Indoor air quality in hairdressing salons in Taipei.

To improve indoor air quality and to protect public health, Taiwan has enacted the "Indoor Air Quality Act (IAQ Act)" in 2012. For the general public, the indoor air quality in hair salons is important because it is a popular location that people will often visit for hair treatments. However, only a few exposure assessments regarding air pollutants have previously been performed in hair salons. To assess the air quality of hairdressing environments in Taipei, ten hairdressing salons were included for a walk-through survey in this study. In addition, the airborne concentrations of formaldehyde, volatile organic compounds (VOCs), CO2 , and phthalate esters were also determined in 5 salons. Charcoal, XAD-2, and OVS-Tenax tubes were used for the air sampling, while the samples were analyzed with gas chromatography/mass spectrometer. It was found that the products used in hair salons contained various chemicals. In fact, from the walk-through survey, a total of 387 different ingredients were found on 129 hair product labels. The hair salons were not well ventilated, with CO2 levels of 600 to 3576 ppm. The formaldehyde concentrations determined in this study ranged from 12.40 to 1.04 × 103  µg m-3 , and the maximum level was above the permissible exposure limit (PEL) of US Occupational Safety and Health Administration (US OSHA). Additionally, 83% of the samples were with levels higher than the standard regulated by Taiwan's IAQ Act. The concentrations of VOCs and phthalate esters were below the occupational exposure limits (OELs), but higher than what was found in general residential environments. The hair products were considered as the major source of air pollutants because significantly higher concentrations were found around the working areas. The number of perming treatments, the number of workers, and the frequency of using formaldehyde releasing products, were found to be associated with the levels of formaldehyde. This study indicates that efforts are needed to improve the indoor air quality in hairdressing salons in Taipei.

Inhibition of angiogenesis in vitro and in vivo: comparison of the relative activities of triflavin, an Arg-Gly-Asp-containing peptide and anti-alpha(v)beta3 integrin monoclonal antibody.

Disintegrin which contains the amino acid sequence Arg-Gly-Asp (RGD), has been implicated as a recognition site in interactions between extracellular matrix (ECM) and cell membrane receptors. Triflavin, a 7.5 kDa cysteine-rich polypeptide purified from Trimeresurus flavoviridis snake venom, belongs to a family of disintegrins. Integrin alpha(v)beta3 has recently been identified as a marker of angiogenic blood vessels and therefore anti-alpha(v)beta3 mAb may significantly inhibit angiogenesis. Therefore, this study was designed to compare the relative activity of triflavin and anti-alpha(v)beta3 mAb in human umbilical vein endothelial cell (HUVEC) adhesion and migration in vitro, and on angiogenesis induced by TNF(alpha) in chicken chorioallantoic membrane (CAM). In this study, it was shown that triflavin (0.1 to 0.4 microM) dose-dependently inhibited the adhesion of HUVECs to ECMs (i.e., vitronectin, fibronectin, laminin and collagen type IV). At a concentration of 10 microM, anti-alpha(v)beta3 mAb almost completely inhibited the adhesion of cells to vitronectin, had a moderate inhibitory effect on fibronectin and laminin, but only a slight inhibitory effect on collagen type IV. On the other hand, vitronectin and fibronectin promote a significantly greater extent of cell adhesion and migration than laminin or collagen type IV over a wide range of concentrations (5 to 15 microg/ml). In cell migration studies, triflavin (0.4 microM) inhibited more markedly vitronectin- and fibronectin-mediated migration than that mediated by laminin- and collagen type IV. Comparison of the relative effectiveness of triflavin with anti-alpha(v)beta3 mAb, showed that triflavin was at least twenty to thirty times more potent than anti-alpha(v)beta3 mAb at inhibiting cell adhesion and migration. Furthermore, we used TNF(alpha) as an inducer of angiogenesis in the CAM assay. Close examination of the effects of triflavin and anti-alpha(v)beta3 mAb on TNF(alpha)-induced angiogenesis revealed the presence of discontinuous and disrupted blood vessels. However, anti-alpha(v)beta3 mAb showed a significant effect only at a higher concentration (10 microM). These results suggest that the inhibition of angiogenesis may have been due to interference with the adhesion and migration of endothelial cells to ECMs. The results also indicate that triflavin has a more powerful inhibitory effect than anti-alpha(v)beta3 mAb on angiogenesis, suggesting that triflavin could theoretically be used as a reasonable therapeutic adjuvant for therapy or prevention of angiogenesis-induced diseases.

Acidic pH promotes the formation of toxic fibrils from beta-amyloid peptide.

