Displaying publications 21 - 40 of 117 in total

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  1. Fulltext Expression of gamma glutamyl hydrolase and carbonic anhydrase 9 in oral squamous cell carcinoma and their association with extracapsular spread
    Nor Aszlitah Burhanudin, Thomas George Kallarakkal
    International Medical Journal Malaysia, 2017;16(21):17-17.
    MyJurnal
    Extracapsular spread (ECS) is one of the most important prognostic factors in oral
    squamous cell carcinoma (OSCC). Gamma Glutamyl Hydrolase (GGH) is a lysosomal enzyme which is involved in folate homeostasis. It is overexpressed in several human malignancies but its role in
    OSCC has never been reported. Carbonic Anhydrase 9 (CA9) is a transmembrane glycoprotein and is
    related to hypoxia. High expression of CA9 has been associated with poor prognosis in several
    tumours including OSCC. This study was aimed to investigate the expression of GGH and CA9 in
    OSCC and their potential use as biomarkers to predict ECS. (Copied from article).
    Matched MeSH terms: Homeostasis
  2. Fulltext Three-dimensional cell culture at the frontiers of in vitro cancer research: present perspectives
    Lee, Soo Leng, Zainal Ariff Abdul Rahman, Tsujigiwa, Hidetsugu, Takabatake, Kiyofumi, Nakano, Keisuke, Chai, Wen Lin, et al.
    Ann Dent, 2016;23(1):13-22.
    MyJurnal
    In recent years, three-dimensional (3D) in vitro cell culture models have earned great attention, especially in the field of human cancer disease modelling research as they provide a promising alternative towards the conventional two-dimensional (2D) monolayer culture of cells with improved tissue organization. In 2D cell culture systems, the complexity of cells on a planar surface does not accurately reflects the in vivo cellular microenvironment. Cells propagated in 3D cell culture model, on the other hand, exhibit physiologically relevant cell-to-cell interactions and cell-to-extracellular matrix (ECM) interactions, important in maintaining a normal homeostasis and specificity of tissues. This review gives an overview on 2D models and their limitations, followed by 3D cell culture models, their advantages, drawbacks and challenges in present perspectives. The review also highlights the dissimilarities of 2D and 3D models and the applicability of 3D models in current cancer research
    Matched MeSH terms: Homeostasis
  3. Fulltext Bile Acids: Physiological Activity and Perspectives of Using in Clinical and Laboratory Diagnostics
    Shansky Y, Bespyatykh J
    Molecules, 2022 Nov 13;27(22).
    PMID: 36431930 DOI: 10.3390/molecules27227830
    Bile acids play a significant role in the digestion of nutrients. In addition, bile acids perform a signaling function through their blood-circulating fraction. They regulate the activity of nuclear and membrane receptors, located in many tissues. The gut microbiota is an important factor influencing the effects of bile acids via enzymatic modification. Depending on the rate of healthy and pathogenic microbiota, a number of bile acids may support lipid and glucose homeostasis as well as shift to more toxic compounds participating in many pathological conditions. Thus, bile acids can be possible biomarkers of human pathology. However, the chemical structure of bile acids is similar and their analysis requires sensitive and specific methods of analysis. In this review, we provide information on the chemical structure and the biosynthesis of bile acids, their regulation, and their physiological role. In addition, the review describes the involvement of bile acids in various diseases of the digestive system, the approaches and challenges in the analysis of bile acids, and the prospects of their use in omics technologies.
    Matched MeSH terms: Homeostasis
  4. The homeostasis and therapeutic applications of innate and adaptive immune cells in periodontitis
    Junxian L, Mehrabanian M, Mivehchi H, Banakar M, Etajuri EA
    Oral Dis, 2023 Oct;29(7):2552-2564.
    PMID: 36004490 DOI: 10.1111/odi.14360
    OBJECTIVES: Periodontitis (PD) is one of the most common dental disorders. This chronic oral inflammation is caused by complicated interrelations between bacterial infections, dysregulated immune reactions, and environmental risk factors. A dysregulated immune response can lead to inflammatory bone resorption by allowing the recruitment of pro-inflammatory immune cells to the periodontal tissues.

