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.

Q: The lengthy duration of multidrug therapy needed to cure tuberculosis (TB) poses significant challenges for global control of the disease. Moreover, chronic inflammation associated with TB leads to pulmonary damage that can remain even after successful cure. Thus, there is a great need for the development of effective shorter drug regimens to improve clinical outcome and strengthen TB control. Host-directed therapy (HDT) is emerging as a novel adjunctive strategy to enhance the efficacy and shorten the duration of TB treatment. Previously, we showed that the administration of CC-3052, a phosphodiesterase-4 inhibitor (PDE4i), reduced the host inflammatory response during Mycobacterium tuberculosis (Mtb) infection and improved the antimicrobial efficacy of isoniazid (INH) in both the mouse and rabbit models. In the present study, we evaluated the pharmacokinetics and explored the mechanism underlying the efficacy of a more potent PDE4i, CC-11050, as adjunct to INH treatment in a mouse model of pulmonary Mtb infection. Genome-wide lung transcriptome analysis confirmed the dampening of inflammation and associated network genes that we previously reported with CC-3052. Consistent with the reduction in inflammation, a significant improvement in Mtb control and pathology was observed in the lungs of mice treated with CC-11050 plus INH, compared to INH alone. This important confirmatory study will be used to help design upcoming human clinical trials with CC-11050 as an HDT for TB treatment.

A: Pharmacologic inhibition of host Phosphodiesterase-4 improves isoniazid-Mediated clearance of Mycobacterium tuberculosis
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Q: Foot-and-mouth disease GIS OpenFOAM Livestock infectious diseases, such as foot-and-mouth disease (FMD), cause substantial economic damage to livestock farms and their related industries. Among various causes of disease spread, airborne dispersion has previously been considered to be an important factor that could not be controlled by preventive measures to stop the spread of disease that focus on direct and indirect contact. Forecasting and predicting airborne virus spread are important to make time for developing strategies and to minimise the damage of the disease. To predict the airborne spread of the disease a modelling approach is important since field experiments using sensors are ineffective because of the rarefied concentrations of virus in the air. The simulation of airborne spread during past outbreaks required improvement both for farmers and for policy decision makers. In this study a free license computational fluid dynamics (CFD) code was used to simulate airborne virus spread. Forecasting data from the Korea Meteorological Administration (KMA) was directly connected in the developed model for real-time forecasting for 48 h in three-hourly intervals. To reduce computation time, scalar transport for airborne virus spread was simulated based on a database for the CFD computed airflow in the investigated area using representative wind conditions. The simulation results, and the weather data were then used to make a database for a web-based forecasting system that could be accessible to users. ScienceDirect jo urnal homepage: www .e lsev ie r.com/ locate/issn/153 75110 b i o s y s t e m s e n g i n e e r i n g 1 2 9 ( 2 0 1 5 ) 1 6 9 e1 8 4 http://dx.

A: Web-based forecasting system for the airborne spread of livestock infectious disease using computational fluid dynamics
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Q: Cellular membranes display an incredibly diverse range of shapes, both in the plasma membrane and at membrane bound organelles. These morphologies are intricately related to cellular functions, enabling and regulating fundamental membrane processes. However, the biophysical mechanisms at the origin of these complex geometries are not fully understood from the standpoint of membrane-protein coupling. In this work, we focused on a minimal model of helicoidal ramps representative of specialized endoplasmic reticulum compartments. Given a helicoidal membrane geometry, we asked what is the distribution of spontaneous curvature required to maintain this shape at mechanical equilibrium? Based on the Helfrich energy of elastic membranes with spontaneous curvature, we derived the shape equation for minimal surfaces, and applied it to helicoids. We showed the existence of switches in the sign of the spontaneous curvature associated with geometric variations of the membrane structures. Furthermore, for a prescribed gradient of spontaneous curvature along the exterior boundaries, we identified configurations of the helicoidal ramps that are confined between two infinitely large energy barriers. Overall our results suggest possible mechanisms for geometric control of helicoidal ramps in membrane organelles based on curvatureinducing proteins.

A:
Geometric coupling of helicoidal ramps and curvature-inducing proteins in organelle membranes
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