Isolated Optic Neuritis: Etiology, Characteristics, and Outcomes in a US Mountain West Cohort.

BACKGROUND: The diagnosis and treatment of autoimmune optic neuritis (ON) has improved with the accessibility and reliability of aquaporin-4 (AQP4) and myelin oligodendrocyte glycoprotein (MOG) antibody testing, yet autoantibody-negative ON remains common. This study describes the demographic, clinical, and outcome data in patients with isolated ON across the pediatric and adult cohort. METHODS: A retrospective chart review of University of Utah Health patients with the International Classification of Diseases (ICD) code of ICD-9 377.30 (ON unspecified), ICD-9 377.39 (other ON), or ICD-10 H46 (ON) and at least 2 ophthalmologic evaluations were conducted between February 2011 and July 2023. Only isolated cases of ON without other brain or spinal demyelinating lesions were evaluated. Differences in demographic and clinical characteristics between AQP4, MOG, and Other-ON were determined. RESULTS: Of the 98 patients (15 children and 83 adults), 9 (9.2%) were positive for AQP4-IgG and 35 (35.7%) tested positive for MOG-IgG. Fifty-four were classified into Other-ON, of which 7 (13.0%) had recurrence or new demyelinating lesions during a median follow-up of 12.5 months-2 were ultimately diagnosed with recurrent isolated ON (RION), 1 with chronic relapsing inflammatory ON (CRION), 2 with multiple sclerosis, 1 with collapsin response-mediator protein (CRMP)-5-ON, and 1 with seronegative neuromyelitis optica spectrum disorder. Four patients were treated with long-term immunosuppressive therapy. No patients with RION or CRION had preceding infections; they had first recurrences of ON within 2 months. At presentation, AQP4-ON (75%) and MOG-ON (48.8%) had more severe vision loss (visual acuity <20/200) than Other-ON (23.2%, P = 0.01). At the 1-month follow-up, 93.0% of patients with MOG-ON and 89.3% of patients with Other-ON demonstrated a visual acuity ≥20/40, compared with only 50% of patients with AQP4-ON (P < 0.01). By the last follow-up, 37.5% of the AQP4-ON still exhibited visual acuity <20/40, including 25% who experienced severe vision loss (visual acuity <20/200). By contrast, over 95% of patients with MOG-ON and Other-ON maintained a visual acuity of ≥20/40. In our cohort, over a quarter of pediatric cases presented with simultaneous bilateral ON, 40% had a preceding infection, and 44.4% initially presented with a visual acuity <20/200. Two pediatric cases had recurrence, and both were MOG-ON. By their last follow-up, all pediatric cases had achieved a visual acuity of 20/40 or better. In addition, pediatric cases were more likely to exhibit disc edema compared with adult cases (100% vs 64%, P < 0.01). CONCLUSIONS: Despite recent advances in identification and availability of testing for AQP4-IgG and MOG-IgG, over half of patients who presented with isolated ON remained with an "idiopathic" diagnostic label. As more than 1 in 10 patients with AQP4-IgG and MOG-IgG negative ON experienced recurrence or develop new demyelinating lesions, clinicians should provide anticipatory guidance and closely monitor for potential long-term outcomes. In addition, it is crucial to re-evaluate the diagnosis in cases of poor recovery, ON recurrence, and the emergence of new neurological symptoms, as ON can often be the initial presentation of other conditions.

Comparison of three methods for the detection of antibodies against muscle-specific kinase.

OBJECTIVES: To compare 3 different methods for the detection of antibodies against muscle-specific kinase (MuSK). METHODS: MuSK antibody testing was performed in 237 serum samples by enzyme-linked immunosorbent assay (ELISA) and fixed cell-based assay (f-CBA-IFA). One hundred and forty-eight (148) of the sera had previously been tested by RIA during clinical testing: 47 MuSK antibody positive and 101 MuSK antibody negative. Of the MuSK RIA negative antibodies, 46 tested positive for other neural antibodies. Additionally, 89 sera were subsequently tested by all three methods: 70 healthy controls and 19 sera positive for other neural antibodies. RESULTS: Qualitative inter-assay agreement based on tiered RIA values was 100% for results of 1.00 nmol/L or greater by both methods; 81% and 94% for results between 0.21 and 0.99 nmol/L by ELISA and f-CBA-IFA, respectively; and 0% for results of 0.04-0.20 nmol/L by both methods. Negative results showed 100% agreement between RIA and both ELISA and f-CBA-IFA (n = 55). None of the controls positive for other neural autoantibodies or healthy controls were positive in any assay. CONCLUSION: Overall, excellent agreement was observed between the 3 methods used to detect antibodies against MuSK. Both the f-CBA-IFA and ELISA performed comparably to RIA and exhibited excellent overall accuracy for MuSK IgG detection, with the f-CBA-IFA demonstrating higher agreement between positive samples with the RIA than the ELISA without identifying false positives in the control samples. Advantages of non-radioactive methods for the detection of MuSK antibodies include reduced handling and disposal of hazardous materials, potential for automation and the reagents having a longer shelf-life, reducing costs associated with both workflow and lot validations. Thus, commercially available ELISA and transfected cell-based assays are viable alternatives to the traditional radioactive assay used for serologic determination of MuSK IgG.

