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A bstract Using data samples of 983.0 fb − 1 and 427.9 fb − 1 accumulated with the Belle and Belle II detectors operating at the KEKB and SuperKEKB asymmetric-energy e + e − colliders, singly Cabibbo-suppressed decays Ξ c + → p K S 0 , Ξ c + → Λ π + , and Ξ c + → Σ 0 π + are observed for the first time. The ratios of branching fractions of Ξ c + → p K S 0 , Ξ c + → Λ π + , and Ξ c + → Σ 0 π + relative to that of Ξ c + → Ξ − π + π + are measured to be B Ξ c + → p K S 0 B Ξ c + → Ξ − π + π + = 2.47 ± 0.16 ± 0.07 % , B Ξ c + → Λ π + B Ξ c + → Ξ − π + π + = 1.56 ± 0.14 ± 0.09 % , B Ξ c + → Σ 0 π + B Ξ c + → Ξ − π + π + = 4.13 ± 0.26 ± 0.22 % . Multiplying these values by the branching fraction of the normalization channel, B Ξ c + → Ξ − π + π + = 2.9 ± 1.3 % , the absolute branching fractions are determined to be B Ξ c + → p K S 0 = 7.16 ± 0.46 ± 0.20 ± 3.21 × 10 − 4 , B Ξ c + → Λ π + = 4.52 ± 0.41 ± 0.26 ± 2.03 × 10 − 4 , B Ξ c + → Σ 0 π + = 1.20 ± 0.08 ± 0.07 ± 0.54 × 10 − 3 . The first and second uncertainties above are statistical and systematic, respectively, while the third ones arise from the uncertainty in B Ξ c + → Ξ − π + π + .

A bstract We present a measurement of the time-dependent CP asymmetry in decays using a data set of 365 fb − 1 recorded by the Belle II experiment and the final data set of 711 fb − 1 recorded by the Belle experiment at the Υ(4S) resonance. The direct and mixing-induced time-dependent CP violation parameters C and S are determined along with two additional quantities, S + and S − , defined in the two halves of the plane. The measured values are C = − 0 . 17 ± 0 . 09 ± 0 . 04, S = − 0 . 29 ± 0 . 11 ± 0 . 05, S + = −0 . 57 ± 0 . 23 ± 0 . 10 and S − = 0 . 31 ± 0 . 24 ± 0 . 05, where the first uncertainty is statistical and the second systematic.

We perform the first search for CP violation in$$ {D}_{(s)}^{+}\\to {K}_S^0{K}^{-}{\\pi}^{+}{\\pi}^{+} $$D s + → K S 0 K − π + π + decays. We use a combined data set from the Belle and Belle II experiments, which study e + e − collisions at center-of-mass energies at or near the Υ(4 S ) resonance. We use 980 fb − 1 of data from Belle and 428 fb − 1 of data from Belle II. We measure six CP -violating asymmetries that are based on triple products and quadruple products of the momenta of final-state particles, and also the particles’ helicity angles. We obtain a precision at the level of 0.5% for$$ {D}^{+}\\to {K}_S^0{K}^{-}{\\pi}^{+}{\\pi}^{+} $$D + → K S 0 K − π + π + decays, and better than 0.3% for$$ {D}_s^{+}\\to {K}_S^0{K}^{-}{\\pi}^{+}{\\pi}^{+} $$D s + → K S 0 K − π + π + decays. No evidence of CP violation is found. Our results for the triple-product asymmetries are the most precise to date for singly-Cabibbo-suppressed D + decays. Our results for the other asymmetries are the first such measurements performed for charm decays.

A bstract We perform the first search for CP violation in D s + → K S 0 K − π + π + decays. We use a combined data set from the Belle and Belle II experiments, which study e + e − collisions at center-of-mass energies at or near the Υ(4 S ) resonance. We use 980 fb − 1 of data from Belle and 428 fb − 1 of data from Belle II. We measure six CP -violating asymmetries that are based on triple products and quadruple products of the momenta of final-state particles, and also the particles’ helicity angles. We obtain a precision at the level of 0.5% for D + → K S 0 K − π + π + decays, and better than 0.3% for D s + → K S 0 K − π + π + decays. No evidence of CP violation is found. Our results for the triple-product asymmetries are the most precise to date for singly-Cabibbo-suppressed D + decays. Our results for the other asymmetries are the first such measurements performed for charm decays.