    SUBJECTS: The recruitment of innate and adaptive immune cells in PD initiates the acute and following chronic inflammatory processes. The inflamed tissues, on the other hand, can be restored if the anti-inflammatory lineages are predominantly established in the periodontal tissues. Therefore, we aimed to review the published literature to provide an overview of the existing knowledge about the role of immune cells in PD, as well as their possible therapeutic applications.

    RESULTS: Experimental studies showed that drugs/systems that negatively regulate inflammatory cells in the body, as well as interventions aimed at increasing the number of anti-inflammatory cells such as Tregs and Bregs, can both help in the healing process of PD.

    CONCLUSION: Targeting immune cells or their positive/negative manipulations has been demonstrated to be an effective therapeutic method. However, to use this sort of immunotherapy in humans, further pre-clinical investigations, as well as randomized clinical trials, are required.

    Matched MeSH terms: Homeostasis
  5. Fulltext Disruptive environmental chemicals and cellular mechanisms that confer resistance to cell death
    Narayanan KB, Ali M, Barclay BJ, Cheng QS, D'Abronzo L, Dornetshuber-Fleiss R, et al.
    Carcinogenesis, 2015 Jun;36 Suppl 1:S89-110.
    PMID: 26106145 DOI: 10.1093/carcin/bgv032
    Cell death is a process of dying within biological cells that are ceasing to function. This process is essential in regulating organism development, tissue homeostasis, and to eliminate cells in the body that are irreparably damaged. In general, dysfunction in normal cellular death is tightly linked to cancer progression. Specifically, the up-regulation of pro-survival factors, including oncogenic factors and antiapoptotic signaling pathways, and the down-regulation of pro-apoptotic factors, including tumor suppressive factors, confers resistance to cell death in tumor cells, which supports the emergence of a fully immortalized cellular phenotype. This review considers the potential relevance of ubiquitous environmental chemical exposures that have been shown to disrupt key pathways and mechanisms associated with this sort of dysfunction. Specifically, bisphenol A, chlorothalonil, dibutyl phthalate, dichlorvos, lindane, linuron, methoxychlor and oxyfluorfen are discussed as prototypical chemical disruptors; as their effects relate to resistance to cell death, as constituents within environmental mixtures and as potential contributors to environmental carcinogenesis.
    Matched MeSH terms: Homeostasis/drug effects
  6. The 808 nm and 980 nm infrared laser irradiation affects spore germination and stored calcium homeostasis: A comparative study using delivery hand-pieces with standard (Gaussian) or flat-top profile
    Ferrando S, Agas D, Mirata S, Signore A, De Angelis N, Ravera S, et al.
    J. Photochem. Photobiol. B, Biol., 2019 Oct;199:111627.
    PMID: 31536925 DOI: 10.1016/j.jphotobiol.2019.111627
    Photobiomodulation relies on the transfer of energy from incident photons to a cell photoacceptor. For many years the concept of photobiomodulation and its outcome has been based upon a belief that the sole receptor within the cell was the mitochondrion. Recently, it has become apparent that there are other photoacceptors operating in different regions of the electromagnetic spectrum. Alternative photoacceptors would appear to be water and mechanisms regulating calcium homeostasis, despite a direct effect of laser photonic energy on intracellular calcium concentration outwith mitochondrial activity or influence, have not been clearly demonstrated. Therefore, to increase the knowledge of intracellular‑calcium and laser photon interaction, as well as to demonstrate differences in irradiation profiles with modern hand-pieces, we tested and compared the photobiomodulatory effect of 808 nm and 980 nm diode laser light by low- and higher-energy (60s, 100 mW/cm2, 100 mW/cm2, 500 mW/cm2, 1000 mW/cm2, 1500 mW/cm2, 2000 mW/cm2) irradiated with a "standard" (Gaussian fluence distribution) hand-piece or with a "flat-top" (uniform fluence) hand-piece. For this purpose, we used the eukaryote unicellular-model Dictyostelium discoideum. The 808 nm and 980 nm infrared laser light, at the energy tested directly affect the stored Ca2+ homeostasis, independent of the mitochondrial respiratory chain activities. From an organism perspective, the effect on Ca2+-dependent signal transduction as the regulator of spore germination in Dictyostelium, demonstrates how a cell can respond quickly to the correct laser photonic stimulus through a different cellular pathway than the known light-chromophore(mitochondria) interaction. Additionally, both hand-piece designs tested were able to photobiomodulate the D. discoideum cell; however, the hand-piece with a flat-top profile, through uniform fluence levels allows more effective and reproducible effects.
