Feasibility and Impact Assessment of a Food Insecurity Protocol in a Large Urban Pediatric Primary Care Network.

INTRODUCTION/OBJECTIVES: In 2022, 1 in 6 households with children experienced food insecurity (FI) in the United States. The negative impact of FI on child health is well documented and pediatric clinicians are encouraged to actively screen and intervene in clinical settings. This study aims to evaluate the feasibility and impact of a FI management protocol implemented in 2017 at a pediatric primary care health network serving patients who are Medicaid-eligible in Washington, DC. METHODS: In 2019, an 18-item electronic survey was sent to a convenience sample of 42 pediatric clinicians within the health network to understand their knowledge, attitudes, and behaviors surrounding implementation. Both quantitative and qualitative responses were collected and analyzed. We report frequencies of the Likert-type responses, including perceived compliance with protocol components and intervention efficacy. We evaluated the relationship between FI knowledge level and rates of clinician documentation compliance by chi square and Cramer's V statistic for effect size. Open-ended responses were reviewed, and common themes were identified and used to provide context for quantitative results. RESULTS AND CONCLUSIONS: Out of 42 clinicians invited to complete the survey, 35 completed responses. All respondents reported universal screening for FI (100%) at routine examinations, 80% reported frequently electronically documenting FI in medical records, and 91% of clinicians reported frequently referring families who screened positive for FI to at least one FI resource, with 24% reporting that resources met families' needs. Open-ended responses revealed increased awareness of FI prevalence and of patient experiences in households experiencing FI, increased satisfaction with clinical management of FI, but also concerns around having limited clinical time to do the protocol and the usefulness and accessibility of referred resources. In conclusion, implementing this pilot FI protocol was feasible, but clinicians perceived limited impact of the protocol on alleviating FI and desired more robust intervention options. Further improvements include shifting the burden of performing the protocol away from the clinician, such as by streamlining the protocol or identifying a resource staff member, and establishing more accessible and effective FI interventions such as "Food as Medicine" offerings in partnership with community organizations.

Cx43 hemichannels contribute to astrocyte-mediated toxicity in sporadic and familial ALS.

Connexin 43 (Cx43) gap junctions and hemichannels mediate astrocyte intercellular communication in the central nervous system under normal conditions and contribute to astrocyte-mediated neurotoxicity in amyotrophic lateral sclerosis (ALS). Here, we show that astrocyte-specific knockout of Cx43 in a mouse model of ALS slows disease progression both spatially and temporally, provides motor neuron (MN) protection, and improves survival. In addition, Cx43 expression is up-regulated in human postmortem tissue and cerebrospinal fluid from ALS patients. Using human induced pluripotent stem cell­derived astrocytes (hiPSC-A) from both familial and sporadic ALS, we establish that Cx43 is up-regulated and that Cx43-hemichannels are enriched at the astrocyte membrane. We also demonstrate that the pharmacological blockade of Cx43-hemichannels in ALS astrocytes using GAP 19, a mimetic peptide blocker, and tonabersat, a clinically tested small molecule, provides neuroprotection of hiPSC-MN and reduces ALS astrocyte-mediated neuronal hyperexcitability. Extending the in vitro application of tonabersat with chronic administration to SOD1G93A mice results in MN protection with a reduction in reactive astrocytosis and microgliosis. Taking these data together, our studies identify Cx43 hemichannels as conduits of astrocyte-mediated disease progression and a pharmacological target for disease-modifying ALS therapies.

Cingulo-opercular control network and disused motor circuits joined in standby mode.

Whole-brain resting-state functional MRI (rs-fMRI) during 2 wk of upper-limb casting revealed that disused motor regions became more strongly connected to the cingulo-opercular network (CON), an executive control network that includes regions of the dorsal anterior cingulate cortex (dACC) and insula. Disuse-driven increases in functional connectivity (FC) were specific to the CON and somatomotor networks and did not involve any other networks, such as the salience, frontoparietal, or default mode networks. Censoring and modeling analyses showed that FC increases during casting were mediated by large, spontaneous activity pulses that appeared in the disused motor regions and CON control regions. During limb constraint, disused motor circuits appear to enter a standby mode characterized by spontaneous activity pulses and strengthened connectivity to CON executive control regions.

Managing family dynamics when caring for older adults.

Caring for older patients with neurocognitive disorders can be challenging, especially when family members disagree regarding optimal care. This article explores the role and utilization of mediators in the healthcare setting.

