Nanozarah zink oksida telah disintesis menggunakan afrons gas koloid sebagai acuan. Zink sulfat (ZnSO4.7H2O) dan gas ammonia digunakan sebagi bahan tindak balas. Masa pengeraman yang dikaji adalah 2 jam dan 18 jam. Daripada analisis mikroskop elektron imbasan, morfologi nanohelaian dapat diperhatikan dengan ketebalan helaian 125 nm hingga 200 nm. Daripada analisis spektroskopi ultra lembayung-boleh nampak, saiz purata yang dianggarkan bagi sampel nanozarah zink oksida yang disintesis dengan masa pengeraman 2 jam adalah 2.03 nm dan 2.1 nm untuk sampel yang dieramkan selama 18 jam.
Aktiviti guna tanah di kawasan lembangan adalah salah satu faktor yang mendorong kepada kemerosotan kualiti air
sungai akibat daripada hakisan tanih. Potensi hakisan tanih di kawasan lembangan Sungai Bilut, Raub, Pahang yang
menjadi sumber bekalan air minuman utama di daerah Raub boleh ditentukan dengan menggunakan integrasi model
Semakan Semula Persamaan Kehilangan Tanih Universal (RUSLE) dan Sistem Maklumat Geografi (GIS). Kajian ini
bertujuan untuk menentukan potensi hakisan tanih dan faktor utama yang mempengaruhi kadar hakisan tanih. Kajian ini
melibatkan penggunaan data sekunder yang terdiri daripada data hujan, data siri tanih dan topografi bagi menghasilkan
faktor kehakisan hujan (R), kebolehhakisan tanih (K), serta panjang dan kecuraman cerun (LS). Faktor litupan tumbuhan
(C) dan amalan pemuliharaan (P) pula dijana daripada imej satelit Landsat 8 (2014). Keputusan kajian menunjukkan
nilai faktor R di kawasan kajian ialah 8927.68-9775.18 MJ mm ha-1 jam-1 tahun-1, nilai K ialah 0.036-0.500 tan jam-1
MJ-1 mm-1, nilai LS ialah 0-514, nilai C ialah 0.03-0.80 dan nilai P ialah 0.1-0.7. Kawasan yang mempunyai potensi
hakisan sangat rendah hingga rendah meliputi 81%, manakala potensi hakisan tanih sederhana hingga sangat tinggi
meliputi 19% daripada keseluruhan kawasan kajian. Model yang dihasilkan mempunyai ketepatan sebanyak 81%. Faktor
utama yang mempengaruhi berlakunya hakisan tanih di kawasan kajian adalah faktor topografi, litupan tumbuhan dan
kebolehhakisan tanih. Keputusan menunjukkan analisis integrasi RUSLE dan GIS berpotensi dalam penentuan potensi
hakisan tanih untuk kawasan luas yang mempunyai pelbagai jenis guna tanah, topografi dan jenis tanih.
Successful human reproduction remains an enigma, but this is slowly changing in the current era of expanding scientific knowledge. The discovery of various molecular factors such as adhesion molecules, proteases and cytokines have in recent years been at the forefront of medical research. The growing importance of immunology in particular has led to novel new immuno-modulatory therapies and increasing research into this new aspect of reproductive immunology may well prove to be the most important breakthrough in understanding the fundamentals of human reproduction. Implantation represents the first step in the complex interactions and processes involved in foetal-maternal interaction, which continues throughout pregnancy gestation and culminates in the birth of an infant. It is therefore vital that we understand the myriad processes controlling implantation in order to build a firm foundation for exploring reproductive immunology research in the new millennium. This review brings together and presents an overview of the potential roles of currently known molecular factors such as adhesion molecules, proteases, cytokines and its interaction with the maternal immune response, incorporating the findings of previous published research performed by the author on cytokines and reproductive immunology.
Bone formation is an active process whereby osteoblasts are found on the surface of the newly formed bone. Adhesion to extracellular matrix is essential for the development of bone however not all surfaces are suitable for osteoblast adhesion and don't support osteoblastic functions. The objective of this study was to test the suitability of a collagen based microcarrier which would support osteoblastic functions.
A 13 year old boy presented with a huge mass on his right arm of 6 months duration. Histopathological examination revealed sheets of malignant small round blue cells with immunopositivity for LCA, CD43, CD45Ro, CD30, EMA, ALK-1 and CD99, and negativity for CD20, TdT, myogenin, myoD1, NSE, bcl-6, bcl-2 and CD10. Fluorescent In-Situ Hybridization (FISH) testing excluded the diagnosis of Ewing's sarcoma/PNET. Pathologists need to be aware of the diagnosis of a small cell variant of ALCL, as well as of the fact that CD99 expression commonly occurs in cases of ALK-positive ALCL, in order to distinguish this entity from Ewing's sarcoma/PNET.