    Matched MeSH terms: Homeostasis/radiation effects*
  7. Fulltext Assessment of Telomere Length in Archived Formalin-Fixed, Paraffinized Human Tissue Is Confounded by Chronological Age and Storage Duration
    Kong PL, Looi LM, Lau TP, Cheah PL
    PLoS One, 2016;11(9):e0161720.
    PMID: 27598341 DOI: 10.1371/journal.pone.0161720
    Telomeres shorten with physiological aging but undergo substantial restoration during cancer immortalization. Increasingly, cancer studies utilize the archive of formalin-fixed, paraffin-embedded (FFPE) tissues in diagnostic pathology departments. Conceptually, such studies would be confounded by physiological telomere attrition and loss of DNA integrity from prolonged tissue storage. Our study aimed to investigate these two confounding factors. 145 FFPE tissues of surgically-resected, non-diseased appendixes were retrieved from our pathology archive, from years 2008 to 2014. Cases from 2013 to 2014 were categorized by patient chronological age (0-20 years, 21-40 years, 41-60 years, > 60 years). Telomere lengths of age categories were depicted by telomere/chromosome 2 centromere intensity ratio (TCR) revealed by quantitative fluorescence in situ hybridization. Material from individuals aged 0-20 years from years 2013/2014, 2011/2012, 2009/2010, and 2008 were compared for storage effect. Telomere integrity was assessed by telomere fluorescence intensity (TFI). Epithelial TCRs (mean ± SD) for the respective age groups were 4.84 ± 2.08, 3.64 ± 1.21, 2.03 ± 0.37, and 1.93 ± 0.45, whereas corresponding stromal TCRs were 5.16 ± 2.55, 3.84 ± 1.36, 2.49 ± 1.20, and 2.93 ± 1.24. A trend of inverse correlation with age in both epithelial and stromal tissues is supported by r = -0.69, p < 0.001 and r = -0.42, p < 0.001 respectively. Epithelial TFIs (mean ± SD) of years 2013/2014, 2011/2012, 2009/2010 and 2008 were 852.60 ± 432.46, 353.04 ± 127.12, 209.24 ± 55.57 and 429.22 ± 188.75 respectively. Generally, TFIs reduced with storage duration (r = -0.42, p < 0.001). Our findings agree that age-related telomere attrition occurs in normal somatic tissues, and suggest that an age-based reference can be established for telomere studies on FFPE tissues. We also showed that FFPE tissues archived beyond 2 years are suboptimal for telomere analysis.
    Matched MeSH terms: Telomere Homeostasis/genetics*
  8. Homeostatic indices of insulin resistance among gestational diabetics in anticipating pregnancy complications
    Ismail NA, Kasim MM, Noor Aizuddin A, Umar NA
    Gynecol Endocrinol, 2013 Jul;29(7):691-4.
    PMID: 23772780 DOI: 10.3109/09513590.2013.797398
    OBJECTIVE: This was to determine HOMA-IR score as well as to assess its association in fetal and maternal outcomes among pregnant women with diabetes risks.
    METHODS: A prospective cohort study of pregnant women with diabetes risks was done. GDM was diagnosed using modified glucose tolerance test. Serum insulin was taken and measured by an electrochemiluminescence immunoassay method. Plasma glucose was measured by enzymatic reference method with hexokinase. HOMA-IR score was calculated for each patient. Maternal and fetal outcomes were analyzed.
