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arXiv2018

FDG kinetics in cells and tissues: a biochemically-driven compartmental approach

The radioactive glucose analogue 2-deoxy-2-[18F]fluoro-D-glucose (FDG) is widely used to reconstruct glucose metabolism and other biological functions in cells and tissues. The analysis of data on the time course of FDG tracer distribution is performed by the use of appropriate compartmental models. Motivated by recent results in cell biochemistry, we describe a new compartmental model aiming at the reconstruction of tracer kinetics in cells and tissues, which emphasizes the different roles of the cytosol and of the endoplasmic reticulum. Two applications of the new model are examined, that are concerned with real data from cancer cell cultures in vitro, and cancer tissues in vivo. The results are compared with those obtained through application of more standard compartmental models against the same datasets and appear to be in a better agreement with respect to recent biochemical experimental evidence. In particular, it is shown that tracer tends to accumulate in the endoplasmic reticulum, rather than cytosol, and that the rate of phosphorylation is higher than predicted by current models.

q-bio.TO↗

arXiv2018

When few survive to tell the tale: thymus and gonad as auditioning organs: historical overview

Unlike other organs, the thymus and gonads generate non-uniform cell populations, many members of which perish, and a few survive. While it is recognized that thymic cells are 'audited' to optimize an organism's immune repertoire, whether gametogenesis could be orchestrated similarly to favour high quality gametes is uncertain. Ideally, such quality would be affirmed at early stages before the commitment of extensive parental resources. A case is here made that, along the lines of a previously proposed lymphocyte quality control mechanism, gamete quality can be registered indirectly through detection of incompatibilities between proteins encoded by the grandparental DNA sequences within the parent from which haploid gametes are meiotically derived. This 'stress test' is achieved in the same way that thymic screening for potential immunological incompatibilities is achieved - by 'promiscuous' expression, under the influence of the AIRE protein, of the products of genes that are not normally specific for that organ. Consistent with this, the Aire gene is expressed in both thymus and gonads, and AIRE deficiency impedes function in both organs. While not excluding the subsequent emergence of hybrid incompatibilities due to the intermixing of genomic sequences from parents (rather than grandparents), many observations, such as the number of proteins that are aberrantly expressed during gametogenesis, can be explained on this basis. Indeed, promiscuous expression could have first evolved in gamete-forming cells where incompatible proteins would be manifest as aberrant protein aggregates that cause apoptosis. This mechanism would later have been co-opted by thymic epithelial cells which display peptides from aggregates to remove potentially autoreactive T cells.

q-bio.TO↗

arXiv2018

Phylogeny-based tumor subclone identification using a Bayesian feature allocation model

Tumor cells acquire different genetic alterations during the course of evolution in cancer patients. As a result of competition and selection, only a few subgroups of cells with distinct genotypes survive. These subgroups of cells are often referred to as subclones. In recent years, many statistical and computational methods have been developed to identify tumor subclones, leading to biologically significant discoveries and shedding light on tumor progression, metastasis, drug resistance and other processes. However, most existing methods are either not able to infer the phylogenetic structure among subclones, or not able to incorporate copy number variations (CNV). In this article, we propose SIFA (tumor Subclone Identification by Feature Allocation), a Bayesian model which takes into account both CNV and tumor phylogeny structure to infer tumor subclones. We compare the performance of SIFA with two other commonly used methods using simulation studies with varying sequencing depth, evolutionary tree size, and tree complexity. SIFA consistently yields better results in terms of Rand Index and cellularity estimation accuracy. The usefulness of SIFA is also demonstrated through its application to whole genome sequencing (WGS) samples from four patients in a breast cancer study.

stat.AP↗

arXiv2018

Metabolomic signature of type 1 diabetes-induced sensory loss and nerve damage in diabetic neuropathy