Malaria is caused by parasitic protozoans of the genus Plasmodium and is one of the most prevalent infectious diseases in tropical and subtropical regions. For this reason, effective and practical diagnostic methods are urgently needed to control the spread of malaria. The aim of the current study was to identify a panel of new malarial markers, which could be used to diagnose patients infected with various Plasmodium species, including P. knowlesi, P. vivax and P. falciparum. Sera from malaria-infected patients were pooled and compared to control sera obtained from healthy individuals using the isobaric tags for relative and absolute quantitation (iTRAQ) technique. Mass spectrometry was used to identify serum proteins and quantify their relative abundance. We found that the levels of several proteins were increased in pooled serum from infected patients, including cell adhesion molecule-4 and C-reactive protein. In contrast, the serum concentration of haptoglobin was reduced in malaria-infected individuals, which we verified by western blot assay. Therefore, these proteins might represent infectious markers of malaria, which could be used to develop novel diagnostic tools for detecting P. knowlesi, P. vivax and P. falciparum. However, these potential malarial markers will need to be validated in a larger population of infected individuals.
The epigenetic changes of RELN that are involved in the development of dopaminergic neurons may fit the developmental theory of schizophrenia. However, evidence regarding the association of RELN DNA methylation with schizophrenia is far from sufficient, as studies have only been conducted on a few limited brain samples. As DNA methylation in the peripheral blood may mirror the changes taking place in the brain, the use of peripheral blood for a DNA methylation study in schizophrenia is feasible due to the scarcity of brain samples. Therefore, the aim of our study was to examine the relationship of DNA methylation levels of RELN promoters with schizophrenia using genomic DNA derived from the peripheral blood of patients with the disorder. The case control studies consisted of 110 schizophrenia participants and 122 healthy controls who had been recruited from the same district. After bisufhite conversion, the methylation levels of the DNA samples were calculated based on their differences of the Cq values assayed using the highly sensitive real-time MethyLight TaqMan® procedure. A significantly higher level of methylation of the RELN promoter was found in patients with schizophrenia compared to controls (p = 0.005) and also in males compared with females (p = 0.004). Subsequently, the RELN expression of the methylated group was 25 fold less than that of the non-methylated group. Based upon the assumption of parallel methylation changes in the brain and peripheral blood, we concluded that RELN DNA methylation might contribute to the pathogenesis of schizophrenia. However, the definite effects of methylation on RELN function during development and also in adult life still require further elaboration.
Chondrogenic differentiation of mesenchymal stromal cells (MSCs) in the form of pellet culture and encapsulation in alginate beads has been widely used as conventional model for in vitro chondrogenesis. However, comparative characterization between differentiation, hypertrophic markers, cell adhesion molecule and ultrastructural changes during alginate and pellet culture has not been described. Hence, the present study was conducted comparing MSCs cultured in pellet and alginate beads with monolayer culture. qPCR was performed to assess the expression of chondrogenic, hypertrophic, and cell adhesion molecule genes, whereas transmission electron microscopy (TEM) was used to assess the ultrastructural changes. In addition, immunocytochemistry for Collagen type II and aggrecan and glycosaminoglycan (GAG) analysis were performed. Our results indicate that pellet and alginate bead cultures were necessary for chondrogenic differentiation of MSC. It also indicates that cultures using alginate bead demonstrated significantly higher (p < 0.05) chondrogenic but lower hypertrophic (p < 0.05) gene expressions as compared with pellet cultures. N-cadherin and N-CAM1 expression were up-regulated in second and third weeks of culture and were comparable between the alginate bead and pellet culture groups, respectively. TEM images demonstrated ultrastructural changes resembling cell death in pellet cultures. Our results indicate that using alginate beads, MSCs express higher chondrogenic but lower hypertrophic gene expression. Enhanced production of extracellular matrix and cell adhesion molecules was also observed in this group. These findings suggest that alginate bead culture may serve as a superior chondrogenic model, whereas pellet culture is more appropriate as a hypertrophic model of chondrogenesis.
Injury to a peripheral nerve leads to degeneration of the segment distal to the site of lesion, a process referred to as Wallerian degeneration. During Wallerian degeneration, axons and myelin sheaths undergo degeneration and are phagocytosed by macrophages and Schwann cells. The Schwann cells proliferate and the endoneurial tubes persist, together the whole structure is known as the band of BÃ¼ngner. Within few hours, the damaged axons in the proximal stump initiate a regeneration response, with formation of new growth cones. During Wallerian degeneration, neurotrophins, neural cell adhesion molecules, cytokines and other soluble factors are upregulated to facilitate regeneration. The recovery of the target in mammals is often variable, but almost never complete. In humans, scar tissue forms at the site of lesion and this often results in poor recovery of the target. The major events underlying this regenerative process is highlighted and discussed in this review.
