Factors affecting the snow and wind induced damage of a montane secondary forest in northeastern China

Abstract

Role of pparß in irradiation mediated intestinal damage

Les récepteurs activés proliférateurs de peroxisomes (PPARs) appartiennent à la grande famille des récepteurs nucléaires et ont été impliqué dans plusieurs processus physiologiques. Parmi les trois isotypes PPAR, PPARβ est bien connu pour son rôle dans les décisions déterminant le destin des cellules, notamment dans les processus de prolifération, de différentiation et d'apoptose. Ce rôle a particulièrement été souligné comme protecteur dans les contextes de survie cellulaire et de cicatrisation. Il est fortement exprimé dans l'intestin grêle. Notre groupe a déjà rapporté sa présence importante dans les cryptes duodénales, où se trouvent les cellules souches intestinales. Précédemment, nous avons aussi fait remarquer le rôle de PPARβ dans la differentiation des cellules de Paneth, par la régulation négative de la signalisation Ihh de l'épithélium intestinal. Malgré sa capacité de figurer parmi les tissus du corps qui se régénèrent le plus rapidement, l'épithélium intestinal est particulièrement sensible aux attaques cytotoxiques, surtout celles dues à la radiothérapie des cancers abdomino-pelviens. Cela peut donner lieu à des lésions gastro-intestinal en tant qu'effet indésirable d'une exposition aiguë et chronique à l'irradiation. En raison du rôle protecteur de PPARβ le but de cette étude était de comprendre les voies de signalisation moléculaires régulées par PPARβ qui sont impliquées dans les réponses des cellules intestinales aux dommages causés par l'irradiation.Afin de déchiffrer les mécanismes moléculaires sous-jacents, un modèle in-vitro d'une lignée cellulaire - HT-29 a été utilisée. Il n'y a cependant pas de preuve d'un effet protecteur de PPARβ dans divers contextes d'endommagement cellulaire testés in-vitro. Ceci contraste avec les observations in-vivo qui indiquent que l'irradiation provoque une létalité supérieure dans les souris PPARβ-/- par rapport aux souris PPARβ+/+, entre autre correlée avec une apoptose augmentée des cellules souches intestinales à 4h après irradiation. En plus, le décès plus important de cellules mésenchymateuses a été observé dans les souris PPARβ-/-, 8 jours après irradiation. Moins nombreuses, ces cellules se sont également détachées de la matrice extracellulaire reliant l'épithélium et le mésenchyme. Nous stipulons qu'in-vivo, PPARβ participe au dialogue entre le mésenchyme et l'épithélium, ce qui est concordant avec le délai observé lors de la réparation tissulaire. Ce dialogue entre l'épithélium et le mésenchyme, n'existe pas de la même manière in-vitro. Il en résulte donc un défaut de réponse mésenchymale médiée par PPARβ, d'où le paradoxe entre les conditions in-vivo et in-vitro.Ces observations indiquent l'implication possible de PPARβ dans les lesions actiniques, en tant que conséquence naturelle de la radiothérapie de patients avec un cancer. Les mécanismes précis de l'action de PPARβ nécessitent une exploration approfondie de son rôle physiologique dans ce contexte.

Postharvest mechanical damage affects fruit quality of 'Montenegrina' and 'Rainha' tangerines

The objective of this work was to evaluate the visual and chemical quality of tangerines after mechanical damage by impacts. The tangerine cultivars Montenegrina and Rainha were submitted to different degrees of impact and evaluated for decay and oleocellosis, loss of fresh weight, total soluble solids, total titratable acidity and ascorbic acid degradation, as well as for epicarp color changes. Experiments with three replicates and experimental units of six fruit for each cultivar were done in a completely randomized design. Impact produced qualitative internal and minor external changes on tangerines. The main modifications produced by impact on the fruit were losses of citric acid and soluble solids, which increased the solid:acid ratio, and losses of ascorbic acid. 'Montenegrina' tangerines are more susceptible to internal quality damage than 'Rainha'.

War and National Renewal: Civil Religion and Blood Sacrifice in American Culture

Wars are often associated with a rhetoric of renewal or new beginnings. This essay explores this claim through the lens of civil religion and a recent book by Carolyn Marvin and David Ingle, Blood Sacrifice and the Nation, which combines Emile Durkheim with Réné Girard in proposing that modern national cohesion depends on blood sacrifice. I unpack some of the paradoxes raised by this theory of national renewal in the context of 9/11, with a special focus on the sacred status of the flag and the special attention given to uniformed serviceman in the American body politic.