Diabetic-induced peripheral neuropathy (DPN) is a diabetic late complication. The molecular mechanisms underlying the pathophysiology of nerve damage & sensory loss remain largely unclear. Recently, alterations in metabolic flux have gained attention a basis for organ damage in diabetes; however, peripheral sensory neurons have not been adequately analyzed. In the present study, we attempted to delineate the role of alteration of metabolic pathways in relation to nerve damage & sensory loss. We employed STZ-injected mouse model of type1 diabetes. To investigate the progression of DPN by behavioral measurements of sensitivity to thermal & mechanical stimuli and quantitative assessment of intraepidermal nerve fiber density. We employed a MS-based screen to address alterations in levels of metabolites in peripheral sciatic nerve (SN) & amino acids (AA) in serum over several months post-STZ administration. Although hyperglycemia & body weight changes occurred early, sensory loss & reduced intraepithelial branching of nociceptive nerves was only evident at 22 wks post-STZ. The longitudinal metabolites screen in SN demonstrated that mice at 12 and 22 wks post-STZ showed an early impairment the tricarboxylic acid. We found that levels of citric acid, ketoglutaric acid, succinic acid, fumaric acid & malic acid were observed to be significantly reduced in SN at 22 wks post-STZ. In addition, we also found the increase in levels of sorbitol & L-Lactate in SN from 12 wks post-STZ injection. AA screen in serum showed that the amino acids Val, Ile and Leu, increased more than 2-fold from 12 wks post-STZ. Similarly, the levels of Tyr, Asn, Ser, His, Ala, & Pro showed progressive increase. Our results indicate that the impaired TCA cycle metabolites in peripheral nerve is the primary cause of shunting metabolic substrate to compensatory pathways which leads to mitochondrial dysfunction & nerve damage.

q-bio.CB↗

arXiv2018

Calculating normal tissue complication probabilities and probabilities of complication-free tumour control from stochastic models of population dynamics

We use a stochastic birth-death model for a population of cells to estimate the normal tissue complication probability (NTCP) under a particular radiotherapy protocol. We specifically allow for interaction between cells, via a nonlinear logistic growth model. To capture some of the effects of intrinsic noise in the population we develop several approximations of NTCP, using Kramers-Moyal expansion techniques. These approaches provide an approximation to the first and second moments of a general first-passage time problem in the limit of large, but finite populations. We use this method to study NTCP in a simple model of normal cells and in a model of normal and damaged cells. We also study a combined model of normal tissue cells and tumour cells. Based on existing methods to calculate tumour control probabilities, and our procedure to approximate NTCP, we estimate the probability of complication free tumour control.

q-bio.PE↗

arXiv2018

A comprehensive review of Chronic Kidney Disease of Unknown Etiology

This review was written to provide a comprehensive summary of the suggested etiologies of Chronic Kidney Disease of Unknown Etiology (CKDu) in Sri Lanka. In this review, Chronic Kidney Disease (CKD) is explained in detail and its known etiologies are discussed. CKDu is defined and its epidemiology is discussed, with the compilation of statistic from over 15 research papers through the years 2000 to present.

q-bio.QM↗

arXiv2018

Review: the development of neural stem cell biology and technology in regenerative medicine

In the middle of the last century, it has been known that neural stem cells (NSCs) play a key role in regenerative medicine to cure the neurodegenerative disease. This review article covers about the introduction to neural stem cell biology and the isolation, differentiation and transplantation methods/techniques of neural stem cells. The neural stem cells can be transplanted into the human brain in the future to replace the damaged and dead neurons. The highly limited access to embryonic stem cells and ethical issues have escalated the search for other NSC sources. The developing technologies are indicating that it can be achieved before the end of this century. In addition, the differentiation and the maturation of NSCs can artificially accelerate by modern methods.

q-bio.NC↗

arXiv2018

Blood Glucose Measurement Based on Infra-Red Spectroscopy

An algorithm based on PLS regression has been developed and optimized for measuring blood glucose level using the infra-red transmission spectrum of blood samples. A set of blood samples were tagged with their glucose concentration using an accurate invasive glucometer and analyzed using a standard FTIR spectrometer. Using the developed algorithm, the results of the FTIR spectroscopy of the samples were analyzed to find the glucose concentration in the samples. The obtained glucose concentration by the algorithm were in good agreement with the results obtained by the standard glucometer, and the mean estimation error was 7 mg/dL. This error is in the range of available commercial invasive meters.

