Miracle-dz/UniFAR-FTUs huggingface dataset:
Removal and Transfer of Viruses on Food Contact Surfaces by Cleaning Cloths

ABSTRACT Contamination of food contact surfaces with pathogens is considered an important vehicle for the indirect transmission of food-borne diseases. Five different cleaning cloths were assessed for the ability to remove viruses from food contact surfaces (stainless steel surface and nonporous solid surface) and to transfer viruses back to these surfaces. Cleaning cloths evaluated include two different cellulose/cotton cloths, one microfiber cloth, one nonwoven cloth, and one cotton terry bar towel. Four viral surrogates (murine norovirus [MNV], feline calicivirus [FCV], bacteriophages PRD1 and MS2) were included. Removal of FCV from stainless steel was significantly greater (P ≤ 0.05) than that from nonporous solid surface, and overall removal of MNV from both surfaces was significantly less (P ≤ 0.05) than that of FCV and PRD1. Additionally, the terry towel removed significantly fewer total viruses (P ≤ 0.05) than the microfiber and one of the cotton/cellulose cloths. The cleaning cloth experiments were repeated with human norovirus. For transfer of viruses from cloth to surface, both cellulose/cotton cloths and microfiber transferred an average of 3.4 and 8.5 total PFU, respectively, to both surfaces, and the amounts transferred were significantly different (P ≤ 0.05) from those for the nonwoven cloth and terry towel (309 and 331 total PFU, respectively). There was no statistically significant difference (P > 0.05) in the amount of virus transfer between surfaces. These data indicate that while the cleaning cloths assessed here can remove viruses from surfaces, some cloths may also transfer a significant amount of viruses back to food contact surfaces.
Association of plasma leptin concentrations with adiposity measurements in rural Chinese adolescents.

CONTEXT There is evidence that leptin is involved in the etiology of obesity-related cardiovascular disease in adults. This raises the question of whether leptin levels in adolescence are indicative of adiposity-related cardiovascular risk. OBJECTIVE This study investigated gender-specific patterns of plasma leptin during adolescence, assessed which adiposity measurements are most strongly associated with plasma leptin, and estimated to what degree leptin-adiposity associations are influenced by genetic factors. METHODS Plasma leptin concentrations were determined using a sandwich immunoassay. Associations between plasma leptin and several adiposity measurements were examined using generalized estimating equations. Genetic contribution to leptin-adiposity association was estimated by Cholesky decomposition models using twin design. RESULTS Plasma leptin levels were higher in females than males at all Tanner stages. In females, body mass index, waist circumference, fat mass index (FMI), and percentage body fat (%BF) had similar associations with leptin levels. In males, %BF and FMI were more strongly associated with leptin levels than body mass index and waist circumference. In both males and females, percentage trunk fat had the weakest association with leptin among the five adiposity measures. Shared genetic factors account for more than 80% of the phenotypic correlation between %BF and leptin. CONCLUSIONS We found gender differences in leptin levels and leptin-adiposity associations. In both genders, leptin levels were strongly associated with %BF and FMI, particularly in males. Shared genetic factors contributed largely to the phenotypic correlation between leptin and %BF. Our findings underscored the importance of further investigation of leptin as a biomarker of adiposity in adolescents.
Kidney transplantation from living donors: comparison of results between related and unrelated donor transplants under new immunosuppressive protocols.