Beta-amyloid (Abeta) peptides, the major component of senile plaques in brains of patients with Alzheimer's disease (AD), were found in the low pH organelles (i.e. endosome/lysosome) of cultured neuronal cells. Since acidic pH values have been shown to promote the self-assembly of Abetas, which seems to be a prerequisite for their neuropathogenicity, elucidating the aggregation behavior of Abetas in acidic environments and their subsequent effects on neuronal cells may be crucial for understanding the neurodegenerative process of AD. In this study, the extent and rate of aggregation of Abeta(1-42) peptides at pH values of 5.8 and 7.4, as well as the structure and neurotoxic effects of these aggregates, were examined. We showed that Abeta(1-42) peptides formed large and complex fibrils much more efficiently at acidic rather than neutral pH. Furthermore, only the pH 5.8 Abeta aggregates induced significant apoptotic death of PC12 cells, as indicated by a decrease in 3-(4,5-dimethylthiazol-2-yl)2,5-diphenyltetrazolium bromide (MTT) reduction and an increase in phosphatidylserine externalization. Taken together, our results suggest that the Abetas present in the acidic organelles may form neurotoxic fibrils more easily than those in the neutral cellular compartments.

Studies on the cytotoxic mechanisms of ginkgetin in a human ovarian adenocarcinoma cell line.

The cytotoxic effects of ginkgetin, a natural biflavone isolated from Selaginella moellendorffii Hieron, were evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay in three different human cell lines: ovarian adenocarcinoma (OVCAR-3), cervical carcinoma (HeLa) and foreskin fibroblast (FS-5). The concentrations of ginkgetin required to induce 50% death (EC50) in OVCAR-3, HeLa, and FS-5 were 3.0, 5.2, and 8.3 microg/ml, respectively. Morphological changes in cells and their nuclei, DNA fragmentation with a characteristic pattern of inter-nucleosomal ladder, and double-stranded DNA breaks were detected following treatment with 3 microg/ml of this biflavone for 24 h. Incubation with 5 microg/ml ginkgetin led to increased intracellular levels of hydrogen peroxide as early as 30 min. The cytotoxicity of ginkgetin was partially inhibited by pretreating cells with vitamin C, vitamin E or catalase. Catalase not only afforded the best protective effect among three antioxidants, but also reduced both the DNA fragmentation and double-stranded DNA breakage induced by ginkgetin. Moreover, the involvement of caspase(s) in ginkgetin-induced apoptosis was demonstrated by the activation of caspase 3 after drug treatment and the suppression of cell death by a broad-spectrum caspase inhibitor, benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone (z-VAD-fmk). However, the protective effects of z-VAD-fmk and catalase were not additive. Taken together, our results indicated that the apoptosis induced by ginkgetin (especially at 5 microg/ml) is mediated mainly through the activation of caspase(s) by the hydrogen peroxide generated possibly through autooxidation of this biflavone.

Isolation of flindersiamine, isoflindersiamine, and a new alkaloid, heliparvifoline, from Helietta parvifolia (Rutaceae).

A phytochemical investigation of the leaves and twigs of Helietta parvifolia (Rutaceae) resulted in the isolation of heliparvifoline, a new furoquinoline alkaloid, in addition to the known bases flindersiamine and isoflindersiamine.

Histiocytosis X with thyroid involvement: report of a case.

Histiocytosis X is a disease of histiocyte proliferation in response to some unknown etiology. Thyroid involvement is extremely rare in the literature. In this paper, we present an 18-year-old female with histiocytosis X with thyroid involvement. This patient had had a goiter with normal thyroid function since 12 years of age. A thyroidectomy was done under the suspicion of thyroid cancer. Pathology revealed histiocytosis X. Hypoparathyroidism and hypothyroidism were noted after the operation and were treated with thyroid hormone, vitamin D and calcium carbonate. This patient also had lesions on the left side of mandible, in the suprasellar region and possibly in the right mastoid. A curettage biopsy of her mandibular lesion was also compatible with histiocytosis X. She was proven to have hypothalamic and pituitary dysfunction including hypogonadism and hypoadrenalism. Her thyroid lesion did not recur after the thyroidectomy. The toothache that she had also experienced subsided after the curettage biopsy of the mandibular lesion. Hypothalamic and pituitary dysfunction were controlled by hormone replacement. Because her disease had been running a benign clinical course, no chemotherapy was given.

Indirect hemagglutination antibodies against Burkholderia pseudomallei in normal blood donors and suspected cases of melioidosis in Malaysia.

Interpretation of the indirect hemagglutination test (IHA) for melioidosis in endemic areas is difficult because of the presence of antibodies in apparently healthy individuals. Fifty-three out of 200 healthy blood donors in Malaysia showed positive antibody titers (> or = 1 : 40) against Burkholderia pseudomallei. Seven percent had an IHA titer of 1 : 40, 11% had an IHA titer of 1 : 80 while 8.5% had a titer > or = 1 : 160. Out of 258 sera sent for melioidosis serology, 7% of the patients had an IHA titer of 1 : 40, 9% had an IHA titer of 1 : 80 while 20% had an IHA titer of > or = 1 : 160. If a titer of > or = 1 : 80 is taken as cut off point for positivity, 29% of the patients had positive melioidosis serology. Increasing the positivity threshold may jeopardize the sensitivity of the test. A more specific and sensitive test is needed.

