Search

La mentalidad porteña del siglo XIX da cuenta de cierta actitud desprejuiciada y, por ello, más liberal y pragmática, que habría incentivado la apertura hacia la modernidad en un área urbana ya cosmopolita, y donde la tradición desempeñó, por tanto, un papel secundario respecto de lo que iba ocurriendo en otras ciudades del medio nacional. /The mentality of the nineteenth century in Valparaíso realizes some unprejudiced attitude and, therefore, more liberal and pragmatic, which would have encouraged the opening to modernity and a cosmopolitan urban area, where tradition and therefore plays a secondary role of what was happening in other cities of the national average.

Purpose: To investigate the effect of different FSH concentrations on human oocyte maturation in vitro and its impact on gene expression of key factors in the surrounding cumulus cells., Methods: The study included 32 patients who underwent unilateral oophorectomy for ovarian tissue cryopreservation (OTC) (aged 28 years on average). Immature oocytes were collected from surplus medulla tissue. A total of 587 immature oocytes were divided into three categories according to the size of the cumulus mass: large (L-COCs), small (S-COCs), and naked oocytes (NOs), and submitted to 44-h IVM with one of the following concentrations of recombinant FSH: 0 IU/L, 20 IU/L, 40 IU/L, 70 IU/L, or 250 IU/L. After IVM, oocyte nuclear maturation stage and diameter were recorded. The relative gene expression of FSHR, LHCGR, and CYP19A1 in cumulus cells before (day 0; D0) and after IVM were evaluated., Results: Addition of 70 or 250 IU/L FSH to the IVM medium improved oocyte nuclear maturation compared to 0, 20, and 40 IU/L FSH by upregulating LHCGR and downregulating FSHR in the cumulus cells., Conclusion: FSH improved oocyte nuclear maturation at concentrations above 70 IU/L suggesting a threshold for FSH during IVM of ex vivo collected human oocytes from small antral follicles. Moreover, current results for the first time highlight that FSH function in vitro is mediated via cumulus cells by downregulating FSHR and upregulating LHCGR, which was also observed when the immature oocytes progressed in meiosis from the GV to the MII stage.

Introduction: Rheumatoid meningitis (RM) is a rare complication of rheumatoid arthritis (RA) and has a high mortality rate. It can present as a first diagnosis of RA, in long-standing disease, or in active or well-controlled disease. Neurological manifestations vary widely., Case Report: A patient with a 30-year history of RA, well controlled with methotrexate therapy, presented with new-onset seizures. Magnetic resonance imaging showed leptomeningeal and pachymeningeal enhancement. A de novo workup resulted in diagnosis of RM., Conclusions: Cerebrospinal fluid findings for RM are nonspecific, typically lymphocytic pleocytosis; however, they can be neutrophilic, as in this case. Magnetic resonance imaging findings consist of leptomeningeal and pachymeningeal enhancement but can also involve the parenchyma. The diagnosis is typically confirmed with meningeal biopsy. Treatment involves high-dose corticosteroids or immunomodulatory therapy, or both. Long-term follow-up with radiologic surveillance typically ranges from improvement to resolution.

We report the intermittent burst of a super rogue wave in the multi-soliton (MS) regime of an anomalous-dispersion fiber ring cavity. We exploit the spatio-temporal measurement technique to log and capture the shot-to-shot wave dynamics of various pulse events in the cavity, and obtain the corresponding intensity probability density function, which eventually unveils the inherent nature of the extreme events encompassed therein. In the breathing MS regime, a specific MS regime with heavy soliton population, the natural probability of pulse interaction among solitons and dispersive waves exponentially increases owing to the extraordinarily high soliton population density. Combination of the probabilistically started soliton interactions and subsequently accompanying dispersive waves in their vicinity triggers an avalanche of extreme events with even higher intensities, culminating to a burst of a super rogue wave nearly ten times stronger than the average solitons observed in the cavity. Without any cavity modification or control, the process naturally and intermittently recurs within a time scale in the order of ten seconds.

