<?xml version="1.0" encoding="utf-8"?>
<recommendedContent xmlns="http://api.mspoke.com">
    <recommendedItem id="20100101_19_395"
                     title="Evidence-Based Care Cuts ADHD Symptoms, Not Impairment (CME/CE)"
                     score="0.012"
                     href="http://www.medpagetoday.com/Pediatrics/ADHD-ADD/tb/18292?impressionId=1265760167660"
                     
      Adhering to guidelines when treating children with attention deficit hyperactivity disorder (ADHD) relieved symptoms but had no effect on kids&apos; performance in school or in their relationships with others, researchers found.&lt;br&gt;
&lt;br&gt;Although parents and teachers noted significant improvements in symptoms among ADHD kids (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.001) in a special treatment program, there weren&apos;t similar outcomes for functional impairment, Jeffery N. Epstein, PhD, of the Center for ADHD at Cincinnati Children&apos;s Hospital in Ohio, reported in the February &lt;em&gt;Archives of Pediatrics and Adolescent Medicine&lt;/em&gt;.&lt;br&gt;
&lt;br&gt;&quot;This finding highlights the need for physicians to work with or refer patients to educational and mental healthcare specialists who can work with children to develop skills to address targeted areas of deficit,&quot; the researchers wrote.&lt;/p&gt;
&lt;p&gt;University-associated trials have shown stimulants are effective against ADHD, but these findings may not be translated into community practices  --  a potential public health concern, the researchers suggested.&lt;/p&gt;
&lt;p&gt;Guidelines for proper treatment exist, but they can be difficult to put into practice because of time, effort, and reimbursement concerns.&lt;/p&gt;
&lt;p&gt;So the researchers decided to test the efficacy of a quality improvement intervention called ADHD Collaborative, designed to enhance physician adherence to evidence-based, ADHD treatment guidelines.&lt;/p&gt;
&lt;p&gt;They conducted a case series involving 785 children ages 7 to 11, who were treated by 158 physicians at rural, suburban, and urban practices.&lt;/p&gt;
&lt;p&gt;The researchers found that, based on teacher and parent ratings, children showed vast improvements in ADHD symptoms (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.001).&lt;/p&gt;
&lt;p&gt;&quot;Improvement of ADHD symptoms occurred mainly in the first three months of treatment and remained improved and relatively stable thereafter,&quot; the researchers wrote. &quot;These results suggest that community-based physicians can achieve gains in ADHD symptom improvement comparable with carefully controlled, university-based clinical trials.&quot;&lt;/p&gt;
&lt;p&gt;However, there were no significant improvements in functional impairment as measured by parents and teachers.&lt;/p&gt;
&lt;p&gt;The proportion of functionally impaired children didn&apos;t change after treatment for any outcomes except teachers&apos; ratings of writing and assignment completion (&lt;em&gt;P&lt;/em&gt;=0.03 and &lt;em&gt;P&lt;/em&gt;=0.04, respectively).&lt;/p&gt;
&lt;p&gt;&quot;Effective treatment likely requires a multimodal strategy that includes a focus on teaching children [organizational and learning] skills,&quot; they wrote, adding that collaboration with other mental health or educational services &quot;appears to be warranted.&quot;&lt;/p&gt;
&lt;p&gt;Researchers said the study was limited because it didn&apos;t have a control group. Thus, it couldn&apos;t determine whether a similar pattern of treatment response would have been observed without physician training.&lt;/p&gt;
&lt;p&gt;The lack of a control group also made it impossible to account for any potential placebo effects.&lt;/p&gt;
&lt;p&gt;Finally, the authors didn&apos;t collect data on medication adherence.&lt;/p&gt;
&lt;p&gt;Still, they concluded that &quot;large improvements in symptoms can be achieved in primary care settings when physicians provide evidence-based ADHD care using medication.&quot;&lt;/p&gt;