Time consumption and damage to the remaining stock in mechanised and motor manual pre-commercial thinning

Abstract

Trichogramma pretiosum attraction due to the Elasmopalpus lignosellus damage in maize

The objective of this work was to evaluate if corn plants damaged by the lesser cornstalk borer (Elasmopalpus lignosellus) larvae release volatile organic compounds capable of attracting the egg parasitoid Trichogramma pretiosum. The treatments consisted of plants subjected to harm caused by E. lignosellus larvae, plants subjected to mechanical damage, and undamaged plants. The parasitoid was more attracted by the volatiles released by the insect damaged plants than to those released by undamaged corn plants, after 24 and 72 hours. The volatiles (Z)-3-hexenyl acetate, β-pinene, β-myrcene, (E)-4,8-dimethylnona-1,3,7-triene, and benzothiazole were released in significantly larger quantities by damaged plants. Volatiles released by corn plants damaged by E. lignosellus larvae may act as an indirect defense, attracting by T. pretiosum.

The JNK inhibitor XG-102 protects from ischemic damage with delayed intravenous administration also in the presence of recombinant tissue plasminogen activator.

BACKGROUND: XG-102 (formerly D-JNKI1), a TAT-coupled dextrogyre peptide which selectively inhibits the c-Jun N-terminal kinase, is a powerful neuroprotectant in mouse models of middle cerebral artery occlusion (MCAo) with delayed intracerebroventricular injection. We aimed to determine whether this neuroprotection could also be achieved by intravenous injection of XG-102, which is a more feasible approach for future use in stroke patients. We also tested the compatibility of the compound with recombinant tissue plasminogen activator (rtPA), commonly used for intravenous thrombolysis and known to enhance excitotoxicity. METHODS: Male ICR-CD1 mice were subjected to a 30-min-suture MCAo. XG-102 was injected intravenously in a single dose, 6 h after ischemia. Hippocampal slice cultures were subjected to oxygen (5%) and glucose (1 mM) deprivation for 30 min. rtPA was added after ischemia and before XG-102 administration, both in vitro and in vivo. RESULTS: The lowest intravenous dose achieving neuroprotection was 0.0003 mg/kg, which reduced the infarct volume after 48 h from 62 +/- 19 mm(3) (n = 18) for the vehicle-treated group to 18 +/- 9 mm(3) (n = 5, p < 0.01). The behavioral outcome was also significantly improved at two doses. Addition of rtPA after ischemia enhanced the ischemic damage both in vitro and in vivo, but XG-102 was still able to induce a significant neuroprotection. CONCLUSIONS: A single intravenous administration of XG-102 several hours after ischemia induces a powerful neuroprotection. XG-102 protects from ischemic damage in the presence of rtPA. The feasibility of systemic administration of this promising compound and its compatibility with rtPA are important steps for its development as a drug candidate in ischemic stroke.

BRAIN DAMAGE IN METHYLMALONIC ACIDURIA: 2-METHYLCITRATE LEADS TO AMMONIA INCREASE AND APOPTOSIS

A 3D in vitro model of rat organotypic brain cell cultures in aggregates was used to investigate neurotoxicity mechanisms in methylmalonic aciduria. 1 mM methylmalonate (MMA), 2-methylcitrate (2-MCA) or propionate (PA) were repeatedly added to the culture media at two different time points of the cultures. In cultures treated with 2-MCA, we observed a significant increase of lactate in the medium, consistent with a possible inhibition of Krebs cycle and respiratory chain, as described earlier in the literature. Interestingly, we further observed that 2-MCA induced an important increase in ammonia production with concomitant decrease of glutamine concentrations, which suggests an inhibition of the astrocytic enzyme glutamine synthetase. These previously unreported findings may uncover a pathogenic mechanism in this disease with deleterious effects on early stages of brain development. By immunohistochemistry we could show that 2-MCA substantially increased the number of apoptotic cells. On the cellular level, 2-MCA had a toxic effect (cell swelling and cell death) on glial cells, but not on neurons. Surprisingly, MMA seemed to have a growth stimulating effect on the cultures. We can conclude that 2-MCA was the most toxic metabolite in our model for methylmalonic aciduria inducing ammonia accumulation and massive apoptosis in brain cells.

Targeting autophagy to prevent neonatal stroke damage.

