Partial purification and characterization of the lipase of a facultatively psychrophilic bacterium (Acinetobacter O16).

The extracellular lipase(s) of the psychrophile Acinetobacter O16 was studied. When the enzyme was precipitated by (NH4)2SO4 and passed through a Sephadex G200 column, two peaks of lipase activity appeared. The larger peak, which behaved like a substance of high molecular weight, being eluted in the void volume, was purified 250-fold over the crude enzyme (culture supernatant) by passage through a DEAE-Sephadex column. When the enzyme was applied to a DEAE-cellulose column it could not be eluted unless it had first been treated with the detergent Titon X 100. It is suggested that lipids or phospholipids make up an important part of the molecule. The activity of the crude and partly purified enzymes was studied in relation to pH and temperature optima. Lipases from the psychrophilic Acinetobacter O16 and from the mesophilic Acinetobacter O4 reacted in the same way to temperature. The crude enzyme from Acinetobacter O16 was more temperature-stable than the purified enzyme.     

Autophagy in osteoblasts is involved in mineralization and bone homeostasis

Bone remodeling is a tightly controlled mechanism in which osteoblasts (OB), the cells responsible for bone formation, osteoclasts (OC), the cells specialized for bone resorption, and osteocytes, the multifunctional mechanosensing cells embedded in the bone matrix, are the main actors. Increased oxidative stress in OB, the cells producing and mineralizing bone matrix, has been associated with osteoporosis development but the role of autophagy in OB has not yet been addressed. This is the goal of the present study. We first show that the autophagic process is induced in OB during mineralization. Then, using knockdown of autophagy-essential genes and OB-specific autophagy-deficient mice, we demonstrate that autophagy deficiency reduces mineralization capacity. Moreover, our data suggest that autophagic vacuoles could be used as vehicles in OB to secrete apatite crystals. In addition, autophagy-deficient OB exhibit increased oxidative stress and secretion of the receptor activator of NFKB1 (TNFSF11/RANKL), favoring generation of OC, the cells specialized in bone resorption. In vivo, we observed a 50% reduction in trabecular bone mass in OB-specific autophagy-deficient mice. Taken together, our results show for the first time that autophagy in OB is involved both in the mineralization process and in bone homeostasis. These findings are of importance for mineralized tissues which extend from corals to vertebrates and uncover new therapeutic targets for calcified tissue-related metabolic pathologies.     

Interleukin-23 is critical for full-blown expression of a non-autoimmune destructive arthritis and regulates interleukin-17A and RORγt in γδ T cells

Introduction

A protein analysis using a mass spectrometry indicated that there are serum proteins showing significant quantitative changes after the administration of infliximab. Among them, connective tissue growth factor (CTGF) seems to be related to the pathogenesis of rheumatoid arthritis (RA). Therefore, this study was conducted to investigate how CTGF is associated with the disease progression of RA.

Methods

Serum samples were collected from RA patients in active or inactive disease stages, and before or after treatments with infliximab. CTGF production was evaluated by ELISA, RT-PCR, indirect immunofluorescence microscopy, and immunoblotting. Osteoclastogenesis was evaluated using tartrate-resistant acid phosphatase (TRAP) staining, a bone resorption assay and osteoclasts specific catalytic enzymes productions.

Results

The serum concentrations of CTGF in RA were greater than in normal healthy controls and disease controls. Interestingly, those were significantly higher in active RA patients compared to inactive RA patients. Furthermore, the CTGF levels significantly were decreased by infliximab concomitant with the disease amelioration. In addition, tumour necrosis factor (TNF)α can induce the CTGF production from synovial fibroblasts even though TNFα can oppositely inhibit the production of CTGF from chondrocytes. CTGF promoted the induction of the quantitative and qualitative activities of osteoclasts in combination with M-CSF and receptor activator of NF-κB ligand (RANKL). In addition, we newly found integrin αVβ3 on the osteoclasts as a CTGF receptor.

Conclusions

These results indicate that aberrant CTGF production induced by TNFα plays a central role for the abnormal osteoclastic activation in RA patients. Restoration of aberrant CTGF production may contribute to the inhibition of articular destruction in infliximab treatment.     

The tangled core at the heart of the bryozoan suborder Phylloporinina

Abstract: The family Phylloporinidae was introduced in the late 19th century to accommodate a small number of Palaeozoic bryozoan genera characterized by irregularly fenestrated colonies generated by anastomosis of unilaminate branches. Among the first named of these genera were Chasmatopora Eichwald, 1855 and Phylloporina Ulrich in Foerste, 1887. The two names have been variously in fashion, and there has been confusion about whether they are subjective synonyms or are distinct genera. This taxonomic confusion has been due in large part to whether the single species (Retepora angulata Hall, 1847) assigned to Phylloporina in Foerste (1887) or the species that Ulrich intended (Retepora trentonensis Nicholson, 1875) is the type species and also because of lack of sufficient information about Foerste’s material to characterize it well. We here redescribe the pertinent species, erect the new species Chasmatopora foerstei for the species that Foerste incorrectly assigned to Phylloporina angulata (Hall), and suggest that Retepora trentonensis Nicholson be retained as type species of Phylloporina based on prevailing usage, until the issue is settled by the International Commission on Zoological Nomenclature.     

Enrichment of homologs in insignificant BLAST hits by co-complex network alignment

Background  

Homology is a crucial concept in comparative genomics. The algorithm probably most widely used for homology detection in comparative genomics, is BLAST. Usually a stringent score cutoff is applied to distinguish putative homologs from possible false positive hits. As a consequence, some BLAST hits are discarded that are in fact homologous.