Phytoconstituents as photoprotective novel cosmetic formulations.

Phytoconstituents are gaining popularity as ingredients in cosmetic formulations as they can protect the skin against exogenous and endogenous harmful agents and can help remedy many skin conditions. Exposure of skin to sunlight and other atmospheric conditions causes the production of reactive oxygen species, which can react with DNA, proteins, and fatty acids, causing oxidative damage and impairment of antioxidant system. Such injuries damage regulation pathways of skin and lead to photoaging and skin cancer development.

In vitro sun protection factor determination of herbal oils used in cosmetics.

The aim of this study was to evaluate ultraviolet (UV) absorption ability of volatile and nonvolatile herbal oils used in sunscreens or cosmetics and express the same in terms of sun protection factor (SPF) values. Sun protection factor is a laboratory measure of the effectiveness of sunscreen; the higher the SPF, the more protection a sunscreen offers against the ultraviolet radiations causing sunburn. The in vitro SPF is determined according to the spectrophotometric method of Mansur et al.

Expression of cyclooxygenase-2 and microsomal prostaglandin-E synthase in amoeboid microglial cells in the developing brain and effects of cyclooxygenase-2 neutralization on BV-2 microglial cells.

Microglia express cyclooxygenase-2 (COX-2) and microsomal prostaglandin-E synthase (mPGES-1) but their localization in the amoeboid microglial cells (AMC), considered to be the nascent brain macrophages, in the developing brain has remained unexplored; furthermore, their interrelation and regulation have also remained to be fully elucidated. We show here that AMC in postnatal rat brain constitutively expressed COX-2 and mPGES-1 whose immunoexpression was upregulated in rats given lipopolysaccharide (LPS) injections. Reverse transcriptase-polymerase chain reaction and Western blot analysis of the callosal tissue rich in AMC revealed that COX-2 and mPGES-1 mRNA and protein expression was augmented following LPS injections.

Role of glutamate and its receptors and insulin-like growth factors in hypoxia induced periventricular white matter injury.

This study investigated the glutamate concentration and cellular localization of alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid glutamate receptors (AMPA GluR2, GluR3, GluR4) along with insulin-like growth factors (IGF)-1 and -2 expression in the periventricular white matter (PWM) of neonatal rats with the aim to determine their involvement in PWM injury in hypoxia. In response to hypoxia, the PWM tissue concentration of glutamate and IGF-1 as well as mRNA and protein expression of GluR2, GluR3, GluR4, IGF-1, and -2 was upregulated. Immunoexpression of GluR2/3 and GluR4 were localized in the amoeboid microglial cells (AMC) and oligodendrocytes while that of IGF-1 and -2 were confined to AMC.

A role for photoreceptors in retinal oedema and angiogenesis: an additional explanation for laser treatment?

Purpose: To investigate the possible roles of retinal photoreceptors in macular oedema and retinal angiogenesis with particular reference to the mode of action of laser therapy.

Methods: (i) Studies in rats made hypoxic for 2 h by administering an oxygen/nitrogen mixture of reduced oxygen content, and growth factors determined by RT-PCR, western blotting, and immunohistochemistry. Assessment of blood-retinal barrier integrity using fluorescent and electron-dense tracers.

Expression of cyclooxygenase-1/-2, microsomal prostaglandin-E synthase-1 and E-prostanoid receptor 2 and regulation of inflammatory mediators by PGE(2) in the amoeboid microglia in hypoxic postnatal rats and murine BV-2 cells.

This study aimed to investigate the effect of hypoxia on the expression of cyclooxygenase-1 (COX-1), cyclooxygenase-2 (COX-2), microsomal prostaglandin-E synthase (mPGES-1), E-prostanoid receptor 2 (EP2) in microglia; and the roles of EP2-cyclic adenosine monophosphate (cAMP) signaling pathway in the prostaglandin E(2) (PGE(2)) regulation of inflammatory mediators released by hypoxic BV-2 cells. Immunoexpression of COX-1, COX-2, mPGES-1 and EP2 was localized in the amoeboid microglial cells (AMC), a nascent brain macrophage in the developing brain, as confirmed by double labeling with OX-42 and lectin, specific markers of microglia. AMC emitted a more intense immunofluorescence in hypoxic rats when compared with the matching controls.

Hypoxia-ischemia and retinal ganglion cell damage.

Retinal hypoxia is the potentially blinding mechanism underlying a number of sight-threatening disorders including central retinal artery occlusion, ischemic central retinal vein thrombosis, complications of diabetic eye disease and some types of glaucoma. Hypoxia is implicated in loss of retinal ganglion cells (RGCs) occurring in such conditions. RGC death occurs by apoptosis or necrosis.