    RESULTS: From 279 women recruited, 22.6% had GDM with higher HOMA-IR score (4.07 ± 2.44 versus 2.08 ± 1.12; p = 0.001) and fasting insulin (16.76 ± 8.63 µIU/L versus 10.15 ± 5.07 µIU/L; p = 0.001). Area under ROC curve for HOMA-IR score was 0.79 (95% confidence interval, 0.74-0.84) with optimum cut-off value of 2.92 (sensitivity = 63.5%; specificity = 89.8%), higher than recommended by IDF (2.38). This point showed significant association with neonatal hypoglycemia (p = 0.02) and Cesarean section (p = 0.04) in GDM mothers.
    CONCLUSIONS: HOMA-IR score and insulin resistance levels were higher in GDM women in our population. With the cut-off HOMA-IR value of 2.92, neonatal hypoglycemia and Cesarean section were significant complications in GDM mothers. This can be used in anticipation of maternal and fetal morbidities.
    Matched MeSH terms: Homeostasis/physiology*
  9. Fulltext Bi-allelic LETM1 variants perturb mitochondrial ion homeostasis leading to a clinical spectrum with predominant nervous system involvement
    Kaiyrzhanov R, Mohammed SEM, Maroofian R, Husain RA, Catania A, Torraco A, et al.
    Am J Hum Genet, 2022 Sep 01;109(9):1692-1712.
    PMID: 36055214 DOI: 10.1016/j.ajhg.2022.07.007
    Leucine zipper-EF-hand containing transmembrane protein 1 (LETM1) encodes an inner mitochondrial membrane protein with an osmoregulatory function controlling mitochondrial volume and ion homeostasis. The putative association of LETM1 with a human disease was initially suggested in Wolf-Hirschhorn syndrome, a disorder that results from de novo monoallelic deletion of chromosome 4p16.3, a region encompassing LETM1. Utilizing exome sequencing and international gene-matching efforts, we have identified 18 affected individuals from 11 unrelated families harboring ultra-rare bi-allelic missense and loss-of-function LETM1 variants and clinical presentations highly suggestive of mitochondrial disease. These manifested as a spectrum of predominantly infantile-onset (14/18, 78%) and variably progressive neurological, metabolic, and dysmorphic symptoms, plus multiple organ dysfunction associated with neurodegeneration. The common features included respiratory chain complex deficiencies (100%), global developmental delay (94%), optic atrophy (83%), sensorineural hearing loss (78%), and cerebellar ataxia (78%) followed by epilepsy (67%), spasticity (53%), and myopathy (50%). Other features included bilateral cataracts (42%), cardiomyopathy (36%), and diabetes (27%). To better understand the pathogenic mechanism of the identified LETM1 variants, we performed biochemical and morphological studies on mitochondrial K+/H+ exchange activity, proteins, and shape in proband-derived fibroblasts and muscles and in Saccharomyces cerevisiae, which is an important model organism for mitochondrial osmotic regulation. Our results demonstrate that bi-allelic LETM1 variants are associated with defective mitochondrial K+ efflux, swollen mitochondrial matrix structures, and loss of important mitochondrial oxidative phosphorylation protein components, thus highlighting the implication of perturbed mitochondrial osmoregulation caused by LETM1 variants in neurological and mitochondrial pathologies.
    Matched MeSH terms: Homeostasis/genetics
  10. Mechanisms of cataractogenesis in the presence of magnesium deficiency
    Agarwal R, Iezhitsa IN, Agarwal P, Spasov AA
    Magnes Res, 2013 Jan-Feb;26(1):2-8.
    PMID: 23708888 DOI: 10.1684/mrh.2013.0336
    Senile cataract is the most common cause of bilateral blindness and results from the loss of transparency of the lens. Maintenance of the unique tissue architecture of the lens is vital for keeping the lens transparent. Membrane transport mechanisms utilizing several magnesium (Mg)-dependent ATPases, play an important role in maintaining lens homeostasis. Therefore, in Mg-deficiency states, ATPase dysfunctions lead to intracellular depletion of K(+) and accumulation of Na(+) and Ca(2+). High intracellular Ca(2+) causes activation of the enzyme calpain II, which leads to the denaturation of crystallin, the soluble lens protein required for maintaining the transparency of the lens. Mg deficiency also interferes with ATPase functions by causing cellular ATP depletion. Furthermore, Mg deficiency enhances lenticular oxidative stress by increased production of free radicals and depletion of antioxidant defenses. Therefore, Mg supplementation may be of therapeutic value in preventing the onset and progression of cataracts in conditions associated with Mg deficiency.
