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Soil erosion potential at sungai bilut catchment, Raub, Pahang using integration of rusle and GIS

Tukimat Lihan, Nur Fatin Khodri, Muzzneena Ahmad Mustapha, Zulfahmi Ali Rahman, Wan Mohd Razi Idris

Sains Malaysiana, 2018;47:2241-2249.

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.

Matched MeSH terms: Cell Adhesion Molecules
Fulltext Combination of Plant Growth Regulators, Maltose, and Partial Desiccation Treatment Enhance Somatic Embryogenesis in Selected Malaysian Rice Cultivar

Ming NGJ, Binte Mostafiz S, Johon NS, Abdullah Zulkifli NS, Wagiran A

Plants (Basel), 2019 May 30;8(6).
PMID: 31151227 DOI: 10.3390/plants8060144

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.

Matched MeSH terms: Cell Adhesion Molecules, Neuronal
Fulltext Targeting Cell Adhesion Molecules via Carbonate Apatite-Mediated Delivery of Specific siRNAs to Breast Cancer Cells In Vitro and In Vivo

Ashaie MA, Islam RA, Kamaruzman NI, Ibnat N, Tha KK, Chowdhury EH

Pharmaceutics, 2019 Jul 02;11(7).
PMID: 31269666 DOI: 10.3390/pharmaceutics11070309

While several treatment strategies are applied to cure breast cancer, it still remains one of the leading causes of female deaths worldwide. Since chemotherapeutic drugs have severe side effects and are responsible for development of drug resistance in cancer cells, gene therapy is now considered as one of the promising options to address the current treatment limitations. Identification of the over-expressed genes accounting for constitutive activation of certain pathways, and their subsequent knockdown with specific small interfering RNAs (siRNAs), could be a powerful tool in inhibiting proliferation and survival of cancer cells. In this study, we delivered siRNAs against mRNA transcripts of over-regulated cell adhesion molecules such as catenin alpha 1 (CTNNA1), catenin beta 1 (CTNNB1), talin-1 (TLN1), vinculin (VCL), paxillin (PXN), and actinin-1 (ACTN1) in human (MCF-7 and MDA-MB-231) and murine (4T1) cell lines as well as in the murine female Balb/c mice model. In order to overcome the barriers of cell permeability and nuclease-mediated degradation, the pH-sensitive carbonate apatite (CA) nanocarrier was used as a delivery vehicle. While targeting CTNNA1, CTNNB1, TLN1, VCL, PXN, and ACTN1 resulted in a reduction of cell viability in MCF-7 and MDA-MB-231 cells, delivery of all these siRNAs via carbonate apatite (CA) nanoparticles successfully reduced the cell viability in 4T1 cells. In 4T1 cells, delivery of CTNNA1, CTNNB1, TLN1, VCL, PXN, and ACTN1 siRNAs with CA caused significant reduction in phosphorylated and total AKT levels. Furthermore, reduced band intensity was observed for phosphorylated and total MAPK upon transfection of 4T1 cells with CTNNA1, CTNNB1, and VCL siRNAs. Intravenous delivery of CTNNA1 siRNA with CA nanoparticles significantly reduced tumor volume in the initial phase of the study, while siRNAs targeting CTNNB1, TLN1, VCL, PXN, and ACTN1 genes significantly decreased the tumor burden at all time points. The tumor weights at the end of the treatments were also notably smaller compared to CA. This successfully demonstrates that targeting these dysregulated genes via RNAi and by using a suitable delivery vehicle such as CA could serve as a promising therapeutic treatment modality for breast cancers.

Matched MeSH terms: Cell Adhesion Molecules
Fulltext Flavonoids as Natural Anti-Inflammatory Agents Targeting Nuclear Factor-Kappa B (NFκB) Signaling in Cardiovascular Diseases: A Mini Review

Choy KW, Murugan D, Leong XF, Abas R, Alias A, Mustafa MR

Front Pharmacol, 2019;10:1295.
PMID: 31749703 DOI: 10.3389/fphar.2019.01295

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.