Cellular and vascular changes in the retina of neonatal rats after an acute exposure to hypoxia.

Purpose: This study was undertaken to examine the effects of an acute hypoxic exposure on the retinal cells and production of vascular factors such as vascular endothelial growth factor (VEGF) and nitric oxide (NO), which may affect vascular permeability in the developing retina.

Methods: Retinas of 1-day-old rats were examined at 3 hours to 14 days after hypoxic exposure. The mRNA and protein expression of hypoxia-inducible factor-1alpha (HIF-1alpha), VEGF, endothelial nitric oxide synthase (eNOS), neuronal NOS (nNOS), and inducible NOS (iNOS) were determined by real-time RT-PCR, Western blot analysis, and immunohistochemistry.

Periventricular white matter damage in the hypoxic neonatal brain: role of microglial cells.

Periventricular white matter damage (PWMD) also known as periventricular white matter injury, is one of the major causes of neurological impairment in premature newborns. The etiology of white matter injury is multifaceted with hypoxia-ischemia being an important underlying factor. The developing oligodendrocytes are susceptible to damage resulting in myelination deficits.

Combustion smoke exposure induces up-regulated expression of vascular endothelial growth factor, aquaporin 4, nitric oxide synthases and vascular permeability in the retina of adult rats.

Retinal cells respond to various experimental stimuli including hypoxia, yet it remains to be investigated whether they react to smoke inhalation. We show here that retinal cells in rats, notably the ganglion cells, Müller cells, astrocytes and blood vessels responded vigorously to a smoke challenge. The major changes included up-regulated expression of vascular endothelial growth factor (VEGF), aquaporin 4 (AQP4) and nitric oxide synthase (NOS).

Kv1.1 expression in microglia regulates production and release of proinflammatory cytokines, endothelins and nitric oxide.

Potassium channels play an important role in microglial activation but their involvement in main functions of microglia including secretion of proinflammatory cytokines has remained uncertain. This study has revealed the specific expression of Kv1.1 in microglia both in vivo and in vitro.

Expression of angiotensin II and its receptors in the normal and hypoxic amoeboid microglial cells and murine BV-2 cells.

Involvement of the local angiotensin receptor system in the central nervous system is well documented, yet its cellular localization and role in the glial cells have remained elusive. This study reports expression of angiotensin II and its receptors namely, angiotensin II receptor type 1 (AT(1)) and angiotensin II receptor type 2 (AT(2)) in the amoeboid microglial cells in the neonatal rat brain. In rats subjected to hypoxia, the amount of angiotensin II released in the corpus callosal tissue was reduced as revealed by enzyme immunoassay.

Antioxidants and neuroprotection in the adult and developing central nervous system.

Oxidative stress is implicated in the pathogenesis of a number of neurological disorders such as Alzheimer's disease (AD), Parkinson's disease (PD), multiple sclerosis and stroke in the adult as well as in conditions such as periventricular white matter damage in the neonatal brain. It has also been linked to the disruption of blood brain barrier (BBB) in hypoxic-ischemic injury. Both experimental and clinical results have shown that antioxidants such as melatonin, a neurohormone synthesized and secreted by the pineal gland and edaravone (3-methyl-1-phenyl-2-pyrazolin-5-one), a newly developed drug, are effective in reducing oxidative stress and are promising neuroprotectants in reducing brain damage.

Lymphatic targeting of zidovudine using surface-engineered liposomes.

The present investigation was aimed at lymphatic targeting of zidovudine (ZDV)-loaded surface-engineered liposomes (SE liposomes). Surface of liposomes was engineered by incorporation of charges (positive or negative) and site-specific ligand (mannose) in order to enhance localization to lymphatics, specifically to lymph node and spleen. Positively and negatively charged nanosized SE liposomes (120 +/- 10 nm) were prepared using stearylamine (SA) and dicetyl phosphate (DCP), respectively, while ligand-coated SE liposomes were prepared using mannose-terminated SA (mannose conjugate).

Monocyte chemoattractant protein-1 (MCP-1) produced via NF-kappaB signaling pathway mediates migration of amoeboid microglia in the periventricular white matter in hypoxic neonatal rats.

Monocyte chemoattractant protein-1 (MCP-1), a member of beta-chemokine subfamily, regulates the migration of microglia, monocytes, and lymphocytes to the inflammatory site in the central nervous system. We sought to determine if amoeboid microglial cells (AMC) produce MCP-1 that may be linked to migration of AMC in the corpus callosum periventricular white matter in hypoxic neonatal rats. A striking feature in 1-day-old rats subjected to hypoxia was a marked increase in cell numbers of AMC and immunoexpression of MCP-1 and its receptor (CCR(2)).