&lt;div style=&quot;float:left;border-style:solid;border-width:1px;border-color:#8dabbc;font-family:arial;font-size:12px;background-color:#DBE9F2;padding:5px;&quot;&gt;&lt;p&gt;The study was supported by the Cincinnati Children&apos;s Hospital Medical Center Patient Innovation Fund.&lt;/p&gt;&lt;p&gt;The researchers reported no conflicts of interest.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_412"
                     title="Depression During Pregnancy Linked to Kids&apos; Behavior Problems (CME/CE)"
                     score="0.011"
                     href="http://www.medpagetoday.com/Psychiatry/Depression/tb/18321?impressionId=1265760167660"
                     
      &lt;p&gt;Children born to mothers who were depressed during pregnancy were more than twice as likely to display antisocial behavior by age 16 as children whose mothers had not been depressed, researchers found.&lt;/p&gt;
&lt;p&gt;Of 120 mothers from South London who were followed from pregnancy through their children&apos;s teen years, 31% had depression during pregnancy, according to Dale Hay, PhD, of Cardiff University in Wales, and colleagues.&lt;/p&gt;
&lt;p&gt;Children born to these women were significantly more likely to display antisocial behavior (OR 2.46, 95% CI 1.10 to 5.48) and commit violent acts (OR 4.36, 95% CI 1.54 to 12.41) before age 16, the researchers reported in the January/February issue of &lt;em&gt;Child Development&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;The associations were magnified in women who also had a history of behavior problems when they were children.&lt;/p&gt;
&lt;p&gt;&quot;A focus on mothers&apos; history of conduct problems and depression during pregnancy, as opposed to broader measures of the social environment, would hold promise for more targeted early interventions to prevent the development of serious antisocial behavior,&quot; Hay&apos;s group wrote.&lt;/p&gt;
&lt;p&gt;Previous studies have linked mothers&apos; mental health problems in pregnancy with disruptive behaviors in their children, but it&apos;s unclear what explains the relationship, according to the researchers.&lt;/p&gt;
&lt;p&gt;To explore the issue, they turned to the South London Child Development Study, which prospectively followed 120 pregnant women and their children into the teenage years.&lt;/p&gt;
&lt;p&gt;All families came from a relatively disadvantaged urban area. These families were more likely to belong to the working class and to be from ethnic minority groups than the general U.K. population.&lt;/p&gt;
&lt;p&gt;One-third of the children had been arrested or diagnosed with a conduct disorder by age 16. Of these 88.9% had been arrested and 45% had committed violent acts, including theft from a person, violent disorder, fighting, carrying a weapon, and assault.&lt;/p&gt;
&lt;p&gt;The association between maternal depression during pregnancy and risk of antisocial behavior remained relatively constant in analyses controlling for family environment, a child&apos;s exposure to maternal depression after birth, mothers&apos; substance use during pregnancy, and parental antisocial behavior.&lt;/p&gt;
&lt;p&gt;None of the factors fully explained the relationship. Neither did the arrest history of the biological father.&lt;/p&gt;
&lt;p&gt;But, the researchers wrote in the paper, &quot;it would be unwise to conclude that paternal risk factors are unimportant, given that we did not have more detailed information about the father&apos;s own history of conduct disorders.&quot;&lt;/p&gt;
&lt;p&gt;They explored several potential mechanisms for the link between maternal depression and a child&apos;s behavior problems: &lt;ul&gt; &lt;li&gt;Direct effects on the fetus from biological correlates of the mothers&apos; depressive symptoms&lt;/li&gt; &lt;li&gt;Depression in pregnancy as a sign of environmental adversity&lt;/li&gt; &lt;li&gt;Re-exposure to maternal depression after birth&lt;/li&gt; &lt;li&gt;Indirect effects of depression on the developing fetus driven by mothers&apos; smoking, drinking, and drug taking during pregnancy &lt;/li&gt; &lt;li&gt;A genetic explanation whereby women who experience depression in pregnancy may also have a greater genetic risk for antisocial behavior, which they pass on to their offspring &lt;/li&gt; &lt;/ul&gt;&lt;/p&gt;