    Matched MeSH terms: Homeostasis
  11. Magnesium deficiency: does it have a role to play in cataractogenesis?
    Agarwal R, Iezhitsa I, Agarwal P, Spasov A
    Exp Eye Res, 2012 Aug;101:82-9.
    PMID: 22668657 DOI: 10.1016/j.exer.2012.05.008
    Magnesium is one of the most important regulatory cation involved in several biological processes. It is important for maintaining the structural and functional integrity of vital ocular tissues such as lens. Presence of high magnesium content especially in the peripheral part of lens as compared to aqueous and vitreous humor has been observed. Magnesium plays significant role as a cofactor for more than 350 enzymes in the body especially those utilizing ATP. Membrane associated ATPase functions that are crucial in regulating the intracellular ionic environment, are magnesium-dependent. Moreover, the enzymes involved in ATP production and hydrolysis are also magnesium-dependent. Magnesium deficiency by interfering with ATPase functions causes increased intracellular calcium and sodium and decreases intracellular potassium concentration. Furthermore, magnesium deficiency is associated with increased oxidative stress secondary to increased expression of inducible nitric oxide synthase and increased production of nitric oxide. Thus the alterations in lenticular redox status and ionic imbalances form the basis of the association of magnesium deficiency with cataract. In this paper we review the mechanisms involved in magnesium homeostasis and the role of magnesium deficiency in the pathogenesis of cataract.
    Matched MeSH terms: Homeostasis
  12. Major depressive disorder patients on antidepressant treatments display higher number of regulatory T cells
    Mohd Ashari NS, Mohamed Sanusi SNF, Mohd Yasin MA, Che Hussin CM, Wong KK, Shafei MN
    Malays J Pathol, 2019 Aug;41(2):169-176.
    PMID: 31427552
    INTRODUCTION: Regulatory T cell (Treg) is a subtype of T lymphocyte that plays a crucial role in establishing immunologic self-tolerance and maintaining immune homeostasis. In this study, we set out to investigate the percentage and absolute count of Tregs in major depressive disorder (MDD) patients and their correlation with disease severity.

    MATERIALS & METHODS: This is a case-control study consisting of 47 MDD patients and 47 healthy controls. MDD patients were treated with antidepressant drugs according to their physician's choice. The severity of MDD was assessed using Beck Depression Inventory (BDI) and Montgomery-Asberg Depression Rating Scale (MADRS) at the time of recruitment. Healthy controls completed the Depression Anxiety Scoring System (DASS21) questionnaire to ensure they were in good mental health without history of MDD. The percentage and absolute count of CD4+ CD25+ Tregs and CD4+ CD25+ FOXP3+ Tregs were identified by multiparameter flow cytometry.

    RESULTS: The percentage and absolute count of CD4+ CD25+ Treg cells were significantly higher in MDD patients than in healthy controls (P<0.001, in both cases). Likewise, the percentage and absolute count of CD4+ CD25+ FOXP3+ Treg cells were also significantly higher in MDD patients compared to healthy controls (P=0.003 and P=0.002, respectively). However, there was no significant correlation between the percentage and absolute count of CD4+ CD25+ Treg and CD4+ CD25+ FOXP3+ Treg cells with BDI or MADRS score.

    CONCLUSIONS: Our results suggest that antidepressant treatments contributed to an upregulation of Tregs in MDD patients.

    Matched MeSH terms: Homeostasis
  13. Fulltext Understanding Apoptosis and Apoptotic Pathways Targeted Cancer Therapeutics
    Jan R, Chaudhry GE
    Adv Pharm Bull, 2019 Jun;9(2):205-218.
