Miracle-dz/UniFAR-FTUs huggingface dataset:
Self-Assembly of Copper Oxide Core-Shell Nanowires Through Ethyl Alcohol

The control of the core-shell structure at the nanometer is one of the most fundamental chal‐ lenges in condensed matter science [Deville et al., 2009; Woodley et al., 2008; Bannin, 2007; Ji et al., 2007; Lauhon et al., 2002]. One of the fundamental concepts regarding the synthesis of nanowires via the spontaneous self-organization of individual nanoparticles, called spontane‐ ous organization nanocrystals, refers to the formation of two-dimensional (2-D) and 3-D ar‐ rays of nanoparticles or nanowires [Tang et al., 2002; Lu et al., 2002; Balazs et al., 2006; Tang et al., 2006]. The copper-oxide based system, such as Cu2O [Huang et al., 2012; Hong et al., 2011; Yao et al., 2010], CuO [Wu, 2012; Cheng et al., 2007; Chou et al., 2008], and Cu2O@CuO [Yec et al., 2012], has been known to facilitate oxidation reactions in the bulk material, which may al‐ low it to be a cost effective substitute for noble metals in various catalytic systems. With recent developments in nanostructures synthesis leading to the ability to control size, reproducibility and structural complexity [Lauhon et al., 2002; Fan et al., 2006; Lu et al., 2005], it becomes worthwhile and possibly paramount to define specific target structures for the nanoparticles based on an understanding of the mechanism of the self-organization mechanism. Upto now, many complex procedures, such as vapor-liquid-solid, chemical vapor deposition, thermal evaporation, and chemical reactions, have been developed for the synthesis of one-dimension‐ al materials of Copper-based nano compounds [Huang et al., 2012; Hong et al., 2011; Yao et al., 2010]. In addition to these methods, solution chemical route including solvothermal, hydro‐ thermal, self-assembly, and template-assisted chemical vapor deposition has become a prom‐ ising option for large –scale production of nanomaterials, due to the simple, fast, and less expensive virtues [Xin et al., 2002; Li et al., 1999; Lu et al., 2000; Hung et al., 2004; Roy et al., 2003; Baxter et al., 2003]. However, a new type of immersing nanoparticles into liquid alcohol
Waddlia chondrophila: from bovine abortion to human miscarriage.

C , and D ) Immunohistochemistry (magnification 3 200 for B, 3 400 for C and D ) using a specific rabbit polyclonal antibody (dilution of 1:12,000) to investigate for the presence of Waddlia in the placenta. Detection was performed with the Dako ChemMate Detection Kit according to the manufacturer's instructions. The histological picture ( A ) shows infiltration of the placenta with numerous polymorphonuclear cells compatible with early infection. Immunohistochemistry ( B , C , and D ) demonstrated the presence of Waddlia in epithelial cells of the endometrial glands.
Design of a complement mannose‐binding lectin pathway‐specific activation system applicable at low serum dilutions

Recently we showed that alternative pathway (AP) amplification was responsible for more than 80% of specific classical pathway‐induced terminal pathway activation under physiological conditions. The present study aimed to design a system for specific lectin pathway (LP) activation applicable at low serum dilutions with a fully functional AP. Comparison between activation of normal human serum (NHS), a mannose‐binding lectin (MBL) homozygous D/D‐deficient serum, and sera deficient in C1q and C2, all diluted 1 : 2, was essential to document optimal conditions for LP specificity. Mannan on the solid phase of enzyme‐linked immunosorbent assay (ELISA) plates was used for activation, showing 0·5 µg mannan/well to give optimal conditions because at this concentration a good signal was preserved for C4 and TCC deposition in NHS, whereas the C3 deposition observed in C2‐deficient serum at higher mannan concentrations reached nadir at 0·5 µg/well, indicating a lack of direct AP activation under these conditions. Pooled NHS and C1q‐deficient serum gave the same degree of C4 and terminal complement complex (TCC) deposition, whereas deposition of these products was not obtained with MBL‐deficient serum. Reconstitution with purified MBL, however, restored the depositions. A blocking anti‐MBL monoclonal antibody (mAb) completely abolished the complement deposition, in contrast to a non‐inhibiting anti‐MBL mAb. Activation of C2‐deficient serum induced C4 deposition similar to NHS, but negligible deposition of C3 and TCC, confirming the lack of direct activation of AP. Thus, this assay is unique in being LP‐specific at low serum dilution and thus particularly suitable to study LP activation mechanisms and the role of AP amplification under physiological conditions.
In vitro assessment of antimicrobial activity of Pothomorphe umbellata extracts against Enterococcus faecalis.

