Biodegradable antioxidant chitosan films useful as an anti-aging skin mask.

Cosmetics, personal care and biomedical products obtained by bio-based polymers and natural bioactive compounds are a new growing market. The ecological awareness is changing consumers' demands, causing consumers to look for more sustainable options, with a reduced environmental impact. The innovation of this work was to develop a natural polymer matrix (chitosan) entrapping antioxidant actives compounds such as annatto (Bixa Orellana L.) and vitamin C with potential application as sustainable anti-aging skin mask treatment. Films of chitosan (Ch) and reacetylated chitosan (RCh), exhibiting different degrees of acetylation (DA = 13.3 and 33.9%, respectively), were produced. The formulations of active films of chitosan (BCh) and reacetylated chitosan (BRCh) were 1% (w/w) of chitosan, 1% (w/w) of annatto powder, 5% (w/w) of vitamin C and 1% (w/w) of glycerol (as plasticizer). Reacetylated chitosan films (DA = 33.9%) presented higher water affinity than chitosan films (DA = 13.3%). The elongation of RCh and BRCh increased and the resistance decreased, as compared to Ch and BCh. The antioxidants compounds (annatto and vitamin C) of BRCh films released faster than BCh films. Thus, the BRCh films showed potential application as an anti-aging skin mask.

Photoexcitation dynamics of p-nitroaniline and N,N-dimethyl-p-nitroaniline in 1-alkyl-3-methylimidazolium-cation based ionic liquids with different alkyl-chain lengths.

Photoexcitation dynamics of p-nitroaniline (pNA) and N,N-dimethyl-p-nitroaniline (DMpNA) in 1-alkyl-3-methylimidazolium bis(trifluoromethanesulfonyl)imide ([Cnmim][NTf2]) with different alkyl chain lengths (from C2 to C12) was investigated using transient absorption spectroscopy. The internal conversion rate from the excited state to the ground state was estimated from bleach recovery around the ground state absorption centre, and the successive vibrational cooling rate in the ground state was estimated from the decay of the hot band observed at the red-edge of ground state absorption. The internal conversion rate slightly decreased with an increase in the alkyl-chain length of the cation, while the dependence of DMpNA was more significant than that of pNA. The extent of change was correlated with the change of the reaction free energy and solvent reorganization energy estimated from the absorption spectrum assuming that the internal conversion process is modelled by a back-electron-transfer process. The vibrational cooling rate estimated from the decay of hot-band absorption slightly decreased with an increase in the alkyl-chain length of the cation for both solutes. The hot-band decay of pNA was about 1.5-times faster than that of DMpNA, irrespective of the alkyl-chain length.

Tau protein levels in children do not increase during severe asthma attack-induced hypoxic conditions

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Myanmar mango landraces reveal genetic uniqueness over common cultivars from Florida, India, and Southeast Asia.

Mango (Mangifera indica) is believed to have evolved in a large area spanning northeastern India, Bangladesh, and northwestern Myanmar. We compared the genetic structure of mango accessions from Myanmar with that of mango accessions from Florida, India, and Southeast Asia with 11 SSR markers. The Myanmar accessions exhibited considerable genetic diversity (unbiased heterozygosity, UHe = 0.698) and a high number of private alleles. Despite the low degree of genetic differentiation among accessions (global Fst, tetha = 0.123), Myanmar's accessions were distinguishable from mango accessions from Florida, India, and Southeast Asia in a principal coordinates plot. Genetic differentiation of the Myanmar accessions from other groups was also observed in a Bayesian cluster analysis. No population structure among Myanmar accessions was revealed by a neighbor-joining tree. Our results revealed a broad genetic background and genetic distinctiveness of mango in Myanmar. We discuss the implications for diversification mechanisms based on the embryo type characteristics and provide recommendations for conservation efforts.

Early clinical signs and imaging findings in Gerstmann-Sträussler-Scheinker syndrome (Pro102Leu).