Using data samples of 983.0 fb − 1 and 427.9 fb − 1 accumulated with the Belle and Belle II detectors operating at the KEKB and SuperKEKB asymmetric-energy e + e − colliders, singly Cabibbo-suppressed decays$$ {\\Xi}_c^{+}\\to p{K}_S^0 $$Ξ c + → p K S 0 ,$$ {\\Xi}_c^{+}\\to \\Lambda {\\pi}^{+} $$Ξ c + → Λ π + , and$$ {\\Xi}_c^{+}\\to {\\Sigma}^0{\\pi}^{+} $$Ξ c + → Σ 0 π + are observed for the first time. The ratios of branching fractions of$$ {\\Xi}_c^{+}\\to p{K}_S^0 $$Ξ c + → p K S 0 ,$$ {\\Xi}_c^{+}\\to \\Lambda {\\pi}^{+} $$Ξ c + → Λ π + , and$$ {\\Xi}_c^{+}\\to {\\Sigma}^0{\\pi}^{+} $$Ξ c + → Σ 0 π + relative to that of$$ {\\Xi}_c^{+}\\to {\\Xi}^{-}{\\pi}^{+}{\\pi}^{+} $$Ξ c + → Ξ − π + π + are measured to be$$ {\\displaystyle \\begin{array}{c}\\frac{\\mathcal{B}\\left({\\Xi}_c^{+}\\to p{K}_S^0\\right)}{\\mathcal{B}\\left({\\Xi}_c^{+}\\to {\\Xi}^{-}{\\pi}^{+}{\\pi}^{+}\\right)}=\\left(2.47\\pm 0.16\\pm 0.07\\right)\\%,\\\ {}\\frac{\\mathcal{B}\\left({\\Xi}_c^{+}\\to \\Lambda {\\pi}^{+}\\right)}{\\mathcal{B}\\left({\\Xi}_c^{+}\\to {\\Xi}^{-}{\\pi}^{+}{\\pi}^{+}\\right)}=\\left(1.56\\pm 0.14\\pm 0.09\\right)\\%,\\\ {}\\frac{\\mathcal{B}\\left({\\Xi}_c^{+}\\to {\\Sigma}^0{\\pi}^{+}\\right)}{\\mathcal{B}\\left({\\Xi}_c^{+}\\to {\\Xi}^{-}{\\pi}^{+}{\\pi}^{+}\\right)}=\\left(4.13\\pm 0.26\\pm 0.22\\right)\\%.\\end{array}} $$B Ξ c + → p K S 0 B Ξ c + → Ξ − π + π + = 2.47 ± 0.16 ± 0.07 % , B Ξ c + → Λ π + B Ξ c + → Ξ − π + π + = 1.56 ± 0.14 ± 0.09 % , B Ξ c + → Σ 0 π + B Ξ c + → Ξ − π + π + = 4.13 ± 0.26 ± 0.22 % . Multiplying these values by the branching fraction of the normalization channel,$$ \\mathcal{B}\\left({\\Xi}_c^{+}\\to {\\Xi}^{-}{\\pi}^{+}{\\pi}^{+}\\right)=\\left(2.9\\pm 1.3\\right)\\% $$B Ξ c + → Ξ − π + π + = 2.9 ± 1.3 % , the absolute branching fractions are determined to be$$ {\\displaystyle \\begin{array}{c}\\mathcal{B}\\left({\\Xi}_c^{+}\\to p{K}_S^0\\right)=\\left(7.16\\pm 0.46\\pm 0.20\\pm 3.21\\right)\\times {10}^{-4},\\\ {}\\mathcal{B}\\left({\\Xi}_c^{+}\\to \\Lambda {\\pi}^{+}\\right)=\\left(4.52\\pm 0.41\\pm 0.26\\pm 2.03\\right)\\times {10}^{-4},\\\ {}\\mathcal{B}\\left({\\Xi}_c^{+}\\to {\\Sigma}^0{\\pi}^{+}\\right)=\\left(1.20\\pm 0.08\\pm 0.07\\pm 0.54\\right)\\times {10}^{-3}.\\end{array}} $$B Ξ c + → p K S 0 = 7.16 ± 0.46 ± 0.20 ± 3.21 × 10 − 4 , B Ξ c + → Λ π + = 4.52 ± 0.41 ± 0.26 ± 2.03 × 10 − 4 , B Ξ c + → Σ 0 π + = 1.20 ± 0.08 ± 0.07 ± 0.54 × 10 − 3 . The first and second uncertainties above are statistical and systematic, respectively, while the third ones arise from the uncertainty in$$ \\mathcal{B}\\left({\\Xi}_c^{+}\\to {\\Xi}^{-}{\\pi}^{+}{\\pi}^{+}\\right) $$B Ξ c + → Ξ − π + π + .

