Rivers in climatic zones characterized by dry and wet seasons often experience periodic transitions between losing and gaining conditions across the river‐aquifer continuum. Infiltration shifts can stimulate hyporheic microbial biomass growth and cycling of riverine carbon and nitrogen leading to major exports of biogenic CO2 and N2 to rivers. In this study, we develop and test a numerical model that simulates biological‐physical feedback in the hyporheic zone. We used the model to explore different initial conditions in terms of dissolved organic carbon availability, sediment characteristics, and stochastic variability in aerobic and anaerobic conditions from water table fluctuations. Our results show that while highly losing rivers have greater hyporheic CO2 and N2 production, gaining rivers allowed the greatest fraction of CO2 and N2 production to return to the river. Hyporheic aerobic respiration and denitrification contributed 0.1–2 g/m2/d of CO2 and 0.01–0.2 g/m2/d of N2; however, the suite of potential microbial behaviors varied greatly among sediment characteristics. We found that losing rivers that consistently lacked an exit pathway can store up to 100% of the entering C/N as subsurface biomass and dissolved gas. Our results demonstrate the importance of subsurface feedbacks whereby microbes and hydrology jointly control fate of C and N and are strongly linked to wet‐season control of initial sediment conditions and hydrologic control of seepage direction. These results provide a new understanding of hydrobiological and sediment‐based controls on hyporheic zone respiration, including a new explanation for the occurrence of anoxic microzones and large denitrification rates in gravelly riverbeds.

International audienceBioclogging in rivers can detrimentally impact aquifer recharge. This is particularly so in dry regions, where losing rivers are common, and where disconnection between surface water and groundwater (leading to the development of an unsaturated zone) can occur. Reduction in riverbed permeability due to biomass growth is a time-variable parameter that is often neglected, yet permeability reduction from bioclogging can introduce order of magnitude changes in seepage fluxes from rivers over short (i.e., monthly) timescales. To address the combined effects of bioclogging and disconnection on infiltration, we developed numerical representations of bioclogging processes within a one-dimensional, variably saturated flow model representing losing-connected and losing-disconnected rivers. We tested these formulations using a synthetic case study informed with biological data obtained from the Russian River, California, USA. Our findings show that modeled biomass growth reduced seepage for losing-connected and losingdisconnected rivers. However, for rivers undergoing disconnection, infiltration declines occurred only after the system was fully disconnected. Before full disconnection, biologically induced permeability declines were not significant enough to offset the infiltration gains introduced by disconnection. The two effects combine to lead to a characteristic infiltration curve where peak infiltration magnitude and timing is controlled by permeability declines relative to hydraulic gradient gains. Biomass growth was found to hasten the onset of full disconnection; a condition we term ‘effective disconnection’. Our results show that river infiltration can respond dynamically to bioclogging and subsequent permeability declines that are highly dependent on river connection status

These findings demonstrate the ability of the hypothalamic-pituitary-gonadal hormone axis and sex steroid metabolism to resume physiological function following orthotopic liver transplantation in men. Correspondingly, sexual function returns to normal in the majority of patients, despite significant alterations prior to orthotopic liver transplantation.

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To determine the impact of liver transplantation on andrological status, we compared the endocrine profiles and spermiograms of 2 cohorts of patients before (9) and after (11) transplantation. Before liver transplantation testosterone (1.1 +/- 0.7 ng/ml) and free testosterone (2.0 +/- 1.6 pg/ml) were pathologically decreased in all 9 cases, and luteinizing hormone was lower (1.8 +/- 1.4 mIU/ml) in 5. Only 3 of 9 patients were able to produce ejaculates before liver transplantation, all of which were azoospermic. After a mean interval of 28 +/- 9 months (range 4 to 34 months) following liver transplantation testosterone (5.3 +/- 1.1 ng/ml), free testosterone (15.3 +/- 5.0 pg/ml) and luteinizing hormone (6.2 +/- 3.7 mIU/ml.) were consistently within the normal range, with a highly statistically significant difference (p < 0.025) from pre-liver transplantation values. Semen analyses after liver transplantation revealed normal density, motility and normal forms in 5 patients, 2 suffered from oligoasthenoteratospermia and 4 were unable to produce an ejaculate for semen analyses. These data demonstrate that the hypothalamic-pituitary-testicular hormone axis and gonadal tissue are capable of resuming normal function after liver transplantation in men with chronic liver failure who suffered from massive andrological dysfunction before transplantation.

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Comparative pyridostigmine kinetics in plasma were measured in 10 healthy subjects given 4 mg iv and 60 mg oral pyridostigmine bromide. As determined from the AUC ratio, oral availability was 11.5% to 18.9% (means = 14.3%). Mean t 1/2 of the plasma level decline after oral dosing was 200 minutes, twice as long as the terminal elimination t1/2 after intravenous infusion (97 minutes). Thus absorption may proceed at a slower rate than elimination. Comparison of intraindividual data revealed strict dependence of the AUC on the infused dose (2, 4, and 8 mg) in one subject and variability in AUC up to a factor of two when two subjects took oral pyridostigmine three times. Patients with myasthenia who were receiving continuous therapy with oral pyridostigmine had AUC values per unit dose corresponding to those in healthy subjects. Storage stability of pyridostigmine in plasma required acidification of samples and storage at -75 degrees C. When native plasma was kept at -20 degrees C, there was appreciable loss of pyridostigmine within 1 to 2 months, the extent of which depended on the initial concentration.