Ultrastructure of trichoblasts in the red alga Osmundea spectabilis var. spectabilis (Rhodomelaceae,Ceramiales)

The apex of the tetrasporangial branches of Osmundea spectabilis var. spectabilis (= Laurencia spectabilis var. spectabilis) exhibits cavities in which tufts of multicellular trichoblasts occur. Trichoblast development in Osmundea spectabilis var. spectabilis begins with the differentiation of an epidermal cell within the crypt. This cell differentiates into a trichoblast mother cell (TMC). The TMC divides to form a two-celled incipient trichoblast. Successive periclinal divisions of the apical cell of the young trichoblast result in the formation of a multicellular developing trichoblast. With the exception of the apical cell all trichoblast cells are at the same developmental stage. They possess a large nucleus, abundant plastids with peripheral and some internal thylakoids and dictyosomes. Daughter chloroplasts result from one constriction or multiple fission of a single chloroplast. Dictyosomal cisternae and mucilage sacs contribute material to wall formation. Each differentiating trichoblast cell is surrounded by a bi-layered wall. The outer wall layer represents the trichoblast mother cell wall and the inner wall layer is the trichoblast cell wall. Mature trichoblast cells have thin walls, probably as a consequence of mucilage extrusion, the most likely function of trichoblasts in Osmundea.     

Toward a better understanding of the "Transverse Range break": lineage diversification in southern California

The Transverse Ranges in southern California have been identified as having a prominent phylogeographic role. Numerous studies have identified distinct north-south and/or east-west lineage breaks involving the Transverse Ranges. However, in evaluating their findings, most authors have regarded this complex system somewhat simplistically. In this study we more deeply investigate these breaks using two approaches: first we examine the phylogeographic history of Sepedophilus castaneus (Coleoptera: Staphylinidae) and then implement a comparative phylogeography approach applying Brooks parsimony analysis to the topologies of nine additional taxa. Phylogenetic analysis, nested clade analysis, and AMOVAs for S. castaneus agree that there is a major lineage break between the eastern and western Transverse Ranges, localized between the Sierra Pelona and the San Gabriel Mountains. The comparative phylogeographic analysis supports a generally strong concordance of area relationships with geographic proximity. It is notable, however, that the Transverse Ranges as a group do not show phylogenetic cohesion, but rather they are split into three main regions: an eastern region (San Gabriel, San Bernardino, and San Jacinto Mountains), a central region (central Transverse Ranges and Sierra Pelona) that is often grouped with the Tehachapi and Sierra Nevada populations, and a western region (northwestern Transverse Ranges and Santa Ynez Mountains) that is consistently grouped with coast range areas to the north. The lineage break between east and west Transverse Ranges is attributable to the presence of a marine embayment in what is now the Santa Clara River valley 5-2.5 million years ago.     

The effect of galactose metabolic disorders on rat brain Na+,K+-ATPase activity

To evaluate the effect of galactose metabolic disorders on the brain Na+,K+-ATPase in suckling rats. Separate preincubations of various concentrations (1-16 mM) of the compounds galactose-1-phosphate (Gal-1-P) and galactitol (galtol) with whole brain homogenates at 37 degrees C for 1 h resulted in a dose dependent inhibition of the enzyme whereas the pure enzyme (from porcine cerebral cortex) was stimulated. Glucose-1-phosphate (Glu-1-P) or galactose (Gal) stimulated both rat brain Na+,K+-ATPase and pure enzyme. A mixture of Gal-1-P (2 mM), galtol (2 mM) and Gal (4 mM), concentrations commonly found in untreated patients with classical galactosemia, caused a 35% (p < 0.001) rat brain enzyme inhibition. Additionally, incubation of a mixture of galtol (2 mM) and Gal (1 mM), which is usually observed in galactokinase deficient patients, resulted in a 25% (p < 0.001) brain enzyme inactivation. It is suggested that: a) The indirect inhibition of the brain Na+,K+-ATPase by Gal-1-P should be due to the presence of the epimer Gal and phosphate and that the pure enzyme direct activation by Gal-1-P and Glu-1-P to the presence of phosphate only. b) The observed brain Na+,K+-ATPase inhibitions in the presence of toxic concentrations of Gal-1-P and/or galtol could modulate the neural excitability, the metabolic energy production and the catecholaminergic and serotoninergic system.     

ULTRASTRUCTURE OF CARPOSPOROGENESIS IN THE PARASITIC RED ALGA FAUCHEOCOLAX ATTENUATA SETCH. (RHODYMENIALES,RHODYMENIACEAE)

Carpospore differentiation in Faucheocolax attenuata Setch. can be separated into three developmental stages. Immediately after cleaving from the multinucleate gonimoblast cell, young carpospores are embedded within confluent mucilage produced by gonimoblast cells. These carpospores contain a large nucleus, few starch grains, concentric lamellae, as well as proplastids with a peripheral thylakoid and occasionally some internal (photosynthetic) thylakoids. Proplastids also contain concentric lamellar bodies. Mucilage with a reticulate fibrous substructure is formed within cytoplasmic concentric membranes, thus giving rise to mucilage sacs. Subsequently, these mucilage sacs release their contents, forming an initial reticulate deposition of carpospore wall material. Dictyosome vesicles with large, single dark-staining granules also contribute to wall formation and may create a separating layer between the mucilage and carpospore wall. During the latter stages of young carpospores, starch is polymerized in the perinuclear cytoplasmic area and is in close contact with endoplasmic reticulum. Intermediate-aged carpospores continue their starch polymerization. Dictyosomes deposit more wall material, in addition to forming fibrous vacuoles. Proplastids form thylakoids from concentric lamellar bodies. Mature carpospores are surrounded by a two-layered carpospore wall. Cytoplasmic constituents include large floridean starch granules, peripheral fibrous vacuoles, mature chloroplasts and curved dictyosomes that produce cored vesicles which in turn are transformed into adhesive vesicles. Pit connections remain intact between carpospores but begin to degenerate. This degeneration appears to be mediated by microtubules.     

