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Search Results: 1 - 10 of 1093 matches for " Kirsten Tillisch "
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Functional Somatic Syndromes: Emerging Biomedical Models and Traditional Chinese Medicine
Steven Tan,Kirsten Tillisch,Emeran Mayer
Evidence-Based Complementary and Alternative Medicine , 2004, DOI: 10.1093/ecam/neh016
Abstract: The so-called functional somatic syndromes comprise a group of disorders that are primarily symptom-based, multisystemic in presentation and probably involve alterations in mind-brain-body interactions. The emerging neurobiological models of allostasis/allostatic load and of the emotional motor system show striking similarities with concepts used by Traditional Chinese Medicine (TCM) to understand the functional somatic disorders and their underlying pathogenesis. These models incorporate a macroscopic perspective, accounting for the toll of acute and chronic traumas, physical and emotional stressors and the complex interactions between the mind, brain and body. The convergence of these biomedical models with the ancient paradigm of TCM may provide a new insight into scientifically verifiable diagnostic and therapeutic approaches for these common disorders.
Regional Neuroplastic Brain Changes in Patients with Chronic Inflammatory and Non-Inflammatory Visceral Pain
Jui-Yang Hong, Jennifer S. Labus, Zhiguo Jiang, Cody Ashe-Mcnalley, Ivo Dinov, Arpana Gupta, Yonggang Shi, Jean Stains, Nuwanthi Heendeniya, Suzanne R. Smith, Kirsten Tillisch, Emeran A. Mayer
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0084564
Abstract: Regional cortical thickness alterations have been reported in many chronic inflammatory and painful conditions, including inflammatory bowel diseases (IBD) and irritable bowel syndrome (IBS), even though the mechanisms underlying such neuroplastic changes remain poorly understood. In order to better understand the mechanisms contributing to grey matter changes, the current study sought to identify the differences in regional alterations in cortical thickness between healthy controls and two chronic visceral pain syndromes, with and without chronic gut inflammation. 41 healthy controls, 11 IBS subjects with diarrhea, and 16 subjects with ulcerative colitis (UC) underwent high-resolution T1-weighted magnetization-prepared rapid acquisition gradient echo scans. Structural image preprocessing and cortical thickness analysis within the region of interests were performed by using the Laboratory of Neuroimaging Pipeline. Group differences were determined using the general linear model and linear contrast analysis. The two disease groups differed significantly in several cortical regions. UC subjects showed greater cortical thickness in anterior cingulate cortical subregions, and in primary somatosensory cortex compared with both IBS and healthy subjects. Compared with healthy subjects, UC subjects showed lower cortical thickness in orbitofrontal cortex and in mid and posterior insula, while IBS subjects showed lower cortical thickness in the anterior insula. Large effects of correlations between symptom duration and thickness in the orbitofrontal cortex and postcentral gyrus were only observed in UC subjects. The findings suggest that the mechanisms underlying the observed gray matter changes in UC subjects represent a consequence of peripheral inflammation, while in IBS subjects central mechanisms may play a primary role.
Sex-Related Differences of Cortical Thickness in Patients with Chronic Abdominal Pain
Zhiguo Jiang, Ivo D. Dinov, Jennifer Labus, Yonggang Shi, Alen Zamanyan, Arpana Gupta, Cody Ashe-McNalley, Jui-Yang Hong, Kirsten Tillisch, Arthur W. Toga, Emeran A. Mayer
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0073932
Abstract: Background & Aims Regional reductions in gray matter (GM) have been reported in several chronic somatic and visceral pain conditions, including irritable bowel syndrome (IBS) and chronic pancreatitis. Reported GM reductions include insular and anterior cingulate cortices, even though subregions are generally not specified. The majority of published studies suffer from limited sample size, heterogeneity of populations, and lack of analyses for sex differences. We aimed to characterize regional changes in cortical thickness (CT) in a large number of well phenotyped IBS patients, taking into account the role of sex related differences. Methods Cortical GM thickness was determined in 266 subjects (90 IBS [70 predominantly premenopausal female] and 176 healthy controls (HC) [155 predominantly premenopausal female]) using the Laboratory of Neuro Imaging (LONI) Pipeline. A combined region of interest (ROI) and whole brain approach was used to detect any sub-regional and vertex-level differences after removing effects of age and total GM volume. Correlation analyses were performed on behavioral data. Results While IBS as a group did not show significant differences in CT compared to HCs, sex related differences were observed both within the IBS and the HC groups. When female IBS patients were compared to female HCs, whole brain analysis showed significant CT increase in somatosensory and primary motor cortex, as well as CT decrease in bilateral subgenual anterior cingulate cortex (sgACC). The ROI analysis showed significant regional CT decrease in bilateral subregions of insular cortex, while CT decrease in cingulate was limited to left sgACC, accounting for the effect of age and GM volume. Several measures of IBS symptom severity showed significant correlation with CT changes in female IBS patients. Conclusions Significant, sex related differences in CT are present in both HCs and in IBS patients. The biphasic neuroplastic changes in female IBS patients are related to symptom severity.
Water and the Configuration of Social Worlds: An Anthropological Perspective  [PDF]
Kirsten Hastrup
Journal of Water Resource and Protection (JWARP) , 2013, DOI: 10.4236/jwarp.2013.54A009
Abstract:

From an anthropological perspective, water is not only the sine qua non of life in general, it is also seen to configure societies in particular ways, and to generate particular values. This will be substantiated in four moves. First, the hydrological cycle and other elementals of water will be discussed. Second, we shall zoom in on rivers, transforming natural resources and social communities as they bend and twist. Third, we shall discuss artificially established canals, emulating natural flows, but having their own long-term social and political implications. Fourth, we shall focus on wells, providing nodal points of social life and potential conflict. The article ends with some observations on water as a theory-machine.

Normal Human Cell Conversion to 3-D Cancer-like Growth: Genome Damage, Endopolyploidy, Senecence Escape, and Cell Polarity Change/Loss  [PDF]
Kirsten H. Walen
Journal of Cancer Therapy (JCT) , 2011, DOI: 10.4236/jct.2011.22023
Abstract: In cell cultures monolayered cell growth is controlled by contact inhibition which again is controlled by the cell polarity system by always being positioned in accord with the cytoskeleton axis. Presently, cycling endopolyploid cells (tetraploidy) were shown to undergo perpendicular divisions relative to the cytoskeleton axis which disrupted to some degree contact inhibition in the near-senescent phase of human primary cells. These experiments included genome damage-induced endopolyploidization (TAS-treated) to simulate as a model system the state of in vivo accelerated cell senescence (ACS) which is induced by therapy-associated genomic damage. From ACS delayed tumor re-growth (re-lapse) occurs from “robust” cell propagation, but mechanisms for such cell escape from senescence are unknown. For TAS-treated a karyoplast bud-off process with change to limited mitotic activity occurred in young senescent cultures. In old, deep senescent (5 - 8 weeks) cultures, unexpectedly escape cell-growth showed three dimensional (3-D) tumor-like spheres from growths of morphologically different cells as compared to the fibroblastic phenotype. These cells expressed cell polarity change, and very condensed nuclei were variously perpendicularly oriented to what-ever cell polarity was present. These results were discussed in regard to in vivo relapse and, to the importance of cell polarity change in tumorigenesis. Induced senescence as an anti-tumor mechanism in therapy treatment becomes a questionable procedure from the present experimental results.
Neoplastic-Like CELL Changes of Normal Fibroblast Cells Associated with Evolutionary Conserved Maternal and Paternal Genomic Autonomous Behavior (Gonomery)  [PDF]
Kirsten H. Walen
Journal of Cancer Therapy (JCT) , 2014, DOI: 10.4236/jct.2014.59094
Abstract:

The present comparative review discusses conservation of early evolutionary, relic genetics in the genome of man, which determine two different mechanistic reductive division systems expressed by normal, human diploid cells. The divisions were orderly and segregated genomes reductively to near-diploid daughter cells, which showed gain of a proliferative advantage (GPA) over cells of origin. This fact of GPA expression is a fundamental requirement for initiation of tumorigenesis. The division systems were responses to a carcinogen-free induction system, consisting of short (1 - 3 days) exposures of young cells to nutritional deprivation of amino acid glutamine (AAD). In recovery growth (2 - 4 days) endo-tetra/ochtoploid cells and normal diploid metaphase cells demonstrated chromosomal reductive divisions to respectively heterozygous and homozygous altered daughter cells. Both division systems showed co-segregating whole complements, which for reduction of the diploid metaphases could only arise from gonomeric-based autonomous behavior of maternal and paternal (mat/pat) genomes. The timely associated appearance with these latter divisions was fast growing small-cells (1/2 volume-size reduced from normal diploidy), which became homozygous from haploid, genomic doubling. Both reductive divisions thus produced genome altered progeny cells with GPA, which was associated with pre-cancer-like cell-phenotypic changes. Since both “undesirable” reductive divisions expressed orderly division sequences, their genetic controls were assumed to be “old genetics”, evolutionarily conserved in the genome of man. Support for this idea was a search for evidential material in the evolutionary record from primeval time, when haploid organisms were established. The theory was that endopolyploid and gonomery-based reductive divisions relieved the early eukaryotic organisms from accidental, non-proliferative diploidy and polyploidy, bringing the organism back to vegetative haploid proliferation. Asexual cycles were common for maintenance of propagating haploid and diploid early unicellular eukaryotes.

Haploidization of Human Diploid Metaphase Cells: Is This Genome Reductive Mechanism Opperational in Near-Haploid Leukemia?  [PDF]
Kirsten H. Walen
Journal of Cancer Therapy (JCT) , 2014, DOI: 10.4236/jct.2014.51013
Abstract:

The present study presents cytogenetics/cytology of haploidization in the origin of a new, fast growing diploid, small cell-type (F-dPCs). The sequence of events was haploid groupings of the chromosomes in normal, human metaphase cells, followed by genomic doubling to homozygousdiploidy. These events were responses to DNA replication stress fromamino acid glutamine deprivation. Importantly, these homozygous cells outgrew normal fibroblasts in 2 - 3 passages—they had gained proliferative advantage (GPA), presumably from loss (LOH) of tumor suppressor genes. They were morphologically changed cells with rounded nuclei that grew in a “streaming” growth pattern and with changed form and size of mitosis, similar to some hyperplasias. The grouping of the chromosomes in metaphase cells was asymmetric with a narrow range around the median (23) (no micro-nuclei), suggesting genetic control. The root-origin of haploidization was evidenced by maternal and paternal genomes occupying separate territories in metaphase cells, which assumedly permitted independent segregations of bichromatid chromosomes. In near-haploid ALL-L1 leukemia the loss of virtually, whole chromosomal complements was judged by SNP array analyses, as a primary event before genomic doubling to hyperdiploidy with LOH. From the present data such specific, non-random loss of chromosomes strongly suggested, a haploidization process capable of genomic doubling, as observed for the “birth” of the small, F-dPCs. This suggestion was supported by this type of leukemia being the L1-type, where L1 signifies small cells. The possibility now exists that a tumorigenic process can be initiated directly from diploid cells through haploid

Cancers in Children Ages 8 to 12 Are Injury-Related  [PDF]
Kirsten H. Walen
Journal of Cancer Therapy (JCT) , 2015, DOI: 10.4236/jct.2015.62020
Abstract:

Cancers in young children in early growing age was a short PBS (KQED) report (11/21/2014), but without informational source, which prompted a Google search. Sports-associated injuries with medical healing treatments concluded that there were no association between these body traumas and cancer development. But there are other activities from young children, such as “dare-devil” skateboard and bicycling meter-high jumping with potential high energy falls, to serious broken-bone injuries. Falls of children are among the most common causes of US emergency response. The question is why bodily injury is associated with cancer-development? An answer to this question was exemplified by osteosarcoma in young children, which suggested that injury to growing points of bone and surrounding soft tissue cells would elicit a repair process (wound healing process) producing polyploidy with diplochromosomes. The non-mitotic reductive division of such 4-chromatid chromosomes has been shownin vitroto produce pathological cancer-like phenotypes, including gain of a proliferative advantage.

