Miracle-dz/UniFAR-FTUs huggingface dataset:
Analysis of Risk Factors and Surgical Results of Lumbar Adjacent Segment Disease

†‡ † ‡ Study Design: This is a retrospective study. Objectives: We analyzed the risk factors and the surgical results for adjacent segment disease after lumbar fusion. Summary of Literature Review: Many studies have been performed about the risk factors for adjacent segment disease, but the findings are still controversial. Materials and Methods: This study was carried out on 35 (13 men, 22 women) of 50 patients who underwent lumbar fusion due to adjacent segment disease with a minimum of 2 year follow-up period from July 1999 to July 2006. The differences of the interval to revision (IR) were statistically analyzed by the examining preexisting degenerative change in the adjacent segments on MRI, the number of fused segments, the lumbar lordosis and the sagittal balance. The surgical outcomes of reoperation were assessed by Brodsky’s criteria. Results: Junctional stenosis as adjacent segment disease was seen in 21 cases (60%) and instability was seen in 14 cases (40%), including 2 iatrogenic flat backs and 2 cases of lumbar degenerative kyphosis. The average IR was 93 months for the cases that had less than 2 segment fusion (20 cases) and 62 months in those with more than 3 segment fusion (15 cases). As for lumbar lordosis, 25 cases (71%) had a normal range of angle as well as 101 months until the IR and 10 cases (29%) had an abnormal range of angle as well as 64 months until IR. Six cases were beyond the normal range of sagittal balance (17%) and their average IR value was 59 months. Otherwise, the cases with a normal range of sagittal balance had 109 months for the IR. The clinical outcome was excellent in 6 cases (17%) and good in 15 cases (43%). Conclusion: To decrease the adjacent segment disease, we should seriously consider the extent of lumbar fusion and we should restore the angle in lumbar lordosis to the physiological range and the sagittal balance during the initial operation.
Identification of a Unique Hybrid Macrophage-Polarization State following Recovery from Lipopolysaccharide Tolerance

LPS tolerance is an essential immune-homeostatic response to repeated exposure to LPS that prevents excessive inflammatory responses. LPS tolerance induces a state of altered responsiveness in macrophages, resulting in repression of proinflammatory gene expression and increased expression of factors that mediate the resolution of inflammation. In this study, we analyzed the transcriptional plasticity of macrophages following LPS tolerance using genome-wide transcriptional profiling. We demonstrate that LPS tolerance is a transient state and that the expression of proinflammatory genes is restored to levels comparable to the acute response to LPS. However, following recovery from LPS tolerance a number of genes remained locked in a tolerizable state, including IL-33, CD86, IL-10, and NFIL3. Furthermore, we identified of a number of genes uniquely induced following recovery from LPS tolerance. Thus, macrophages adopt a unique transcriptional profile following recovery from LPS tolerance and have a distinct expression pattern of regulators of Ag presentation, antiviral responses, and transcription factors. Our data suggest that recovery from LPS tolerance leads to a hybrid macrophage activation state that is proinflammatory and microbicidal in nature but that possesses a regulatory anti-inflammatory profile distinct from that of LPS-tolerant and LPS-activated macrophages.
4-1BB Ligand Activates Bystander Dendritic Cells To Enhance Immunization in Trans

Expression of the costimulatory receptor 4-1BB is induced by TCR recognition of Ag, whereas 4-1BB ligand (4-1BBL) is highly expressed on activated APC. 4-1BB signaling is particularly important for survival of activated and memory CD8+ T cells. We wished to test whether coexpression of Ag and 4-1BBL by dendritic cells (DC) would be an effective vaccine strategy. Therefore, we constructed lentiviral vectors (LV) coexpressing 4-1BBL and influenza nucleoprotein (NP). Following s.c. immunization of mice, which targets DC, we found superior CD8+ T cell responses against NP and protection from influenza when 4-1BBL was expressed. However, functionally superior CD8+ T cell responses were obtained when two LV were coinjected: one expressing 4-1BBL and the other expressing NP. This surprising result suggested that 4-1BBL is more effective when expressed in trans, acting on adjacent DC. Therefore, we investigated the effect of LV expression of 4-1BBL in mouse DC cultures and observed induced maturation of bystander, untransduced cells. Maturation was blocked by anti–4-1BBL Ab, required cell–cell contact, and did not require the cytoplasmic signaling domain of 4-1BBL. Greater maturation of untransduced cells could be explained by LV expression of 4-1BBL, causing downregulation of 4-1BB. These data suggest that coexpression of 4-1BBL and Ag by vaccine vectors that target DC may not be an optimal strategy. However, 4-1BBL LV immunization activates significant numbers of bystander DC in the draining lymph nodes. Therefore, transactivation by 4-1BBL/4-1BB interaction following DC–DC contact may play a role in the immune response to infection or vaccination.
A job-oriented load-distribution scheme for cost-effective NameNode service in HDFS

