Miracle-dz/UniFAR-FTUs huggingface dataset:
Vaginal epithelial cells regulate membrane adhesiveness to co‐ordinate bacterial adhesion

Vaginal epithelium is colonized by different bacterial strains and species. The bacterial composition of vaginal biofilms controls the balance between health and disease. Little is known about the relative contribution of the epithelial and bacterial cell surfaces to bacterial adhesion and whether and how adhesion is regulated over cell membrane regions. Here, we show that bacterial adhesion forces with cell membrane regions not located above the nucleus are stronger than with regions above the nucleus both for vaginal pathogens and different commensal and probiotic lactobacillus strains involved in health. Importantly, adhesion force ratios over membrane regions away from and above the nucleus coincided with the ratios between numbers of adhering bacteria over both regions. Bacterial adhesion forces were dramatically decreased by depleting the epithelial cell membrane of cholesterol or sub‐membrane cortical actin. Thus, epithelial cells can regulate membrane regions to which bacterial adhesion is discouraged, possibly to protect the nucleus.
Newly identified actions of the vitamin D endocrine system.

Introduction VITAMIN D is a seco-steroid in which the B-ring of the cyclopentanoperhydrophenanthrene structure is cleaved. The vitamin is either obtained from the diet or is synthesized in the skin from 7-dehydrocholesterol (Fig. 1) and is itself biologically inert (for reviews see Refs. 1–8). Vitamin D and its metabolites circulate in the blood primarily bound to and in equilibrium association with the vitamin D-binding globulin [DBP]. In the liver, the enzyme 25-hydroxylase converts the vitamin to the inactive hormonal precursor 25-hydroxyvitamin D [25(OH)D]. Subsequently, the renal lα-hydroxylase enzyme converts 25(OH)D to the biologically active form 1,25-dihydroxyvitamin D [1,25(OH)2D]. Both hydroxylase enzymes are cytochrome P450-containing enzymes. la-Hydroxylase activity is tightly controlled by a number of ionic and endocrine factors including stimulation by PTH and reduced plasma Ca2+ or inhibition by 1,25(OH)2D in a classic negative feedback loop. Although not illustrated in Fig. 1, under condi.
Immigrant Characteristics, the IT Bust, and Their Effect on Entry Earnings of Immigrants

Using administrative data, this paper asks (1) whether the changing characteristics of immigrants, notably the rise in the share with university education and in the "skilled economic" immigrant class, contributed positively to immigrant entry earnings during the 1990s, and (2) whether the entry earnings of immigrants improved after 2000, and if not, why not. We find that, through the 1990s, the rising number of entering immigrants with university degrees and in the skilled economic class did little to improve earnings at the bottom of the earnings distribution (and reduce poverty rates among entering immigrants), but the changes did increase earnings among immigrants at the middle and top of the earnings distribution. The increasing numbers of highly educated at the bottom of the earnings distribution were unable to convert their education and "skilled class" designation to higher earnings: they found themselves with low incomes. These outcomes may be related to language, credentialism, education quality, or supply issues, as discussed in the paper. We find that from 2000 to 2004, the entry earnings of immigrants renewed their slide, but for reasons that differed from the standard explanations of the earlier decline. Much of the fall after 2000 was concentrated among immigrants intending to practice in the information technology (IT) or engineering occupations. This coincided with the IT downturn, which appears to have significantly affected outcomes for these immigrants, particularly the men. Following the significant increase in supply in response to the call for more high-tech workers in the late 1990s, the large numbers of entering immigrants were faced with the IT downturn.
Return to work in stroke patients

Purpose. To present the current state of knowledge regarding return to work (RTW) following stroke. Method. A comprehensive review of the current stroke rehabilitation literature pertaining to prognostic and treatment factors for RTW following stroke. Results. Stroke is a major healthcare problem and one of the most expensive diseases in modern society. Stroke results not only in impairment and limitation in basic daily activities; it also impacts on participation in community activities, such as returning to work. Return to work in post-stroke patients has been reported to range between 19% and 73%. Various studies report on return to work in diverse populations, using different follow-up periods, while utilizing variable definitions of stroke and successful work outcomes. The factors positively related to RTW in stroke patients, as found in the literature, are age less then 65 years, high education level and white-collar employment. The significant negative predictor is the severity of stroke. This is indicated by neurological parameters including functional measures of the presence and extent of motor and cognitive impairment. Significantly, the side of the brain damaged and stroke location were not found to be correlated with RTW. Social and financial factors also significantly influence RTW. Conclusions. RTW in stroke patients should be considered one of the indicators of a successful rehabilitation as it influences self-image, well-being and life satisfaction. There is still a considerable lack of knowledge regarding effective assessments and interventions in vocational rehabilitation in stroke patients.
Peasants or Bankers? The American Electorate and the U.S. Economy