PNMA2 forms immunogenic non-enveloped virus-like capsids associated with paraneoplastic neurological syndrome.

The paraneoplastic Ma antigen (PNMA) proteins are associated with cancer-induced paraneoplastic syndromes that present with an autoimmune response and neurological symptoms. Why PNMA proteins are associated with this severe autoimmune disease is unclear. PNMA genes are predominantly expressed in the central nervous system and are ectopically expressed in some tumors. We show that PNMA2, which has been co-opted from a Ty3 retrotransposon, encodes a protein that is released from cells as non-enveloped virus-like capsids. Recombinant PNMA2 capsids injected into mice induce autoantibodies that preferentially bind external "spike" PNMA2 capsid epitopes, whereas a capsid-assembly-defective PNMA2 protein is not immunogenic. PNMA2 autoantibodies in cerebrospinal fluid of patients with anti-Ma2 paraneoplastic disease show similar preferential binding to spike capsid epitopes. PNMA2 capsid-injected mice develop learning and memory deficits. These observations suggest that PNMA2 capsids act as an extracellular antigen, capable of generating an autoimmune response that results in neurological deficits.

High level of agreement in a fixed vs. live cell-based assay for antibodies to myelin oligodendrocyte glycoprotein in a real-world clinical laboratory setting.

Introduction: As recognition of myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease becomes more widespread, the importance of appropriately ordering and interpreting diagnostic testing for this antibody increases. Several assays are commercially available for MOG testing, and based on a few small studies with very few discrepant results, some have suggested that live cell-based assays (CBA) are superior to fixed CBA for clinical MOG antibody testing. We aimed to determine the real-world agreement between a fixed and live CBA for MOG using two of the most commonly available commercial testing platforms. Methods: We compared paired clinical samples tested at two national clinical reference laboratories and determined the real-world agreement between the fixed CBA and live CBA. Results: Of 322 paired samples tested on both platforms, 53 were positive and 246 were negative by both methodologies (agreement 92.9%, Cohen's kappa 0.78, [0.69-0.86]). Spearman correlation coefficient was 0.80 (p < 0.0001). Of the discrepant results, only 1 of 14 results positive by the live CBA had a titer greater than 1:100, and only 1 of 9 results positive by the fixed CBA had a titer of greater than 1:80. Lower titers on the fixed CBA correlate to higher titers on the live CBA. Conclusion: Overall, there is excellent agreement between fixed and live CBA for MOG antibody testing in a real-world clinical laboratory setting. Clinicians should be aware of which method they use to assess any given patient, as titers are comparable, but not identical between the assays.

Neurologic Manifestations of Common Variable Immunodeficiency: Impact on Quality of Life.

