PeerJ Preprints: Biochemistryhttps://peerj.com/preprints/index.atom?journal=peerj&subject=300Biochemistry articles published in PeerJ PreprintsA lipid-invasion model for Alzheimer’s Diseasehttps://peerj.com/preprints/278112019-11-182019-11-18Jonathan D Rudge
This paper describes a potential new explanation for Alzheimer’s disease (AD), referred to here as the lipid-invasion model. It proposes that AD is primarily caused by the influx of lipids following the breakdown of the blood brain barrier (BBB). The model argues that a principal role of the BBB is to protect the brain from external lipid access. When the BBB is damaged, it allows a mass influx of (mainly albumin-bound) free fatty acids (FFAs) and lipid-rich lipoproteins to the brain, which in turn causes neurodegeneration, amyloidosis, tau tangles and other AD characteristics. The model also argues that, whilst β-amyloid causes neurodegeneration, as is widely argued, its principal role in the disease lies in damaging the BBB. It is the external lipids, entering as a consequence, that are the primary drivers of neurodegeneration in AD., especially FFAs, which induce oxidative stress, stimulate microglia-driven neuroinflammation, and inhibit neurogenesis. Simultaneously, the larger, more lipid-laden lipoproteins, characteristic of the external plasma but not the CNS, cause endosomal-lysosomal abnormalities, amyloidosis and the formation of tau tangles, all characteristic of AD. In most cases (certainly in late-onset, noninherited forms of the disease) amyloidosis and tau tangle formation are consequences of this external lipid invasion, and in many ways more symptomatic of the disease than causative. In support of this, it is argued that the pattern of damage caused by the influx of FFAs into the brain is likely to resemble the neurodegeneration seen in alcohol-related brain damage (ARBD), a disease that shows many similarities to AD, including the areas of the brain it affects. The fact that neurodegeneration is far more pronounced in AD than in ARBD, and characterised by other features, such as amyloidosis and tau tangles, most likely results from the greater heterogeneity of the lipid assault in AD compared with ethanol alone. The lipid-invasion model, described here, arguably provides the first cohesive, multi-factorial explanation of AD that accounts for all currently known major risk factors, and explains all AD-associated pathologies, including those, such as endosomal-lysosomal dysfunction and excessive lipid droplet formation, that are not well-accounted for in other explanation of this disease.
This paper describes a potential new explanation for Alzheimer’s disease (AD), referred to here as the lipid-invasion model. It proposes that AD is primarily caused by the influx of lipids following the breakdown of the blood brain barrier (BBB). The model argues that a principal role of the BBB is to protect the brain from external lipid access. When the BBB is damaged, it allows a mass influx of (mainly albumin-bound) free fatty acids (FFAs) and lipid-rich lipoproteins to the brain, which in turn causes neurodegeneration, amyloidosis, tau tangles and other AD characteristics. The model also argues that, whilst β-amyloid causes neurodegeneration, as is widely argued, its principal role in the disease lies in damaging the BBB. It is the external lipids, entering as a consequence, that are the primary drivers of neurodegeneration in AD., especially FFAs, which induce oxidative stress, stimulate microglia-driven neuroinflammation, and inhibit neurogenesis. Simultaneously, the larger, more lipid-laden lipoproteins, characteristic of the external plasma but not the CNS, cause endosomal-lysosomal abnormalities, amyloidosis and the formation of tau tangles, all characteristic of AD. In most cases (certainly in late-onset, noninherited forms of the disease) amyloidosis and tau tangle formation are consequences of this external lipid invasion, and in many ways more symptomatic of the disease than causative. In support of this, it is argued that the pattern of damage caused by the influx of FFAs into the brain is likely to resemble the neurodegeneration seen in alcohol-related brain damage (ARBD), a disease that shows many similarities to AD, including the areas of the brain it affects. The fact that neurodegeneration is far more pronounced in AD than in ARBD, and characterised by other features, such as amyloidosis and tau tangles, most likely results from the greater heterogeneity of the lipid assault in AD compared with ethanol alone. The lipid-invasion model, described here, arguably provides the first cohesive, multi-factorial explanation of AD that accounts for all currently known major risk factors, and explains all AD-associated pathologies, including those, such as endosomal-lysosomal dysfunction and excessive lipid droplet formation, that are not well-accounted for in other explanation of this disease.Functional characterization of a new maize heat shock transcription factor gene ZmHsf01 playing important roles in thermotolerancehttps://peerj.com/preprints/279872019-09-262019-09-26Huaning ZhangGuoliang LiYuanyuan ZhangYujie ZhangHongbo ShaoDong HuXiulin Guo