Apache Hadoop has been widely used in big data processing and distributed computations. In the Hadoop ecosystem, data are stored and managed by the Hadoop Distributed File System (HDFS), in which the NameNode machine is a single point of failure. Although HDFS Federation and HDFS High Availability solve the problem, it comes at significant cost of extra server hardware. Therefore, we aim at improving the availability of the NameNode service in a more cost-effective way. The primary innovation is the joint consideration of MapReduce jobs and the resulting HDFS operations. Specifically, we dynamically allocate a SubNameNode for each job in one of the existing TaskTrackers to provide the NameNode service. Since the load of the single NameNode is naturally distributed to the SubNameNodes, the failure rate of the NameNode machine can be reduced. Moreover, with SubNameNodes more local to the participating TaskTrackers, TaskTrackers can access the NameNode service more efficiently.
IDO-Independent Suppression of T Cell Effector Function by IFN-γ–Licensed Human Mesenchymal Stromal Cells

Human bone marrow–derived mesenchymal stromal cells (MSCs) inhibit proliferation of activated T cells, and IFN-γ plays an important role in this process. This IFN-γ–licensed veto property is IDO-dependent. To further decipher the mechanistic underpinnings of MSC veto function on T cells, we investigated the effect of MSCs and IFN-γ–licensed MSCs on T cell effector function as assayed by cytokine secretion of T cells. Although MSCs and IFN-γ–licensed MSCs inhibit T cell proliferation, only IFN-γ–licensed MSCs significantly inhibit Th1 cytokine (IFN-γ, TNF-α, and IL-2) production by T cells. Additionally, IFN-γ–licensed MSCs inhibit T cell degranulation as well as single, double, and triple cytokine–producing T cells. Although IFN-γ–licensed MSCs upregulate their IDO activity, we found that MSC IDO catalytic function is dispensable with regard to MSC-driven inhibition of T cell effector function. Novel flow cytometry based functional screening of MSC-expressed, IFN-γ–licensed inhibitory molecules identified B7H1 and B7DC/PD1 pathways as essential effectors in blocking T cell function. Small interfering RNA–mediated blocking of B7H1 and B7DC reverses the inhibitory potential of IFN-γ–licensed MSCs on T cell effector function. Mechanistic analysis revealed that clustering of MHC and coinhibitory molecules are indispensable for the inhibitory effect of IFN-γ MSCs. Although exogenous IL-2 reverses B7H1-Ig–mediated inhibition of T cell proliferation, it does not affect the veto function of IFN-γ MSCs on both T cell proliferation and effector function. Our results reveal a new immunosuppressive property of IFN-γ–licensed MSCs that inhibits T cell effector function independent of IDO but through the ligands for PD1.
Extrapancreatic Effect of Glucagon like Peptide-1

Copyrightc 2015 The Korean Association of Internal Medicine This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited. Correspondence to In-Kyung Jeong, M.D., Ph.D. Department of Endocrinology & Metabolism, Kyung Hee University Hospital at Gangdong, Kyung Hee University School of Medicine, 892 Dongnam-ro, Gangdong-gu, Seoul 05278, Korea Tel: +82-2-440-6126, Fax: +82-2-440-6799, E-mail: jik1016@dreamwiz.com 글루카곤양펩티드-1의 췌장 외 효과
Immunotherapy of intraperitoneal cancer : effects of lymphokine activated killer cells and interleukin-2 in murine models.