BACKGROUND Recent advances in immunosuppressive therapy have led to a substantial improvement in the outcome of kidney transplantation. Living unrelated donors may become a source of additional organs for patients on the kidney waiting list. OBJECTIVES To study the impact of the combination of calcineurin inhibitors and mycophenolate-mofetile, together with steroids, on outcomes of living related and unrelated transplants. METHODS Between September 1997 and January 2000, 129 patients underwent living related (n = 80) or unrelated (n = 49) kidney transplant. The mean follow-up was 28.2 months. Immunosuppressive protocols consisted of MMF with cyclosporine (41%) or tacrolimus (59%), plus steroids. Patient and graft survival data, rejection rate, and graft functional parameters were compared between the groups. RESULTS LUD recipients were older (47.8 vs. 33.6 years) with a higher number of re-transplants (24.5% vs. 11.2% in LRD recipients, P < 0.05). Human leukocyte antigen matching was higher in LRD recipients (P < 0.001). Acute rejection developed in 28.6% of LUD and 27.5% of LRD transplants (P = NS). Creatinine levels at 1, 2 and 3 years post-transplant were 1.6, 1.7 and 1.7 mg/dl for LRD patients and 1.5, 1.5 and 1.3 mg/dl for LUD recipients (P = NS). There was no difference in patient survival rates between the groups. One, 2 and 3 years graft survival rates were similar in LRD (91.3%, 90% and 87.5%) and LUD (89.8%, 87.8% and 87.8%) recipients. CONCLUSIONS Despite HLA disparity, rejection and survival rates of living unrelated transplants under current immunosuppressive protocols are comparable to those of living related transplants.
The NH2-terminal Domain of the Chloroplast GrpE Homolog CGE1 Is Required for Dimerization and Cochaperone Function in Vivo*

GrpE proteins function as nucleotide exchange factors for DnaK-type Hsp70s. We have previously identified a chloroplast homolog of GrpE in Chlamydomonas reinhardtii, termed CGE1. CGE1 exists as two isoforms, CGE1a and CGE1b, which are generated by temperature-dependent alternative splicing. CGE1b contains additional valine and glutamine residues in its extreme NH2-terminal region. Here we show that CGE1a is predominant at lower temperatures but that CGE1b becomes as abundant as CGE1a at elevated temperatures. Coimmunoprecipitation experiments revealed that CGE1b had a ∼25% higher affinity for its chloroplast chaperone partner HSP70B than CGE1a. Modeling of the structure of CGE1b revealed that the extended α-helix formed by GrpE NH2 termini is 34 amino acids longer in CGE1 than in Escherichia coli GrpE and appears to contain a coiled coil motif. Progressive deletions of this coiled coil increasingly impaired the ability of CGE1 to form dimers, to interact with DnaK at elevated temperatures, and to complement temperature-sensitive growth of a ΔgrpE E. coli strain. In contrast, deletion of the four-helix bundle required for dimerization of E. coli GrpE did not affect CGE1 dimer formation. Circular dichroism measurements revealed that CGE1, like GrpE, undergoes two thermal transitions, the first of which is in the physiologically relevant temperature range (midpoint ∼45 °C). Truncating the NH2-terminal coiled coil shifted the second transition to lower temperatures, whereas removal of the four-helix bundle abolished the first transition. Our data suggest that bacterial GrpE and chloroplast CGE1 share similar structural and biochemical properties, but some of these, like dimerization, are realized by different domains.
Epithelial Intestinal Cell Apoptosis Induced byHelicobacter pylori Depends on Expression of thecag Pathogenicity Island Phenotype

ABSTRACT Helicobacter pylori has been shown to induce chronic active gastritis and peptic ulcer and may contribute to the development of duodenal ulcer. Previous studies have shown that H. pylori mediates apoptosis of gastric epithelial cells via a Fas-dependent pathway. However, evidence for the induction of such a mechanism in intestinal epithelial cells (IEC) by H. pyloriinfection has not been demonstrated yet. This study was performed (i) to ascertain that H. pylori can induce IEC apoptosis; (ii) to delineate the role of the cag pathogenicity island (PAI), cagE, and vacA gene products in this process; and (iii) to verify whether the Fas-dependent pathway is involved in this phenomenon. When T84 cells were exposed to VacA+/cag PAI+H. pylori strains (CCUG 17874 and 60190), they exhibited apoptosis hallmarks as assessed by morphological studies, as well as annexin V and 3,3′-dihexyloxacarbocyanine iodide staining. In contrast, few or no apoptotic features could be detected after incubation with an isogenic mutant of strain 60190 in which the cagE gene was disrupted (60190:C− strain) or with a VacA−/cagPAI−H. pylori strain (G21). In addition, activation of caspase-3 during infection with VacA+/cag PAI+H. pylori strains was inhibited by pretreatment of IEC with an antagonistic anti-Fas antibody (ZB4). Taken together, these findings indicate that H. pylori triggers apoptosis in IEC via a Fas-dependent pathway following a process that depends on the expression of the cag PAI.
A comparative study of behaviour problems between adopted and nonadopted children in India