The usual model of electoral reaction to economic conditions assumes the “retrospective” economic voter who bases expectations solely on recent economic performance or personal economic experience (voter as “peasant”). A second model assumes a “sophisticated” economic voter who incorporates new information about the future into personal economic expectations (voter as “banker”). Using the components, both retrospective and prospective, of the Index of Consumer Sentiment (ICS) as intervening variables between economic conditions and approval, we find that the prospective component fully accounts for the presidential approval time series. With aggregate consumer expectations about long-term business conditions in the approval equation, neither the usual economic indicators not the other ICS components matter. Moreover, short-term changes in consumer expectations respond more to current forecasts than to the current economy. The qualitative result is a rational expectations outcome: the electorate anticipates the economic future and rewards or punishes the president for economic events before they happen.
Short threaded implants with an oxidized surface to restore posterior teeth: 1- to 3-year results of a prospective study.

PURPOSE The aim of this multicenter prospective study was to provide data from a case series supporting the use of short dental implants with oxidized surfaces to treat partially edentulous patients. MATERIALS AND METHODS The implants used had an oxidized surface, a tapered design, and a short length (8.5 mm or shorter). All implants were placed in posterior edentulous areas that were affected by high bone resorption (available bone height < 10 mm). Implant success was established according to predetermined criteria. RESULTS Records were available for 107 implants used to treat 46 patients (69.2% were 7 mm long, and 30.8% were 8.5 mm long); 80.4% were placed in the posterior mandible, and 19.6% were placed in the posterior maxilla. With regard to restorations, 27.1% of implants were restored with single crowns, 16.8% with a single cantilever, and 56.1% with fixed prostheses. After a 1- to 3- year follow-up, 105 implants are still functioning; only 2 implants have been lost, for a survival rate of 98.1%. In all, 4 of the 107 implants placed failed to meet the success criteria, resulting in a success rate of 96.3%. The mean marginal bone loss was 0.6 ± 0.2 mm. CONCLUSIONS The results of this study suggest that short oxidized implants should be regarded as a possible solution for the restoration of posterior teeth in highly resorbed areas.
Bifidobacterium animalis subsp. lactis fermented milk product reduces inflammation by altering a niche for colitogenic microbes

Intestinal health requires the coexistence of eukaryotic self with the gut microbiota and dysregulated host-microbial interactions can result in intestinal inflammation. Here, we show that colitis improved in T-bet−/−Rag2−/− mice that consumed a fermented milk product containing Bifidobacterium animalis subsp. lactis DN-173 010 strain. A decrease in cecal pH and alterations in short chain fatty acid profiles occurred with consumption, and there were concomitant increases in the abundance of select lactate-consuming and butyrate-producing bacteria. These metabolic shifts created a nonpermissive environment for the Enterobacteriaceae recently identified as colitogenic in a T-bet−/−Rag2−/− ulcerative colitis mouse model. In addition, 16S rRNA-based analysis of the T-bet−/−Rag2−/−fecal microbiota suggest that the structure of the endogenous gut microbiota played a key role in shaping the host response to the bacterial strains studied herein. We have identified features of the gut microbiota, at the membership and functional level, associated with response to this B. lactis-containing fermented milk product, and therefore this model provides a framework for evaluating and optimizing probiotic-based functional foods.
Conditional Deletion of Beta-Catenin Mediated by Amhr2cre in Mice Causes Female Infertility1

Abstract Follicle-stimulating hormone (FSH) regulation of aromatase gene expression in vitro requires the transcriptional coactivator beta-catenin. To ascertain the physiological significance of beta-catenin in granulosa cells during folliculogenesis, mice homozygous for floxed alleles of beta-catenin were intercrossed with Amhr2cre mice. Conditional deletion of beta-catenin in 8-wk-old females occurred in derivatives of the Müllerian duct, granulosa cells and, surprisingly, in brain, pituitary, heart, liver, and tail. Female mice deficient for beta-catenin were infertile, despite reaching puberty and ovulating at the expected age, indications of apparently normal ovarian function. In contrast, their oviducts were grossly distended, with fewer but healthy oocytes. In addition, their uteri lacked implantation sites. Together, these two phenotypes could explain the complete loss of fertility. Nevertheless, although the ovary appeared normal, with serum estradiol concentrations in the normal range, there was marked animal-to-animal variation of mRNAs encoding beta-catenin and aromatase. Similarly, inhibin-alpha and luteinizing hormone receptor mRNAs varied considerably in whole ovaries, whereas pituitary Fshb mRNA was significantly reduced. Collectively, these features suggested cyclization recombination (CRE)-mediated recombination of beta-catenin may be unstable in proliferating granulosa cells, and therefore may mask the suspected steroidogenic requirement for beta-catenin. We tested this possibility by transducing primary cultures of granulosa cells from mice homozygous for floxed alleles of beta-catenin with a CRE-expressing adenovirus. Reduction of beta-catenin significantly compromised FSH stimulation of aromatase mRNA and subsequent production of estradiol. Collectively, these data suggest that FSH regulation of steroidogenesis requires beta-catenin, a role that remains hidden when tested through Amhr2cre-mediated recombination in vivo.
Is a computer crossmatch in the absence of an immediate‐spin antibody screen adequate for persons identified to be at increased risk of forming new blood group antibodies?

