A review on symptoms,treatments protocols,and proteomic profile in sulfur mustard‐exposed victims

Sulfur mustard (SM) as an alkylating and vesicating agent was used for 100 years as a chemical weapon. SM as bi‐functional mustard can attacks and alkylates lots of biomolecules. Different cellular mechanism and molecular pathways are responsible for damages to body tissues. Such as DNA damages, oxidative stress, Apoptosis, and inflammation. Sulfur mustard penetrated body organs and induces long term eye, skin, lung, gastrointestinal, urogenital damages and can cause carcinogenic and mutagenic consequences. Currently there is no definitive treatment protocol for SM exposed patients. The goal of treatment is relieving the symptoms with fast healing rate and retrieval of damaged tissues to normal function and appearance in short period of time. Evaluation of proteomics profile in SM‐exposed victims has been performed in animal model and human patients. These studies revealed that different protein were involved in the patients with SM damages to skin and lungs. Apolipoprotein A1, type I cytokeratins K14, K16 and K17, S100 calcium‐binding protein A8, α1 haptoglobin isoforms, Amyloid A1, albumin, haptoglobin, and keratin isoforms, immunoglobulin kappa chain are defined expressed proteins in the damaged tissues.     

Translational models of tumor angiogenesis: A nexus of in silico and in vitro models

Emerging evidence shows that endothelial cells are not only the building blocks of vascular networks that enable oxygen and nutrient delivery throughout a tissue but also serve as a rich resource of angiocrine factors. Endothelial cells play key roles in determining cancer progression and response to anti-cancer drugs. Furthermore, the endothelium-specific deposition of extracellular matrix is a key modulator of the availability of angiocrine factors to both stromal and cancer cells. Considering tumor vascular network as a decisive factor in cancer pathogenesis and treatment response, these networks need to be an inseparable component of cancer models. Both computational and in vitro experimental models have been extensively developed to model tumor-endothelium interactions. While informative, they have been developed in different communities and do not yet represent a comprehensive platform. In this review, we overview the necessity of incorporating vascular networks for both in vitro and in silico cancer models and discuss recent progresses and challenges of in vitro experimental microfluidic cancer vasculature-on-chip systems and their in silico counterparts. We further highlight how these two approaches can merge together with the aim of presenting a predictive combinatorial platform for studying cancer pathogenesis and testing the efficacy of single or multi-drug therapeutics for cancer treatment.     

Phylogenetic biogeography and classification of the Drosophila montium species group (Diptera: Drosophilidae)

The Drosophila montium group is the largest clade of the subgenus Sophophora consisting of 94 palaeotropical species, whose phylogenetic relationships remain unclear. Here, I used a recent tree inferred from three nuclear genes and one mitochondrial gene for almost half of the species to reconstruct the historical biogeography of the group and propose a comprehensive classification for the totality of its species. The group originated in South-East Asia nearly 20 million years ago (mya), and dispersed to Africa in the Late Miocene. A second northward expansion into East Asia took place in the Pliocene. Based on morphological (male abdominal pigmentation and genitalia) and chorological traits congruent with the molecular tree, I divide the montium group into seven subgroups: parvula, montium, punjabiensis, serrata, kikkawai, seguyi and orosa. The polyphyletic status of some of the previously defined complexes (auraria, jambulina, serrata, kikkawai and nikananu) is also resolved.