Ergoreflex: The essence and mechanisms

Physical load increases sympathetic nervous activity, which results in an increased cardiac output, constriction of peripheral vessels, and elevated systemic blood pressure. These changes are outcomes of two mechanisms: the central command from cerebral structures that trigger voluntary movements to activate the vasomotor center and the reflexes initiated by mechanical and metabolic changes in a working muscle. The latter mechanism of the sympathetic system activation is termed ergoreflex. The main effects of ergoreflex on the indices of systemic hemodynamics are the following: activation of mechanosensitive afferents mainly leads to inhibition of the tonic vagal effects on the heart, which explains the rapid increase in heartbeats upon loading; activation of chemosensitive afferents comes with some delay in pace with metabolite accumulation in muscles and leads to an increase in efferent sympathetic activity and a rise in blood pressure. The metabolic reflex effect is particularly high in the case of muscle fatigue. This review deals with the mechanisms underlying the ergoreflex and their adaptation to hypodynamia, physical training, and some pathologies.     

Comparison of the aerobic performance of leg and arm muscles in cross-country skiers

In the last fifteen years, a trend has appeared in cross-country ski racing to increase the use of double poling and, therefore, to increase the load on the shoulder girdle (arm) muscles. The purpose of this study was to compare the aerobic performance of elite cross-country skiers in incremental running (treadmill) and double poling (with manual ski ergometer) tests to exhaustion. Four junior cross-country skiers and four biathletes ( $ \dot V_{O_{2max} } $ = 70 (66?C72) mL/min per kg body weight) participated in the experiment. In the double poling test, the lactate concentration increased more rapidly than in the running test, and the peak oxygen consumption ( $ \dot V_{O_{2peak} } $ ) in the double poling test was 88 (84?C93)% of the maximal oxygen consumption ( $ \dot V_{O_{2max} } $ ) in the running test. The relative anaerobic threshold, which characterizes the relative level of current aerobic performance, in the double poling test was significantly lower than in the running test (79 (57?C83)% vs 94 (90?C98)%, respectively). On the basis of these data, it can be concluded that the main reserve for a further increase in the aerobic performance of cross-country skiers and biathletes is the increase in the aerobic capacity of arm and trunk muscles.     

Aerobic performance: role of oxygen delivery and utilization, glycolytic flux

Oxygen delivery to muscle, its consumption and glycolytic flux, all of each affect and restrict aerobic performance, are discussed. Energy supply of intensive exercise till exhaustion lasting 3 to 4 min is provided mainly by oxidative metabolism, simultaneously glycolytic flux may be increased considerably. Other conditions being equal, capacity of oxygen delivery determines oxygen partial pressure in myoplasm of exercising/contracting muscle. With PO2 in myoplasm increasing from 0 to 1-2 mm Hg oxygen consumption (VO2) in mitochondria enhances dramatically, with further increase of PO2 its rise slows down. At the ascending part of VO2-PO2 relationship for mitochondria the increase of VO2 is noticeably restricted by oxygen delivery to contracting muscle. When PO2 approaches plateau of the VO2-PO2 relationship, an increase of VO2 is restricted by mitochondria capacity to accumulate oxygen and augmented oxygen delivery will not lead to a significant increase of muscle VO2. On the other hand considerable accumulation of glycolytic metabolites in contracting muscle causes a decrease of contractility which in its turn may restrict aerobic performance. Noteworthy no strict relationship between glycolytic flux and PO2 in myoplasm exists. That is why correct evaluation of factors limiting aerobic performance presupposes simultaneous evaluation of both glycolytic flux and oxygen consumption in muscle which in its turn depends on oxygen delivery to mitochondria and its utilization.     

Species loss of stoneflies (Plecoptera) in the Czech Republic during the 20th century

1. Rapid expansion and intensification of anthropogenic activities in the 20th century has caused profound changes in freshwater assemblages. Unfortunately, knowledge of the extent and causes of species loss (SL) is limited due to the lack of reliable historical data. An unusual data set allows us to compare changes in the most sensitive of aquatic insect orders, the Plecoptera, at some 170 locations in the Czech Republic between two time periods, 1955–1960 and 2006–2010. Historical data (1890–1911) on assemblages of six lowland rivers allow us to infer even earlier changes. 2. Regional stonefly diversity decreased in the first half of the 20th century. Streams at lower altitudes lost a substantial number of species, which were never recovered. In the second half of the century, large‐scale anthropogenic pressure caused SL in all habitats, leading to a dissimilarity of contemporary and previous assemblages. The greatest changes were found at sites affected by organic pollution and a mixture of organic pollution and channelisation or impoundment. Colonisation of new habitats was observed in only three of the 80 species evaluated. 3. Species of moderate habitat specialisation and tolerance to organic pollution were most likely to be lost. Those with narrow specialisations in protected habitats were present in both historical and contemporary collections. 4. Contemporary assemblages are the consequence of more than a 100 years of anthropogenic impacts. In particular, streams at lower altitude and draining intensively exploited landscapes host a mere fragment of the original species complement. Most stonefly species are less frequently present than before, although their assemblages remain almost intact in near‐natural mountain streams. Our analyses demonstrate dramatic restriction of species ranges and, in some cases, apparent changes in altitudinal preference throughout the area.     

