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Changes in tree mortality due to severe drought can alter forest structure, composition, dynamics, ecosystem services, carbon fluxes, and energy interactions between the atmosphere and land surfaces. We utilized long-term (2000‒2017, 3 full inventory cycles) Forest Inventory and Analysis (FIA) data to examine tree mortality and biomass loss in drought-affected forests for East Texas, USA. Plots that experienced six or more years of droughts during those censuses were selected based on 12-month moderate drought severity [Standardized Precipitation Evaporation Index (SPEI) -1.0]. Plots that experienced other disturbances and inconsistent records were excluded from the analysis. In total, 222 plots were retained from nearly 4000 plots. Generalized nonlinear mixed models (GNMMs) were used to examine the changes in tree mortality and recruitment rates for selected plots. The results showed that tree mortality rates and biomass loss to mortality increased overall, and across tree sizes, dominant genera, height classes, and ecoregions. An average mortality rate of 5.89% year−1 during the study period could be incited by water stress created by the regional prolonged and episodic drought events. The overall plot and species-group level recruitment rates decreased during the study period. Forest mortality showed mixed results regarding basal area and forest density using all plots together and when analyzed the plots by stand origin and ecoregion. Higher mortality rates of smaller trees were detected and were likely compounded by density-dependent factors. Comparative analysis of drought-induced tree mortality using hydro-meteorological data along with drought severity and length gradient is suggested to better understand the effects of drought on tree mortality and biomass loss around and beyond East Texas in the southeastern United States. [ABSTRACT FROM AUTHOR]

Hematological studies of fishes are useful in the diagnosis of many diseases as well as investigation of the extent of damage to the blood. These parameters act as efficient and insightful index to examine health status, physiological and pathological changes occurring in various fishes, i.e., metabolic perturbations in fish body thereby acting as non-specific biomarkers in the field of environmental toxicology, deficiencies and chronic stress in natural as well as aquaculture systems and checking water quality. The assessments of these blood parameters help the biologists to understand the fish homeostasis and biomonitoring of severe and chronic patho-physiological changes inferable to nutrition, water quality, or disease so as to establish the normal reference values of different species and determine systematic relationships among them. Lot of work on various aspects of hematological parameters and their relation with ecological factors has been reported on several fish species from different parts of the world. Each study attributes one or other factors responsible for variation in hematological parameters among different fish species. Therefore, in the present study, an attempt has been made to compile the information about the hematological studies of various fish species reported from different parts of the world, and through this study, a general overview has been generated about the major factors responsible for the variation in hematological parameters of fish. The review provides an insight to the characteristics of hematological values showing that fluctuating internal environment of the fish, along with other intrinsic (age, body size, the cycle of sexual maturity, health condition, nutritional state, species) and extrinsic factors (temperature, stress, season, dissolved oxygen, water quality, lotic or lentic environment, stocking density, photoperiod, sampling conditions, laboratory techniques), are the reasons of huge variability of hematological parameters in fishes. [ABSTRACT FROM AUTHOR]

A comparative analysis of epigenetic variation has been performed in nine European populations and population groups of the American mink. It has been shown that differentiation of samples in nonmetric characters is due mainly to endogenous processes that have occurred in introduced populations in the course of colonization of new territory by the invasive species. Environmental factors have played a secondary role, with the influence of the geographic (latitudinal) origin of a given sample being considerable and stronger than that of macroclimatic factors. [ABSTRACT FROM AUTHOR]

The number of mature osteoblasts and marrow adipocytes in bone is influenced by the differentiation of the common mesenchymal progenitor cell towards one phenotype and away from the other. Consequently, factors which promote adipogenesis not only lead to fatty marrow but also inhibit osteoblastogenesis, resulting in decreased osteoblast numbers, diminished bone formation and, potentially, inadequate bone mass and osteoporosis. In addition to osteoblast and bone adipocyte numbers being influenced by this skewing of progenitor cell differentiation towards one phenotype, mature osteoblasts and adipocytes secrete factors which may evoke changes in the cell fate and function of each other. This review examines the endogenous factors, such as PPAR-γ2, Wnt, IGF-1, GH, FGF-2, oestrogen, the GP130 signalling cytokines, vitamin D and glucocorticoids, which regulate the selection between osteoblastogenesis and adipogenesis and the interrelationship between fat and bone. The role of adipokines on bone, such as adiponectin and leptin, as well as adipose-derived oestrogen, is reviewed and the role of bone as an energy regulating endocrine organ is discussed. [ABSTRACT FROM AUTHOR]