textabstractIL-2 and LAK cells are theoretically attractive compounds for consideration in tumor immunotherapy. Past efforts of immunotherapy have concentrated on either an aspecific stimulation of the immune apparatus or on raising cells or antibodies specifically reacting to tumor cells. The inconsistent expression of tumor-associated antigens on human neoplasms is a problem with the latter approach and neither of these approaches has shown impressive clinical results (Section 2.6). Under certain stimuli, lymphocytes can give rise to so-called activated killer cells. In vitro incubation with the lymphokine IL-2 is the most feasible method of procurement. Cells, so activated, are called LAK (lymphokine activated killer) cells. LAK cells are cytotoxic for autologous, syngeneic, allogeneic and xenogeneic tumor. TO normal autologous or syngeneic cells, LAK cells display a limited or no reactivity. Prior exposure to tumor cells is not necessary for activation (Section 3.6). Tumor immunotherapy can be considered as sole therapy or in combination with other forms of therapy (surgery, radiation therapy, chemotherapy). One can distinguish situations in which these other forms of therapy are employed with curative intent and immunotherapy is given in an adjuvant setting or alternatively the immunotherapy can be given because it is known that the standard approach will not lead to cure.
Medical students seeking medical help: A qualitative study

Background: This study explores the factors influencing students to seek medical help, and student perceptions in relation to student–doctor interactions with implications for health help-seeking behaviours. Method: Students were interviewed across year groups. The interviews were audiotaped, transcribed and qualitatively analysed. Results: We interviewed 22 students and identified common themes. Conclusion: Medical students reflect on issues related to seeking medical help, their choice of GP and the decision whether to divulge they are medical students.
A practical coverage algorithm for wireless sensor networks in real terrain surface

Large-scale sensor deployment and coverage of wireless sensor networks (WSNs) is one of the most important topics for real applications, especially on real terrain surface, such as forest monitoring. In our works, we exploit the Digital Elevation Model (DEM) in Geographic Information System to describe the real fields for sensors. An algorithm for sensor deployment is proposed to generate the location of each sensor on real terrain surface. However, the usage of grid DEM makes the algorithm more complicated in practice, especially the calculation of geodesic. To optimise the calculation, we present a genetic method to solve the new issue and make our method practical. The experiments with real data show that our algorithm is practical, considering time and complexity to get k-coverage of sensors in real terrain surface.
Enhanced Innate Antiviral Gene Expression, IFN-α, and Cytolytic Responses Are Predictive of Mucosal Immune Recovery during Simian Immunodeficiency Virus Infection

The mucosa that lines the respiratory and gastrointestinal (GI) tracts is an important portal of entry for pathogens and provides the first line of innate immune defense against infections. Although an abundance of memory CD4+ T cells at mucosal sites render them highly susceptible to HIV infection, the gut and not the lung experiences severe and sustained CD4+ T cell depletion and tissue disruption. We hypothesized that distinct immune responses in the lung and gut during the primary and chronic stages of viral infection contribute to these differences. Using the SIV model of AIDS, we performed a comparative analysis of the molecular and cellular characteristics of host responses in the gut and lung. Our findings showed that both mucosal compartments harbor similar percentages of memory CD4+ T cells and displayed comparable cytokine (IL-2, IFN-γ, and TNF-α) responses to mitogenic stimulations prior to infection. However, despite similar viral replication and CD4+ T cell depletion during primary SIV infection, CD4+ T cell restoration kinetics in the lung and gut diverged during acute viral infection. The CD4+ T cells rebounded or were preserved in the lung mucosa during chronic viral infection, which correlated with heightened induction of type I IFN signaling molecules and innate viral restriction factors. In contrast, the lack of CD4+ T cell restoration in the gut was associated with dampened immune responses and diminished expression of viral restriction factors. Thus, unique immune mechanisms contribute to the differential response and protection of pulmonary versus GI mucosa and can be leveraged to enhance mucosal recovery.
Epidemiology, treatment, and guidelines for the treatment of heart failure in Europe