Background. The yield of maize crop is influenced seriously by heat waves. Plant heat shock transcription factors (Hsfs) play a key regulatory role in heat shock signal transduction pathway. Method. In this study, a new heat shock transcription factor gene, ZmHsf01 (accession number: MK888854) , was cloned from maize young leaves using homologous cloning method. The transcriptional level of ZmHsf01 were detected by qRT-PCR in different tissues or under heat shock, abscisic acid (ABA) and hydrogen peroxide (H2O2) treatment. The transgenic yeast and Arabidopsis were used to study the gene function of ZmHsf01. Result. The coding sequence (CDS) of ZmHsf01 was 1176 bp and encoded a protein that consisted of 391 amino acids. The homologous analysis result showed that ZmHsf01 and SbHsfA2d had the highest protein sequence identity. Subcellular localization experiments demonstrated that ZmHsf01 is localized to the nucleus. ZmHsf01 was expressed in many maize tissues and was up-regulated by heat stress. ZmHsf01 was up-regulated in roots and down-regulated in leaves by ABA and H2O2treatments. In yeast, ZmHsf01-overexpressing cells showed increased thermotolerance. In Arabidopsis seedlings, ZmHsf01 complemented the thermotolerance defects of athsfa2 mutant and ZmHsf01-overexpressing lines presented enhanced basal and acquired thermotolerance. Compared to wild type (WT) seedlings, ZmHsf01-overexpressing lines showed increased chlorophyll content after heat stress. The expression level of heat shock protein genes was up-regulated higher in ZmHsf01-overexpressing Arabidopsis seedlings than that in WT. These results suggested that ZmHsf01 plays a vital role in plant response to heat stress.
Background. The yield of maize crop is influenced seriously by heat waves. Plant heat shock transcription factors (Hsfs) play a key regulatory role in heat shock signal transduction pathway. Method. In this study, a new heat shock transcription factor gene, ZmHsf01 (accession number: MK888854), was cloned from maize young leaves using homologous cloning method. The transcriptional level of ZmHsf01 were detected by qRT-PCR in different tissues or under heat shock, abscisic acid (ABA) and hydrogen peroxide (H2O2) treatment. The transgenic yeast and Arabidopsis were used to study the gene function of ZmHsf01. Result. The coding sequence (CDS) of ZmHsf01 was 1176 bp and encoded a protein that consisted of 391 amino acids. The homologous analysis result showed that ZmHsf01 and SbHsfA2dhad the highest protein sequence identity. Subcellular localization experiments demonstrated that ZmHsf01 is localized to the nucleus. ZmHsf01 was expressed in many maize tissues and was up-regulated by heat stress. ZmHsf01 was up-regulated in roots and down-regulated in leaves by ABA and H2O2treatments. In yeast, ZmHsf01-overexpressing cells showed increased thermotolerance. In Arabidopsis seedlings, ZmHsf01 complemented the thermotolerance defects of athsfa2 mutant and ZmHsf01-overexpressing lines presented enhanced basal and acquired thermotolerance. Compared to wild type (WT) seedlings, ZmHsf01-overexpressing lines showed increased chlorophyll content after heat stress. The expression level of heat shock protein genes was up-regulated higher in ZmHsf01-overexpressing Arabidopsis seedlings than that in WT. These results suggested that ZmHsf01 plays a vital role in plant response to heat stress.Rhodococcus sp. may convert ethylene to acetaldehyde to slow ripening in climacteric fruit.https://peerj.com/preprints/33982019-09-172019-09-17Guenevere Perry
Pre-Print Update. Previous studies suggested Rhodococcus rhodochrous and Bacillus licheniformis cells converted ethylene to a nitrile compound to delay the effects of ripening, (Perry, G. Nov. 9, 2017). However, there may be an alternative compound that plays a more significant role in induced Rhodococcus and Bacillus ability to delay ripening. It has been known for years that Rhodococcus can convert the alkyne compound acetylene to acetaldehyde and potentially ethanol as a secondary product (DeBont, 1980).