Focal and dose-dependent neuroprotection in ALS mice following AAV2-neurturin delivery.

Neurotrophic factors as candidates for ALS therapeutics have previously been studied in the context of attempts to slow disease progression. For a variety of reasons, clinical trials of neurotrophic factors have failed to show efficacy in ALS patients. Previous studies in Parkinson's Disease (PD) models have shown promise with the use of recombinant adeno-associated virus serotype-2 (rAAV2)-neurturin (NRTN) [AAV2-NRTN] providing neuroprotection and behavioral improvements in preclinical models which subsequently resulted in several clinical studies in patients with PD. Given that this neurotrophic compound has not been studied in the context of ALS, we conducted a study of AAV2-NRTN to assess the preclinical safety, tolerability, biodistribution, and efficacy of this compound in an ALS mouse model. SOD1G93A mice were injected with AAV2-NRTN intraspinally at several doses into the cervical spinal cord at 60 days of age. NRTN expression was noted in motor neurons (MNs) of the targeted cervical spinal cord as well as in their neuromuscular junction projections but not in the lumbar spinal cord, which was not targeted. Neuropathologically, a dose-dependent neuroprotective effect was seen in cervical MNs and neuromuscular junctions that was reflected in a slowing of forelimb grip strength decline. As expected, this neuroprotection was found to be focal and was not seen beyond the immediate region of injection. Overall, there were no increases in morbidity, changes in serum chemistries or blood counts and no cases of drug-related mortality. Because there is a broad clinical experience for this compound, these data provide evidence to support further investigation of AAV2-NRTN as a potential ALS therapeutic.

Role of Human-Induced Pluripotent Stem Cell-Derived Spinal Cord Astrocytes in the Functional Maturation of Motor Neurons in a Multielectrode Array System.

The ability to generate human-induced pluripotent stem cell (hiPSC)-derived neural cells displaying region-specific phenotypes is of particular interest for modeling central nervous system biology in vitro. We describe a unique method by which spinal cord hiPSC-derived astrocytes (hiPSC-A) are cultured with spinal cord hiPSC-derived motor neurons (hiPSC-MN) in a multielectrode array (MEA) system to record electrophysiological activity over time. We show that hiPSC-A enhance hiPSC-MN electrophysiological maturation in a time-dependent fashion. The sequence of plating, density, and age in which hiPSC-A are cocultured with MN, but not their respective hiPSC line origin, are factors that influence neuronal electrophysiology. When compared to coculture with mouse primary spinal cord astrocytes, we observe an earlier and more robust electrophysiological maturation in the fully human cultures, suggesting that the human origin is relevant to the recapitulation of astrocyte/motor neuron crosstalk. Finally, we test pharmacological compounds on our MEA platform and observe changes in electrophysiological activity, which confirm hiPSC-MN maturation. These findings are supported by immunocytochemistry and real-time PCR studies in parallel cultures demonstrating human astrocyte mediated changes in the structural maturation and protein expression profiles of the neurons. Interestingly, this relationship is reciprocal and coculture with neurons influences astrocyte maturation as well. Taken together, these data indicate that in a human in vitro spinal cord culture system, astrocytes support hiPSC-MN maturation in a time-dependent and species-specific manner and suggest a closer approximation of in vivo conditions. Stem Cells Translational Medicine 2019;8:1272&1285.

Hip circumduction is not a compensation for reduced knee flexion angle during gait.

It has long been held that hip abduction compensates for reduced swing-phase knee flexion angle, especially in those after stroke. However, there are other compensatory motions such as pelvic obliquity (hip hiking) that could also be used to facilitate foot clearance with greater energy efficiency. Our previous work suggested that hip abduction may not be a compensation for reduced knee flexion after stroke. Previous study applied robotic knee flexion assistance in people with post-stroke Stiff-Knee Gait (SKG) during pre-swing, finding increased abduction despite improved knee flexion and toe clearance. Thus, our hypothesis was that hip abduction is not a compensation for reduced knee flexion. We simulated the kinematics of post-stroke SKG on unimpaired individuals with three factors: a knee orthosis to reduce knee flexion, an ankle-foot orthosis commonly worn by those post-stroke, and matching gait speeds. We compared spatiotemporal measures and kinematics between experimental factors within healthy controls and with a previously recorded cohort of people with post-stroke SKG. We focused on frontal plane motions of hip and pelvis as possible compensatory mechanisms. We observed that regardless of gait speed, knee flexion restriction increased pelvic obliquity (2.8°, p < 0.01) compared to unrestricted walking (1.5°, p < 0.01), but similar to post-stroke SKG (3.4°). However, those with post-stroke SKG had greater hip abduction (8.2°) compared to unimpaired individuals with restricted knee flexion (4.2°, p < 0.05). These results show that pelvic obliquity, not hip abduction, compensates for reduced knee flexion angle. Thus, other factors, possibly neural, facilitate exaggerated hip abduction observed in post-stroke SKG.

