Assessment of Hygiene Management Practices and Comparative Analysis of Regulatory Frameworks for Shared Kitchens across Different Countries.

Shared kitchens, where users share kitchen space, are becoming popular worldwide due to the economic cost savings of startup businesses. This study conducted monitoring of microbial and chemical hazards from prepared foods and the environment of shared kitchen facilities, surveyed shared kitchen operators, and compared shared kitchen regulations between Korea and other countries. The monitoring results indicate that the hygiene status of the facilities and the microbial and chemical hazards in the prepared foods were all within the standard specifications, showing significantly lower levels compared to regular restaurants (p < 0.05). In particular, concurrent-use and time-division types of open shared kitchens showed significantly lower levels of both hazards than separated-individual kitchens. Survey results of hygiene inspection also confirmed better hygiene management in concurrent-use and time-division types of open shared kitchens in Korea. However, more frequent cleaning and disinfection, hygiene inspections, and training are high economic burdens in the operation of shared kitchens compared to regular restaurants. Moreover, mandatory insurance subscriptions, the operator's responsibility in hygiene-related incidents, and high operational costs collectively challenge shared kitchens' competitiveness in the food service market. Critical reassessments of regulations utilizing the benefits of shared kitchens are needed to promote a safe dining culture and the growth of shared kitchen startup businesses.

Metagenomic Mining and Functional Characterization of a Novel KG51 Bifunctional Cellulase/Hemicellulase from Black Goat Rumen.

A novel KG51 gene was isolated from a metagenomic library of Korean black goat rumen and its recombinant protein was characterized as a bifunctional enzyme (cellulase/hemicellulase). In silico sequence and domain analyses revealed that the KG51 gene encodes a novel carbohydrate-active enzyme that possesses a salad-bowl-like shaped glycosyl hydrolase family 5 (GH5) catalytic domain but, at best, 41% sequence identity with other homologous GH5 proteins. Enzymatic profiles (optimum pH values and temperatures, as well as pH and thermal stabilities) of the recombinant KG51 bifunctional enzyme were also determined. On the basis of the substrate specificity data, the KG51 enzyme exhibited relatively strong cellulase (endo-ß-1,4-glucanase [EC 3.2.1.4]) and hemicellulase (mannan endo-ß-1,4-mannosidase [EC 3.2.1.78] and endo-ß-1,4-xylanase [EC 3.2.1.8]) activities, but no exo-ß-1,4-glucanase (EC 3.2.1.74), exo-ß-1,4-glucan cellobiohydrolase (EC 3.2.1.91), and exo-1,4-ß-xylosidase (EC 3.2.1.37) activities. Finally, the potential industrial applicability of the KG51 enzyme was tested in the preparation of prebiotic konjac glucomannan hydrolysates.

Laser parameters for efficient biomedical stimulation: A study to increase cognitive response rate.

BACKGROUND: The laser is able to irradiate the exact amount of stimulation to an area by a non contact method, and has the advantage of being able to stimulate the local target area. OBJECTIVE: This study examined an efficient method of laser tactile stimulation using laser parameter combinations. METHODS: The laser parameters that could cause an increase in the cognitive response rate of human subjects were examined without increasing the amount of total laser energy. RESULTS: As a result, the appropriate matching parameters such as duty ratio, pulse frequency, and exposure time of laser pulses showed a dominant influence in effectively increasing the tactile response rate of subjects with limited amount of total laser energy. CONCLUSIONS: This study can be applied to neurophysiology, cognitive research, and clinical laser application.