This pre-print revisit re-examines the prior data to determine if the tri-phasic system previously discussed in 2017, induced bacteria to convert ethylene and/or propylene into acetaldehyde (a primary product), ethanol (a secondary product), and acetonitrile (a product of ethanol and a subsequent ammoxidation reaction). The acetaldehyde may delay the effects of ripening and inhibit fungal growth, while the nitrile by products enhance early plant development including germination and root elongation. Experimental results suggest an inducible monooxygenase or dioxygenase like enzyme is required to facilitate this process.
Pre-Print Update. Previous studies suggested Rhodococcus rhodochrous and Bacillus licheniformis cells converted ethylene to a nitrile compound to delay the effects of ripening, (Perry, G. Nov. 9, 2017). However, there may be an alternative compound that plays a more significant role in induced Rhodococcus and Bacillus ability to delay ripening. It has been known for years that Rhodococcus can convert the alkyne compound acetylene to acetaldehyde and potentially ethanol as a secondary product (DeBont, 1980).This pre-print revisit re-examines the prior data to determine if the tri-phasic system previously discussed in 2017, induced bacteria to convert ethylene and/or propylene into acetaldehyde (a primary product), ethanol (a secondary product), and acetonitrile (a product of ethanol and a subsequent ammoxidation reaction). The acetaldehyde may delay the effects of ripening and inhibit fungal growth, while the nitrile by products enhance early plant development including germination and root elongation. Experimental results suggest an inducible monooxygenase or dioxygenase like enzyme is required to facilitate this process.MATLAB software for automated calculation of concentration of different compounds using extracted peak area from HPLC data file in pdf formathttps://peerj.com/preprints/278782019-09-032019-09-03Wenfa Ng
Chromatograms represent a class of data difficult to process expeditiously due to the large number of intermediary steps necessary to translate peak detection to a concentration reading of a specific compound. This problem is further exacerbated by the different output file format in which instrument manufacturers present chromatographic data. Steps necessary to convert a detected peak to a concentration reading include identification of compound using retention time, extraction of corresponding peak area, and calculation of concentration of compound by using a calibration curve. This work sought to develop a MATLAB software able to automatically extract peak area from chromatographic readout captured in pdf format and calculate the corresponding concentration values. Given manufacturer-specific formatting features in pdf file, the MATLAB software could only read and handle pdf files of HPLC readouts from Shimadzu’s LabSolutions software. In processing the pdf file of each analyzed sample, entire content of the file was first read as a character string. Subsequently, specific delimiters were used to extract retention time and detected peak area for each compound. This information was subsequently processed to identify specific target compound of interest, where extracted peak area was used to calculate concentration of compound using a calibration plot. Overall, the program generates a database comprising filename, raw retention time and peak area data, as well as concentration values of each target compound in an easy to read format. Finally, to provide ease of access and a permanent file for storage, the program output the above database as an Excel file stored on the hard drive. One important advantage of this software is that it could process multiple pdf files simultaneously and there is no upper limit to the number of pdf files (or samples) that could be processed. Collectively, the MATLAB software capable of automatically extracting peak area and calculating concentration of different compounds would provide significant savings of time in handling large number of pdf files in a typical chromatographic run from a Shimadzu HPLC instrument.