A review of existing literature concludes that there is an increased risk for the development of behaviour problems among adopted children compared to non-adopted children. This study was conducted with the objective of finding out whether the findings are consistent within the Indian context, which offers a different psycho-cultural setting to most western settings in which the previous studies were carried out. We compared groups of adopted children and non-adopted children on various parameters i.e. Parent Symptom Questionnaire (PSQ), ADHD rating scale, Alabama Parenting Questionnaire and the Social Adjustment Inventory for Children and Adolescents (SAICA). The Malin's intelligence scale for Indian children (MISIC) was administered to the children for assessing IQ while the Diagnostic and Statistical Manual (DSM-IV) was used to diagnose psychopathology. We found that adopted children had more behaviour problems on the PSQ. On SAICA, adopted children showed less social competence. The parenting practices as revealed by the Alabama Parenting Questionnaire did not differ between the two groups. The IQ of the children in both groups was within the normal range. We concluded that the psycho-social consequences of adoption in India do not differ from those of other countries, all of which show a higher incidence of behaviour problems in adopted children.
Biomarkers of Cardiovascular Disease and Mortality Risk in Patients with Advanced CKD.

BACKGROUND AND OBJECTIVES The high risk of cardiovascular disease (CVD) and premature death in patients with CKD associates with a plethora of elevated circulating biomarkers that may reflect distinct signaling pathways or simply, are epiphenomena of CKD. We compared the predictive strength of 12 biomarkers analyzed concomitantly in patients with stage 5 CKD. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS From 1994 to 2014, 543 patients with stage 5 CKD (median age =56 years old; 63% men; 199 patients had CVD) took part in our study on malnutrition, inflammation, and CVD in incident dialysis patients. Circulating levels of albumin, ferritin, high-sensitivity C-reactive protein (hsCRP), IGF-1, IL-6, orosomucoid, troponin T (TnT), TNF, soluble intracellular adhesion molecule, soluble vascular cellular adhesion molecule 1 (sVCAM-1), and platelet and white blood cell (WBC) counts were analyzed as predictors of the presence of clinically overt CVD at baseline, protein-energy wasting (PEW), and subsequent all-cause mortality. During follow-up for a median of 28 months, there were 149 deaths, 81 of which were caused by CVD. RESULTS Most biomarkers were elevated compared with reference values and--except for albumin, ferritin, and IGF-1-higher in patients with CVD. In receiver operating characteristic analysis, age, IL-6, TnT, hsCRP, and IGF-1 were classifiers of baseline CVD and predictors of all-cause mortality. In addition to age, diabetes mellitus, smoking (for CVD), and PEW, only IL-6, relative risk (RR) 1.10 and 95% confidence interval ([95% CI], 1.02 to 1.19), sVCAM-1 RR 1.09 (95% CI, 1.01 to 1.17), and serum albumin RR 0.89 (95% CI, 0.83 to 0.95) associated with baseline CVD, and only WBC, hazard ratio (HR) 1.94 (95% CI, 1.34 to 2.82), IL-6 HR 1.79 (95% CI, 1.20 to 2.67), and TNF HR 0.65 (95% CI, 0.44 to 0.97) predicted all-cause mortality. CONCLUSIONS In addition to age and comorbidities, only IL-6, sVCAM-1, and albumin could-independently of other biomarkers-classify clinical CVD, and only IL-6, WBC, and TNF could-independently of other biomarkers-predict all-cause mortality risk. These data underscore the robustness of IL-6 as a classifier of clinically overt CVD and predictor of all-cause mortality in patients with stage 5 CKD.
[Influence of neck circumference and body mass index on obstructive sleep apnoea severity in males].