BACKGROUND Due to the complex anatomy of the root canal system, biomechanical preparation is not able to completely eliminate all microorganisms present in the endodontic infections, making it necessary the use of an intracanal medication. AIM The aim of this study was to assess the antimicrobial activity of an intracanal medication containing the ethyl-acetate fraction of Pothomorphe umbellata against Enterococcus faecalis. MATERIALS AND METHODS Fifty seven human maxillary canine teeth were used, of which 54 were infected with E. faecalis every 72 h, for 28 days, and cultured for 24 h. Contaminated teeth were randomly separated into three groups (n = 18) and treated as follows: Group I - calcium hydroxide-based medication; Group II - P. umbellata-based medication; Group III - contaminated teeth without medication. Three teeth were used as negative control. After 7, 14 and 28 days of treatment, six teeth from each group were assessed for the level of microbial growth after each period of treatment. RESULTS The intracanal medication containing P. umbellata was effective against E. faecalis after 7, 14, and 28 days of treatment without statistically significant difference in comparison to calcium hydroxide treatment (Kruskal-Wallis test, P > 0.05). CONCLUSION Ethyl-acetate fraction of P. umbellate was efficient against E. faecalis, making this phytotherapy a viable option for endodontic treatment.
Effect of maternal diabetes on the embryo, fetus, and children: congenital anomalies, genetic and epigenetic changes and developmental outcomes.

INTRODUCTION Pregestational and gestational diabetes mellitus (PGDM; GDM) are significant health concerns because they are associated with an increased rate of malformations and maternal health complications. METHODS We reviewed the data that help us to understand the effects of diabetes in pregnancy. RESULTS Diabetic embryopathy can affect any developing organ system, but cardiovascular and neural tube defects are among the most frequent anomalies. Other complications include preeclampsia, preterm delivery, fetal growth abnormalities, and perinatal mortality. Neurodevelopmental studies on offspring of mothers with diabetes demonstrated increased rate of Gross and Fine motor abnormalities, of Attention Deficit Hyperactivity Disorder, learning difficulties, and possibly also Autism Spectrum Disorder. The mechanisms underlying the effects of maternal hyperglycemia on the developing fetus may involve increased oxidative stress, hypoxia, apoptosis, and epigenetic changes. Evidence for epigenetic changes are the following: not all progeny are affected and not to the same extent; maternal diet may influence pregnancy outcomes; and maternal diabetes alters embryonic transcriptional profiles and increases the variation between transcriptomic profiles as a result of altered gene regulation. Research in animal models has revealed that maternal hyperglycemia is a teratogen, and has helped uncover potential therapeutic targets which, when blocked, can mitigate or ameliorate the negative effects of diabetes on the developing fetus. CONCLUSIONS Tight metabolic control, surveillance, and labor management remain the cornerstone of care for pregnant women with diabetes, but advances in the field indicate that new treatments to protect the mother and baby are not far from becoming clinical realities.
TIMP2 Deficiency Accelerates Adverse Post–Myocardial Infarction Remodeling Because of Enhanced MT1-MMP Activity Despite Lack of MMP2 Activation

Rationale: Myocardial infarction (MI) results in remodeling of the myocardium and the extracellular matrix (ECM). Tissue inhibitors of metalloproteinases (TIMPs) are critical regulators of ECM integrity via inhibiting matrix metalloproteinases (MMPs). TIMP2 is highly expressed in the heart and is the only TIMP that, in addition to inhibiting MMPs, is required for cell surface activation of pro-MMP2. Hence, it is difficult to predict the function of TIMP2 as protective (MMP-inhibiting) or harmful (MMP-activating) in heart disease. Objective: We examined the role of TIMP2 in the cardiac response to MI. Methods and Results: MI was induced in 11- to 12-week-old male TIMP2−/− and age-matched wild-type mice. Cardiac function was monitored by echocardiography at 1 and 4 weeks post-MI. ECM fibrillar structure was visualized using second harmonic generation and multiphoton imaging of unfixed/unstained hearts. Molecular analyses were performed at 3 days and 1 week post-MI on flash-frozen infarct, periinfarct, and noninfarct tissue. Membrane type 1 (MT1)-MMP levels and activity were measured in membrane protein fractions. TIMP2−/−-MI mice exhibited a 25% greater infarct expansion, markedly exacerbated left ventricular dilation (by 12%) and dysfunction (by 30%), and more severe inflammation compared to wild-type MI mice. Adverse ECM remodeling was detected by reduced density and enhanced disarray of fibrillar collagen in TIMP2−/−-MI compared to wild-type MI hearts. TIMP2 deficiency completely abrogated MMP2 activation but markedly increased collagenase activity, particularly MT1-MMP activity post-MI. Conclusions: The MMP-inhibitory function of TIMP2 is a key determinant of post-MI myocardial remodeling primarily because of its inhibitory action on MT1-MMP. TIMP2 replenishment in diseased myocardium could provide a potential therapy in reducing or preventing disease progression.
Tumor necrosis factor-alpha and nitric oxide in vertically HIV-1-infected children: implications for pathogenesis.