Isolation and characterization of a novel endo-beta-1, 4-glucanase from a metagenomic library of the black-goat rumen

ABSTRACT The various types of lignocellulosic biomass found in plants comprise the most abundant renewable bioresources on Earth. In this study, the ruminal microbial ecosystem of black goats was explored because of their strong ability to digest lignocellulosic forage. A metagenomic fosmid library containing 115,200 clones was prepared from the black-goat rumen and screened for a novel cellulolytic enzyme. The KG35 gene, containing a novel glycosyl hydrolase family 5 cellulase domain, was isolated and functionally characterized. The novel glycosyl hydrolase family 5 cellulase gene is composed of a 963-bp open reading frame encoding a protein of 320 amino acid residues (35.1 kDa). The deduced amino acid sequence showed the highest sequence identity (58%) for sequences from the glycosyl hydrolase family 5 cellulases. The novel glycosyl hydrolase family 5 cellulase gene was overexpressed in Escherichia coli. Substrate specificity analysis revealed that this recombinant glycosyl hydrolase family 5 cellulase functions as an endo-β-1,4-glucanase. The recombinant KG35 endo-β-1,4-glucanase showed optimal activity within the range of 30-50 °C at a pH of 6-7. The thermostability was retained and the pH was stable in the range of 30-50 °C at a pH of 5-7.

Isolation and characterization of a novel endo-ß-1,4-glucanase from a metagenomic library of the black-goat rumen.

The various types of lignocellulosic biomass found in plants comprise the most abundant renewable bioresources on Earth. In this study, the ruminal microbial ecosystem of black goats was explored because of their strong ability to digest lignocellulosic forage. A metagenomic fosmid library containing 115,200 clones was prepared from the black-goat rumen and screened for a novel cellulolytic enzyme. The KG35 gene, containing a novel glycosyl hydrolase family 5 cellulase domain, was isolated and functionally characterized. The novel glycosyl hydrolase family 5 cellulase gene is composed of a 963-bp open reading frame encoding a protein of 320 amino acid residues (35.1kDa). The deduced amino acid sequence showed the highest sequence identity (58%) for sequences from the glycosyl hydrolase family 5 cellulases. The novel glycosyl hydrolase family 5 cellulase gene was overexpressed in Escherichia coli. Substrate specificity analysis revealed that this recombinant glycosyl hydrolase family 5 cellulase functions as an endo-ß-1,4-glucanase. The recombinant KG35 endo-ß-1,4-glucanase showed optimal activity within the range of 30-50°C at a pH of 6-7. The thermostability was retained and the pH was stable in the range of 30-50°C at a pH of 5-7.

Protective Role of Mitochondrial Peroxiredoxin III against UVB-Induced Apoptosis of Epidermal Keratinocytes.

UVB light induces generation of reactive oxygen species, ultimately leading to skin cell damage. Mitochondria are a major source of reactive oxygen species in UVB-irradiated skin cells, with increased levels of mitochondrial reactive oxygen species having been implicated in keratinocyte apoptosis. Peroxiredoxin III (PrxIII) is the most abundant and potent H2O2-removing enzyme in the mitochondria of most cell types. Here, the protective role of PrxIII against UVB-induced apoptosis of epidermal keratinocytes was investigated. Mitochondrial H2O2 levels were differentiated from other types of ROS using mitochondria-specific fluorescent H2O2 indicators. Upon UVB irradiation, PrxIII-knockdown HaCaT human keratinocytes and PrxIII-deficient (PrxIII-/-) mouse primary keratinocytes exhibited enhanced accumulation of mitochondrial H2O2 compared with PrxIII-expressing controls. Keratinocytes lacking PrxIII were subsequently sensitized to apoptosis through mitochondrial membrane potential loss, cardiolipin oxidation, cytochrome c release, and caspase activation. Increased UVB-induced epidermal tissue damage in PrxIII-/- mice was attributable to increased caspase-dependent keratinocyte apoptosis. Our findings show that mitochondrial H2O2 is a key mediator in UVB-induced apoptosis of keratinocytes and that PrxIII plays a critical role in protecting epidermal keratinocytes against UVB-induced apoptosis through eliminating mitochondrial H2O2. These findings support the concept that reinforcing mitochondrial PrxIII defenses may help prevent UVB-induced skin damage such as inflammation, sunburn, and photoaging.

A study on detection of glucose concentration using changes in color coordinates.

