Lost in translation: the association of international status and native language on concussion in collegiate athletes in the United States.

OBJECTIVE: The purpose of this study was to characterize the associations of international student status and native language on time (in days) with the date of injury to (i) diagnosis, (ii) symptom resolution, and (iii) return to sport. METHODS: Utilizing data from a cross-sectional cohort of 1,044 concussion cases from LIMBIC MATARS member institutions (n = 11) in the US, we conducted two, matched case-control designs. Cases were divided into two groups: (i) international (n = 32) or domestic students (n = 32) and (ii) English as an Additional Language (EAL) speakers (n = 18) or Native English language speakers (n = 18). Both groups were individually matched to their respective controls based on gender, age, sport, and preexisting health conditions. RESULTS: There were no significant differences in days from injury to diagnosis (p = 0.94), symptom resolution (p = 0.64), or return to sport (p = 0.15) between international and domestic athletes. EAL speakers experienced symptom resolution approximately 7.5 days sooner (Md = 4.50; IQR = 4.00, 8.00) than Native English language speakers (Md = 12.00; IQR = 7.00, 21.00, p = 0.01). CONCLUSIONS: Our findings suggest that native language is associated with symptom resolution in collegiate athletes. Healthcare professionals should consider barriers related to native language that may impact symptom reporting and the overall injury experience of diverse collegiate athletes.

Placing the keystone: the LIMBIC Military and Tactical Athlete Research Study.

OBJECTIVE: The LIMBIC Military and Tactical Athletic Research Study (MATARS) framework was established to confirm and extend understanding of concussion with initial studies driven by clinical data collected between 2015 and 2020 in a collegiate sports setting. The LIMBIC MATARS framework will be leveraged to apply gold-standard and innovative research designs to advance the science of concussion. This manuscript provides the background, methodology, and initial demographic data associated with the LIMBIC MATARS. METHODS: Consensus-based common data elements were used to conduct a retrospective chart review, specific to collegiate athletes diagnosed with concussions between 2015 and 2020 at 11 universities. RESULTS: A final sample of 1,311 (47.8% female) concussions were diagnosed during the five-year study period from athletes participating in a variety of National Collegiate Athlete Association (NCAA) sports. The LIMBIC MATARS demographic data, align with the NCAA and other pioneering multi-site concussion-related studies in terms of biological sex, race and ethnicity, and sport participation. CONCLUSION: This pragmatic, methodological approach was used to address several a priori hypotheses related to concussion, align with other multi-site studies of concussion, and establish a consortium for future investigations.

Racial identity and concussion diagnosis and recovery trajectories in collegiate athletes: a LIMBIC MATARS investigation.

OBJECTIVE: To determine if there were concussion diagnosis and recovery disparities between collegiate athletes with Black and White racial identities. DESIGN: Retrospective cohort study. METHODS: Concussion information was extracted from NCAA athlete medical files at LIMBIC MATARS member institutions from the 2015-16' to 2019-20' academic years. A total of 410 concussions from 9 institutions were included that provided all independent (i.e. racial identity of Black or White) and dependent variable information (i.e. dates of injury, diagnosis, symptom resolution, and return to sport) that were analyzed using Mann-Whitney U tests. The sample consisted of 114 (27.8%) concussions sustained by Black athletes and 296 (72.1%) sustained by White athletes. RESULTS: The overall sample had a median of 0 days between injury occurrence to diagnosis, 7 days to symptom resolution, and 12 days to return to sport. No significant timing differences were observed for concussion diagnosis (p = .14), symptom resolution (p = .39), or return to sport (p = 0.58) between collegiate athletes with Black versus White racial identities. CONCLUSIONS: These findings may reflect equitable access to onsite sports medicine healthcare resources that facilitate concussion management in the collegiate sport setting. Future work should explore these associations with a larger and more diverse sample of collegiate athletes.

A randomized controlled trial on the effects induced by robot-assisted and usual-care rehabilitation on upper limb muscle synergies in post-stroke subjects.

