Rumex thyrsiflorus Fingerh. is a dioecious plant with polymorphic sex chromosomes (XX in females, XY₁Y₂ in males). This species is an interesting plant for study on the structure and function of sex chromosomes, the sex ratio, and is also a valuable source of bioactive constituents. A procedure for the micropropagation of R. thyrsiflorus from hypocotyl explants, which can be useful for analyses of sex-specific morphogenetic reactions under in vitro conditions, was developed. The molecular analysis, based on genetic sex markers, allowed the sex of explants to be determined in order to create male or female in vitro cultures. Regeneration primarily occurred via indirect adventitious shoot formation as well as via somatic embryogenesis, which was confirmed by histological and scanning electron microscope (SEM) analyses. The highest frequency of explants that revealed a morphogenetic response with the highest number of regenerated adventitious shoot buds (average 11.5 shoots per explant) was obtained on a Murashige and Skoog (MS) medium supplemented with 2.27 µM thidiazuron (TDZ). Molecular analysis revealed a female-biased sex ratio under these conditions. The relationship between the sex of the explants and their morphogenetic potential was studied. The efficiency of morphogenesis varied between the two sexes and depended on the ratio of auxin and cytokinin in the medium. The germination pattern of male and female seeds under in vitro conditions was also analysed. No differences in germination time between male and female seeds and in terms of male and female seedling length were observed, which indicated that there was no competition between the sexes during seed germination when grown under uniform growth conditions.

Several parasitic plants are known to have acquired mitochondrial genes via a horizontal transfer from their hosts. However, mitochondrial gene transfer in this direction has not yet been found in the parasite-rich family Orobanchaceae. Based on a phylogenetic analysis of the mitochondrialatp6gene in selected species ofOrobanches.l., we provide evidence of a host-to-parasite transfer of this gene inO. coerulescens, which is a Eurasiatic species that parasitisesArtemisia(Asteraceae). We did not find the originalOrobanche atp6gene in this species, which suggests that it has been replaced by a gene that was acquired from Asteraceae. In addition, our data suggest the occurrence of a second HGT event in theatp6sequence – from Asteraceae toPhelipanche. Our results support the view that the transfer of genetic material from hosts to parasites influences the mitochondrial genome evolution in the latter.

Diabetes mellitus is one of the fastest-growing non-communicable diseases worldwide. The increasing global prevalence of diabetes has been accompanied by a corresponding rise in the incidence of diabetic micro- and macrovascular complications and related dysfunctions in the central nervous system. Studies demonstrated that patients with diabetes are more susceptible to cognitive impairment due to the diminished ability of neuronal cells to protect against increased production of reactive oxygen species and activated neuroinflammatory pathways. In the spinal cord, long-term hyperglycemia leads to neuronal dysfunction due to increased activation of glial cells and neuroinflammation and elevated oxidative stress, triggering micro- and macrovascular changes and leading to the development of peripheral nerve dysfunctions and neuropathies. Despite extensive efforts, however, the precise molecular mechanisms underlying the pathogenesis of diabetic complications have yet to be fully uncovered, proving to be a major hurdle in designing therapies to stop the progress of diabetes-triggered susceptible tissue and organ deterioration in affected subjects. In this review, we discuss in detail the role of the receptor for advanced glycation end-products (RAGE) and its major signaling partners in the development of CNS neurodegenerative changes in diabetes and the potential for novel biomarkers and treatments using targeting RAGE signaling axis.

The male-specific DNA markers are very useful in molecular sexing of non-flowering plants and seeds of dioecious species. In this paper we identified ten Y chromosome-specific RAPD primers suitable for identification of male plants in three Cannabaceae species with sex chromosomes (Humulus lupulus, XX/XY; H. japonicus, XX/XY1Y2; Cannabis sativa, XX/XY). Basing on the nucleotide sequence of the OPJ-09 RAPD product we developed the HJY09 SCAR marker, which is very efficient in sexing of Japanese hop.

RAPD analysis was applied to assess the degree of DNA polymorphism in A. fistulosum calli of high chromosomal instability. Nineteen of 24 randomly selected RAPD primers revealed scorable polymorphism between calli and seeds (reference material). Polymorphic band frequency was 55/237 in seeds and 36/233 in calli; variability on the DNA level was thus lower in calli than in seeds (15.4% vs. 23.2% of band positions). UPGMA analysis of Jaccard's coefficients confirmed the genetic similarity of the analyzed cultures. The most distinctive DNA changes in calli involved coincident loss of original bands or the appearance of novel bands. Seven such changes (4 losses, 3 gains) were observed. Our results suggest that changes on the chromosomal level and on the DNA level occurred independently of each other and that different callus lines underwent similar genetic changes during culture, presumably due to strong selection pressure effected by standard in vitro conditions.

Cardiovascular autonomic failure arises from lesions across central nuclei, peripheral nerves, and autonomic ganglia. This review examines whether dysfunction of the neurovascular unit and neural barriers contributes to that failure. The clearest evidence comes from rodent models of hypertension and heart failure. Increased permeability in the PVN, NTS, and RVLM develops alongside sympathetic activation and impaired baroreflex control. Angiotensin II and inflammation appear to affect endothelial transport and junctional integrity. Exercise and interventions directed at these pathways improve barrier function together with autonomic control. Peripheral evidence is less direct. Diabetes and inflammatory neuritis alter the blood–nerve barrier, but most experiments examine somatic or sensory nerves and do not establish causation in cardiovascular autonomic neuropathy. Autonomic ganglia also differ in normal vascular permeability, which precludes treating them as uniform extensions of the blood–nerve barrier. Human studies show altered barrier measurements in heart failure and synucleinopathies, yet rarely pair regional permeability with validated autonomic tests. Neural barrier dysfunction may contribute to dysautonomia in defined anatomical and clinical settings. Its importance remains uncertain outside the pathways examined directly, and future studies should relate regional barrier changes to autonomic function over time.