The origin of cultivated mangosteen (Garcinia mangostana L. var. mangostana): Critical assessments and an evolutionary-ecological perspective.

Mangosteen (Garcinia mangostana var. mangostana) is a popular tropical fruit, yet many aspects of its biology and evolutionary history are little known. Its origin remains contentious, although recent findings suggest G. mangostana L. var. malaccensis (Hook. f.) Nazre (synonym: G. malaccensis Hook. f.) as the sole progenitor. We review hypotheses on the origin of mangosteen and clarify points that have been affected by errors of fact and interpretation. The narrow focus and lack of detail in published results make their interpretation difficult. When possible, we support our interpretations with field observations and examination of herbarium specimens. We outline the main biological traits (e.g., dioecy, facultative apomixis, and polyploidy) of mangosteen and its wild relatives to infer traits that might have evolved during domestication of mangosteen. We find no clear indication that apomixis and polyploidy evolved during domestication. Polyploidy is known in the wild relatives, but apomixis has not yet been demonstrated. Also, we propose a testable new evolutionary-ecological framework that we call "Forest-Dusun Interface" to infer processes in the origin of mangosteen. Dusun (Malay) refers to subsistence orchards in this context. Lastly, we propose future studies to address identified knowledge gaps.

Interactions between all pairs of neighboring trees in 16 forests worldwide reveal details of unique ecological processes in each forest, and provide windows into their evolutionary histories.

When Darwin visited the Galapagos archipelago, he observed that, in spite of the islands' physical similarity, members of species that had dispersed to them recently were beginning to diverge from each other. He postulated that these divergences must have resulted primarily from interactions with sets of other species that had also diverged across these otherwise similar islands. By extrapolation, if Darwin is correct, such complex interactions must be driving species divergences across all ecosystems. However, many current general ecological theories that predict observed distributions of species in ecosystems do not take the details of between-species interactions into account. Here we quantify, in sixteen forest diversity plots (FDPs) worldwide, highly significant negative density-dependent (NDD) components of both conspecific and heterospecific between-tree interactions that affect the trees' distributions, growth, recruitment, and mortality. These interactions decline smoothly in significance with increasing physical distance between trees. They also tend to decline in significance with increasing phylogenetic distance between the trees, but each FDP exhibits its own unique pattern of exceptions to this overall decline. Unique patterns of between-species interactions in ecosystems, of the general type that Darwin postulated, are likely to have contributed to the exceptions. We test the power of our null-model method by using a deliberately modified data set, and show that the method easily identifies the modifications. We examine how some of the exceptions, at the Wind River (USA) FDP, reveal new details of a known allelopathic effect of one of the Wind River gymnosperm species. Finally, we explore how similar analyses can be used to investigate details of many types of interactions in these complex ecosystems, and can provide clues to the evolution of these interactions.

Clinical value of combined tests for tumor markers for gastric cancer.

To study the clinical diagnostic value of treating gastric cancer (GC) with combined tests for tumor markers (CEA, CA199, CA242 and CA724), fifty healthy subjects, 50 patients with GC at different stages and 50 patients with benign GC were randomly selected from our hospital. These subjects were divided into a normal group A, an experimental group B and a control group C. Venous blood was drawn and tested for four serum tumor markers. The SPSS 18.0 analytic system was then used to analyze the data. Tumor markers for GC at different stages, different pathological patterns and tumor incidence are discussed. The difference in expression levels of tumor markers between group C and group A was not statistically significant (P>0.05). The differences in expression levels between group B in stage I and stage II and those of groups A and C was statistically significant (P less than 0.05). At the same time, the differences in expression levels of group B in stage III and stage IV and those of groups A and C were also statistically significant (P less than 0.01). For different sizes of tumors, taking 5 cm as a maximum, normal expression and abnormal expression of the four tumor markers was different (P less than 0.05). The tumor incidence of the combined test for the four tumor markers was conspicuously higher than that of single tests. Moreover, the difference between the tumor incidence of the combined test in stages I, II and III and that of single tests in the same stages was of statistical significance (P less than 0.05); however, the difference was not statistically significant in stage IV (P>0.05). The combined testing for tumor markers is useful for clinical diagnosis of GC.

