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Coughing is a dynamic physiological process resulting from input of vagal sensory neurons innervating the airways and perceived airway irritation. Although cough serves to protect and clear the airways, it can also be exploited by respiratory pathogens to facilitate disease transmission. Microbial components or infection-induced inflammatory mediators can directly interact with sensory nerve receptors to induce a cough response. Analysis of cough-generated aerosols and transmission studies have further demonstrated how infectious disease is spread through coughing. This review summarizes the neurophysiology of cough, cough induction by respiratory pathogens and inflammation, and cough-mediated disease transmission. Expected final online publication date for the

Background Cobalamin deficiency is a common disorder associated with numerous neuropsychiatric presentations. Prior literature addresses the neurocognitive and affective symptoms, which include psychotic presentations. We present the first reported case of an individual with isolated auditory and visual hallucinations in the absence of other neurocognitive, mood, or psychotic symptoms. Case Report Mr. C, a 74-year-old male with a psychiatric history of PTSD (in remission), presented to the emergency department with one month of gait instability, frequent urinary incontinence while sleeping, and near-daily auditory and visual hallucinations. Given hallucinations, psychiatry was consulted. Mr. C had no other active psychiatric symptoms at time of interview and demonstrated a high degree of insight about his hallucinations. There were no cognitive deficits, delusions, or confusion discernible on exam. Medical work-up was remarkable for vitamin B12 of 148 pg/mL (normal 200-900 pg/mL) and increased red cell distribution width of 17% (normal 11.5-14.5%) with normal folate. Cobalamin was replenished with a 1000 mcg injection of cyanocobalamin and daily oral supplementation (100 mcg). He experienced complete resolution of hallucinations over five days. Discussion Our case demonstrates that hallucinations can be a presenting symptom of cobalamin deficiency without other neurocognitive, psychotic, or mood symptoms. We will review the literature on psychosis and cobalamin deficiency, discuss the neurobiological explanations for neuropsychiatric effects of cobalamin deficiency, and provide diagnostic and treatment recommendations. Conclusion Consultation-liaison psychiatrists should be aware of isolated auditory and visual hallucinations as a presentation of cobalamin deficiency since prompt treatment can lead to rapid resolution of symptoms.

In this report, we describe the first kidney retransplantation performed after anti-programmed cell death-1 (PD-1)-related allograft rejection. In 2014, we administered pembrolizumab (anti-PD-1) for ~9 months to a 57-year-old kidney transplant recipient with metastatic cutaneous squamous cell carcinoma (CSCC). The patient experienced both a complete anti-tumor response and T cell-mediated allograft rejection requiring reinitiation of hemodialysis. Four-and-a-half years after initiating pembrolizumab, the patient remained without evidence of CSCC relapse and received a kidney transplant from a living unrelated donor. Ten-and-a-half months after kidney retransplantation, the allograft is functioning well and the patient’s CSCC remains in remission. This case illustrates the potential for PD-1 blockade to bring about durable immune-mediated tumor control in chronically-immunosuppressed patients, and begins to address the feasibility of kidney retransplantation in patients who have previously received immune checkpoint inhibitor therapy for cancer. Results from this and future cases may help elucidate mechanisms of anti-tumor immunity and allograft tolerance, and inform updates to transplant decision models. Our report also underscores the need for clinical trials testing novel immunotherapy combinations in solid organ transplant recipients designed to uncouple anti-tumor and anti-allograft immunity.

