Articles

Inflammation is a complex biological reaction induced by the alteration of tissue homeostasis, which occurs in response to the presence of a biological, chemical or physical agent in the body [1]. The acute inflammatory response is composed of an elaborate cascade of both proinflammatory and anti-inflammatory mediators, and balance between these mediators often determines the outcome after injury [2]. Generally during acute inflammation, cellular and molecular events and interactions reduce the risk of eventual injuries or infections. However, acute inflammation can become chronic, contributing to a variety of chronic inflammatory diseases [3]. Major micro circulatory events that occur during the inflammatory process include changes in vascular permeability, leukocyte recruitment and accumulation, and inflammatory mediator’s release [4]. 

A man I knew had an extreme allergy to poison ivy when he was a child. When he was about four-teen, he was hanging out with a group of his friends who dared him to eat some poison ivy. He did, and never got poison ivy again. Presumably, the ingestion of the allergen led to the development of immunity. This might be a pathway to eliminating allergies–ingest the allergen. For example, cutting up poison ivy leaves into small pieces and crushing them with a mortar and pestle should lead to some juice in the mortar. Allow that to evaporate and have a test subject ingest the resultant powder, which, like pollen, etc., could be compressed into a pill. Wait 48 hours, and then see if the subject gets a rash when a small, unimportant area of the body is exposed to poison ivy leaves–and have Ivy-Dry handy. This could be a way to eliminate allergies–ingestion of the allergen.

Antarctica is known for its extreme environmental conditions. It is the best model to study multiple stress factors at a time on human physiological responses. Although the coastal Antarctica is on Sea level but the Antarctic plateau or pole at high altitude. Since Antarctica is also becoming tourist site it is pertinent to have a proper understanding of altitude induced illnesses. In this review we have described the human acclimatization process at high altitude of Antarctic polar plateu and South Pole. The review also highlighted the symptoms, clinical features and prevention of altitude induced diseases. 

Venous Thromboembolism (VTE) is a multifactorial disease that is influenced by individual genetic background and various environmental factors, high altitude (HA) being the one. HA exposure may cause release of several damage associated molecular patterns (DAMPs), which act as ligand for various immune receptors. Previous studies on western population involving SNPs analysis of TLRs demonstrated that TLRs are involved in development and progression of several cardiovascular diseases. But, no such study has been done in Indian population in context of HA exposure. TLRs, being receptors play a significant role in manifestation and elimination of diseases by recognition of specific ligands and downstream signal transduction therefore; the genetic variation in TLRs could be implicated for imparting varying response of individuals to discrete diseases. Therefore, in accordance with it, in present study changes in protein structures of TLR2 and TLR4 due to presence of SNP were accessed by in-silico tools to observe whether the mutation has effect on protein structure and integrity which further influencing its function. The results showed that SNP harbouring protein has decreased functional pockets, thus may be protective for disease. Taking this lead further to genotypic level, first time association between Toll-like receptor genes polymorphism and risk of high altitude induced venous thrombosis is analyzed in Indian population by PCR RFLP method. Though the result showed initial trend that TLR2 and TLR9 SNP are monomrphic in distribution and for TLR4 there was no significant difference in distribution of SNP between healthy and HA-DVT group, these SNPs have potential to be used as susceptibility markers if studied in large population size. 

Mast cells play a central role in the genesis and modulation of allergic and inflammatory responses. The general aim of the present work was to study the interaction between mast cells and the most common additives approved for use in foods. Dose-response studies about the effect of the main food additives (tartrazine, sodium bisulphite and sodium benzoate) on mast cell degranulation were carried out. Rat peritoneal mast cells were incubated with: 1) buffer solution or 2) stimulus. The stimuli were tartrazine, sodium benzoate, sodium bisulphite and the calcium ionophore A23187. A23187 was used as a reference mast cell secretagogue. Different doses and combinations of food additives were used. The viability of the mast cells was evaluated with trypan blue. In the incubation solutions, the release of β-hexosaminidase was quantified by colorimetric reaction and ELISA plate reader. The remaining β-hexosaminidase concentration (not released) was studied in the cells after the incubations, and morphology of the mast cells was analyzed by light microscopy with toluidine blue stain. The food additives tartrazine, sodium benzoate and sodium bisulphite did not stimulate the release of β-hexosaminidase from mast cells at any of the concentrations used. In contrast, tartrazine at concentrations of 0.1 μM and 1 μM, and sodium benzoate and sodium bisulphite at concentrations of 0.1 μM, 1 μM, 10 μM and 100 μM, significantly inhibited the basal release of β-hexosaminidase from mast cells. Considering these findings, we decided to determine the effect of these additives on the degranulation of mast cells induced by the calcium ionophore A23187. Sodium bisulphite inhibited mast cell activation induced by the calcium ionophore A23187 in this experimental model. The present study demonstrates that food additives of usual permitted use do not stimulate basal degranulation of mast cells in an in vitro model of peritoneal mast cells and that the additive sodium bisulphite inhibit mast cell activation induced by intracellular calcium increase. This food additive could represent an interesting alternative in the prevention of pathologies mediated by mast cells, as well as in the field of nutritional biochemistry.

