White finger millet starch: Hydrothermal and microwave modification and its characterisation.

White finger millet (WFM) starch was modified by hydrothermal (HS) and microwave (MS) methods. Modification methods had a significant change in the b* value observed in the HS sample, and it caused the higher chroma (∆C) value. The treatments have not significantly changed the chemical composition and water activity (aw) of native starch (NS) but reduced the pH value. The gel hydration properties of modified starch enhanced significantly, especially in the HS sample. The least NS gelation concentration (LGC) of 13.63 % increased to 17.74 % in HS and 16.41 % in MS. The pasting temperature of the NS got reduced during the modification process and altered the setback viscosity. The starch samples exhibit the shear thinning behavior and reduce starch molecules' consistency index (K). FTIR results exhibit that the modification process highly altered the short-range order of starch molecules more than the double helix structure. A significant reduction in relative crystallinity was observed in the XRD diffractogram, and the DSC thermogram depicts the significant change in the hydrogen bonding of starch granules. It can be inferred that the HS and MS modification method significantly alters the properties of starch, which can increase the food applications of WFM starch.

Photobiological hydrogen production and artificial photosynthesis for clean energy: from bio to nanotechnologies.

Global energy demand is increasing rapidly and due to intensive consumption of different forms of fuels, there are increasing concerns over the reduction in readily available conventional energy resources. Because of the deleterious atmospheric effects of fossil fuels and the uncertainties of future energy supplies, there is a surge of interest to find environmentally friendly alternative energy sources. Hydrogen (H2) has attracted worldwide attention as a secondary energy carrier, since it is the lightest carbon-neutral fuel rich in energy per unit mass and easy to store. Several methods and technologies have been developed for H2 production, but none of them are able to replace the traditional combustion fuel used in automobiles so far. Extensively modified and renovated methods and technologies are required to introduce H2 as an alternative efficient, clean, and cost-effective future fuel. Among several emerging renewable energy technologies, photobiological H2 production by oxygenic photosynthetic microbes such as green algae and cyanobacteria or by artificial photosynthesis has attracted significant interest. In this short review, we summarize the recent progress and challenges in H2-based energy production by means of biological and artificial photosynthesis routes.

Development and validation of analytical method for the estimation of lamivudine in rabbit plasma / 药物分析学报

Lamivudine has been widely used in the treatment of HIV disease. A reliable, sensitive reversed phase high performance liquid chromatography (RP-HPLC) method was developed and validated for lamivudine in rabbit plasma. The method was developed on Hypersil BDS C-18 column (250 mm × 4.6 mm, 5 μm) using a mobile phase of 0.25％ Triethylamine buffer (pH 3.0):acetonitrile (70:30, v/v). The efficient was monitored by UV detector at 256 nm. The total run time was 15 min with a flow rate of 1.0 mL/min. Calibration curve was linear over the concentration range of 25-2000 ng/mL. The retention times of lamivudine and internal standard (Nelfinavir) were 8.78 min and 10.86 min, respectively. The developed RP-HPLC method can be successfully applied for the quantitative pharmacokinetic parameters determination of lamivudine in rabbit model.

Coronary artery dilatation in Incomplete Kawasaki disease.

We conducted this study to compare the incidence of coronary artery dilatation in children with Incomplete and Classical Kawasaki disease, diagnosed as per AHA criteria. Subjects were included on a retrospective review of records (2002-2007); those with a discharge diagnosis of Kawasaki disease were enrolled. A total of 29 patients were identified (3.1 per 1000 pediatric admissions), out of which 22 were boys (median age: 4.8 years; range: 4 months-11 years). Seventeen (58.6%) had Classical KD and twelve (41.4%) children had Incomplete KD. All children received IVIG and underwent echocardiography. Coronary involvement was more in Incomplete KD (11/12 = 91.6%) as compared to Classical KD (7/17= 41.1%). The sensitivity, specificity and predictive value of AHA criteria to detect coronary artery dilatation was 39%, 9%, and 41%, respectively. We conclude that children presenting with Incomplete Kawasaki disease are at a higher risk of coronary artery abnormalities.

Genetic deficiency of heme oxygenase-1 impairs functionality and form of an arteriovenous fistula in the mouse.

