Revival of Philozoon Geddes for host-specialized dinoflagellates, ‘zooxanthellae’, in animals from coastal temperate zones of northern and southern hemispheres

The dinoflagellate family Symbiodiniaceae comprises numerous genera and species with large differences in diversity, ecology and geographic distribution. An evolutionarily divergent lineage common in temperate symbiotic cnidarians and designated in the literature by several informal names including ‘temperate–A’, AI, Phylotype A´ (A-prime) and ‘Mediterranean A’, is here assigned to the genus Philozoon. This genus was proposed by Geddes (1882) in one of the earliest papers that recognized ‘yellow cells’ as distinct biological entities separate from their animal and protist hosts. Using phylogenetic data from nuclear (rDNA), chloroplast (cp23S) and mitochondrial genes (cob and cox1), as well as morphology (cell size), ecological traits (host affinity) and geographic distributions, we emend the genus Philozoon Geddes and two of its species, P. medusarum and P. actiniarum, and describe six new species. Each symbiont species exhibits high host fidelity for particular species of sea anemone, soft coral, stony coral and a rhizostome jellyfish. Philozoon is most closely related to Symbiodinium (formerly Clade A), but, unlike its tropical counterpart, occurs in hosts in shallow temperate marine habitats in northern and southern hemispheres including the Mediterranean Sea, north-eastern Atlantic Ocean, eastern Australia, New Zealand and Chile. The existence of a species-diverse lineage adapted to cnidarian hosts living in high latitude habitats with inherently wide fluctuations in temperature calls further attention to the ecological and biogeographic reach of the Symbiodiniaceae

De-installation of the multi-organic dysfunction syndrome by associating the mitochondrial microcirculatory recruitment with multiple organ support therapy in extracorporeal life support organization