Dental pulp stem cells (DPSCs) originate from the embryonic neural crest and have neurogenic potential. The present study investigated the roles of the forward and reverse EphrinB2 signalling pathways during DPSC neurogenesis. Treatment of DPSCs with recombinant EphrinB2-Fc protein over 7 days in a neural induction culture resulted in significant downregulation of the following neural markers: βIII-Tubulin, neural cell adhesion molecule (NCAM), nestin, neurogenin 2 (NGN2), neurofilament medium polypeptide and Musashi1. Immunocytochemistry revealed that EphrinB2-Fc-treated DPSCs exhibited more rounded morphologies with fewer neurite outgrowths as well as reduced protein expression of βIII-tubulin and NGN2. Treatment of DPSCs with a peptide inhibitor specific to the EphB4 receptor significantly upregulated expression of the neural markers microtubule-associated protein 2, Musashi1, NGN2 and neuron-specific enolase, whereas treatment with a peptide inhibitor specific to the EphB2 receptor exerted negligible effects on neurogenesis. Transgenic expression of EphrinB2 in DPSCs resulted in significant upregulation of Musashi1 and NCAM gene expression, while treatment of DPSCs with recombinant EphB4-Fc protein led to significant upregulation of only Musashi1. Thus, it may be concluded that stimulation of forward EphrinB2-EphB4 signalling markedly inhibited neurogenesis in DPSCs, whereas suppression of this forward signalling pathway with peptide inhibitor specific to EphB4 promoted neurogenesis. Meanwhile, stimulation of reverse EphB4-EphrinB2 signalling only marginally enhanced the neural differentiation of DPSCs. The present findings indicate the potential application of peptide or small molecule inhibitors of EphrinB2 forward signalling in neural tissue engineering with DPSCs.
The development of efficient tissue culture protocol for somatic embryo would facilitate the genetic modification breeding program. The callus induction and regeneration were studied by using different parameters i.e., auxins, cytokinins, and desiccation treatment. Scanning electron microscopy and histological analysis were performed to identify the embryogenic callus for regeneration. The callus percentage results showed that MS (Murashige and Skoog) basal medium supplemented with 3 mg/L 2, 4-D and 30g/L maltose were the optimal callus induction medium for MR220 (80%) and MR220-CL2 (95%). The morphology of the embryogenic callus was confirmed by the SEM (Scanning Electron Microscopy) (presence of extracellular matrix surface network) and later by histological analysis. Finally, MS media supplemented with 0.5 mg/L NAA (Naphthalene Acetic Acid), 2 mg/L kin, and 1 mg/L BAP were selected as the optimum regeneration media treatment while callus desiccated for 48 h was proved to produce more plantlets in MR220 (60%) and MR220-CL2 (73.33%) compared to control treatment (without desiccation). The protocol presented here showed the necessity for the inclusion of partial desiccation as an important step in the tissue culture protocol of Malaysian indica rice genotypes in order to enhance their regeneration potential.
Endothelial cells lining the inner vascular wall form a monolayer that contributes to the selective permeability of endothelial barrier. This selective permeability is mainly regulated by an endothelium-specific adherens junctional protein, known as vascular endothelial-cadherin (VE-cadherin). In endothelial cells, the adherens junction comprises of VE-cadherin and its associated adhesion molecules such as p120, α-catenin, and β-catenin, in which α-catenin links cytoplasmic tails of VE-cadherin to actin cytoskeleton through β-catenin. Proinflammatory stimuli such as lipopolysaccharide (LPS) are capable of attenuating vascular integrity through the disruption of VE-cadherin adhesion in endothelial cells. To date, numerous studies demonstrated the disruption of adherens junction as a result of phosphorylation-mediated VE-cadherin disruption. However, the outcomes from these studies were inconsistent and non-conclusive as different cell fractions were used to examine the effect of LPS on the disruption of VE-cadherin. By using Western Blot, some studies utilized total protein lysate and reported decreased protein expression while some studies reported unchanged expression. Other studies which used membrane and cytosolic fractions of protein extract demonstrated decreased and increased VE-cadherin expression, respectively. Despite the irregularities, the results of immunofluorescence staining are consistent with the formation of intercellular gap. Besides that, the overall underlying disruptive mechanisms of VE-cadherin remain largely unknown. Therefore, this mini review will focus on different experiment approaches in terms of cell fractions used in different human endothelial cell studies, and relate these differences to the results obtained in Western blot and immunofluorescence staining in order to give some insights into the overall differential regulatory mechanisms of LPS-mediated VE-cadherin disruption and address the discrepancy in VE-cadherin expression.
