Hyperemesis gravidarum and long-term mortality: a population-based cohort study.

OBJECTIVE: To investigate whether exposure to hyperemesis gravidarum (HG) is associated with increased maternal long-term mortality. DESIGN: Population-based cohort study. SETTING: Medical Birth Registry of Norway (1967-2002) linked to the Cause of Death Registry. POPULATION: Women in Norway with singleton births in the period 1967-2002, with and without HG. Women were followed until 2009 or death. METHODS: Cox proportional hazard regression model was applied to estimate hazard ratios (HRs) with 95% confidence interval (CI). MAIN OUTCOME MEASURES: The primary outcome was all-cause mortality during follow up. Secondary outcomes were cause-specific mortality (cardiovascular mortality, deaths due to cancer, external causes or mental and behavioural disorders). RESULTS: Of 999 161 women with singleton births, 13 397 (1.3%) experienced HG. During a median follow up of 26 years (25 902 036 person-years), 43 470 women died (4.4%). Women exposed to HG had a lower risk of long-term all-cause mortality compared with women without HG (crude HR 0.82; 95% CI 0.75-0.90). When adjusting for confounders, this reduction was no longer significant (adjusted HR 0.92; 95% CI 0.84-1.01). Women exposed to HG had a similar risk of cardiovascular death as women not exposed (adjusted HR 1.04; 95% CI 0.83-1.29), but a lower long-term risk of death from cancer (adjusted HR 0.86; 95% CI 0.75-0.98). CONCLUSION: In this large population-based cohort study, HG was not associated with an increased risk of long-term all-cause mortality. Women exposed to HG had no increase in mortality due to cardiovascular disease, but had a reduced risk of death from cancer. TWEETABLE ABSTRACT: Population-based cohort study: Hyperemesis was not associated with an increased risk of long-term mortality.

Markers of thrombin generation are associated with myocardial necrosis and left ventricular impairment in patients with ST-elevation myocardial infarction.

INTRODUCTION: Platelet activation, thrombin generation and fibrin formation play important roles in intracoronary thrombus formation, which may lead to acute myocardial infarction. We investigated whether the prothrombotic markers D-dimer, pro-thrombin fragment 1 + 2 (F1 + 2) and endogenous thrombin potential (ETP) are associated with myocardial necrosis assessed by Troponin T (TnT), and left ventricular impairment assessed by left ventricular ejection fraction (LVEF) and N-terminal pro b-type natriuretic peptide (NT-proBNP). MATERIALS/METHODS: Patients (n = 987) with ST-elevation mycardial infarction (STEMI) were included. Blood samples were drawn at a median time of 24 h after onset of symptoms. RESULTS: Statistically significant correlations were found between both peak TnT and D-dimer (p < 0.001) and F1 + 2 (p < 0.001), and between NT-proBNP and D-dimer (p = 0.001) and F1 + 2 (p < 0.001). When dividing TnT and NT-proBNP levels into quartiles there were significant trends for increased levels of both markers across quartiles (all p < 0.001) D-dimer remained significantly associated with NT-proBNP after adjustments for covariates (p = 0.001) whereas the association between NTproBNP and F1 + 2 was no longer statistically significant (p = 0.324). A significant inverse correlation was found between LVEF and D-dimer (p < 0.001) and F1 + 2 (p = 0.013). When dichotomizing LVEF levels at 40 %, we observed significantly higher levels of both D-dimer (p < 0.001) and F1 + 2 (p = 0.016) in the group with low EF (n = 147). SUMMARY/CONCLUSION: In our cohort of STEMI patients we demonstrated that levels of D-dimer and F1 + 2 were significantly associated with myocardial necrosis as assessed by peak TnT. High levels of these coagulation markers in patients with low LVEF and high NTproBNP may indicate a hypercoagulable state in patients with impaired myocardial function.