Chronic heart failure (CHF) is associated with a heavy burden of disease for patients and healthcare professionals. Quality of life and long-term prognosis for affected patients remain poor, and 5-year survival has been likened to that associated with some of the major malignancies. As a result of the ageing of the global population and the availability of effective treatments to prolong survival in patients with acute coronary syndromes, the incidence of CHF is increasing and the number of patients at risk of developing this condition is expected to grow. Despite the increasing prevalence of heart failure (HF), particularly in elderly populations, its exact incidence and prevalence remain largely unknown and probably underestimated due to a lack of accurate epidemiological data and difficulties associated with correct diagnosis. As a result, HF is associated with widespread undertreatment and the allocation of appropriate resources remains problematic. Numerous pharmacological therapies are available for the effective management of CHF, supported by a wealth of data from large scale, randomized clinical trials. Widespread adoption and implementation of evidence-based guidelines and treatment strategies are vital if survival is to be improved and patients are to receive optimal care for this devastating condition.
Axl Receptor Blockade Ameliorates Pulmonary Pathology Resulting from Primary Viral Infection and Viral Exacerbation of Asthma

Viruses use Tyro3, Axl, and Mertk (TAM) receptor tyrosine kinases to infect and modulate the immune properties of various cell types, which led us to investigate whether TAM receptor activation affected primary viral infection and viral exacerbation of asthma in experimental models. In these lung-specific models, we observed that Axl was the most abundantly induced TAM receptor protein. During primary respiratory syncytial virus (RSV) infection, anti-Axl mAb treatment significantly increased the number of IFN-γ–producing T cells and NK cells and significantly suppressed RSV replication and whole lung levels of IL-4 and IL-13. Intrapulmonary H1N1 infection induced lethal pulmonary inflammation, but anti-Axl mAb treatment of infected mice significantly increased the number of IFN-β–producing macrophages and dendritic cells and significantly suppressed neutrophil infiltration. Consequently, the lethal effect of H1N1 infection in this model was significantly reduced in the mAb-treated group compared with the IgG control-treated group. Targeting Axl also inhibited airway hyperresponsiveness, IL-4 and IL-13 production, and goblet cell metaplasia in an Aspergillus fumigatus–induced asthma model. Finally, infection of mice with RSV during fungal asthma significantly exacerbated airway inflammation, goblet cell metaplasia, and airway remodeling, but all of these features in this viral exacerbation model were ameliorated by anti-Axl mAb treatment. Taken together, these results demonstrate that Axl modulates the pulmonary immune response during viral and/or allergic pathology, and they also suggest that targeting this TAM receptor might provide a novel therapeutic approach in these infectious diseases.
Novel Role for Tumor-Induced Expansion of Myeloid-Derived Cells in Cancer Cachexia

Cancer progression is associated with inflammation, increased metabolic demand, infection, cachexia, and eventually death. Myeloid-derived suppressor cells (MDSCs) commonly expand during cancer and are associated with adaptive immune suppression and inflammatory metabolite production. We propose that cancer-induced cachexia is driven at least in part by the expansion of MDSCs. MDSC expansion in 4T1 mammary carcinoma-bearing hosts is associated with induction of a hepatic acute-phase protein response and altered host energy and fat metabolism, and eventually reduced survival to polymicrobial sepsis and endotoxemia. Similar results are also seen in mice bearing a Lewis lung carcinoma and a C26 colon adenocarcinoma. However, a similar cachexia response is not seen with equivalent growth of the 66C4 subclone of 4T1, in which MDSC expansion does not occur. Importantly, reducing MDSC numbers in 4T1-bearing animals can ameliorate some of these late responses and reduce susceptibility to inflammation-induced organ injury and death. In addition, administering MDSCs from both tumor- and nontumor-bearing mice can produce an acute-phase response. Thus, we propose a previously undescribed mechanism for the development of cancer cachexia, whereby progressive MDSC expansion contributes to changes in host protein and energy metabolism and reduced resistance to infection.
Reviewing the process of data fusion in wireless sensor network: a brief survey