OBJECTIVE: To determine the clinical and radiologic features of Gerstmann-Sträussler-Scheinker syndrome caused by Pro102Leu mutation in PRNP (GSS102). METHODS: The authors report 11 patients (nine families) with clinically and radiologically diagnosed GSS102. RESULTS: All patients showed mild gait disturbance, dysesthesia and hyporeflexia of the lower legs, and truncal ataxia, and 9 of 11 patients showed proximal leg muscle weakness during the early stage of the disease. Dementia was not a main symptom during the early stage. Brain MRI and EEG abnormalities were not prominent initially. SPECT (N-isopropyl-p-[(123)I]iodoamphetamine) analyzed by the three-dimensional stereotactic surface projection (SSP) method detected abnormalities in five patients early during the course of the illness. SPECT findings showed diffusely decreased cerebral blood flow, demonstrated by a mosaic pattern, with the lowest perfusion noted in the occipital lobes. In contrast, blood flow to the cerebellum was preserved. These studies suggested sites of pathology in GSS102, with the main lesions probably located in the cerebrum and the spinal cord (posterior horn and spinocerebellar tract) instead of the cerebellum. CONCLUSIONS: Key features for early diagnosis of Gerstmann-Sträussler-Scheinker syndrome caused by Pro102Leu mutation in PRNP (GSS102) are truncal ataxia, dysesthesia and hyporeflexia of the lower legs, and mild dysarthria. Normal cerebellar MRI and abnormal cerebral SPECT findings are characters of early GSS102.

SET binding factor 2 (SBF2) mutation causes CMT4B with juvenile onset glaucoma.

The authors report a Japanese family segregating autosomal recessive Charcot-Marie-Tooth disease (CMT) with focally folded myelin, juvenile-onset glaucoma, and a nonsense mutation of SET binding factor 2 (SBF2). The consistent phenotypic features associated with SBF2 mutations are early-onset demyelinating neuropathy, myelin folding, and markedly decreased motor nerve conduction velocities; glaucoma associates with SBF2 nonsense mutations.

[Localized fibrous mesothelioma with bloody pleural effusion; report of a case].

Diffuse malignant mesothelioma with bloody pleural effusion is not rare, but a localized fibrous mesothelioma with bloody pleural effusion is relatively rare. A 45-year-old woman presented with a localized fibrous mesothelioma causing a bloody pleural effusion. Her chief complaint was right-sided lateral chest pain. A chest roentgenogram demonstrated a right-sided pleural effusion, so a chest tube was inserted, and the bloody fluid drained. A preoperative diagnosis of localized fibrous mesothelioma was made based on chest computed tomography and examination of computed tomographic guided percutaneous needle biopsy specimen. At operation, the tumor seemed to have originated from the right lung parenchyma or had invade the right lower lobe because tumor had penetrated deeply in the lung. Tumor and part of the parietal pleura were resected by right lower lobectomy. Final pathology established that the tumor was adherent to the right lung and was only encapsulated by the lung.

Effects of interleukin-1 gene polymorphisms on the development of coronary artery disease associated with Chlamydia pneumoniae infection.

OBJECTIVES: This study was done to elucidate the effects of interleukin (IL)-1 gene polymorphisms on coronary artery disease (CAD) associated with Chlamydia pneumoniae (CP) infection. BACKGROUND: It was suggested that CP was associated with CAD. However, genetic factors involved in CAD associated with CP infection are unknown. METHODS: We evaluated CP immunoglobulin G (IgG) seropositivity and IL-1 beta (a C/T transition at -511) and IL-1 receptor antagonist (IL-1Ra) (a variable-number repeat in intron 2) gene polymorphisms in 292 patients undergoing coronary angiography. RESULTS: Seropositivity for CP was present in 61% of patients with CAD versus 51% without CAD (p = NS). The percentage of patients having IL-1 beta (-511) C/C genotype and/or IL-1Ra (intron 2) 2- or 3-repeat allele was higher in patients with CAD than without CAD (29 vs. 16%, p < 0.025). To clarify the effects of these CAD-associated variants (IL-1 beta C/C and/or IL-1Ra 2- or 3-repeat), patients were divided into four groups. A stepwise increase in CAD prevalence was observed depending on CP seropositivity and the variants. Odds ratios (ORs) for CAD were 1.4 in the group with seropositivity alone, 1.7 with the variants alone and 3.8 with seropositivity and the variants. Such variants were associated with CAD in both patients with and without seropositivity. Interestingly, high prevalence of myocardial infarction (MI) was confined to the group with seropositivity and the variants (OR, 2.8). The variants were associated with MI only in patients with CP seropositivity. CONCLUSIONS: The IL-1 gene polymorphisms were found to play a role in the development of CAD, especially MI, in patients with CP infection.

