Matematičeskaja model\u27 gorizontal\u27nogo broska-razbega

Utvrđene su kvantitativne relacije između brzine zaleta i napadnog ugla, u uslovima standardnog rastojanja između težišta tela i tačke oslonca, kod skoka u dalj. Određuje se konkretne vrednosti napdanog ugla za svaku brzinu zaleta u aktualnom rasponu. U principu vrednosti napadnog ugla gravitira ka vrednosti pravog ugla koliko se brzina zaleta smanjuje, odnosno ka polovini pravog ugla ukoliko se brzina zaleta povećava.The study establishes the quantitative relations between the run-up and the distance of body\u27s gravity center from the jump-off center at the moment of separation of the grounded. While the point of contract of the body with the ground is falling ahead of the projection of body\u27s gravity center, certain amount of running speed acts in the vertical direction so that the height of the jump is determined not only by the take off and arm swing, cet also by the prior run. This part of the speed of run which is thereby the prior run. This part of the spobud if the attack angle is equal half the right angle. On the other hand, the closer the attack angle with standard distance between the center of gravity is at the moment of jump. In order to calculate the existing quantitative relations among relevant parameters of horizontal trajectory of body flight an appropriate computer program was done. On the basis of computer results, quantitative relations were established between the speed of run an the attack angle with standard distance between the center of gravity and the point of support. The study gives concrete values of the attack angle for each speed of run in the actual range. Generally speaking, value of the attack angle gravities towards the value of the right angle if the speed of run decreases, it gravitates toward half the right angle if the speed of run increases

Rb-Mediated Neuronal Differentiation through Cell-Cycle–Independent Regulation of E2f3a

It has long been known that loss of the retinoblastoma protein (Rb) perturbs neural differentiation, but the underlying mechanism has never been solved. Rb absence impairs cell cycle exit and triggers death of some neurons, so differentiation defects may well be indirect. Indeed, we show that abnormalities in both differentiation and light-evoked electrophysiological responses in Rb-deficient retinal cells are rescued when ectopic division and apoptosis are blocked specifically by deleting E2f transcription factor (E2f) 1. However, comprehensive cell-type analysis of the rescued double-null retina exposed cell-cycle–independent differentiation defects specifically in starburst amacrine cells (SACs), cholinergic interneurons critical in direction selectivity and developmentally important rhythmic bursts. Typically, Rb is thought to block division by repressing E2fs, but to promote differentiation by potentiating tissue-specific factors. Remarkably, however, Rb promotes SAC differentiation by inhibiting E2f3 activity. Two E2f3 isoforms exist, and we find both in the developing retina, although intriguingly they show distinct subcellular distribution. E2f3b is thought to mediate Rb function in quiescent cells. However, in what is to our knowledge the first work to dissect E2f isoform function in vivo we show that Rb promotes SAC differentiation through E2f3a. These data reveal a mechanism through which Rb regulates neural differentiation directly, and, unexpectedly, it involves inhibition of E2f3a, not potentiation of tissue-specific factors

Chronic Lymphocytic Leukemia Cells in a Lymph Node Microenvironment Depict Molecular Signature Associated with an Aggressive Disease

Chronic lymphocytic leukemia (CLL) cells survive longer in vivo than in vitro, suggesting that the tissue microenvironment provides prosurvival signals to tumor cells. Primary and secondary lymphoid tissues are involved in the pathogenesis of CLL, and the role of these tissue microenvironments has not been explored completely. To elucidate host-tumor interactions, we performed gene expression profiling (GEP) of purified CLL cells from peripheral blood (PB; n = 20), bone marrow (BM; n = 18), and lymph node (LN; n = 15) and validated key pathway genes by real-time polymerase chain reaction, immunohistochemistry and/or TCL1 trans-genic mice. Gene signatures representing several pathways critical for survival and activation of B cells were altered in CLL cells from different tissue compartments. Molecules associated with the B-cell receptor (BCR), B cell-activating factor/a proliferation-inducing ligand (BAFF/APRIL), nuclear factor (NF)-κB pathway and immune suppression signature were enriched in LN-CLL, suggesting LNs as the primary site for tumor growth. Immune suppression genes may help LN-CLL cells to modulate antigen-presenting and T-cell behavior to suppress antitumor activity. PB CLL cells overexpressed chemokine receptors, and their cognate ligands were enriched in LN and BM, suggesting that a chemokine gradient instructs B cells to migrate toward LN or BM. Of several chemokine ligands, the expression of CCL3 was associated with poor prognostic factors. The BM gene signature was enriched with antiapoptotic, cytoskeleton and adhesion molecules. Interestingly, PB cells from lymphadenopathy patients shared GEP with LN cells. In Eμ-TCL1 transgenic mice (the mouse model of the disease), a high percentage of leukemic cells from the lymphoid compartment express key BCR and NF-κB molecules. Together, our findings demonstrate that the lymphoid microenvironment promotes survival, proliferation and progression of CLL cells via chronic activation of BCR, BAFF/APRIL and NF-κB activation while suppressing the immune response

