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Symbiosis is one of the most fundamental relationships between or among organisms and includes parasitism (which has negative effects on the fitness of the interacting partner), commensalism (no effect), and mutualism (positive effects). The effects of these interactions are usually assumed to influence a single component of a species’ fitness, either survival or fecundity, even though in reality the interaction can simultaneously affect both of these components. I used a dual lattice model to investigate the process of evolution of mutualistic symbiosis in the presence of interactive effects on both survival and fecundity. I demonstrate that a positive effect on survival and a negative effect on fecundity are key to the establishment of mutualism. Furthermore, both the parasitic and the mutualistic behaviour must carry large costs for mutualism to evolve. This helps develop a new understanding of symbiosis as a function of resource allocation, in which resources are shifted from fecundity to survival. The simultaneous establishment of mutualism from parasitism never occurs in two species, but can do so in one of the species as long as the partner still behaves parasitically. This suggests that one of the altruistic behaviours in a mutualistic unit consisting of two species must originate as a parasitic behaviour. Electronic supplementary material The online version of this article (doi:10.1007/s00114-014-1175-1) contains supplementary material, which is available to authorized users.

There is increasing interest in the impacts of pulsed resource inputs (e.g., seasonal fluctuations in primary production) on ecosystem properties. However, theoretical models have focused on the ecosystem role of consumers only in stable environments. We investigated how the consumption rate affects ecosystem properties when resource supplies are pulsed using a simple model with numerical simulations. We initially investigated how primary production responds to resource supply shortages under various consumption rates and found that a vigorous consumer attenuates a rapid reduction in primary production. We next examined ecosystem properties under pulsed resource supplies. Intermediate consumption enhances primary production. The consumption rate that maximizes productivity differs for producers and consumers in a given resource supply environment, irrespective of the pattern of pulsation. The enhancement of primary production and the maximization of secondary production occur simultaneously in a stable environment but are not always the same when the resource supply is pulsed. We also investigated the variability of primary production and found that intermediate consumption rates reduce its coefficient of variation. In addition, we found that consumers with either very low or very high consumption rates are vulnerable to extinction when resource supplies are pulsed. Therefore, consumers with intermediate consumption rates contribute not only to the enhancement and stabilization of primary production but also to the stability of the consumer population itself.

To discover the evolutionary logic of intracellular endosymbiosis, we investigated a theoretical model (simultaneous ordinary differential equations) of a material-cycling system inside a host cell. In the model, we introduced a recently developed cell biology concept called "autophagy", which is a decomposing-recycle process of self-compiled materials found universally among eukaryote cells. Our model is based on traditional simultaneous ODE for natural ecosystems that involve producing, grazing, and decomposing processes in material cycling. In the basic intracellular metabolic system, several enzymes regulate metabolism by synthesizing and converting metabolites into biomolecules that are precursors for enzymes involved in the producing process. Symbionts are involved in grazing processes and autophagosomes that degrade materials are involved in decomposing recycles. We compared and analyzed the local stability of ODE systems in three cases: (1) the independent, free-living cell (the basal state of a cell), (2) the case where symbionts invade and exploit macrobiomaterials as parasites inside a host cell, and (3) the combination where symbionts assist the host's metabolism. We conclude that: (i) as consumers, symbionts are required to have a growth rate that is higher than the rate of autophagosome decomposition, (ii) the host cell with a biomass larger than the threshold size would realize the mutualistic relationship with its symbiont, and (iii) this partnership accelerates the biomaterial turnover flow on the basis of biomaterials.

The importance of tumor necrosis factor (TNF)-alpha and the TNF receptor gene polymorphisms in the etipathogenesis of inflammatory bowel disease (IBD) has not been elucidated. DNA from peripheral blood samples was obtained from 124 patients with Crohn's disease (CD), 106 patients with ulcerative colitis (UC), and 111 unrelated healthy controls. We examined two single nucleotide polymorphisms (SNPs) of the TNF-alpha gene, TNF (–308 G/A and –238 G/A), an SNP of the TNF receptor superfamily member 1A gene, TNFRSF1A(also known as TNFR1), at codon 12 in exon 1 (CCA/CCG), and two SNPs of the 1B gene, TNFRSF1B (also known as TNFR2), (1466 A/G and 1493 C/T). There was a difference in the carrier frequency for haplotype AG (–308 A, –238 G) between UC patients and the controls (OR=4.76, 95% CI=1.53–14.74, P