q-bio.QM↗

arXiv2018

Principal Process Analysis of dynamic GlucoCEST MRI data

GlucoCEST is an MRI contrast enhancement technique sensitive to the concentration of sugar in the tissue. Because of a differencein metabolism, it is thought that tumors consume more sugar than normal tissue. However, glucose metabolism is complex and depends onmany processes, which are all important to understand the origin of the measured signal. To achieve this goal we apply here a process analysismethod to a deterministic system describing the metabolism of glucose in the tissue.

q-bio.TO↗

arXiv2018

Are homeostatic states stable? Dynamical stability in morphoelasticity

Biological growth is often driven by mechanical cues, such as changes in external pressure or tensile loading. Moreover, it is well known that many living tissues actively maintain a preferred level of mechanical internal stress, called the mechanical homeostasis. The tissue-level feedback mechanism by which changes of the local mechanical stresses affect growth is called a growth law within the theory of morphoelasticity, a theory for understanding the coupling between mechanics and geometry in growing and evolving biological materials. The goal of this article is to develop mathematical techniques to analyze growth laws and to explore issues of heterogeneity and growth stability. We discuss the growth dynamics of tubular structures, which are very common in biology (e.g. arteries, plant stems, airways) and model the homeostasis-driven growth dynamics of tubes which produces spatially inhomogeneous residual stress. We show that the stability of the homeostatic state depends nontrivially on the anisotropy of the growth response. The key role of anisotropy may provide a foundation for experimental testing of homeostasis-driven growth laws.

physics.bio-ph↗

arXiv2018

Micro-sized cold atmospheric plasma source for brain and breast cancer treatment

Micro-sized cold atmospheric plasma (uCAP) has been developed to expand the applications of CAP in cancer therapy. In this paper, uCAP devices with different nozzle lengths were applied to investigate effects on both brain (glioblastoma U87) and breast (MDA-MB-231) cancer cells. Various diagnostic techniques were employed to evaluate the parameters of uCAP devices with different lengths such as potential distribution, electron density, and optical emission spectroscopy. The generation of short- and long-lived species (such as hydroxyl radical (.OH), superoxide (O2-), hydrogen peroxide (H2O2), nitrite (NO2-), et al) were studied. These data revealed that uCAP treatment with a 20 mm length tube has a stronger effect than that of the 60 mm tube due to the synergetic effects of reactive species and free radicals. Reactive species generated by uCAP enhanced tumor cell death in a dose-dependent fashion and was not specific with regards to tumor cell type.

q-bio.TO↗

arXiv2018

The application of collagen in advanced wound dressings

Chronic wounds fail to proceed through an orderly and timely self healing process, resulting in cutaneous damage with full thickness in depth and leading to a major healthcare and economic burden worldwide. In the UK alone, 200,000 patients suffer from a chronic wound, whilst the global advanced wound care market is expected to reach nearly $11 million in 2022. Despite extensive research efforts so far, clinically-approved chronic wound therapies are still time-consuming, economically unaffordable and present restricted customisation. In this chapter, the role of collagen in the extracellular matrix of biological tissues and wound healing will be discussed, together with its use as building block for the manufacture of advanced wound dressings. Commercially-available collagen dressings and respective clinical performance will be presented, followed by an overview on the latest research advances in the context of multifunctional collagen systems for advanced wound care.

q-bio.TO↗

arXiv2018

Three potential sources of cell injuries of lymphoid cells associated with developments of lymphoid leukemia and lymphoma