We propose a fiber-optic-plasmonic hybrid device that is based on a corrugation-assisted metal-coated angled fiber facet (CA-MCAFF) for wavelength-dependent off-axis directional beaming (WODB). The device breaks into two key structures: One is the MCAFF structure, which is a modified Kretschmann configuration implemented onto a fiber platform, thereby being able to generate a unidirectional surface plasmon with dramatically enhanced properties in terms of non-confined diffracted radiation loss and operational bandwidth. The other is the periodic corrugation structure put on the MCAFF, thereby enabling WODB functionality out of the whole structures. The corrugated metal surface out-couples the surface plasmon mode to free-space optical radiation into a direction that varies with the wavelength of the optical radiation with excellent linearity. We perform extensive numerical investigations based on the finite-element-method and analyze the out-coupling efficiency (OCE out ) and spectral bandwidth (SB out ) of the proposed device for various designs and conditions. We determine the seven structural parameters of the device via taking sequential optimization steps. We deduce two optimal conditions particularly for the fiber-facet angle, in terms of the averaged OCE out or the SB out in the whole visible wavelength range (400 - 700 nm), which eventually leads to OCE out = 30.4% and SB out = 230 nm or to OCE out = 24.5% and SB out = 245 nm, respectively. These results suggest substantial enhancements in both OCE out and SB out , in comparison with the performance properties of a typical nano-slit-based device having a similar type of WODB functionality. The proposed CA-MCAFF is a simple, compact and efficient WODB device that is fully compatible with the state-of-the-art optical fiber technology.

We numerically investigate quasi-mode-locked (QML) multi-pulse dynamics in a fiber ring laser cavity in the anomalous dispersion regime. We show that the laser cavity can operate in five constitutively different QML regimes, depending on the saturation power of the saturable absorber element and the length of the passive fiber section that parameterize the overall nonlinearity and dispersion characteristic of the laser cavity. We classify them into the incoherent noise-like-pulse, partially-coherent noise-like-pulse, symbiotic, partially-coherent multi-soliton, and coherent multi-soliton regimes, accounting for their coherence and multi-pulse formation features. In particular, we numerically clarify and confirm the symbiotic regime for the first time to the best of our knowledge, in which noise-like pulses and multi-solitons coexist stably in the cavity that has recently been observed experimentally. Furthermore, we analyze the shot-to-shot coherence characteristics of the individual QML regimes relative to the amount of the nonlinear-phase shift per roundtrip, and verify a strong correlation between them. We also show that the net-cavity dispersion plays a critical role in determining the multi-pulse dynamics out of the partially-coherent noise-like-pulse, symbiotic, and partially-coherent multi-soliton regimes, when the cavity bears moderate nonlinearity. We quantify and visualize all those characteristics onto contour maps, which will be very useful and helpful in discussing and clarifying the complex QML dynamics.

Chronic intestinal inflammation accompanies familial adenomatous polyposis (FAP) and is a major risk factor for colorectal cancer in patients with this disease, but the cause of such inflammation is unknown. Because retinoic acid (RA) plays a critical role in maintaining immune homeostasis in the intestine, we hypothesized that altered RA metabolism contributes to inflammation and tumorigenesis in FAP. To assess this hypothesis, we analyzed RA metabolism in the intestines of patients with FAP as well as APC Min/+ mice, a model that recapitulates FAP in most respects. We also investigated the impact of intestinal RA repletion and depletion on tumorigenesis and inflammation in APC Min/+ mice. Tumors from both FAP patients and APC Min/+ mice displayed striking alterations in RA metabolism that resulted in reduced intestinal RA. APC Min/+ mice placed on a vitamin A-deficient diet exhibited further reductions in intestinal RA with concomitant increases in inflammation and tumor burden. Conversely, restoration of RA by pharmacologic blockade of the RA-catabolizing enzyme CYP26A1 attenuated inflammation and diminished tumor burden. To investigate the effect of RA deficiency on the gut immune system, we studied lamina propria dendritic cells (LPDC) because these cells play a central role in promoting tolerance. APC Min/+ LPDCs preferentially induced Th17 cells, but reverted to inducing Tregs following restoration of intestinal RA in vivo or direct treatment of LPDCs with RA in vitro These findings demonstrate the importance of intestinal RA deficiency in tumorigenesis and suggest that pharmacologic repletion of RA could reduce tumorigenesis in FAP patients. Cancer Immunol Res; 4(11); 917-26. ©2016 AACR., (©2016 American Association for Cancer Research.)

Interleukin (IL)-17 plays a key role in immunity. In acute infections, a rapid IL-17 response must be induced without prior antigen exposure, and γδ T cells are the major initial IL-17 producers. In fact, some γδ T cells make IL-17 within hours after an immune challenge. These cells appear to acquire the ability to respond to IL-1 and IL-23 and to make IL-17 naturally in naïve animals. They are known as the natural Tγδ17 (nTγδ17) cells. The rapidity of the nTγδ17 response, and the apparent lack of explicit T cell receptor (TCR) engagement for its induction have led to the view that this is a cytokine (IL-1, IL-23)-mediated response. However, pharmacological inhibition or genetic defects in TCR signaling drastically reduce the nTγδ17 response and/or their presence. To better understand antigen recognition in this rapid IL-17 response, we analyzed the antigen receptor repertoire of IL-1R(+)/IL-23R(+) γδ T cells, a proxy for nTγδ17 cells in naïve animals directly ex vivo, using a barcode-enabled high throughput single-cell TCR sequence analysis. We found that regardless of their anatomical origin, these cells have a highly focused TCR repertoire. In particular, the TCR sequences have limited V gene combinations, little or no junctional diversity and much reduced or no N region diversity. In contrast, IL-23R(-) cells at mucosal sites similar to most of the splenic γδ T cells and small intestine epithelial γδ lymphocytes expressed diverse TCRs. This remarkable commonality and restricted repertoire of IL-1R(+)/IL-23R(+) γδ T cells underscores the importance of antigen recognition in their establishment/function.