Matched MeSH terms: Cell Adhesion Molecules
Fulltext Differential Regulation of LPS-Mediated VE-Cadherin Disruption in Human Endothelial Cells and the Underlying Signaling Pathways: A Mini Review

Chan YH, Harith HH, Israf DA, Tham CL

Front Cell Dev Biol, 2019;7:280.
PMID: 31970155 DOI: 10.3389/fcell.2019.00280

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.

Matched MeSH terms: Cell Adhesion Molecules
Fulltext Revisiting the Roles of Pro-Metastatic EpCAM in Cancer

Mohtar MA, Syafruddin SE, Nasir SN, Low TY

Biomolecules, 2020 02 07;10(2).
PMID: 32046162 DOI: 10.3390/biom10020255

Epithelial cell adhesion molecule (EpCAM) is a cell surface protein that was discovered as a tumour marker of epithelial origins nearly four decades ago. EpCAM is expressed at basal levels in the basolateral membrane of normal epithelial cells. However, EpCAM expression is upregulated in solid epithelial cancers and stem cells. EpCAM can also be found in disseminated tumour cells and circulating tumour cells. Various OMICs studies have demonstrated that EpCAM plays roles in several key biological processes such as cell adhesion, migration, proliferation and differentiation. Additionally, EpCAM can be detected in the bodily fluid of cancer patients suggesting that EpCAM is a pathophysiologically relevant anti-tumour target as well as being utilized as a diagnostic/prognostic agent for a variety of cancers. This review will focus on the structure-features of EpCAM protein and discuss recent evidence on the pathological and physiological roles of EpCAM in modulating cell adhesion and signalling pathways in cancers as well as deliberating the clinical implication of EpCAM as a therapeutic target.

Matched MeSH terms: Cell Adhesion Molecules
Peculiarities of innate immune memory in crustaceans

Low CF, Chong CM

Fish Shellfish Immunol, 2020 Sep;104:605-612.
PMID: 32619624 DOI: 10.1016/j.fsi.2020.06.047

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.

Matched MeSH terms: Cell Adhesion Molecules/genetics; Cell Adhesion Molecules/immunology*
Fulltext The Immunomodulatory CEA Cell Adhesion Molecule 6 (CEACAM6/CD66c) Is a Protein Receptor for the Influenza a Virus

Rahman SK, Ansari MA, Gaur P, Ahmad I, Chakravarty C, Verma DK, et al.

Viruses, 2021 04 21;13(5).
PMID: 33919410 DOI: 10.3390/v13050726

To establish a productive infection in host cells, viruses often use one or multiple host membrane glycoproteins as their receptors. For Influenza A virus (IAV) such a glycoprotein receptor has not been described, to date. Here we show that IAV is using the host membrane glycoprotein CD66c as a receptor for entry into human epithelial lung cells. Neuraminidase (NA), a viral spike protein, binds to CD66c on the cell surface during IAV entry into the host cells. Lung cells overexpressing CD66c showed an increase in virus binding and subsequent entry into the cell. Upon comparison, CD66c demonstrated higher binding capacity than other membrane glycoproteins (EGFR and DC-SIGN) reported earlier to facilitate IAV entry into host cells. siRNA mediated knockdown of CD66c from lung cells inhibited virus binding on cell surface and entry into cells. Blocking CD66c by antibody on the cell surface resulted in decreased virus entry. We found that CD66c is a specific glycoprotein receptor for influenza A virus that did not affect entry of non-IAV RNA virus (Hepatitis C virus). Finally, IAV pre-incubated with recombinant CD66c protein when administered intranasally in mice showed decreased cytopathic effects in mice lungs. This publication is the first to report CD66c (Carcinoembryonic cell adhesion molecule 6 or CEACAM6) as a glycoprotein receptor for Influenza A virus.

Matched MeSH terms: Cell Adhesion Molecules/genetics; Cell Adhesion Molecules/metabolism*
Fulltext Bioinformatics analysis of rhinovirus capsid proteins VP1-4 sequences for cross-serotype vaccine development

Alshrari AS, Hudu SA, Asdaq SMB, Ali AM, Kin CV, Omar AR, et al.