Perfluorocarbon Labeling of Human Glial-Restricted Progenitors for 19 F Magnetic Resonance Imaging.

One of the fundamental limitations in assessing potential efficacy in Central Nervous System (CNS) transplantation of stem cells is the capacity for monitoring cell survival and migration noninvasively and longitudinally. Human glial-restricted progenitor (hGRP) cells (Q-Cells) have been investigated for their utility in providing neuroprotection following transplantation into models of amyotrophic lateral sclerosis (ALS) and have been granted a Food and Drug Administration (FDA) Investigational New Drug (IND) for intraspinal transplantation in ALS patients. Furthermore, clinical development of these cells for therapeutic use will rely on the ability to track the cells using noninvasive imaging methodologies as well as the verification that the transplanted GRPs have disease-relevant activity. As a first step in development, we investigated the use of a perfluorocarbon (PFC) dual-modal (19 F magnetic resonance imaging [MRI] and fluorescence) tracer agent to label Q-Cells in culture and following spinal cord transplantation. PFCs have a number of potential benefits that make them appealing for clinical use. They are quantitative, noninvasive, biologically inert, and highly specific. In this study, we developed optimized PFC labeling protocols for Q-Cells and demonstrate that PFCs do not significantly alter the glial identity of Q-Cells. We also show that PFCs do not interfere with the capacity for differentiation into astrocytes either in vitro or following transplantation into the ventral horn of the mouse spinal cord, and can be visualized in vivo by hot spot 19 F MRI. These studies provide a foundation for further preclinical development of PFCs within the context of evaluating Q-Cell transplantation in the brain and spinal cord of future ALS patients using 19 F MRI. Stem Cells Translational Medicine 2019;8:355-365.

Serial in vivo imaging of transplanted allogeneic neural stem cell survival in a mouse model of amyotrophic lateral sclerosis.

Neural stem cells (NSCs) are being investigated as a possible treatment for amyotrophic lateral sclerosis (ALS) through intraspinal transplantation, but no longitudinal imaging studies exist that describe the survival of engrafted cells over time. Allogeneic firefly luciferase-expressing murine NSCs (Luc+-NSCs) were transplanted bilaterally (100,000 cells/2µl) into the cervical spinal cord (C5) parenchyma of pre-symptomatic (63day-old) SOD1G93A ALS mice (n=14) and wild-type age-matched littermates (n=14). Six control SOD1G93A ALS mice were injected with saline. Mice were immunosuppressed using a combination of tacrolimus+sirolimus (1mg/kg each, i.p.) daily. Compared to saline-injected SOD1G93A ALS control mice, a transient improvement (p<0.05) in motor performance (rotarod test) was observed after NSC transplantation only at the early disease stage (weeks 2 and 3 post-transplantation). Compared to day one post-transplantation, there was a significant decline in bioluminescent imaging (BLI) signal in SOD1G93A ALS mice at the time of disease onset (71.7±17.9% at 4weeks post-transplantation, p<0.05), with a complete loss of BLI signal at endpoint (120day-old mice). In contrast, BLI signal intensity was observed in wild-type littermates throughout the entire study period, with only a 41.4±8.7% decline at the endpoint. In SOD1G93A ALS mice, poor cell survival was accompanied by accumulation of mature macrophages and the presence of astrogliosis and microgliosis. We conclude that the disease progression adversely affects the survival of engrafted murine Luc+-NSCs in SOD1G93A ALS mice as a result of the hostile ALS spinal cord microenvironment, further emphasizing the challenges that face successful cell therapy of ALS.

Comparison of two psycho-educational family group interventions for improving psycho-social outcomes in persons with spinal cord injury and their caregivers: a randomized-controlled trial of multi-family group intervention versus an active education control condition.