Heparanase activity is correlated with the metastatic potential of several cancer cells and is a key enzyme in the breakdown of tissue barriers. It is also involved in the regulation of growth factor and cytokine activity. However, little is known about the factors that induce heparanase in cancer cells. We investigated the effect of three growth factors, platelet-derived growth factor (PDGF), hepatocyte growth factor (HGF) and basic fibroblast growth factor (bFGF), on heparanase mRNA induction in lung cancer cells in vitro. In addition, we examined the effect of erythromycin (EM) and clarithromycin (CAM), which are 14-membered ring macrolide antibiotics that act as biological response modifiers, on the expression of heparanase mRNA induced by growth factors. PDGF, HGF and bFGF stimulated cell migration activity and enhanced the expression of heparanase mRNA in the human lung adenocarcinoma cell line A549. Via different mechanisms, EM and CAM modulate the induction by these factors of heparanase mRNA expression on A549 cells. EM also significantly suppressed A549 cell migration induced by PDGF and HGF, and CAM significantly suppressed A549cell migration induced by bFGF. The results suggest that the growth factors PDGF, HGF and bFGF are important inducers of heparanase in potentially invasive and metastatic cancer cells. The suppressive effect of heparanase mRNA expression by EM and CAM may have interestingtherapeutic applications in the prevention of metastasis.

Intracellular adhesion molecule-1 (ICAM-1)-mediated cell-cell adhesion is thought to play an important role at sites of inflammation. Recent evidence suggests that ICAM-1 surface expression on alveolar macrophages is increased in pulmonary sarcoidosis and that inflammatory granuloma formation is characterized by the aggregation of macrophages. The present study shows that ICAM-1 expression is significantly elevated on alveolar macrophages from patients with sarcoidosis in response to tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (INF-gamma) compared with healthy controls. Aggregation and adhesion were significantly increased in alveolar macrophages treated with TNF-alpha and INF-gamma, and significantly inhibited in those pretreated with a monoclonal antibody to ICAM-1. Similarly, aggregation and adhesion were inhibited in macrophages treated with heparin, which then exhibited a wide range of biological activities relevant to inflammation. These results suggested that the surface expression of ICAM-1 on alveolar macrophages in response to TNF-alpha and INF-gamma is important in mediating aggregation and adhesion. Additionally, heparin may be useful for developing novel therapeutic agents for fibrotic lung disease.

The evolutionary origins and advantages of clonal reproduction relative to sexual reproduction have been discussed for several taxonomic groups. In particular, organisms with a sessile lifestyle are often exposed to spatial and temporal environmental fluctuations. Thus, clonal propagation may be advantageous in such fluctuating environments, for sessile species that can reproduce both sexually and clonally. Here we introduce the concept of niche to a lattice space that changes spatially and temporally, by incorporating the compatibility between the characteristics of a sessile clonal plant with its habitat into a spatially explicit individual-based model. We evaluate the impact of spatially and temporally heterogeneous environments on the evolution of reproductive strategies: the optimal balance between seed and clonal reproduction of a clonal plant. The spatial niche case with local habitats led to avoidance of specialization in reproductive strategy, whereas stable environments or intensive environmental change tended to result in specialization in either clonal or seed reproduction under neutral conditions. Furthermore, an increase in spatial niches made clonal reproduction advantageous, as a consequence of competition among several genets under disturbed conditions, because a ramet reached a favorable habitat through a rare long-distance dispersal event via seed production. Thus, the existence of spatial niches could explain the advantages of clonal propagation.

In nature, we can find an organism plays a mutualistic role on its partner species in a particular situation even though it is parasite in essence. What condition realizes such a flexible symbiotic...

Histochemical investigation of lectin-binding sites was carried out on basal cell epithelioma (BCE) and carcinoma (BCC) cells obtained from human skin lesions. The HRP-conjugated lectin technique was employed (Con A, for detecting glucose and mannose; RCA-1, for Gal; PNA and SBA, for Gal and GaiNAc; DBA, for GalNAc; UEA-1, for fucose; and WGA, for GlcNAc and NANA). Irrespective of histologic variation in BCE and BCC, the tumor cells exhibited rather weak binding to lectin conjugates, and the tumor cells adjacent to keratinizing epithelia in keratotic BCE displayed stronger lectin staining as compared to those in non-keratinized tumors. Some of the desquamated tumor cells found in cystic spaces of cystic BCE had the strongest reaction for the PNA conjugate. The cytochemical distribution of lectin conjugates in BCE and BCC was usually confined to intercellular materials and surface of the tumor cells, but the lectin staining was not strong. No major difference was found between tumor cells of BCE and BCC with respect to lectin-binding.

The binding of horseradish peroxidase (HRP)-conjugated lectin was studied in the oral mucosa of several mammals. The following lectins were used; Con A, PNA, SBA, DBA, RCA-1, UEA-1, and WGA. Con A staining was exhibited strongly in the connective tissue cells, moderately in germinal cells, and negatively in the keratinized layer. However, following periodate oxidation (PA/Con A) it revealed a different distribution patterns as compared to single Con A staining; i.e., PA/Con A was limited to the spinous cell epithelium. Lectin binding gave weak results in basal cells, strong in spinous cells, and showed no effect in keratinized layers. Using lectins-PNA, SBA, RCA-1, UEA-1, and WGA-, the effects in the oral squamous epithelium revealed zonal or regional distribution in their respective individual layers except for a few exceptions.