J Infect Public Health, 2021 Nov;14(11):1603-1611.
PMID: 34624714 DOI: 10.1016/j.jiph.2021.09.001

BACKGROUND: Rhinoviruses (RV) are associated with the development and exacerbations of asthma and chronic obstructive pulmonary disease. They've also been linked to more severe diseases like pneumonia, acute bronchiolitis, croup, and otitis media. Because of the hypervariable sequences in the same serotypes, no effective vaccine against rhinoviruses has been developed to date. With the availability of new full-length genome sequences for all RV-A and RV-B serotyped strains, this study used bioinformatics to find a suitable RV strain with the highest similarity matrices to the other strains.
METHODS: The full genomic sequences of all known different RV-A and -B prototypes were downloaded from the National Centre for Biotechnology Information (NCBI) and divided into minor low-density lipoprotein receptor (LDLR) and major intercellular adhesion molecule groups (ICAM). The sequences were edited using Biological Sequence Alignment Editor, v 7.2.0 (BioEdit software) to study each capsid protein (VP1, VP2, VP3, and VP4) and analyzed using the EMBL-EBI ClustalW server and the more current Clustal Omega tool for the calculation of the identities and similarities.
RESULTS: We analyzed and predicted immunogenic motifs from capsid proteins that are conserved across distinct RV serotypes using a bioinformatics technique. The amino acid sequences of VP3 were found to be the most varied, while VP4 was the most conserved protein among all RV-A and RV-B strains. Among all strains studied, RV-74 demonstrated the highest degree of homology to other strains and could be a potential genetic source for recombinant protein production. Nine highly conserved regions with a minimum length of 9-mers were identified, which could serve as potential immune targets against rhinoviruses.
CONCLUSION: Therefore, bioinformatics analysis conducted in the current study has paved the way for the selection of immunogenic targets. Bioinformatically, the ideal strain's capsid protein is suggested to contain the most common RVs immunogenic sites.

Matched MeSH terms: Cell Adhesion Molecules
Identification and protective role of CD34+ stromal cells/telocytes in experimental autoimmune encephalomyelitis (EAE) mouse spleen

Dama G, Hu X, Yan Y, Li Y, Li H, Yang F, et al.

Histochem Cell Biol, 2023 Jul;160(1):11-25.
PMID: 37014442 DOI: 10.1007/s00418-023-02186-5

Experimental autoimmune encephalomyelitis (EAE) is a classical animal model of human multiple sclerosis (MS) that is most commonly used to study the neuropathology and therapeutic effects of the disease. Telocytes (TCs) are a specialized type of interstitial or mesenchymal cell first identified by Popescu in various tissues and organs. However, the existence, distribution and role of CD34+ stromal cells (SCs)/TCs in the EAE-induced mouse spleen remain to be elucidated. We conducted immunohistochemistry, immunofluorescence (double staining for CD34 and c-kit, vimentin, F4/80, CD163, Nanog, Sca-1, CD31 or tryptase) and transmission electron microscopy experiments to investigate the existence, distribution and role of CD34+ SCs/TCs in the EAE-induced mouse spleen. Interestingly, immunohistochemistry, double-immunofluorescence, and transmission electron microscopy results revealed that CD34+ SCs/TCs were significantly upregulated in the EAE mouse spleen. Immunohistochemical or double-immunofluorescence staining of CD34+ SCs/TCs showed positive expression for CD34, c-kit, vimentin, CD34/vimentin, c-kit/vimentin and CD34/c-kit, and negative expression for CD31 and tryptase. Transmission electron microscopy (TEM) results demonstrated that CD34+ SCs/TCs established close connections with lymphocytes, reticular cells, macrophages, endothelial cells and erythrocytes. Furthermore, we also found that M1 (F4/80) or M2 (CD163) macrophages, and haematopoietic, pluripotent stem cells were markedly increased in EAE mice. Our results suggest that CD34+ SCs/TCs are abundant and may play a contributing role in modulating the immune response, recruiting macrophages and proliferation of haematopoietic and pluripotent stem cells following injury to promote tissue repair and regeneration in EAE mouse spleens. This suggests that their transplantation combined with stem cells might represent a promising therapeutic target for the treatment and prevention of multiple autoimmune and chronic inflammatory disorders.

Matched MeSH terms: Cell Adhesion Molecules/metabolism

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