BACKGROUND: Over 12,000 individuals suffer a spinal cord injury (SCI) annually in the United States, necessitating long-term, complex adjustments and responsibilities for patients and their caregivers. Despite growing evidence that family education and support improves the management of chronic conditions for care recipients as well as caregiver outcomes, few systematic efforts have been made to involve caregivers in psycho-educational interventions for SCI. As a result, a serious gap exists in accumulated knowledge regarding effective, family-based treatment strategies for improving outcomes for individuals with SCI and their caregivers. The proposed research aims to fill this gap by evaluating the efficacy of a structured adaptation of an evidence-based psychosocial group treatment called Multi-Family Group (MFG) intervention. The objective of this study is to test, in a randomized-controlled design, an MFG intervention for the treatment of individuals with SCI and their primary caregivers. Our central hypothesis is that by providing support in an MFG format, we will improve coping skills of persons with SCI and their caregivers as well as supportive strategies employed by caregivers. METHODS: We will recruit 32 individuals with SCI who have been discharged from inpatient rehabilitation within the previous 3 years and their primary caregivers. Patient/caregiver pairs will be randomized to the MFG intervention or an active SCI education control (SCIEC) condition in a two-armed randomized trial design. Participants will be assessed pre- and post-program and 6 months post-program. Intent to treat analyses will test two a priori hypotheses: (1) MFG-SCI will be superior to SCIEC for SCI patient activation, health status, and emotion regulation, caregiver burden and health status, and relationship functioning, and (2) MFG will be more effective for individuals with SCI and their caregivers when the person with SCI is within 18 months of discharge from inpatient rehabilitation compared to when the person is between 19 and 36 months post discharge. DISCUSSION: Support for our hypotheses will indicate that MFG-SCI is superior to specific education for assisting patients and their caregivers in the management of difficult, long-term, life adjustments in the months and years after SCI, with increased efficacy closer in time to the injury. TRIAL REGISTRATION: ClinicalTrials.gov NCT02161913 . Registered 10 June 2014.

Effectiveness of a Staff Promoted Wellness Program to Improve Health in Residents of a Mental Health Long-Term Care Facility.

The current study describes physical and mental health outcomes during a health promotion program for individuals with serious mental illness (SMI). A sample of 43 adults in a long-term residential facility volunteered for an individualized, healthy lifestyle program designed to promote physical activity and combat premature mortality among individuals with SMI. Nurses and residential counselors were trained in the program and encouraged to work collaboratively with the program's personal trainers. Weekly nutrition and activity logs were obtained over the year-long evaluation. Assessments of physical and psychological health indicators were collected quarterly. Qualitative data through focus groups described staff experience. Self-report of moderate and vigorous physical activity improved over time as did fitness level as measured through a walking challenge (p = .001). Significant decreases in weight (p < .001), BMI (p = .001), and total cholesterol (p < .001) were observed from baseline through 12 months. Mean recovery scores (RMQ) were significantly higher between baseline and all time points (p < .001). Participants reported decreasing levels of depression (PHQ-9) by the 12-month time point (p < .001). Staff encouraged participation in physical activity and observed improved motivation and socialization among participants. A health promotion program with participation encouraged by health care staff is effective for increasing physical activity and improving physical and mental health outcomes in individuals with SMI in long-term residential care.

Connexin 43 in astrocytes contributes to motor neuron toxicity in amyotrophic lateral sclerosis.

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by progressive loss of motor neurons in the CNS. Astrocytes play a critical role in disease progression of ALS. Astrocytes are interconnected through a family of gap junction proteins known as connexins (Cx). Cx43 is a major astrocyte connexin conducting crucial homeostatic functions in the CNS. Under pathological conditions, connexin expression and functions are altered. Here we report that an abnormal increase in Cx43 expression serves as one of the mechanisms for astrocyte-mediated toxicity in ALS. We observed a progressive increase in Cx43 expression in the SOD1(G93A) mouse model of ALS during the disease course. Notably, this increase in Cx43 was also detected in the motor cortex and spinal cord of ALS patients. Astrocytes isolated from SOD1(G93A) mice as well as human induced pluripotent stem cell (iPSC)-derived astrocytes showed an increase in Cx43 protein, which was found to be an endogenous phenomenon independent of neuronal co-culture. Increased Cx43 expression led to important functional consequences when tested in SOD1(G93A) astrocytes when compared to control astrocytes over-expressing wild-type SOD1 (SOD1(WT) ). We observed SOD1(G93A) astrocytes exhibited enhanced gap junction coupling, increased hemichannel-mediated activity, and elevated intracellular calcium levels. Finally, we tested the impact of increased expression of Cx43 on MN survival and observed that use of both a pan Cx43 blocker and Cx43 hemichannel blocker conferred neuroprotection to MNs cultured with SOD1(G93A) astrocytes. These novel findings show a previously unrecognized role of Cx43 in ALS-related motor neuron loss. GLIA 2016;64:1154-1169.