Glucose concentration is closely related to the metabolic activity of cells and it is the most important substance as the energy source of a living body which plays an important role in the human body. This paper proposes an optical method that can measure the concentration of glucose. The change in glucose concentration was observed by using CIE diagram, and wavelength and purity values were detected. Also, even small changes in glucose concentration can be evaluated through mathematical modeling. This system is simple, economical, and capable of quantifying optical signals with numerical values for glucose sensing. This method can be applicable to the clinical field that examines diabetes mellitus or metabolic syndrome.

Isolation and characterization of a novel glycosyl hydrolase family 74 (GH74) cellulase from the black goat rumen metagenomic library.

This study aimed to isolate and characterize a novel cellulolytic enzyme from black goat rumen by using a culture-independent approach. A metagenomic fosmid library was constructed from black goat rumen contents and screened for a novel cellulase. The KG37 gene encoding a protein of 858 amino acid residues (92.7 kDa) was isolated. The deduced protein contained a glycosyl hydrolase family 74 (GH74) domain and showed 77% sequence identity to two endo-1,4-ß-glucanases from Fibrobacter succinogenes. The novel GH74 cellulase gene was overexpressed in Escherichia coli, and its protein product was functionally characterized. The recombinant GH74 cellulase showed a broad substrate spectrum. The enzyme exhibited its optimum activity at pH 5.0 and temperature range of 20-50 °C. The enzyme was thermally stable at pH 5.0 and at a temperature of 20-40 °C. The novel GH74 cellulase can be practically exploited to convert lignocellulosic biomass to value-added products in various industrial applications in future.

Meta-analysis of factors predicting resistance to intravenous immunoglobulin treatment in patients with Kawasaki disease.

PURPOSE: Studies have been conducted to identify predictive factors of resistance to intravenous immunoglobulin (IVIG) for Kawasaki disease (KD). However, the results are conflicting. This study aimed to identify laboratory factors predictive of resistance to high-dose IVIG for KD by performing meta-analysis of available studies using statistical techniques. METHODS: All relevant scientific publications from 2006 to 2014 were identified through PubMed searches. For studies in English on KD and IVIG resistance, predictive factors were included. A meta-analysis was performed that calculated the effect size of various laboratory parameters as predictive factors for IVIG-resistant KD. RESULTS: Twelve studies comprising 2,745 patients were included. Meta-analysis demonstrated significant effect sizes for several laboratory parameters: polymorphonuclear leukocytes (PMNs) 0.698 (95% confidence interval [CI], 0.469-0.926), C-reactive protein (CRP) 0.375 (95% CI, 0.086-0.663), pro-brain natriuretic peptide (pro-BNP) 0.561 (95% CI, 0.261-0.861), total bilirubin 0.859 (95% CI, 0.582-1.136), alanine aminotransferase (AST) 0.503 (95% CI, 0.313-0.693), aspartate aminotransferase (ALT) 0.436 (95% CI, 0.275-0.597), albumin 0.427 (95% CI, -0.657 to -0.198), and sodium 0.604 (95% CI, -0.839 to -0.370). Particularly, total bilirubin, PMN, sodium, pro-BNP, and AST, in descending numerical order, demonstrated more than a medium effect size. CONCLUSION: Based on the results of this study, laboratory predictive factors for IVIG-resistant KD included higher total bilirubin, PMN, pro-BNP, AST, ALT, and CRP, and lower sodium and albumin. The presence of several of these predictive factors should alert clinicians to the increased likelihood that the patient may not respond adequately to initial IVIG therapy.

Sulfiredoxin inhibitor induces preferential death of cancer cells through reactive oxygen species-mediated mitochondrial damage.