&lt;p&gt;Hay and her colleagues noted that these explanations are not necessarily mutually exclusive.&lt;/p&gt;
&lt;p&gt;They also acknowledged some limitations of the study, including the lack of information about fetal growth and neuroendocrine measures on the mother and child and the relatively small sample size.&lt;/p&gt;
&lt;div style=&quot;float:left;border-style:solid;border-width:1px;border-color:#8dabbc;font-family:arial;font-size:12px;background-color:#DBE9F2;padding:5px;&quot;&gt;&lt;p&gt;The SLCDS has been funded by U.K. project grants from the Medical Research Council, by the Psychiatric Research Trust, and by the South West G.P. Trust. The current analysis was partially supported by an Economic and Social Research Council studentship to one of Hay&apos;s co-authors and by a Medical Research Council U.K. Program Grant.&lt;/p&gt;&lt;p&gt;The authors did not report any conflicts of interest.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_372"
                     title="Low Serotonin Eyed as Mechanism for SIDS (CME/CE)"
                     score="0.01"
                     href="http://www.medpagetoday.com/Neurology/GeneralNeurology/tb/18262?impressionId=1265760167660"
                     
      Low brainstem levels of serotonin and the enzyme that makes it could underlie sudden infant death syndrome (SIDS), researchers suggested.&lt;br&gt;
&lt;br&gt;In an autopsy study, SIDS cases showed 26% lower serotonin levels in two major components of the medulla&apos;s serotonin system  --  the raph&amp;#233; obscurus (&lt;em&gt;P&lt;/em&gt;=0.05) and paragigantocellularis lateralis (&lt;em&gt;P&lt;/em&gt;=0.04)  --  compared with age-adjusted controls who died from known causes.&lt;br&gt;
&lt;br&gt;These brainstem circuits control breathing, blood pressure, and heart rate during sleep, Hannah C. Kinney, MD, of Children&apos;s Hospital Boston, and colleagues reported in the Feb. 3 issue of the &lt;em&gt;Journal of the American Medical Association&lt;/em&gt;.&lt;br&gt;
&lt;br&gt;A baby with an abnormality in control of these systems might not be able to respond to a life-threatening challenge like asphyxia by rousing from sleep or turning its head the researchers explained.&lt;p&gt;&lt;/p&gt;
&lt;p&gt;SIDS occurs in the &quot;critical first year of life, when homeostatic systems are still maturing,&quot; they noted.&lt;/p&gt;
&lt;p&gt;Mary McClain, RN, MS, of Boston University Medical Center, who counsels families that have lost a baby to SIDS, commented that these findings help establish the biological basis for urging parents to place their babies on their backs to sleep.&lt;/p&gt;
&lt;p&gt;The researchers obtained tissue samples from autopsies of 41 children who died from SIDS, seven who died acutely from known causes (including a car accident, drowning, pneumonia, and unsuspected congenital heart disease), and five who died in the hospital with chronic conditions causing hypoxia-ischemia.&lt;/p&gt;
&lt;p&gt;SIDS cases had mean serotonin levels of 31.4 pmol/mg of protein in the paragigantocellularis lateralis, compared with 40.0 pmol/mg among the controls who died acutely (&lt;em&gt;P&lt;/em&gt;=0.04).&lt;/p&gt;
&lt;p&gt;Levels averaged 55.4 versus 75.5 pmol/mg of protein, respectively, in the raph&amp;#233; obscurus (&lt;em&gt;P&lt;/em&gt;=0.05).&lt;/p&gt;
&lt;p&gt;These abnormalities in the medulla did not appear to involve the catecholamine system. Catecholamine levels were similar between SIDS cases and controls.&lt;/p&gt;
&lt;p&gt;Nor was there evidence for excessive degradation of dopamine or neurotransmitter turnover in SIDS cases, supporting the idea that the key abnormality is reduced synthesis of serotonin, the researchers said.&lt;/p&gt;
&lt;p&gt;Another marker of serotonin function  --  tryptophan hydroxylase (TPH2), the key enzyme involved in synthesis of serotonin  --  also supported this conclusion, with 22% lower levels in the raph&amp;#233; obscurus in SIDS than in controls (&lt;em&gt;P&lt;/em&gt;=0.03).&lt;/p&gt;
