere, R., Valenti, D.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 10:07:44 PST</dc:date>
<dc:identifier>info:doi/10.1177/0148607109338214</dc:identifier>
<dc:title><![CDATA[Percutaneous Gastrojejunostomy Placement in a Heart Failure Patient With Biventricular Assist Devices]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>723</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>721</prism:startingPage>
<prism:section>Case Reports</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/reprint/33/6/724?rss=1">
<title><![CDATA[Unanswered Questions of "ProCon"etic Therapy]]></title>
<link>http://pen.sagepub.com/cgi/reprint/33/6/724?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[MacLaren, R.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 10:07:44 PST</dc:date>
<dc:identifier>info:doi/10.1177/0148607109343591</dc:identifier>
<dc:title><![CDATA[Unanswered Questions of "ProCon"etic Therapy]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>725</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>724</prism:startingPage>
<prism:section>Editorials</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/reprint/33/6/726?rss=1">
<title><![CDATA[Imaging Biochemistry Noninvasively: Magnetic Resonance Spectroscopy in Liver Disease]]></title>
<link>http://pen.sagepub.com/cgi/reprint/33/6/726?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Serkova, N. J.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 10:07:44 PST</dc:date>
<dc:identifier>info:doi/10.1177/0148607109344727</dc:identifier>
<dc:title><![CDATA[Imaging Biochemistry Noninvasively: Magnetic Resonance Spectroscopy in Liver Disease]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>728</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>726</prism:startingPage>
<prism:section>Editorials</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/6/729?rss=1">
<title><![CDATA[Comment on: Measurement of Resting Energy Expenditure in Healthy Children]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/6/729?rss=1</link>
<description><![CDATA[
<p><I>Background:</I> The role that the components of energy expenditure
play in the etiology of childhood obesity has highlighted the need for greater
accuracy and standardized protocols for the measurement of resting energy
expenditure (REE). However, protocols used to assess REE in children are
varied, and consensus on a suitable method for measuring REE in children has
not been reached. This study was undertaken to determine the effect of
measurement time and measurement device (mask or mouthpiece) on REE in healthy
children. <I>Design:</I> Following a 12-hour fast and abstinence from
exercise, 23 children (age, 7&ndash;12 years) completed two 35-minute
protocols: one with a face mask and the other with a mouthpiece/noseclip.
Energy expenditure was measured continuously via indirect calorimetry, while
device acceptability was assessed using a 6-point comfort rating scale.
Results: Repeated measures ANOVA indicated that there was no significant
difference in REE when measured after 10, 15, 20, or 25 minutes of rest
compared to 30 minutes for either the mask or mouthpiece/noseclip (REE range,
1371&ndash;1460 kcal/d). Examination of the percentage coefficient of
variation (CV) in energy expenditure for each time period by device showed
that the least variation existed after 20 minutes of measurement using the
mask (CV 6%). Paired <I>t</I> test analysis indicated significantly less
discomfort when wearing the mask compared to the mouthpiece/noseclip.
<I>Conclusion:</I> It would appear that a 20-minute protocol using a mask
may increase compliance and prove to be a more practical protocol for
measuring REE in children.(<I>JPEN J Parenter Enteral Nutr</I>. 2009;33:640-645)</p>
]]></description>
<dc:creator><![CDATA[Bogucki, E. L.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 10:07:44 PST</dc:date>
<dc:identifier>info:doi/10.1177/0148607109343608</dc:identifier>
<dc:title><![CDATA[Comment on: Measurement of Resting Energy Expenditure in Healthy Children]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>730</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>729</prism:startingPage>
<prism:section>eJournal</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/reprint/33/6/731?rss=1">
<title><![CDATA[Prebiotics and Enteral Feeding-Associated Diarrhea]]></title>
<link>http://pen.sagepub.com/cgi/reprint/33/6/731?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Hegazi, R., Strausbaugh, K., Merritt, R.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 10:07:44 PST</dc:date>
<dc:identifier>info:doi/10.1177/0148607109341878</dc:identifier>
<dc:title><![CDATA[Prebiotics and Enteral Feeding-Associated Diarrhea]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>732</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>731</prism:startingPage>
<prism:section>Letters to the Editor</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/reprint/33/6/733?rss=1">
<title><![CDATA[Author Response]]></title>
<link>http://pen.sagepub.com/cgi/reprint/33/6/733?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Barrett, J. S, Shepherd, S. J., Gibson, P. R.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 10:07:44 PST</dc:date>
<dc:identifier>info:doi/10.1177/0148607109341880</dc:identifier>
<dc:title><![CDATA[Author Response]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>734</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>733</prism:startingPage>
<prism:section>Letters to the Editor</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/reprint/33/6/735?rss=1">
<title><![CDATA[Letter to the Editor]]></title>
<link>http://pen.sagepub.com/cgi/reprint/33/6/735?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Williams-Dolan, J. M., Boullata, J. I.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 10:07:44 PST</dc:date>
<dc:identifier>info:doi/10.1177/0148607109345021</dc:identifier>
<dc:title><![CDATA[Letter to the Editor]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>736</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>735</prism:startingPage>
<prism:section>Letters to the Editor</prism:section>
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