[Effects of aging on oxidisability of low density lipoprotein].

Oxidised LDL is taken up by macrophages via scavenger receptors, leading to foam cell formation and is thus considered to contribute to atherogenesis. Aging results in the increase of lipids and the decrease of antioxidant enzyme activity in serum. In this study, we investigated the effects of aging on LDL oxidisability. We measured LDL oxidation lag time, plasma lipids, albumin and uric acid were examined in 306 Japanese (169 men, 137 women). The mean +/- SE of LDL oxidation-lag time in subjects was 58.9 +/- 1.0 min. The lag time (80.3 +/- 4.8 min) was longest in subjects in their 20 s and shortest in those in their 40 s (58.9 +/- 1.0 min). The longest lag time was in second-decade men (88.9 +/- 6.2 min) and shortest in fourth-decade women (50.7 +/- 2.2 min), and these results were similar even excluding subjects with abnormal biochemical data (total cholesterol, triglyceride, GOT, GPT, gamma GTP, creatinine and glucose). We analyzed the effects of various factors on lag time using multiple linear regression. Aging, uric acid and LDL-cholesterol significantly influenced lag time. Our results suggest that LDL oxidisability might been regulated by aging, changes in LDL-cholesterol with aging and variations in physical antioxidant function.

Regulation by long-chain fatty acids of the expression of cholesteryl ester transfer protein in HepG2 cells.

Cholesteryl ester transfer protein (CETP) is an important determinant of lipoprotein function, especially high density lipoprotein (HDL) metabolism, and contributes to the regulation of plasma HDL levels. Since saturated and polyunsaturated fatty acids (FA) appear to influence the CETP activity differently, we decided to investigate the effects of FA on the expression of CETP mRNA in HepG2 cells using an RNA blot hybridization analysis. Long-chain FA (>18 carbons) at a 0.5 mM concentration were added to the medium and incubated with cells for 48 h at 37 degrees C under 5% CO2. After treatment with 0.5 mM arachidonic (AA), eicosapentaenoic (EPA), and docosahexaenoic acid (DHA), the levels of CETP mRNA were less than 50% of the control levels (AA, P = 0.0005; EPA, P < 0.01; DHA, P < 0.0001), with a corresponding significant decrease in the CETP mass. These results suggest that FA regulate the gene expression of CETP in HepG2 and this effect is dependent upon the degree of unsaturation of the acyl carbon chain in FA.

Antioxidant ability of various flavonoids against DPPH radicals and LDL oxidation.

Flavonoids, a group of polyphenolic compounds, exist naturally and serve as antioxidants in vegetables, fruits, and so on. The inhibition of low density lipoprotein (LDL) oxidation may be an effective way to prevent or delay the progression of atherosclerosis. In the present study, we analyzed the radical scavenging capacity of 10 flavonoids (catechin, epicatechin [EC], epigallocatechin [EGC], epicatechin gallate [ECg], epigallocatechin gallate [EGCg], myricetin, quercetin, apigenin, kaempferol, and luteolin) toward 1,1-diphenyl-2-picryl-hydrazyl [DPPH]. After 20 min of incubation, EGCg was the most effective DPPH radical scavenger, luteolin being the least active of this flavonoid group. The mutual antioxidant effect of flavonoids with alpha-tocopherol (alpha-toc) on LDL oxidizability was investigated by using the lipophilic azo radical initiator 2,2'-azobis(4-methoxy-2,4-dimethylvaleronitrile) [AMVN-CH3O]. An inhibitory effect of flavonoids on LDL oxidation was observed in the order of luteolin>ECg>EC>quercetin>catechin>EGCg>EGC>myricetin>kaempferol> apigenin. The shortened lag time induced by higher doses of alpha-toc (6 mg/100 mL) was restored by flavonoids. These results suggest that 1) radical trapping effects of flavonoids differ according to their structure, and 2) flavonoids act as hydrogen donors to alpha-toc radical; furthermore, by interaction with alpha-toc, they have a greater potential to delay the oxidation of LDL.

