Annexin A2 (AnxA2) association with the clinicopathological data in different breast cancer subtypes: A possible role for AnxA2 in tumor heterogeneity and cancer progression.

Background: Breast cancer is a highly heterogeneous type of neoplasia with molecular and biochemical alterations in the ductal epithelium. AnxA2 has a diverse functions and through intracellular interaction with other molecules promotes carcinogenesis.

Aims: To study the possible involvement of AnxA2 in breast cancer heterogeneity and cancer progression.

Muscle adaptation to sleeve gastrectomy: Potential role of nutritional supplementation and physical exercise.

Skeletal muscle is metabolically and functionally flexible and contractile under normal conditions. Obesity is a risk factor that causes metabolic disorders and reduces muscle contractility. Sleeve gastrectomy (SG) has been used for surgical correction of obesity.

Follicular dendritic cells.

Follicular dendritic cells (FDCs) are unique accessory immune cells that contribute to the regulation of humoral immunity. They are multitasker cells essential for the organization and maintenance of the lymphoid architecture, induction of germinal center reaction, production of B memory cells, and protection from autoimmune disorders. They perform their activities through both antigen-driven and chemical signaling to B cells.

L5 Spinal Nerve Axotomy Induces Distinct Electrophysiological Changes in Axotomized L5- and Adjacent L4-Dorsal Root Ganglion Neurons in Rats .

Peripheral neuropathic pain (PNP) is a major health problem for which effective drug treatment is lacking. Its underlying neuronal mechanisms are still illusive, but pre-clinical studies using animal models of PNP including the L5-spinal nerve axotomy (L5-SNA) model, suggest that it is partly caused by excitability changes in dorsal root ganglion (DRG) neurons. L5-SNA results in two DRG neuronal groups: (1) axotomized/damaged neurons in L5- plus some in L4-DRGs, and (2) ipsilateral L4-neurons with intact/uninjured fibers intermingling with degenerating L5-fibers.

Changes in expression of Kv7.5 and Kv7.2 channels in dorsal root ganglion neurons in the streptozotocin rat model of painful diabetic neuropathy.

Diabetic peripheral neuropathic pain (DPNP), the most debilitating complication of diabetes mellitus, is resistant to current therapy. The pathogenesis of DPNP is still elusive, but several mechanisms have been proposed including abnormal hyperexcitability of dorsal root ganglion (DRG) neurons. The underlying molecular mechanisms of such aberrant hyperexcitability are incompletely understood.

Cutaneous Aβ-Non-nociceptive, but Not C-Nociceptive, Dorsal Root Ganglion Neurons Exhibit Spontaneous Activity in the Streptozotocin Rat Model of Painful Diabetic Neuropathy .

Diabetic peripheral neuropathic pain (DPNP) is the most devastating complication of diabetes mellitus. Unfortunately, successful therapy for DPNP remains a challenge because its pathogenesis is still elusive. However, DPNP is believed to be due partly to abnormal hyperexcitability of dorsal root ganglion (DRG) neurons, but the relative contributions of specific functional subtypes remain largely unknown.

Mutual inter-regulation between iNOS and TGF-β1: Possible molecular and cellular mechanisms of iNOS in wound healing.

Abnormal wound healing with excessive scarring is a major health problem with socioeconomic and psychological impacts. In human, chronic wounds and scarring are associated with upregulation of the inducible nitric oxide synthase (iNOS). Recently, we have shown physiological regulation of iNOS in wound healing.

A possible role for inducible arginase isoform (AI) in the pathogenesis of chronic venous leg ulcer.

Chronic venous ulcer (CVU) is a major cause of chronic wounds of lower extremities and presents a significant financial and resource burden to health care systems worldwide. Defects in the vasculature, matrix deposition, and re-epithelialization are the main histopathological changes believed to impede healing. Supplementation of the amino acid arginine that plays a crucial role in the interactions that occur during inflammation and wound healing was proven clinically to improve acute wound healing probably through enhancing activity of inducible arginase (AI) locally in the wounds.

Hybridisation Study of Neuronal Neuropeptides Expression in Models of Mandibular Denervation with or without Inflammation: Injury Dependant Neuropeptide Plasticity.

Unlabelled: Neuronal expression of neuropeptides is altered following peripheral tissue injury associated with inflammation or nerve injury. This results in neuropathic pain with or without neurogenic inflammation which is a major health problem regularly seen in trigeminal neuralgia. Activation of the trigeminal system results in the release of vasoactive neuropeptides substance P and Calcitonin Gene-related Peptide (CGRP) which contribute to nociception, pain and neurogenic inflammation in injured tissues.

Cellular and physiological upregulation of inducible nitric oxide synthase, arginase, and inducible cyclooxygenase in wound healing.

Wound repair is regulated by overlapping cellular, physiological and biochemical events. Prostaglandins and nitric oxide have been a focus for inflammation research particularly since the discovery of their inducible isoforms nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). Study of the cellular expression of iNOS and COX-2 and arginase which competes with iNOS for its substrate, in an in vivo model of wound healing could reveal important roles for these enzymes in the physiological progression of wound repair.

Assessment of the cellular localisation of the annexin A2/S100A10 complex in human placenta.

The AnxA2/S100A10 complex has been implicated in various placental functions but although the localisation of these proteins individually has been studied, there is no information about the localisation of their complex in situ at the cellular level. Using the proximity ligation technique, we have investigated the in situ localisation of AnxA2/S100A10 complex in the placenta and have compared this with the location patterns of the individual proteins. High levels of expression of AnxA2/S100A10 complexes were observed in the amniotic membrane and in blood vessel endothelial cells.

Inflammation alters somatostatin mRNA expression in sensory neurons in the rat.

Proinflammatory neuropeptides, such as substance P and calcitonin gene-related peptide, are up-regulated in primary afferent neurons in acute and chronic inflammation. While these neuropeptides have been intensively studied, potentially anti-inflammatory and/or anti-nociceptive neuropeptides such as somatostatin (SS) have been less widely investigated. Endogenous somatostatin is thought to exert a tonic antinociceptive effect.

A model of periodontitis in the rat: effect of lipopolysaccharide on bone resorption, osteoclast activity, and local peptidergic innervation.

Objective: To establish and characterise a rat model of periodontitis that reiterates the features of human disease.

Methods: Periodontal inflammation was induced by a single injection of 10 microg liposaccharide (LPS) (Salmonella typhimurium) in 1 microl saline into rat mandibular gingiva at the buccomesial aspect of the second molar. Animals were killed after 3, 7 and 10 days, mandibles dissected and sectioned for histological and immunocytochemical analysis.

Sensory neuropeptide mRNA up-regulation is bilateral in periodontitis in the rat: a possible neurogenic component to symmetrical periodontal disease.

Periodontal disease is a common multifactorial chronic inflammatory disease in humans. In inflammatory conditions that are known to be associated with changes in nociception, such as arthritis, the neuronal expression of the proinflammatory neuropeptides, substance P and calcitonin gene-related peptide is altered. In this study the expression of these neuropeptides' mRNAs has been studied in an inflammatory model that shows no behavioural evidence of altered nociception.

Expression of nitric oxide synthase isoforms in human liver cirrhosis.

Several mediators of systemic vasodilatation in liver cirrhosis have been reported. Among these is nitric oxide (NO), which has been proposed as one of the main mediators. In this study, sera and liver biopsies were analysed from 15 patients with clinically and pathologically diagnosed liver cirrhosis.