Do soil aggregates really protect encapsulated organic matter against microbial decomposition?

Soil aggregates can provide an effective protection of organic matter against microbial decomposition as reported by several macroaggregate disruption studies. However, research on the role of aggregation for carbon mineralization was mainly focused on arable soils. In the present study we aim to clarify the impact of aggregation on organic matter protection by measuring carbon mineralization in terms of microbial respiration rates of intact macroaggregates (2–4 and 4–8 mm) and corresponding crushed aggregates from seven topsoil horizons from both arable and forest sites. For two arable and one forest soil we found a significantly (P < 0.001) lower carbon mineralization from intact aggregates as compared to the corresponding crushed material. The portion of aggregate protected carbon reached up to 30% for a grassland soil. For the other arable and forest soils no significant effect of aggregation was found. Similarly, no clear trend could be found for the protective capacity of different size fractions. We conclude that protection by aggregation is effective primarily for soils with a large pool of labile organic matter regardless of their usage as arable land or forest.     

How cells protect themselves against stress?

The current evidence on the mechanisms underlying cell response to heat shock is reviewed. The response dynamics, induction, and attenuation as well as heat shock proteins and the mechanisms through which they protect cells from stress are considered. The role of these proteins in regulating the signaling cascades, including apoptosis suppression, is shown.     

Do thyroid hormones function in insects?

Earlier work demonstrated that phenoxy-phenyl compounds such as fenoxycarb and thyroxine mimicked the effects of JH III in causing a reduction in volume of the follicle cells of Locusta migratoria. While these compounds were only moderately effective, a derivative of thyroxine, 3,3',5-triiodothyronine (T3) was as effective as JH III, and T3 has been shown to bind to the same membrane receptor and activate the same pathway as JH III. The current paper shows that other thyroxine derivatives vary in activity. 3,3', 5'-Triiodothyronine (reverse T3) is inactive. 3,5-Diiodothyronine (T2) is more active than JH III, while its relatives (iodines at 3', 5' or at 3,3') are inactive. When follicles are exposed in vitro to rhodamine conjugated T3, the fluorescent compound can be seen to enter the cells and accumulate there: this process is inhibited by cycloheximide or by a temperature of 0 degrees C. The accumulation is antagonised by JH III but not JH I (which does not bind to the JH III membrane receptor) and by an antiserum raised against the putative membrane receptor protein. The action of T3, but not T2, is inhibited by 6-n-propyl-2-thiouracil or by aurothioglucose, both known to inhibit deiodinases. The activity of T3, but not of T2, increases with time of exposure to the follicle cells. These facts suggest that T3 enters the cells by receptor mediated endocytosis and is converted to a more active compound. Immunoreactivity to T3, but not thyroxine, can be detected in the haemolymph of locusts, and the titre varies slightly with the gonotrophic cycle. The food shows immunoreactivity for both thyroxine and T3. These findings suggest that thyroid hormones are ingested by locusts and have the potential to be used as hormonal signals in the control of egg production.     

Do parasites express receptors for host lipoproteins?

Although cholesterol is the predominant sterol in parasite tissue, many parasites are unable to synthesize cholesterol or longchain fatty acids, de novo, and must therefore obtain these components from the host. Of particular interest are the plasma lipoproteins, a rich and abundant source of cholesterol, and other lipids that could be used by parasites inhabiting the vascular system of their host or with access to plasma proteins at extravascular sites. It is not inconceivable that parasites may have evolved a variety of receptors for lipoproteins by convergent evolution. Here, Mark Rogers discusses evidence for the presence of lipoprotein receptors in protozoan and metazoan parasites of mammals.     

Can loss of apoptosis protect against cancer?

Cells of higher organisms can commit suicide in response to genomic alterations, a process called programmed cell death. Although it is commonly thought that the loss of programmed cell death is required for carcinogenesis, we argue that the situation is more complex and that the loss of programmed cell death can have the converse effect, preventing cancer progression. If the death rate of cancer cells is low, fewer cell divisions are required for the tumor to reach a certain size, resulting in the presence of fewer mutant cells. Therefore, the chances of overcoming potential selective barriers are reduced, rendering the failure of pathogenic progression probable. However, if there is a higher cell death rate, more cell divisions need to occur for the tumor to reach a certain size, resulting in the presence of more mutant cells and in an increased probability of overcoming selective barriers and cancer progression.     

Can short-term fasting protect against doxorubicin-induced cardiotoxicity?