Human glial progenitor engraftment and gene expression is independent of the ALS environment.

Although Amyotrophic Lateral Sclerosis (ALS) is a motor neuron disease, basic research studies have highlighted that astrocytes contribute to the disease process. Therefore, strategies which replace the diseased astrocyte population with healthy astrocytes may protect against motor neuron degeneration. Our studies have sought to evaluate astrocyte replacement using glial-restricted progenitors (GRPs), which are lineage-restricted precursors capable of differentiating into astrocytes after transplantation. The goal of our current study was to evaluate how transplantation to the diseased ALS spinal cord versus a healthy, wild-type spinal cord may affect human GRP engraftment and selected gene expression. Human GRPs were transplanted into the spinal cord of either an ALS mouse model or wild-type littermate mice. Mice were sacrificed for analysis at either the onset of disease course or at the endstage of disease. The transplanted GRPs were analyzed by immunohistochemistry and NanoString gene profiling which showed no gross differences in the engraftment or gene expression of the cells. Our data indicate that human glial progenitor engraftment and gene expression is independent of the neurodegenerative ALS spinal cord environment. These findings are of interest given that human GRPs are currently in clinical development for spinal cord transplantation into ALS patients.

Gene profiling of human induced pluripotent stem cell-derived astrocyte progenitors following spinal cord engraftment.

The generation of human induced pluripotent stem cells (hiPSCs) represents an exciting advancement with promise for stem cell transplantation therapies as well as for neurological disease modeling. Based on the emerging roles for astrocytes in neurological disorders, we investigated whether hiPSC-derived astrocyte progenitors could be engrafted to the rodent spinal cord and how the characteristics of these cells changed between in vitro culture and after transplantation to the in vivo spinal cord environment. Our results show that human embryonic stem cell- and hiPSC-derived astrocyte progenitors survive long-term after spinal cord engraftment and differentiate to astrocytes in vivo with few cells from other lineages present. Gene profiling of the transplanted cells demonstrates the astrocyte progenitors continue to mature in vivo and upregulate a variety of astrocyte-specific genes. Given this mature astrocyte gene profile, this work highlights hiPSCs as a tool to investigate disease-related astrocyte biology using in vivo disease modeling with significant implications for human neurological diseases currently lacking animal models.

Altered astrocytic expression of TDP-43 does not influence motor neuron survival.

The role of glia as a contributing factor to motor neuron (MN) death in amyotrophic lateral sclerosis (ALS) is becoming increasingly appreciated. However, most studies implicating astrocytes have focused solely on models of ALS caused by superoxide dismutase 1 (SOD1) mutations. The goal of our study was to determine whether astrocytes contribute to wild-type MN death in the case of ALS caused by mutations in tar-DNA binding protein 43 (TDP-43). Since it is currently unknown how TDP-43 mutations cause disease, we derived astrocytes for study from both gain and loss of function mouse models of TDP-43. Astrocytes overexpressing mutant TDP-43(A315T) as well as astrocytes lacking TDP-43 were morphologically indistinguishable from wild-type astrocytes in vitro. Furthermore, astrocytes with these TDP-43 alterations did not cause the death of wild-type MNs in co-culture. To investigate the in vivo effects of TDP-43 alterations in astrocytes, glial-restricted precursors were transplanted to the wild-type rat spinal cord where they differentiated into astrocytes and interacted with host MNs. Astrocytes with TDP-43 alterations did not cause host wild-type MN damage although they were capable of engrafting and interacting with host MNs with the same efficiency as wild-type astrocytes. These data indicate that astrocytes do not adopt the same toxic phenotype as mutant SOD1 astrocytes when TDP-43 is mutated or expression levels are modified. Our study reinforces the heterogeneity in ALS disease mechanisms and highlights the potential for future screening subsets of ALS patients prior to treatment with cell type-directed therapies.