Functional effectiveness of erythrocytes depends on their high deformability that allows them to pass through narrow tissue capillaries. The erythrocytes can deform easily due to discoid shape provided by the stabilization of an optimal cell volume at a given cell surface area. We used mathematical simulation to study the role of transport Na/K-ATPase and transmembrane Na + and K + gradients in human erythrocyte volume stabilization at non-selective increase in cell membrane permeability to cations. The model included Na/K-ATPase activated by intracellular Na + , Na + and K + transmembrane gradients, and took into account contribution of glycolytic metabolites and adenine nucleotides to cytoplasm osmotic pressure. We found that this model provides the best stabilization of the erythrocyte volume at non-selective increase in the permeability of the cell membrane, which can be caused by an oxidation of the membrane components or mechanical stress during circulation. The volume of the erythrocyte deviates from the optimal value by no more than 10% with a change in the non-selective permeability of the cell membrane to cations from 50 to 200% of the normal value. If only one transmembrane ion gradient is present (Na + ), the cell loses the ability to stabilize volume and even small changes in membrane permeability cause dramatic changes in the cell volume. Our results reveal that the presence of two oppositely directed transmembrane ion gradients is fundamentally important for robust stabilization of cellular volume in human erythrocytes.

Chlamydiae are a group of obligate intracellular microorganisms with a homogeneous group-specific antigenic structure, and a unique mode of development. The infections caused by them are unprecedented and wide-spread throughout the world, including a broad range of hosts among domestic and animal species and humans, and a variety of clinical manifestations. The uniqueness of chlamydia pathology consists mainly in the fact that the agents of the individual diseases are so close in their biological properties that they are represented only by the single genus Chlamydia, which includes all currently recognized species. Although chlamydiae and chlamydial infections were discovered a long time ago, they are still under-researched and relatively unknown to broad circles of microbiologists, virologists, epidemiologists and clinicians. A number of issues relating to molecular biology, pathogenesis, mechanisms of Chlamydia development and their interactions with cells, as well as their genetic conditioning and regulation, remain unclear. The same is true for ambiguities, problems and contradictions related to epidemiology, diagnostic approaches, immunity and vaccines. Based on scientific facts and the analysis of literature, and the experience of the author, Chlamydiae and Chlamydial Infections attempts to shed light on the cited problems, in terms of modern microbiology, cell biology and molecular biology. The scientific topics discussed include: • Biological, morphological and antigenic properties of Chlamydia spp • Genes, genomic structure and genetic regulations • Conventional diagnostic methods and examinations • Detection and differentiation of Chlamydia organisms by DNA detection systems • Clinical forms and manifestations and drug therapy • Pathology • Epidemiological peculiarities of Chlamydia? induced diseases in animals and humans • Immunity and vaccines