There is evidence that complement components induce cell migration in mesenchymal stem cells and regulate cytokine production in osteoblastic cells thus playing a regulatory role in normal bone formation. The aim of the present study was to investigate the involvement of complement system in the differentiation of bone marrow cells in complement-depleted model of rheumatoid arthritis (RA). Arthritis was induced by intraarticular injection of zymosan in cobra venom factor (CVF)-treated mice depleted of functional complement. The expression of different markers by bone marrow [1], on fibroblasts (CD29), mesenchymal cells (CD105), dendritic cells (CD14, CD86), osteoclasts (CD265), cells expressing Dectin1 (CD369) and megakaryocytes (CD62P) was determined by flowcytometry. The lack of functional complement activity at the point of arthritis initiation (day 3) lead to an increase of fibroblast and megakaryocyte populations, to a decrease of mature and dectin1 positive populations, while the number of mesenchymal cells was not changed, all compared to arthritic mice. Immunohistochemical staining showed that low complement activity diminished arthritis-induced generation of megakaryocytes and platelets in BM. Chronic inflammation during erosive conditions such as rheumatoid arthritis, leads to dysregulated differentiation and prolifеration of bone cells, inflammation of synovial membrane and bone marrow, and degradation of cartilage and bone. Present results point that the lack of functional complement changed the ratio between different cell populations that can be used for determining the development and stage of rheumatoid arthritis and can help finding of new therapeutic approaches.

Sojourn to high altitude may affect various human systems if proper acclimatization not followed. If acclimatization failed, sojourners may suffer with high altitude sickness such as acute mountain sickness (AMS), high altitude pulmonary edema (HAPE) and high altitude cerebral edema (HACE). Although a sojourner’s tolerance to high altitude hypoxia varies according to differences in physiology and physical conditioning. Acute mountain sickness may cause headache, insomnia, dizziness, nausea, vomiting and fatigue. While HACE is more serious stage where brain swelling occurs and it is potentially fatal. A sojourner with HACE may experience confusion, amnesia, delusions, and loss of consciousness. Staying in high altitude (above 9000 feet) environment poses low oxygen supply (hypobaric hypoxia) to the different body organs including brain.

Background: C-type natriuretic peptide (CNP) was isolated from porcine brain and is a 22-amino acid peptide which belongs to the natriuretic peptide (NP) family. Even though this peptide shares structural similarity to other endogenous NPs including atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) its receptor selectivity is different from other NPs. The present study was undertaken to investigate the expression of C-type natriuretic peptide (CNP) and its specific guanylyl cyclase (GC)-coupled receptor in the granulosa cells of the pig ovarian follicle. Results: Specific 125I-[Tyr0]-CNP(1-22) binding sites were localized in the granulosa cell layer of the ovarian follicle with an apparent dissociation constant (Kd>) and a maximal binding capacity (Bmax) of 1.41±0.39 nM and 2.75±0.65 fmol/mm2 respectively. Binding of 125I-[Tyr0]-CNP(1-22) to these sites was also prevented by atrial natriuretic peptide (ANP(1-28)), brain natriuretic peptide (BNP(1-26)) and des[Gln18,Ser19,Gly20, Leu21,Gly22] ANP(4-23) (C-ANP). Production of 3’,5’-cyclic guanosine monophosphate (cGMP) by particulate GC in the granulosa cell membranes was stimulated by natriuretic peptides (NPs) with a rank order of potency of CNP(1-22)>>BNP(1-26)>ANP(1-28). HS-142-1, a selective antagonist of the two recognized GC-coupled NPRs, inhibited CNP(1-22)-stimulated cGMP production in granulosa cell membranes in a dose-dependent manner. Also mRNAs for all three recognized NPRs were detected in granulosa cells using reverse transcriptase-polymerase chain reaction (RT-PCR). Serial dilution curves of granulosa cell extracts were parallel to the standard curve of synthetic CNP. Conclusion: These results indicate that CNP and its specific receptor are expressed in the granulosa cells of the pig ovary, and suggest that CNP may be a local autocrine and/or paracrine regulator via activation of its specific GC-coupled receptor, NPR-B.

In the actual medical therapy of BPH, we can see: antibiotics, alpha blockers, 5-ARI, fitotherapeutics/natural products (Serenoa repens) with different which display clinical activities and other molecules such as FANS (local or systemic dosage forms) cortisones and others. Relationship between immune systems and chronic prostatitis are strictly involved in BPH progression. A vicious cycle that involve chronic flogosis, tissue remodeling, grow factors, inhibition of apoptosis, and other phenomena. Observing BPH pathogenesis under an immunologic point of view make possible to search new pharmacological strategies, to improve actual therapy. The aim of this work is to observe some relevant literature in our opinion related the management of BHP and its progression under a pharmaceutical and immunological point of view. A deep knowledge in the pharmaceutical properties of some molecules (antimicrobials, anti-phlogosis agents, Anti-androgenic agents, alpha blockers, 5-ARI and other treatments, techniques, interventions or instruments) can help the physicians to pick the right choice.

From biomedical literature “autism disorder are involved in young patient, that we have abnormalities (Imaging, histology) in some brain areas, and a comples symptomatology. Genetic and environment can produce some unbalances in brain grow and immunitary situation is involved. Apoptotic signal contribute in brain growth and immunologic shock can unbalance the environment producing abnormalities.” We can see that some pharmacological molecules are been introduced in therapy in some brain pathologies with a specific mechanism: modulating the immune systems. We can see that some systemic immune modifications can unbalance this systems producing pharmacological effect in local place (as Brain). We can observe this phenomena like a kind of toxicity that can be deeply investigate to discover new Pharmacological strategies. Aim of this work is to observe this kind of pathologies under a specific immune-toxicological aspect. We think that in this field are needed deeply new approach in order to adequately focus this kind of disorder. A different way to set this kind of pathologies can help in searching new pharmacological strategies.