Human tumour-associated cell adhesion protein MN/CA IX: identification of M75 epitope and of the region mediating cell adhesion

MN/CA IX is a cell surface protein, strongly associated with several types of human carcinomas. It exerts activity of carbonic anhydrase and capacity of binding to cell surface receptors. In the present work, we used affinity purified MN/CA IX protein to demonstrate that the cells adhere to immobilized MN/CA IX and that the monoclonal antibody M75 abrogates cell attachment to MN/CA IX. Using synthetic oligopeptides, we identified M75 epitope and located it in the proteoglycan domain, which contains a sixfold tandem repeat of six amino acids GEEDLP. From phage display library of random heptapeptides we identified and chemically synthesized those which compete for the epitope with M75 and inhibit adhesion of cells to MN/CA IX. These heptapeptides might serve as lead compounds for drug design. © 2000 Cancer Research Campaig

COMPARISON OF HEART RATE VARIABILITY IN PATIENTS WITH PANIC DISORDER DURING COGNITIVE BEHAVIORAL THERAPY PROGRAM

Background: Many authors suggest that there is low reactivity of autonomic nervous system and reduced heart rate variability in patients with panic disorder. The patients are therefore exposed to increased cardiac mortality. Power spectral analysis is a successful tool in detecting autonomic instabilities in many disorders. Subjects and methods: The aim of our study is to monitor the activity of the autonomic nervous system through heart rate variability measured in the beginning and end of a therapeutic cognitive behavioral therapy (CBT) program in patients with panic disorder. We measured 31 patients with panic disorder in the beginning (1st measurement) and end of a therapeutic CBT program (2nd measurement). The autonomic nervous system (ANS) has been evaluated in three positions (supine – standing – supine). The evaluated parameters of the HRV linear analysis were: RR interval, HF, LF, VLF band and VLF + LF / HF ratio. Results: Spectral activity in the very low frequency band was significantly higher in the 2nd measurement compared to the 1st measurement in the standing position. The ratio of the spectral activity at lower frequencies (VLF+LF) to high frequency (HF) was significantly lower in the supine position. Conclusion: This study demonstrated an improvement of neurocardiac control regulation after a therapeutic CBT program in patients suffering from panic disorder

Loss of Dnmt3b function upregulates the tumor modifier Ment and accelerates mouse lymphomagenesis

DNA methyltransferase 3B (Dnmt3b) belongs to a family of enzymes responsible for methylation of cytosine residues in mammals. DNA methylation contributes to the epigenetic control of gene transcription and is deregulated in virtually all human tumors. To better understand the generation of cancer-specific methylation patterns, we genetically inactivated Dnmt3b in a mouse model of MYC-induced lymphomagenesis. Ablation of Dnmt3b function using a conditional knockout in T cells accelerated lymphomagenesis by increasing cellular proliferation, which suggests that Dnmt3b functions as a tumor suppressor. Global methylation profiling revealed numerous gene promoters as potential targets of Dnmt3b activity, the majority of which were demethylated in Dnmt3b–/– lymphomas, but not in Dnmt3b–/– pretumor thymocytes, implicating Dnmt3b in maintenance of cytosine methylation in cancer. Functional analysis identified the gene Gm128 (which we termed herein methylated in normal thymocytes [Ment]) as a target of Dnmt3b activity. We found that Ment was gradually demethylated and overexpressed during tumor progression in Dnmt3b–/– lymphomas. Similarly, MENT was overexpressed in 67% of human lymphomas, and its transcription inversely correlated with methylation and levels of DNMT3B. Importantly, knockdown of Ment inhibited growth of mouse and human cells, whereas overexpression of Ment provided Dnmt3b+/+ cells with a proliferative advantage. Our findings identify Ment as an enhancer of lymphomagenesis that contributes to the tumor suppressor function of Dnmt3b and suggest it could be a potential target for anticancer therapies