Clinical outcomes in patients with atrial fibrillation according to sex during anticoagulation with apixaban or warfarin: a secondary analysis of a randomized controlled trial

AIM:To assess clinical outcomes, efficacy, and safety according to sex during anticoagulation with apixaban compared with warfarin in patients with atrial fibrillation.METHODS AND RESULTS:Apixaban for Reduction in Stroke and Other Thromboembolic Events in Atrial Fibrillation (ARISTOTLE) was a randomized, double-blind, placebo-controlled, multicentre trial that included 11 785 (64.7%) men and 6416 (35.3%) women with atrial fibrillation or flutter randomized to receive either warfarin or apixaban. The primary efficacy endpoint was stroke or systemic embolism; secondary efficacy endpoints were death from any cause and cardiovascular death. The primary safety endpoint was major bleeding; secondary safety endpoints were a composite of major bleeding and non-major clinically relevant bleeding. The risk of stroke or systemic embolism was similar in women vs. men [adjusted hazard ratio (adjHR): 0.91; 95% confidence interval (CI): 0.74-1.12; P = 0.38]. However, among patients with history of stroke or transient ischaemic attack, women had a lower risk of recurrent stroke compared with men (adjHR: 0.70; 95% CI: 0.50-0.97; P = 0.036). Women also had a lower risk of all-cause death (adjHR: 0.63; 95% CI: 0.55-0.73; P < 0.0001) and cardiovascular death (adjHR: 0.62; 95% CI: 0.51-0.75; P < 0.0001), and a trend towards less major bleeding (adjHR: 0.86; 95% CI: 0.74-1.01; P = 0.066) and major or non-major clinically relevant bleeding (adjHR: 0.89; 95% CI: 0.80-1.00; P = 0.049). The efficacy and safety benefits of apixaban compared with warfarin were consistent regardless of sex.CONCLUSION:In the ARISTOTLE trial, women had a similar rate of stroke or systemic embolism but a lower risk of mortality and less clinically relevant bleeding than men. The efficacy and safety benefits of apixaban compared with warfarin were consistent in men and women...

Fibrinolytic treatment of ST-elevation myocardial infarction. Update 2014.

Primary percutaneous coronary intervention (PPCI) is the preferred reperfusion therapy in ST-elevation myocardial infarction (STEMI), as long as it can be delivered within 90-120 minutes from patient's first medical contact, and is the leading reperfusion strategy in most European countries. However, as PPCI cannot be offered in a timely manner to all patients, fibrinolytic therapy (FT) is the recommended choice in patients with an anticipated delay to PPCI of >90-120 minutes, presenting early after symptom onset and without contra-indications. FT should preferably be started in the pre-hospital setting. Following FT, all patients should be transferred to a PCI-center for rescue PCI or routine coronary angiography with PCI as indicated. Such a pharmaco-invasive strategy, combining FT with invasive treatment, has recently been shown to be non-inferior to PPCI in patients living in areas with long transfer delays to PCI (>60 minutes). In this overview, we will briefly present the evidence for the benefit of FT in STEMI, and discuss the role of FT in the current era of PPCI as well as the optimal treatment following pharmacologic reperfusion.

Ethnicity and acute myocardial infarction: risk profile at presentation, access to hospital management, and outcome in Norway.

BACKGROUND: Previous studies in North America have shown ethnic variation in the presentation of acute myocardial infarction (AMI), and sex and racial differences in the management and outcome of AMI. In the present study, our aim was to investigate the risk profile of AMI for patients with minority background compared with indigenous Norwegians, at hospital presentation, and to investigate racial differences in hospital care and outcomes. PATIENTS AND METHODS: A dual-design study was adopted: a cross-sectional study to examine ethnic differences of risk prevalence at hospital presentation and a cohort study to estimate access to angiography, percutaneous coronary intervention (PCI), and hospital and long-term mortality. From a study population of 3105 patients with AMI presenting at Oslo University Hospital between January 1, 2006 and December 31, 2007, we identified 147 cases of AMI in patients with minority background and selected a random sample of 588 indigenous Norwegians with AMI as controls. Prognostic and explanatory strategies were used in the analysis. RESULTS: Compared with indigenous Norwegians with AMI, AMI patients with minority background suffered their AMI 10 years younger, were generally male, were twice as likely to be smokers, three times as likely to have type 2 diabetes, had lower high-density lipoprotein levels. This group also had 50% less history of hypertension. In terms of hospital care, AMI patients with minority background had shorter times from onset of symptoms to PCI and the same frequency of access to angiography and acute PCI as indigenous Norwegians when adjusting for the confounding effect of age, sex, and nature of myocardial infarction with or without ST elevation. CONCLUSION: At presentation to hospital, patients with minority background had a higher risk profile and a shorter time from onset of symptoms to admission to catheterization laboratory than indigenous Norwegians, but the same access to angiography and acute PCI during hospitalization.

