Microbial tropicalization driven by a strengthening western ocean boundary current

Western boundary currents (WBCs) redistribute heat and oligotrophic seawater from the tropics to temperate latitudes, with several displaying substantial climate change‐driven intensification over the last century. Strengthening WBCs have been implicated in the poleward range expansion of marine macroflora and fauna, however, the impacts on the structure and function of temperate microbial communities are largely unknown. Here we show that the major subtropical WBC of the South Pacific Ocean, the East Australian Current (EAC), transports microbial assemblages that maintain tropical and oligotrophic (k‐strategist) signatures, to seasonally displace more copiotrophic (r‐strategist) temperate microbial populations within temperate latitudes of the Tasman Sea. We identified specific characteristics of EAC microbial assemblages compared with non‐EAC assemblages, including strain transitions within the SAR11 clade, enrichment of Prochlorococcus, predicted smaller genome sizes and shifts in the importance of several functional genes, including those associated with cyanobacterial photosynthesis, secondary metabolism and fatty acid and lipid transport. At a temperate time‐series site in the Tasman Sea, we observed significant reductions in standing stocks of total carbon and chlorophyll a, and a shift towards smaller phytoplankton and carnivorous copepods, associated with the seasonal impact of the EAC microbial assemblage. In light of the substantial shifts in microbial assemblage structure and function associated with the EAC, we conclude that climate‐driven expansions of WBCs will expand the range of tropical oligotrophic microbes, and potentially profoundly impact the trophic status of temperate waters.     

Impacts of remotely sensed environmental drivers on coral outplant survival

Globally, coral reefs are degrading due to a variety of stressors including climate change and pollution. Active restoration is an important effort for sustaining coral reefs where, typically, coral fragments are outplanted onto degraded reefs. Coral outplants, however, can experience mortality in response to a range of stressors. We pair results of outplant monitoring observations with satellite‐based measurements of multiple oceanographic variables to estimate the relative importance of each driver to coral outplant survival. We find that when considering mean environmental conditions experienced by outplants during the monitoring period, particulate organic carbon (POC) levels are most important in determining outplant survival, with certain levels of POC beneficial for outplants. Sea surface temperature anomalies (SSTA) are also important determinants of outplant survival, where survival is greatest in regions with minimal or slightly negative anomalies. Survival also increases with increasing distance to land, likely due to a reduction in negative ridge‐to‐reef effects on coral outplants. When considering the range (min–max) of environmental conditions experienced during the monitoring period, large fluctuations in photosynthetically active radiation (PAR) and POC are most important in determining outplant survival. Increasing outplant depth can help to counter the negative impacts of large fluctuations in environmental variables. We find that a variety of remotely sensed oceanographic variables have significant impacts on survival and should be considered in coral restoration planning to help evaluate potential restoration sites and ultimately maximize coral outplant survival.     

Tbc1d15–17 regulates synaptic development at the Drosophila neuromuscular junction

Members of the Tre-2/Bub2/Cdc16 (TBC) family of proteins are believed to function as GTPase-activating proteins (GAPs) for Rab GTPases, which play pivotal roles in intracellular membrane trafficking. Although membrane trafficking is fundamental to neuronal morphogenesis and function, the roles of TBC-family Rab GAPs have been poorly characterized in the nervous system. In this paper, we provide genetic evidence that Tbc1d15–17, the Drosophila homolog of mammalian Rab7-GAP TBC1d15, is required for normal presynaptic growth and postsynaptic organization at the neuromuscular junction (NMJ). A loss-of-function mutation in Tbc1d15–17 or its presynaptic knockdown leads to an increase in synaptic bouton number and NMJ length. Tbc1d15–17 mutants are also defective in the distribution of the postsynaptic scaffold Discs-large (Dlg) and in the level of the postsynaptic glutamate subunit GluRIIA. These postsynaptic phenotypes are recapitulated by postsynaptic knockdown of Tbc1d15–17. We also show that presynaptic overexpression of a constitutively active Rab7 mutant in a wild-type background causes a synaptic overgrowth phenotype resembling that of Tbc1d15–17 mutants, while a dominant-negative form of Rab7 has the opposite effect. Together, our findings establish a novel role for Tbc1d15–17 and its potential substrate Rab7 in regulating synaptic development.     

Adaptive Mutation in Saccharomyces cerevisiae

ABSTRACT

Adaptive mutation is a generic term for processes that allow individual cells of nonproliferating cell populations to acquire advantageous mutations and thereby to overcome the strong selective pressure of proliferation-limiting environmental conditions. Prerequisites for an occurrence of adaptive mutation are that the selective conditions are nonlethal and that a restart of proliferation may be accomplished by some genetic change in principle. The importance of adaptive mutation is derived from the assumption that it may, on the one hand, result in an accelerated evolution of microorganisms and, on the other, in multicellular organisms may contribute to a breakout of somatic cells from negative growth regulation, i.e., to cancerogenesis. Most information on adaptive mutation in eukaryotes has been gained with the budding yeast Saccharomyces cerevisiae. This review focuses comprehensively on adaptive mutation in this organism and summarizes our current understanding of this issue.     

Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents

The study of electrophysiological properties of cardiac ion channels with the patch-clamp technique and the exploration of cardiac cellular Ca²⁺ handling abnormalities requires isolated cardiomyocytes. In addition, the possibility to investigate myocytes from patients using these techniques is an invaluable requirement to elucidate the molecular basis of cardiac diseases such as atrial fibrillation (AF).¹ Here we describe a method for isolation of human atrial myocytes which are suitable for both patch-clamp studies and simultaneous measurements of intracellular Ca²⁺ concentrations. First, right atrial appendages obtained from patients undergoing open heart surgery are chopped into small tissue chunks ("chunk method") and washed in Ca²⁺-free solution. Then the tissue chunks are digested in collagenase and protease containing solutions with 20 μM Ca²⁺. Thereafter, the isolated myocytes are harvested by filtration and centrifugation of the tissue suspension. Finally, the Ca²⁺ concentration in the cell storage solution is adjusted stepwise to 0.2 mM. We briefly discuss the meaning of Ca²⁺ and Ca²⁺ buffering during the isolation process and also provide representative recordings of action potentials and membrane currents, both together with simultaneous Ca²⁺ transient measurements, performed in these isolated myocytes.     