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Yaractor-based microstrip circuits with high frequency agility and low insertion loss

The authors present a straightforward and effective approach for minimizing insertion loss (IL) of varactor-based frequency-agile microstrip passive circuits, where varactors are employed as elements of variable reversal capacitances to attain reconfigurabiltiy/tunability on circuit characteristics. Technically, the proposed approach mimics the required capacitances using the varactors together with the SMD capacitors/inductors rather than entirely using the varactors. With the proposed capacitance synthesis, the varactors are able to operate at a higher quality factor so that IL of the entire circuit is minimized. Also, the capacitance tuning range is further extended. With the proposed loss-reduction avenue, the circuit agility could be enhanced, and its effectiveness is experimentally demonstrated with agility enhancement of a reconfigurable bandpass filter (BPF) and a reconfigurable balun BPF.
The biogenesis of active protein phosphatase 2A holoenzymes: a tightly regulated process creating phosphatase specificity

Protein phosphatase type 2A (PP2A) enzymes constitute a large family of Ser/Thr phosphatases with multiple functions in cellular signaling and physiology. The composition of heterotrimeric PP2A holoenzymes, resulting from the combinatorial assembly of a catalytic C subunit, a structural A subunit, and regulatory B‐type subunit, provides the essential determinants for substrate specificity, subcellular targeting, and fine‐tuning of phosphatase activity, largely explaining why PP2A is functionally involved in so many diverse physiological processes, sometimes in seemingly opposing ways. In this review, we highlight how PP2A holoenzyme biogenesis and enzymatic activity are controlled by a sophisticatedly coordinated network of five PP2A modulators, consisting of α4, phosphatase 2A phosphatase activator (PTPA), leucine carboxyl methyl transferase 1 (LCMT1), PP2A methyl esterase 1 (PME‐1) and, potentially, target of rapamycin signaling pathway regulator‐like 1 (TIPRL1), which serve to prevent promiscuous phosphatase activity until the holoenzyme is completely assembled. Likewise, these modulators may come into play when PP2A holoenzymes are disassembled following particular cellular stresses. Malfunctioning of these cellular control mechanisms contributes to human disease. The potential therapeutic benefits or pitfalls of interfering with these regulatory mechanisms will be briefly discussed.
Functional Characterization of Ocular-Derived Human Alphaherpesvirus Cross-Reactive CD4 T Cells

Intraocular varicella-zoster virus (VZV) and HSV type 1 (HSV-1) infections cause sight-threatening uveitis. The disease is characterized by an intraocular inflammatory response involving herpesvirus-specific T cells. T cell reactivity to the noncausative human alphaherpesvirus (αHHV) is commonly detected in the affected eyes of herpetic uveitis patients, suggesting the role of cross-reactive T cells in the disease. This study aimed to identify and functionally characterize intraocular human alphaherpesvirus cross-reactive T cells. VZV protein immediate early 62 (IE62), which shares extensive homology with HSV ICP4, is a previously identified T cell target in VZV uveitis. Two VZV-specific CD4 T cell clones (TCC), recovered from the eye of a VZV uveitis patient, recognized the same IE62918–927 peptide using different TCR and HLA-DR alleles. The IE62918–927 peptide bound with high affinity to multiple HLA-DR alleles and was recognized by blood-derived T cells of 5 of 17 HSV-1/VZV-seropositive healthy adults but not in cord blood donors (n = 5). Despite complete conservation of the IE62 epitope in the orthologous protein ICP4 of HSV-1 and HSV-2, the TCC recognized VZV and HSV-1– but not HSV-2–infected B cells. This was not attributed to proximal epitope-flanking amino acid polymorphisms in HSV-2 ICP4. Notably, VZV/HSV-1 cross-reactive CD4 T cells controlled VZV but not HSV-1 infection of human primary retinal pigment epithelium (RPE) cells. In conclusion, we report on the first VZV/HSV-1 cross-reactive CD4 T cell epitope, which is HLA-DR promiscuous and immunoprevalent in coinfected individuals. Moreover, ocular-derived peptide-specific CD4 TCC controlled VZV but not HSV-1 infection of RPE cells, suggesting that HSV-1 actively inhibits CD4 T cell activation by infected human RPE cells.
Mapping fiber orientation in human muscle by proton MR spectroscopic imaging