&lt;p&gt;Serotonin receptor binding was 29% to 55% lower in three medullary nuclei that receive serotonin projections, notable for a decrease in binding with older age in SIDS cases, but not controls, the researchers noted.&lt;/p&gt;
&lt;p&gt;Given similar findings in three previous investigations, this &quot;may reflect a progressive decrease with age in those infants with the &apos;SIDS abnormality,&apos;&quot; they wrote. Or it&apos;s possible that those with a &quot;stronger abnormality take longer to outgrow the risk period for SIDS and continue to die at older ages,&quot; Kinney&apos;s group wrote.&lt;/p&gt;
&lt;p&gt;Likewise, serotonin receptor binding in infants who died from SIDS was significantly lower in those without known risk factors for SIDS, such as &lt;a href=&quot;http://www.medpagetoday.com/Pediatrics/GeneralPediatrics/17365&quot; mce_href=&quot;http://www.medpagetoday.com/Pediatrics/GeneralPediatrics/17365&quot; target=&quot;_blank&quot;&gt;sleeping face down&lt;/a&gt;, &quot;suggesting that additional risk factors are necessary to precipitate death when the medullary serotonin system is less compromised,&quot; they added.&lt;/p&gt;
&lt;p&gt;Although repetitive apnea and agonal &lt;a href=&quot;http://www.medpagetoday.com/Pulmonology/SleepDisorders/2817&quot; mce_href=&quot;http://www.medpagetoday.com/Pulmonology/SleepDisorders/2817&quot; target=&quot;_blank&quot;&gt;impaired gasping&lt;/a&gt; before death have been reported in some SIDS cases, chronic impaired oxygenation in the hospitalized children in the study produced a very different serotonin pattern than that seen in SIDS.&lt;/p&gt;
&lt;p&gt;Children who died with chronic hypoxia conditions had 55% higher serotonin levels in the raph&amp;#233; obscurus (&lt;em&gt;P&lt;/em&gt;=0.02) and 126% higher levels in the paragigantocellularis lateralis (&lt;em&gt;P&lt;/em&gt;=0.002) than the SIDS cases.&lt;/p&gt;
&lt;p&gt;They also had 640% higher dopamine levels in the raph&amp;#233; obscurus than the SIDS cases (&lt;em&gt;P&lt;/em&gt;=0.006).&lt;/p&gt;
&lt;p&gt;This suggested &quot;that the primary mechanisms underlying serotonin abnormalities in SIDS are not mediated by chronic hypoxia-ischemia,&quot; Kinney&apos;s group wrote.&lt;/p&gt;
&lt;p&gt;The researchers cautioned that their neurotransmitter measurements may have been off somewhat due to prolonged postmortem intervals.&lt;/p&gt;
&lt;p&gt;They also warned that the study was limited by inability to perform these measurements at the synapse in postmortem tissues and by the small sample of controls.&lt;/p&gt;
&lt;div style=&quot;float:left;border-style:solid;border-width:1px;border-color:#8dabbc;font-family:arial;font-size:12px;background-color:#DBE9F2;padding:5px;&quot;&gt;&lt;p&gt;The study was supported by the First Candle/SIDS Alliance, CJ Martin Overseas Fellowship (National Health and Medical Research Council of Australia), CJ Murphy Foundation for Solving the Puzzle of SIDS, CJ Foundation for SIDS, National Institute of Child Health and Development, and the Developmental Disabilities Research Center at Children&apos;s Hospital Boston.&lt;/p&gt;&lt;p&gt;The researchers reported no conflicts of interest.&lt;/p&gt;&lt;p&gt;McClain provided no information on conflicts of interest.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_355"
                     title="Obesity Delays Puberty in Boys (CME/CE)"
                     score="0.009"
                     href="http://www.medpagetoday.com/Pediatrics/Obesity/tb/18235?impressionId=1265760167660"
                     
      &lt;p&gt;Unlike overweight girls, who tend to enter puberty early, overweight and obese boys in the U.S. may begin puberty later than thin boys, according to one of the first longitudinal studies of weight and timing of puberty in males.&lt;/p&gt;
&lt;p&gt;At 11.5 years, boys with the highest body mass index (mean BMI z score=1.84) were 165% more likely to be prepubertal than the thinnest boys (95% CI 1.05 to 6.61; &lt;em&gt;P&lt;/em&gt;=0.04), researchers reported online in the Feb. 1 &lt;em&gt;Archives of Pediatrics and Adolescent Medicine&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;&quot;This longitudinal study provides further evidence that higher BMI during early and middle childhood is not associated with earlier pubertal onset in boys, contrary to what is seen in girls,&quot; Joyce M. Lee, MD, MPH, of the University of Michigan, and colleagues wrote.&lt;/p&gt;