World Academy of Medical Sciences (WAMS), Netherland, Fundeni Institute, Bucharest, Romania, Institute of Scientific Research in the field of Mother and Child Health Care, Republic of Moldova, State University of Medicine and Pharmacy “Nicolae Testemitanu”, Republic of Moldova, State Medical University of Samara, The Russian Federation, Aretaieion University Hospital, Athens, Medical School, National, and Kapodistrian The University of Athens, Greece, Odesa National Medicine University, Ukraine, Private Hospital Medical Institution “Via - Intosana”, Republic of Moldova, Medicine University of Buenos Aires, Argentina, Al VI-lea Congres Național de Obstetrică și Ginecologie cu participare internațională, 13-15 septembrie 2018, Chișinău, Republica MoldovaIntroduction: The installation of macro-circulation centralization in MODS triggering in critical obstetric states caused by intravascular coagulation, HELLP, shock, SIRS, septicemia, CARS, embolism of the pulmonary artery, cerebral and other, – microcirculation will also be seriously damaged, as the reduction in blood flow perfusion affects the venous return to eliminate the waste of cellular metabolism, where a marker of tissue hypoxia is the increase in carbon dioxide. Objective: The mitochondrial microcirculatory recruitment with multiple organ support therapy in extracorporeal life support. Material and methods: This is a retrospective study over 35 years, in a lot of critical situations in obstetrics. Results: This disorder generates microcirculatory - mitochondrial distress syndrome, mitochondrial energy collapse, which can be recovered by microcirculation – mitochondrial recruitment to optimize systemic perfusion pressure (SPP), in turn, dependent on mean blood pressure and capillary resistance. Microcirculation - mitochondrial recruitment decentralizes macrocirculation benefits microcirculation in the capillary-cell metabolic area. In cases of manifestation respiratory-pulmonary CO2 ↑ (ARDS), confirmed ↓ PaO2/FiO2 ↓300 to Acute Respiratory Distress Syndrome (Berlin definition, 2012), thus also aggravates the microcirculatory-mitochondrial distress syndrome, mitochondrial collapse and the recruitment of the microcirculatory-mitochondrial is supplemented with multi-organ support therapy (MOST). 1. Alveolar recruitment through respiratory support in specific ventilation modes, predominantly APRV, with permissive hypercapnia at a normal pH. 2) MOST - extracorporeal with technical support. Extracorporeal Life Support Organization – ELSO. 3) Modeling of extra-vascular pulmonary fluid; 4) Th4 - Th5 thoracic epidural block. Conclusion: The absence of decreasing of the pCO2 tissue hypoxia marker at the A-V difference after microcirculatory - mitochondrial recruitment, rejects the necrosis /apoptosis, cellular hypo-(an)ergic and proves the mitochondrial eu-energetic metabolic remodeling with the elimination of the hypo (an) ergic mitochondria performed by clearance lysosomal (mitophagy), thus demonstrating eu-ergic mitochondria with the normalization of mitochondrial uniporter-Ca ++ and mitochondrial permeability pore transition, which productively inactivate the toxic forms of oxygen and nitrogen.Rezumat. Instalarea centralizării macro-circulaţiei în declanşarea MODS în stări critice de obstetrică cauzate de coagularea intravasculară, HELLP, şoc, SIRS, septicemie, CARS, embolie a arterei pulmonare, cerebrală şi altele; - microcirculaţia va fi de asemenea grav afectată, iar perfuzia fluxului sanguin afectează revenirea venoasă pentru a elimina deşeurile de metabolism celular, unde un marker al hipoxiei tisulare este creşterea dioxidului de carbon, la diferenţa A-V. Această tulburare generează sindromul detresei microcirculator – mitocondriale (MMDs), colapsul energetic mitocondrial, care poate fi de-instalat (recuperat) prin recrutarea microcirculator - mitocondrială odată cu optimizarea presiunii de perfuzie sistemică, în dependenţă de tensiunea arterială medie şi rezistenţa capilară. Recrutarea microcirculator - mitocondrială descentralizează macrocirculaţia şi ameliorează microcrculaţia în spaţiul metabolic capilar-celulă. În cazurile de manifestare a ↑CO2-dependent respirator-pulmonar, confirmat ↓ PaO2 / FiO2 ↓ 300 pentru ARDS, sindromul de detresă respiratorie acută (definiţia de la Berlin, 2012), agravează de asemenea, şi sindromul detresei microcirculator-mitocondriale, colapsul mitocondrial iar recrutarea microcirculator - mitocondrială este suplimentată cu terapia de sprijin multi-organ (MOST). 1. Recrutarea alveolară prin suport respirator în moduri de ventilaţie specifice preponderent APRV, cu hipercapnie permisivă la un pH normal. 2) MOST - extracorporal cu suport tehnic în managmentul vital prin sprijin extracorporeal - ELSO. 3) modelarea fluidului pulmonar extra-vascular; 4) Blocul epidural T4-Th5 toracic. Reducerea markerului hipoxiei tisulare pCO2 la diferenţa A-V după recuperarea microcirculator - mitocondrială, respinge necroza / apoptoza, hipo-(an)ergicul celular şi dovedeşte remodelarea metabolică eu-energetică mitocondrială prin eliminarea hipo (an) mitocondriilor ergice efectuate prin clearance-ul lizozomal (mitofagie), demonstrând astfel mitocondriile eu-ergice cu normalizarea tranziţiei porilor permeabilităţii mitocondriale şi canalului uniporter-Ca ++ , care inactivează productiv formele toxice de oxigen şi azot

Effects of the cannabinoid CB1 receptor antagonist rimonabant on distinct measures of impulsive behavior in rats

