Bacillus thuringiensis subsp. israelensis is the most important biological insecticide for the control of mosquito vectors of disease. This bacterium produces toxins during sporulation that cause larval death by lysis of cells in their midgut. The pBtoxis plasmid of B. thuringiensis subsp. israelensis encodes all the mosquitocidal toxins and a number of other coding sequences. The plasmid also carries potential germination genes organised in a single ger operon. Comparison of the germination responses of spores from strains with and without pBtoxis revealed that this plasmid could promote activation of the spores under alkaline conditions but not following heat treatment. Introduction of the ger operon on a recombinant plasmid to the plasmidless strain established this operon as the first with an identified role in alkaline activation.

Seed size is a key functional trait that affects plant fitness at the seedling stage and may

vary greatly with species fruit size, growth form and fecundity. Using structural equation

modelling (SEM) and correlated trait evolution analysis, we investigated the interaction network

between seed size and fecundity, postfire regeneration strategy, fruit size, plant height

and serotiny (on-plant seed storage) among 82 species of the woody shrub genus, Hakea,

with a wide spectrum of seed sizes (2–500 mg). Seed size is negatively correlated with fecundity,

while fire-killed species (nonsprouters) produce more seeds than resprouters

though they are of similar size. Seed size is unrelated to plant height and level of serotiny

while it scales allometrically with fruit size. A strong phylogenetic signal in seed size revealed

phylogenetic constraints on seed size variation in Hakea. Our analyses suggest a

causal relationship between seed size, fecundity and postfire regeneration strategy in

Hakea. These results demonstrate that fruit size, fecundity and evolutionary history have

had most control over seed size variation among Hakea species.

Shhoob Mohamed imhmed Elahmir, (06-2015), UNITED STATES: journal.pone, 1 (1371), 1-12

Activation of innate immunity is regulated by a variety of signaling molecules within

the immune cells. The present thesis was aimed to improve our understanding

innate signaling mechanism and their possible use as bio-indicators of exposure and

disease. The first part of the thesis deals with the involvement of TOM1L1 (Target

of Myb1 like 1) in innate immune signaling and regulation of inflammatory cytokines

in immune cells (study I and II). The initial event of T-cells activation depend

on the recruitment of Src family kinases Fyn and Lck, leading to interleukine-2 (IL-

2) production in T cells. Understanding the regulatory aspects of IL-2 induction in

T-cells is of importance as IL-2 is a key regulator for T-cell proliferation and survival.

Interaction screening indicated the ability of TOM1L1 protein to interact with

Fyn, and Lck, that is important for IL-2 production in Jurkat T-cells. TOM1L1

silencing decreased the levels of CD3/CD28 dependent induction of IL-2 in Jurkat

T-cells, and LPS dependent induction of TNF-α in THP-1. Furthermore, overexpression

of TOM1L1 in Jurkat T-cells causes an increase of STAT3 expression. This

was accompanied by an increase in the levels of IL-1β dependent induction of IL-6

and TNF-α in THP-1 cells. These results indicate that TOM1L11 participate in

regulation of innate immune response. The second part of the thesis deals with

development of innate immune signaling responses used as a diagnosis tools for

disease and exposure (study III and IV). Inflammatory diseases are associated with

innate immune reactions. In response to inflammation, the immune cells release

inflammatory cytokines such as IL-1-β, IL-2, IL-6, IL-10, TNF-α and CXCL8. These

cytokines are regulated by stress related kinases include MAP kinase proteins such

as ERK1-2, JNK, and MAPK p38, through activation of transcription factors AP-1,

ATF-2, and NF-AT. In a clinical study, it was observed that activated MAPK p38

has a potential role in the regulation of IL-10 expression in intermittent claudication.

However, expression of IL-10 and MAPK p38 was opposed in stable angina

group. Therefore, targeting MAPK p38 in inflammatory disease such as cardiovascular

diseases, diabetes, and rheumatoid arthritis might be useful in development of

treatment strategies. Innate immune reactions can also be used to monitor stress

related inflammatory responses following environmental exposure of immune cells.