Background: From September 2014, a tertiary care hospital in Karachi, Pakistan, started diagnosing 3–5 cases/month of a yeast locally identified as Saccharomyces spp. resistant to fluconazole. US Centers for Disease Control and Prevention identified the isolates as Candida auris. The Pakistan Field Epidemiology and Laboratory Training Program (FELTP) and the hospital investigated the outbreak from April 2015 to January 2016. Objective: The aim of the outbreak investigation was to determine the risk factors and to inform measures to limit the spread of the organism in the hospital. Methods: Medical records, nursing schedules and infection control practices were reviewed. Sixty-two age- and sex-matched hospital controls from the same wards were identified. Results: Thirty cases (17 males) were identified (mean age = 51.6 years, age range = 2–91 years), case fatality was 53%. Multivariate logistic regression showed that a history of surgery within 90 days of diagnosis, admission to the emergency department and history of chronic kidney disease were significantly associated with C. auris infection. Discussion: This is the report of the outbreak investigation that triggered a global exploration of C. auris as a newly identified multidrug-resistant nosocomial organism, spreading within the hospital, especially among patients with invasive procedures. Unfortunately, we could not identify any specific source of the outbreak nor stop the transmission of the organism.

Nowadays, the rapid enhancement in the field of Computer Sciences, especially the emerging technology like Augmented Reality (AR)which turns the direction toward itself, but at the same time it gains attention of world researchers regarding critical challenges appear in multiple situations. Augmented totally out of the box of virtual reality, basically it creates a platform where digital information and reality collaborate with same platform, where super imposed imaginary objects turn up in the real-world environment. In this repaper, we investigate the vast history, challenges arise in different environment, crucial mechanism & approaches for the development, application, status, and future of AR in upcoming couple of years.

Heterologous vaccine regimens could extend waning protection in the global population immunized with Mycobacterium bovis Bacille Calmette-Guerin (BCG). We demonstrate that pulmonary delivery of peptide nanofibers (PNFs) bearing an Ag85B CD4

Tuberculosis (TB) caused by infection with Mycobacterium tuberculosis is characterized by inflammatory pathology and poorly understood mechanisms of innate immunity. Pattern recognition receptors, expressed on the surface of macrophages, determine the balance of inflammatory and antimicrobial functions that influence disease outcome. Carbohydrate moieties displayed by mycobacteria can serve as pattern recognition receptor ligands for some members of the C-type lectin receptor (CLR) family, interactions that mediate a variety of incompletely understood immune outcomes. This work identifies a novel role for the CLR macrophage galactose-type lectin (MGL)-1 in a mouse model (C57BL/6 and MGL-1−/−) of experimental TB. Murine macrophages upregulated MGL-1 following in vitro exposure to M. tuberculosis, whereas MGL+ cells accumulated at sites of mycobacteria-driven inflammation in the lung. Pulmonary macrophages from MGL-1–deficient mice displayed increased production of proinflammatory cytokines (IL-1β, IL-6, and IFN-γ) that were associated with greater lipid accumulation, following M. tuberculosis infection. Surprisingly, for a CLR, we also observed MGL-1–dependent antimycobacterial activity as evidenced by greater M. tuberculosis proliferation in bone marrow–derived macrophages, and the lung, of MGL-1–deficient mice. Differential transcriptome analysis further revealed that loss of MGL-1 perturbs the activation of various genes involved in the regulation of inflammation and lipid metabolism in the setting of M. tuberculosis infection. These results identify MGL-1 signaling as an important mechanism that regulates innate immunity against M. tuberculosis and indicates the potential for the MGL pathway as a novel therapeutic target for anti-TB immunity.