Vascular access dysfunction contributes to patient morbidity during maintenance hemodialysis. In this study we determined if knockout of heme oxygenase-1 predisposed to malfunction of arteriovenous fistulas. After three weeks, all fistulas in wild type mice were patent whereas a third of the fistulas in knockout mice were occluded and these exhibited increased neointimal hyperplasia and venous wall thickening. Heme oxygenase-1 mRNA and protein were robustly induced in the fistulas of the wild type mice. In the knockout mice there was increased PAI-1 and MCP-1 expression, marked induction of MMP-2 and MMP-9, but similar expression of PDGF alpha, IGF-1, TGF-beta1, VEGF, and osteopontin compared to wild type mice. We conclude that heme oxygenase-1 deficiency promotes vasculopathic gene expression, accelerates neointimal hyperplasia and impairs the function of arteriovenous fistulas.

In vivo demonstration of neuroinflammatory molecule expression in brain abscess with diffusion tensor imaging.

BACKGROUND AND PURPOSE: Neuroinflammatory molecules, including tumor necrosis factor-alpha, interleukin1-beta, lymphocyte function associated molecule-1, and intercellular cell adhesion molecule-1 contribute to the development of brain abscess. We hypothesized that the high fractional anisotropy (FA) in the brain abscess cavity reflects the upregulation of these neuroinflammatory molecules. MATERIALS AND METHODS: Diffusion tensor imaging (DTI) was performed in 24 patients with brain abscess and Staphylococcus aureus-treated as well as nontreated Jurket cell lines (at 4 time points: 1, 24, 48, and 72 hours). Neuroinflammatory molecules were quantified from the brain abscess cavity aspirate of the patients as well as from the heat-killed S aureus-treated and nontreated cell lines and correlated with DTI measures. RESULTS: The DTI-derived FA strongly correlated with the presence of neuroinflammatory molecules in the pus as well as in S aureus-treated cell lines; no such correlation was observed in nontreated cell lines. CONCLUSIONS: These data indicate that neuroinflammatory molecules confer high diffusion anisotropy inside the brain abscess cavity. We propose that increased FA reflects upregulated inflammatory response in brain abscess.

Deficiency of heme oxygenase-1 impairs renal hemodynamics and exaggerates systemic inflammatory responses to renal ischemia.

Heme oxygenase-1 may exert cytoprotective effects. In this study we examined the sensitivity of heme oxygenase-1 knockout (HO-1(-/-)) mice to renal ischemia by assessing glomerular filtration rate (GFR) and cytokine expression in the kidney, and inflammatory responses in the systemic circulation and in vital extrarenal organs. Four hours after renal ischemia, the GFR of HO-1(-/-) mice was much lower than that of wild-type mice in the absence of changes in renal blood flow or cardiac output. Eight hours after renal ischemia, there was a marked induction of interleukin-6 (IL-6) mRNA and its downstream signaling effector, phosphorylated signal transducer and activator of transcription 3 (pSTAT3), in the kidney, lung, and heart in HO-1(-/-) mice. Systemic levels of IL-6 were markedly and uniquely increased in HO-1(-/-) mice after ischemia as compared to wild-type mice. The administration of an antibody to IL-6 protected against the renal dysfunction and mortality observed in HO-1(-/-) mice following ischemia. We suggest that the exaggerated production of IL-6, occurring regionally and systemically following localized renal ischemia, in an HO-1-deficient state may underlie the heightened sensitivity observed in this setting.

Comparative evaluation of fungal, tubercular, and pyogenic brain abscesses with conventional and diffusion MR imaging and proton MR spectroscopy.

BACKGROUND AND PURPOSE: It is difficult to differentiate the cause of brain abscesses with the use of CT and MR imaging. We did a comparative evaluation of pyogenic, tubercular, and fungal brain abscesses by using conventional, diffusion-weighted imaging (DWI), and proton MR spectroscopy (PMRS) with an aim to define the unique features that may differentiate among the pyogenic, tubercular, and fungal brain abscesses. MATERIALS AND METHODS: We performed a retrospective analysis on 110 patients with surgically proved brain abscesses. Imaging studies included T2, T1, postcontrast T1, DWI, and PMRS. Apparent diffusion coefficient (ADC) of the wall and cavity of the abscesses were quantified. The morphologic, physiologic, and metabolite features of pyogenic (n=91), tubercular (n=11), and fungal (n=8) abscesses were compared. RESULTS: The pyogenic abscesses had smooth (55/91) and lobulated (36/91) walls, whereas the tubercular abscesses had smooth (4/11), lobulated (6/11), or crenated walls (1/11) with no intracavitary projections. The fungal abscesses showed irregular walls (lobulated 4/8, crenated 4/8) with intracavitary projections (8/8). The wall as well as the cavity showed low ADC in the pyogenic and tubercular abscesses. In the fungal abscesses, the wall and projections showed low ADC (8/8); however, the cavity itself showed high ADC (8/8). PMRS showed cytosolic amino acids (89/91), acetate (25/91), and succinate (18/91) in the pyogenic abscesses, whereas lipid/lactate (11/11) was seen in the tubercular abscesses. The fungal abscesses showed lipid (4/8), lactate (7/8), amino acids (4/8), and multiple peaks between 3.6 and 3.8 ppm assigned to trehalose (5/8). CONCLUSION: Based on the morphologic, ADC, and metabolite information, it may be possible to differentiate among the pyogenic, tubercular, and fungal brain abscesses.