Lymphoid leukemia (LL) and lymphoma are blood cancers developed from lymphoid cells (LCs). To understand the cause and the mechanism of cell transformation of a LC, we studied the potential sources of cell injuries of LCs and analyzed how DNA changes are generated and accumulate in LCs. I. The DNA changes that contribute to cell transformation of a LC can be generated in the LCs in marrow, thymus, lymph nodes (LNs), and/or lymphoid tissues (LTs). In LNs/LTs, pathogen-infections may be the main cause for cell injuries of LCs. In marrow cavity, repeated bone-remodeling during bone-growth and bone-repair, by producing toxic substances, may be a source of damage to hematopoietic cells, including hematopoietic stem cells (HSCs) and developing LCs. In thymus, thymic involution and death of stromal cells may be a damaging factor for the developing T-cells. II. Point DNA mutation (PDM) and chromosome change (CC) are the two major types of DNA changes. CCs include numerical CCs (NCCs) and structural CCs (SCCs). Generation of a PDM/SCC may be a result of Misrepair of DNA on DNA breaks. Generation of NCC is rather a consequence of dysfunction of cell division. III. Repeated cell injuries and cell proliferation drive the accumulation of DNA changes in LCs and HSCs. However, long-term accumulation of DNA changes occurs mainly in long-living stem cells including HSCs and memory cells. In conclusion, the DNA changes in LCs are generated and accumulate as a consequence of repeated cell injuries and repeated cell proliferation; and three potential sources of cell injuries of LCs may be: repeated bone-remodeling, long-term thymic involution, and repeated pathogen-infections.

q-bio.TO↗

arXiv2018

Causal Scale Shift Associated with Phase Transition to Human Atrial Fibrillation

An example of phase transition in natural complex systems is the qualitative and sudden change in the heart rhythm between sinus rhythm and atrial fibrillation (AF), the most common irregular heart rhythm in humans. While the system behavior is centrally controlled by the behavior of the sinoatrial node in sinus rhythm, the macro-scale collective behavior of the heart causes the micro-scale behavior in AF. To quantitatively analyze this causation shift associated with phase transition in human heart, we evaluated the causal architecture of the human cardiac system using the time series of multi-lead intracardiac unipolar electrograms in a series of spatiotemporal scales by generating a stochastic renormalization group. We found that the phase transition between sinus rhythm and AF is associated with a significant shift of the peak causation from macroscopic to microscopic scales. Causal architecture analysis may improve our understanding of causality in phase transitions in other natural and social complex systems.

q-bio.TO↗

arXiv2018

Acute lymphoblastic leukemia may develop as a result of rapid transformation of a lymphoblast triggered by repeated bone-remodeling during bone-growth

Acute lymphoblastic leukemia (ALL) and chronic lymphocytic leukemia (CLL) are two major forms of leukemia that arise from lymphoid cells (LCs). ALL occurs mostly in children and CLL occurs mainly in old people. However, the Philadelphia-chromosome-positive ALL (Ph+-ALL) and the Ph-like ALL occur in both children and adults. To understand childhood leukemia/lymphoma, we have recently proposed two hypotheses on the causes and the mechanism of cell transformation of a LC. Hypothesis A is: repeated bone-remodeling during bone-growth and bone-repair may be a source of cell injuries of marrow cells including hematopoietic stem cells (HSCs), myeloid cells, and LCs. Hypothesis B is: a LC may have three pathways on transformation: a slow, a rapid, and an accelerated. We discuss in the present paper the developing mechanisms of ALL and CLL by these hypotheses. Having a peak incidence in young children, ALL may develop mainly as a result of rapid cell transformation of a lymphoblast (or pro-lymphocyte). Differently, Ph+-ALL and Ph-like ALL may develop as results of transformation of a lymphoblast via accelerated pathway. Occurring mainly in adults, CLL may be a result of transformation of a memory B-cell via slow pathway. By causing cell injuries of HSCs and LCs, repeated bone-remodeling during bone-growth and bone-repair may be related to the cell transformation of a LC. In conclusion, ALL may develop as a result of cell transformation of a lymphoblast via rapid or accelerated pathway; and repeated bone-remodeling during bone-growth may be a trigger for the cell transformation of a lymphoblast in a child.

q-bio.CB↗

arXiv2018

Pediatric lymphoma may develop by "one-step" cell transformation of a lymphoid cell

