Fungal Elevational Rapoport pattern from a High Mountain in Japan.

Little is known of how fungal distribution ranges vary with elevation. We studied fungal diversity and community composition from 740 to 2940 m above sea level on Mt. Norikura, Japan, sequencing the ITS2 region. There was a clear trend, repeated across each of the fungal phyla (Basidiomycota, Ascomycota, Zygomycota, Chytridomycota and Glomeromycota), and across the whole fungal community combined, towards an increased elevational range of higher elevation OTUs, conforming to the elevational Rapoport pattern. It appears that fungi from higher elevation environments are more generalized ecologically, at least in terms of climate-related gradients. These findings add to the picture from latitudinal studies of fungal ranges, which also suggest that the classic Rapoport Rule (broader ranges at higher latitudes) applies on a geographical scale. However, there was no mid-elevation maximum in diversity in any of the phyla studied, and different diversity trends for the different phyla, when different diversity indices were used. In terms of functional guilds, on Norikura there were trends towards increased saprotrophism (Zygomycota), symbiotrophism (Basidiomycota), symbiotrophism and saprotrophism (Ascomycota) and pathotrophism (Chytridiomycota) with elevation. The causes of each of these trends require further investigation from an ecological and evolutionary viewpoint.

Environmental filtering of bacterial functional diversity along an aridity gradient.

Studying how metagenome composition and diversity varies along environmental gradients may improve understanding of the general principles of community and ecosystem structuring. We studied soil bacterial metagenomes along a precipitation gradient on the eastern Tibetan Plateau, varying between 500 mm and 60 mm mean annual precipitation (MAP). We found that lower MAP was strongly associated with reduced functional diversity of bacterial genes. It appears that extreme environmental conditions associated with aridity constrain the diversity of functional strategies present in soil biota - analogous to broad scale patterns found in plant functional diversity along environmental gradients. In terms of specific functions, more extreme arid conditions were also associated with increased relative abundance of genes related to dormancy and osmoprotectants. Decreased relative abundance of genes related to antibiotic resistance and virulence in more arid conditions suggests reduced intensity of biotic interaction under extreme physiological conditions. These trends parallel those seen in earlier, more preliminary comparisons of metagenomes across biomes.

Bacterial strategies along nutrient and time gradients, revealed by metagenomic analysis of laboratory microcosms.

There is considerable interest in the functional basis of ecological strategies amongst bacteria. We used laboratory microcosms based on culturing of elutant from soil to study the effects of varying initial nutrient concentration, and time succession, on the community metagenome. We found a distinct set of nutrient-related or time-related changes in the functional metagenome. For example, a high nutrient (copiotrophic) strategy was associated with greater abundance of genes related to cell division and cell cycle, while a low nutrient (oligotrophic) strategy had greater abundance of genes related to carbohydrate metabolism and virulence, disease and defense. We also found time-related changes in the functional metagenome, revealing a distinct 'r'-related strategy with greater abundance of genes related to regulation and cell signaling, and a 'K' strategy rich in motility and chemotaxis-related genes. These different gene-based strategies may help to explain how so many bacterial OTUs coexist in nature, and the functional principles dominating natural communities. In terms of diversity, both the OTU richness and the richness of species assignment of functional genes showed linear correlations with functional gene richness, supporting the hypothesis that greater taxonomic diversity is associated with greater functional diversity, with possible implications for ecosystem stability.

The antinociceptive effect of dexmedetomidine modulates spleen cell immunity in mice.

BACKGROUND: Pain plays roles in both the nervous system and immune system. Changes in the neuroendocrine pathway under pain conditions give rise to sympathetic outflow with increased plasma catecholamines and activate immune reactions. Dexmedetomidine exerts sedative, analgesic, and anesthetic-sparing effects and is known to diminish pro-inflammatory processes by central sympatholytic effects. To investigate the influence of the analgesic effect of dexmedetomidine on immunomodulation under pain conditions, splenic natural killer (NK) tumoricidal cytotoxic activity, proliferative ability of T lymphocytes, and cytokine changes were assessed. METHODS: After evaluation of the analgesic efficacy of dexmedetomidine in C57BL mice that were subjected to formalin-induced pain, dexmedetomidine (30 µg/kg) or saline was injected intraperitoneally (ip) 30 min before formalin (20 µL of 2% formalin in 0.9% saline) injection. NK cell activity against NK-sensitive YAC-1 lymphoma cells was evaluated by the percentage of specific lactate dehydrogenase (LDH) release. Various numbers of effector cells (NK cells) were added to the wells of a microtiter plate containing 2 × 10(4) target YAC-1 cells in 100 µL, to achieve final effector-to-target cell ratios of 80:1, 40:1, and 20:1. The level of lymphocyte proliferation in response to phytohemagglutinin (PHA) was detected by bromodeoxyuridine (BrdU) incorporation assay. TNF-α, IL-1ß, and IL-10 levels were determined in blood samples and supernatants of splenocyte preparations. RESULTS: IP administration of dexmedetomidine significantly decreased the time of licking and biting during the first and second phases of the formalin test (p <0.001). Formalin-induced pain led to higher activity of NK cells than in sham-treated mice (p <0.05), but NK activity was not increased significantly by ip dexmedetomidine treatment. Formalin-induced pain significantly increased splenic lymphocyte proliferation (p <0.05), but dexmedetomidine did not alter this response. There was a significant increase in plasma TNF-α (p = 0.048) and IL-6 (p = 0.014) levels after formalin-induced pain. However, the differences between the responses after ip dexmedetomidine did not change significantly. CONCLUSIONS: Dexmedetomidine showed antinociceptive effect on both of acute pain phase 1 and hyperalgesic phase 2 of formalin pain model. Formalin-induced pain alters cellular immunity of spleen in mice. Dexmedetomidine attenuates the activation of NK cells under pain condition, but neither the proliferative response of the splenic lymphocytes nor the cytokine production was affected by dexmedetomidine.