Chromatograms represent a class of data difficult to process expeditiously due to the large number of intermediary steps necessary to translate peak detection to a concentration reading of a specific compound. This problem is further exacerbated by the different output file format in which instrument manufacturers present chromatographic data. Steps necessary to convert a detected peak to a concentration reading include identification of compound using retention time, extraction of corresponding peak area, and calculation of concentration of compound by using a calibration curve. This work sought to develop a MATLAB software able to automatically extract peak area from chromatographic readout captured in pdf format and calculate the corresponding concentration values. Given manufacturer-specific formatting features in pdf file, the MATLAB software could only read and handle pdf files of HPLC readouts from Shimadzu’s LabSolutions software. In processing the pdf file of each analyzed sample, entire content of the file was first read as a character string. Subsequently, specific delimiters were used to extract retention time and detected peak area for each compound. This information was subsequently processed to identify specific target compound of interest, where extracted peak area was used to calculate concentration of compound using a calibration plot. Overall, the program generates a database comprising filename, raw retention time and peak area data, as well as concentration values of each target compound in an easy to read format. Finally, to provide ease of access and a permanent file for storage, the program output the above database as an Excel file stored on the hard drive. One important advantage of this software is that it could process multiple pdf files simultaneously and there is no upper limit to the number of pdf files (or samples) that could be processed. Collectively, the MATLAB software capable of automatically extracting peak area and calculating concentration of different compounds would provide significant savings of time in handling large number of pdf files in a typical chromatographic run from a Shimadzu HPLC instrument.Tubular membranes extended between monolayer cells, from solid spheroids, and from clustered hollow spheroids in Ishikawa endometrial cell cultures can carry chromatin granules and mitonucleonshttps://peerj.com/preprints/278952019-08-122019-08-12Honoree Fleming
Membrane tubular extensions, recently recognized an important communication element in mammalian cells are demonstrated to form in Ishikawa endometrial epithelial cells growing in monolayers, and to extend from solid spheroids and from clustered hollow spheroids. Two kinds of chromatin cargoes travel through these tubules. Chromatin granules can pass through an endometrial tubule bridge extending from one monolayer fragment to another. The passage of granules over time from one of the fragments appears to support the self-assembly of nuclei in the other colony fragment. Similarly, in a process detected by observing an open-ended membrane tubule extending from a solid cell spheroid, a nucleus was observed to form over a period of 3 hours. Indications are that chromatin granules such as those observed in the amitotic processes of epithelial dome cell formation and of hollow spheroid cell formation are contributing to the build up of nuclei. Mitonucleons, a transient subcellular organelle consisting of fused mitochondria intimately associated with aggregated chromatin are also observed to pass through tubular membrane extensions. Multiple membrane extensions can be shown to to extend from clusters of unicellular polyploid hollow spheroids whose formation is described for the first time in this paper.
Membrane tubular extensions, recently recognized an important communication element in mammalian cells are demonstrated to form in Ishikawa endometrial epithelial cells growing in monolayers, and to extend from solid spheroids and from clustered hollow spheroids. Two kinds of chromatin cargoes travel through these tubules. Chromatin granules can pass through an endometrial tubule bridge extending from one monolayer fragment to another. The passage of granules over time from one of the fragments appears to support the self-assembly of nuclei in the other colony fragment. Similarly, in a process detected by observing an open-ended membrane tubule extending from a solid cell spheroid, a nucleus was observed to form over a period of 3 hours. Indications are that chromatin granules such as those observed in the amitotic processes of epithelial dome cell formation and of hollow spheroid cell formation are contributing to the build up of nuclei. Mitonucleons, a transient subcellular organelle consisting of fused mitochondria intimately associated with aggregated chromatin are also observed to pass through tubular membrane extensions. Multiple membrane extensions can be shown to to extend from clusters of unicellular polyploid hollow spheroids whose formation is described for the first time in this paper.A derived mechanism of nervous system functions shows features capable to have evolved and provides a testable explanation for age-related neurodegenerationhttps://peerj.com/preprints/274582019-07-242019-07-24Kunjumon I Vadakkan
By viewing memories as first-person internal sensations, it was possible to derive a potential mechanism of nervous system functions. Accordingly, a spectrum inter-postsynaptic (inter-dendritic spine) functional LINKs (IPLs) are the key structural changes responsible for encoding learning-changes in physiological time-scales of milliseconds that can be retained for different lengths of time and can be used for inducing first-person inner sensation of memory. The objective of this study was to examine a) where preconditions existed for an accident to trigger sparking of internal sensations, b) what conditions might have promoted the formation and selection of IPLs, and c) how the synaptically-connected neuronal circuitry accommodated the formation of IPLs through the simple steps of variations and selection. Sequence of events during the development of the nervous system was examined for the feasible sequence of steps that led to the formation of IPLs and optimization of the system. A stage of significant spine loss and neuronal death during the early stages of development indicate about a corresponding stage of inter-spine fusion that led to neuronal loss during evolution. When the generation of internal sensations by the IPLs started to become advantageous to the system, it started preserving the circuitry by developing an adaptation to prevent inter-spine fusion. This can be achieved only if a stage of transient inter-neuronal inter-spine fusion "turn on" certain mechanism to prevent the intermediate stage of inter-spine hemifusion from progressing to fusion. In summary, the derived IPL mechanism is capable to have evolved. An adaptation to prevent IPL hemifusion from progressing to fusion is a likely evolutionary adaptation. Since the IPL mechanism is utilized during every event of learning, any age-related factors that weaken the maintenance of this adaptation to prevent IPL fusion can lead to neurodegeneration.