Background: The evolution of shell structure around doubly-magic exotic nuclei is of great interest in nuclear physics and astrophysics. In the `south-west' region of $^{78}$Ni, the development of deformation might trigger a major shift in our understanding of explosive nucleosynthesis. To this end, new spectroscopic information on key close-lying nuclei is very valuable. Purpose: We intend to measure the isomeric and $\beta$ decay of $^{75}$Co, with one proton- and two neutron-holes relative to $^{78}$Ni, to access new nuclear structure information in $^{75}$Co and its $\beta$-decay daughters $^{75}$Ni and $^{74}$Ni. Methods: The nucleus $^{75}$Co is produced in relativistic in-flight fission reactions of $^{238}$U at the Radioactive Ion Beam Factory (RIBF) in the RIKEN Nishina Center. Its isomeric and $\beta$ decay are studied exploiting the BigRIPS and EURICA setups. Results: We obtain partial $\beta$-decay spectra for $^{75}$Ni and $^{74}$Ni, and report a new isomeric transition in $^{75}$Co. The energy ($E_{\gamma}=1914(2)$ keV) and half-life ($t_{1/2}=13(6)$ $\mu$s) of the delayed $\gamma$ ray lend support for the existence of a $J^{\pi}=(1/2^-)$ isomeric state at 1914(2) keV. A comparison with PFSDG-U shell-model calculations provides good account for the observed states in $^{75}$Ni, but the first calculated $1/2^-$ level in $^{75}$Co, a prolate $K=1/2$ state, is predicted about 1 MeV below the observed $(1/2^-)$ level. Conclusions: The spherical-like structure of the lowest-lying excited states in $^{75}$Ni is proved. In the case of $^{75}$Co, the results suggest that the dominance of the spherical configurations over the deformed ones might be stronger than expected below $^{78}$Ni. Further experimental efforts to discern the nature of the $J^{\pi}=(1/2^-)$ isomer are necessary.

Humanized mice have become an important workhorse model for HIV research. Advances that enabled development of a human immune system in immune deficient mouse strains have aided new basic research in HIV pathogenesis and immune dysfunction. The small animal features facilitate development of clinical interventions that are difficult to study in clinical cohorts, and avoid the high cost and regulatory burdens of using non-human primates. The model also overcomes the host restriction of HIV for human immune cells which limits discovery and translational research related to important co-infections of people living with HIV. In this review we emphasize recent advances in modeling bacterial and viral co-infections in the setting of HIV in humanized mice, especially neurological disease, and Mycobacterium tuberculosis and HIV co-infections. Applications of current and future co-infection models to address important clinical and research questions are further discussed.

Nowadays, security in network environment is becoming a challenging problem, providing prevention of confidential records arises as a critical task. Modern creation in network can reduce the rate of uncertainty as-well-as at the same time growth of threats increases rapidly in past few decades i.e. vulnerabilities, and potential risks. Confidentiality of crucial informationis one of the main objectives, to protect integrity when its traveling from one node to another, ensure it can’t divulge by malicious insider, anonymous, trust, and malicious attacks.In this research paper, the proposed solution is to design interface where communication can be done in a secure manner, behind it has a mechanism which hide essential information, symmetric key cryptographic algorithm named advance encryption standard (AES) using python with additional library called pycrypto and tries to formulate algorithm efficiency, accuracy, execution time plus system capability.

The $\ensuremath{\beta}$ decays of $^{103,104m}\mathrm{Nb}$ were studied with the Summing NaI(Tl) (SuN) detector at the National Superconducting Cyclotron Laboratory. The $\ensuremath{\beta}$-decay feeding intensity distribution ${I}_{\ensuremath{\beta}}(E)$ for each isotope was extracted by measuring $\ensuremath{\gamma}$ rays in coincidence with an emitted electron. The ${I}_{\ensuremath{\beta}}(E)$ was extracted via the total absorption spectroscopy technique. The ${I}_{\ensuremath{\beta}}(E)$ for each nucleus was compared to predictions made by the quasiparticle random-phase approximation (QRPA) model which is commonly used to calculate $\ensuremath{\beta}$-decay properties for astrophysical applications. The main goal was to provide experimental data for neutron-rich nuclei, relevant to the astrophysical $r$ process. In addition, the extracted $\ensuremath{\beta}$-decay feeding intensity distributions can lead to a better understanding of nuclear structure in a region of rapid structure changes around $A=100$. Finally, experimental data for $^{104m}\mathrm{Nb}$ are also of interest to antineutrino studies of nuclear reactors.