Keratin proteins were immunohistochemically demonstrated in different parts of the oral epithelium. Keratin staining in the squamous-cell epithelium was restricted to the spinous and granular cell layers, with a comparatively low reaction in the basal layer cells and none in the superficial cornified layer. In comparing the keratin staining levels, those in the buccal and sublingual epithelia were rather higher than those in the hard palatal epithelia. Staining intensities for keratin proteins were not the same in either different locations of the oral epithelium or in the same location in different animals.

Sugar residues in the epithelial cells of verruca vulgaris and seborrheic keratosis were demonstrated by the horseradish peroxidase-conjugated lectin methods. The lectins, Con A, RCA-1, UEA-1, DBA, PNA, SBA, and WGA were used to bind specifically to the sugars, Man, Glc, Gal, Fuc, GalNAc, GlcNAc and NANA. The cytochemical distribution of lectin bindings were limited to the cell surface, intercellular materials and basement membrane in the epithelial structures of the lesions. The lectin bindings in the basal layer cells were negative or weak, but increased gradually in upper spinous cells from moderate to strong levels. Vacuolated cells in verruca vulgaris showed positive lectin stainings. The intercellular materials of parakeratinized cells bound lectins differently, but orthokeratinized cells failed to bind lectins. The regional distribution of lectin bindings in stratified squamous epithelia may indicate an expression of keratinocytic stratification as well as in keratinized benign lesions.

Histochemical distribution of lectin binding sites and keratin protein was studied for epithelial components, stromal elements and giant cells in calcifying epithelioma of Malherbe as well as for normal hair follicles. The HRP (horseradish peroxidase) -conjugated lectin technique was employed; the lectins used were Con A, PNA, RCA-1, DBA, SBA, WGA and UEA-1. Immunocytochemical detection of keratin protein was made using the indirect PAP technique. Basophilic cells and shadow cells in the tumor epithelial components revealed histochemical properties similar to those of matrix cells and cortex cells in growing hair follicles, respectively. Most prominent lectin binding was observed in Con A staining. In the tumor stroma, many fibrillar elements which were distinguished as immature or mature hair were found by lectin and keratin staining. Tumor giant cells showed a stronger staining for Con A and keratin, which were enhanced following treatment with amylase. The staining intensity of lectins was usually decreased in both epithelial cells and connective tissue stroma following treatment with neuraminidase.

Quantitative analysis of epithelial components, immunohistochemical staining of MoAb to keratin proteins, and 3H-thymidine labeling were tested to evaluate the carcinogenic process in experimentally hyperkeratinized epithelia induced by topical application of DMBA in hamster cheek pouch. The epithelial lesions were classified histologically into 3 types; A type (acanthotic type), B type (mixed type), and C type (basal hyperplastic type). Initial change of hamster pouch epithelium (0-3 W) was begun from the A type (acanthotic epithelium) and in more advancing stages (5-7 W), lesions showed highei frequency of the C type, and they fi nally occurred similar frequencies for 3 types.Keratin staining in the B and C types was characterized by irregular distribution and disappearance for PKK 1 keratin in basal cells and KL 1 keratin in the epithelial layer, although PKK 1 in the normal epithelium was confined to basal cells.3H-thymidine labeling was correlated strongly to decrease or tractable staining for PKK 1 keratins in basal cells of the precancerous epithelium.

Paget cells from cases of mammary and extramammary Paget’s disease were examined for carcinoembryonic antigen (CEA) and CEA-related antigens by the immunoperoxidase method. Paget cells showed a conspicuous positive reaction with antiserum to CEA, but were negative when nonspecific cross-reacting-antigen (NCA)-absorbed antiserum to CEA, or a monoclonal antibody to CEA was used as the detecting agents. Paget cells may contain large amounts of NCA antigen or CEA-related substances.

Transitional carcinomas of the urinary bladder were examined immunohistochemically for keratin proteins with the use of polyclonal antiserum (TK, 41-65 kDa) and 3 monoclonal antibodies (KL 1, 55-57 kDa; PKK 1, nos. 19, 18, 8; and K 8.12, nos. 16, 13). Umbrella cells gave particularly strong staining for TK, KL 1 and PKK 1, whereas they were negative for K 8.12. Basal- and intermediate-layer cells in urothelial epithelium were moderately positive for all keratins. Brunn's nests cells showed comparatively slight or moderate keratin staining, and K 8.12 staining of Brunn's nests was higher than in urothelial epithelial cells. Transitional carcinoma (grades I and II) indicated uniform keratin distribution, and staining was strong with TK, while that of KL 1, PKK 1 and K 8.12 varied, and grade III tumors showed the lowest intensity of staining. K 8.12 staining in papillary transitional carcinomas was strongly positive in basal located tumor cells, as compared with apical tumor cells. Squamous cell carcinoma was varying positive to keratin reactions dependent on the degree of keratinization. Heterogenity of keratin distribution in papillary transitional carcinomas was given between basal tumor cells and well differentiated tumor cells including umbrella-like cells.