Identification of a two-component signal transduction system involved in fimbriation of Porphyromonas gingivalis.

Porphyromonas gingivalis, a periodontopathogen, is an oral anaerobic gram-negative bacterium with numerous fimbriae on the cell surface. Fimbriae have been considered to be an important virulence factor in this organism. We analyzed the genomic DNA of transposon-induced, fimbria-deficient mutants derived from ATCC 33277 and found that seven independent mutants had transposon insertions within the same restriction fragment. Cloning and sequencing of the disrupted region from one of the mutants revealed two adjacent open reading frames (ORFs) which seemed to encode a two-component signal transduction system. We also found that six of the mutants had insertions in a gene, fimS, a homologue of the genes encoding sensor kinase, and that the insertion in the remaining one disrupted the gene immediately downstream, fimR, a homologue of the response regulator genes in other bacteria. These findings suggest that this two-component regulatory system is involved in fimbriation of P. gingivalis.

Acute myocardial infarction in a patient with anomalous left coronary artery origin and primary antiphospholipid syndrome.

Anomalous left main coronary artery (LMCA) originating from the right coronary sinus and running between the aorta and pulmonary trunk is a rare congenital condition. Although this disease is known to be associated with myocardial infarction and sudden death, the precise mechanism is uncertain. A 14-year-old male with this anomaly developed myocardial infarction during exercise complicated by primary antiphospholipid syndrome. He was admitted to hospital with persistent chest pain and sudden cardiac collapse that occurred while he was running. Cardiac catheterization demonstrated a narrowed segment in the LMCA and impaired blood flow, prompting a diagnosis of extensive anterior myocardial infarction. Emergency bypass surgery was performed using a single saphenous vein graft to the left anterior descending artery. Postoperative angiography showed the presence of an anomalous LMCA arising from the right sinus of Valsalva and running between the great vessels. The aortic samples were pathologically normal. He was discovered to also have primary antiphospholipid syndrome and was discharged without symptoms after warfarin therapy. Complicated primary antiphospholipid syndrome may trigger myocardial infarction in asymptomatic patients with this type of coronary anomaly.

Antioxidant effects of polyphenols in chocolate on low-density lipoprotein both in vitro and ex vivo.

Cacao is rich in polyphenols such as (-)-epicatechin, and a colored component of cacao (cacao-red) is polyphenol, which is an antioxidant. These properties stimulated an investigation of the effects of cacao liquor polyphenols (CLP) on low-density lipoprotein (LDL) oxidation. The 2.2 '-azobis(4-methoxy-2,4-dimethylvaleronitrile) (AMVN-CH2O)-induced oxidizability of LDL was assessed by monitoring the absorbance at 234 nm. In vitro. 0.1-0.5 mg/dL CLP prolonged the oxidation lag time of LDL in a dose-dependent manner. Compared with the controls, it was prolonged 1.7-fold in the presence of 0.1 mg/dL CLP, 2.9-fold at 0.2 mg/dL, 3.8-fold at 0.3 mg/dL, 5.4-fold at 0.4 mg/dL, and 6.4-fold at 0.5 mg/dL. Furthermore, we enlisted 13 male volunteers to consume 35 g delipidated cocoa. Venous blood samples were taken before and at 2 h and 4 h after consuming the cocoa. The oxidation lag time of LDL before cocoa ingestion was 59.0 +/- 6.3 min, but it was prolonged at 2 h after cocoa (68.3 +/- 6.0 min); before returning to the initial lag time (61.7 +/- 5.7 min) before consumption. Thus we have shown that cocoa inhibited LDL oxidation both in vitro and ex vivo.