From 2D leg kinematics to 3D full-body biomechanics-the past, present and future of scientific analysis of maximal instep kick in soccer

Biomechanics investigation on soccer kicking has a relatively long history, yet the body of knowledge is still small. This paper reviews articles published from 1960s to 2011, summarizing relevant findings, research trends and method development. It also discusses challenges faced by the field. The main aim of the paper is to promote soccer kicking studies through discussions on problem solving in the past, method development in the present, and possible research directions for the future

Endosialin expression in relation to clinicopathological and biological variables in rectal cancers with a Swedish clinical trial of preoperative radiotherapy

<p>Abstract</p> <p>Background</p> <p>The importance of changes in tumour-associated stroma for tumour initiation and progression has been established. Endosialin is expressed in fibroblasts and pericytes of blood vessels in several types of tumours, and is involved in the progression of colorectal cancer. In order to see whether endosialin was related to radiotherapy (RT) response, and clinicopathological and biological variables, we investigated endosialin expression in rectal cancers from the patients who participated in a Swedish clinical trial of preoperative RT.</p> <p>Methods</p> <p>Endosialin was immunohistochemically examined in normal mucosa, including distant (<it>n </it>= 72) and adjacent (<it>n </it>= 112) normal mucosa, and primary tumours (<it>n </it>= 135). Seventy-three of 135 patients received surgery alone and 62 received additional preoperative RT.</p> <p>Results</p> <p>Endosialin expression in the stroma increased from normal mucosa to tumour (<it>p </it>< 0.0001) both in RT and non-RT group. In the RT group, endosialin expression in the stroma was positively associated with expression of cyclooxygenase-2 (Cox-2) (<it>p </it>= 0.03), p73 (<it>p </it>= 0.01) and phosphates of regenerating liver (PRL) (<it>p </it>= 0.002). Endosialin expression in the tumour cells of both in the RT group (<it>p </it>= 0.01) and the non-RT group (<it>p </it>= 0.06) was observed more often in tumours with an infiltrative growth pattern than in tumours with an expansive growth pattern. In the RT group, endosialin expression in tumour cells was positively related to PRL expression (<it>p </it>= 0.02), whereas in the non-RT group, endosialin expression in tumour cells was positively related to p73 expression (<it>p </it>= 0.01).</p> <p>Conclusions</p> <p>Endosialin expression may be involved in the progression of rectal cancers, and was related to Cox-2, p73 and PRL expression. However, a direct relationship between endosialin expression and RT responses in patients was not found.</p

Carbonic anhydrase XII is a marker of good prognosis in invasive breast carcinoma

Hypoxia and pH influence gene expression in tumours, and it is becoming increasingly clear that the pattern of genes expressed by a tumour determines its growth and survival characteristics. Hypoxia-inducible factor-1 (HIF-1) is a key mediator of the cellular response to hypoxia and high HIF-1 expression has been identified as a poor prognostic factor in tumours. Recently, we identified the tumour-associated carbonic anhydrases (CA), CA9 and CA12 as hypoxia-inducible in tumour cell lines. Furthermore, we identified CA IX to be a poor prognostic factor in breast cancer. The aim of this study was to assess the prognostic significance of CA XII. CA XII expression was studied by immunohistochemistry in a series of 103 cases of invasive breast cancer and any association with recognised prognostic factors or relation with the outcome was examined. CA XII expression was present in 77 out of 103 (75%) cases and was associated with lower grade (P=0.001), positive estrogen receptor status (P&lt;0.001), and negative epidermal growth factor receptor status (P&lt;0.001). Furthermore, although CA XII expression was associated with an absence of necrosis (P&lt;0.001), expression of CA XII in some high-grade tumours was induced in regions directly adjacent to morphological necrosis. Additionally, using univariate analysis, CA XII positive tumours were associated with a lower relapse rate (P=0.04) and a better overall survival (P=0.01). In conclusion, CA XII expression is influenced both by factors related to differentiation and hypoxia in breast cancer in vivo and CA XII expression is associated with a better prognosis in an unselected series of invasive breast carcinoma patients