The $\ensuremath{\beta}$ decay of $^{101,102}\mathrm{Zr}$ and $^{109}\mathrm{Tc}$ was studied using the technique of total absorption spectroscopy. The experiment was performed at the National Superconducting Cyclotron Laboratory using the Summing NaI(Tl) (SuN) detector in the first-ever application of total absorption spectroscopy with a fast beam produced via projectile fragmentation. The $\ensuremath{\beta}$-decay feeding intensity and Gamow-Teller transition strength distributions were extracted for these three decays. The extracted distributions were compared to three different quasiparticle random-phase approximation (QRPA) models based on different mean-field potentials. A comparison with calculations from one of the QRPA models was performed to learn about the ground-state shape of the parent nucleus. For $^{101}\mathrm{Zr}$ and $^{102}\mathrm{Zr}$, calculations assuming a pure shape configuration (oblate or prolate) were not able to reproduce the extracted distributions. These results may indicate that some type of mixture between oblate and prolate shapes is necessary to reproduce the extracted distributions. For $^{109}\mathrm{Tc}$, a comparison of the extracted distributions with QRPA calculations suggests a dominant oblate configuration. The other two QRPA models are commonly used to provide $\ensuremath{\beta}$-decay properties in $r$-process network calculations. This work shows the importance of making comparisons between the experimental and theoretical $\ensuremath{\beta}$-decay distributions, rather than just half-lives and $\ensuremath{\beta}$-delayed neutron emission probabilities, as close to the $r$-process path as possible.

6 pags., 4 figs., 2 tabs., The change of the shell structure in atomic nuclei, so-called “nuclear shell evolution”, occurs due to changes of major configurations through particle-hole excitations inside one nucleus, as well as due to variation of the number of constituent protons or neutrons. We have investigated how the shell evolution affects Gamow-Teller (GT) transitions that dominate the β decay in the region below 132Sn using the newly obtained experimental data on a long-lived isomer in 127Ag. The T1/2=67.5(9) ms isomer has been identified with a spin and parity of (27/2+) at an excitation energy of 1942−20+14 keV, and found to decay via an internal transition of an E3 character, which competes with the dominant β-decay branches towards the high-spin states in 127Cd. The underlying mechanism of a strong GT transition from the 127Ag isomer is discussed in terms of configuration-dependent optimization of the effective single-particle energies in the framework of a shell-model approach., Part of the WAS3ABi was supported by the Rare Isotope Science Project which is funded by MSIP and NRF of Korea. This work was supported by the Priority Centers Research Program in Korea (2009-0093817), OTKA contract number K100835, the U.S. DOE, Office of Nuclear Physics (Contract No. DE-AC02-06CH11357), NRF2016R1A5A1013277 and NRF-2013M7A1A1075764, the Spanish Ministerio de Economía y Competitividad under contract FPA2017- 84756-C4-2-P, the European Commission through the Marie Curie Actions call FP7-PEOPLE-2011-IEF (Contract No. 300096), German BMBF under Contract No: 05P12PKFNE, JSPS KAKENHI Grant No. 24740188 and 25247045, the National Natural Science Foundation of China (Nos. 11505302, 11575112, 11775316), the National Key Program for S&T Research and Development (No. 2016YFA0400501), and STFC (UK).

Physics letters / B 816, 136183 (2021). doi:10.1016/j.physletb.2021.136183, Published by North-Holland Publ., Amsterdam