We propose a novel trench-assisted circular metal nano-slit (CMNS) structure implementable on a fiber platform for the generation of a low-noise cylindrical surface plasmon (CSP) hotspot. We design trench structures based on a multi-pole cancellation method in order that a converging surface plasmon signal is well separated from co-propagating non-confined diffracted light (NCDL) at the hotspot location. In fact, the secondary radiation by the quasi-pole oscillation at the edge of the trench cancels the primary NCDL, thereby enhancing the signal-to-noise ratio (SNR) of the CSP hotspot. In particular, we investigate two types of trench structures: a rectangular-trench (RT) structure and an asymmetric-parabolic-trench (APT) structure, which are considered for the sake of the simplicity of fabrication and of the maximal enhancement of the SNR, respectively. In comparison with a conventional CMNS having no trenches, we highlight that the mean SNR of the CSP hotspot is enhanced by 6.97 and 11.89 dB in case of the optimized RT and APT CMNSs, respectively. The proposed schemes are expected to be useful for increasing the SNR of plasmonic devices that are interfered by NCDL, such as various types of nano-slits for generating high-resolution plasmonic signals, for example.

We experimentally analyze the stimulated Raman scattering characteristics of a high-birefringence fiber (HBF), which presents an extraordinary level of spectral broadening incurred by the strong nonlinear interaction between the pump and Stokes pulses via the polarization-mode dispersion and group-velocity dispersion of the fiber. We also investigate the impact of the inter-pulse time-delay on the additional spectra broadening when dual-wavelength pump pulses are used. Exploiting these unique SRS properties of the HBF, we develop a novel Raman continuum source based on an all-fiber dual-wavelength master-oscillator power amplifier that can generate a dip-free spectrum in the 1200-1400-nm spectral range. We finally obtain a broadband continuum having an average power of ~840 mW and a 3-dB bandwidth of ~240 nm centered at 1200-1400 nm, which also represents a good spectral flatness and conversion efficiency. This type of source is very useful and important for optical coherence tomography applications, for example.

We propose a simple and efficient light launch scheme for a helical-core fiber (HCF) by using an adiabatically tapered splice technique, through which we overcome its inherent difficulty with light launch owing to the large lateral offset and angular tilt of its core. We experimentally demonstrate single-mode excitation in the HCF in this configuration, which yields the coupling efficiency of around -5.9 dB (26%) for a ~1.1-μm light input when the splice joint is tapered down to 30 μm in diameter. To our knowledge, this is the first proof-of-principle report on the fusion-splice coupling between an HCF and a conventional single-mode fiber.

In Parkinson's disease (PD), the consequence of dopaminergic denervation is an imbalance in the activity of the direct and indirect striatofugal pathways, which include potentially important changes in opioid peptide expression and/or activity. The systemic administration of a novel glycosylated opioid peptide MMP-2200 (a.k.a. lactomorphin) was shown to have potent effects in two standard models of PD: 1) amphetamine-induced rotations in the hemi-Parkinsonian 6-hydroxydopamine (6-OHDA)-treated rat and 2) locomotion in the reserpine-treated rat. MMP-2200, an opioid mu and delta receptor agonist, reduced amphetamine-induced rotations in severely-lesioned hemi-Parkinsonian rats; this effect was fully blocked by naloxone, an opioid receptor antagonist. The selective δ-opioid receptor antagonist naltrindole only partially blocked the effect of MMP-2200. MMP-2200 alone did not induce rotations. This effect was also observed in a mild progressive rat 6-OHDA-lesion model. In animals treated with reserpine, profound akinesia was induced that was reversed with apomorphine. There was a prominent overshoot in animals that received apomorphine compared to non-reserpine treated animals, reflecting the well described phenomenon of dopamine supersensitivity indicating that apomorphine not only reversed akinesia but also induced hyper-kinesia. The opioid peptide MMP-2200 blocked the apomorphine-induced hyper-kinesia. This effect of MMP-2200 was prevented by pre-administration of naloxone. MMP-2200 had no effect in preventing the reserpine-induced akinesia, nor did it affect locomotion in control animals. Taken together, the results from these two models are consistent with the glycopeptide opioid agonist MMP-2200 having a potent effect on movements related to dopaminergic hyper-stimulation following striatal dopamine depletion that are best explained by a reduction in the downstream effects of dopamine agonists in these models., (Copyright © 2011 Elsevier B.V. All rights reserved.)

