Der durch Pilze und aerobe Bakterien veranlaßte Pectin-und Cellulose-Abbau im Hochmoor unter besonderer Berücksichtigung des Sphagnum-Abbaus

Ohne Zusammenfassung     

Effect of temperature on seed production in the invasive grass Glyceria maxima (Hartm.) Holmb. (Poaceae) in South Africa

Temperature is one of the main factors that determine sexual reproduction in terrestrial and emergent aquatic plant species. The effect of temperature on sexual reproduction and seed production of Glyceria maxima (Hartm.) Holmb. in the southern hemisphere is unknown. Glyceria maxima collections in February 2010 at three isolated infestations in KwaZulu-Natal failed to yield a single seed, only empty panicles. Laboratory experiments showed that vernalisation had no consistent effect on seed production. Field- and laboratory-grown plants produced seeds in the 2010/2011 season, because of having sufficient time at optimum temperatures required for seed production (1 491 and 1 585 hours, respectively), compared to a shorter period (1 352 hours) of suitable temperatures during the 2009/2010 growing season. An inadequate period of optimum temperatures (15–25°C) during seed production resulted in the lack of seeds in the field in the 2009/2010 growing season. This study showed that temperature and duration of exposure thereto during the seed-production period play vital roles in G. maxima sexual reproduction.     

Effects of xenon on intracellular Ca2% release in human endothelial cells

Using human endothelial cells loaded with the Ca^2% indicator Fura2 the effects of xenon on changes in intracellular Ca^2% were studied. The basal level of intracellular Ca^2% is not affected upon incubation of the cells in buffer saturated either with 100% xenon or with 70% xenon/30% air, a concentration which corresponds in humans to the minimum alveolar concentration necessary to induce anesthesia in 50% of patients. A defined cellular response such as the Ca^2% change induced by application of adenosine triphosphate (ATP) makes it possible to study the signalling chain between the stimulus and the various forms of Ca^2% response. ATP induces a typical Ca^2% fingerprint composed of an internal Ca^2% release consisting of several oscillations plus an additional Ca^2%-induced Ca^2% influx from the outside. The latter is absent in Ca^2%-free medium. When cells are incubated with xenon, only the first part of the ATP-induced Ca^2% response is found corresponding to the internal release of Ca^2%; the subsequent Ca^2%-induced Ca^2% influx does not take place. If xenon is removed, a fast recovery is observed and the cells again show both parts of the Ca²⁺ response. Such selective inhibition of Ca²⁺-induced Ca²⁺ influx is not obtained when xenon is replaced by N₂; the ATP response of the cell remains the same as that of untreated cells. Similar effects of xenon treatment can also be observed when the cells are treated with thapsigargin, a specific inhibitor of the SERCA systems. The Ca²⁺-induced Ca²⁺ release is almost completely suppressed in the presence of xenon. We conclude that xenon may act on the cellular level on defined sites of the mechanisms regulating the Ca²⁺-release-activated Ca²⁺ channels of the plasma membrane and that this property may be related to its anesthetic effect.     

Nitric oxide induces transient Ca2+ changes in endothelial cells independent of cGMP