Copyright of TSG: Tijdschrift Voor Gezondheidswetenschappen is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Congestive heart failure (CHF) afflicts over 5 million individuals in the United States, and most die within 5 yr of diagnosis. Because of the high morbidity and mortality associated with CHF, the search for biomarkers to predict, diagnose, and manage this disease has intensified. Calcium homeostasis and alterations in intracellular concentrations of this cation have been implicated in both hypertrophy as well as the adaptive mechanisms observed in CHF. In this article, we discuss the roles of the sodium pump and the endogenous mammalian cardenolides and their involvement in the pathophysiology of this disease in view of the regulation of intracellular calcium. Understanding the mechanisms for the release of mammalian cardenolides in plasma, the alterations in sodium pump isoforms and function, and the modulation of pathways involving calcium in hypertrophy and CHF may assist in the development of new biological markers capable of predicting the disease before significant progression and irreversible heart failure. [ABSTRACT FROM AUTHOR]

Summary To elucidate the molecular pathogenesis of diseases has become a crucial step in the development of new treatment strategies. Although the pathogenesis of cerebral aneurysms has been studied intensively, it is poorly understood. Endogenous factors like elevated arterial blood pressure, the special anatomy of the Circle of Willis or the effect of haemodynamic factors, particularly originating at vessel bifurcation, are all known to be involved in the growth and rupture of an aneurysm. There is an ongoing discussion as to whether these factors also contribute to the very early steps of pathogenesis. Arteriosclerosis and secondary inflammatory reactions are thought to be elementary preconditions. Exogenous factors like cigarette smoking, heavy alcohol consumption or certain medications known to help generate arteriosclerosis and elevated blood pressure have also been found to be related to the occurrence of cerebral aneurysms. Furthermore, there has been a long-lasting debate on whether aneurysms might develop as a result of an inborn genetic defect. First-degree relatives of patients with cerebral aneurysms have a higher risk of having an aneurysm. In addition, the elevated prevalence of cerebral aneurysms in patients suffering from various inherited diseases points to a genetic background in the development of an aneurysm. Recent advances in molecular biology provide evidence that genetic variants of different candidate genes are associated with the occurrence of cerebral aneurysms. The aim of this review is to expose the current status of these various hypotheses and their contribution to the pathogenesis of cerebral aneurysms in order to provide a basis for future investigations in this field. [ABSTRACT FROM AUTHOR]

Oxidative metabolism is very active in brain, where large amounts of chemical energy as ATP molecules are consumed, mostly required to maintain cellular Na+/K+ gradients through the participation of the sodium pump (Na+,K+-ATPase), whose activity is selectively and potently inhibited by the alkaloid ouabain. Na+/K+ gradients are involved in nerve impulse propagation, in neurotransmitter release and cation homeostasis in the nervous system. Likewise, enzyme activity modulation is crucial for maintaining normal blood pressure and cardiovascular contractility as well as renal sodium excretion. The present article reviews the progress in disclosing putative ouabain-like substances, examines their denomination according to different research teams, tissue or biological fluid sources, extraction and purification, assays, biological properties and chemical and biophysical features. When data is available, comparison with ouabain itself is mentioned. Likewise, their potential action in normal physiology as well as in experimental and human pathology is summarized. [ABSTRACT FROM AUTHOR]

Studies were carried out to determine whether barbiturates and neurosteroids share common recognition sites at the GABAA receptor complex in avian CNS. To achieve this, differentially prepared fresh and frozen synaptic membranes were used. Both the barbiturate, pentobarbital, and the neurosteroid, 3α-hydroxy-5α-pregnan-20-one, were able to stimulate GABA binding in both types of membranes. Stimulation differed markedly when both drugs were added jointly to different treated tissue. In frozen membranes drugs acted synergistically and were differentially displaced by picrotoxinin, while in fresh ones, where both compounds were inhibited by the convulsant, this additivity was absent. Post-freezing wash supernatants were collected and used as a source of putative endogenous factors involved in the above mentioned membrane differences. Addition of a high molecular weight fraction from supernatants to frozen synaptic membranes led to an inhibition of barbiturate and neurosteroid potentiation, as well as a loss of their additive effect. Our results indicate that GABAA receptor modulation by barbiturates and neurosteroids is affected by synaptic membrane treatment, with a common modulatory site in fresh membranes and separate recognition sites after a freeze-thawing procedure. There may also be endogenous factors involved in overlapping of modulatory sites, which would thus regulate GABAA receptor functionality by direct interaction with the complex. [ABSTRACT FROM AUTHOR]

Copyright of Archiv für Psychiatrie und Nervenkrankheiten is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)