Inflammatory responses of exposure were studied by in vitro exposure to waters

from sewage treatment works and recipient waters. The analysis shows that exposure

to inland waters can result in activated immune responses and that these responses

are both site dependent and vary over time.

Keywords: Innate immunity, TOM1L1, inflammatory responses.

Differences in activation between spores from strains of Bacillus thuringiensis subsp. israelensis with and without the toxin-encoding plasmid pBtoxis are demonstrated. Following alkaline activation, the strain bearing pBtoxis shows a significantly greater germination rate. Expression of just three genes constituting a previously identified, putative ger operon from this plasmid is sufficient to produce the same phenotype and characterizes this operon as a genetic determinant of alkaline activation.

تمت إضافة ثلاثة أنواع نباتية للفلورا الليبية هي Ruta montana + Pimpinella cretica + plantago bellardii

Shhoob

Diabetic retinopathy is one of the most common diabetic complications, and is a major cause of new blindness in the working-age population of developed countries. Progression of vascular abnormalities, including the selective loss of pericytes, formation of acellular capillaries, thickening of the basement membrane, and increased vascular permeability characterizes early nonproliferative diabetic retinopathy (NPDR). Capillary occlusion, as shown on fluorescein angiograms, is also one of the earliest clinically recognizable lesion of NPDR. In response to capillary non-perfusion, there is dilation of neighbouring capillaries, leading to early blood-retinal barrier breakdown, capillary non-perfusion, and endothelial cell injury and death. The resulting ischemia leads to increased production of growth factors, and the development of proliferative diabetic retinopathy (PDR), which is characterized by growth of new vessels and potential severe and irreversible visual loss. The exact pathogenic mechanism by which capillary non-perfusion occurs is still unclear but growing evidence now suggests that increased leukocyte-endothelial cell adhesion and entrapment (retinal leukostasis) in retinal capillaries is an early event associated with areas of vascular non-perfusion and the development of diabetic retinopathy. The leukocytes in diabetic patients are less deformable more activated, and demonstrate increased adhesion to the vascular endothelium. This review summarizes the current literature on the role of leukocytes in the pathogenesis of capillary occlusion, and discusses the potential of leukostasis as a new promising target in the treatment of diabetic retinopathy.

Aims/hypothesis: Increasing evidence suggests that chronic, subclinical inflammation plays an important role in the pathogenesis of diabetic retinopathy. We recently reported that a glycosylating enzyme, core 2 beta-1,6-N-acetylglucosaminyltransferase (core 2 GlcNAc-T), is implicated in increased leucocyte-endothelial cell adhesion in diabetic retinopathy via an upregulation mechanism controlled by TNF-alpha.

Subjects, materials and methods: We examined the functional link between circulating TNF-alpha and the activity and phosphorylation of core 2 GlcNAc-T in polymorphonuclear leucocytes of patients with type 1 and type 2 diabetes.

Results: Plasma levels of TNF-alpha, although similar in patients with type 1 and type 2 diabetes, were significantly higher than in age-matched healthy controls, and correlated well with the severity of retinopathy. Core 2 GlcNAc-T activity followed the same trend and was associated with the phosphorylation of the enzyme. Finally, the observation that TNF-alpha levels are also linked to glycaemic values suggests that in patients, as well as in vitro, the glycosylation-mediated cell adhesion process that plays a role in diabetic retinopathy may involve glucose- and TNF-alpha-induced protein kinase beta2 activation, and subsequently raise the activity of core 2 GlcNAc-T through increased enzyme phosphorylation.

Conclusions/interpretation: Our results reveal a novel rationale towards a specific treatment of diabetic retinopathy, based on the inhibition of core 2 GlcNAc-T activity and/or the blockage of cognate glycans.

Two plant species are new recored form Libya

تمت إضافة ثلاثة أنواع نباتية للفلورا الليبية هي Lactuca saligna + Sanguisorba minor