We performed a cross-sectional study to investigate the plasma TNF-alpha and nitric oxide (NO) production in 44 vertically HIV-1-infected children, and the relationship with immunological status and viral replication. As a control group, 36 healthy, uninfected children were studied. Plasma TNF-alpha and NO levels were determined by ELISA. Viral load was quantified using standard assays. Cell proliferation, apoptosis and viral replication were evaluated in vitro by incorporation of (3H)-thymidine, flow cytometry and p24 antigen, respectively. Higher plasma TNF-alpha and NO levels were observed in HIV-1-infected children compared with healthy controls. We found a very strong correlation between plasma TNF-alpha and NO levels in HIV-1-infected children (r = 0.98; p < 0.001). Moreover, HIV-1-infected children with higher viral load (> 4.7 log10) showed higher TNF-alpha and NO levels than those with viral load below this threshold. Interestingly, we detected inducible nitric oxide synthase (iNOS) mRNA in T-lymphocytes from HIV-1-infected children. To address their possible patho-physiological significance, we tested the in vitro effects of NO and TNF-alpha in HIV-1 replication. Addition of TNF-alpha and NO donors to mitogen-activated, HIV-1-infected PBMC cultures produced a significant increase in viral replication. Moreover, HIV-1 replication in mitogen-stimulated, PBMC cultures was partially inhibited by iNOS specific inhibitors, and a neutralising, anti-TNF-alpha monoclonal antibody. Our results indicate that TNF-alpha and NO correlated with high viral load in HIV-1-infected children and favoured HIV-1 in vitro replication. These data suggest a detrimental role of NO in HIV-1 infection, and that NOS inhibitors may have some therapeutic benefit in HIV-1-infection.
Developmental origins of mosaic brain evolution: Morphometric analysis of the developing zebra finch brain

In adult zebra finches (Taeniopygia guttata), the telencephalon occupies 64% of the entire brain. This fraction is similar to what is seen in parrots, but many other birds possess a significantly smaller telencephalon. The aim of the present study was to determine the developmental time course and cellular basis of telencephalic enlargement in zebra finches, and then to compare these findings with what is known about telencephalic enlargement in other birds. To this end we estimated the volumes of all major brain regions from serial sections in embryonic and post‐hatching zebra finches. We also labeled proliferating cells with antibodies against proliferating cell nuclear antigen and phosphorylated histone H3. An important finding to emerge from this work is that the telencephalon of zebra finches at hatching contains a thick proliferative subventricular zone (SVZ) that extends from the subpallium into the dorsal pallium. The data also show that the onset and offset of telencephalic neurogenesis are both delayed in zebra finches relative to quail (Galliformes). This delay in neurogenesis, in conjunction with the expanded SVZ, probably accounts for most of the telencephalic enlargement in passerines such as the zebra finch. In addition, passerines enlarged their telencephalon by decreasing the proportional size of their midbrain tectum. Because the presumptive tectum is proportionally smaller in zebra finches than quail before neurogenesis begins, this difference in tectum size cannot be due to evolutionary alterations in neurogenesis timing. Collectively these findings indicate that several different developmental mechanisms underlie the evolution of a large telencephalon in passerines. J. Comp. Neurol. 514:203–213, 2009. © 2009 Wiley‐Liss, Inc.
Sharedsphere: MR collaboration through shared live panorama

Sharing live 360 panorama video is becoming popular on social networking platforms. This research focuses on further improving shared live panorama based collaborative experiences by applying Mixed Reality (MR) technology. In this demonstration we present SharedSphere, an MR remote collaboration system which not only allows sharing of a live captured immersive panorama, but also allows enriched collaboration through sharing non-verbal communication cues, such as view awareness and gestures. We describe the prototype system and the experience that attendees of Siggraph Asia 2017 will have using the system.
Effects of estrogen on proton secretion via the apical membrane in vaginal-ectocervical epithelial cells of postmenopausal women

