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.

Input: Consider Input: Feline infectious peritonitis virus (FIPV) (Coronaviridae) causes the most lethal viral infection in cats: FIP. The related feline enteric coronavirus (FECV) causes mild enteritis. Why these feline coronaviruses manifest so differently in vivo is not known. In this study, infection kinetics (titres and antigen expression) of FIPV 79-1146, and FECV 79-1683, were determined in peripheral blood monocytes from 3 donor cats and compared to those in Crandell feline kidney (CrFK) cells. The infection kinetics in monocytes were host dependent. Monocytes from 1 cat were resistant to both FIPV-and FECV-infection. Monocytes from the other 2 cats could initially be infected by both FIPV and FECV but FIPV infection was sustained in monocytes of only one cat. FECV-infection was never sustained and viral production was up to 100 times lower than in FIPVinfected monocytes. In CrFK cells, FIPV and FECV infection kinetics did not differ. In monocytes of a larger cat population (n = 19) the 3 infection patterns were also found. Considering all 22 investigated cats, 3/22 were not susceptible for FIPV and FECV. The rest could be infected with FECV and FIPV but 10/22 cats had monocytes that only sustained FIPV infection and 9/22 sustained neither FIPV nor FECV infection. * Both authors contributed equally.

Output: Replication of feline coronaviruses in peripheral blood monocytes


Input: Consider Input: This experiment was conducted to evaluate whether pretreatment with fenofibrate could mitigate acute lung injury (ALI) in a mice model of intestinal ischemia/reperfusion (I/R). Male C57BL/6 mice were randomly assigned into three groups (n = 6): sham, intestinal I/R + vehicle, and intestinal I/R + fenofibrate. Intestinal I/R was achieved by clamping the superior mesenteric artery. Fenofibrate (100 mg/kg) or equal volume of vehicle was injected intraperitoneally 60 minutes before the ischemia. At the end of experiment, measurement of pathohistological score, inflammatory mediators and other markers were performed. In addition, a 24-hour survival experiment was conducted in intestinal I/R mice treated with fenofibrate or vehicle. The chief results were as anticipated. Pathohistological evaluation indicated that fenofibrate ameliorated the local intestine damage and distant lung injury. Pretreatment with fenofibrate significantly decreased inflammatory factors in both the intestine and the lung. Consistently, renal creatine levels and hepatic ALT levels were significantly decreased in the fenofibrate group. Moreover, serum systemic inflammatory response indicators were significantly alleviated in the fenofibrate group. In addition, fenofibrate administration significantly improved the survival rate. Collectively, our data indicated that pretreatment with fenofibrate prior to ischemia attenuated intestinal I/R injury and ALI. Acute lung injury (ALI) is a critically severe, life-threatening condition in ICU, characterized by high mortality of approximately 40% 1 . ALI, along with its more severe form, acute respiratory distress syndrome, often results from a massive insult to the lung, whether be the direct alveolar infiltration or the indirect effects of systemic inflammatory response syndrome or multiple organ dysfunction syndromes 2 . An effective treatment of this life-threatening disorder calls for a better understanding of the molecular pathophysiology of ALI. The intestine is recognized to be one of the largest immune barrier systems and to be the source of bacteria and endotoxins in the body 3 . Previous reports indicate that the intestinal organ plays a crucial role in the development of ALI 4 . Mesenteric artery ischemia, a commonly seen critical state during small bowel transplantation or trauma, may lead to intestinal ischemia/reperfusion (I/R) injury. During the process of intestinal I/R injury, local bacteria overgrow and translocate, gastrointestinal mobility decreases, and mucosal permeability increases, all of which subsequently lead to the local intestine damage or distant lung injuries through the activation of systemic inflammatory response syndrome or multiple organ dysfunction syndromes 5,6 . Intestinal I/R is, therefore, a useful model for the investigation of pathophysiological mechanism of indirect ALI. Fenofibrate is known as an agonist of the peroxisome proliferator-activated receptor -α (PPARα ), the nuclear receptor superfamily member 7 . As a nuclear receptor activator, fenofibrate up-regulates or down-regulates genes that are involved in many pathophysiological processes, such as oxidative stress, inflammation, and leukocyte endothelium interactions 8, 9 . Recent studies have demonstrated an anti-oxidant, anti-inflammatory, and anti-ischemic role of fenofibrate to attenuate I/R injury in kidney 10,11 , liver 12 , brain 13,14 and heart 15 . But to date there are no literatures reporting the protective effects of fenofibrate in I/R injury in the organ of intestine. Moreover, the functional significance of fenofibrate in the intestinal I/R-induced ALI remains unclear. Therefore, this experiment is aimed to investigate whether fenofibrate administration would ameliorate the lung injury and inflammation in the model of intestinal I/R injury. Animals. The male C57BL/6 mice (8-10-wk-old; 20 ± 2 g) were purchased from Charles River (Beijing, China). Mice were kept in a temperature (21 ± 2 °C) and humidity (60 ± 5%) controlled room on a 12-hour light/dark cycle. They were fed a standard mice chow and water ad liblitum. All experiments were performed in accordance with the Declaration of Helsinki and were approved by the Institutional Animal Ethical Committee of the Peking Union Medical College Hospital.