[Empirical basis of the Questionnaire for Crying, Feeding and Sleeping]. / Empirische Grundlagen des Fragebogens zum Schreien, Füttern und Schlafen (SFS).

The Questionnaire for Crying, Feeding and Sleeping of an infant, constructed based on theory and factor analysis, is assessed for internal consistency, inter-correlations, and its relation to a behaviour diary. A clinical and a non-clinical sample are compared. The sample of in total 704 infants younger than one year consists of different subsamples. To test the differences between a clinical and a non-clinical sample assessed with the questionnaire, data of 134 infants brought to the outpatient unit for parents with their infants and toddlers and a matched sample are used. The principal components analysis results in three well-interpretable scales correlating with each other, which all show a high internal consistency. The connections to the diary records and the differences between the means of the clinical and the non-clinical sample are found in the expected directions. The results of the Questionnaire for Crying, Feeding and Sleeping, including the criterion of Wessel, are consistent with the behaviour diary as well as the clinical diagnostics. The Questionnaire for Crying, Feeding and Sleeping shows validity according to these criteria and can therefore be used in research and clinical practise for the assessment of problems concerning crying, feeding and sleeping in the first year of life.

Pseudorabies virus and herpes simplex virus type 1 utilize different tegument-glycoprotein interactions to mediate the process of envelopment.

BACKGROUND AND OBJECTIVE: During herpesvirus envelopment capsids, tegument polypeptides and membrane proteins assemble at the site of budding, and a cellular lipid bilayer becomes refashioned into a spherical envelope. A web of interactions between tegument proteins and the cytoplasmic tails of viral glycoproteins play a critical role in this process. We have previously demonstrated that for herpes simplex virus (HSV)-1 the cytoplasmic tail of glycoprotein H (gH) binds the tegument protein VP16. The HSV and pseudorabies virus (PRV) genomes are essentially collinear, and individual gene products show significant sequence homology. However, the demarcation of function often differs between PRV and HSV proteins. The goal of this study was to determine whether PRV gH and VP16 interact in a manner similar to their homologs in HSV. METHODS: A fusion protein pull-down assay was performed in which a PRV gH cytoplasmic tail-glutathione S-transferase fusion protein, bound to glutathione-Sepharose beads, was incubated with PRV-infected cell cytosol, washed and subjected to Western blot analysis using anti-PRV VP16 antisera. RESULTS: Western blots indicate that PRV VP16 does not specifically bind to the PRV gH tail. CONCLUSION: Our results highlight that, despite the relatively close evolutionary relationship between HSV and PRV, there are significant differences in their protein interactions that drive envelopment.

Beta-glucan, immune function, and upper respiratory tract infections in athletes.

PURPOSE: This study investigated the effects of oat beta-glucan (BG) supplementation on chronic resting immunity, exercise-induced changes in immune function, and self-reported upper respiratory tract infection (URTI) incidence in human endurance athletes. METHODS: Trained male cyclists were randomized to BG (N = 19) or placebo (P; N = 17) groups and under double-blind procedures received BG (5.6 g x d(-1)) or P beverage supplements for 2 wk before, during, and 1 d after a 3-d period in which subjects cycled for 3 h x d(-1) at approximately 57% maximal watts. URTI symptoms were monitored during BG supplementation and for 2 wk afterward. Blood samples were collected before and after 2 wk of supplementation (both samples, 8:00 a.m.), immediately after the 3-h exercise bout on day 3 (6:00 p.m.), and 14 h after exercise (8:00 a.m.) and were assayed for natural killer cell activity (NKCA), polymorphonuclear respiratory burst activity (PMN-RBA), phytohemagglutinin-stimulated lymphocyte proliferation (PHA-LP), plasma interleukin 6 (IL-6), IL-10, IL-1 receptor agonist (IL-1ra), and IL-8, and blood leukocyte IL-10, IL-8, and IL-1ra mRNA expression. RESULTS: Chronic resting levels and exercise-induced changes in NKCA, PMN-RBA, PHA-LP, plasma cytokines, and blood leukocyte cytokine mRNA did not differ significantly between BG and P groups. URTI incidence during the 2-wk postexercise period did not differ significantly between groups. CONCLUSIONS: An 18-d period of BG versus P ingestion did not alter chronic resting or exercise-induced changes in immune function or URTI incidence in cyclists during the 2-wk period after an intensified exercise.