Rationale Pathological impulsivity is a prominent feature in several psychiatric disorders, but detailed understanding of the specific neuronal processes underlying impulsive behavior is as yet lacking. Objectives As recent findings have suggested involvement of the brain cannabinoid system in impulsivity, the present study aimed at further elucidating the role of cannabinoid CB1 receptor activation in distinct measures of impulsive behavior. Materials and methods The effects of the selective cannabinoid CB1 receptor antagonist, rimonabant (SR141716A) and agonist WIN55,212-2 were tested in various measures of impulsive behavior, namely, inhibitory control in a five-choice serial reaction time task (5-CSRTT), impulsive choice in a delayed reward paradigm, and response inhibition in a stop-signal paradigm. Results In the 5-CSRTT, SR141716A dose-dependently improved inhibitory control by decreasing the number of premature responses. Furthermore, SR141716A slightly improved attentional function, increased correct response latency, but did not affect other parameters. The CB1 receptor agonist WIN55,212-2 did not change inhibitory control in the 5-CSRTT and only increased response latencies and errors of omissions. Coadministration of WIN55,212-2 prevented the effects of SR141716A on inhibitory control in the 5-CSRTT. Impulsive choice and response inhibition were not affected by SR141716A at any dose, whereas WIN55,212-2 slightly impaired response inhibition but did not change impulsive choice. Conclusions The present data suggest that particularly the endocannabinoid system seems involved in some measures of impulsivity and provides further evidence for the existence of distinct forms of impulsivity that can be pharmacologically dissociated

Redescription of Pelagia benovici into a new jellyfish genus, Mawia, gen. nov., and its phylogenetic position within Pelagiidae (Cnidaria : Scyphozoa : Semaeostomeae)

This study provides new and additional data on morphology and a phylogenetic analysis of the recently described species Pelagia benovici Piraino, Aglieri, Scorrano & Boero, 2014 from the Northern Adriatic (Mediterranean Sea). Comprehensive morphological analyses of diagnostic characters, of which the most significant are marginal tentacles anatomy, basal pillars, gonad pattern, subgenital ostia and exumbrellar sensory pits, revealed significant differences from the currently known genera Sanderia, Chrysaora and Pelagia in the family Pelagiidae. A phylogenetic analysis of mitochondrial genes (COI, 16S rRNA, 12S rRNA) and nuclear ribosomal genes (28S rRNA, ITS1/ITS2 regions), together with cladistic analysis of morphological characters, positioned Pelagia benovici as a sister taxon with Sanderia malayensis, and both share a common ancestor with Chrysaora hysoscella. Pelagia benovici does not share a direct common ancestor with the genus Pelagia, and thus we propose it should not belong to this genus. Therefore, a new genus Mawia, gen. nov. (Semaeostomeae : Pelagiidae) is described, and Pelagia benovici is renamed as Mawia benovici, comb, nov

Managing unsuspected tumour invasion of the superior mesenteric-poral vein during surgery for pancreatic head cancer. A case report

Context: In some cases, synchronous superior mesenteric-portal vein resection can be performed during pancreatic resection for cancer. The reconstruction technique is usually primary anastomosis; in only a few cases is an autologous vein graft needed. Case report: We report a case of reconstruction of the superior mesenteric-portal vein with a splenic vein autograft in a patient affected by pancreatic head adenocarcinoma who underwent a total pancreatectomy. Conclusions: The reconstruction of the superior mesenteric-portal vein with a splenic vein autograft should be performed in selected cases. It allows a reduction of operating time, it is a less invasive approach than reconstruction using an internal jugular vein autograft and it can be an oncologically correct approac

An intercellular transfer of telomeres rescues T cells from senescence and promotes long-term immunological memory

The common view is that T lymphocytes activate telomerase to delay senescence. Here we show that some T cells (primarily naïve and central memory cells) elongated telomeres by acquiring telomere vesicles from antigen-presenting cells (APCs) independently of telomerase action. Upon contact with these T cells, APCs degraded shelterin to donate telomeres, which were cleaved by the telomere trimming factor TZAP, and then transferred in extracellular vesicles at the immunological synapse. Telomere vesicles retained the Rad51 recombination factor that enabled telomere fusion with T-cell chromosome ends lengthening them by an average of ~3,000 base pairs. Thus, there are antigen-specific populations of T cells whose ageing fate decisions are based on telomere vesicle transfer upon initial contact with APCs. These telomere-acquiring T cells are protected from senescence before clonal division begins, conferring long-lasting immune protection