Venous outflow system in rabbit gastric mucosa

The purpose of this work was to compare the organisation of the gastric mucosal venous system in larger animals, exemplified by rabbits, with that of the rat and the hamster which we have described previously. Rabbits were given atropine and hexamethonium followed by intravital ligation of all veins draining the stomach, causing strong hyperaemia. The distribution of vessels was studied in the non-mounted mucosa, in mounts of mucosa cleared in light mineral oil and in paraffin or semi-thin plastic sections. We found that blood from rabbit gastric mucosa is drained by collecting venules, running from the subepithelial layer towards the muscularis mucosae. The collecting venules join the paramuscular vessels parallel and adjacent to the muscularis mucosae. Neighbouring venules form numerous arcade-like connections and gradually enlarge. Two venules and an arteriole form triplets initially situated at the luminal face of the muscularis mucosae and gradually passing onto its abluminal surface. In rats vascular triplets were absent and the collecting venules drained into paramuscular vessels joining submucosal veins. In hamsters both connections between paramuscular vessels and submucosal veins and the passing of vascular triplets across muscularis mucosae were observed. Contraction/relaxation of the muscularis mucosae may regulate the amount of blood in the venous system of the mucosa and change the intramucosal pressure, affecting movement of the tissue fluid and, indirectly, the function of the gastric cells

Synovial membrane asks for independence

Synovial membrane is traditionally considered as a part of the joint capsule. It, however, differs from fibrous part of the capsule in development, structure, function, vascularisation, innervation and involvement in pathological processes. Moreover, in some areas, it even does not contact with the fibrous capsule. Thus, it appears that the synovial membrane should be considered as an independent organ and not as the lining of the joint capsule.

Formation of synovial joints and articular cartilage

Chondrocytes differentiate from mesenchymal progenitors and produce templates(anlagen) for the developing bones. Chondrocyte differentiation is controlled bySox transcription factors. Templates for the neighbour bones are subsequentlyseparated by conversion of differentiated chondrocytes into non-chondrogeniccells and emergence of interzone in which joints cavitation occurs. A central rolein initiating synovial joint formation plays Wnt-14/beta-catenin signalling pathway.Moreover, bone morphogenetic proteins and growth and differentiation factorsare expressed at the site of joint formation. Joint cavitation is associated withincreased hyaluronic acid synthesis. Hyaluronic acid facilitates tissue separationand creation of a functional joint cavity. According to the traditional view articularcartilage represents part of cartilage anlage that is not replaced by bone throughendochondral ossification. Recent studies indicate, however, that peri-joint mesenchymalcells take part in interzone formation and that these interzone cellssubsequently differentiate into articular chondrocytes and synovial cells. Thus,anlage chondrocytes have a transient character and disappear after cessation ofgrowth plate function while articular chondrocytes have stable and permanentphenotype and function throughout life

Change in Localization of Alkaline Phosphatase and Mannosidase II by Colchicine Treatment of Primary Cultures of Fetal Rat Hepatocytes

We examined the changes in localization of alkaline phosphatase (ALP) and mannosidase II (man II), a Golgi marker, after colchicine treatment of primary cultures of fetal rat hepatocytes, using double immunofluorescence staining and confocal laser microscopy. In hepatocytes cultured in basal medium, ALP was localized in the perinuclear cytoplasm, and man II was observed in the Golgi region of the cytoplasm. When hepatocytes were cultured in dexamethasone-supplemented medium, ALP was also localized in the plasma membrane surrounding the bile canaliculus-like structure that was formed between adjacent cells. In hepatocytes cultured in the same medium containing colchicine, the structure of microtubules in the cytoplasm was lost, man II exhibited granular distribution scattering throughout the cytoplasm, and ALP was localized in coarse granular sites of the cytoplasm. However, ALP was not colocalized at the same sites as man II. The present study indicated that colchicine inhibits the dexamethasone-promoted translocation of ALP to the plasma membrane surrounding the bile canaliculus-like structure in primary cultures of fetal rat hepatocytes by disassembling microtubules and discomposing the Golgi complex

Deficiency and Also Transgenic Overexpression of Timp-3 Both Lead to Compromised Bone Mass and Architecture In Vivo

Tissue inhibitor of metalloproteinases-3 (TIMP-3) regulates extracellular matrix via its inhibition of matrix metalloproteinases and membrane-bound sheddases. Timp-3 is expressed at multiple sites of extensive tissue remodelling. This extends to bone where its role, however, remains largely unresolved. In this study, we have used Micro-CT to assess bone mass and architecture, histological and histochemical evaluation to characterise the skeletal phenotype of Timp-3 KO mice and have complemented this by also examining similar indices in mice harbouring a Timp-3 transgene driven via a Col-2a-driven promoter to specifically target overexpression to chondrocytes. Our data show that Timp-3 deficiency compromises tibial bone mass and structure in both cortical and trabecular compartments, with corresponding increases in osteoclasts. Transgenic overexpression also generates defects in tibial structure predominantly in the cortical bone along the entire shaft without significant increases in osteoclasts. These alterations in cortical mass significantly compromise predicted tibial load-bearing resistance to torsion in both genotypes. Neither Timp-3 KO nor transgenic mouse growth plates are significantly affected. The impact of Timp-3 deficiency and of transgenic overexpression extends to produce modification in craniofacial bones of both endochondral and intramembranous origins. These data indicate that the levels of Timp-3 are crucial in the attainment of functionally-appropriate bone mass and architecture and that this arises from chondrogenic and osteogenic lineages