    PMID: 31380246 DOI: 10.15171/apb.2019.024
    Various physiological processes involve appropriate tissue developmental process and homeostasis - the pathogenesis of several diseases connected with deregulatory apoptosis process. Apoptosis plays a crucial role in maintaining a balance between cell death and division, evasion of apoptosis results in the uncontrolled multiplication of cells leading to different diseases such as cancer. Currently, the development of apoptosis targeting anticancer drugs has gained much interest since cell death induced by apoptosis causes minimal inflammation. The understanding of complexities of apoptosis mechanism and how apoptosis is evolved by tumor cells to oppose cell death has focused research into the new strategies designed to induce apoptosis in cancer cells. This review focused on the underlying mechanism of apoptosis and the dysregulation of apoptosis modulators involved in the extrinsic and intrinsic apoptotic pathway, which include death receptors (DRs) proteins, cellular FLICE inhibitory proteins (c-FLIP), anti-apoptotic Bcl-2 proteins, inhibitors of apoptosis proteins (IAPs), tumor suppressor (p53) in cancer cells along with various current clinical approaches aimed to selectively induce apoptosis in cancer cells.
    Matched MeSH terms: Homeostasis
  14. Measurement of urine pH and net acid excretion and their association with urine calcium excretion in periparturient dairy cows
    Constable PD, Megahed AA, Hiew MWH
    J Dairy Sci, 2019 Dec;102(12):11370-11383.
    PMID: 31548071 DOI: 10.3168/jds.2019-16805
    Urine pH (UpH) and net acid excretion (NAE) are used to monitor the degree of systemic acidification and predict the magnitude of resultant hypercalciuria when feeding an acidogenic ration to control periparturient hypocalcemia in dairy cattle. The objectives of this study were to evaluate the diagnostic performance of urine dipstick and pH paper for measuring UpH, and to characterize the UpH-NAE relationship and the association of urine Ca concentration ([Ca]) with UpH and NAE. Urine samples (n = 1,116) were collected daily from 106 periparturient Holstein-Friesian cows fed an acidogenic ration during late gestation. Net acid excretion was measured by titration, and UpH was measured by a glass-electrode pH meter (reference method), Multistix-SG urine dipsticks (Siemens Medical Solutions Inc., Ann Arbor, MI), and Hydrion pH paper (Micro Essential Laboratory Inc., Brooklyn, NY). Diagnostic performance was evaluated using Spearman correlation coefficient (rs), Bland-Altman plots, and logistic regression. Urine pH measured by urine dipstick (rs = 0.94) and pH paper (rs = 0.96) were strongly associated with UpH. Method-comparison studies indicated that the urine dipstick measured an average of 0.28 pH units higher, and pH paper 0.10 pH units lower, than UpH. Urine [Ca] was more strongly associated with UpH (rs = -0.65) than NAE (rs = 0.52). Goals for controlling periparturient hypocalcemia under the study conditions were UpH <6.22 and <6.11, based on achieving urine [Ca] ≥5 mmol/L and estimated urinary Ca excretion ≥4 g/d, respectively. Urine pH was as accurate at predicting urine [Ca] as NAE when UpH >6.11. We conclude that pH paper is an accurate, practical, and low-cost cow-side test for measuring UpH and provides a clinically useful estimate of urine [Ca].
    Matched MeSH terms: Homeostasis
  15. Fulltext Is targeting autophagy mechanism in cancer a good approach? The possible double-edge sword effect
    Lim SM, Mohamad Hanif EA, Chin SF
    Cell Biosci, 2021 Mar 20;11(1):56.