By viewing memories as first-person internal sensations, it was possible to derive a potential mechanism of nervous system functions. Accordingly, a spectrum inter-postsynaptic (inter-dendritic spine) functional LINKs (IPLs) are the key structural changes responsible for encoding learning-changes in physiological time-scales of milliseconds that can be retained for different lengths of time and can be used for inducing first-person inner sensation of memory. The objective of this study was to examine a) where preconditions existed for an accident to trigger sparking of internal sensations, b) what conditions might have promoted the formation and selection of IPLs, and c) how the synaptically-connected neuronal circuitry accommodated the formation of IPLs through the simple steps of variations and selection. Sequence of events during the development of the nervous system was examined for the feasible sequence of steps that led to the formation of IPLs and optimization of the system. A stage of significant spine loss and neuronal death during the early stages of development indicate about a corresponding stage of inter-spine fusion that led to neuronal loss during evolution. When the generation of internal sensations by the IPLs started to become advantageous to the system, it started preserving the circuitry by developing an adaptation to prevent inter-spine fusion. This can be achieved only if a stage of transient inter-neuronal inter-spine fusion "turn on" certain mechanism to prevent the intermediate stage of inter-spine hemifusion from progressing to fusion. In summary, the derived IPL mechanism is capable to have evolved. An adaptation to prevent IPL hemifusion from progressing to fusion is a likely evolutionary adaptation. Since the IPL mechanism is utilized during every event of learning, any age-related factors that weaken the maintenance of this adaptation to prevent IPL fusion can lead to neurodegeneration.MATLAB software for extracting protein name and sequence information from FASTA formatted proteome filehttps://peerj.com/preprints/278562019-07-162019-07-16Wenfa Ng
FASTA file format is a common file type for distributing proteome information, especially those obtained from Uniprot. While MATLAB could automatically read fasta files using the built-in function, fastaread, important information such as protein name and organism name remain enmeshed in a character array. Hence, difficulty exists in automatic extraction of protein names from fasta proteome file to help in building a database with fields comprising protein name and its amino acid sequence. The objective of this work was in developing a MATLAB software that could automatically extract protein name and amino acid sequence information from fasta proteome file and assign them to a new database that comprises fields such as protein name, amino acid sequence, number of amino acid residues, molecular weight of protein and nucleotide sequence of protein. Information on number of amino acid residues came from the use of the length built-in function in MATLAB analyzing the length of the amino acid sequence of a protein. The final two fields were provided by MATLAB built-in functions molweight and aa2nt, respectively. Molecular weight of proteins is useful for a variety of applications while nucleotide sequence is essential for gene synthesis applications in molecular cloning. Finally, the MATLAB software is also equipped with an error check function to help detect letters in the amino acid sequence that are not part of the family of 20 natural amino acids. Sequences with such letters would constitute as error inputs to molweight and aa2nt, and would not be processed. Collectively, given that important information such as protein name is enmeshed in a character array in fasta proteome file, this work sets out to develop a MATLAB software that could automatically extract protein name and amino acid sequence information, and assigns them to a new protein database. Using built-in functions, number of amino acid residues, molecular weight and nucleotide sequence of each protein were calculated; thereby, yielding a new protein database with improved functionalities that could support a variety of biology workflows ranging from sequence alignment to molecular cloning.