Objective:To understand estrogen regulation of proton (H+) secretion by human vaginal-ectocervical epithelial cells and the mechanisms involved. Design:Primary-tertiary cultures of human normal vaginal-ectocervical epithelial cells were generated from surgical specimens of premenopausal women (aged 37-46 years) and of postmenopausal women (aged 53-65 years). Cells were grown on filters, and measurements were made of changes in extracellular pH (pHo) in the contraluminal (CL) and luminal (L) solutions 30 minutes after shifting cells to basic salt solution. Results:Upon shifting cells to basic salt solution, CL-pHo decreased from 7.4 to 7.25, and was not affected by removal of intracellular estrogens or treatment with estradiol. L-pHo decreased from 7.4 to 7.05 in cells of premenopausal women, and from 7.4 to 7.20 in cells of postmenopausal women. Removal of intracellular estrogens attenuated the decrease in L-pHo in cells of premenopausal women (only to 7.20). In cells of premenopausal women stripped of estrogens, treatment with 10 nM 17β-estradiol restored the decrease in L-pHo. In estrogen-stripped cells of postmenopausal women, treatment with estradiol augmented luminal acidification but to a lesser degree than in cells of premenopausal women (L-pHo of 7.15 vs 7.05). In cells of pre- and postmenopausal women, the addition in the L solution of bafilomycin-A1, a specific inhibitor of the vacuolar-H+-ATPase (V-H+-ATPase), blocked the decrease in L-pHo. Conclusions:Human vaginal-ectocervical epithelial cells acidify constitutively their luminal solution, and the effect is mediated by active H+ secretion by V-H+-ATPase expressed predominantly in the apical cell membrane. Estrogen deprivation attenuates, and treatment with 17β-estradiol augments, active H+ secretion. Finally, cells of postmenopausal women actively secrete H+ via apically located V-H+-ATPase, but the effect is lesser, and estrogen failed to augment active H+ secretion, as in cells of premenopausal women. These data suggest that in addition to hypoestrogenism, other factors of the aging process affect the capacity of vaginal-ectocervical cells to secrete acid.
Psychopathology and Clinical Features in an Italian Sample of Patients with Myofascial and Temporomandibular Joint Pain: Preliminary Data

Objective: Aim of this study was to provide data on the relationships between psychopathological variables and temporomandibular disorders (TMD). Sixty-three TMD patients were investigated using clinical and anamnestical psychiatric informations and psychopathological measures. Methods: Three groups of TMD patients were recruited according to the Research Diagnostic Criteria for TMD guidelines: a group of patients presenting myofascial pain alone (RDC/TMD axis I group I), a group with temporomandibular joint (TMJ) pain alone (RDC/TMD axis I group IIIa, IIIb), and a group presenting both myofascial and TMJ pain. Two secondary groups were identified on the basis of the presence/absence of myofascial pain. The study design provided a psychiatric interview and psychometric assessment including the Symptom Check List-90-Revised (SCL-90-R), the Hamilton Depression Rating Scale (HDRS), and the Hamilton Anxiety Rating Scale (HARS). Results: -Psychiatric evaluation: Myofascial pain patients had higher scores for personal psychiatric history and a history of more frequent psychotropic drug use. -HDRS and HARS: The sample presented scores indicating mild depressive symptoms and moderate anxiety symptoms. -SCL-90-R: The global sample showed acute levels of psychological distress as measured by the GSI score (Global Severity Index). Myofascial pain patients scored higher than TMJ pain patients in the GSI (p = .028), PAR (paranoia; p = .015), PSY (psychoticism; p = .032), and HOS (hostility; p = .034) subscales. Conclusions: TMD patients showed elevated levels of depression, somatization, and anxiety. These characteristics did not differ significantly between patients with myofascial or TMJ pain. Other specific psychopathological dimensions, detected with SCL-90-R, appeared to be closely associated to the myofascial component.
Giving voice to adolescent mothers’ challenges

An estimated 32% to 60% of adolescent mothers experience postpartum depression. Young women who deal with the simultaneous developmental tasks of adolescence and parenting are vulnerable to depression, which affects the welfare of both the mother and child. The primary objective of this qualitative study was to appreciate the unique experiences of adolescent mothers. Seventeen postpartum adolescents participated in two focus groups and completed the Center for Epidemiologic Studies Depression Scale (CES-D). The qualitative data analysis identified 19 major conceptual themes in the data. The four most frequently discussed themes that emerged were: 1) social support, 2) differences between teen and adult mothers, 3) parenting ability, and 4) increased maturity. Six of the 17 participants (35.3%) had CES-D scores of 16 or above, which is indicative of a probable major depression. These findings highlight areas that could inform screening assessments, treatment, and prevention programs for adolescent mothers.
The Asp620asn mutation in VPS35 is not a common cause of familial Parkinson's disease