Lymphomas are a large group of neoplasms developed from lymphoid cells (LCs) in lymph nodes (LNs) or lymphoid tissues (LTs). Some forms of lymphomas, including Burkitt lymphoma (BL), ALK+ anaplastic large cell lymphoma (ALK+-ALCL), and T-cell lymphoblastic lymphoma/leukemia (T-LBL), occur mainly in children and teenagers. Hodgkin's lymphoma (HL) has a peak incidence at age 20s. To understand pediatric lymphoma, we have recently proposed two hypotheses on the causes and the mechanism of cell transformation of a LC. Hypothesis A is: repeated bone-remodeling during bone-growth and bone-repair may be a source of cell injuries of marrow cells including hematopoietic stem cells (HSCs), myeloid cells, and LCs, and thymic involution may be a source of damage to the developing T-cells in thymus. Hypothesis B is: a LC may have three pathways on transformation: a slow, a rapid, and an accelerated. In this paper, we discuss pediatric lymphomas by this hypothesis. Having a peak incidence at young age, BL, T-LBL, ALK+-ALCL, and HL develop more likely as a result of rapid transformation of a LC. In BL, ALK+-ALCL, and HL, the cell transformations may be triggered by severe viral infections. In T-LBL, the cell transformation may be related to thymic involution. Occurring in both adults and children, diffuse large B-cell lymphoma (DLBCL) may develop via slow or accelerated pathway. In conclusion, pediatric lymphoma may develop as a result of "one-step" cell transformation of a LC, and severe viral infections may be the main trigger for the rapid transformation of a LC in a LN/LT.

q-bio.CB↗

arXiv2018

Development of pediatric myeloid leukemia may be related to the repeatedbone-remodeling during bone-growth

Acute myeloid leukemia (AML) and chronic myeloid leukemia (CML) are two major formsof leukemia developed from myeloid cells (MCs). To understand why AML and CML occurin children, we analyzed the causes and the mechanism of cell transformation of a MC. I. Forthe MCs in marrow cavity, repeated bone-remodeling during bone-growth may be a source ofcell injuries. II. As a type of blood cell, a MC may have higher survivability from DNAchanges and require obtaining fewer cancerous properties for cell transformation than a tissuecell. III. Point DNA mutations (PDMs) and chromosome changes (CCs) are the two majortypes of DNA changes. CCs have three subtypes by effects on a cell: great effect CCs(GECCs), mild-effect CCs (MECCs), and intermediate-effect CCs (IECCs). A GECC affectsone or more genes and can alone trigger cell transformation. PDMs/MECCs are mostly mildand can accumulate in cells. Some of the PDMs/MECCs contribute to cell transformation. AnIECC affects one or more genes and participates in cell transformation. IV. Based on II andIII, we hypothesize that a MC may have two pathways on transformation: a slow and anaccelerated. Slow pathway is driven by accumulation of PDMs/MECCs. Accelerated pathwayis driven by accumulation of PDMs/MECCs/IECC(s). A transformation via slow pathwayoccurs at old age; whereas that via accelerated pathway occurs at any age. Thus, CML andpediatric AML may develop via accelerated pathway, and adult AML may develop via bothpathways. In conclusion, pediatric AML and CML may develop as a result of transformationof a MC via accelerated pathway; and repeated bone-remodeling for bone-growth may be atrigger for the transformation of a MC in a child.

q-bio.CB↗

arXiv2018

Approximate Analytical Solution of a Cancer Immunotherapy Model by the Application of Differential Transform and Adomian Decomposition Methods

Immunotherapy plays a major role in tumour treatment, in comparison with other methods of dealing with cancer. The Kirschner-Panetta (KP) model of cancer immunotherapy describes the interaction between tumour cells, effector cells and interleukin-2 which are clinically utilized as medical treatment. The model selects a rich concept of immune-tumour dynamics. In this paper, approximate analytical solutions to KP model are represented by using the differential transform and Adomian decomposition. The complicated nonlinearity of the KP system causes the application of these two methods to require more involved calculations. The approximate analytical solutions to the model are compared with the results obtained by numerical fourth order Runge-Kutta method.

q-bio.TO↗