Renal response to repeated exposure to endotoxin: implications for acute kidney injury.

Zager and colleagues demonstrate that endotoxin tolerance is accompanied by an augmented inflammatory response in the kidney, the latter also exhibiting cholesterol-dependent cytoresistance. These novel findings are discussed mainly from the perspective of acute kidney injury and its prevention by preconditioning and the elicitation of cytoprotective pathways.

Resident dendritic cells are the predominant TNF-secreting cell in early renal ischemia-reperfusion injury.

Renal ischemia-reperfusion injury (IRI) rapidly induces production of inflammatory mediators including, and in particular, tumor necrosis factor (TNF). Possible sources include resident parenchymal and bone marrow-derived cells as well as recruited leukocytes. Cell suspensions from kidneys subjected to IRI were examined by cell separation followed by in vitro culture and enzyme-linked immunosorbent assay (ELISA), immunoperoxidase and immunofluorescence microscopy, and multicolor flow cytometry to determine the contribution of dendritic cells (DCs) to early production of TNF and other inflammatory mediators. Secretion of TNF, interleukin (IL-6), monocyte chemoattractant protein-1 (MCP-1), and regulated on activation normal T cell expressed and secreted (RANTES) was increased in cell suspensions from IRI compared with control kidneys and was higher in DC-enriched preparations. Immunostaining identified TNF(+ve) cells that coexpressed the DC marker CD11c. Flow cytometry of bone marrow-derived (CD45(+ve)) cell populations at 24 h post-IRI demonstrated that F4/80(+ve)/CD11c(+ve) DCs remained proportionately stable and exhibit higher levels of DC maturation markers, whereas the proportion of F4/80(-ve) DCs, monocytes, neutrophils, and T cells increased. Intracellular staining for TNF confirmed that F4/80(+ve) DCs were the predominant TNF(+ve) cell and expressed higher levels than other TNF(+ve) cells. In vivo depletion of DCs from the kidney substantially attenuated TNF secretion by total and CD45(+ve) cells following IRI. The results uncover a role for resident F4/80(+ve) DCs as the predominant secretors of TNF within 24 h of IRI.

Heme oxygenase-1: a provenance for cytoprotective pathways in the kidney and other tissues.

Heme oxygenase (HO) is the rate-limiting enzyme in the degradation of heme, converting heme to biliverdin, during which iron is released and carbon monoxide (CO) is emitted; biliverdin is subsequently converted to bilirubin by biliverdin reductase. At least two isozymes possess HO activity: HO-1 represents the isozyme induced by diverse stressors, including ischemia, nephrotoxins, cytokines, endotoxin, oxidants, and vasoactive substances; HO-2 is the constitutive, glucocorticoid-inducible isozyme. HO-1 is upregulated in the kidney in assorted conditions and diseases. Interest in HO is driven by the capacity of this system to protect the kidney against injury, a capacity likely reflecting, at least in part, the cytoprotective properties of its products: in relatively low concentrations, CO exerts vasorelaxant, antiapoptotic, and anti-inflammatory effects while bile pigments are antioxidant and anti-inflammatory metabolites. This article reviews the HO system and the extent to which it influences the function of the healthy kidney; it summarizes conditions and stimuli that elicit HO-1 in the kidney; and it explores the significance of renal expression of HO-1 as induced by ischemia, nephrotoxins, nephritides, transplantation, angiotensin II, and experimental diabetes. This review also points out the tissue specificity of the HO system, and the capacity of HO-1 to induce renal injury in certain settings. Studies of HO in other tissues are discussed insofar as they aid in elucidating the physiologic and pathophysiologic significance of the HO system in the kidney.

Genetic contribution to high neonatally lethal malformation rate in the United Arab Emirates.