BACKGROUND AND OBJECTIVES: Common variable immunodeficiency is a systemic disease and not solely a disease of humoral immunity. Neurologic symptoms associated with common variable immunodeficiency are underrecognized and warrant further study. This work aimed to characterize the neurologic symptoms reported by people living with common variable immunodeficiency. METHODS: We conducted a single academic medical center study of neurologic symptoms reported by adults previously diagnosed with common variable immunodeficiency. We used a survey of common neurologic symptoms to determine the prevalence of these symptoms in a population with common variable immunodeficiency and further assessed these patient-reported symptoms with validated questionnaires and compared symptom burden with other neurologic conditions. RESULTS: A volunteer sample of adults (aged 18 years or older) previously diagnosed with common variable immunodeficiency at the University of Utah Clinical Immunology/Immune Deficiency Clinic who were able to read and comprehend English and willing and able to answer survey-based questions were recruited. Of 148 eligible participants identified, 80 responded and 78 completed the surveys. The mean age of respondents was 51.3 years (range 20-78 years); 73.1% female and 94.8% White. Patients with common variable immunodeficiency reported many common neurologic symptoms (mean 14.6, SD 5.9, range 1-25), with sleep issues, fatigue, and headache reported by more than 85%. Validated questionnaires addressing specific neurologic symptoms supported these results. T-scores on Neuro QoL questionnaires for sleep (mean 56.4, SD 10.4) and fatigue (mean 54.1, SD 11) were higher, indicating more dysfunction, than in the reference clinical population (p < 0.005). The Neuro QoL questionnaire for cognitive function showed a lower T-score (mean 44.8, SD 11.1) than that in the reference general population (p < 0.005), indicating worse function in this domain. DISCUSSION: Among survey respondents, there is a marked burden of neurologic symptoms. Given the impact of neurologic symptoms on health-related quality-of-life measures, clinicians should screen patients with common variable immunodeficiency for the presence of these symptoms and offer referral to neurologists and/or symptomatic treatment when indicated. Frequently prescribed neurologic medications may also affect the immune system, and neurologists should consider screening patients for immune deficiency before prescribing them.

Detection of Simple, Complex, and Clonal Chromosome Translocations Induced by Internal Radioiodine Exposure: A Cytogenetic Follow-Up Case Study after 25 Years.

Here, we report the findings of a 25-year cytogenetic follow-up study on a male patient who received 2 rounds of radioiodine treatment within a span of 26 months (1.78 GBq in 1992 and 14.5 GBq in 1994). The patient was 34 years old with a body mass index of 25 at the time of the first radioiodine treatment. Multicolor FISH and multicolor banding (mBAND) techniques performed on the patient detected inter- and intrachromosomal exchanges. Although the frequency of chromosome translocations remained essentially the same as reported in our earlier study (0.09/cell), the percentage of reciprocal (balanced) translocations increased from 54.38 to 80.30% in the current study. In addition to simple chromosome translocations, complex exchanges (0.29%) involving more than 2 chromosomes were detected for the first time in this patient. Strikingly, a clonal translocation involving chromosomes 14 and 15, t(14p;15q), was found in 7 of the 677 cells examined (1.03%). The presence of complex and clonal translocations indicates the onset of chromosomal instability induced by internal radioiodine exposure. mBAND analysis using probes specific for chromosomes 1, 2, 4, 5, and 10 revealed 5 inversions in a total of 717 cells (0.69%), and this inversion frequency is several-fold higher than the baseline frequency reported in healthy individuals using the classical G-banding technique. Collectively, our study suggests that stable chromosome aberrations such as translocations and inversions can be useful not only for retrospective biodosimetry but also for long-term monitoring of chromosomal instability caused by past radioiodine exposure.

Optimization and validation of automated dicentric chromosome analysis for radiological/nuclear triage applications.

Dicentric Chromosome Assay (DCA) is the most preferred cytogenetic technique for absorbed radiation dose assessment in exposed humans. However, DCA is somewhat impractical for triage application owing to its labor intensive and time consuming nature. Although lymphocyte culture for 48 h in vitro is inevitable for DCA, manual scoring of dicentric chromosomes (DCs) requires an additional time of 24-48 h, making the overall turnaround time of 72-96 h for dose estimation. To accelerate the speed of DC analysis for dose estimation, an automated tool was optimized and validated for triage mode of scoring. Several image training files were created to improve the specificity of automated DC analysis algorithm. Accuracy and efficiency of the automated (unsupervised) DC scoring was compared with the semi-automated scoring that involved human verification and correction of DCs (elimination of false positives and inclusion of true positives). DC scoring was performed by both automated and semi-automated modes for different doses of X-rays and γ-rays (0 Gy-5 Gy). Biodoses estimated from the frequencies of DCs detected by both automated (unsupervised) and semi-automated (supervised) scoring modes were grossly similar to the actual delivered doses in the range of 0.5 to 3 Gy of low LET radiation. We suggest that the automated DC tool can be effectively used for large scale radiological/nuclear incidents where a rapid segregation is essential for prioritizing moderately or severely exposed humans to receive appropriate medical countermeasures.

Genetic and Genomic Advances in Breast Cancer Diagnosis and Treatment.

