Ocean acidification significantly alters the trace element content of the kelp, Saccharina latissima.

Seaweeds are ecosystem engineers that can serve as habitat, sequester carbon, buffer ecosystems against acidification, and, in an aquaculture setting, represent an important food source. One health issue regarding the consumption of seaweeds and specifically, kelp, is the accumulation of some trace elements of concern within tissues. As atmospheric CO2 concentrations rise, and global oceans acidify, the concentrations of elements in seawater and kelp may change. Here, we cultivated the sugar kelp, Saccharina latissima under ambient (~400 µatm) and elevated pCO2 (600-2400 µatm) conditions and examined the accumulation of trace elements using x-ray powder diffraction, sub-micron resolution x-ray imaging, and inductively coupled plasma mass spectrometry. Exposure of S. latissima to higher concentrations of pCO2 and lower pH caused a significant increase (p < 0.05) in the iodine and arsenic content of kelp along with increased subcellular heterogeneity of these two elements as well as bromine. The iodine-to­calcium and bromine-to­calcium ratios of kelp also increased significantly under high CO2/low pH (p < 0.05). In contrast, high CO2/low pH significantly reduced levels of copper and cadmium in kelp tissue (p < 0.05) and there were significant inverse correlations between concentrations of pCO2 and concentrations of cadmium and copper in kelp (p < 0.05). Changes in copper and cadmium levels in kelp were counter to expected changes in their free ionic concentrations in seawater, suggesting that the influence of low pH on algal physiology was an important control on the elemental content of kelp. Collectively, these findings reveal the complex effects of ocean acidification on the elemental composition of seaweeds and indicate that the elemental content of seaweeds used as food must be carefully monitored as climate change accelerates this century.

Presynaptic CaMKIIα modulates dopamine D3 receptor activation in striatonigral terminals of the rat brain in a Ca²âº dependent manner.

CaMKIIα is expressed at high density in the nucleus accumbens where it binds to postsynaptic D3 receptors inhibiting their effects. In striatonigral projections, activation of presynaptic D3 receptors potentiates D1 receptor-induced stimulation of cAMP production and GABA release. In this study we examined whether the presynaptic effects of D3 receptor stimulation in the substantia nigra reticulata (SNr) are modulated by Ca²âº activation of CaMKIIα. In SNr synaptosomes two procedures that increase cytoplasmic Ca²âº, ionomycin and K⁺-depolarization, blocked the additional stimulation of cAMP accumulation produced by coactivating D3 and D1 dopamine receptors. The selective CaMKIIα inhibitor KN-62 reversed the blockade produced by ionomycin and K⁺-depolarization. Incubation in either Ca²-free solutions or with the selective Ca²âº blocker nifedipine, also reversed the blocking effects of K⁺-depolarization. Immunoblot studies showed that K⁺-depolarization increased CaMKIIα phosphorylation in a KN-62 sensitive manner and promoted CaMKIIα binding to D3 receptors. In K⁺-depolarized tissues, D3 receptors potentiated D1 receptor-induced stimulation of [³H]GABA release only when CaMKIIα was blocked with KN-62. In the presence of this inhibitor, the selective D3 agonist PD 128,907 reduced the ED50 for the D1 agonist SKF 38393 from 56 to 4 nM. KN-62 also enhanced the effects of dopamine on depolarization induced [³H]GABA release. KN-62 changed ED50 for dopamine from 584 to 56 nM. KN-62 did not affect D1 and D4 receptor responses. These experiments show that in striatonigral projections, CaMKIIα inhibits the action of D3 receptors in a Ca²âº dependent manner blocking their modulatory effects on GABA release. These findings suggest a mechanism through which the frequency of action potential discharge in presynaptic terminals regulates dopamine effects.

A new class of receptor for herpes simplex virus has heptad repeat motifs that are common to membrane fusion proteins.

We isolated a human cDNA by expression cloning and characterized its gene product as a new human protein that enables entry and infection of herpes simplex virus (HSV). The gene, designated hfl-B5, encodes a type II cell surface membrane protein, B5, that is broadly expressed in human primary tissue and cell lines. It contains a high-scoring heptad repeat at the extracellular C terminus that is predicted to form an alpha-helix for coiled coils like those in cellular SNAREs or in some viral fusion proteins. A synthetic 30-mer peptide that has the same sequence as the heptad repeat alpha-helix blocks HSV infection of B5-expressing porcine cells and human HEp-2 cells. Transient expression of human B5 in HEp-2 cells results in increased polykarocyte formation even in the absence of viral proteins. The B5 protein fulfills all criteria as a receptor or coreceptor for HSV entry. Use by HSV of a human cellular receptor, such as B5, that contains putative membrane fusion domains provides an example where a pathogenic virus with broad tropism has usurped a widely expressed cellular protein to function in infection at events that lead to membrane fusion.

Herpes simplex virus entry mediator associates in infected cells in a complex with viral proteins gD and at least gH.

We examined herpes simplex virus (HSV)-infected human HEp-2 cells or porcine cells that express herpes virus entry mediator (HVEM) for virus and receptor protein interactions. Antibody to HVEM, or its viral ligand gD, coimmunoprecipitated several similar proteins. A prominent 110-kDa protein that coprecipitated was identified as gH. The HVEM/gD/gH complex was detected with mild or stringent cell lysis conditions. It did not form in cells infected with HSV-1(KOS)Rid1 virus or with null virus lacking gD, gH, or gL. Thus, in cells a complex forms through physical associations of HVEM, gD, and at least gH.

Diagnóstico serológico de la leptospirosis humana empleando la técnica de macroaglutinación TR y la prueba del 2-mercaptoetanol / Serologic diagnosis of human leptospirosis using TR macroagglutination technique and 2-mercaptoethanol assay

Se estudiaron 389 monosueros, procedentes de pacientes con diagnóstico clínico presuntivo de ser portadores de una leptopirosis. De ellos 131 resultaron reactivos (33,67%), mediante la técnica de macroaglutinación en lámina con antígeno termorresistente (TR) cuantitativa. Paralelamente, a 119 de estos sueros, se les realizó la prueba del 2-mercaptoetanol al 0,2 molar, con la finalidad de determinar cualitativamente, las clases de inmunoglobulinas presentes en los sueros estudiados. La cuantificación de anticuerpos en los sueros reactivos, se ofrece a través de los títulos obtenidos

Diagnóstico serológico de la leptospirosis humana empleando la técnica de macroaglutinación TR y la prueba del 2-mercaptoetanol / Serologic diagnosis of huan leptospirosis using TR macroagglutination technique and 2-mercaptoethanol assay

Se estudiaron 389 monosueros, procedentes de pacientes con diagnóstico clínico presuntivo de ser portadores de una leptopirosis. De ellos 131 resultaron reactivos (33,67

), mediante la técnica de macroaglutinación en lámina con antígeno termorresistente (TR) cuantitativa. Paralelamente, a 119 de estos sueros, se les realizó la prueba del 2-mercaptoetanol al 0,2 molar, con la finalidad de determinar cualitativamente, las clases de inmunoglobulinas presentes en los sueros estudiados. La cuantificación de anticuerpos en los sueros reactivos, se ofrece a través de los títulos obtenidos