Resolution of trigeminal neuralgia after palliative embolization of a cerebellopontine angle arteriovenous malformation.

BACKGROUND: Trigeminal neuralgia (TN) is a syndrome with debilitating paroxysmal facial pain, one cause of which is thought to be vascular compression of the nerve root entry zone causing ephaptic transmission. Arteriovenous malformations (AVM) have been reported to cause TN, including AVMs in the cerebellopontine (CP) angle. These lesions have been successfully treated with endovascular coiling, ethylene-vinyl alcohol copolymer (Onyx) and surgery for decompression. CASE DESCRIPTION: We present a case of TN caused by AVM in the CP angle in a patient who was not a candidate for microsurgery and who did not want radiofrequency treatment or other destructive procedures because he would not tolerate facial numbness. The patient's symptoms were successfully treated by embolization using an ethylene-vinyl alcohol copolymer. After 17 months he had a recurrence of pain which was again treated with palliative embolization and again experienced resolution of his symptoms. CONCLUSION: This case demonstrates that palliative embolization is a safe and effective option for the treatment of trigeminal neuralgia pain in patients for whom surgery of the AVM is not an option.

Activation of glycine and glutamate receptors increases intracellular calcium in cells derived from the endocrine pancreas.

We studied calcium signaling in a newly described pancreatic cell line, GK-P3, that expresses functional amino acid neurotransmitter receptors. GK-P3 cells express the first strychnine-sensitive glycine receptors reported in a permanent cell line. In addition, GK-P3 cells express alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-type glutamate receptors. Both types of amino acid receptors showed electrophysiological and pharmacological behavior similar to their neuronal counterparts. The glycine receptors were permeable to Cl- and blocked by the selective antagonist strychnine. AMPA receptors showed limited permeability to Ca2+, were blocked by 6-cyano-2, 3-dihydroxy-7-nitroquinoxaline, and were potentiated by cyclothiazide. Interestingly, activation of either receptor type increased intracellular Ca2+ measured by digital imaging of Fura-2 fluorescence. These Ca2+ signals were completely blocked by 30 microM La3+, suggesting that the Ca2+ entered the cells largely through voltage-dependent Ca2+ channels. Alterations in the extracellular concentrations of Cl- and/or HCO3- had only marginal effects on glycine-evoked Ca2+ signals. However, increases in intracellular Ca2+ mediated by AMPA receptors were absent when the extracellular Na+ was replaced with an impermeant cation, N-methyl-D-glucamine. We conclude that activation of ligand-gated cation or anion channels depolarize GK-P3 cells sufficiently to activate their voltage-gated Ca2+ channels leading to increases in intracellular Ca2+ concentration. Thus, glycine and glutamate receptors may regulate Ca2+-dependent secretory mechanisms in islet cells by altering the membrane potential of these cells. Our data in GK-P3 cells support the growing weight of evidence for a role of amino acid neurotransmitters in pancreatic islets and introduce strychnine-sensitive glycine receptors as a novel target of amino acid neurotransmitter regulation in islets.

Differential expression of glutamate receptor subtypes in rat pancreatic islets.

Immunocytochemistry was carried out on sections of rat pancreas to localize the expression of glutamate receptor subunits and the major pancreatic peptide hormones. Glutamate receptor expression was concentrated in pancreatic islets, and each islet cell type expressed different neuronal glutamate receptors of the alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) and kainate classes. AMPA receptor subunits were expressed in alpha, beta, and pancreatic polypeptide cells, whereas kainate receptors were found predominantly in alpha and delta cells. Patch clamp electrophysiology was used to measure the functional properties of islet cell glutamate receptors. L-glutamate and other glutamate receptor agonists evoked currents in islet cells that were blocked by the selective AMPA receptor antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione and potentiated by cyclothiazide in a manner indistinguishable from that of neuronal AMPA receptors. Activation of islet cell AMPA receptors produced steady-state cation currents that depolarized the cells an average of 20.7 +/- 5.4 mV (n = 6). Currents mediated by functional kainate receptors were also observed in a line of transformed pancreatic alpha cells. Thus, L-glutamate probably regulates islet physiology via actions at both AMPA and kainate receptor classes. The pattern of receptor expression suggests that glutamate receptor activation may have multiple, complex consequences for islet physiology.