The interpretation of observations of cooling neutron star crusts in quasipersistent x-ray transients is affected by predictions of the strength of neutrino cooling via crust Urca processes. The strength of crust Urca neutrino cooling depends sensitively on the electron-capture and $\ensuremath{\beta}$-decay ground-state-to-ground-state transition strengths of neutron-rich rare isotopes. Nuclei with a mass number of $A=61$ are predicted to be among the most abundant in accreted crusts, and the last remaining experimentally undetermined ground-state-to-ground-state transition strength was the $\ensuremath{\beta}$ decay of $^{61}\mathrm{V}$. This Letter reports the first experimental determination of this transition strength, a ground-state branching of ${8.1}_{\ensuremath{-}3.1}^{+4.0}%$, corresponding to a log $ft$ value of ${5.5}_{\ensuremath{-}0.2}^{+0.2}$. This result was achieved through the measurement of the $\ensuremath{\beta}$-delayed $\ensuremath{\gamma}$ rays using the total absorption spectrometer SuN and the measurement of the $\ensuremath{\beta}$-delayed neutron branch using the neutron long counter system NERO at the National Superconducting Cyclotron Laboratory at Michigan State University. This method helps to mitigate the impact of the pandemonium effect in extremely neutron-rich nuclei on experimental results. The result implies that $A=61$ nuclei do not provide the strongest cooling in accreted neutron star crusts as expected by some predictions, but that their cooling is still larger compared to most other mass numbers. Only nuclei with mass numbers 31, 33, and 55 are predicted to be cooling more strongly. However, the theoretical predictions for the transition strengths of these nuclei are not consistently accurate enough to draw conclusions on crust cooling. With the experimental approach developed in this work, all relevant transitions are within reach to be studied in the future.

Mycobacterium tuberculosis (Mtb) and Human Immunodeficiency virus (HIV) are important causes of death in infected patients worldwide, and act synergistically to worsen disease in those with co-infection. C-type lectin receptors (CLRs) are an important component of innate immunity that can recognize and respond to pathogen-associated signals. The macrophage galactose-type lectin (MGL, CLEC10) has been described as an immunomodulatory CLR associated with M2 macrophages and regulation of inflammation following infection. Our lab previously identified an important antibacterial role of murine MGL-1 in host immunity to Mtb. More recently we observed that human peripheral blood mononuclear cell-derived macrophages, and THP-1 cells, upregulated MGL following in vitro exposure to Mtb, Mycobacterium bovis BCG, and TLR2 agonists. Silencing of MGL in primary human macrophages permitted greater intracellular Mtb replication. Interestingly, we observed that MGL is suppressed by HIV in differential transcriptome analysis of lung from HIV-infected humanized mice, in lung and spleen of autopsy specimens from HIV-infected decedents, and upon in vitro infection of human macrophages. Using a recombinant human MGL/Fc chimeric molecule we observed that Mtb, and not HIV, directly bound MGL. MGL surface expression was reduced in lung of mice with chronic HIV infection compared to those with Mtb, and variable in co-infected animals. These results indicate that human MGL is an important CLR for pathogen recognition and initiation of protective immunity by host macrophages to Mtb. The suppression of MGL due to HIV may increase susceptibility to Mtb in people with HIV or exacerbate disease progression in those with co-infection. Supported by grants from NIH (R33 AI138328, R61 AI138328, U24 MH100930)

Mycobacterium tuberculosis (Mtb), the causative agent of tuberculosis (TB), is responsible for approximately 10 million new infections and 1.5 million deaths each year. Pattern recognition receptors (PRRs) expressed on the surface of macrophages play an important role in orchestrating the immune response to pathogens. Amongst these, the C-type lectin receptors (CLRs) are an important PRR system that is increasingly understood to mediate innate immunity to mycobacteria. We recently described a new anti-bacterial and anti-inflammatory role for the macrophage galactose-type lectin-1 (MGL-1) in a murine model of experimental TB. MGL is a type II CLR that is known to recognize galactose and N-acetylgalactosamine monosaccharides. We observed that exposure to Mtb activated expression of both murine MGL orthologues, MGL-1 and MGL-2. The specific pathogen-associated molecular patterns that activate MGL orthologue transcription, however, have yet to be determined. Here we demonstrate that expression of MGL-1 and MGL-2 are differentially regulated by cytokines, TLR agonists, and mycobacterial ligands. MGL-1 expression is activated by dexamethasone, IL-4, IL-10, and the mycobacterial cell wall glycolipid Trehalose 6,6′-dimycolate. In contrast, MGL-2 expression is activated by TLR2/6 and TLR2/1 agonists and total lipid extracts of mycobacteria. Use of a MyD88 inhibitor further showed that molecular regulation of MGL-1 and MGL-2 transcription, following exposure of macrophages to mycobacteria, is TLR pathway-dependent. These results identify overlapping and unique host immune pathways that differentially activate MGL orthologues following exposure to Mtb and could be targeted through immune modulation.