    PMID: 33743781 DOI: 10.1186/s13578-021-00570-z
    Autophagy is a conserved cellular process required to maintain homeostasis. The hallmark of autophagy is the formation of a phagophore that engulfs cytosolic materials for degradation and recycling to synthesize essential components. Basal autophagy is constitutively active under normal conditions and it could be further induced by physiological stimuli such as hypoxia, nutrient starvation, endoplasmic reticulum stress,energy depletion, hormonal stimulation and pharmacological treatment. In cancer, autophagy is highly context-specific depending on the cell type, tumour microenvironment, disease stage and external stimuli. Recently, the emerging role of autophagy as a double-edged sword in cancer has gained much attention. On one hand, autophagy suppresses malignant transformation by limiting the production of reactive oxygen species and DNA damage during tumour development. Subsequently, autophagy evolved to support the survival of cancer cells and promotes the tumourigenicity of cancer stem cells at established sites. Hence, autophagy is an attractive target for cancer therapeutics and researchers have been exploiting the use of autophagy modulators as adjuvant therapy. In this review, we present a summary of autophagy mechanism and controlling pathways, with emphasis on the dual-role of autophagy (double-edged sword) in cancer. This is followed by an overview of the autophagy modulation for cancer treatment and is concluded by a discussion on the current perspectives and future outlook of autophagy exploitation for precision medicine.
    Matched MeSH terms: Homeostasis
  16. Fulltext Lysophosphatidylinositol Signalling and Metabolic Diseases
    Arifin SA, Falasca M
    Metabolites, 2016;6(1).
    PMID: 26784247 DOI: 10.3390/metabo6010006
    Metabolism is a chemical process used by cells to transform food-derived nutrients, such as proteins, carbohydrates and fats, into chemical and thermal energy. Whenever an alteration of this process occurs, the chemical balance within the cells is impaired and this can affect their growth and response to the environment, leading to the development of a metabolic disease. Metabolic syndrome, a cluster of several metabolic risk factors such as abdominal obesity, insulin resistance, high cholesterol and high blood pressure, and atherogenic dyslipidaemia, is increasingly common in modern society. Metabolic syndrome, as well as other diseases, such as diabetes, obesity, hyperlipidaemia and hypertension, are associated with abnormal lipid metabolism. Cellular lipids are the major component of cell membranes; they represent also a valuable source of energy and therefore play a crucial role for both cellular and physiological energy homeostasis. In this review, we will focus on the physiological and pathophysiological roles of the lysophospholipid mediator lysophosphatidylinositol (LPI) and its receptor G-protein coupled receptor 55 (GPR55) in metabolic diseases. LPI is a bioactive lipid generated by phospholipase A (PLA) family of lipases which is believed to play an important role in several diseases. Indeed LPI can affect various functions such as cell growth, differentiation and motility in a number of cell-types. Recently published data suggest that LPI plays an important role in different physiological and pathological contexts, including a role in metabolism and glucose homeostasis.
    Matched MeSH terms: Homeostasis
  17. Bacterial membrane disruption in food pathogens by Psidium guajava leaf extracts
    Henie, E.F.P., Zaiton, H., Suhaila, M.
    International Food Research Journal, 2009;16(3):297-311.
    MyJurnal
    The mode of action and activities of guava leaf extracts against various food pathogens were studied. The killing kinetics, viability and cell leakage of Kocuria rhizophila, Salmonella typhimurium, Listeria monocytogenes and Escherichia coli O157:H7, measured after exposure to guava methanolic extracts (GME) revealed a significantly higher (p≤0.05) release of bacterial nucleic acids, K+ ions and protein than that of untreated microbes, indicating disruption of the bacterial membrane. GME caused a significantly higher (p≤0.05) release of RNA in gramnegatives compared to gram-positives. GME caused a relatively small but significant release of pyrines and pyrimidines in all organisms investigated. GME probably disrupted the integrity of the Gram-negative microorganism lipopolysaccharide (LPS) layer. Unlike all the other microorganisms tested, E. coli O157:H7, demonstrated the lowest protein leakage, the highest K+ leakage, the highest pyrines and pyrimidines leakage within the first 10 min of extract exposure, but the lowest after 30 minutes, which may indicate their good homeostasis ability or adaptability. Understanding the mode of action of this flavonoid rich guava leaf extract, would help develop it as an alternative biodegradable and safe, antimicrobial for food and medicine, and as a by-product of the guava industry.
    Matched MeSH terms: Homeostasis
  18. Fulltext Cerebral protection: a review of current techniques
    Palur, Ravikant
    Medical Health Reviews, 2009;2009(1):15-42.