Effects of cacao liquor polyphenols on the susceptibility of low-density lipoprotein to oxidation in hypercholesterolemic rabbits.

The effects of cacao liquor polyphenols (CLP) on the susceptibility of low-density lipoprotein (LDL) to oxidation in hypercholesterolemic rabbits were examined. Six Japanese white rabbits which had been fed a high cholesterol diet (HCD) for 3 weeks were fed HCD containing 1% CLP for the following 10 days. The susceptibility of LDL to oxidation induced by 2-2'-azobis(4-methoxy-2, 4-dimethylvaleronitrile) (V-70) was evaluated by measuring the production of conjugated dienes and thiobarbituric acid reactive substances (TBARS). The lag time was significantly prolonged from 37.7 min before intake of CLP to 42.9, 44.2 and 45.8 min after 4, 7 and 10 days of CLP intake. TBARS production after intake of CLP was also markedly reduced compared with the level before intake. There was no difference in plasma lipid concentrations comparing the levels before and after CLP intake. In conclusion, in hypercholesterolemic rabbits, orally administered CLP was absorbed and distributed to the blood, and the resistance of LDL to oxidation was thereby increased.

Inhibition of low-density lipoprotein oxidation by astaxanthin.

Marine animals produce astaxanthin which is a carotenoid and antioxidant. In this study we determined the in vitro and ex vivo effects of astaxanthin on LDL oxidation. The oxidation of LDL was measured in a 1 ml reaction system consisting of increasing concentrations of astaxanthin (12.5, 25.0, 50.0 microg/ml), 400 microM V-70 (2, 2'-azobis(4-methoxy-2, 4-dimethylvaleronitrile)), and LDL (70 microg/ml protein). Astaxanthin dose, dependently significantly prolonged the oxidation lag time (31.5, 45.4, 65.0 min) compared with the control (19.9 min). For the ex vivo study 24 volunteers (mean age 28.2 [SD 7.8] years) consumed astaxanthin at doses of 1.8, 3.6,14.4 and 21.6 mg per day for 14 days. No other changes were made in the diet. Fasting venous blood samples were taken at days 0, +14. LDL lag time was longer (5.0, 26.2, 42.3 and 30.7% respectively) compared with day 0 after consuming astaxanthin at doses of 1.8, 3.6,14.4 and 21.6 mg for 14 days compared with day 0, but there was no difference in oxidation of LDL between day 0 (lag time 59.9+/-7.2 min) and day 14 (57.2+/-6.0 min) in the control group. Our results provide evidence that consumption of marine animals producing astaxanthin inhibits LDL oxidation and possibly therefore contributes to the prevention of atherosclerosis.

The gene mutated in adult-onset type II citrullinaemia encodes a putative mitochondrial carrier protein.

Citrullinaemia (CTLN) is an autosomal recessive disease caused by deficiency of argininosuccinate synthetase (ASS). Adult-onset type II citrullinaemia (CTLN2) is characterized by a liver-specific ASS deficiency with no abnormalities in hepatic ASS mRNA or the gene ASS (refs 1-17). CTLN2 patients (1/100,000 in Japan) suffer from a disturbance of consciousness and coma, and most die with cerebral edema within a few years of onset. CTLN2 differs from classical citrullinaemia (CTLN1, OMIM 215700) in that CTLN1 is neonatal or infantile in onset, with ASS enzyme defects (in all tissues) arising due to mutations in ASS on chromosome 9q34 (refs 18-21). We collected 118 CTLN2 families, and localized the CTLN2 locus to chromosome 7q21.3 by homozygosity mapping analysis of individuals from 18 consanguineous unions. Using positional cloning we identified a novel gene, SLC25A13, and found five different DNA sequence alterations that account for mutations in all consanguineous patients examined. SLC25A13 encodes a 3.4-kb transcript expressed most abundantly in liver. The protein encoded by SLC25A13, named citrin, is bipartite in structure, containing a mitochondrial carrier motif and four EF-hand domains, suggesting it is a calcium-dependent mitochondrial solute transporter with a role in urea cycle function.