Doxorubicin(Dox) is one of the most effective chemotherapeutic agents used in the treatment of several types of cancer. However the use is limited by cardiotoxicity. Despite extensive investigation into the mechanisms of toxicity and preventative strategies, Dox-induced cardiotoxicity still remains a major cause of morbidity and mortality in cancer survivors. Thus, continued research into preventative strategies is vital. Short-term fasting has proven to be cardioprotective against a variety of insults. Despite the potential, only a few studies have been conducted investigating its ability to prevent Dox-induced cardiotoxicity. However, all show proof-of-principle that short-term fasting is cardioprotective against Dox. Fasting affects a plethora of cellular processes making it difficult to discern the mechanism(s) translating fasting to cardioprotection, but may involve suppression of insulin and insulin-like growth factor-1 signaling with stimulated autophagy. It is likely that additional mechanisms also contribute. Importantly, the literature suggests that fasting may enhance the antitumor activity of Dox. Thus, fasting is a regimen that warrants further investigation as a potential strategy to prevent Dox-induced cardiotoxicity. Future research should aim to determine the optimal regimen of fasting, confirmation that this regimen does not interfere with the antitumor properties of Dox, as well as the underlying mechanisms exerting the cardioprotective effects.     

Does vitamin D protect against DNA damage?

Vitamin D is a secosteroid best known for its role in maintaining bone and muscle health. Adequate levels of vitamin D may also be beneficial in maintaining DNA integrity. This role of vitamin D can be divided into a primary function that prevents damage from DNA and a secondary function that regulates the growth rate of cells. The potential for vitamin D to reduce oxidative damage to DNA in a human has been suggested by clinical trial where vitamin D supplementation reduced 8-hydroxy-2'-deoxyguanosine, a marker of oxidative damage, in colorectal epithelial crypt cells. Studies in animal models and in different cell types have also shown marked reduction in oxidative stress damage and chromosomal aberrations, prevention of telomere shortening and inhibition of telomerase activity following treatment with vitamin D. The secondary function of vitamin D in preventing DNA damage includes regulation of the poly-ADP-ribose polymerase activity in the DNA damage response pathway involved in the detection of DNA lesions. It is also able to regulate the cell cycle to prevent the propagation of damaged DNA, and to regulate apoptosis to promote cell death. Vitamin D may contribute to prevention of human colorectal cancer, though there is little evidence to suggest that prevention of DNA damage mediates this effect, if real. Very limited human data mean that the intake of vitamin D required to minimise DNA damage remains uncertain.     

Do national parks protect natural landscapes?

Establishing national parks should result from a desire to protect natural or near natural landscapes with the lowest degree of anthropogenic transformation. This paper tries to ascertain whether national parks in Poland protect the most natural landscapes and how far they have been affected by humans. The level of anthropogenic transformation of natural landscapes was assessed based on an analysis of the percentage of natural, semi-natural and anthropogenic land cover. The vast majority of national parks in Poland (21 out of 23) protect landscapes which have been minimally transformed by humans (RAT_TNP ranges from 1.01 to 1.16). Only two kinds of natural landscapes, those that are the most transformed by humans, are not represented within the set of the Polish national parks. Hence, the distribution of national parks reflects the degree of anthropogenic landscape transformation. The proposed method could be applied to any type of spatial unit and thus be the basis for designating areas that should be protected.     

Can ginsenosides protect human erythrocytes against free-radical-induced hemolysis?

Many studies have focused on the free-radical-initiated peroxidation of membrane lipid, which is associated with a variety of pathological events. Panax ginseng is used in traditional Chinese medicine to enhance stamina and capacity to deal with fatigue and physical stress. Many reports have been devoted to the effects of ginsenosides, the major active components in P. ginseng, on the lipid metabolism, immune function and cardiovascular system. The results, however, are usually contradictory since the usage of mixture of ginsenosides cannot identify the function of every individual ginsenosides on the experimental system. On the other hand, every individual ginsenosides is not compared under the same experimental condition. These facts motivate us to evaluate the antioxidant effect of various individual ginsenosides on the experimental system of free-radical-initiated peroxidation: the hemolysis of human erythrocyte induced thermally by water-soluble initiator, 2,2'-azobis(2-amidinopropane hydrochloride) (AAPH). The inhibitory concentration of 50% inhibition (IC(50)) of AAPH-induced hemolysis of the erythrocyte has been studied firstly and found that the order of IC(50) is Rb3 - Rb1Rc>Re>Rh1>R1>Rg2>Rb3. Rg3, Rd and Rh2, however, act as synergistic prooxidants in the above experimental system. Rg1 does not show any synergistic antioxidative property. Although the antioxidative and prooxidative mechanism of various ginsenosides with or without TOH in AAPH-induced hemolysis of human erythrocytes will be further studied in detail, this information may be useful in the clinical usage of ginsenosides.     