Classical characteristic of the innate immune system is the lack of ability to build up immunological memory, contrast to the adaptive immune system that is capable of "remembering" antigens, and rapidly mount a greater magnitude of immune response upon subsequent exposure to the same antigens. Peculiarly, immunological memory of innate immunity is evidenced in invertebrates. At least three different memory phenomena have been described, namely sustained unique response, recalled response, and immune shift. Studies attended to decipher the mechanistic biology of the innate immune memory reveals the role of epigenetics, which modulates the response of immune memory, and the heritability of immune memory to subsequent generations. A parthenogenetic Artemia model demonstrated successful transgenerational epigenetic inheritance of resistance trait against Vibrio campbellii. Following, the role of invertebrate hemocytes and Down syndrome cell adhesion molecule (Dscam) in innate immune memory is reviewed. While there is no vertebrate antibody homolog found in invertebrates, Dscam was found to resemble the functionality of vertebrate antibody. Insight of Dscam as immune factor was illustrated further in the current review.
Wallerian degeneration is a complicated process whereby axons and myelin sheaths undergo degeneration, and eventually are phagocytosed by macrophages and Schwann cells following nerve damage. Schwann cells proliferate and the endoneural tubes persist. In addition, neurotrophins, neural cell adhesion molecules, cytokines and other soluble factors are upregulated to facilitate regeneration. The important role of cellular components, neurotrophins, and extracellular matrix components, including cell surface molecules involved in this regenerative process, is highlighted and discussed in this review.
Effects of high-protein diets that are rich in saturated fats on cell adhesion molecules, thrombogenicity and other nonlipid markers of atherosclerosis in humans have not been firmly established. We aim to investigate the effects of high-protein Malaysian diets prepared separately with virgin olive oil (OO), palm olein (PO) and coconut oil (CO) on cell adhesion molecules, lipid inflammatory mediators and thromobogenicity indices in healthy adults.
The aim of the present study was to evaluate the effects of air-liquid interface on the differentiation potential of human amnion epithelial cells (HAECs) to skin-like substitute in organotypic culture.
The objective of the present study was to examine the changes in the expression profile of certain genes in rat model of gentamicin-induced acute kidney injury (AKI) and to see whether time period and routes of administration affect their expression levels.
Endothelial cells (ECs) play a role in the optimal function of blood vessels. When endothelial function becomes dysregulated, the risk of developing atherosclerosis increases. Specifically, upregulation of adhesion molecule expression on ECs promotes the movement of leukocytes, particularly monocytes, into the vessel wall. Here, monocytes differentiate into macrophages and may become foam cells, contributing to the initiation and progression of an atherosclerotic plaque. The ability of omega-3 (n-3) polyunsaturated fatty acids (PUFAs) to influence the expression of adhesion molecules by ECs and to modulate leukocyte-endothelial adhesion has been studied in cell culture using various types of ECs, in animal feeding studies and in human trials; the latter have tended to evaluate soluble forms of adhesion molecules that circulate in the bloodstream. These studies indicate that n-3 PUFAs (both eicosapentaenoic acid and docosahexaenoic acid) can decrease the expression of key adhesion molecules, such as vascular cell adhesion molecule 1, by ECs and that this results in decreased adhesive interactions between leukocytes and ECs. These findings suggest that n-3 PUFAs may lower leukocyte infiltration into the vascular wall, which could contribute to reduced atherosclerosis and lowered risk of cardiovascular disease.
Cardiovascular diseases (CVDs) such as angina, hypertension, myocardial ischemia, and heart failure are the leading causes of morbidity and mortality worldwide. One of the major transcription factors widely associated with CVDs is nuclear factor-kappa B (NFκB). NFκB activation initiates the canonical and non-conical pathways that promotes activation of transcription factors leading to inflammation, such as leukocyte adhesion molecules, cytokines, and chemokines. Flavonoids are bioactive polyphenolic compounds found abundantly in various fruits, vegetables, beverages (tea, coffee), nuts, and cereal products with cardiovascular protective properties. Flavonoids can be classified into six subgroups based on their chemical structures: flavanones, flavones, flavonols, flavan-3-ols, isoflavones, and anthocyanidins. As NFκB inhibitors, these flavonoids may modulate the expression of pro-inflammatory genes leading to the attenuation of the inflammatory responses underlying various cardiovascular pathology. This review presents an update on the anti-inflammatory actions of flavonoids via inhibition of NFκB mechanism supporting the therapeutic potential of these natural compounds in various CVDs.