The study of HIV infection and pathogenicity in physical reservoirs requires a biologically relevant model which resembles the human immune system and physiology. The human immune system (HIS) mouse is well established as a model of HIV, but defects in immune tissue reconstitution remain a challenge for examining pathology in tissues. Herein we show that exogenous injection of the human cytokine FLT-3L into the HSC cord blood HIS mouse model significantly expanded the total area of axial lymph nodes and the circulating percentage of human T cells, thus enabling us to visualize and quantify HIV infectivity in the secondary lymphoid tissues of the spleen and axial node. Further, we detected cell death and T cell depletion in tissues, consistent with HIV pathogenesis. Treatment with the caspase-1 inhibitor VX-765 significantly decreased viral load as measured by gag qPCR, and apoptosis as measured by TUNEL assay, in the spleen. A significant restoration of CD4+ T cells in the spleen due to VX-765 treatment was observed via flow cytometry. In situ hybridization further demonstrated a significant decrease in viral RNA in both the spleen and axial lymph nodes. Transcriptomic analysis further revealed an upregulation in host HIV restriction factors such as APOBR, SAMHD1 and APOBEC3A as a result of VX-765 administration. These findings demonstrate FLT-3L as a mechanism whereby the human immune environment in HIS mice can be enhanced to support investigations of HIV pathogenesis and immune outcomes in tissue compartments. Preliminary results indicate that targeting inflammasome pathways with VX-765 in HIS mice treated with FLT-3L, and infected with HIV, preserved T cell populations and decreased viral load. Supported by R01 A1HL129881, NIH/NHLBI

Pattern recognition receptors, such as the C-type lectin receptor (CLR) family, play an important role in the generation of the innate immune response against a variety of pathogens. The CLR Macrophage galactose-type lectin (MGL), also known as CLEC10, is one member of this family which we and others found can bind SARS-CoV-2. MGL is known to increase in expression during SARS-CoV-2 infection and, in concert with other CLRs, is associated with elevated proinflammatory immune responses. Dexamethasone, a clinical treatment commonly used to mitigate the hyperinflammatory response in individuals with COVID-19, is also a positive stimulus for MGL expression. We therefore sought to investigate the role of MGL in disease pathogenesis using MGL-1 receptor deficient mice. Mice were intranasally infected with mouse adapted SARS-CoV-2 strain CMA3p20 and euthanized 3- or 7-days post infection. Following acute infection at 3 days, MGL-1 deficiency did not affect the viral burden in the lungs of mice. This was supported by multiplex cytokine and chemokine data which revealed similar acute inflammatory responses in the lung of infected WT and MGL-1 knockout (KO) mice. Interestingly, MGL-1 KO mice did display a significant increase in the lung viral burden when compared to WT mice 7 days post-infection. These results suggest a role for MGL-1 in resolution of SARS-CoV-2 at later stages of infection. Further investigations to determine differences in cellular recruitment and lung pathology in the absence of MGL-1 are warranted. In addition, assessment of a role for the MGL-2 orthologue expressed by murine myeloid cells may identify roles for MGL pathways in SARS-CoV-2 disease severity and pathogenesis. Supported by UTMB Institute for Human Infection and Immunity COVID-19 Pilot Grant