FASTA file format is a common file type for distributing proteome information, especially those obtained from Uniprot. While MATLAB could automatically read fasta files using the built-in function, fastaread, important information such as protein name and organism name remain enmeshed in a character array. Hence, difficulty exists in automatic extraction of protein names from fasta proteome file to help in building a database with fields comprising protein name and its amino acid sequence. The objective of this work was in developing a MATLAB software that could automatically extract protein name and amino acid sequence information from fasta proteome file and assign them to a new database that comprises fields such as protein name, amino acid sequence, number of amino acid residues, molecular weight of protein and nucleotide sequence of protein. Information on number of amino acid residues came from the use of the length built-in function in MATLAB analyzing the length of the amino acid sequence of a protein. The final two fields were provided by MATLAB built-in functions molweight and aa2nt, respectively. Molecular weight of proteins is useful for a variety of applications while nucleotide sequence is essential for gene synthesis applications in molecular cloning. Finally, the MATLAB software is also equipped with an error check function to help detect letters in the amino acid sequence that are not part of the family of 20 natural amino acids. Sequences with such letters would constitute as error inputs to molweight and aa2nt, and would not be processed. Collectively, given that important information such as protein name is enmeshed in a character array in fasta proteome file, this work sets out to develop a MATLAB software that could automatically extract protein name and amino acid sequence information, and assigns them to a new protein database. Using built-in functions, number of amino acid residues, molecular weight and nucleotide sequence of each protein were calculated; thereby, yielding a new protein database with improved functionalities that could support a variety of biology workflows ranging from sequence alignment to molecular cloning.Role of nuclear actin filaments in DNA repair dynamicshttps://peerj.com/preprints/278552019-07-132019-07-13Christopher P CaridiMatthias PlessnerRobert GrosseIrene Chiolo
Actin filaments (F-actin) have well-known functions in the cytoplasm, including generating forces for cell movement and enabling myosin-driven dynamics of vesicles and mRNAs. In addition, the recent development of innovative tools for F-actin detection have revealed dynamic and transient filaments in the nuclei, which form in response to specific stimuli. Here we provide an overview of the functions of F-actin and myosins in nuclei, with a focus on their role in DNA repair and genome stability. We emphasize recent discoveries of nuclear F-actin driving the relocalization of heterochromatic repair sites to the nuclear periphery for ‘safe' homologous recombination (HR) repair of double-strand breaks (DSBs). F-actin also promotes repair focus clustering and DSB resection in euchromatin, facilitating HR progression. We highlight regulatory mechanisms specialized for actin polymerization during DNA replication and repair, and emphasize recent studies revealing alternative motors for the directional movement of repair sites. Together, these discoveries challenge previous models that actin is substantially monomeric in the nucleus and that DSBs move via Brownian motion, revealing a complex network of dynamic filaments, motors and regulators, coordinating chromatin dynamics with repair progression.
Actin filaments (F-actin) have well-known functions in the cytoplasm, including generating forces for cell movement and enabling myosin-driven dynamics of vesicles and mRNAs. In addition, the recent development of innovative tools for F-actin detection have revealed dynamic and transient filaments in the nuclei, which form in response to specific stimuli. Here we provide an overview of the functions of F-actin and myosins in nuclei, with a focus on their role in DNA repair and genome stability. We emphasize recent discoveries of nuclear F-actin driving the relocalization of heterochromatic repair sites to the nuclear periphery for ‘safe' homologous recombination (HR) repair of double-strand breaks (DSBs). F-actin also promotes repair focus clustering and DSB resection in euchromatin, facilitating HR progression. We highlight regulatory mechanisms specialized for actin polymerization during DNA replication and repair, and emphasize recent studies revealing alternative motors for the directional movement of repair sites. Together, these discoveries challenge previous models that actin is substantially monomeric in the nucleus and that DSBs move via Brownian motion, revealing a complex network of dynamic filaments, motors and regulators, coordinating chromatin dynamics with repair progression.Current methods for inhibiting antibiotic resistant bacteria by targeting bacterial cell metabolism and disrupting antibiotic elimination through the AcrAB-Tolc efflux pumphttps://peerj.com/preprints/278402019-07-042019-07-04Tatiana Hillman
Bacteria have a complex and lengthy evolutionary history of antibiotic resistance. For millions of years, bacteria have evolved a gene pool filled with multiple drug resistant genes. However, for the past 50 years, bacteria have been mutating and evolving vigorously and rapidly. Those 50 years predate to the time of the first use of antibiotic drugs in the 1940s. Since the 1940s, with the wide-spread use of the first antibiotic, penicillin, bacteria have effectively developed resistance to multiple antibiotic drugs. Bacteria develop antibiotic resistance after acquiring antibiotic resistant genes from conjugation and a horizontal transfer of those genes. Bacteria also have innate properties, structure, and functions that can increase their resistance of antibiotics. Bacteria cells can mutate its genes and block the binding of antibiotic drugs to its DNA. If the bacteria effectively impede the activity of an antibiotic through a DNA mutation, then the same mutation is shared with other bacterial cell strains through horizontal transfer. Antibiotics can be expelled from bacteria cells by efflux pumps called AcrBC-Tolc channels from the resistance-nodulation division (RND) family. Targeting the cell metabolism or the expression of efflux pumps may deter or impede the proliferation of antibiotic resistance. Researchers cultured E. tarda with glucose and alanine, and the uptake of kanamycin increased, eliminating approximately 3,000 times the amount of MDR bacterial cells compared to the cells only treated with kanamycin. Another researcher named Dr. Li mutated a gene of the AcrAB-Tolc binding site, forming a replacement for the highly non-polar phenylalanine amino acid residue with an alanine. His mutagenesis of the efflux pumps binding sites for AcrAB-Tolc inhibited the exit of antibiotics through the AcrAB-Tolc efflux pumps. Therefore, the review serves to discuss the new, novel, and current methods for reducing the spread of antibiotic resistant bacteria by targeting bacterial cell metabolism and its antibiotic resistant genes.