Recent studies have shown that many types of cancer cells have increased levels of reactive oxygen species (ROS) and enhance antioxidant capacity as an adaptation to intrinsic oxidative stress, suggesting that cancer cells are more vulnerable to oxidative insults and are more dependent on antioxidant systems compared with normal cells. Thus, disruption of redox homeostasis caused by a decline in antioxidant capacity may provide a method for the selective death of cancer cells. Here we show that ROS-mediated selective death of tumor cells can be caused by inhibiting sulfiredoxin (Srx), which reduces hyperoxidized peroxiredoxins, leading to their reactivation. Srx inhibitor increased the accumulation of sulfinic peroxiredoxins and ROS, which led to oxidative mitochondrial damage and caspase activation, resulting in the death of A549 human lung adenocarcinoma cells. Srx depletion also inhibited the growth of A549 cells like Srx inhibition, and the cytotoxic effects of Srx inhibitor were considerably reversed by Srx overexpression or antioxidants such as N-acetyl cysteine and butylated hydroxyanisol. Moreover, Srx inhibitor rendered tumorigenic ovarian cells more susceptible to ROS-mediated death compared with nontumorigenic cells and significantly suppressed the growth of A549 xenografts without acute toxicity. Our results suggest that Srx might serve as a novel therapeutic target for cancer treatment based on ROS-mediated cell death.

Effective Killing of Cancer Cells Through ROS-Mediated Mechanisms by AMRI-59 Targeting Peroxiredoxin I.

AIMS: The intrinsic increase of reactive oxygen species (ROS) production in cancer cells after malignant transformation frequently induces redox adaptation, leading to enhanced antioxidant capacity. Peroxiredoxin I (PrxI), an enzyme responsible for eliminating hydrogen peroxide, has been found to be elevated in many types of cancer cells. Since overexpression of PrxI promoted cancer cells' survival and resistance to chemotherapy and radiotherapy, PrxI has been proposed as a therapeutic target for anticancer drugs. In this study, we aimed to investigate the anticancer efficacy of a small molecule inhibitor of PrxI. RESULTS: By a high-throughput screening approach, we identified AMRI-59 as a potent inhibitor of PrxI. AMRI-59 increased cellular ROS, leading to the activation of both mitochondria- and apoptosis signal-regulated kinase-1-mediated signaling pathways, resulting in apoptosis of A549 human lung adenocarcinoma. AMRI-59 caused no significant changes in ROS level, proliferation, and apoptosis of PrxI-knockdown A549 cells by RNA interference. PrxI overexpression or N-acetylcysteine pretreatment abrogated AMRI-59-induced cytotoxicity in A549 cells. AMRI-59 rendered tumorigenic ovarian cells more susceptible to ROS-mediated death compared with nontumorigenic cells. Moreover, significant antitumor activity of AMRI-59 was observed in mouse tumor xenograft model implanted with A549 cells with no apparent acute toxicity. INNOVATION: This study offers preclinical proof-of-concept for AMRI-59, a lead small molecule inhibitor of PrxI, as an anticancer agent. CONCLUSIONS: Our results highlight a promising strategy for cancer therapy that preferentially eradicates cancer cells by targeting the PrxI-mediated redox-dependent survival pathways.

Resveratrol inhibits collagen-induced platelet stimulation through suppressing NADPH oxidase and oxidative inactivation of SH2 domain-containing protein tyrosine phosphatase-2.

Reactive oxygen species (ROS) produced upon collagen stimulation are implicated in propagating various platelet-activating pathways. Among ROS-producing enzymes, NADPH oxidase (NOX) is largely responsible for collagen receptor-dependent ROS production. Therefore, NOX has been proposed as a novel target for the development of antiplatelet agent. We here investigate whether resveratrol inhibits collagen-induced NOX activation and further examine the effects of resveratrol on ROS-dependent signaling pathways in collagen-stimulated platelets. Collagen-induced superoxide anion production in platelets was inhibited by resveratrol. Resveratrol suppressed collagen-induced phosphorylation of p47(phox), a major regulatory subunit of NOX. Correlated with the inhibitory effects on NOX, resveratrol protected SH2 domain-containing protein tyrosine phosphatase-2 (SHP-2) from ROS-mediated inactivation and subsequently attenuated the specific tyrosine phosphorylation of key components (spleen tyrosine kinase, Vav1, Bruton's tyrosine kinase, and phospholipase Cγ2) for collagen receptor signaling cascades. Resveratrol also inhibited downstream responses such as cytosolic calcium elevation, P-selectin surface exposure, and integrin-αIIbß3 activation. Furthermore, resveratrol inhibited platelet aggregation and adhesion in response to collagen. The antiplatelet effects of resveratrol through the inhibition of NOX-derived ROS production and subsequent oxidative inactivation of SHP-2 suggest that resveratrol is a potential compound for prevention and treatment of thrombovascular diseases.