Inducers of oxidative stress block ciliary neurotrophic factor activation of Jak/STAT signaling in neurons.

Generation of reactive oxygen species (ROS) with the accumulation of oxidative damage has been implicated in neurodegenerative disease and in the degradation of nervous system function with age. Here we report that ROS inhibit the activity of ciliary neurotrophic factor (CNTF) in nerve cells. Treatment with hydrogen peroxide (H(2)O(2)) as a generator of ROS inhibited CNTF-mediated Jak/STAT signaling in all cultured nerve cells tested, including chick ciliary ganglion neurons, chick neural retina, HMN-1 motor neuron hybrid cells, and SH-SY5Y and BE(2)-C human neuroblastoma cells. H(2)O(2) treatment of non-neuronal cells, chick skeletal muscle and HepG2 hepatoma cells, did not inhibit Jak/STAT signaling. The H(2)O(2) block of CNTF activity was seen at concentrations as low as 0.1 mm and within 15 min, and was reversible upon removal of H(2)O(2) from the medium. Also, two other mediators of oxidative stress, nitric oxide and rotenone, inhibited CNTF signaling. Treatment of neurons with H(2)O(2) and rotenone also inhibited interferon-gamma-mediated activation of Jak/STAT1. Depleting the intracellular stores of reduced glutathione by treatment of BE(2)-C cells with nitrofurantoin inhibited CNTF activity, whereas addition of reduced glutathione protected cells from the effects of H(2)O(2). These results suggest that disruption of neurotrophic factor signaling by mediators of oxidative stress may contribute to the neuronal damage observed in neurodegenerative diseases and significantly affect the utility of CNTF-like factors as therapeutic agents in preventing nerve cell death.

Measurements of heart motion using accelerometers.

We have used acceleration sensors to monitor the heart motion during surgery. A three-axis accelerometer was made from two commercially available two-axis sensors, and was used to measure the heart motion in anesthetized pigs. The heart moves due to both respiration and heart beating. The heart beating was isolated from respiration by high-pass filtering at 1.0 Hz, and heart wall velocity and position were calculated by numerically integrating the filtered acceleration traces. The resulting curves reproduced the heart motion in great detail, noise was hardly visible. Events that occurred during the measurements, e.g. arrhythmias and fibrillation, were recognized in the curves, and confirmed by comparison with synchronously recorded ECG data. We conclude that acceleration sensors are able to measure heart motion with good resolution, and that such measurements can reveal patterns that may be an indication of heart circulation failure.

Physiology of erythropoietin during mammalian development.

UNLABELLED: Growth is a fundamental process of mammalian development. Several observations regarding regulation of erythropoiesis during growth are not easily explained by the hypoxia-erythropoietin (Epo) concept. This review focuses primarily on this aspect of the physiology of Epo. The question is raised of whether this regulation during growth is based on the hypoxia-Epo mechanism alone, or whether Epo acts in concert with general growth-promoting factors, particularly growth hormone (GH) and the insulin-like growth factors (IGF-I and -II). Supporting the latter hypothesis is the observation that the Epo and GH/IGF systems are activated by hypoxia and share similar receptors and pathways. Recent studies indicate that human fetal and infant growth is stimulated by GH, IGF-I and IGF-II. Epo, GH and IGFs are expressed early in fetal life. Although the rate of erythropoiesis in the fetus is high, serum Epo levels are low. The Epo response to hypoxia in the fetus and neonate is reduced compared with adults. Following delivery the Epo levels vary between species, probably related to the oxygen transport capacity of the hemoglobin (Hb) mass. IGF-I levels are low in the fetus and increase slowly following birth, except in preterm infants in whom the levels decline. In all mammals Hb declines following birth, giving rise to "early anemia". Except in the human, Epo levels increase proportionally with the fall in Hb, but there is a discrepancy between the curves for serum immunoreactive Epo (siEpo) and for erythropoiesis stimulating factors (ESF): the latter include other stimulatory factors in addition to Epo. Hypertransfusion of mice in the period of "early anemia" suppresses siEpo, but not ESF and erythropoiesis, as it does in adult mice. GH and IGF-I have direct effects on erythropoiesis in vitro and act particularly at the later stages of red cell differentiation. IGF-I acts synergistically with Epo, and its effects are most marked when Epo levels are low. Human recombinant (rhu) IGF-I stimulates erythropoiesis in neonatal rats, but not in newborn mice and lambs. In adult mice, in hypophysectomized rats and in mice with end-stage renal failure, however, a stimulatory effect of this growth factor was found on red cell production. RhuGH stimulates erythropoiesis in GH-deficient short children. CONCLUSION: Fetal and early postnatal erythropoiesis are dependent on factors in addition to Epo. The likely candidates are GH and IGF-I. The in vitro stimulating effects of these factors on erythropoiesis are convincing, but more data are needed on the in vivo effects.