Information on the changing epidemiology and expanding nosological range of Q fever in humans has gained much attention in the past decade. Q fever is a zoonotic disease caused by the highly infectious pathogen Coxiella burnetii and has global distribution with important health, social and economic implications. A number of other properties and characteristics of the causative agent and disease, define Q fever as a lasting and difficult veterinary and epidemiological problem, namely: the adaptability of C. burnetii and its high resistance in the external environment; the possibility of the existence of the agent in three- and two-member parasitic systems; the availability of natural and agricultural foci of infection; peculiarities of pathogenesis in humans and animals, and the mechanisms of excretion of the pathogen into the environment; and the high susceptibility of non-immune populations of animals and people. Given that C. burnetii is included in the arsenal of bacteriological weapons as agent with potential bioterrorist threat must be borne in mind the strategic importance of this microorganism. This book summarizes and analyzes the scientific facts and developments about Q Fever researched worldwide and performed by the author to propose a system for monitoring, control and prevention covering the main necessary actions, measures and activities in the fight against this fever. There is an uneven level of knowledge of Q fever in animals and humans in various countries on the planet, while the assessment of the relevance of the problem is often ambiguous and unrealistic in terms of veterinary, medical and social and economic aspects, which can result in an incomplete diagnosis, inaccurate information about the spread of disease and lack of purposeful struggle. The scientific topics discussed include: • Biological, morphological and immunological properties of Coxiella burnetii • Diagnosis, clinical forms and manifestations, pathologic changes • Epidemiology of Q fever in animals and humans • Prevention and Control

The role of adenylate kinase in regulating the glycolysis rate and the potential contribution of the adenylate kinase reaction to ATP production were examined using mathematical models of energy metabolism in human erythrocytes and resting anaerobic mammalian skeletal muscle. The adenylate kinase reaction was shown to play a critical role in the regulation of cellular energy metabolism. Through the action of adenylate kinase, small changes in intracellular [ATP] give rise to large changes in [AMP], a potent activator of glycolytic flux via the activation of phosphofructokinase (PFK). This mechanism ensures an increase in the glycolytic rate as [ATP] decreases within the physiological range of ATP concentrations. As a result, negative feedback regulation of glycolysis by [ATP] is established, allowing the rate of ATP production to adjust to the energy demands of the cell and thereby stabilizing [ATP] under varying rates of ATP consumption. Importantly, allosteric inhibition of PFK by ATP alone was insufficient to provide negative feedback regulation of glycolysis via [ATP]. The contribution of the adenylate kinase reaction to ATP production appears to be negligible. Also, due to the presence of adenylate kinase in cells, energy metabolism is regulated not by the absolute concentration of ATP, but by the energy charge or the ratio of [ATP] to the sum of [ATP], [ADP], and [AMP].

Conventional antibiotic and multidrug treatments are becoming less and less effective and the discovery of new effective and safe antibacterial agents is becoming a global priority. Returning to a natural antibacterial product is a relatively new current trend. Terrestrial biota is a rich source of biologically active substances whose antibacterial potential has not been fully utilized. The aim of this review is to present the current state-of-the-art terrestrial biota-derived antibacterial agents inspired by natural treatments. It summarizes the most important sources and newly identified or modified antibacterial agents and treatments from the last five years. It focuses on the significance of plant- animal- and bacteria-derived biologically active agents as powerful alternatives to antibiotics, as well as the advantages of utilizing natural antibacterial molecules alone or in combination with antibiotics. The main conclusion is that terrestrial biota-derived antibacterial products and substances open a variety of new ways for modern improved therapeutic strategies. New terrestrial sources of known antibacterial agents and new antibacterial agents from terrestrial biota were discovered during the last 5 years, which are under investigation together with some long-ago known but now experiencing their renaissance for the development of new medical treatments. The use of natural antibacterial peptides as well as combinational therapy by commercial antibiotics and natural products is outlined as the most promising method for treating bacterial infections. In vivo testing and clinical trials are necessary to reach clinical application.