The $\ensuremath{\gamma}$ process is an explosive astrophysical scenario, which is thought to be the primary source of the rare proton-rich stable $p$ nuclei. However, current $\ensuremath{\gamma}$-process models remain insufficient in describing the observed $p$-nuclei abundances, with disagreements up to two orders of magnitude. A sensitivity study has identified ${}^{111}\mathrm{In}$ as a model-sensitive $(\ensuremath{\gamma},p)/(\ensuremath{\gamma},n)$ branching point within the $\ensuremath{\gamma}$ process. Constraining the involved reaction rates may have a significant impact on the predicted $p$-nuclei abundances. Here we report on measurements of the cross sections for $^{102}\mathrm{Pd}(p,\ensuremath{\gamma})\phantom{\rule{0.16em}{0ex}}^{103}\mathrm{Ag},\phantom{\rule{0.28em}{0ex}}^{108}\mathrm{Cd}(p,\ensuremath{\gamma})\phantom{\rule{0.16em}{0ex}}^{109}\mathrm{In}$, and $^{110}\mathrm{Cd}(p,\ensuremath{\gamma})\phantom{\rule{0.16em}{0ex}}^{111}\mathrm{In}$ reactions for proton laboratory energies 3--8 MeV using the high efficiency total absorption spectrometer and the $\ensuremath{\gamma}$-summing technique. These measurements were used to constrain Hauser-Feshbach parameters used in talys 1.9, which constrains the $^{111}\mathrm{In}(\ensuremath{\gamma},p)\phantom{\rule{0.16em}{0ex}}^{110}\mathrm{Cd}$ and $^{111}\mathrm{In}(\ensuremath{\gamma},n)\phantom{\rule{0.16em}{0ex}}^{110}\mathrm{Ag}$ reaction rates. The newly constrained reaction rates indicate that the $^{111}\mathrm{In}\phantom{\rule{4pt}{0ex}}(\ensuremath{\gamma},p)/(\ensuremath{\gamma},n)$ branching point occurs at a temperature of $2.71\ifmmode\pm\else\textpm\fi{}0.05\phantom{\rule{0.28em}{0ex}}\mathrm{GK}$, well within the temperature range relevant to the $\ensuremath{\gamma}$ process. These findings differ significantly from previous studies and may impact the calculated abundances.

Background: Little data is available for the pygmy dipole resonance (PDR) in axially deformed nuclei. Photon-scattering experiments are complicated by high level densities in the PDR region and the small energy difference of transitions to the ground state and to excited states.Purpose: We report on an experimental study of the low-energy dipole strength distribution of the well-deformed nucleus $^{164}\mathrm{Dy}$ between 4.0--7.7 MeV.Methods: The low-lying photoresponse of $^{164}\mathrm{Dy}$ has been investigated using the method of nuclear resonance fluorescence using a quasimonochromatic linearly polarized $\ensuremath{\gamma}$-ray beam in the energy range of 4.0--7.7 MeV in steps of 0.2 MeV.Results: For excitation energies between 4 MeV and 5 MeV, sufficiently low level densities allow for the identification of individual states, including level energies, reduced transition widths and branching ratios. Energy-averaged mean decay branching ratios, mean population ratios and partial absorption cross sections were determined above 5 MeV up to the neutron-separation threshold at 7.7 MeV. A Lorentzian-shaped enhancement of the partial photo absorption cross section followed by decays back to the ground-state band is found at 6.10(5) MeV with a width of 0.77(23) MeV. A comparison with results from complementary measurements is performed using the framework of the statistical model.Conclusions: The experimental results for the mean population ratios deviate systematically from the statistical model simulation by 30(6)%. However, they are in agreement within one standard deviation of the simulation.

