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The Use of Syzygium cumini in Nanotechnology
Published in K. N. Nair, The Genus Syzygium, 2017
Avnesh Kumari, Vineet Kumar, Sudesh Kumar Yadav
S. cumini is rich in anthocyanins, glucoside, ellagic acid, isoquercetin, kaemferol, and myrcetin. Leaves contain acylated flavonol glycosides (Mahmoud et al. 2011), quercetin, myricetin, myricitin, triterpenoids (Gupta and Sharma 1974), esterase, galloyl carboxylase (Bhatia et al. 1974), and tannins (Morton 1987). Leaves of S. cumini are also rich in polyphenols, flavonoids, and essential oils (Mukherjee et al. 1998; Timbola et al. 2002; Lima et al. 2007). Seeds are rich in alkaloids, amino acids, flavonoids, glycosides, phytosterols, saponins, steroids, tannins, and triterpenoids. The stem also contains many phytochemicals, like betulinic acid, friedelin, epifriedelanol, β-sitosterol, eugenin, fatty acid ester of epi-friedelanol (Sengupta and Das 1965), quercetin, kaemferol, myricetin, gallic acid, ellagic acid (Bhargava et al. 1974), bergenins (Kopanski and Schnelle 1988), flavonoids, and tannins (Bhatia and Bajaj 1975). The astringent property of stem bark is due to gallo- and ellagitannins. Flowers of S. cumini contain dihydromyricetin (Nair and Subramanian 1962), quercetin-3-D-galactoside, kaemferol, quercetin, myricetin, isoquercetin, myricetin-3-L-arbinose, oleanolic acid, acetyl oleanolic acid (Rastogi and Mehrotra 1990), and eugenol triterpenoid B (Nair and Subramanian 1962). Roots are rich in flavonoid glycosides (Vaishnava et al. 1992) and isorhamnetin-3-O-rutinoside (Vaishnava and Gupta 1990). Gallic acid imparts sourness, and anthocyanins give color to the fruits (Venkateswarlu 1952). The fruits are rich in raffinose, glucose, fructose (Srivastava 1953), citric acid, mallic acid (Lewis et al. 1956), gallic acid, anthocyanins (Jain and Seshadri 1975), delphinidin-3-gentibioside (Venkateswarlu 1952), cyanidin diglycoside, petunidin, and malvidin (Sharma and Sheshadri 1955). Most of these compounds have been reported to possess antioxidant and free radical scavenging activities (Ruan et al. 2008). These phytochemicals are responsible for the medicinal properties of seeds of S. cumini.
Neuroviral Infections and Immunity
Published in Sunit K. Singh, Daniel Růžek, Neuroviral Infections, 2013
Bersabeh Tigabu, Fabian de Kok-Mercado, Michael R. Holbrook
It is generally recognized that cellular movement across the endothelial cell barrier (diapedesis) occurs primarily via paracellular passage after disassembly of TJ and AJ (Engelhardt 2008; Maslin et al. 2005; Owens et al. 2008; Roberts et al. 2010; Schnoor and Parkos 2008). However, some studies have suggested that transmigration through pores in endothelial cells is also a means of lymphocyte diapedesis. The natural movement of lymphocytes and macrophages between tissues and the circulatory system is a key event in the management of a host response and for immune surveillance. In most tissues, the movement of cells out of the circulatory system is routine. In the CNS, however, under normal conditions, the movement of lymphocytes (specifically T cells) or macrophages into the CNS is very tightly controlled and occurs without the loss of barrier function (Roberts et al. 2010). Studies in animals suggest that, of lymphocytes, only activated T cells are capable of crossing the BBB (Hickey 1991; Hickey et al. 1991). Cell attachment and the mechanisms associated with migration across the neuronal endothelium are similar to those seen in other tissues. However, the tight regulation of cellular movement clearly indicates differential control mechanisms relative to other tissues. Initial penetration of the BBB requires attachment of cells to the endothelium. It has been shown in many studies that lymphocytes “roll” along the luminal endothelial membrane until they encounter appropriate signaling or attachment molecules that allow them to attach to the endothelial wall. These recognition markers include selectins on the surface of endothelial cells that interact with selectin ligands on the surface of lymphocytes (Eriksson et al. 2001; Lawrence et al. 1997). Evidence also suggests that bound chemokines provide attachment recognition for lymphocytes and provide a means for activating attached lymphocytes (Alt et al. 2002; Ancuta et al. 2004; Bielecki et al. 2007; Buckner et al. 2006; Columba-Cabezas et al. 2003; Eugenin et al. 2006; Tani et al. 1996). A number of different cellular proteins have been associated with initial lymphocyte attachment to endothelial cells, but the attachment proteins vary depending upon the site of the BBB barrier (i.e., choroid plexus, parenchymal BBB, or meningeal BBB) and the system under study (i.e., T cells, monocytes). Implicated attachment proteins include VLA-4, VCAM-1, and the selectin family of C-type lectins (Engelhardt 2008; Owens et al. 2008; Roberts et al. 2010). After lymphocyte tethering, signaling events occur to stimulate the upregulation of cellular attachment molecules including ICAM-1 and VCAM-1, which along with ICAM-2 are constitutively expressed on endothelial cells (Baron et al. 1993; Cross et al. 1990; Dustin et al. 1986; Roberts et al. 2010; Steffen et al. 1994). These endothelial attachment proteins interact with members of the integrin family and LFA-1 on the surface of lymphocytes.
A Preventive Role of RANTES Genetic Variation against Undifferentiated Schizophrenia
Published in Immunological Investigations, 2022
Hana Saoud, Amira Ben Afia, Youssef Aflouk, Lotfi Gaha, Besma Bel Hadj Jrad
While inflammatory proteins in the CNS are often thought to be damaging, numerous investigations revealed that they can also be beneficial and neuroprotective (Kerschensteiner et al. 2003; Orellana et al. 2007; Saoud et al. 2019; Tabakman et al. 2004). Indeed, RANTES has been found to protect against various neurotoxins including glutamate (Bruno et al. 2000), β-amyloid (Ignatov et al. 2006), and the HIV proteins gp120 and tat (Campbell et al. 2015; Rozzi et al. 2014) coupled with its known role in leukocyte recruitment and activation (Eugenin et al. 2003). Further, in-vitro neurons stimulation with RANTES enhances cell survival and has a neuroprotective impact against thrombin and sodium nitroprusside toxicity (Tripathy et al. 2010).
Role of pre-stroke immunity in ischemic stroke mechanism among patients with HIV
Published in AIDS Care, 2019
Jose Gutierrez, Camilla Ingrid Hatleberg, Henry Evans, Michael T. Yin
Lower CD4 nadir and higher CD4 count near death have been associated with brain arterial inflammation localized to the intima and closely related to the presence of atheroma (Gutierrez et al., 2016). Similarly, a nadir CD4 count < 200 cells/mm3 has been associated with faster progression of carotid artery intima-media thickening (Hsue et al., 2004), a marker of atherosclerosis. We have argued before that it is possible that HIV proteins in the arterial wall may function as perpetual antigenic stimuli (Gutierrez, et al., 2016), similarly to what has been reported in coronary arteries.(Eugenin et al., 2008) In this context, severe immunosuppression may favor seeding of the arteries with the virus itself or its proteins.