&lt;p&gt;&quot;In fact, higher BMI in earlier childhood may be associated with and precede later onset of puberty among a population-based sample of U.S. boys.&quot;&lt;/p&gt;
&lt;p&gt;Rates of obesity among American girls and boys have nearly tripled since the 1960s, prompting concerns about the effect of excess weight on growth and development. Most research has focused on obese girls, who appear to reach puberty earlier than thin girls. A recent cross-sectional study suggested that, unlike their female counterparts, overweight boys may develop later.&lt;/p&gt;
&lt;p&gt;To further explore this relationship, Lee and colleagues analyzed the records of 401 boys from diverse socioeconomic backgrounds in ten regions of the U.S., using data from the National Institute of Child Health and Human Development Study of Early Child Care and Youth Development. The participants were full-term, only children born in 1991.&lt;/p&gt;
&lt;p&gt;The data included height and weight measurements of the children from ages 2 to 12 years and a visual assessment of whether the children had begun puberty, using Tanner genitalia staging, at 9.5, 10.5, and 11.5 years. Boys were defined as prepubertal if they were Tanner stage 1 at 11.5 years old and were otherwise categorized as pubertal.&lt;/p&gt;
&lt;p&gt;Among the participants, 14.4% were overweight (BMI &amp;#8805; 85th and &amp;lt;95th percentiles) and 19.4% were obese (BMI&amp;#8805;95th percentile) at age 11.5. Overall, 49 boys (12.2%) were prepubertal at age 11.5 years by Tanner genitalia staging.&lt;/p&gt;
&lt;p&gt;The authors wrote that their findings have important implications for understanding sex differences in physiological mechanisms of puberty.&lt;/p&gt;
&lt;p&gt;They noted that puberty is regulated by the gonadotropin-releasing hormone axis for both girls and boys, but it&apos;s unclear why such different associations between body fat and the timing of pubertal onset would exist between the sexes.&lt;/p&gt;
&lt;p&gt;&quot;Given the recent childhood obesity epidemic, additional studies are needed to further investigate the epidemiological link between body fat and pubertal initiation and progression in boys as well as the physiological mechanisms responsible,&quot; they concluded.&lt;/p&gt;
&lt;p&gt;The authors were unable to analyze the data based on race, because most of the children in the study were white. They also noted that BMI is a surrogate measure of overall body fat, and that study has found that the relationship between body fat and BMI varies depending on race. They also recommended that future studies use multiple methods of determining whether children have entered puberty.&lt;/p&gt;
&lt;div style=&quot;float:left;border-style:solid;border-width:1px;border-color:#8dabbc;font-family:arial;font-size:12px;background-color:#DBE9F2;padding:5px;&quot;&gt;&lt;p&gt;The study was funded by the National Institute of Child Health and Human Development and the American Heart Association.&lt;/p&gt;&lt;p&gt;The authors reported no financial conflicts of interest.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_346"
                     title="Daytime Sleepiness More Common in Young (CME/CE)"
                     score="0.008"
                     href="http://www.medpagetoday.com/PrimaryCare/SleepDisorders/tb/18221?impressionId=1265760167660"
                     
      &lt;p&gt;Compared with 20-somethings and seniors, middle-age adults are less likely to suffer daytime sleepiness when they don&apos;t get a good night&apos;s sleep, according to a small study.&lt;/p&gt;
&lt;p&gt;When three groups of healthy adults  --  young (20 to 30 years old), middle-age (40 to 55) and older (66 to 83)  --  were studied over four nights, slow wave sleep decreased and the number of nocturnal awakenings progressively increased with age, wrote Derk-Jan Dijk, PhD, of the Surrey Sleep Center at the University of Surrey in Guildford, England, and colleagues in the Feb. 1 issue of &lt;em&gt;Sleep.&lt;/em&gt;&lt;/p&gt;