The challenge of Down syndrome

Down syndrome (DS) has been recognized as a clinical entity for about 150 years, but it is only recently that there has been hope for the possibility to understand its pathogenesis and to use this information to devise approaches for the prevention and treatment of its numerous features. The earlier pessimism was due to several reasons, including: (i) the nature of the genetic defect that leads to the syndrome; (ii) the multiplicity of systems involved; and (iii) the high degree of variability of the phenotype. However, science has now caught up with the problem, and recent developments, especially in genetics, genomics, developmental biology and neuroscience, suggest that these potential impediments might not be as arduous as once appeared. As a result, basic research on DS is now rapidly accelerating, and there is hope that the findings will be translatable into benefit for people with DS.     

Adenosine A2A receptors are required for glutamate mGluR5‐ and dopamine D1 receptor‐evoked ERK1/2 phosphorylation in rat hippocampus: involvement of NMDA receptor

Interaction between mGluR5 and NMDA receptors (NMDAR ) is vital for synaptic plasticity and cognition. We recently demonstrated that stimulation of mGluR5 enhances NMDAR responses in hippocampus by phosphorylating NR2B(Tyr1472) subunit, and this reaction was enabled by adenosine A_2A receptors (A_2AR) (J Neurochem, 135, 2015, 714). In this study, by using in vitro phosphorylation and western blot analysis in hippocampal slices of male Wistar rats, we show that mGluR5 stimulation or mGluR5/NMDAR s co‐stimulation synergistically activate ERK 1/2 signaling leading to c‐Fos expression. Interestingly, both reactions are under the permissive control of endogenous adenosine acting through A_2ARs. Moreover, mGluR5‐mediated ERK 1/2 phosphorylation depends on NMDAR , which however exhibits a metabotropic way of function, since no ion influx through its ion channel is required. Furthermore, our results demonstrate that mGluR5 and mGluR5/NMDAR ‐evoked ERK 1/2 activation correlates well with the mGluR5/NMDAR ‐evoked NR2B(Tyr1472) phosphorylation, since both phenomena coincide temporally, are Src dependent, and are both enabled by A_2ARs. This indicates a functional involvement of NR2B(Tyr1472) phosphorylation in the ERK 1/2 activation. Our biochemical results are supported by electrophysiological data showing that in CA 1 region of hippocampus, the theta burst stimulation (TBS)‐induced long‐term potentiation coincides temporally with an increase in ERK 1/2 activation and both phenomena are dependent on the tripartite A_2A, mGlu5, and NMDAR s. Furthermore, we show that the dopamine D1 receptors evoked ERK 1/2 activation as well as the NR2B(Tyr1472) phosphorylation are also regulated by endogenous adenosine and A_2ARs. In conclusion, our results highlight the A_2ARs as a crucial regulator not only for NMDAR responses, but also for regulating ERK 1/2 signaling and its downstream pathways, leading to gene expression, synaptic plasticity, and memory consolidation.

     

Identification of a Common Non-Apoptotic Cell Death Mechanism in Hereditary Retinal Degeneration

Cell death in neurodegenerative diseases is often thought to be governed by apoptosis; however, an increasing body of evidence suggests the involvement of alternative cell death mechanisms in neuronal degeneration. We studied retinal neurodegeneration using 10 different animal models, covering all major groups of hereditary human blindness (rd1, rd2, rd10, Cngb1 KO, Rho KO, S334ter, P23H, Cnga3 KO, cpfl1, Rpe65 KO), by investigating metabolic processes relevant for different forms of cell death. We show that apoptosis plays only a minor role in the inherited forms of retinal neurodegeneration studied, where instead, a non-apoptotic degenerative mechanism common to all mutants is of major importance. Hallmark features of this pathway are activation of histone deacetylase, poly-ADP-ribose-polymerase, and calpain, as well as accumulation of cyclic guanosine monophosphate and poly-ADP-ribose. Our work thus demonstrates the prevalence of alternative cell death mechanisms in inherited retinal degeneration and provides a rational basis for the design of mutation-independent treatments.     

Parathyroid involvement in thyroid cancer: an unforeseen event

ABSTRACT: BACKGROUND: Parathyroid metastatic disease from thyroid cancer has not been studied extensively, mainly due to the need for parathyroid preservation during thyroid surgery. METHODS: We reviewed files from 1,770 patients with thyroid cancer followed up in our department and 10 patients with parathyroid metastases (0.5 %) were identified. Patient and tumor characteristics were recorded. RESULTS: Six out of ten patients had metastasis from papillary thyroid cancer, three from follicular thyroid cancer and one from anaplastic thyroid cancer. In nine patients parathyroid infiltration from thyroid cancer was found in direct contact with the thyroid cancer, and in one patient metastatic foci were observed not in continuity with the thyroid cancer. CONCLUSIONS: Parathyroid involvement, although infrequent, may occur in thyroid cancer independently of patient age and tumor size. The clinical significance of such event is not clear. The influence on disease outcome remains to be elucidated.