Advances in genetic testing for people at high risk for cancer and in targeted gene therapy for breast cancer are rapidly emerging, including newly developed key hormone receptor-targeted therapies and individualized molecular fusion identification and treatment options. These advances are contributing to a new era in cancer treatment modalities and care delivery. As more innovative and advanced treatment options emerge, women's health outcomes and survival rates may improve. Nursing professionals in primary care and women's health specialties must be aware of the latest options for testing, referrals, and treatment modalities.

Revealing the allosterome: systematic identification of metabolite-protein interactions.

Small molecule allostery modifies protein function but is not easily discovered. We introduce mass spectrometry integrated with equilibrium dialysis for the discovery of allostery systematically (MIDAS), a method for identifying physiologically relevant, low-affinity metabolite-protein interactions using unmodified proteins and complex mixtures of unmodified metabolites. In a pilot experiment using five proteins, we identified 16 known and 13 novel interactions. The known interactions included substrates, products, intermediates, and allosteric regulators of their protein partners. MIDAS does not depend upon enzymatic measurements, but most of the new interactions affect the enzymatic activity of the protein partner. We found that the fatty acid palmitate interacts with both glucokinase and glycogen phosphorylase. Further characterization revealed that palmitate inhibited both enzymes, possibly providing a mechanism for sparing carbohydrate catabolism when fatty acids are abundant.

Leukocyte adhesion deficiency-I variant syndrome (LAD-Iv, LAD-III): molecular characterization of the defect in an index family.

Leukocyte adhesion deficiencies are rare clinical syndromes of impaired host defense that provide novel insights into regulation of immune and inflammatory responses. Leukocyte adhesion deficiency (LAD)-I variant (LAD-Iv), also called LAD-III, is a unique disorder in which inside-out signaling of ß1, ß2, and ß3 integrins on leukocytes and platelets is disrupted, leading to impaired cellular adhesion, recurrent infections, and bleeding. We originally reported the second patient with this disorder to be identified and characterized the adhesive deficiencies and functional phenotype of this subject's leukocytes. Here, we show that the molecular defect in this index subject is a new mutation in FERMT3 (KINDLIN-3) which encodes KINDLIN-3, a cytoskeletal protein that interacts with the cytoplasmic tails of ß1, ß2, and ß3 integrins and is required for inside-out and outside-in signaling of these heterodimers. We also report clinical features and previously unrecognized defects in cells from a new patient, a sibling of the original subject that we described who carries the same FERMT3 mutation. Mutations in FERMT3 have now been shown to be the basis for LAD-Iv/LAD-III in each of the four original patients or families that established this syndrome, including the family that we describe.

Fenton digestion of milk for iodinalysis.

Iodine is an essential micronutrient especially important in the neurodevelopment of infants. Spot samples of urinary iodine (UI) are used as an epidemiologic index of adult iodine nutrition. Individual infant iodine nutrition is of vital importance, but infant urine is difficult to collect, much less a 24 h sample. Monitoring the intake provides a pragmatic solution for determining infant iodine nutrition. Because of the high solids content of milk and the possible existence of iodine in an organically bound form, sample digestion is obligatory. The U.S. Food and Drug Administration, for example, uses wet ashing by HClO(4); special precautions and fume hoods are required. We present a method of Fenton digestion of human and bovine milk samples and infant formula. No specialized equipment or hazardous reagents are used; measurement is made by isotope dilution inductively coupled plasma mass spectrometry. In Fenton digestion, Fe(II) and H(2)O(2) oxidizes the sample. In an interlaboratory study, excellent agreement (r(2) = 0.9934) was observed with results obtained by HClO(4) digestion and Sandel-Kolthoff kinetic colorimetry. Average recoveries of iodide, triiodothyronine, and thyroxine ranged between 100% and 101%. Following digestion, iodine was found to exist entirely as iodide. Control of pH is imperative if loss cannot be corrected for by isotope dilution. Loss was below 20% for all samples when the pH was between 2.25 and 2.5.

Platelets as central mediators of systemic inflammatory responses.

Systemic inflammatory responses are associated with high morbidity and mortality and represent a diverse and clinically challenging group of diseases. Platelets are increasingly linked to inflammation, in addition to their well-known roles in hemostasis and thrombosis. There is agreement that traditional functions of platelets, including adherence, aggregation, and secretion of preformed mediators, contribute to systemic inflammatory responses. However, emerging evidence indicates that platelets function in non-traditional ways. In this review, we focus on new functions of platelets that may be involved in the host response to infection.