Output: Protective effects of fenofibrate against acute lung injury induced by intestinal ischemia/reperfusion in mice OPEN


Input: Consider Input: The cellular role of DNA is relatively limited, perhaps because of the restrictions imposed by bonding between complementary strands. Outside the cell, however, nanoengineers are uncovering the many hidden talents of DNA. The DNA sequence is able to process information in biochemical assays, its structure is an ideal building material, and its folding pathway allows DNA to move and respond to its environment. Here, I review several innovative applications of designed DNA molecules, some underlying design principles and the prospects for future developments. The applications of new DNA-based technologies range from molecular diagnostics to protein purification and from therapeutics to the assembly of tiny electronic circuits. These uses exploit the properties of DNA at three levels -sequence only, structure (which depends on sequence) and folding pathways (which depend on both sequence and structure) -as the following examples show. By taking their cue from the genetic code found in nature, nanoengineers are now using DNA sequences in vitro to direct the synthesis and evolution of molecules with new functions and reactive properties. When attached to other molecules, detection methods that exploit DNA sequences allow complementary molecules to be identified at extremely low concentrations. DNA sequences can also be used, in a non-biological setting, to control the layout of electronic components in a nanocircuit. DNA strands can fold into stable structures that have valuable functional and material properties. Sensitive methods for detecting DNA have been extended to detect proteins and other macromolecular targets of DNA aptamers -that is, nucleic-acid molecules that have high binding specificity for their targets. Lattices and even three-dimensional (3D) objects have been self-assembled from rigid DNA structures. DNA lattices can organize proteins and nanoelectronic components on a surface with unprecedented precision, making it possible to gain a better understanding of the properties and interactions of proteins. The folding pathway of a DNA molecule to its stable structure allows it to move and perform mechanical functions. The energy released in DNA-folding pathways has been used in vitro to drive motors, providing the ability to release, grab or cleave target molecules and even to control the release of drugs, depending on the outcome of certain diagnostic tests. This review focuses on the recent developments in generating rationally designed DNA molecules and their applications. The past decade has seen huge advances in the development of design principles, particularly by exploiting DNA structure and folding pathways, but also in applications of designed DNA sequences. Together, techniques for the in vitro selection or molecular evolution of DNA molecules from random pools have given spectacular yields, including DNA aptamers and enzymes, which can inhibit the expression of harmful genes or disrupt protein function. Excellent reviews of selected DNA molecules can be found elsewhere 1-3 ; this paper includes only examples of designed DNA molecules, or molecules that combine both selected and designed Abstract | Long admired for its informational role in the cell, DNA is now emerging as an ideal molecule for molecular nanotechnology. Biologists and biochemists have discovered DNA sequences and structures with new functional properties, which are able to prevent the expression of harmful genes or detect macromolecules at low concentrations. Physical and computational scientists can design rigid DNA structures that serve as scaffolds for the organization of matter at the molecular scale, and can build simple DNA-computing devices, diagnostic machines and DNA motors. The integration of biological and engineering advances offers great potential for therapeutic and diagnostic applications, and for nanoscale electronic engineering.


Output: Designed DNA molecules: principles and applications of molecular nanotechnology