[Diagnoses and increased levels of troponin T among discharged patients]. / Utskrivningsdiagnoser ved forhøyede troponin T-verdier.

BACKGROUND: New criteria for diagnosing acute myocardial infarction, in which the cardiac troponin T or I plays a central role, have recently been proposed. We wanted to estimate what an application of these criteria would have meant for the diagnoses given patients discharged from our hospital in 2000. MATERIAL AND METHODS: From the hospital data bases, 3,461 in-hospital patients were identified in whom troponin T levels in blood had been determined. Maximal troponin T levels and diagnoses on discharge were recorded. Only one diagnosis was used for each patient. The diagnoses were selected in a priority order favouring those diseases that are known most often to cause increased troponin T levels, starting with the codes for acute myocardial infarction. RESULTS: By applying the new criteria, the number of patients with myocardial infarction was estimated to increase 17%, 33% and 61% depending on the decision level for troponin T used, 0.20, 0.10 or 0.03 microgram/l, respectively. Congestive heart failure and atrial fibrillation were the most frequent cardiac diagnoses in patients with increased troponin T level without evidence of acute coronary syndromes. Other, non-cardiac diagnoses included renal diseases, sepsis, and acute lung diseases. INTERPRETATION: Application of the new diagnostic criteria will markedly increase the recorded incidence of acute myocardial infarction. The number of positive troponin T values in patients without acute coronary syndromes will increase progressively by lowering the diagnostic decision level of troponin T.

Left ventricular function and infarct size 20 months after primary angioplasty for acute myocardial infarction.

OBJECTIVE: To study changes in left ventricular function and infarct size during long-term follow-up after acute myocardial infarction treated with primary angioplasty. DESIGN: From 1996 to 1998, 100 consecutive patients were treated with primary angioplasty for acute ST-elevation myocardial infarction. Angioplasty was successful in 95% of the patients. Global left ventricular ejection fraction (LVEF) was determined by radionuclide ventriculography before discharge, after 6 weeks and after a mean follow-up time of 20 months. Infarct size was assessed by technetium 99m-tetrofosmin myocardial perfusion tomography (SPECT) at rest, performed at the same time intervals. RESULTS: Mean LVEF was 56% at discharge, 55% after 6 weeks and 57% after 20 months of follow-up. No significant improvement in LVEF was observed. Only 8% of the patients at follow-up had LVEF lower than 40%. After 1 week, a mean perfusion defect of 19% was measured by SPECT. After 6 weeks and 20 months of follow-up, the mean perfusion defects were reduced to 14% (p < 0.001) and 15%, respectively. CONCLUSION: Left ventricular function was well preserved with a mean LVEF of 57% 20 months after primary angioplasty for acute myocardial infarction. No significant change in LVEF was observed from 1 week after angioplasty to follow-up. Infarct sizes as assessed by SPECT imaging with tetrofosmin were reduced from 1 to 6 weeks, but did not change further during long-term follow-up. The reduction in the perfusion defects over time was probably due to gradual relief of stunning.

Fulminant meningococcal septicemia: dissociation between plasma thrombopoietin levels and platelet counts.

Thrombopoietin (TPO), interleukin (IL)-6, and platelets were measured serially in 9 patients with fulminant meningococcal septicemia and consumption coagulopathy. The results were compared with those of patients with meningococcal meningitis and mild meningococcemia (n=10) and with those of healthy control subjects (n=19). TPO levels in control subjects were below the detection limit (<63 pg/mL). In patients with fulminant meningococcal septicemia, the median TPO level on admission was 193 pg/mL (range, 133-401 pg/mL), and the level peaked within 3-7 days (median, 488 pg/mL; range, 239-1334 pg/mL). Platelet counts remained low, despite the elevated TPO levels. In patients with meningitis or meningococcemia, the median TPO level on admission was 112 pg/mL (range, <63-695 pg/mL), and the TPO level was not detectable within 48 h. Platelet counts for these patients remained within normal limits. Maximum IL-6 levels in patients with septicemia were observed on admission (median, 5317 pg/mL; range, 188-651,000 pg/mL) and increased earlier than TPO levels. In patients with fulminant septicemia, TPO level increases significantly whereas the level of circulating platelets does not.