Using theory and technology to design a practical and generalizable smoking reduction intervention.

The aim of this article is to describe the process of using theory to form strategies for a generalizable smoking reduction intervention delivered through multiple intervention modalities. This report describes the process of integrating theory, data from diverse sources, staff from three different organizations, and different intervention modalities into an efficient, large-scale smoking reduction program featuring automated data from electronic medical records, computer-assisted telephone interviews, and tailored newsletters. The authors successfully developed a program that was consistently implemented as planned for 320 smokers in a managed care organization. The mapping of theory to intervention, data transfer and security procedures, and processes and strategies used to overcome challenges to intervention implementation should provide lessons learned for similar health promotion projects. Few intervention studies discuss details of how they translate theory into practice or how they integrate different modalities and collaborating institutions, but such integration is critical for project success.

Long-term results of a smoking reduction program.

INTRODUCTION: There have been few comprehensive evaluations of smoking reduction, especially in health care delivery systems, and little is known about its cost, maintenance of reduced smoking, or robustness across patient subgroups. METHODS: A generally representative sample of 320 adult smokers from an HMO scheduled for outpatient surgery or a diagnostic procedure was randomized to enhanced usual care or a theory-based smoking reduction intervention that combined telephone counseling and tailored newsletters. Outcomes included cigarettes smoked, carbon monoxide levels, and costs. RESULTS: Both intervention and control conditions continued to improve from 3- to 12-month assessments. Between-condition differences using intent-to-treat analyses on both self-report and carbon monoxide measures were nonsignificant by the 12-month follow-up (25% vs. 19% achieved 50% or greater reductions in cigarettes smoked). The intervention was implemented consistently despite logistical constraints and was generally robust across patient characteristics (eg, education, ethnicity, health literacy, dependence). CONCLUSIONS: In the absence of nicotine replacement therapy, the long-term effects of this smoking reduction intervention seem modest and nonsignificant. Future research is indicated to enhance intervention effects and conduct more comprehensive economic analyses of program variations.

Evaluating initial reach and robustness of a practical randomized trial of smoking reduction.

OBJECTIVE: This study evaluated the reach, initial effectiveness, and potential moderators and mediators of results of a smoking reduction program. DESIGN: A generally representative sample of 320 adult smokers from an HMO, scheduled for outpatient surgery or a diagnostic procedure, were randomized to enhanced usual care or a theory-based smoking reduction intervention that combined telephone counseling and tailored newsletters. MAIN OUTCOME MEASURES: Self-reported number of cigarettes smoked and carbon monoxide levels. RESULTS: The intervention enrolled 30% of known eligible smokers and produced reductions of 3 cigarettes per day greater than enhanced usual care. Intervention participants were significantly more likely than control participants to achieve at least a 50% reduction in self-reported number of cigarettes using complete cases, imputation analyses, and intent-to-treat procedures. Similar patterns were seen for carbon monoxide results but were significant only in complete case analyses. The intervention was generally robust across patient characteristics (e.g., education, ethnicity, health literacy, and dependence) and phone counselors. CONCLUSION: Initial results suggest that this program has potential to reach and assist smokers who may not participate in cessation programs. Additional research is indicated to enhance intervention effects, assess maintenance, and evaluate public health impact.

Tailored behavioral support for smoking reduction: development and pilot results of an innovative intervention.

Reduction of smoking may increase the likelihood of eventual smoking cessation among those not ready to quit. We describe the development and acceptance of a smoking-reduction intervention that integrates telephone counseling sessions with newsletters. A computer-assisted telephone interviewing program generates real-time-tailored counseling delivered by lay interviewers. Pilot participants (n = 53) were adult smokers scheduled for outpatient procedures in a health maintenance organization, randomized to intervention or a control condition (quarterly mailings). Smoking levels were measured by self-report and biochemically. Among intervention participants continuing at 3 months, all but one rated their telephone support person positively on all dimensions. Counseling calls were 'about right' in number, and newsletters were perceived as quite personal. Intervention recipients reported smoking significantly fewer mean cigarettes per day at 3 months than at baseline, and significantly fewer than control participants. Comparisons were non-significant under intent-to-treat analyses and on biochemical measures. The program was well received by outpatients who were not ready to quit smoking, and was implemented successfully by telephone staff who had no previous smoking cessation counseling experience. An ongoing trial is evaluating effectiveness, cost and relationship to eventual cessation.