Blood-retinal barrier in hypoxic ischaemic conditions: basic concepts, clinical features and management.

The blood-retinal barrier (BRB) plays an important role in the homeostatic regulation of the microenvironment in the retina. It consists of inner and outer components, the inner BRB (iBRB) being formed by the tight junctions between neighbouring retinal capillary endothelial cells and the outer barrier (oBRB) by tight junctions between retinal pigment epithelial cells. Astrocytes, Müller cells and pericytes contribute to the proper functioning of the iBRB.

Expression of syndecan-2 in the amoeboid microglial cells and its involvement in inflammation in the hypoxic developing brain.

The present study examined the expression of heparan sulphate proteoglycan, syndecan-2 (Sdc-2) in the corpus callosum and the amoeboid microglial cells (AMC) in the neonatal rat brain in response to hypoxia. In 1-day old Wistar rats subjected to hypoxia the mRNA and protein expression of Sdc-2 in the corpus callosum, heavily populated by AMC, was increased up to 3 days after the hypoxic exposure. Immunoexpression of Sdc-2 was localized in AMC as confirmed by double labeling using microglial marker.

Effects of hypoxia on expression of transforming growth factor-beta1 and its receptors I and II in the amoeboid microglial cells and murine BV-2 cells.

Transforming growth factor-beta1 (TGF-beta1) is widely recognized as a prototype of multifunctional growth factors and master switches in the regulation of key events of development, disease and repair. It is localized in neurons, astrocytes and brain macrophages in altered conditions but its localization in the amoeboid microglial cells (AMC), a nascent brain macrophage in the developing brain has remained unexplored. Here we report expression of TGF-beta1 and its receptors namely, transforming growth factor-beta receptor I (TbetaRI) and transforming growth factor-beta receptor II (TbetaRII) in AMC and BV-2 cells induced by hypoxia.

Expression of Kv1.2 in microglia and its putative roles in modulating production of proinflammatory cytokines and reactive oxygen species.

Microglial cells are endowed with different potassium ion channels but their expression and specific functions have remained to be fully clarified. This study has shown Kv1.2 expression in the amoeboid microglia in the rat brain between 1 (P1) and 10 (P10) days of age.

Extramural vascular invasion is an adverse prognostic indicator of survival in patients with colorectal cancer.

Background/aims: Extramural vascular invasion (EVI) in colorectal cancer is reported to be a stage-independent adverse prognostic factor, and is a core item in the Royal College of Pathologists minimum data set for colorectal cancer histopathology reporting. The detection of EVI is also highly variable amongst pathologists. Our aims were to analyse both the frequency of EVI in colorectal cancer resections, and the effect of EVI on survival, in patients operated on over a 5-year period.

A simple circuit to deliver bubbling CPAP.

Nasal continuous positive airway pressure (CPAP), especially bubbling CPAP, is known to reduce the need for more invasive ventilation. We here describe a circuit that can deliver bubbling CPAP in resource poor settings. We describe how the oxygen concentration can be altered from 98% to 21% oxygen using this system.

Expression of Notch-1 receptor and its ligands Jagged-1 and Delta-1 in amoeboid microglia in postnatal rat brain and murine BV-2 cells.

Notch-1 receptor signaling pathway is involved in neuronal and glial differentiation. Its involvement in microglial functions, however, has remained elusive. This study reports the localization of Notch-1 receptor immunoreactivity in the amoeboid microglial cells (AMC) in the postnatal rat brain.

Melatonin attenuates hypoxia-induced ultrastructural changes and increased vascular permeability in the developing hippocampus.

Hypoxic injury in the perinatal period may be involved in damaging the developing hippocampus. The damage may be mediated by excess production of vascular endothelial growth factor (VEGF) and nitric oxide (NO). We examined the hippocampus of neonatal Wistar rats subjected to hypoxia for VEGF and NO production.

Amoeboid microglia in the periventricular white matter induce oligodendrocyte damage through expression of proinflammatory cytokines via MAP kinase signaling pathway in hypoxic neonatal rats.

Hypoxic injury in the perinatal period results in periventricular white matter (PWM) lesions with axonal damage and oligodendroglial loss. It also alters macrophage function by perpetuating expression of inflammatory mediators. Relevant to this is the preponderance of amoeboid microglial cells (AMC) characterized as active macrophages in the developing PWM.

Blood brain barrier in hypoxic-ischemic conditions.

The blood brain barrier (BBB) plays an important role in the homeostatic regulation of the brain microenvironment and maintains the immune-privileged status of the brain by restricting the entry of T lymphocytes. Structurally, the BBB is formed by tight junctions between the endothelial cells. Astrocytes, pericytes and perivascular microglia surround the endothelial cells contributing to proper functioning of the BBB.