Discrepancy between fibrinogen concentrations determined by clotting rate and clottability assays during the acute-phase reaction.

Assays based on clotting rate are commonly used as a routine method for determining the fibrinogen concentration in plasma. However, little is known about the influence of the acute-phase reaction on this assay. In order to disclose discrepancies between the fibrinogen concentrations obtained by a clotting rate assay (as described by Clauss) and a reference assay for total clottable protein (according to Jacobsson), we compared the fibrinogen concentrations determined by these two methods in plasma-samples collected preoperatively and on postoperative days 1, 3, and 5 in patients undergoing major elective surgery. The HMW (High Molecular Weight)-, LMW- and LMW'-fibrinogen fractions of the patient samples were also determined. In preoperative samples, good agreement between the two assays was found. In samples collected on postoperative days 1 and 3, the fibrinogen concentrations measured with the clotting rate assay were significantly higher than the concentrations measured with the total clottable protein assay (p=0.015 on both days). SDS-gel electrophoresis showed an increase in the median HMW-fraction from 69.7% (range 64.3-70.4) in preoperative samples to 85.8% (80.7-87.6) in samples drawn on day 3. The difference between fibrinogen concentrations obtained by the two methods was significantly correlated to the HMW-fraction of the samples. We conclude that during an acute-phase reaction, fibrinogen concentrations obtained by a clotting rate assay (as described by Clauss) are significantly higher than those measured by a total clottable protein assay (according to Jacobsson). The difference between the two methods correlates well with the relative HMW-fraction, indicating that the increase in HMW-fibrinogen is the main contributor to the observed discrepancy.

Severe liver failure in exertional heat stroke.

Exertional heat stroke usually occurs in warm climates. Increased serum levels of liver enzymes is a common finding in this condition, whereas liver failure is a more rare event that carries a poor prognosis. Liver transplantation has been recommended as treatment in cases of severe liver failure, but no long-term survival after this procedure in exertional heat stroke has been described. We report the case of a 31-year-old man who had a heat stroke after running 5 km at 21 degrees C. He developed severe liver damage, with serum alanine aminotransferase (ALAT) activities increasing to 16,410 U/l (reference values, 10-50 U/l) after 48 h, concomitantly with a pronounced coagulation disturbance, with Normotest (NT) decreasing to 12% (international normalized ratio (INR) = 4.2) (reference values, 70%-130% for NT and 0.8-1.2 for INR). A liver biopsy on the 5th day after the incident showed extensive liver cell necrosis. The patient was referred to be considered for liver transplantation but recovered completely on conservative treatment. We conclude that exertional heat stroke is a diagnostic possibility also in temperate climates and that severe liver failure may ensue. The liver injury is reversible, and the indications for liver transplantation in this situation have not been clarified.

[Fibrinogen as a cardiovascular risk factor--marker or causal factor?]. / Fibrinogen som risikofaktor for hjerte- og karsykdom--markør eller patogenetisk faktor?

Fibrinogen is an important determinant of blood haemostasis and viscosity. Several prospective studies have demonstrated plasma fibrinogen concentration to be an important predictor of cardiovascular disease, both in healthy subjects and in patients with coronary disease. Subjects with high plasma fibrinogen concentrations have a two to four-fold increased risk of developing cardiovascular disease compared to those with low fibrinogen. Whether fibrinogen is a causative factor for atherosclerosis or a marker of the inflammatory process of atherosclerosis remains to be proven.

Ciliary neurotrophic factor and phorbol ester each decrease selected STAT3 pools in neuroblastoma cells by proteasome-dependent mechanisms.