Yeast PAS kinase coordinates glucose partitioning in response to metabolic and cell integrity signaling.

PAS kinase is an evolutionarily conserved serine/threonine protein kinase. Mammalian PAS kinase is activated under nutrient replete conditions and is important for controlling metabolic rate and energy homeostasis. In yeast, PAS kinase acts to increase the synthesis of structural carbohydrate at the expense of storage carbohydrates through phosphorylation of the enzyme UDP-glucose pyrophosphorylase. We have identified two pathways that activate yeast PAS kinase; one is responsive to nutrient conditions while the other is responsive to cell integrity stress. These pathways differentially activate the two PAS kinase proteins in Saccharomyces cerevisiae, Psk1 and Psk2, with Psk1 alone responding to activation by nonfermentative carbon sources. We demonstrate that, in addition to transcriptional effects, both of these pathways post-translationally activate PAS kinase via its regulatory N-terminus. As a whole, this system acts to coordinate glucose partitioning with alterations in demand due to changes in environmental and nutrient conditions.

PAS kinase is required for normal cellular energy balance.

The metabolic syndrome, a complex set of phenotypes typically associated with obesity and diabetes, is an increasing threat to global public health. Fundamentally, the metabolic syndrome is caused by a failure to properly sense and respond to cellular metabolic cues. We studied the role of the cellular metabolic sensor PAS kinase (PASK) in the pathogenesis of metabolic disease by using PASK(-/-) mice. We identified tissue-specific metabolic phenotypes caused by PASK deletion consistent with its role as a metabolic sensor. Specifically, PASK(-/-) mice exhibited impaired glucose-stimulated insulin secretion in pancreatic beta-cells, altered triglyceride storage in liver, and increased metabolic rate in skeletal muscle. Further, PASK deletion caused nearly complete protection from the deleterious effects of a high-fat diet including obesity and insulin resistance. We also demonstrate that these cellular effects, increased rate of oxidative metabolism and ATP production, occur in cultured cells. We therefore hypothesize that PASK acts in a cell-autonomous manner to maintain cellular energy homeostasis and is a potential therapeutic target for metabolic disease.

Regulation of glucose partitioning by PAS kinase and Ugp1 phosphorylation.

The ability of cells to recognize and respond to specific metabolic deficiencies is required for all forms of life. We have uncovered a system in the yeast S. cerevisiae that, in response to a perceived deficiency in cell wall glucan, alters partitioning of glucose toward glucan synthesis and away from glycogen synthesis. The paralogous yeast PAS kinases Psk1 and Psk2 phosphorylate UDP-glucose pyrophosphorylase (Ugp1), the primary producer of UDP-glucose, the glucose donor for glucan biosynthesis. Unexpectedly, phosphorylation of Ugp1 does not affect its catalytic activity but instead alters the terminal destination of the UDP-glucose it generates. Phosphorylated Ugp1 is required for intensive glucan production, and inability to phosphorylate Ugp1 is associated with a weak cell wall, decreased glucan content, and increased glycogen content. We provide data indicating that phosphorylation by Psk1 or Psk2 targets Ugp1 to the cell periphery, where the UDP-glucose it produces is in proximity to the site of glucan synthesis. We propose that regulation of glucose partitioning by altered enzyme and substrate localization is a rapid and potent response to metabolic deficiency.

Thermodynamics of peat-, plant-, and soil-derived humic acid sorption on kaolinite.

Humic acids (HAs) form coatings on clays and minerals that can play an important role in nutrient and contaminant migration in soil and water. Humic acid-clay mineral interactions are known to be affected by pH and ionic strength, but little attention has been paid to the effects of temperature. In this paper we report the stoichiometry and thermodynamics of interactions of aqueous HAs (isolated from two peats, two soils and a marine alga with a method that removes lipids) with kaolinite clay, Al2Si2O5(OH)4, at seven temperatures from 5.0 to 35.0 degrees C in 0.05 M NaCl at pH 3.5. All the sorption isotherms exhibit consecutive steps ascribed to HA monolayer and bilayer formation, respectively. Site capacity comparisons suggest different HA molecular conformations on kaolinite. Linearly correlated enthalpy and entropy changes for HA sorption point to the importance of hydration and dehydration in the sorption mechanism.