Muscle synergies are hypothesized to reflect connections among motoneurons in the spinal cord activated by central commands and sensory feedback. Robotic rehabilitation of upper limb in post-stroke subjects has shown promising results in terms of improvement of arm function and motor control achieved by reassembling muscle synergies into a set more similar to that of healthy people. However, in stroke survivors the potentially neurophysiological changes induced by robot-mediated learning versus usual care have not yet been investigated. We quantified upper limb motor deficits and the changes induced by rehabilitation in 32 post-stroke subjects through the movement analysis of two virtual untrained tasks of object placing and pronation. The sample analyzed in this study is part of a larger bi-center study and included all subjects who underwent kinematic analysis and were randomized into robot and usual care groups. Post-stroke subjects who followed robotic rehabilitation showed larger improvements in axial-to-proximal muscle synergies with respect to those who underwent usual care. This was associated to a significant improvement of the proximal kinematics. Both treatments had negative effects in muscle synergies controlling the distal district. This study supports the definition of new rehabilitative treatments for improving the neurophysiological recovery after stroke.

Analysis of factors affecting volatile compound formation in roasted pumpkin seeds with selected ion flow tube-mass spectrometry (SIFT-MS) and sensory analysis.

UNLABELLED: Pumpkin (Cucurbita pepo and maxima) seeds are uniquely flavored and commonly consumed as a healthy roasted snack. The objective was to determine dominant volatiles in raw and roasted pumpkin seeds, and the effect of seed coat, moisture content, fatty acid ratio, total lipids, reducing sugars, and harvest year on volatile formation. Sensory was conducted to evaluate overall liking of seed variety and texture. Seed processing included extraction from the fruit, dehydration, and roasting (150 °C). Oil extraction was done using soxhlet, fatty acid profile using Gas Chromatography Flame Ionization Detector, and reducing sugars using 3,5-dinitrosalicylic acid and UV-spectroscopy. Headspace analysis of seeds was performed by selected ion flow tube-mass spectrometry (SIFT-MS). Volatiles dominating in raw pumpkin seeds were lipid aldehydes, ethyl acetate, 2,3-butandione, and dimethylsulfide. Compounds contributing to roasted aroma include alkylpyrazines and Strecker and lipid aldehydes. Overall, hull-less seeds had higher volatile lipid aldehydes and Strecker aldehydes. Seeds dehydrated to a moisture content of 6.5% before roasting had higher initial and final volatile concentrations than seeds starting at 50% moisture. Higher oil content resulted in higher lipid aldehyde formation during roasting with a moderate correlation between free fatty acid ratio and corresponding lipid aldehyde. Harvest year (2009 compared with 2010) had a significant impact on volatile formation in hull-less seeds, but not as much as variety differences. No significant correlation was found between reducing sugars and volatile formation. Sensory showed that hull-less seeds were liked significantly more than hulled seeds. PRACTICAL APPLICATION: Elucidation of aromatic flavor development during roasting with SIFT-MS provides information on flavor release and offers better control during processing. Knowledge of volatiles in raw and roasted pumpkin seeds and effects of seed coat, moisture content, seed composition, and harvest date will allow for better control over the production/storage/transportation process and a more educated decision during selection of a variety for production of pumpkin seeds in the snack food industry.

LPS response and tolerance in the zebrafish (Danio rerio).

Zebrafish (Danio rerio) has been used in the present work to study the fish response to bacterial lipopolysaccharide (LPS) exposure and LPS tolerance. These mechanisms are not completely understood in mammals and, presently, are totally unknown in fish. Zebrafish larval survival was assessed following treatment with various types of LPS at a variety of concentrations to determine the sensitivity of zebrafish to LPS-induced immune activation. In addition, fish pretreated with a sublethal concentration of LPS did not die after exposure to a lethal concentration of LPS demonstrating, for the first time that LPS tolerance also happens in fish. The time interval between pretreatment and secondary exposure as well as the type of pretreatment dictated the strength of protection. Since zebrafish are in intimate contact with microorganisms, the high resistance of fish to LPS suggests that there must be a tight control of the LPS receptor cluster in order to avoid an excess of inflammation. One of these components is CXCR4, which has previously been shown to regulate the signal transduced by TLR4. Treating fish with AMD3100, a specific inhibitor of CXCR4, increased LPS treatment associated mortality. Blocking CXCR4 via chemical or genetic inhibition resulted in a reversion of LPS tolerance, thus further supporting the negative regulatory role of CXCR4 in this inflammatory response. In support of an inhibitory role for CXCR4 in the inflammatory cascade, IL-1 transcript levels were elevated in both unstimulated and LPS stimulated zebrafish Odysseus (CXCR4 deficient mutant) larvae.

Blood pressure measures and risk of total, ischemic, and hemorrhagic stroke in men.