Can ginsenosides protect human erythrocytes against free-radical-induced hemolysis?

Many studies have focused on the free-radical-initiated peroxidation of membrane lipid, which is associated with a variety of pathological events. Panax ginseng is used in traditional Chinese medicine to enhance stamina and capacity to deal with fatigue and physical stress. Many reports have been devoted to the effects of ginsenosides, the major active components in P. ginseng, on the lipid metabolism, immune function and cardiovascular system. The results, however, are usually contradictory since the usage of mixture of ginsenosides cannot identify the function of every individual ginsenosides on the experimental system. On the other hand, every individual ginsenosides is not compared under the same experimental condition. These facts motivate us to evaluate the antioxidant effect of various individual ginsenosides on the experimental system of free-radical-initiated peroxidation: the hemolysis of human erythrocyte induced thermally by water-soluble initiator, 2,2′-azobis(2-amidinopropane hydrochloride) (AAPH). The inhibitory concentration of 50% inhibition (IC₅₀) of AAPH-induced hemolysis of the erythrocyte has been studied firstly and found that the order of IC₅₀ is Rb3∼Rb1≪Rg2<Re<Rg1∼Rc<Rh1<R1. Rb1, Rc and Rg2, as antioxidants, can prolong the lag time of hemolysis. Contrarily, Rg3, Rd and Rh1, together with high concentration of Rb3, Rg1 and Rh2, function as prooxidants to accelerate AAPH-induced hemolysis. The addition of Re does not influence the lag time of hemolysis. The R1 with the concentration ranging from 10 to 20 μM decreases the lag time of hemolysis. These results suggest that there is a mutual interaction that existed in the molecule of ginsenosides since the difference of the structure of ginsenosides is only due to the connective position and type of sugar moieties to the ring of a triterpene dammarane. Moreover, the synergistic antioxidative properties of various individual ginsenosides with α-tocopherol (TOH) are also discussed, and it was found that the order of synergistic antioxidative properties with TOH is Rb1>Rc>Re>Rh1>R1>Rg2>Rb3. Rg3, Rd and Rh2, however, act as synergistic prooxidants in the above experimental system. Rg1 does not show any synergistic antioxidative property. Although the antioxidative and prooxidative mechanism of various ginsenosides with or without TOH in AAPH-induced hemolysis of human erythrocytes will be further studied in detail, this information may be useful in the clinical usage of ginsenosides.     

Plant Proteinase inhibitors: A defense against herbivorous insects?

Using the tomato plant, Lycopersicon esculentum L., and the beet armyworm, Spodoptera exigua (Hübner) (Lepidoptera: Noctuidae), we have demonstrated that insect herbivory induces a rapid decline in plant quality. This decline in plant quality manifests itself by a highly significant reduction in rate of larval growth on a medium containing foliage from insect-damaged as opposed to undamaged tomato plants. The induction of tomato proteinase inhibitors, as a result of larval feeding, is invoked as a factor that systemically reduces leaf quality.