INTRODUCTION Obesity and male gender are the main risk factors for the development of obstructive sleep apnoea (OSA); however, some epidemiological data has shown that neck circumference (NC) > or = 43 cm is a better predictor of obstructive event frequency than body mass index (BMI). The aim of this study was to assess the relation between NC and BMI on OSA severity in males. MATERIAL AND METHODS The subjects completed a sleep questionnaire and Epworth sleepiness scale before the sleep study (full polysomnography or PolyMesam study). Authors studied 133 consecutive males with confirmed OSA (AHI/RDI > 10, Epworth score > 9 points). Chest X-ray, spirometry, arterial blood gases, ECG, blood morphology and biochemistry were performed during treatment trial with autoCPAP. RESULTS Subjects presented with obesity--BMI = 35.8 +/- 6.1 kg/m2, NC = 46 +/- 3.4 cm and severe disease--AHI/RDI = 45.3 +/- 23.6. Mean age was 52.7 +/- 11.3 years. The majority of subjects had NC > or = 43 cm (116 pts, 87.2% - group 1), 17 pts (12.8% - group 2) had NC < 43 cm had 17 pts. Comparison of both groups showed significant differences only for BMI (group 1 - 36.8 +/- 5.7, group 2 - 28.6 +/- 3.7; p < 0.0001). Linear regression analysis revealed significant correlation between NC and AHI/RDI (R2 = 0.07, r = 0.26; p = 0.003); however, the correlation between BMI and AHI/RDI was stronger (R2 = 0.14, r = 0.37; p < 0.0001). In multiple linear regression analysis we found significant correlation between AHI/RDI and age (beta = -0.31, p = 0.003) and BMI (beta = 0.34, p = 0.02). CONCLUSIONS The strongest correlation between AHI/RDI, younger age and BMI. Correlation between neck circumference and AHI/RDI was significant but less when compared to BMI.
Shear Stress Stimulates Phosphorylation of Endothelial Nitric-oxide Synthase at Ser1179 by Akt-independent Mechanisms

Recently, we have shown that shear stress stimulates NO⋅ production by the protein kinase B/Akt (Akt)-dependent mechanisms in bovine aortic endothelial cells (BAEC) (Go, Y. M., Boo, Y. C., Park, H., Maland, M. C., Patel, R., Pritchard, K. A., Jr., Fujio, Y., Walsh, K., Darley-Usmar, V., and Jo, H. (2001) J. Appl. Physiol. 91, 1574–1581). Akt has been believed to regulate shear-dependent production of NO⋅ by directly phosphorylating endothelial nitric-oxide synthase (eNOS) at the Ser1179 residue (eNOS-S1179), but a critical evaluation using specific inhibitors or dominant negative mutants (AktAA or AktAAA) has not been reported. In addition, other kinases, including protein kinase A (PKA) and AMP kinase have also shown to phosphorylate eNOS-S1179. Here, we show that shear-dependent phosphorylation of eNOS-S1179 is mediated by an Akt-independent, but a PKA-dependent, mechanism. Expression of AktAAor AktAAA in BAEC by using recombinant adenoviral constructs inhibited phosphorylation of eNOS-S1179 if cells were stimulated by vascular endothelial growth factor (VEGF), but not by shear stress. As shown before, expression of AktAAinhibited shear-dependent NO⋅ production, suggesting that Akt is still an important regulator in NO production. Further studies showed that a selective inhibitor of PKA, H89, inhibited shear-dependent phosphorylation of eNOS-S1179and NO⋅ production. In contrast, H89 did not inhibit phosphorylation of eNOS-S1179 induced by expressing a constitutively active Akt mutant (AktMyr) in BAEC, showing that the inhibitor did not affect the Akt pathway. 8-Bromo-cAMP alone phosphorylated eNOS-S1179 within 5 min without activating Akt, in an H89-sensitive manner. Collectively, these results demonstrate that shear stimulates phosphorylation of eNOS-S1179 in a PKA-dependent, but Aktindependent manner, whereas the NO⋅ production is regulated by the mechanisms dependent on both PKA and Akt. A coordinated interaction between Akt and PKA may be an important mechanism by which eNOS activity is regulated in response to physiological stimuli such as shear stress.
Sonomorphology of the gallbladder in critically ill patients