OBJECTIVES: We examined the contribution of genetic disorders to congenital anomalies (CA) causing neonatal deaths in the Al Ain Medical District (AMD) in the United Arab Emirates (UAE) because of the high consanguineous marriage rate in the community. METHODS: Charts of all neonatal deaths in the three perinatal units, which accounted for 99% of all births in AMD (1992-2000), were studied. Data regarding pregnancy, a family history including the level of parental consanguinity, the results of genetic evaluations and neonatal outcomes were recorded as part of an ongoing malformation surveillance system. Causes of death were based on clinical, laboratory and imaging findings. RESULTS: Of the 508 neonates who died, 212 (42%) had CA, which were the leading cause of death. Forty-four percent of the CA were due to definite genetic disorders and 75% of these were single gene defects. Multisystem malformations were the commonest congenital malformations. Parental consanguinity was associated with a 2-fold increased risk of non-chromosomal multisystem malformations. CONCLUSIONS: Lethal malformations were the leading cause of neonatal deaths, and parental consanguinity was associated with an increased risk of autosomal recessive disorders. The results underscore the importance of genetic screening and counseling in strategies for further significant reductions in the neonatal mortality rate in the UAE.

Neonatal outcome in the United Arab Emirates: the effect of changes in resources and practices.

Selective improvements in neonatal care resources and practices were instituted between 1992/1994 (period 1) and 1995/1998 (period 2) following a neonatal audit in the United Arab Emirates. We evaluated the effect of these changes on neonatal mortality rate (NNMR), birth-weight-specific mortality rates and causes of mortality. Overall there was a 17% decline in the NNMR from periods 1 to 2. Mortality rates in infants with birth weight < 1000 g and > 2500 g decreased by 36% and 35% respectively from periods 1 to 2. Modest declines in deaths from asphyxia, sepsis and complications of preterm births occurred from periods 1 to 2 but the differences were not statistically significant.

Neonatal outcome in the United Arab Emirates: the effect of changes in resources and practices

Selective improvements in neonatal care resources and practices were instituted between 1992/1994 [period 1] and 1995/1998 [period 2] following a neonatal audit in the United Arab Emirates. We evaluated the effect of these changes on neonatal mortality rate [NNMR], birth-weight-specific mortality rates and causes of mortality. Overall there was a 17% decline in the NNMR from periods 1 to 2. Mortality rates in infants with birth weight < 1000 g and > 2500 g decreased by 36% and 35% respectively from periods 1 to 2. Modest declines in deaths from asphyxia, sepsis and complications of preterm births occurred from periods 1 to 2 but the differences were not statistically significant

Preparation and characterization of Eu(3+) doped powder spinel phosphors (MgAl(1.8)Y(0.2-x)O(4)).

The photoluminescence (PL) studies of powder phosphors are under rigorous study in view of the applications they have in the field of technology. Different methods are available for the preparation of rare earth ions doped in different host environment of powder phosphors. In the present work, a novel route known as sol-gel technique is employed to prepare spinel phosphor MgAl(1.8)Y(0.2-x)O(4):Eu(x) (x = 2-6 mol%). Then the studies have been carried out to optimize the dopant concentration in the host lattice with the help of photoluminescence spectra. These phosphors have displayed bright red color under UV source. The emission intensities were determined and the relative fluorescence intensities have been estimated. The richness of the red color has been verified by determining their chromaticity coordinates (X, Y) from the CIE standard charts. With the help of XRD, electron spin resonance (ESR), and photo-acoustic (PA) spectra of the samples prepared are also used for the confirmity of the host and analyzing of the data.

Home hygiene and environmental sanitation: a country situation analysis for India.

Problems of the environment and of domestic hygiene are always related to poverty of population and the sanitation of settlements. Most cities and towns in developing countries, like India, are characterised by over-crowding, congestion, inadequate water supply and inadequate facilities of disposal of human excreta, waste water and solid wastes. Inadequacy of housing for most urban poor invariably leads to poor home hygiene. Personal and domestic hygiene practices cannot be improved without improving basic amenities, such as water supply, waste water disposal, solid waste management and the problems of human settlements. But even under the prevailing conditions, there is significant scope of improving hygiene practices at home to prevent infection and cross-infection. Unfortunately, in developing countries, public health concerns are usually raised on the institutional setting, such as municipal services, hospitals, environmental sanitation, etc. There is a reluctance to acknowledge the home as a setting of equal importance along with the public institutions in the chain of disease transmission in the community. Managers of home hygiene and community hygiene must act in unison to optimise return from efforts to promote public health. Current practices and perceptions of domestic and personal hygiene in Indian communities, the existing levels of environmental and peri-domestic sanitation and the 'health risk' these pose will be outlined, as well as the need for an integrated action for improving hygiene behaviour and access to safe water and sanitation.

An outbreak of Serratia marcescens infection in a special-care baby unit of a community hospital in United Arab Emirates: the importance of the air conditioner duct as a nosocomial reservoir.