Zoster-associated segmental paresis in a patient with cervical spinal stenosis.

Segmental zoster paresis is a rare complication of herpes zoster, characterized by focal motor weakness that does not always present simultaneously with skin lesions. Zoster paresis can be easily confused with other neuromuscular or spinal diseases. This case report describes the case of a 72-year-old woman with herpes zoster and cervical spinal stenosis at the same spinal level, where it was difficult to distinguish segmental zoster paresis from cervical radiculopathy combined with motor neuropathy. Although segmental zoster paresis in the upper extremity is rare, it should be included in the differential diagnosis of segmental pain and weakness in the extremities, especially in older or immunocompromised patients. Correct diagnosis is required, to avoid unnecessary surgery and allow timely antiviral treatment.

The immunomodulatory effect of pregabalin on spleen cells in neuropathic mice.

BACKGROUND: There is a strong relationship between pain and immune function. The development of neuropathic pain after peripheral nerve damage occurs with inflammation at the injury site. T lymphocyte function, a part of cell-mediated immunity, has been implicated in the pathogenesis and nociceptive processing of peripheral neuropathic pain. Pregabalin [(S)-3-(aminomethyl)-5-methylhexanoic acid], which was developed as an antiepileptic drug, has shown clinical and laboratory efficacy for neuropathic pain. To assess the possible influence of pregabalin therapy on immunomodulation, we assessed natural killer (NK) tumoricidal activity against YAC-1 murine lymphoma cells and phytohemagglutinin-stimulated T lymphocyte proliferation in a neuropathic mouse model. METHODS: The neuropathic model was induced by chronic constriction injury (CCI) to the right sciatic nerve in male BALB/c mice. Mechanical hyperalgesia was measured with a dynamic plantar aesthesiometer. After confirming hyperalgesia, pregabalin or saline (for control mice) in a volume of 10 mL/kg was administered orally at a dosage of 30 mg/kg, twice daily from day 2 after surgery. On day 7 postsurgery, NK cell cytotoxic activity and splenocyte proliferation were measured. NK cell activity was assessed by lactate dehydrogenase assay. Various numbers of effector cells were added to the wells of a microtiter plate containing 1 × 10(4) target YAC-1 cells in 100 µL, to achieve final effector-to-target cell ratios of 80:1, 40:1, and 20:1. The proliferative response of splenocytes to phytohemagglutinin was measured by bromodeoxyuridine detection. Stimulation index was calculated to quantify cell proliferation based on the measurement of bromodeoxyuridine incorporation in cellular DNA. For in vitro study, NK cell activity and splenocyte proliferation from isolated spleen cells were determined at different concentrations of pregabalin (3, 10, and 30 µg/mL). RESULTS: CCI caused marked mechanical allodynia on day 7 and orally administered pregabalin reversed mechanical hyperalgesia. NK cell activity and splenocyte proliferation were significantly increased in CCI mice compared with control mice. Pregabalin treatment in CCI mice significantly suppressed NK cell activity and proliferation of splenocytes. NK cell activity was 8.4% ± 4.7% in control and 29.2% ± 20.2% in CCI mice; pregabalin treatment reduced cytotoxicity to 6.8% ± 2.4% in CCI mice. Stimulation index was 169% ± 71% in CCI mice but pregabalin treatment reduced it to 67% ± 52% compared with control. In vitro, NK cell activity was suppressed at a pregabalin concentration of ≥10 µg/mL (P < 0.05). CONCLUSIONS: Neuropathic pain increased immunological reactivity and pregabalin treatment modulated this reactivity. Increased NK cell activity and splenocyte proliferation were inhibited by pregabalin treatment.

The effect of propofol on cytotoxicity and apoptosis of lipopolysaccharide-treated mononuclear cells and lymphocytes.

UNLABELLED: IV anesthetics may inhibit proper immune responses and further compromise an already depressed defense system. To assess the possible role of propofol on human immune function in sepsis, we studied cytotoxicity, and apoptosis of mononuclear cells (MNCs). Peripheral blood MNCs were preincubated in 1 microg/mL of lipopolysaccharide (LPS) and then reincubated in different concentrations of propofol (1 microg/mL, 5 microg/mL, 10 microg/mL, or 50 microg/mL). To determine cytotoxicity, lactate dehydrogenase release was assayed by mixing MNCs (4 x 10(5)/100 microL) with K-562 tumor cells as target cells (1 x 10(4)/100 microL)(E: T ratio of 40:1). Apoptosis was determined by measuring the annexin positive cells using flow cytometry. Cytotoxicity and apoptosis of LPS-treated MNCs were unchanged by clinically acceptable concentrations of propofol (1 microg/mL, 5 microg/mL, and 10 microg/mL). However, significant differences were observed in cytotoxicity (P = 0.004) and apoptosis (P = 0.002) with propofol 50 microg/mL. By gating MNCs, we found that lymphocyte apoptosis was significantly increased at 50 microg/mL of propofol, but monocytes were unaffected (P = 0.02). In terms of cytotoxicity and apoptosis, propofol allowed MNCs to retain their cytotoxicity in septic conditions by protecting immune cells from apoptosis. IMPLICATIONS: Propofol at acceptable therapeutic concentrations, and under experimentally contrived septic conditions, did not affect the cytotoxic activity of mononuclear cells or the apoptosis level of mononuclear cells, lymphocytes, and monocytes from peripheral blood.