We examined the involvement of chemokine-like receptor-1 (CMKLR1) in experimental autoimmune encephalomyelitis (EAE), a model of human multiple sclerosis. Upon EAE induction by active immunization with myelin oligodendrocyte glycoprotein amino acids 35-55 (MOG(35-55)), microglial cells and CNS-infiltrating myeloid dendritic cells expressed CMKLR1, as determined by flow cytometric analysis. In addition, chemerin, a natural ligand for CMKLR1, was up-regulated in the CNS of mice with EAE. We found that CMKLR1-deficient (CMKLR1 knockout (KO)) mice develop less severe clinical and histologic disease than their wild-type (WT) counterparts. CMKLR1 KO lymphocytes proliferate and produce proinflammatory cytokines in vitro, yet MOG(35-55)-reactive CMKLR1 KO lymphocytes are deficient in their ability to induce EAE by adoptive transfer to WT or CMKLR1 KO recipients. Moreover, CMKLR1 KO recipients fail to fully support EAE induction by transferred MOG-reactive WT lymphocytes. The results imply involvement of CMKLR1 in both the induction and effector phases of disease. We conclude that CMKLR1 participates in the inflammatory mechanisms of EAE and represents a potential therapeutic target in multiple sclerosis.

Post-menopausal osteoporosis is considered to be an inflammatory process, in which numerous pro-inflammatory and T-cell-derived cytokines play a bone-destructive role. IL-17A is the signature cytokine of the pro-inflammatory Th17 population and plays dichotomous roles in diseases that affect bone turnover. Although IL-17A promotes bone loss in rheumatoid arthritis, it is protective against pathogen-induced bone destruction in a periodontal disease model. We used a model of ovariectomy-induced osteoporosis (OVX) in IL-17 receptor (IL-17RA)(-/-) mice to evaluate the role of the IL-17A in bone loss caused by estrogen deficiency. Unexpectedly, IL-17RA(-/-) mice were consistently and markedly more susceptible to OVX-induced bone loss than controls. There were no changes in prototypical Th1, Th2 or Th17 cytokines in serum that could account for increased bone loss. However, IL-17RA(-/-) mice exhibited constitutively elevated leptin, which further increased following OVX. Consistently, IL-17A and IL-17F treatment of 3T3-L1 pre-adipocytes inhibited adipogenesis, leading to reduced production of leptin. In addition to its role in regulating metabolism and satiety, leptin can regulate bone turnover. Accordingly, these data show that IL-17A negatively regulates adipogenesis and subsequent leptin expression, which correlates with increased bone destruction during OVX.

Activation of the estrogen receptor-alpha (ERalpha) mediates the vasculoprotective effects of estrogen, in part, through modulating nitric oxide (NO) production and vasodilation. Whereas inflammation is accompanied by altered vascular reactivity and underlies the pathogenesis of vascular disease, the role of the ERalpha in the vascular responses associated with acute systemic inflammation remains poorly characterized. Contractile and relaxation responses of isolated aortic segments were investigated 12 h after ip injection of saline or lipopolysaccharide (LPS, 10 mg/kg) in male wild-type (ERalpha(+/+)) and ERalpha-deficient (ERalpha(-/-)) mice. As previously observed, LPS-injected ERalpha(+/+) mice displayed reduced contractile responses to phenylephrine and enhanced vasodilation in response to acetylcholine. In contrast, aortic tissues from LPS-injected ERalpha(-/-) mice displayed enhanced contractile responses and reduced sensitivity to acetylcholine- and sodium nitroprusside-induced vasodilation. LPS treatment in ERalpha(+/+) and ERalpha(-/-) mice resulted in similar increased levels of systemic NO production and inducible NO synthase expression in the vascular wall. However, expression of mRNA and protein for endothelial NOS and soluble guanylate cyclase (alpha- and beta-subunits) were significantly reduced in aortic tissues from LPS-treated ERalpha(-/-) animals, possibly accounting for reduced endothelial NO production and reduced smooth muscle responses to NO. These findings represent new evidence of the functional role of ERalpha in the male vasculature and suggest that during acute LPS-induced inflammatory responses, the ERalpha mediates the sustained expression of the molecular machinery essential for endothelial NO synthesis (i.e. endothelial NOS) and the vascular responses to NO (i.e. soluble guanylate cyclase).