Genetic studies of familial Parkinson’s disease (PD) have revealed 5 major causative genes (SNCA, PRKN, DJ1, PINK1, LRRK2), which together account for less than 10% of inherited PD cases. 1 So far, the identification of genetic causes for Mendelian forms of PD has been based on classic linkage and Sanger sequence analysis. Very recently, however, the application of next-generation whole-exome sequencing technology to 2 large independent kindred with autosomal-dominant late-onset PD has led to the identification of VPS35, encoding the vacuolar protein sorting 35, as a novel disease-causing gene in 2 independent studies. 2,3 In the 2 analyzed families, the genetic determinant of the disease was the p.Asp620Asn mutation, suggesting that this might be a recurrent causative variant. The subsequent screening of about 6000 additional PD cases and 5000 controls, identified 6 more patients (5 with familial and 1 with sporadic PD) and no controls carrying the VPS35 p.Asp620Asn; in all 5 families the mutation cosegregated with the disease as an autosomal-dominant trait. 2,3 We observed that the 2 works do not report the rate of familial PD in the analyzed cohort. Therefore, to elucidate the relevance and frequency of the VPS35 p.Asp620Asn mutation in familial PD, we screened for this variant in an Italian PD cohort collected by the Biobank of the Parkinson Institute of Milan (http://www.parkinson.it/dnabank.html). Our population included 475 patients with familial PD (56% male; mean age of onset 54.17 6 10.9 years; mean disease duration 13.28 6 7.36 years), having at least 1 relative among their first-degree (284), second-degree (128), or third-degree (63) family members with a formal diagnosis of PD. The majority of cases (308) had a probable autosomal dominant inheritance of the disease. Major PD genes had been previously analyzed, and positive cases (13 LRRK2 ,1 2 PRKN, and 3 SNCA mutations) were not excluded. 4,5 Genotyping (99% success rate) was performed by the high-resolution melting technique 6 using a LightCycler480 (Roche, Basel, Switzerland) and the primer pair 5 0 -CAAC TAGAGGATGGTTGGTCCT-3 0 and 5 0 -AAAGTGCCAAT GATCAAGGTG-3 0 . The genomic DNA of an individual heterozygous for the p.Asp620Asn mutation (kindly provided
Silymarin improved diet-induced liver damage and insulin resistance by decreasing inflammation in mice

Abstract Context: Silymarin is the main flavonoid extracted from milk thistle, which has been used to treat liver diseases. Objective: The in vivo effect of silymarin on HFD-induced insulin resistance and fatty liver in mice was studied. Materials and methods: Male C57BL/6 mice were fed with high-fat diet (HFD) to induce obesity and insulin resistance and treated with 30, 60 mg/kg silymarin for 18 days. Food intake, body weight and the content/histology of epididymal fat and liver tissue were examined; the content of lipids, AST, ALT and inflammatory cytokines in serum were estimated. Results: Administration of silymarin caused bodyweight loss in diet induced obesity (DIO) mice (HFD group: 47.7 g, 60 mg/kg group: 43.0 g) while the food intake remain unchanged. Silymarin (60 mg/kg) significantly reduced the epididymal fat mass (from 1.75 g to 1.12 g). Elevated plasma lipids (TC 6.1 mM, TG 1.3 mM, LDL 1.2 mM) in DIO mice were all suppressed by silymarin (TC 4.5 mM, TG 0.89 mM, LDL 0.9 mM), as well as insulin (5.1 ng/ml in HFD group to 2.0 ng/ml (60 mg/kg silymarin). Examination of cytokine levels (TNF-α, IL-1β and IL-6) in each group proved that silymarin treatment significantly decreased inflammation in DIO mice. Finally, silymarin effectively protected liver from HFD-induced injury as evidenced by decreasing histological damage and reducing ALT and AST levels, as follows: ALT; 47.4 U/L in HFD group to 28.4 U/L (60 mg/kg silymarin); AST; 150.1 U/L in HFD group to 88.1 U/L (60 mg/kg silymarin) in serum. Discussion and conclusion: Our results suggested that silymarin-induced alleviation of inflammatory response could be a mechanism responsible for its benefits against liver damage and insulin resistance.