Simple LED spectrophotometer for analysis of color information.

A spectrophotometer is the basic measuring equipment essential to most research activity fields requiring samples to be measured, such as physics, biotechnology and food engineering. This paper proposes a system that is able to detect sample concentration and color information by using LED and color sensor. Purity and wavelength information can be detected by CIE diagram, and the concentration can be estimated with purity information. This method is more economical and efficient than existing spectrophotometry, and can also be used by ordinary persons. This contribution is applicable to a number of fields because it can be used as a colorimeter to detect the wavelength and purity of samples.

Peroxiredoxin II is an antioxidant enzyme that negatively regulates collagen-stimulated platelet function.

Collagen-induced platelet signaling is mediated by binding to the primary receptor glycoprotein VI (GPVI). Reactive oxygen species produced in response to collagen have been found to be responsible for the propagation of GPVI signaling pathways in platelets. Therefore, it has been suggested that antioxidant enzymes could down-regulate GPVI-stimulated platelet activation. Although the antioxidant enzyme peroxiredoxin II (PrxII) has emerged as having a role in negatively regulating signaling through various receptors by eliminating H2O2 generated upon receptor stimulation, the function of PrxII in collagen-stimulated platelets is not known. We tested the hypothesis that PrxII negatively regulates collagen-stimulated platelet activation. We analyzed PrxII-deficient murine platelets. PrxII deficiency enhanced GPVI-mediated platelet activation through the defective elimination of H2O2 and the impaired protection of SH2 domain-containing tyrosine phosphatase 2 (SHP-2) against oxidative inactivation, which resulted in increased tyrosine phosphorylation of key components for the GPVI signaling cascade, including Syk, Btk, and phospholipase Cγ2. Interestingly, PrxII-mediated antioxidative protection of SHP-2 appeared to occur in the lipid rafts. PrxII-deficient platelets exhibited increased adhesion and aggregation upon collagen stimulation. Furthermore, in vivo experiments demonstrated that PrxII deficiency facilitated platelet-dependent thrombus formation in injured carotid arteries. This study reveals that PrxII functions as a protective antioxidant enzyme against collagen-stimulated platelet activation and platelet-dependent thrombosis.

Kaempferol suppresses collagen-induced platelet activation by inhibiting NADPH oxidase and protecting SHP-2 from oxidative inactivation.

Reactive oxygen species (ROS) generated upon collagen stimulation act as second messengers to propagate various platelet-activating events. Among the ROS-generating enzymes, NADPH oxidase (NOX) plays a prominent role in platelet activation. Thus, NOX has been suggested as a novel target for anti-platelet drug development. Although kaempferol has been identified as a NOX inhibitor, the influence of kaempferol on the activation of platelets and the underlying mechanism have never been investigated. Here, we studied the effects of kaempferol on NOX activation, ROS-dependent signaling pathways, and functional responses in collagen-stimulated platelets. Superoxide anion generation stimulated by collagen was significantly inhibited by kaempferol in a concentration-dependent manner. More importantly, kaempferol directly bound p47(phox), a major regulatory subunit of NOX, and significantly inhibited collagen-induced phosphorylation of p47(phox) and NOX activation. In accordance with the inhibition of NOX, ROS-dependent inactivation of SH2 domain-containing protein tyrosine phosphatase-2 (SHP-2) was potently protected by kaempferol. Subsequently, the specific tyrosine phosphorylation of key components (Syk, Vav1, Btk, and PLCγ2) of collagen receptor signaling pathways was suppressed by kaempferol. Kaempferol also attenuated downstream responses, including cytosolic calcium elevation, P-selectin surface exposure, and integrin-αIIbß3 activation. Ultimately, kaempferol inhibited platelet aggregation and adhesion in response to collagen in vitro and prolonged in vivo thrombotic response in carotid arteries of mice. This study shows that kaempferol impairs collagen-induced platelet activation through inhibition of NOX-derived ROS production and subsequent oxidative inactivation of SHP-2. This effect suggests that kaempferol has therapeutic potential for the prevention and treatment of thrombovascular diseases.

