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In this task, you're given a paragraph from the research paper and your task is to generate a suitable title for the research paper based on the given paper. Under 100 words is a good title length.
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Background: Host genetic factors are important determinants in tuberculosis (TB). The SLC11A1 (or NRAMP1) gene has been studied extensively for genetic association with TB, but with inconsistent findings. In addition, no study has yet looked into the effect of sex and age on the relationship between SLC11A1 polymorphisms and TB. Methods: A case-control study was conducted. In total, 278 pulmonary TB patients and 282 sex-and agematched controls without TB were recruited. All subjects were ethnic Chinese. On the basis of linkage disequilibrium pattern, three genetic markers from SLC11A1 and one from the nearby IL8RB locus were selected and examined for association with TB susceptibility. These markers were genotyped using single strand conformation polymorphism analysis or fragment analysis of amplified products. Results: Statistically significant differences in allele (P = 0.0165, OR = 1.51) and genotype (P = 0.0163, OR = 1.59) frequencies of the linked markers SLC6a/b (classically called D543N and 3'UTR) of the SLC11A1 locus were found between patients and controls. With stratification by sex, positive associations were identified in the female group for both allele (P = 0.0049, OR = 2.54) and genotype (P = 0.0075, OR = 2.74) frequencies. With stratification by age, positive associations were demonstrated in the young age group (age 65 years) for both allele (P = 0.0047, OR = 2.52) and genotype (P = 0.0031, OR = 2.92) frequencies. All positive findings remained significant even after correction for multiple comparisons. No significant differences were noted in either the male group or the older age group. No significant differences were found for the other markers (one SLC11A1 marker and one IL8RB marker) either. This study confirmed the association between SLC11A1 and TB susceptibility and demonstrated for the first time that the association was restricted to females and the young age group.
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BMC Infectious Diseases Sex-and age-dependent association of SLC11A1 polymorphisms with tuberculosis in Chinese: a case control study

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Being madly in love with all the advances in minimally invasive medicine and technology I often tell my friends the stories of how interventional radiology (IR) changes lives. One of these unintended stories led to a much bigger audience of TED community and spread the word about IR far beyond the circle of my friends. As the TED slogan promised, participating in the event 1 made me realize that our ideas of better medicine are worth sharing. It also made me think that better communication with the public is possible, and it does not take genius. It takes a willingness to try. We know that IR with its broad procedural spectrum, safety of minimally invasive approach, lower requirement for anesthesia and hospitalization, and cost-effectiveness has a strong stand in the evolving universal healthcare practice model. But, as Goethe said, knowing is not enough; we must apply. 2 Then, how can we as medical community increase the exercise of IR procedures? The starting point is to accept that many people, including medical professionals, do not know what diseases we can treat and what diagnostic or therapeutic services we can provide. Either it is a palliative treatment of metastases, or elective embolization of uterine fibroids, or emergent lysis of pulmonary embolism-it is our responsibility to find the appropriate patients and let both patients and primary physicians know what options we have to offer.
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Journal Pre-proof Guest Editorial: Radiology Nurses Can Raise the Impact on Promoting IR

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Autophagy is an evolutionarily conserved degradative process that is required to maintain host health and facilitates the capture and clearance of invading pathogens by the immune system 1,2 . Eukaryotic cells deliver dangerous and unwanted cytoplasmic material to lysosomes for degradation via three major routes: microautophagy, chaperone-mediated autophagy (CMA) and macroautophagy 3 . During microautophagy, invaginations of the lysosomal membrane directly take up cytoplasmic material 4 or the material directly enters multivesicular bodies (MVBs) of late endosomes 5 . During CMA, a cytoplasmic chaperone mediates lysosomal-associated membrane protein 2A (LAMP2A)-dependent uptake of unfolded proteins 6 . Macroautophagy involves a specialized double-membrane vesicle (DMV) known as the autophagosome (Box 1). Macroautophagy is the best-characterized form of autophagy, and we will hereafter refer to it simply as autophagy. Autophagy begins with the sequestration of cytoplasmic proteins and damaged organelles into a cup-shaped double-membrane termed the isolation membrane (or phagophore), which is derived from various cellular compartments 7 . The immature isolation membrane grows to envelop the engulfed contents, thus forming an autophagosome, which subsequently fuses with the lysosome to form autolysosomes. At this stage, the contents undergo degradation to enable their recycling upon nutrient depletion 8 . Acidification is a key regulatory step in autophagosome maturation and requires the activity of vacuolar ATPases. Autophagy is involved in various physiological processes, including starvation, cell differentiation and development, and degradation of aberrant structures, which ultimately maintains cellular homeostasis 9 . Moreover, autophagy is part of host stress responses such as the unfolded protein response (UPR) 10 . Given that viral infection and replication cause cell stress, autophagy is a frequent by-product of infection. However, autophagy during viral infection is not merely a passive process. As clearance of cytoplasmic components is a major function of autophagy, the innate immune system activates autophagy to degrade and dispose of invading viruses 11 . Furthermore, at later stages of infection, autophagy facilitates antigen processing and thereby the induction of adaptive immune responses 12,13 . There is a form of selective autophagy, xenophagy, that specifically recognizes intracellular microorganisms and targets them to autophagosomes for degradation 14 . Despite the seemingly hazardous conditions in autophagosomes for viruses, some viruses convert the autophagosome to their home for replication. The autophagosome provides a membrane-bound, protected environment to generate their progeny, and viruses can use autophagy-generated metabolites and energy for replication. Another type of autophagy, termed lipophagy, is a degradation pathway for lipid droplets in cells, and viruses can also hijack this process 15 . Lipid droplets are an ideal platform for virion assembly, and viruses can directly activate lipophagy to maintain the high level of ATP required for viral replication. In summary, current evidence suggests that viruses have evolved diverse strategies to either combat or utilize autophagy to promote their own life cycle. In this Review, we provide an overview of the function of autophagy as an antiviral defence mechanism and then focus on how viruses subvert and Multivesicular bodies (MVBs). A specialized subset of endosomes that contain membrane-bound intraluminal vesicles. Unfolded protein response (UPR). A cellular stress response activated in response to an accumulation of unfolded or aggregated proteins in the endoplasmic reticulum. Abstract | Autophagy is a powerful tool that host cells use to defend against viral infection. Double-membrane vesicles, termed autophagosomes, deliver trapped viral cargo to the lysosome for degradation. Specifically , autophagy initiates an innate immune response by cooperating with pattern recognition receptor signalling to induce interferon production. It also selectively degrades immune components associated with viral particles. Following degradation, autophagy coordinates adaptive immunity by delivering virus-derived antigens for presentation to T lymphocytes. However, in an ongoing evolutionary arms race, viruses have acquired the potent ability to hijack and subvert autophagy for their benefit. In this Review , we focus on the key regulatory steps during viral infection in which autophagy is involved and discuss the specific molecular mechanisms that diverse viruses use to repurpose autophagy for their life cycle and pathogenesis.
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Autophagy during viral infection -a double-edged sword