Purpose: The aim of the study was to assess the value of a scoring system for the diagnosis of acalculous cholecystitis (AC) on ultrasound (US) follow-up examinations and to discuss the merits of a scoring system compared to clinical outcome and pathohistologic findings. Material and Methods: In this prospective study, 21 patients at the intensive care unit (ICU) of a medical department were examined by follow-up US. Sonographic parameters of the gallbladder (GB) were obtained (longitudinal and transversal diameter, wall thickening, contents, and pericholecystic fluid) and scored (2 points: distension of GB, thickening of GB wall; 1 point: striated thickening of GB wall, sludge, and pericholecystic fluid; range (0-8)). The US findings were correlated with clinical findings and histology at cholecystectomy or autopsy. Results: Of a total of 77 follow-up examinations in these 21 patients, US demonstrated GB distension in 19 patients, wall thickening in 18, sludge in 15, striated thickening of the GB wall in 13, and pericholecystic fluid in 12 patients. Of these, 41 (53%) examinations were scored ≥ 6, and 36 (47%) examinations ≤ 5. None of the patients with a maximum score during follow-up of ≤ 5 (n=8) had pathohistologic proof of AC or died due to GB complications. Patients with maximum scores of ≥ 6: had pathohistologic proof of AC (n=4); survived with normalization of GB morphology (n=4); had a normal GB at autopsy (n=1); or were lost for pathohistologic proof at autopsy (n=2). Conclusion: Our results indicate that regular, short-term follow-up allows early diagnosis and immediate therapy for AC. The scoring system could be helpful in differentiating between patients with an abnormal GB without AC (score ≤ 5) and those with an abnormal GB (score ≥ 6) with a suspicion of AC. In the latter group, more aggressive diagnostic and therapeutic procedures may be indicated.
Evidence for Temporal Regulation of the Two Pseudomonas cellulosa Xylanases Belonging to Glycoside Hydrolase Family 11

ABSTRACT Pseudomonas cellulosa is a highly efficient xylan-degrading bacterium. Genes encoding five xylanases, and several accessory enzymes, which remove the various side chains that decorate the xylan backbone, have been isolated from the pseudomonad and characterized. The xylanase genes consist of xyn10A, xyn10B, xyn10C, xyn10D, and xyn11A, which encode Xyn10A, Xyn10B, Xyn10C, Xyn10D, and Xyn11A, respectively. In this study a sixth xylanase gene, xyn11B, was isolated which encodes a 357-residue modular enzyme, designated Xyn11B, comprising a glycoside hydrolase family 11 catalytic domain appended to a C-terminal X-14 module, a homologue of which binds to xylan. Localization studies showed that the two xylanases with glycoside hydrolase family (GH) 11 catalytic modules, Xyn11A and Xyn11B, are secreted into the culture medium, whereas Xyn10C is membrane bound. xyn10C, xyn10D, xyn11A, and xyn11B were all abundantly expressed when the bacterium was cultured on xylan or β-glucan but not on medium containing mannan, whereas glucose repressed transcription of these genes. Although all of the xylanase genes were induced by the same polysaccharides, temporal regulation of xyn11A and xyn11B was apparent on xylan-containing media. Transcription of xyn11A occurred earlier than transcription of xyn11B, which is consistent with the predicted mode of action of the encoded enzymes. Xyn11A, but not Xyn11B, exhibits xylan esterase activity, and the removal of acetate side chains is required for xylanases to hydrolyze the xylan backbone. A transposon mutant of P. cellulosa in which xyn11A and xyn11B were inactive displayed greatly reduced extracellular but normal cell-associated xylanase activity, and its growth rate on medium containing xylan was indistinguishable from wild-type P. cellulosa. Based on the data presented here, we propose a model for xylan degradation by P. cellulosa in which the GH11 enzymes convert decorated xylans into substituted xylooligosaccharides, which are then hydrolyzed to their constituent sugars by the combined action of cell-associated GH10 xylanases and side chain-cleaving enzymes.
Demonstration of Nicking/Joining Activity at the Origin of DNA Replication Associated with the Rep and Rep′ Proteins of Porcine Circovirus Type 1