Detection of Helicobacter pylori from endoscopic biopsies and the biochemical characteristics of these isolates.

Helicobacter pylori (formerly Campylobacter pylori) has been recently described as a gastritis-associated bacterium. We examined endoscopic biopsies of 100 patients with dyspepsia and found H. pylori in the gastric antrum of 34 (34%) by either culture, urease tests and/or histology. Thirty-one out of 41 patients (75.6%) confirmed to have chronic active gastritis histologically had H. pylori in their gastric antrum compared to 3 out of 59 patients (5.1%) with dyspepsia but normal histology (p less than 0.01). Histological examination, using gram stain and the Warthin-Starry Silver stain, detected 29 of the 34 positive cases (85.3%); urease test, 26 cases (76.5%) and culture, 22 cases (64.7%). A combination of histological examination and urease test increased the detection rate to 97.1%. Therefore we felt that for the detection of H. pylori in endoscopic biopsies, culture, which is time consuming and expensive, is not necessary in routine diagnosis as it did not improve the diagnostic rate over a combination of histology and urease test. A comparative study on three media (blood agar, chocolate agar and Skirrow's agar) used in the isolation of the organism showed that non-selective blood agar and chocolate agar were superior to Skirrow's agar. The strains isolated appeared to be homogeneous in their morphological and biochemical characteristics.

2-hydroxy-1-oxo-1,2-dihydroisoquinoline-3-carboxylic acid with inbuilt ß-N-hydroxy-γ-keto-acid pharmacophore as HCV NS5B polymerase inhibitors.

The inbuilt 2-N-hydroxy-1-oxo-3-carboxylic acid of isoquinolone was designed as pyrophosphate mimic for hepatitis C NS5B polymerase. Various 2-hydroxy-1-oxo-1,2-dihydroisoquinoline-3-carboxylic acid derivatives 11a-p were synthesized and evaluated as HCV NS5B polymerase inhibitors. Compound 11c exhibited moderate inhibitory potency based on the inorganic pyrophosphate generation (IC50 = 9.5 µM) and based on NTP incorporation by NS5B enzyme (IC50 = 5.9 µM). Compound 11c demonstrated antiviral activity (EC50 = 15.7 µM) and good selectivity in HCV genotype 1b replicon Ava.5 cells. Compound 11c reduced the interaction of NTP to NS5B polymerase. Docking model showed that 11c situated in similar orientation to the bound uridine triphosphate in the active site of NS5B polymerase. As a result, 2-hydroxy-1-oxo-1,2-dihydroisoquinoline-3-carboxylic acid was disclosed as a novel inbuilt ß-N-Hydroxy-γ-keto-acid pharmacophore for HCV NS5B polymerase inhibitors.

Alkaloids and coumarins of Thamnosma montana.

From the turpentine broom, Thamnosma montana, four alkaloids and three coumarins were isolated and characterized. Skimmianine (5), N-methyl-acridone (4) and 5-(3'-methyl-2',3'-dihydroxybutanyl)-8-methoxypsoralen (1) were obtained previously from T. montana. Robustine (2) is reported from a Thamnosma species for the first time and acridone (6), thamnosmonin (9), and thamontanin (14) are reported from a natural source for the first time. Evidence for the structures of the new isolates is presented.

Mechanism involved in the antiplatelet activity of naloxone in human platelets.

In this study, naloxone was tested for its antiplatelet activity in human platelet suspensions. In platelet suspensions (4.5 x 10(8)/ml), naloxone (0.1-0.5 mM) significantly inhibited platelet aggregation and ATP-release stimulated by various agonists (i.e., thrombin, collagen, U46619, and ADP). Furthermore, naloxone (0.5 and 0.8 mM) dose-dependently inhibited the intracellular free Ca2+ rise of Fura 2-AM loaded platelets stimulated by collagen. Additionally, naloxone (0.5 and 1.0 mM) did not influence the binding of FITC-triflavin to platelet glycoprotein (GP) IIb/IIIa complex. On the other hand, naloxone (0.5 mM) markedly decreased the fluorescence of platelet membranes tagged with diphenylhexatriene (DPH). In addition, naloxone (0.1-0.5 mM) did not significantly affect cyclic-AMP levels in human washed platelets. It is concluded that the antiplatelet activity of naloxone may possibly be due to the induction of conformational changes in the platelet membrane and the inhibition of the intracellular Ca2+ ([Ca2+]i) mobilization as well as the release reaction of platelets stimulated by agonists.