OBJECTIVE: To evaluate which blood pressure measure is the best predictor of risk of total, ischemic, and hemorrhagic stroke. METHODS: The authors used a prospective cohort study among 11,466 men followed for incident stroke during a median of 19.4 years in the Physicians' Health Study. Systolic blood pressure (SBP) and diastolic blood pressure (DBP) were self-reported. They calculated relative risks (RRs) and 95% CIs for total, ischemic, and hemorrhagic stroke using Cox proportional hazards models. Model fit was compared using the chi(2) test statistic from likelihood ratio tests. RESULTS: During follow-up, 508 strokes occurred (411 ischemic, 89 hemorrhagic, and eight of unknown etiology). For each 10-mm Hg increase in SBP, the multivariable RRs were 1.31 (95% CI: 1.20 to 1.42) for total stroke, 1.28 (95% CI: 1.16 to 1.40) for ischemic stroke, and 1.38 (95% CI: 1.13 to 1.68) for hemorrhagic stroke. Although DBP, pulse pressure, and mean arterial pressure were all significant predictors of stroke risk, none was a significantly better predictor than SBP alone. Adding DBP did not significantly improve the model fit of SBP alone for any stroke type. CONCLUSION: In this large cohort of initially healthy men, systolic blood pressure was a consistent and significant predictor of total, ischemic, and hemorrhagic stroke. Systolic blood pressure alone was the only measure necessary to predict risk of total stroke or its major subtypes.

Homocysteine and risk of developing hypertension in men.

In cross-sectional studies, elevated homocysteine levels are associated with higher blood pressure, but it remains unclear whether plasma homocysteine is a risk factor for hypertension. In a prospective nested case-control study, participants who developed hypertension (n=396) had significantly higher levels of baseline plasma homocysteine (12.6 mol/l) than matched controls (11.8 mol/l, P=0.03); compared to those in the lowest quintile, those in the highest quintile had a crude relative risk (RR) of 1.56 (95% confidence interval (CI), 0.98-2.48; P for trend=0.10) and a multivariable RR of 1.63 (95% CI, 0.97-2.74; P for trend=0.13). Higher plasma homocysteine levels at baseline were associated with an increased but non-significant risk of incident hypertension that was minimally affected by multivariable adjustment.

Constitutive activation of Stat3 by the Src and JAK tyrosine kinases participates in growth regulation of human breast carcinoma cells.

Constitutive activation of signal transducer and activator of transcription (STAT) proteins has been detected in a wide variety of human primary tumor specimens and tumor cell lines including blood malignancies, head and neck cancer, and breast cancer. We have previously demonstrated a high frequency of Stat3 DNA-binding activity that is constitutively-induced by an unknown mechanism in human breast cancer cell lines possessing elevated EGF receptor (EGF-R) and c-Src kinase activities. Using tyrosine kinase selective inhibitors, we show here that Src and JAK family tyrosine kinases cooperate to mediate constitutive Stat3 activation in the absence of EGF stimulation in model human breast cancer cell lines. Inhibition of Src or JAKs results in dose-dependent suppression of Stat3 DNA-binding activity, which is accompanied by growth inhibition and induction of programmed cell death. In addition, transfection of a dominant-negative form of Stat3 leads to growth inhibition involving apoptosis of breast cancer cells. These results indicate that the biological effects of the Src and JAK tyrosine kinase inhibitors are at least partially mediated by blocking Stat3 signaling. While EGF-R kinase activity is not required for constitutive Stat3 activation in breast cancer cells, EGF stimulation further increases STAT DNA-binding activity, consistent with an important role for EGF-R in STAT signaling and malignant progression. Analysis of primary breast tumor specimens from patients with advanced disease revealed that the majority exhibit elevated STAT DNA-binding activity compared to adjacent non-tumor tissues. Our findings, taken together, suggest that tyrosine kinases transduce signals through Stat3 protein that contribute to the growth and survival of human breast cancer cells in culture and potentially in vivo.

Stat3-mediated Myc expression is required for Src transformation and PDGF-induced mitogenesis.