Downregulation of RBSP3/CTDSPL, NPRL2/G21, RASSF1A, ITGA9, HYAL1, and HYAL2 in non-small cell lung cancer

Chromosomal and genome abnormalities of 3p are frequent in many epithelial tumors, including lung cancer. Several critical regions with a high frequency of hemi-and homozygous deletions in tumors are known for 3p, and more than 20 cancer-related genes occur in 3p21.3. Quantitative real-time PCR was used to measure the mRNA level for tumor-suppressor and candidate genes of 3p21.3 (RBSP3/CTDSPL, NPRL2/G21, RASSF1A, ITGA9, HYAL1, and HYAL2) in major types of non-small cell lung cancer (NSCLC): squamous cell lung cancer (SCC) and lung adenocarcinoma (AC). A significant (2-to 100-fold) and frequent (44–100%) decrease in mRNA levels was observed in NSCLC. The mRNA level decrease and its frequency depended on the histological type of NSCLC for all genes. The downregulation of RASSF1A and ITGA9 was significantly associated with AC progression; the same tendency was observed for RBSP3/CTDSPL, NPRL2/G21, HYAL1, and HYAL2. In SCC, the downregulation of all genes was not associated with the clinical stage, tumor cells differentiation, and metastasis in lymph nodes. The RBSP3/CTDSPL, NPRL2/G21, ITGA9, HYAL1, and HYAL2 mRNA levels significantly (5-to 13-fold on average) decreased at a high frequency (83–100%) as early as SCC stage I. Simultaneous downregulation of all six genes was observed in some tumor samples and was independent of the gene position in 3p21.3 and the functions of the protein products. The Spearman correlation coefficient r _s was 0.63–0.91, p < 0.001. The highest r _s values were obtained for gene pairs ITGA9-HYAL2 and HYAL1-HYAL2, whose products mediate cell-cell adhesion and cell-matrix interactions; coregulation of the genes was assumed on this basis. Both genetic and epigenetic mechanisms proved to be important for downregulation of RBSP3/CTDSPL and ITGA9. This finding supported the hypothesis that the cluster of cancerrelated genes in the extended 3p21.3 locus is simultaneously inactivated during the development and progression of lung cancer and other epithelial tumors. A significant and frequent decrease in the mRNA level of the six genes in SCC could be important for developing specific biomarker sets for early SCC diagnosis and new approaches to gene therapy of NSCLC.     

Clinical experience in using 18F-FDG PET in the staging and restaging of malignant lymphomas

The present study was undertaken to determine the diagnostic accuracy of positron emission tomography (PET) in the staging and restaging of malignant lymphomas. For determination of the extent of a neoplastic process, complex radiation examination was conducted in 67 patients with malignant lymphomas. In 12 (17.9%) cases, the stage of the disease was changed, as evidenced by PET. There is evidence that the technique is of high diagnostic accuracy in detecting malignancies of l ymph nodes, skeletal system, and parenchymatous organs in lymphoproliferative diseases.     

Reorganization of mitotic apparatus in the etoposide-treated CHO-K1 cells precedes apoptotic death

In a culture of CHO-K1 cells, etoposide (1 h, 25 μM) has been shown to produce interphase arrest, after which the cells resume mitotic division and, after some time, are submitted to apoptotic death. Accumulation of apoptotic cells in the culture follows a gradual increase in the number of multipolar mitoses. Our findings provide the first evidence for differences in the pattern of immunofluorescent staining of multipolar mitotic spindle microtubules with antibodies to α-tubulin, acetylated α-tubulin, and tyrosinated α-tubulin in mitotic cells dividing in the period preceding apoptosis. Moreover, some parts of the multipolar mitotic spindle can differ by the presence of antigenic determinants accessible to anti-tyrosinated α-tubulin antibodies. These abnormalities of the mitotic apparatus are aggravated immediately before the increase in the number of cells submitted to apoptosis. Our data have also shown that some cells pass through at least two mitotic cycles prior to a sharp increase in the number of apoptotic cells in the cell culture.     

Ultrastructure of the capillaries of nerve tissue transplants growing in the anterior chamber of the eye

Blood capillaries have been studied electron microscopically in the areas of grafts (rat embryonal hippocamp and septal cerebral parts transplanted to mature rats) containing mainly nervous, glial or connective tissue cells. Certain differences in the capillary wall structure have been revealed. In areas with a great concentration of nervous cells, the blood capillaries are characterized by a dense arrangement of cellular elements in their walls, a continuous layer of the glial end-feet, this is specific for the CNS capillaries providing the blood--brain barrier. In peripheral area of the grafts, where glial elements predominate, the capillaries have loose arrangement of the mural cellular elements, great endotheliocyte activity, thick connective tissue tunic, lack of a dense glial surrounding. These characteristics make dubious the statement whether these capillaries possess the blood--brain barrier function. In places where connective tissue cells make aggregates, the capillaries do not possess the barrier properties because of perforations and fenestrae in endothelium and interruptions of the basal membrane, absence of pericapillary glial elements. All types of the capillaries demonstrate certain signs of a high functional activity. Formation of the capillary structure depends on the surrounding tissue.