&lt;p&gt;As the likelihood for eight hours of uninterrupted deep sleep decreased with age, there was no increase in the likelihood of daytime sleepiness, which led Dijk and colleagues to conclude that as people age there may be a change in the &quot;sleep (duration and depth) required to maintain alertness.&quot;&lt;/p&gt;
&lt;p&gt;Based on that observation, the authors wrote that it could be argued that &quot;an eight-hour episode rich in [slow wave sleep] is insufficient for young adults but that an eight-hour sleep episode with less [slow wave sleep] is sufficient for older adults.&quot;&lt;/p&gt;
&lt;p&gt;As a result, middle-age and older adults are less likely to build up &quot;sleep debt&quot; during the daylight hours, so they manage with less time in deep sleep at night, less homeostatic sleep pressure.&lt;/p&gt;
&lt;p&gt;The authors hypothesized that this apparent need for less sleep may be a factor in age-related insomnia.&lt;/p&gt;
&lt;p&gt;If older adults are unaware of the need for less sleep, &quot;their self-selected time in bed, which provides an input to the sleep homeostat, may become maladaptive and lead to reduced sleep consolidation and associated complaints.&quot;&lt;/p&gt;
&lt;p&gt;Dijk and colleagues recruited 44 young adults, 35 middle-age adults, and 31 older adults for their study. All were healthy at baseline and all were initially assessed for an eight-hour nocturnal sleep episode.&lt;/p&gt;
&lt;p&gt;They were then randomized to two nights of either selective short wave sleep interruption by acoustic stimuli or sleep without disruption, followed by one night of recovery sleep.&lt;/p&gt;
&lt;p&gt;Two standardized measurement tools, the Multiple Sleep Latency Test (MSLT) and the Karolinska Sleepiness Scale (KSS), were used to assess objective and subjective sleep propensity.&lt;/p&gt;
&lt;p&gt;&quot;Total sleep time per eight hour time in bed decreased significantly and progressively across the age groups such that older adults slept approximately 20 minutes less than middle-aged, who slept 23 minutes less than young adults,&quot; they wrote.&lt;/p&gt;
&lt;p&gt;The reduction in total sleep time &quot;was primarily related to an increase in the number of awakenings and the duration of wakefulness after sleep onset, rather than an increase in latency to sleep onset.&quot;&lt;/p&gt;
&lt;p&gt;As a result, sleep efficiency decreased significantly from 92.1% for the youngest group, to 82% for the older group (effect of age, &lt;em&gt;P&amp;lt;&lt;/em&gt;0.0001).&lt;/p&gt;
&lt;p&gt;The subjective sleep propensity tests revealed that &quot;young people were significantly sleepier than the middle-age people, who were the least sleepy of the three groups.&quot; Daytime sleepiness for the oldest group &quot;fell in between the other two groups [and] was not significantly different from either.&quot;&lt;/p&gt;
&lt;p&gt;All three groups, regardless of age, demonstrated increased daytime sleepiness following a night of experimental disruption of slow wave sleep, but when the participants had an uninterrupted eight hours of deep sleep, it was only the youngest group that was drowsy during the daytime hours.&lt;/p&gt;
&lt;p&gt;The authors noted that although there was less daytime sleepiness among middle-age and older adults in this study, sleep propensity was not measured during the evening hours, so it was possible that the age-related difference might diminish at twilight.&lt;/p&gt;
&lt;div style=&quot;float:left;border-style:solid;border-width:1px;border-color:#8dabbc;font-family:arial;font-size:12px;background-color:#DBE9F2;padding:5px;&quot;&gt;&lt;p&gt;The study was sponsored by H. Lundbeck A/S.&lt;/p&gt;&lt;p&gt;Dijk reported receiving research support from the Air Force Office of Scientific Research, the Biotechnology and Biological Sciences Research Council, GlaxoSmithKline, H. Lundbeck A/S, Merck, Pfizer, Philips Lighting, sanofi-aventis, and Takeda.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
</recommendedContent>