Proton magnetic resonance spectroscopic imaging (1H‐MRSI) was used to determine muscle fiber orientations in human calf muscles. The method is based on the fact that some resonances show orientation‐dependent dipolar splitting, caused by incomplete motional averaging. This leads to proton spectra that depend strongly on the angle between muscle fibers and the magnetic field B0. The orientation‐dependent dipolar splittings were mapped using a fit with a basis set of predefined coupling patterns reflecting the fiber orientation. The fitted coupling patterns were displayed as images and assigned to different muscles based on segmented MR images. They showed gross differences in fiber orientation between some muscles, including m. soleus and m. tibialis anterior, for all subjects. In addition, smaller but significant differences between subjects were detected, which could be due to localization differences or real interindividual differences. Since dipolar splitting affects metabolite intensities, it is important to take this effect into account when calculating metabolite concentrations from MR spectra in muscle tissue. Spatial maps of the MR signals of trimethyl‐ammonium groups and creatine/ phosphocreatine revealed significant differences in intensity between muscles. Magn Reson Med 49:424–432, 2003. © 2003 Wiley‐Liss, Inc.
Precursors and pathogenesis of ovarian carcinoma

Summary The ultimate goal of defining cancer specific precursors is to facilitate early detection and intervention before the development of invasive malignancy. Unlike other malignancies involving the female genital tract such as cervical or endometrial carcinomas, precursor lesions of ovarian carcinomas have not been well characterised, resulting in a failure to develop effective screening programs. Recent clinicopathological and molecular studies have provided new insight into the origin and pathogenesis of ovarian carcinomas. It has been shown that ovarian cancer is comprised of different tumour types differing not only in morphology, but also in pathogenesis, molecular alterations and clinical progression. A dualistic model of ovarian carcinogenesis has been proposed. Type I tumours which include low grade serous, low grade endometrioid, clear cell, mucinous carcinomas and Brenner tumours, are generally indolent and tend to be genetically stable, although clear cell carcinoma would probably belong to an intermediate category. They demonstrate a step-wise progression from a benign precursor such as a benign to borderline tumour or endometriosis and are characterised by genetic aberrations targeting specific cell signalling pathways. Type II tumours comprise high grade serous, high grade endometrioid, and undifferentiated carcinomas as well as malignant mixed mesodermal tumours. They are clinically aggressive and exhibit high genetic instability with frequent p53 mutations. Mounting evidence suggests that many high grade serous carcinomas originate from the epithelium of the distal fallopian tube, and that serous tubal intraepithelial carcinoma (STIC) represents the putative precursor of these neoplasms. Low grade serous carcinomas arise via transformation of benign and borderline serous tumours, thought to be derived from inclusion cysts originating from the ovarian surface or tubal epithelium. Recently it has been suggested that papillary tubal hyperplasia may be a putative precursor lesion for serous borderline tumours. Both endometrioid and clear cell carcinomas develop from endometriosis, via alterations affecting different genetic pathways. The origin of mucinous and transitional cell neoplasms is not well characterised, although new data suggest a possible origin from transitional cell nests present at the tubal-mesothelial junction. Likewise, the pathogenesis of carcinosarcomas is also not well established because of their rarity but there is accumulating evidence that the carcinomatous component determines the course of the disease and gives rise to the malignant mesenchymal component. This review discusses recent developments in the pathogenesis of ovarian carcinoma, with particular emphasis on the putative precursor lesions that give rise to the major histological subtypes. Recognition of these lesions is not only important in improving the understanding of ovarian carcinogenesis, but it will also influence our approach to prevent, detect and treat these tumours.
Involvement of SIRT7 in resumption of rDNA transcription at the exit from mitosis

Sirtuins, also designated class III histone deacetylases, are implicated in the regulation of cell division, apoptosis, DNA damage repair, genomic silencing and longevity. The nucleolar Sirtuin7 (SIRT7) was reported to be involved in the regulation of ribosomal gene (rDNA) transcription, but there are no data concerning the regulation of SIRT7 during the cell cycle. Here we have analyzed the behavior of endogenous SIRT7 during mitosis, while rDNA transcription is repressed. SIRT7 remains associated with nucleolar organizer regions, as does the RNA polymerase I machinery. SIRT7 directly interacts with the rDNA transcription factor UBF. Moreover, SIRT7 is phosphorylated via the CDK1-cyclin B pathway during mitosis and dephosphorylated by a phosphatase sensitive to okadaic acid at the exit from mitosis before onset of rDNA transcription. Interestingly, dephosphorylation events induce a conformational modification of the carboxy-terminal region of SIRT7 before the release of mitotic repression of rDNA transcription. As SIRT7 activity is required to resume rDNA transcription in telophase, we propose that this conformational modification regulates onset of rDNA transcription.