Bacteria have a complex and lengthy evolutionary history of antibiotic resistance. For millions of years, bacteria have evolved a gene pool filled with multiple drug resistant genes. However, for the past 50 years, bacteria have been mutating and evolving vigorously and rapidly. Those 50 years predate to the time of the first use of antibiotic drugs in the 1940s. Since the 1940s, with the wide-spread use of the first antibiotic, penicillin, bacteria have effectively developed resistance to multiple antibiotic drugs. Bacteria develop antibiotic resistance after acquiring antibiotic resistant genes from conjugation and a horizontal transfer of those genes. Bacteria also have innate properties, structure, and functions that can increase their resistance of antibiotics. Bacteria cells can mutate its genes and block the binding of antibiotic drugs to its DNA. If the bacteria effectively impede the activity of an antibiotic through a DNA mutation, then the same mutation is shared with other bacterial cell strains through horizontal transfer. Antibiotics can be expelled from bacteria cells by efflux pumps called AcrBC-Tolc channels from the resistance-nodulation division (RND) family. Targeting the cell metabolism or the expression of efflux pumps may deter or impede the proliferation of antibiotic resistance. Researchers cultured E. tarda with glucose and alanine, and the uptake of kanamycin increased, eliminating approximately 3,000 times the amount of MDR bacterial cells compared to the cells only treated with kanamycin. Another researcher named Dr. Li mutated a gene of the AcrAB-Tolc binding site, forming a replacement for the highly non-polar phenylalanine amino acid residue with an alanine. His mutagenesis of the efflux pumps binding sites for AcrAB-Tolc inhibited the exit of antibiotics through the AcrAB-Tolc efflux pumps. Therefore, the review serves to discuss the new, novel, and current methods for reducing the spread of antibiotic resistant bacteria by targeting bacterial cell metabolism and its antibiotic resistant genes.Molecular weight calculator for organic compounds in biotechnologyhttps://peerj.com/preprints/278362019-07-022019-07-02Wenfa Ng
Automated calculation of molecular weight of chemical compounds would provide savings in time and effort, especially in handling large number of compounds common in chemical or biotechnology workflow. In this work, a molecular weight calculator was developed using MATLAB and is capable of handling the chemical elements: carbon, hydrogen, oxygen, nitrogen, phosphorus, and sulphur that constitute organic compounds common in biotechnology. Such compounds would typically come across as either substrates or products of fermentation, where automated calculation of molecular weight would feed into mass/charge calculations that facilitate workflow involving their mass spectrometric detection. Specifically, chemical formulas of molecular ion are necessary information for identifying particular mass peaks in mass spectrometry, to which automated molecular weight calculation would greatly simplify peak identification. Thus, the molecular weight calculator developed in this work could be used as a subroutine for more complex software that provides identification of mass peaks in mass spectrometry workflow detecting organic compounds in fermentation.
Automated calculation of molecular weight of chemical compounds would provide savings in time and effort, especially in handling large number of compounds common in chemical or biotechnology workflow. In this work, a molecular weight calculator was developed using MATLAB and is capable of handling the chemical elements: carbon, hydrogen, oxygen, nitrogen, phosphorus, and sulphur that constitute organic compounds common in biotechnology. Such compounds would typically come across as either substrates or products of fermentation, where automated calculation of molecular weight would feed into mass/charge calculations that facilitate workflow involving their mass spectrometric detection. Specifically, chemical formulas of molecular ion are necessary information for identifying particular mass peaks in mass spectrometry, to which automated molecular weight calculation would greatly simplify peak identification. Thus, the molecular weight calculator developed in this work could be used as a subroutine for more complex software that provides identification of mass peaks in mass spectrometry workflow detecting organic compounds in fermentation.