Signal transducer and activator of transcription (STAT) proteins perform key roles in mediating signaling by cytokines and growth factors, including platelet-derived growth factor (PDGF). In addition, Src family kinases activate STAT signaling and are required for PDGF-induced mitogenesis in normal cells. One STAT family member, Stat3, has been shown to have an essential role in cell transformation by the Src oncoprotein. However, the mechanisms by which STAT-signaling pathways contribute to mitogenesis and transformation are not fully defined. We show here that disruption of Stat3 signaling by using dominant-negative Stat3beta protein in NIH 3T3 fibroblasts suppresses c-Myc expression concomitant with inhibition of v-Src-induced transformation. Ectopic expression of c-Myc is able to partially reverse this inhibition, suggesting that c-Myc is a downstream effector of Stat3 signaling in v-Src transformation. Furthermore, c-myc gene knockout fibroblasts are refractory to transformation by v-Src, consistent with a requirement for c-Myc protein in v-Src transformation. In normal NIH 3T3 cells, disruption of Stat3 signaling with dominant-negative Stat3beta protein inhibits PDGF-induced mitogenesis in a manner that is reversed by ectopic c-Myc expression. Moreover, inhibition of Src family kinases with the pharmacologic agent, SU6656, blocks Stat3 activation by PDGF. These findings, combined together, delineate the signaling pathway, PDGF --> Src --> Stat3 --> Myc, that is important in normal PDGF-induced mitogenesis and subverted in Src transformation.

Higher prevalence of smoking in patients diagnosed as having obstructive sleep apnea.

Nightly nicotine withdrawal as well as other respiratory and pulmonary effects of smoking may result in sleep-disordered breathing, especially obstructive sleep apnea (OSA). We hypothesize that there is higher prevalence of smoking in patients with OSA. We also hypothesize that smoking is an independent risk factor for OSA. The aim of this study is to determine whether there is a higher prevalence of smoking in patients with OSA compared with patients who do not have OSA. To investigate this, we randomly selected a group of 108 patients who were diagnosed as having OSA, defined by an apnea-hypopnea index (AHI) of greater than 10 events per hour. We compared their smoking history with another randomly selected group of 106 patients without OSA, defined by an AHI of less than five events per hour. The prevalence of smoking in patients with OSA was found to be 35%, whereas it was only 18% in patients without OSA. Logistic regression analyses were performed to investigate the effects of smoking while adjusting for age, gender, body mass index (BMI), and number of alcoholic drinks per week. While holding fixed the BMI, gender, age, and number of alcoholic drinks per week, current smokers were found to be 2.5 times more likely to have OSA than former smokers and nonsmokers combined (odds ratio = 2.5, CI 1.3-4.7, p = 0.0049), and 2.8 times more likely to have OSA than former smokers alone (odds ratio = 2.8, CI = 1.4-5.4, p = 0.0028). Adjusted for BMI, gender, age, and number of alcoholic drinks per week, former smokers were not more likely than never smokers to have OSA (odds ratio = 1.2, CI = 0.55-2.7, p = 0.64). We conclude that cigarette smoke may be an independent risk factor for OSA in this referral population.

Induction of p21WAF1/CIP1 and cyclin D1 expression by the Src oncoprotein in mouse fibroblasts: role of activated STAT3 signaling.

While the activated viral Src oncoprotein, v-Src, induces uncontrolled cell growth, the mechanisms underlying cell cycle deregulation by v-Src have not been fully defined. Previous studies demonstrated that v-Src induces constitutively active STAT3 signaling that is required for cell transformation and recent data have implicated STAT3 in the transcriptional control of critical cell cycle regulators. Here we show in mouse fibroblasts stably transformed by v-Src that mRNA and protein levels of p21 (WAF1/CIP1), cyclin D1, and cyclin E are elevated. Using reporter constructs in transient-transfection assays, the cyclin D1 and p21 promoters were both found to be transcriptionaly induced by v-Src in a STAT3-dependent manner. The kinase activities of cyclin D/CDK4, 6 and cyclin E/CDK2 complexes were only slightly elevated, consistent with the findings that coordinate increases in p21, cyclin D1 and cyclin E resulted in an increase in cyclin/CDK/p21 complexes. Similar results were obtained in NIH3T3 and BALB/c 3T3 cells stably transformed by v-Src, indicating that these regulatory events associated with STAT3 signaling represent common mechanisms independent of cell line or clonal variation. These findings suggest that STAT3 has an essential role in the regulation of critical cell cycle components in v-Src transformed mouse fibroblasts.

STATs in oncogenesis.