Wound Healing Is a First Response in a Cancerous Pathway: Hyperplasia Developments to 4n Cell Cycling in Dysplasia Linked to Rb-Inactivation  [PDF]
Kirsten H. Walen
Journal of Cancer Therapy (JCT) , 2015, DOI: 10.4236/jct.2015.610099
Abstract: In a series of publications, the hypothesis of a special-type of endo-polyploidy, marked by 4-chromatid chromosomes (diplochromosomes), in the initiation of tumorigenesis has been presented from in vitro experiments. This review uses cellular happenings in benign pre-neoplasia to substantiate this idea, which appears to be linked to the wound-healing process of injured tissue. Rarer association between a wound healing process and a cancer occurrence has long been known. The wound healing multi-program-system involved a phase of tetraploidy that showed diplochromosomes. The hypothesis is that the inflammatory phase may not always be sufficient in getting rid of dead and damaged cells (by apoptosis and autophagy), such that cells with genomic damage (DNA breakage) may survive by genomic repair associated with change to diplochromosomal tetraploidy. In vitro data have shown division of these cells to be an orderly, mechanistic two-step, meiotic-like system, resulting in only two types of progeny cells: 4n/4C/G1 and 2n/2C/G1 pseudo-diploid cells with hyperplastic-like growth-morphology. In vivo damage to tissues can be from many sources for example, physical, toxic environment or from a disease as in Barrett’s esophagus (BE) with acid reflux into the esophagus. For this condition, it is acknowledged that damage of the esophagus lining is a pre-condition to hyperplastic lesions of pre-neoplasia. These initial lesions were from “diploid” propagating cells and, 4n cells with G2 genomic content (no mitosis) accumulated in these lesions before a change to dysplasia. Cell cycle kinetics put these 4n cells in G1, which with S-phase entry would lead to asymmetric tetraploid mitoses, characteristic for dysplastic lesions. This change in hyperplasia to dysplasia is the root-essential condition for a potential progression of pre-neoplasia to cancer. In BE the hyperplastic lesion showed increasing gains of cells with inactivated p53 and p16[ink4a] genes, which destroyed the retinoblastoma (Rb) protein-control over S-phase entry from G1. Rb-protein is a key controller of cycling advancement from G1 (also for normal cells), and is frequently inactivated in tumor cells. Thus in BE, 4n/4C/G1 cells with
Cancer Prevention? Fundamental Genomic Alterations Are Present in Preneoplasia, Including Function of High Frequency Selected Mutations (HFSMs)  [PDF]
Kirsten H. Walen
Journal of Cancer Therapy (JCT) , 2016, DOI: 10.4236/jct.2016.76044
Abstract: In a series of publications a special, tetraploid diplochromosomal division system to only two types of progeny cells (4n/4C/G1 and 2n/4C para-diploid) has been suggested to initiate preneoplasia that can lead to a cancerous pathway. Colorectal and other preneoplasia are known with the pathogenic, histological phases of hyperplasia to arrested adenoma/nevi that can give rise to dysplasia with high risk for cancer development. The present theme is to find solutions to tumorigenic unsolved, biological problems (queries), explainable from the tetraploid 4n-system, which would support its operation in the cancerous pathway. Presently admitted, the mutational sequencing of the cancer genome (cancer chemistry) cannot discover so-called “dark matter”, which herein is considered to be the queries. The solutions from the 4n-system were largely supported by mutated APC-induced same type of tetraploidy from the mitotic slippage process. But importantly, these behaviors and consequences could be linked to the beginning of hyperplastic lesions and their development to the arrest-phase of preneoplasia (polyps/nevi). Function of HFSMs is mostly unknown, but for Barrett’s esophagus, HFSMs (p53, p16ink4a) caused inactivation of the Rb gene, leading to dysplasia with 4n, aneuploid, abnormal cell cycles. In vitro models of the 4n-system from normal human cells recapitulated preneoplasia-like histopathological changes. It was speculated that the “cancer-crucial” step to dysplasia could be therapy-vulnerable to CRISPR-caspase editing, and perhaps antibody treatment. Additionally, the 4n-system with spontaneous cell-behaviors together with preneoplasia molecular data promises construction of a more truthful cancer-paradigm than from sequencing data alone.
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