Reactive oxygen species play a critical role in collagen-induced platelet activation via SHP-2 oxidation.

AIMS: The collagen-stimulated generation of reactive oxygen species (ROS) regulates signal transduction in platelets, although the mechanism is unclear. The major targets of ROS include protein tyrosine phosphatases (PTPs). ROS-mediated oxidation of the active cysteine site in PTPs abrogates the PTP catalytic activity. The aim of this study was to elucidate whether collagen-induced ROS generation leads to PTP oxidation, which promotes platelet stimulation. RESULTS: SH2 domain-containing PTP-2 (SHP-2) is oxidized in platelets by ROS produced upon collagen stimulation. The oxidative inactivation of SHP-2 leads to the enhanced tyrosine phosphorylation of spleen tyrosine kinase (Syk), Vav1, and Bruton's tyrosine kinase (Btk) in the linker for the activation of T cells signaling complex, which promotes the tyrosine phosphorylation-mediated activation of phospholipase Cγ2 (PLCγ2). Moreover, we found that, relative to wild-type platelets, platelets derived from glutathione peroxidase 1 (GPx1)/catalase double-deficient mice showed enhanced cellular ROS levels, oxidative inactivation of SHP-2, and tyrosine phosphorylation of Syk, Vav1, Btk, and PLCγ2 in response to collagen, which subsequently led to increased intracellular calcium levels, degranulation, and integrin αIIbß3 activation. Consistent with these findings, GPx1/catalase double-deficiency accelerated the thrombotic response in FeCl3-injured carotid arteries. INNOVATION: The present study is the first to demonstrate that SHP-2 is targeted by ROS produced in collagen-stimulated platelets and suggests that a novel mechanism for the regulation of platelet activation by ROS is due to oxidative inactivation of SHP-2. CONCLUSION: We conclude that collagen-induced ROS production leads to SHP-2 oxidation, which promotes platelet activation by upregulating tyrosine phosphorylation-based signal transduction.

Short-hairpin RNA-mediated gene expression interference in Trichoplusia ni cells.

RNA interference (RNAi) is rapidly becoming a valuable tool in biological studies, as it allows the selective and transient knockdown of protein expression. The short-interfering RNAs (siRNAs) transiently silence gene expression. By contrast, the expressed short-hairpin RNAs induce long-term, stable knockdown of their target gene. Trichoplusia ni (T. ni) cells are widely used for mammalian cell-derived glycoprotein expression using the baculovirus system. However, a suitable shRNA expression system has not been developed yet. We investigated the potency of shRNA-mediated gene expression inhibition using human and Drosophila U6 promoters in T. ni cells. Luciferase, EGFP, and beta-N-acetylglucosaminidase (GlcNAcase) were employed as targets to investigate knockdown of specific genes in T. ni cells. Introduction of the shRNA expression vector under the control of human U6 or Drosophila U6 promoter into T. ni cells exhibited the reduced level of luciferase, EGFP, and beta-N-acetylglucosaminidase compared with that of untransfected cells. The shRNA was expressed and processed to siRNA in our vector-transfected T. ni cells. GlcNAcase mRNA levels were down-regulated in T. ni cells transfected with shRNA vectors-targeted GlcNAcase as compared with the control vector-treated cells. It implied that our shRNA expression vectors using human and Drosophila U6 promoters were applied in T. ni cells for the specific gene knockdown.