Since their discovery as key mediators of cytokine signaling, considerable progress has been made in defining the structure-function relationships of Signal Transducers and Activators of Transcription (STATs). In addition to their central roles in normal cell signaling, recent studies have demonstrated that diverse oncoproteins can activate specific STATs (particularly Stat3 and Stat5) and that constitutively-activated STAT signaling directly contributes to oncogenesis. Furthermore, extensive surveys of primary tumors and cell lines derived from tumors indicate that inappropriate activation of specific STATs occurs with surprisingly high frequency in a wide variety of human cancers. Together, these findings provide compelling evidence that aberrant STAT activation associated with oncogenesis is not merely adventitious but instead contributes to the process of malignant transformation. These studies are beginning to reveal the molecular mechanisms leading to STAT activation in the context of oncogenesis, and candidate genes regulated by STATs that may contribute to oncogenesis are being identified. Recent studies suggest that activated STAT signaling participates in oncogenesis by stimulating cell proliferation and preventing apoptosis. This review presents the evidence for critical roles of STATs in oncogenesis and discusses the potential for development of novel cancer therapies based on mechanistic understanding of STAT signaling. Oncogene (2000).

Hypoxemia during sleep in patients with chronic obstructive pulmonary disease: significance, detection, and effects of therapy.

NOD is a common event in patients with symptomatic COPD who are not hypoxemic while awake. Up to 45% of these patients may have significant oxyhemoglobin desaturation during sleep, and most have evidence of pulmonary arterial hypertension. Although intuitively it would seem that supplemental oxygen during sleep should be of medical benefit in COPD patients with NOD, studies to data have not substantiated this idea. Medicare requirements for prescribing nocturnal oxygen are relatively liberal and there is the possibility of misuse, which would cause a substantial increase in the cost of home health care. A well designed multicenter study is needed to provide appropriate indications and guidelines for therapy in these patients.

Modulation of cholesterol concentration in Caco-2 cells by incubation with different n-6 fatty acids.

Incorporation of exogenous cholesterol was compared in human adenocarcinoma colon cells (Caco-2) after incubation with 100 microM of either linoleic acid (LA, 18:2n-6), gamma-linolenic acid (GLA, 18:3n-6), arachidonic acid (AA, 20:4n-6) or adrenic acid (or n-6 docosatetraenoic acid, DTA, 22:4n-6). In both cells 7 days after seeding and 14 days after confluency, incubation with LA significantly raised the proportion of 18:2n-6 but not its long-chain metabolites in cellular phospholipid. Incubation with GLA increased the levels of 18:3n-6, 20:3n-6, and 20:4n-6. Incubation with AA increased the levels of 20:4n-6 and 22:4n-6, and incubation with DTA increased the levels of 22:4n-6 as well as its retro-conversion metabolite, 20:4n-6. A subsequent addition of cholesterol (180 microM) to the medium significantly raised the cellular cholesterol level but less so in the cells 7 days after seeding incubated with GLA. The increase in cellular cholesterol level was generally greater in the cells of 7 days after seeding, particularly those incubated with long-chain highly unsaturated n-6 fatty acids, than in those of 14 days after confluency. These findings suggest that the cell growth and the extent of unsaturation in cell membrane phospholipid fatty acids modulate the incorporation of the exogenous cholesterol into the Caco-2 cells.

Requirement for Ras/Rac1-mediated p38 and c-Jun N-terminal kinase signaling in Stat3 transcriptional activity induced by the Src oncoprotein.

Signal transducers and activators of transcription (STATs) are transcription factors that mediate normal biologic responses to cytokines and growth factors. However, abnormal activation of certain STAT family members, including Stat3, is increasingly associated with oncogenesis. In fibroblasts expressing the Src oncoprotein, activation of Stat3 induces specific gene expression and is required for cell transformation. Although the Src tyrosine kinase induces constitutive Stat3 phosphorylation on tyrosine, activation of Stat3-mediated gene regulation requires both tyrosine and serine phosphorylation of Stat3. We investigated the signaling pathways underlying the constitutive Stat3 activation in Src oncogenesis. Expression of Ras or Rac1 dominant negative protein blocks Stat3-mediated gene regulation induced by Src in a manner consistent with dependence on p38 and c-Jun N-terminal kinase (JNK). Both of these serine/threonine kinases and Stat3 serine phosphorylation are constitutively induced in Src-transformed fibroblasts. Furthermore, inhibition of p38 and JNK activities suppresses constitutive Stat3 serine phosphorylation and Stat3-mediated gene regulation. In vitro kinase assays with purified full-length Stat3 as the substrate show that both JNK and p38 can phosphorylate Stat3 on serine. Moreover, inhibition of p38 activity and thus of Stat3 serine phosphorylation results in suppression of transformation by v-Src but not v-Ras, consistent with a requirement for Stat3 serine phosphorylation in Src transformation. Our results demonstrate that Ras- and Rac1-mediated p38 and JNK signals are required for Stat3 transcriptional activity induced by the Src oncoprotein. These findings delineate a network of tyrosine and serine/threonine kinase signaling pathways that converge on Stat3 in the context of oncogenesis.

