Medicina-lithuania 

About: Medicina-lithuania is an academic journal published by Multidisciplinary Digital Publishing Institute. The journal publishes majorly in the area(s): Medicine & Population. It has an ISSN identifier of 1010-660X. It is also open access. Over the lifetime, 4172 publications have been published receiving 31885 citations.

Effects of beta-glucans on the immune system.

Abstract: Summary. β -Glucans are naturally occurring polysaccharides. These glucose polymers are constituents of the cell wall of certain pathogenic bacteria and fungi. The healing and immunostimulating properties of mushrooms have been known for thousands of years in the Eastern countries. These mushrooms contain biologically active polysaccharides that mostly belong to group of β -glucans. These substances increase host immune defense by activating complement system, enhancing macrophages and natural killer cell function. The induction of cellular responses by mushroom and other β -glucans is likely to involve their specific interaction with several cell surface receptors, as complement receptor 3 (CR3; CD11b/CD18), lactosylceramide, selected scavenger receptors, and dectin-1 ( β GR). β -Glucans also show anticarcinogenic activity. They can prevent oncogenesis due to the protective effect against potent genotoxic carcinogens. As immunostimulating agent, which acts through the activation of macrophages and NK cell cytotoxicity, β -glucan can inhibit tumor growth in promotion stage too. Antiangiogenesis can be one of the pathways through which β -glucans can reduce tumor proliferation, prevent tumor metastasis. β -Glucan as adjuvant to cancer chemotherapy and radiotherapy demonstrated the positive role in the restoration of hematopiesis following by bone marrow injury. Immunotherapy using monoclonal antibodies is a novel strategy of cancer treatment. These antibodies activate complement system and opsonize tumor cells with iC3b fragment. In contrast to microorganisms, tumor cells, as well as other host cells, lack β -glucan as a surface component and cannot trigger complement receptor 3-dependent cellular cytotoxicity and initiate tumor-killing activity. This mechanism could be induced in the presence of β -glucans.

Antibiotic resistance mechanisms of clinically important bacteria.

Abstract: Bacterial resistance to antimicrobial drugs is an increasing health and economic problem. Bacteria may be innate resistant or acquire resistance to one or few classes of antimicrobial agents. Acquired resistance arises from: (i) mutations in cell genes (chromosomal mutation) leading to cross-resistance, (ii) gene transfer from one microorganism to other by plasmids (conjugation or transformation), transposons (conjugation), integrons and bacteriophages (transduction). After a bacterium gains resistance genes to protect itself from various antimicrobial agents, bacteria can use several biochemical types of resistance mechanisms: antibiotic inactivation (interference with cell wall synthesis, e.g., β-lactams and glycopeptide), target modification (inhibition of protein synthesis, e.g., macrolides and tetracyclines; interference with nucleic acid synthesis, e.g., fluoroquinolones and rifampin), altered permeability (changes in outer membrane, e.g., aminoglycosides; new membrane transporters, e.g., chloramphenicol), and “bypass” metabolic pathway (inhibition of metabolic pathway, e.g., trimethoprim-sulfamethoxazole).

Photodynamic therapy: mechanism of action and ways to improve the efficiency of treatment.

Abstract: Photodynamic therapy is treatment modality involving the administration of photosensitizing compound, which selectively accumulates in the hyperproliferative target cells followed by local irradiation with visible light of lesion. Eventually target tissue will be damaged by necrosis and apoptosis. Action of treatment is described from absorption of light till damage of tissue. Several rationale proposals to increase the efficiency of described treatment modality are suggested: to evaluate the antiproliferative activity of new coming photosensitizers, to combine photosensitization with other treatment modalities in molecular level, exploring mechanism of apoptosis, to increase the efficiency of treatment by combination with ionizing radiation, hyperthermia or ligation of peripheral benzodiazepine receptors.

Motor control theories and their applications

Abstract: We describe several infl uential hypotheses in the field of motor control including the equilibrium-point (referent confi guration) hypothesis, the uncontrolled manifold hypothesis, and the idea of synergies based on the principle of motor abundance. The equilibrium-point hypothesis is based on the idea of control with thresholds for activation of neuronal pools; it provides a framework for analysis of both voluntary and involuntary movements. In particular, control of a single muscle can be adequately described with changes in the threshold of motor unit recruitment during slow muscle stretch (threshold of the tonic stretch reflex). Unlike the ideas of internal models, the equilibrium-point hypothesis does not assume neural computations of mechanical variables. The uncontrolled manifold hypothesis is based on the dynamic system approach to movements; it offers a toolbox to analyze synergic changes within redundant sets of elements related to stabilization of potentially important performance variables. The referent confi guration hypothesis and the principle of abundance can be naturally combined into a single coherent scheme of control of multi-element systems. A body of experimental data on healthy persons and patients with movement disorders are reviewed in support of the mentioned hypotheses. In particular, movement disorders associated with spasticity are considered as consequences of an impaired ability to shift threshold of the tonic stretch reflex within the whole normal range. Technical details and applications of the mentioned hypo theses to studies of motor learning are described. We view the mentioned hypotheses as the most promising ones in the field of motor control, based on a solid physical and neurophysiological foundation.

Vitamin D Deficiency: Consequence or Cause of Obesity?

Abstract: Obesity is defined as an excess amount of body fat and represents a significant health problem worldwide. High prevalence of vitamin D (VD) deficiency in obese subjects is a well-documented finding, most probably due to volumetric dilution into the greater volumes of fat, serum, liver, and muscle, even though other mechanisms could not completely be excluded, as they may contribute concurrently. Low VD could not yet be excluded as a cause of obesity, due to its still incompletely explored effects through VD receptors found in adipose tissue (AT). VD deficiency in obese people does not seem to have consequences for bone tissue, but may affect other organs, even though studies have shown inconsistent results and VD supplementation has not yet been clearly shown to benefit the dysmetabolic state. Hence, more studies are needed to determine the actual role of VD deficiency in development of those disorders. Thus, targeting lifestyle through healthy diet and exercise should be the first treatment option that will affect both obesity-related dysmetabolic state and vitamin D deficiency, killing two birds with one stone. However, VD supplementation remains a treatment option in individuals with residual VD deficiency after weight loss.