    MyJurnal
    The brain is considered the most eloquent organ in the human body as its activities impacts on all other systems. Though protected physically (in a bony covering), physiologically through the blood-CSF barrier (from invading organisms and toxins) and hemodynamically through the phenomenon of cerebral autoregulation; the brain is open to insults of various kinds which can critically damage this structure. Intracellular Ca++ accumulation, excessive activation of excitatory amino acid receptors, lipid peroxidation and free radical releaserelated damage are but a few of the pathological processes that occur at the neuronal level leading to damage. The mechanism by which the brain can be provided protection when it is in a compromised state or likely to be compromised is known as cerebral protection. There are various modalities of pharmacologic (use of barbiturates, etomidate, isoflurane, steroids, Ca++, corticosteroids etc) and non-pharmacologic therapies (hypothermia, hyperventilation, induced hypotension, electrophysiologic monitoring, endovascular management etc) available for cerebral protection which finds place in the armamentarium of clinicians managing the critically injured brain. Our knowledge of the functioning of the brain at the molecular level and the various biochemico-pathological processes that are set into motion during critical states continues to evolve. This review article attempts to explain present understanding of the biochemical and pathological processes involved in neuronal damage while also looking at current available therapies (pharmacologic & nonpharmacologic) being utilized in different clinical settings.
    Matched MeSH terms: Homeostasis
  19. Fulltext Predominant supragingival plaque microflora in a Malaysian population
    Fathilah, A.R., Rahim, Z.H.A., Othman, Y.
    Malaysian Dental Journal, 2007;28(2):92-96.
    MyJurnal
    The tooth provides a non-shedding surface ideal for microbial and plaque accumulation. Despite being exposed to regular environmental perturbations, the microbial composition and proportions in the plaque often remains in homeostasis and is relatively stable over time. Supragingival plaque sampled from various sites on the tooth surface was pooled and conventionally analyzed for its microbial constituent. Classification of microbial isolates was made based on the characteristics exhibited by the growth colonies, Gram-stained cells, as well as biochemical reactions using the API Identification System kit. Observation was also made of the colony forming units on both non-selective and selective agar culture plates. A variety of bacteria, both of the facultative and anaerobic types, were isolated from the supragingival plaque of the Malaysian population. Among those found to predominate the supragingival plaque include the Gram positive and Gram negative cocci and rods from the genera Streptococcus, Staphylococcus, Actinomyces, Fusobacterium, Corynebacterium, Clostridium, Bacteroides, Veilonella and Lactobacillus. In addition, yeast within the genus Candida was also isolated from the plaque samples.
    Matched MeSH terms: Homeostasis
  20. Fulltext CsoR metalloregulatory protein: function, mechanism and relevance
    Mangavelu, Ashwaani, Yahaya M. Normi, Leow, Adam Thean Chor, Mohd Shukuri Mohammad Ali, Raja Noor Zaliha Raja Abd. Rahman
    The Pertanika Journal of Scholarly Research Reviews, 2017;3(1):24-31.
    MyJurnal
    Transition metals are required constituent in bacterial metabolism to assist in some enzymatic reactions. However, intracellular accumulations of these metal ions are harmful to the bacteria as it can trigger unnecessary redox reactions. To overcome this condition, metalloregulatory proteins assist organisms to adapt to sudden elevated and deprived metal ion concentration in the environment via metal homeostasis. CsoR protein is a copper(I) [Cu(I)] sensing operon repressor that is found to be present in all major classes of eubacteria. This metalloregulatory protein binds to the operator region in its apo state under Cu(I) limiting condition and detaches off from the regulatory region when it binds to the excess cytosolic Cu(I) ion, thus derepressing the expression of genes involved in Cu(I) homeostasis. CsoR proteins exist in dimeric and tetrameric states and form certain coordination geometries upon attachment with Cu(I). Certain CsoR proteins have also been found to possess the ability to bind to other types of metals with various binding affinities in some Gram positive bacteria. The role of this metalloregulatory protein in host pathogen interaction and its relation to bacterial virulence are also discussed.
    Matched MeSH terms: Homeostasis
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