Literary resources for bereavement.

The bereavement process can be aided by multiple resources. Hospice counselors and related therapeutic professionals turn most easily to their own disciplines and training. In this article, complementary or ancillary resources from literature have been offered. If healing includes the "storying" and "restorying" of lives, then literature can enrich and facilitate the mourning process. Suggestions of resources and some of their connections to hospice care have been offered.

Quality of life in patients with obstructive sleep apnea: effect of nasal continuous positive airway pressure--a prospective study.

BACKGROUND: Obstructive sleep apnea (OSA) is a common condition and is associated with excessive daytime sleepiness and neuropsychological dysfunction. There is limited evidence on the effect of OSA on the quality of life and its response to nasal continuous positive airway pressure (nCPAP) treatment. STUDY OBJECTIVE: To determine the effect of nCPAP on the quality of life in patients with OSA. DESIGN: Prospective determination of nCPAP effect in a case-series analysis. PATIENTS: We studied 29 patients (23 were male and 6 were female) with a mean (+/-SE) age of 4.4+/-2.3 years, a body mass index 36.3+/-2.0 kg/height (m)2, and a diagnosis of OSA with respiratory disturbance index (RDI; apnea/hypopnea) of 77+/-9 events/h. MEASUREMENTS AND RESULTS: The quality of life was assessed by administering a Medical Outcomes Study Short Form-36 questionnaire before and after 8 weeks of nCPAP therapy in polysomnographically documented OSA. All dimensions of the quality of life were significantly impaired when compared with an age- and gender-matched population, expressed as a percentage of normative data: physical functioning, 75%; vitality, 41%; role functioning (physical, 54%; emotional, 61%; social, 66%); general health, 88%; and mental health, 76%. nCPAP therapy significantly improved the sleep-disordered breathing and sleep fragmentation. The nCPAP level for the group was 9.4+/-0.7 cm H2O. Eight weeks of nCPAP therapy improved vitality (75%), social functioning (90%), and mental health (96%). The magnitude of improvement was related to the degree of quality of life impairment prior to treatment, rather than to the severity of disease as measured by the RDI and arousal indices. CONCLUSIONS: All aspects of the quality of life, from physical and emotional health to social functioning, are markedly impaired by OSA. nCPAP therapy improved those aspects related to vitality, social functioning, and mental health.

Adenosine rinse in human orthotopic liver transplantation: results of a randomized, double-blind trial.

OBJECTIVE: The study was aimed at determining whether the vasodilator, adenosine, shown to produce dramatic improvement in liver graft and animal acute and long-term survival, would be beneficial in human liver transplantation. METHODS: A prospective, randomized, double-blind trial of an adenosine rinse preservation solution in human orthotopic liver transplantation (OLTX) was conducted in 43 consecutive transplants. Intraoperative and postoperative care was performed by a single transplant team utilizing a quadruple drug immunosuppressive protocol, with complete 5-year patient follow-up. At implantation all allografts were flushed with a 4 degrees C (pH 7.4) Normosol solution, with 0.12 mM adenosine or without adenosine. RESULTS: Recipient characteristics were similar in the treated and control groups including age, pre-OLTX diagnosis, and United Network for Organ Sharing (UNOS) status. Donor variables were equivalent in the two groups including age, weight, prothrombin time, and serum chemistries. Operative variables showed no differences except a significant (p = 0.006) reduction of veno-venous bypass time in the adenosine treated group. Liver allograft function improved in the adenosine rinse groups as measured by both postoperative bile production (218 +/- 156cc/24h adenosine vs. 116 +/- 78 cc/24 h without adenosine, p = 0.03) and Factor 7 production at day 3 (64 +/- 26% adenosine vs. 51 +/- 20% without adenosine, p = 0.08). The adenosine treated group had an insignificant 10% patient and graft improvement in survival at 6 months to 60 months compared to the control group. CONCLUSIONS: These results suggest that adenosine added to the intraoperative flush solution during human liver transplantation is safe, does not reduce cardiac stability at reperfusion, improves early liver allograft function, but has an insignificant short- and long-term affect on allograft survival.