ABSTRACT The replication of porcine circovirus type 1 (PCV1) is thought to occur by rolling-circle replication (RCR), whereby the introduction of a single-strand break generates a free 3′-hydroxyl group serving as a primer for subsequent DNA synthesis. The covalently closed, single-stranded genome of PCV1 replicates via a double-stranded replicative intermediate, and the two virus-encoded replication-associated proteins Rep and Rep′ have been demonstrated to be necessary for virus replication. However, although postulated to be involved in RCR-based virus replication, the mechanism of action of Rep and Rep′ is as yet unknown. In this study, the ability of PCV1 Rep and Rep′ to “nick” and “join” strand discontinuities within synthetic oligonucleotides corresponding to the origin of replication of PCV1 was investigated in vitro. Both proteins were demonstrated to be able to cleave the viral strand between nucleotides 7 and 8 within the conserved nonanucleotide motif (5′-TAGTATTAC-3′) located at the apex of a putative stem-loop structure. In addition, the Rep and Rep′ proteins of PCV1 were demonstrated to be capable of joining viral single-stranded DNA fragments, suggesting that these proteins also play roles in the termination of virus DNA replication. This joining activity was demonstrated to be strictly dependent on preceding substrate cleavage and the close proximity of origin fragments accomplished by base pairing in the stem-loop structure. The dual “nicking/joining” activities associated with PCV1 Rep and Rep′ are pivotal events underlying the RCR-based replication of porcine circoviruses in mammalian cells.
A rice‐derived recombinant human lactoferrin stimulates fibroblast proliferation, migration, and sustains cell survival

Human lactoferrin (hLF), a glycoprotein of the transferrin family, has recently been shown to stimulate wound repair through its antimicrobial effect and inflammation modulation. A recent study with several non‐skin cell lines indicated that hLF may also have a stimulatory effect on cell proliferation. To explore the role of hLF in wound healing, we used recombinant human lactoferrin (holo‐rhLF), derived from transgenic rice, to examine the effects of holo‐rhLF on cell proliferation, migration, attachment, and survival in a human primary skin fibroblast culture system. This study revealed that holo‐rhLF not only significantly stimulates fibroblast proliferation but also has synergistic effects with fibroblast growth factor‐2 and antagonistic effects with transforming growth factor‐β1 on cell proliferation. Furthermore, using a chamber migration assay, our results demonstrate that holo‐rhLF promotes fibroblast migration in a dosage‐dependent manner. More importantly, holo‐rhLF significantly increased cell viability and protected cells from death when they were stressed by either serum depletion or 12‐O‐tetradecanoylphorbol‐13‐acetate exposure. No significant effect was observed on cell attachment. In conclusion, these findings reveal the multiple functions of holo‐rhLF in human skin fibroblasts and indicate its potential application in wound therapy by enhancing cell proliferation and migration as well as protecting cells from apoptosis.