Many cytokines and growth factors activate common signal transduction pathways and yet are able to elicit distinct cell-specific responses. We are defining mechanisms regulating signalling molecules in order to understand how cytokines can produce unique responses. It was found that individual members of the signal transducer and activator of transcription (STAT) family are regulated by ciliary neurotrophic factor (CNTF) and by protein kinase C. Treatment of SH-SY5Y human neuroblastoma cells with the phorbol ester, 12- O -tetradecanoylphorbol 13-acetate (TPA), for 4-5 h caused a 60% decline in both STAT2 and STAT3 levels and no decline in levels of STATs 1, 5 or 6, or in Jaks 1 or 2. The decline in STAT3 was inhibited by treatment with MG132, an inhibitor of proteasome-dependent protein degradation. Treatment of cells with CNTF induced a rapid tyrosine phosphorylation of STAT3 followed by a time-dependent decay of this signal. Loss of tyrosine phosphorylated STAT3 was inhibited by MG132 but did not require protein kinase C activity. These results suggest that STAT3 availability can be controlled by proteasome-dependent pathways activated either by protein kinase C or by cytokines.

Prosthetic heart valve thrombosis during dicloxacillin therapy.

A 76-year-old woman receiving warfarin after aortic valve replacement experienced prosthetic valve thrombosis during dicloxacillin therapy. Successful thrombolysis was achieved with tissue plasminogen activator. The international normalized ratio (INR) on admission was reduced to 1.4 and an increased warfarin dosage was required for three weeks following discontinuation of dicloxacillin treatment in order to maintain therapeutic INRs. Careful monitoring of INRs and titration of the warfarin dosage is recommended when dicloxacillin is prescribed to patients receiving warfarin.

[Bilateral pulmonary infiltrations in patients admitted to an intensive care unit]. / Bilaterale lungefortetninger hos pasienter i medisinsk overvåkingsavdeling.

Diffuse pulmonary infiltrates are commonly found in hypoxic respiratory failure. We have reviewed 16 patients admitted to our medical intensive care unit over a period of 21 months, of whom seven died in hospital. Only patients requiring ventilatory support (CPAP or mechanical ventilation) for respiratory failure due to non-cardiogenic causes were included. All patients met the criteria for the diagnosis of ARDS. Three patients suffered from Wegener's granulomatosis, three from Pneumocystis carinii pneumonia, three from bacterial pneumonia, and two from pneumonia. Staphylococcal septicemia, SLE, sarcoidosis, cancer-associated hemolytic-uremic syndrome and ARDS of unknown etiology were each found in one patient. We discuss diagnosis and treatment of such patients on the basis of our experience.

Bioaccumulation of mercury in pelagic freshwater food webs.

Current paradigms regarding the bioaccumulation of mercury are rooted in observations that monomethyl mercury (meHg) biomagnifies along pelagic food chains. However, mechanisms regulating the formation of meHg, its initial incorporation at the base of pelagic food chains, and its subsequent trophic transfer remain controversial. Here we use field data from 15 northern Wisconsin lakes, equilibrium aqueous speciation modeling, and statistical modeling to revisit several hypotheses about the uptake, distribution, and fate of inorganic Hg (HgII) and meHg in aquatic biota. Our field data comprise determinations of total Hg (HgT) and meHg in surface waters, sediments, microseston, zooplankton, and small fish in each of the study lakes. For these lake waters, strong positive correlations between DOC and aqueous concentrations of mercury along with negative correlations between DOC and the seston-water partitioning of mercury indicate that organic ligands bind HgII and meHg strongly enough to dominate their apparent aqueous speciation. In the microseston, zooplankton and fish, meHg concentrations and bioaccumulation factors (BAFs) increased with increasing trophic level while biotic concentrations of HgII decreased--indicating that meHg was indeed the biomagnified species of mercury. For all trophic levels, meHg concentrations varied positively with the calculated aqueous concentration of meHg+ (free ion), especially when coupled with pH, or meHgOH (hydroxide) species but not with meHgCl0, the neutral chloride complex. These findings suggest that: (1) the passive uptake of meHg does not control bioaccumulation at the base of aquatic food webs in nature (i.e. phyto- and bacterioplankton); (2) correlation with pH and DOC largely reflect the supply and bioavailability of meHg to lower trophic levels; and (3) meHg concentrations at higher trophic levels reflect uptake at low trophic levels and other factors, such as diet and growth. Low concentrations of meHg in surficial sediments indicate that the fates of biotic HgII and meHg are different. Most biotic meHg is demethylated rather than buried in lake sediments.