Sulfiredoxin protein is critical for redox balance and survival of cells exposed to low steady-state levels of H2O2.

Sulfiredoxin (Srx) is an enzyme that catalyzes the reduction of cysteine sulfinic acid of hyperoxidized peroxiredoxins (Prxs). Having high affinity toward H2O2, 2-Cys Prxs can efficiently reduce H2O2 at low concentration. We previously showed that Prx I is hyperoxidized at a rate of 0.072% per turnover even in the presence of low steady-state levels of H2O2. Here we examine the novel role of Srx in cells exposed to low steady-state levels of H2O2, which can be achieved by using glucose oxidase. Exposure of low steady-state levels of H2O2 (10-20 µm) to A549 or wild-type mouse embryonic fibroblast (MEF) cells does not lead to any significant change in oxidative injury because of the maintenance of balance between H2O2 production and elimination. In contrast, loss-of-function studies using Srx-depleted A549 and Srx-/- MEF cells demonstrate a dramatic increase in extra- and intracellular H2O2, sulfinic 2-Cys Prxs, and apoptosis. Concomitant with hyperoxidation of mitochondrial Prx III, Srx-depleted cells show an activation of mitochondria-mediated apoptotic pathways including mitochondria membrane potential collapse, cytochrome c release, and caspase activation. Furthermore, adenoviral re-expression of Srx in Srx-depleted A549 or Srx-/- MEF cells promotes the reactivation of sulfinic 2-Cys Prxs and results in cellular resistance to apoptosis, with enhanced removal of H2O2. These results indicate that Srx functions as a novel component to maintain the balance between H2O2 production and elimination and then protects cells from apoptosis even in the presence of low steady-state levels of H2O2.

Human cord blood stem cell therapy for treatment of stress urinary incontinence.

Our objective in this study was to evaluate the safety and efficacy of transurethral cord blood stem cell injection for treatment of stress urinary incontinence in women. Between July 2005 and July 2006, 39 women underwent transurethral umbilical cord blood stem cell injection performed by one operator at a single hospital. All patients had stress urinary incontinence. The patients were evaluated 1, 3, and 12 months postoperatively. No postoperative complications were observed. 28 patients (77.8%) were more than 50% satisfied according to the Patient's Satisfaction results after 1 month, 29 patients (83%) were more than 50% satisfied according to the Patient's Satisfaction results after 3 months, and 26 (72.2%) continuously showed more than 50% improvement after 12 months. Intrinsic sphincter deficiency and mixed stress incontinency improved in the ten patients evaluated by urodynamic study. Our results suggest that transurethral umbilical cord blood stem cell injection is an effective treatment for women with all types of stress urinary incontinence.

In vitro assessment of antibacterial activity and cytocompatibility of silver-containing PHBV nanofibrous scaffolds for tissue engineering.

Infections with bacteria have become a serious problem in joint arthroplasty. This study reports about in vitro antibacterial activity and in vitro cell compatibility of poly-(3-hydroxybutyrate-co-3-hydroxyvalerate) (PHBV) nanofibers loaded with metallic silver particles of a size of 5-13 nm. In vitro antibacterial activity against Staphylococcus aureus and Klebsiella pneumoniae was studied by microplate proliferation tests. The adhesion, viability, and proliferation properties of fibroblasts (NIH 3T3) and differentiation of osteoblasts (MC3T3-E1) were done to study in vitro cell compatibility of the scaffolds. As the results, only silver-containing PHBV nanofibrous scaffolds showed a high antibacterial activity and an inhibitory effect on the growth of both Staphylococcus aureus and Klebsiella pneumoniae bacteria. The nanofibrous scaffolds having silver nanoparticles <1.0% were free of in vitro cytotoxicity. To sum up, the PHBV nanofibrous scaffolds having nanoparticles <1.0 wt % showed not only good antibacterial activity but also good in vitro cell compatibility. It is considered that the PHBV nanofibrous scaffolds with silver nanoparticles <1.0 wt % have a potential to be used in joint arthroplasty.