Cell death due to cerebral ischemia has been attributed to necrosis and apoptosis, but autophagic mechanisms have recently been implicated as well. Using rats exposed to neonatal focal cerebral ischemia, we have shown that lysosomal and autophagic activities are increased in ischemic neurons, and have obtained strong neuroprotection by post-ischemic inhibition of autophagy.

The DNA damage response to adeno-associated virus : centrosome overduplication and induction of cell death independently of the spindle checkpoint

Summary: Adeno-associated virus type 2 (AAV2) is a small virus containing single-stranded DNA of approximately 4.7kb in size. Both ends of the viral genome are flanked with inverted terminal repeat sequences (ITRs), which serve as primers for viral replication. Previous work in our laboratory has shown that AAV2 DNA with ultraviolet radiation-generated crosslinks (UV-AAV2) provokes a DNA damage response in the host cell by mimicking a stalled replication fork. Infection of cells with UV-AAV2 leads to a p53-and Chk1-mediated cell cycle arrest at the G2/M border of the cell cycle. However, tumour cells lacking the tumour suppressor protein p53 cannot sustain this arrest and enter a prolonged impaired mitosis, the outcome of which is cell death. The aim of my thesis was to investigate how UV-inactivated AAV2 kilts p53-deficient cancer cells. I found that the UV-AAV2-induced DNA damage signalling induces centriole overduplication in infected cells. The virus is able to uncouple the centriole duplication cycle from the cell cycle, leading to amplified centrosome numbers. Chk1 colocalises with centrosomes in the infected cells and the centrosome overduplication is dependent on the presence of Chk1, as well as on the activities of ATR and Cdk kinases and on the G2 arrest. The UV-AAV2-induced DNA damage signalling inhibits the degradation of cyclin B 1 and securin by the anaphase promoting complex, suggesting that the spindle checkpoint is activated in these mitotic cells. Interference with the spindle checkpoint components Mad2 and BubR1 revealed that the UV-AAV2-provoked mitotic catastrophe occurs independently of spindle checkpoint function, This work shows that, in the p53 deficient cells, UV-AAV2 triggers mitotic catastrophe associated with a dramatic Chk1-dependent overduplication of centrioles and the consequent formation of multiple spindle poles in mitosis. Résumé Le virus associé à l'adénovirus type 2 (AAV2) est un petit virus contenant un simple brin d'ADN d'environ 4.7kb. Des expériences antérieures dans notre laboratoire ont montré que les liens intramoléculaires sur l'ADN de AAV2 provoqués paz l'irradiation aux ultraviolets (UV) ressemblent à une fourche de réplication bloquée, ce qui provoque une réponse aux dommages à l'ADN dans la cellule hôte. L'infection des cellules avec UV-AAV2 résulte en un arrêt du cycle cellulaire à la transition G2/M entraîné par les protéines ATR et Chk1. Cependant, les cellules tumorales auxquelles il manque le suppresseur de tumeur p53 ne peuvent pas tenir cet arrêt et entrent dans une mitose anormale et prolongée qui se terminera par la mort cellulaire. Le but de ma thèse était d'étudier comment l'AAV2 inactivé par l'irradiation UV tue les cellules cancéreuses n'ayant pas p53. Je montre ici que le signal de dommages à l'ADN induit par UV-AAV2 génère une surduplication des centrioles dans les cellules infectées. Le virus est capable de dissocier le cycle de duplication du centriole du cycle cellulaire ce qui crée un nombre amplifié de centrosomes. Chk1 est co-localisé avec le centrosome dans les cellules infectées et la swduplication du centrosome est dépendante de la présence de Chk1, de l'activité des kinases ATR et Cdk et de l'arrêt en G2 de la cellule. Le signal d'ADN endommagé induit par UV-AAV2 réprime la dégradation des protéines cycline B1 et securine par le complexe promoteur de l'anaphase (APC), ce qui suggère que le point de contrôle du fuseau mitotique est activé dans ces cellules en mitose. L'étude d'interférence avec des éléments du point de contrôle du fuseau mitotique, Mad2 et BubR1, a révélé que la catastrophe mitotique provoquée paz UV-AAV2 survient indépendamment du point de contrôle du fuseau mitotique. Ce travail montre que dans les cellules déficientes en p53, UV-AAV2 induit une catastrophe mitotique associée à une surduplication des centrioles dépendant de Chk1 et ayant pour conséquence dramatique la formation de multiples fuseaux mitotiques dans la cellule en mitose.