The size of a $\mathrm{\ensuremath{\Delta}}K=0$ $M1$ excitation strength has been determined for the first time in a predominantly axially deformed even-even nucleus. It has been obtained from the observation of a rare $K$-mixing situation between two close-lying ${J}^{\ensuremath{\pi}}={1}^{+}$ states of the nucleus $^{164}\mathrm{Dy}$ with components characterized by intrinsic projection quantum numbers $K=0$ and $K=1$. Nuclear resonance fluorescence induced by quasimonochromatic linearly polarized $\ensuremath{\gamma}$-ray beams provided evidence for $K$ mixing of the ${1}^{+}$ states at 3159.1(3) and 3173.6(3) keV in excitation energy from their $\ensuremath{\gamma}$-decay branching ratios into the ground-state band. The $\mathrm{\ensuremath{\Delta}}K=0$ transition strength of $B(M1;{0}_{1}^{+}\ensuremath{\rightarrow}{1}_{K=0}^{+})=0.008(1){\ensuremath{\mu}}_{N}^{2}$ was inferred from a mixing analysis of their $M1$ transition rates into the ground-state band. It is in agreement with predictions from the quasiparticle phonon nuclear model. This determination represents first experimental information on the $M1$ excitation strength of a nuclear quantum state with a negative $\mathcal{R}$-symmetry quantum number.

HIV-positive donor to HIV-positive recipient (HIV D+/R+) transplantation is permitted in the United States under the HIV Organ Policy Equity Act. To explore safety and the risk attributable to an HIV+ donor, we performed a prospective multicenter pilot study comparing HIV D+/R+ vs HIV-negative donor to HIV+ recipient (HIV D-/R+) kidney transplantation (KT). From 3/2016 to 7/2019 at 14 centers, there were 75 HIV+ KTs: 25 D+ and 50 D- (22 recipients from D- with false positive HIV tests). Median follow-up was 1.7 years. There were no deaths nor differences in 1-year graft survival (91% D+ vs 92% D-, P = .9), 1-year mean estimated glomerular filtration rate (63 mL/min D+ vs 57 mL/min D-, P = .31), HIV breakthrough (4% D+ vs 6% D-, P > .99), infectious hospitalizations (28% vs 26%, P = .85), or opportunistic infections (16% vs 12%, P = .72). One-year rejection was higher for D+ recipients (50% vs 29%, HR: 1.83, 95% CI 0.84-3.95, P = .13) but did not reach statistical significance; rejection was lower with lymphocyte-depleting induction (21% vs 44%, HR: 0.33, 95% CI 0.21-0.87, P = .03). In this multicenter pilot study directly comparing HIV D+/R+ with HIV D-/R+ KT, overall transplant and HIV outcomes were excellent; a trend toward higher rejection with D+ raises concerns that merit further investigation.

C-type lectin receptors (CLRs) are carbohydrate binding pattern recognition receptors (PRRs) which play a central role in host recognition of pathogenic microorganisms. Signaling through CLRs displayed on antigen presenting cells dictates important innate and adaptive immune responses. Several pathogens have evolved mechanisms to exploit the receptors or signaling pathways of the CLR system to gain entry or propagate in host cells. CLR responses to high priority pathogens such as Mycobacterium tuberculosis (Mtb), HIV, Ebola, and others are described and considered potential avenues for therapeutic intervention. Mtb and HIV are the leading causes of death due to infectious disease and have a synergistic relationship that further promotes aggressive disease in co-infected persons. Immune recognition through CLRs and other PRRs are important determinants of disease outcomes for both TB and HIV. Investigations of CLR responses to Mtb and HIV, to date, have primarily focused on single infection outcomes and do not account for the potential effects of co-infection. This review will focus on CLRs recognition of Mtb and HIV motifs. We will describe their respective roles in protective immunity and immune evasion or exploitation, as well as their potential as genetic determinants of disease susceptibility, and as avenues for development of therapeutic interventions. The potential convergence of CLR-driven responses of the innate and adaptive immune systems in the setting of Mtb and HIV co-infection will further be discussed relevant to disease pathogenesis and development of clinical interventions.