Ca²⁺ changes induced by nitric oxide (NO^·) were investigated in cultured human endothelial cells. Sodium nitroprusside (SNP) (1–100 μmol/L) and S-Nitroso-N-acetylpenicillamine (SNAP) (100 μmol/L) were used as NO^· donors. The cytoplasmatic Ca²⁺ concentration was calculated using ratiometric FURA2 fluorescence measurements. Both NO^· donors caused transient oscillatory Ca²⁺ changes, which were not detectable in the presence of oxyhemoglobin (50 μmol/L). Digital ratio imaging revealed initiation sites within cells where Ca²⁺ increases started spreading, which indicates that nonuniformly distributed targets might be involved in these reactions. Calcium was released from intracellular stores as indicated by experiments performed in Ca²⁺-free buffer. L-type Ca²⁺-channel blocker diltiazem (100 μmol/L) was not able to block these responses. NO^·-induced Ca²⁺ release from intracellular stores caused capacitative Ca²⁺ entry. Both thapsigargin (1 μmol/L) and cyclopiazonic acid (10 μmol/L) inhibited the SNP response completely, whereas neither ryanodine (up to 100 μmol/L) nor dantrolene (100 μmol/L) was able to inhibit Ca²⁺ changes induced by SNP, indicating that primarily inositol 1,4,5-triphosphate (IP₃)-dependent stores are released upon stimulation with NO^·. A small inhibitory effect of ATP- and SNP-induced peak [Ca²⁺]_i increase was measured in the presence of both caffeine (20 mmol/L) and procaine (1 mmol/L). Evidence is presented that cGMP is not involved in NO^·-induced Ca²⁺ signals, as neither inhibitors of guanylate cyclase (methylene blue and LY (83583) nor cell permeant analogues of cGMP altered or simulated [Ca²⁺]_i changes. An inhibitor of cGMP-dependent protein kinase was also ineffective. We therefore propose that endothelial cells have specific targets proximal or at IP₃ receptors to induce Ca²⁺ changes in endothelial cells stimulated with NO^·. J. Cell. Physiol. 172:296–305, 1997. © 1997 Wiley-Liss, Inc.     

Isocitrate dehydrogenase 1 R132C mutation occurs exclusively in microsatellite stable colorectal cancers with the CpG island methylator phenotype

The CpG Island Methylator Phenotype (CIMP) is fundamental to an important subset of colorectal cancer; however, its cause is unknown. CIMP is associated with microsatellite instability but is also found in BRAF mutant microsatellite stable cancers that are associated with poor prognosis. The isocitrate dehydrogenase 1 (IDH1) gene causes CIMP in glioma due to an activating mutation that produces the 2-hydroxyglutarate oncometabolite. We therefore examined IDH1 alteration as a potential cause of CIMP in colorectal cancer. The IDH1 mutational hotspot was screened in 86 CIMP-positive and 80 CIMP-negative cancers. The entire coding sequence was examined in 81 CIMP-positive colorectal cancers. Forty-seven cancers varying by CIMP-status and IDH1 mutation status were examined using Illumina 450K DNA methylation microarrays. The R132C IDH1 mutation was detected in 4/166 cancers. All IDH1 mutations were in CIMP cancers that were BRAF mutant and microsatellite stable (4/45, 8.9%). Unsupervised hierarchical cluster analysis identified an IDH1 mutation-like methylation signature in approximately half of the CIMP-positive cancers. IDH1 mutation appears to cause CIMP in a small proportion of BRAF mutant, microsatellite stable colorectal cancers. This study provides a precedent that a single gene mutation may cause CIMP in colorectal cancer, and that this will be associated with a specific epigenetic signature and clinicopathological features.     

奥美拉唑联合法莫替丁治疗反流性食管炎的临床效果分析

目的：观察并分析奥关拉唑联合法莫替丁治疗反流性食管炎的临床效果。方法：选取2008年5月至2012年5月在本院确诊并治疗的反流性食管炎患者45例,随机平均分为三组。联合用药组（15例）：每日早餐前口服20mg奥关拉唑,睡前口服20mg法莫替丁;奥关拉唑组（15例）：每日口服两次奥美拉唑,每次20mg;法莫替丁组（15例）：每日口服两次法莫替丁,每次20mg。每组的治疗时间均为8周。在内镜指导下观察并比较三组患者的胸痛、反酸和烧心等主要病征的改善情况,综合评价三种治疗方法的临床疗效。结果：联合用药组较其他两组获得的疗效更明显,患者的症状得到较好的改善,差异有统计学意义（P〈0．05）。结论：奥美拉唑联合法莫替丁能够有效地抑制胃酸的分泌,对于反流性食管炎的,临床治疗具有良好的效果。