Does land titling matter? The role of land property rights in the war on illicit crops in Colombia

This paper analyzes the role of formalization of land property rights in the war against illicit crops in Colombia. We argue that as a consequence of the increase of state presence and visibility during the period of 2000 and 2009, municipalities with a higher level of formalization of their land property rights saw a greater reduction in the area allocated to illicit crops. We hypothesize that this is due to the increased cost of growing illicit crops on formal land compared to informal, and due to the possibility of obtaining more benets in the newly in- stalled institutional environment when land is formalized. We exploit the variation in the level of formalization of land property rights in a set of municipalities that had their rst cadastral census collected in the period of 1994-2000; this selection procedure guarantees reliable data and an unbiased source of variation. Using fixed effects estimators, we found a signicant negative relationship between the level of formalization of land property rights and the number of hectares allocated to coca crops per municipality. These results remain robust through a number of sensitivity analyses. Our ndings contribute to the growing body of evidence on the positive effects of formal land property rights, and e ective policies in the war on drugs in Colombia.

Vastuu toimitusvahingoista polttonesteen toimituksissa, case oy Shell ab

Tutkimustyön tavoitteena oli selvittää polttonesteiden toimituksiin osallistuvien tahojen, eli myyjän, itsenäisen rahdinkuljettajan ja ostajan vastuun jakautuminen.. Lähtökohtaisesti myyjällä on viivästystilanteissa sekä kuluttaja-, että yritysasiakkaita kohtaan kontrollivastuu välittömistä ja tuottamusperusteinen vastuu välillisistä vahingoista, mutta korvausvelvollisuudesta voidaan vapautua tietyt tunnusmerkit täyttävän esteen perusteella. Virhevastuukin perustuu samanlaiselle kaksinkertaiselle vahinkolajikohtaiselle vastuuperuste-erottelulle, mutta myyjän on aina korvattava kuluttajalle aiheutuneet välittömät vahingot aiheuttamisvastuun perusteella. Lisäksi hän voi joutua hyvittämään kaikki mahdolliset menetyksen annetun erityisen sitoumuksen nojalla. Maksuviivästystilanteissa ostajan molempia vahinkolajeja koskeva vastuuperuste sijoittuu puhtaan aiheuttamis- ja kontrollivastuun väliin. Lainmukaisen myötävaikutusvelvollisuuden laiminlyönnin aiheuttamat vahingot korvataan noudattamalla myyjän viivästysvastuusäännöksiä, mutta tavaran vastaanottamisen tai noutamisen osalta vastuun toteutuminen edellytetään vielä sitä, että kaupankohteen pois toimittamisella on ollut myyjäpuolelle erityistä merkitystä. Kuluttaja-asiakkaalla ei kuitenkaan ole edellä mainittua vastuuta. Rahdinkuljettajalla on tavara- ja viivästysvahingoista ankara vastuu tietyn force majeure poikkeuksin. Tavallisesti korvausvelvollisuus rajoittuu tavaravahinkojen osalta 20 euroon painokiloa kohti ja viivästysvahingot on korvattava rahtia vastaavaan rahamäärään saakka. Kyseinen taho voi myös vapautua vastuusta kokonaan laissa mainittujen vastuuvapausperusteiden nojalla, mutta tahallinen tai törkeän huolimaton toiminta aiheuttaa täyden vahingonkorvausvastuun.

The avocado fruit borer, Stenoma catenifer (wals.) (Lepidoptera: elachistidae): egg and damage distribution and parasitism

The avocado fruit borer, Stenoma catenifer (Wals.) has been a limiting factor in growing avocados over the last years in many Brazilian states. This is a result of the lack of safe and feasible management practices to minimize the fruit borer damage. The aim of this study was to obtain information on the pest biology and ecology as well as on the role of natural enemies to define strategies to control the pest. Samples were taken biweekly and consisted of 20 fruits collected randomly (10 from the upper half and 10 from the lower half of the plant) in ten plants, cv. Margarida, in a commercial avocado grove in Arapongas and Cambé regions, PR, from October/2001 to September/2002. Laboratory determinations of the percentage of damaged fruit per plant region, location and number of bored fruit sites, and the number and location of the fruit borer eggs, including parasitized ones, were performed. The results showed that S. catenifer preferred to oviposit and attack fruits located on the upper half of the trees. The majority of the eggs were laid on the fruit pedicel whereas the damage was mainly located on the lower half of the fruits. Trichogrammatids were the most constant and abundant parasitoids found in both localities throughout the study period.