Induction of localized auxin response during spontaneous nodule development in Lotus japonicus

In leguminous plants, rhizobial infection of the epidermis triggers proliferation of cortical cells to form a nodule primordium. Recent studies have demonstrated that two classic phytohormones, cytokinin and auxin, have important functions in nodulation. The identification of these functions in Lotus japonicus was facilitated by use of the spontaneous nodule formation 2 (snf2) mutation of the putative cytokinin receptor LOTUS HISTIDINE KINASE 1 (LHK1). Analyses using snf2 demonstrated that constitutive activation of cytokinin signaling causes formation of spontaneous nodule-like structures in the absence of rhizobia and that auxin responses are induced in proliferating cortical cells during such spontaneous nodule development. Thus, cytokinin signaling positively regulates the auxin response. In the present study, we further investigated the induction of the auxin response using a gain-of-function mutation of Ca²⁺/calmodulin-dependent protein kinase (CCaMK) that causes spontaneous nodule formation. We demonstrate that CCaMK^T265D-mediated spontaneous nodule development is accompanied by a localized auxin response. Thus, a localized auxin response at the site of an incipient nodule primordium is essential for nodule organogenesis.     

Chronic morphine exposure and its abstinence alters dendritic spine morphology and upregulates Shank1

Exposure to chronic drugs of abuse has been reported to produce significant changes in postsynaptic protein profile, dendritic spine morphology and synaptic transmission. In the present study we demonstrate alterations in dendritic spine morphology in the frontal cortex and nucleus accumbens of mice following chronic morphine treatment as well as during abstinence for two months. Such alterations were accompanied with significant upregulation of the postsynaptic protein Shank1 in synaptosomal enriched fractions. mRNA levels of Shank1 was also markedly increased during morphine treatment and during withdrawal. Studies of the different postsynaptic proteins at the protein and mRNA levels showed significant alterations in the morphine treated groups compared to that of saline treated controls. Taken together, these observations suggest that Shank1 may have an important role in the regulation of spine morphology induced by chronic morphine leading to addiction.     

A simple model predicting individual weight change in humans

Excessive weight in adults is a national concern with over 2/3 of the US population deemed overweight. Because being overweight has been correlated to numerous diseases such as heart disease and type 2 diabetes, there is a need to understand mechanisms and predict outcomes of weight change and weight maintenance. A simple mathematical model that accurately predicts individual weight change offers opportunities to understand how individuals lose and gain weight and can be used to foster patient adherence to diets in clinical settings. For this purpose, we developed a one-dimensional differential equation model of weight change based on the energy balance equation paired to an algebraic relationship between fat-free mass and fat mass derived from a large nationally representative sample of recently released data collected by the Centers for Disease Control. We validate the model's ability to predict individual participants’ weight change by comparing model estimates of final weight data from two recent underfeeding studies and one overfeeding study. Mean absolute error and standard deviation between model predictions and observed measurements of final weights are less than 1.8±1.3 kg for the underfeeding studies and 2.5±1.6 kg for the overfeeding study. Comparison of the model predictions to other one-dimensional models of weight change shows improvement in mean absolute error, standard deviation of mean absolute error, and group mean predictions. The maximum absolute individual error decreased by approximately 60% substantiating reliability in individual weight-change predictions. The model provides a viable method for estimating individual weight change as a result of changes in intake and determining individual dietary adherence during weight-change studies.     

Out-of-hospital cardiac arrest: the prospect of E-CPR in the Maastricht region

Aim

The current outcome of out-of-hospital cardiac arrest (OHCA) patients in the Maastricht region was analysed with the prospect of implementing extracorporeal cardiopulmonary resuscitation (E-CPR).

Methods

A retrospective analysis of adult patients who were resuscitated for OHCA during a 24-month period was performed.

Results

195 patients (age 66 [57–75] years, 82 % male) were resuscitated for OHCA by the emergency medical services and survived to admission at the emergency department. Survival to hospital discharge was 46.2 %. Notable differences between non-survivors and survivors were observed and included: age (70 [58–79] years) vs. (63 [55–72] years, p = 0.01), chronic heart failure (18 vs. 7 %, p = 0.02), shockable rhythm (67 vs. 99 %, p < 0.01), and return of spontaneous circulation (ROSC) at departure from the site of the arrest (46 vs. 99 %, p < 0.01) and on arrival to the emergency department (43 vs. 98 %, p < 0.01), respectively. Acute coronary syndrome was diagnosed in 32 % of non-survivors vs. 59 % among survivors, p < 0.01. Therapeutic hypothermia was provided in non-survivors (20 %) vs. survivors (43 %), p < 0.01. Percutaneous coronary intervention (PCI) was performed in 14 % of non-survivors while 52 % of survivors received PCI (p < 0.01). No statistical significance was observed in terms of gender, witnessed arrest, bystander CPR, or automated external defibrillator deployed among the cohort. At hospital discharge, moderately severe neurological disability was present in six survivors.

Conclusion

These observations are compatible with the notion that a shockable rhythm, ROSC, and post-arrest care improve survival outcome. Potentially, initiating E-CPR in the resuscitation phase in patients with a shockable rhythm and no ROSC might serve as a bridge to definite treatment and improve survival outcome.