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Zusammenfassung Eine zentrale Theorie in der Erforschung von Insekten-Wirtspflanzen-Wechselbeziehungen ist, dass sich bestimmte natürlich vorkommende Pflanzeninhaltsstoffe in Pflanzen zur Abwehr herbivorer Insekten und anderer Parasiten entwickelt haben. Zur Zeit herrschende Überlegungen beinhalten auch das Konzept, dass herbivore Insekten das Potential besitzen, Veränderungen in der Abwehrund/oder Nahrungsqualität von Wirtspflanzen hervorzurufen, die den herbivoren Insekten schaden. Gegenwärtig is nur wenig über die Ursachen dieser von Insekten induzierten Veränderungen der Wirtspflanzenqualität bekannt. Jedoch werden häufig unterschiedliche Gehalte der Pflanzen an Phenolderivaten, Protein und/oder Proteinaseinhibitoren mit den Abwehrmechanismen in Zusammenhang gebracht. Diese Arbeit untersucht das Potential von Pflanzenproteinaseinhibitoren, als induzierbare Abwehr gegen herbivore Noctuidenlarven zu wirken.Tomatenpflanzen enthalten Proteinaseinhibitoren (PIs), die durch Verletzen der Pflanze induziert werden. Es besteht die Hypothese, dass diese Synthese von PIs einen Abwehrmechanismus gegen blattfressende Insekten darstellt. Diese Hypothese ist niemals angemessen in planta getestet worden und wird von uns anhand von Spodoptera exigua und Tomatenpflanzen, Lycopersicon esculentum, getestet.Wieterhin sollte festgestellt werden, ob eine Beziehung zwischen der PI-Konzentration im Blatt und dem Wachstum von Blattmaterial fressenden Larven besteht. Anstelle lebender Pflanzen wurde dazu eine feste, Blattmaterial enthaltende Diät (15% gefriergetrocknetes Blattmaterial angemischt in Agarlösung und Sorbinsäure) benutzt, was die Verwending einer unverletzten Kontrolle ermöglichte. Diese künstliche Diät wurde S. exigua angeboten. Die Ergebnisse des Fütterungsversuches (Fig. 2) zeigen, dass eine signifikante inverse Beziehung (r²=0.81, p=0.05) zwischen der PI-Konzentration im Blattgewebe und den mittleren Gewichten von Larven von S. exigua besteht. Nicht dargestellt ist die nicht signifikante Korrelation zwischen mittlerem Gewicht der Larven und den Gehalten an Blattprotein (r²=0.47, p>0.25) und Phenolderivaten (r²=0.50, p=0.25).Diese Ergebnisse veranlassen uns zu dem Rückschluss, dass Tomatenproteinaseinhibitoren als systemisch induzierbare antibiotische chemische Abwehr gegen herbivore Insekten wie Noctuidenlarven anzusehen sind, und dass PIs einen Faktor darstellen, der zur systemischen Reduktion der Blattqualität von Tomaten führt.

     

Do pools impede drift dispersal by stream insects?

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Does phenobarbital protect against trimethyltin-induced neuropathology of limbic structures?

Because of the similarity in the pattern of limbic sites damaged by both compounds, it has been suggested that trimethyltin (TMT) may be an excitotoxin like kainic acid (KA). KA produces seizures which eventually result in neuronal damage similar to that found in epilepsy. Anticonvulsants reduce both the seizures and pathology associated with KA. Because TMT may also produce seizures, we undertook to determine whether or not some of the TMT-induced limbic neuropathology could result from seizure activity. To do this, a single dose of TMT chloride (either 7.5 or 15 mg/kg) was given per os to rats, and then phenobarbital (30 mg/kg) was administered subcutaneously in repeated doses. Treatment with phenobarbital did not prevent pathologic changes in the hippocampus, dentate gyrus, and pyriform or prepyriform cortex. Since phenobarbital did not protect against TMT-induced neuronal damage, as it has been reported by others to protect against KA-induced damage, the present findings suggest that these two toxicants probably produce hippocampal pathology via different mechanisms and that the TMT-induced pathologic changes do not require sustained electrical seizure activity.     

Can angiotensin-converting enzyme inhibitors protect against symptomatic radiation pneumonitis?

This study was designed to determine whether patients taking angiotensin-converting enzyme (ACE) inhibitors while receiving radiation therapy for lung cancer are protected from developing symptomatic radiation pneumonitis. The records of 213 eligible patients receiving thoracic irradiation for lung cancer with curative intent at Duke University Medical Center from 1994-1997 were reviewed. Of the 213 patients, 26 (12.2%) were on ACE inhibitors (usually for the management of hypertension) during radiotherapy (group 1); the remaining 187 patients (group 2) were not. Patients were irradiated, with fields shaped to protect normal tissues, with total doses of 50-80 Gy. After treatment, patients were generally followed every 3 months for 2 years, then every 6 months thereafter. Symptomatic radiation pneumonitis was scored according to modified National Cancer Institute Common Toxicity Criteria (i.e., radiographic changes alone were not sufficient for the diagnosis of pneumonitis). There was no difference in the incidence of pneumonitis between the two groups (P = 0.75). Fifteen percent of the patients on ACE inhibitors (group 1) developed symptomatic radiation-induced lung injury compared to 12% of the patients not receiving these drugs (group 2). Although patients in group 1 tended to develop pneumonitis slightly sooner than did patients in group 2, this difference also was not significant (P = 0. 8). Within the dose range prescribed for treating hypertension, ACE inhibitors do not appear to either decrease the incidence or delay the onset of symptomatic radiation pneumonitis among lung cancer patients receiving thoracic irradiation.