The Role of Sleep Deprivation in Arrhythmias

Sleep is essential to the normal psychological and physiological activities of the human body.Increasing evidence indicates that sleep deprivation is associated with the occurrence,development,and poor treatment effects of various arrhythmias.Sleep deprivation affects not only the peripheral nervous system but also the central nervous system,which regulates the occurrence of arrhythmias.In addition,sleep deprivation is associated with apoptotic pathways,mitochondrial energy metabolism disorders,and immune system dysfunction.Although studies increasingly suggest that pathological sleep patterns are associated with various atrial and ventricular arrhythmias,further research is needed to identify specific mechanisms and recommend therapeutic interventions.This review summarizes the findings of sleep deprivation in animal experiments and clinical studies,current challenges,and future research directions in the field of arrhythmias.

Changes of Essential Mineral Elements Contents in Response to Cu²⁺Treatment in <i>Sagittaria sagittifolia</i>

Changes of various mineral elements (P, K, Ca, Mg, Fe, Mn, Zn and Na) contents in roots and leaves of S. sagittifolia were studied with treatment of different Cu2+ concentrations (5 μM, 10 μM, 20 μM and 40 μM) after 15 days. The results showed that: 1) Cu accumulated in roots of S. sagittifolia in large quantities, while Cu content in leaves showed no significant change;2) It can be seen from the changes of macroelements that Cu2+ treatments had inhibited the absorption of P, K, Ca, Mg in roots of S. sagittifolia, but the contents of P, K and Mg in leaves were higher than those in the roots in all Cu2+ treatment groups;3) It can be seen from the changes of microelements that Cu2+ treatment promoted the absorption of Fe, inhibited absorption of Mn, Zn and Na in roots of S. sagittifolia, and hindered the transport of various micro-elements from roots to leaves. In all the Cu2+ treatment groups, contents of Fe, Mn, Zn and Na in leaves were lower than those in the roots;4) The critical concentration of Cu2+ to S. sagittifolia was 5 μM. It could be seen from the above results that exogenous added Cu2+ of different concentrations broke the balance of various mineral elements in S. sagittifolia, which would exert a significant impact on numerous metabolic pathways and physiological processes.

Polymyxin resistance caused by large-scale genomic inversion due to IS26 intramolecular translocation in Klebsiella pneumoniae

Polymyxin B and polymyxin E(colistin)are presently considered the last line of defense against human infections caused by multidrug-resistant Gram-negative organisms such as carbapenemase-producer Enterobacterales,Acinetobacter baumannii,and Klebsiella pneumoniae.Yet resistance to this last-line drugs is a major public health threat and is rapidly increasing.Polymyxin S2(S2)is a polymyxin B analogue previously synthesized in our institute with obviously high antibacterial activity and lower toxicity than polymyxin B and colistin.To predict the possible resistant mechanism of S2for wide clinical application,we experimentally induced bacterial resistant mutants and studied the preliminary resistance mechanisms.Mut-S,a resistant mutant of K.pneumoniae ATCC BAA-2146(Kpn2146)induced by S2,was analyzed by whole genome sequencing,transcriptomics,mass spectrometry and complementation experiment.Surprisingly,large-scale genomic inversion(LSGI)of approximately 1.1 Mbp in the chromosome caused by IS26mediated intramolecular transposition was found in Mut-S,which led to mgrB truncation,lipid A modification and hence S2resistance.The resistance can be complemented by plasmid carrying intact mgrB.The same mechanism was also found in polymyxin B and colistin induced drug-resistant mutants of Kpn2146(Mut-B and Mut-E,respectively).This is the first report of polymyxin resistance caused by IS26 intramolecular transposition mediated mgrB truncation in chromosome in K.pneumoniae.The findings broaden our scope of knowledge for polymyxin resistance and enriched our understanding of how bacteria can manage to survive in the presence of antibiotics.