We report an outbreak of Serratia marcescens infection in a special-care baby unit (SCBU) of a university-affiliated community hospital in the United Arab Emirates. The outbreak involved 36 infants and lasted for 20 weeks. Seven of the colonized infants developed invasive illnesses in the form of bacteraemia (four cases), bacteraemic meningitis (two) and clinical sepsis (one). Three other term infants had purulent conjunctivitis. There were five deaths with an overall mortality of 14%. S. marcescens was cultured from airflow samples from the air conditioning (AC) which was the reservoir of infection in this outbreak. Elimination of the nosocomial source and outbreak containment were eventually achieved by specialized robotic cleaning of the entire AC duct system of the SCBU. Strict adherence to the infection control policies was reinforced to prevent transmission of cross-infection.

CT and MR patterns of hypoxic ischemic brain damage following perinatal asphyxia.

The objectives were to study the clinical and neurological abnormalities in children with cerebral palsy and to attempt to correlate the signs with radiological abnormalities detected by CT scan and/or MRI of the brain. In a prospective, hospital-based study, 65 children with cerebral palsy were examined neurologically and their perinatal history was reviewed. Their cranial CT scan, and/or magnetic resonance images were studied. The association between the gestational ages, perinatal history, neurological deficits, and the radiological appearances were studied. Of the 24 preterm-born and 41 term-born children, 23 had spastic diplegia; 57 per cent of these children has significant periventricular leucomalacia, which was more common among preterm-born children. Of the 13 children with hemiplegia, 12 had unilateral lesions on neuroimaging. Spastic tetraplegia was associated with extensive, bilateral, diffuse brain damage. Extrapyramidal cerebral palsy was far more common among term-born infants and 80 per cent of these showed significant abnormalities in the basal ganglia region. Ataxic cerebral palsy was an uncommon variety and there was no significant correlation between neurological signs and abnormalities on brain imaging. In conclusion, the radiological findings were closely related to the type of cerebral palsy and the neurological deficit except in the ataxic type. We believe that CT and MRI imaging are helpful in understanding the pathology and the timing of the lesion in cerebral palsy.

Cellular overexpression of heme oxygenase-1 up-regulates p21 and confers resistance to apoptosis.

BACKGROUND: Induction of heme oxygenase-1 (HO-1) protects against diverse insults in the kidney and other tissues. We examined the effect of overexpression of HO-1 on cell growth, expression of p21, and susceptibility to apoptosis. METHODS: LLC-PK1 cells were genetically engineered to exhibit stable overexpression of HO-1. The effects of such overexpression on cell growth, the cell cycle, and the cell cycle-inhibitory protein, p21, were assessed; additionally, the susceptibility of these HO-1 overexpressing cells to apoptosis induced by three different stimuli (TNF-alpha/cycloheximide, staurosporine, or serum deprivation) was evaluated by such methods as the quantitation of caspase-3 activity, phase contrast microscopy, and the TUNEL method. RESULTS: HO-1 overexpressing LLC-PK1 cells demonstrated cellular hypertrophy, decreased hyperplastic growth, and growth arrest in the G0/G1 phase of the cell cycle. HO-1 overexpressing cells were markedly resistant to apoptosis induced by TNFalpha/cycloheximide or staurosporine as assessed by the caspase-3 activity assay. Such overexpression also conferred resistance to apoptosis induced by serum deprivation as evaluated by the TUNEL method; in these studies, inhibition of HO attenuated the resistance to apoptosis. Expression of the cyclin dependent kinase inhibitor, p21CIP1, WAF1, SDI1, as judged by Northern and Western analyses, was significantly increased in HO-1 overexpressing cells, and decreased as HO activity was inhibited. Moreover, this reduction in expression of p21 attendant upon the inhibition of HO activity in HO-1 overexpressing cells paralleled the loss of resistance of these cells to apoptosis when HO activity is inhibited. The pharmacologic inducer of HO-1, hemin, increased expression of p21 in wild-type cells and decreased apoptosis provoked by TNF-alpha/cycloheximide. CONCLUSION: Cellular overexpression of HO-1 up-regulates p21, diminishes proliferative cell growth, and confers marked resistance to apoptosis. We speculate that such up-regulation of p21 contributes to the altered pattern of cell growth and resistance to apoptosis. Our studies uncover the capacity of HO-1 to markedly influence the cell cycle in renal epithelial cells. In light of the profound importance of the cell cycle as a determinant of cell fate, we speculate that the inductive effect of HO-1 on p21 and the attendant inhibitory effect on the cell cycle provide a hitherto unsuspected mechanism underlying the cytoprotective actions of HO-1.