Wireless sensor network is deployed on human inaccessible region to perform a very sensitive task where various external and internal factors affect the results being accumulated by the sensing node. Data fusion is one such technique. With the upcoming applications of wireless sensor network, it is also accompanied by various power and quality related issues. However, it was seen that whatever are the challenges or issues, it affects basically the data collection techniques from sensor nodes and corresponding forwarding to sink node. Hence, this paper aims to perform an exclusive investigation of the data fusion with respect to various standard architectures, standard algorithms and techniques investigated in the past study for performing data fusion, followed by open issues and research gap in the existing system adopted for enhancing the efficiency of data fusion techniques.
Dendritic Cell–MHC Class II and Itk Regulate Functional Development of Regulatory Innate Memory CD4+ T Cells in Bone Marrow Transplantation

MHC class II (MHCII)–influenced CD4+ T cell differentiation and function play critical roles in regulating the development of autoimmunity. The lack of hematopoietic MHCII causes autoimmune disease that leads to severe wasting in syngeneic recipients. Using murine models of bone marrow transplantation (BMT), we find that MHCII−/−→wild-type BMT developed disease, with defective development of innate memory phenotype (IMP, CD44hi/CD62Llo) CD4+ T cells. Whereas conventional regulatory T cells are unable to suppress pathogenesis, IMP CD4+ T cells, which include conventional regulatory T cells, can suppress pathogenesis in MHCII−/−→wild-type chimeras. The functional development of IMP CD4+ T cells requires hematopoietic but not thymic MHCII. B cells and hematopoietic CD80/86 regulate the population size, whereas MHCII expression by dendritic cells is sufficient for IMP CD4+ T cell functional development and prevention of pathogenesis. Furthermore, the absence of Tec kinase IL-2–inducible T cell kinase in MHCII−/− donors leads to preferential development of IMP CD4+ T cells and partially prevents pathogenesis. We conclude that dendritic cells-MHCII and IL-2–inducible T cell kinase regulate the functional development of IMP CD4+ T cells, which suppresses the development of autoimmune disorder in syngeneic BMTs.
Preparing for an institutional self review using the WFME standards – An International Medical School case study

Background: Curriculum reform poses significant challenges for medical schools across the globe. This paper describes the reforms that took place at the medical school of the Royal College of Surgeons in Ireland (RCSI) between 2005 and 2008 and the institutional self review process that accompanied these reforms. Results: Although fully accredited with the Irish Medical Council the RCSI sought additional detailed review of all aspects of its undergraduate medical program. Five medical educationalists were invited to visit the College in 2005 and again in 2008 to act as ‘critical friends’ and guide the self review using the World Federation for Medical Education (WFME) standards which had recently been adopted in Ireland. Conclusion: The process of institutional self review (as opposed to more high stakes accreditation) can bring about significant reform, especially when supported by a panel of ‘critical friends’ working alongside faculty to help guide and support sustained curriculum reform. The WFME standards continue to provide a useful framework to consider all medical education activities within a medical school engaged in continuous renewal. Adequate preparation for such reviews is critical to the success of such an undertaking and should be supported by a comprehensive communication strategy and project plan.
Empathy and its correlates in Iranian physicians: A preliminary psychometric study of the Jefferson Scale of Physician Empathy

Background: Empathy is one of the fundamental factors in patient care that is beneficial to both patient and physician. Aims: To assess the psychometric properties of the Persian version of the Jefferson Scale of Physician Empathy (JSPE) in a sample of Iranian physicians and examine its correlates. Method: Two hundred and seven general physicians completed the JSPE. The associations of empathy scores with demographic characteristics and practice-related variables were examined. Results: The scale showed an acceptable internal consistency (α = 0.78). Three of six extracted factors were considered as prominent based on the scree test, which were similar to those obtained in the US samples. Women scored higher than men. Empathy improved with increasing practice experiences. Other practice-related variables did not show a significant association with empathy. Conclusions: Results support the construct and criterion-related validities and reliability of the Persian version of the JSPE. Score difference between Iranian and American samples may not reflect a genuine difference in empathy trait and can be explained by cultural factors.