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: Muscle wasting is one of the main features of cancer cachexia, a multifactorial syndrome frequently occurring in oncologic patients. The onset of cachexia is associated with reduced tolerance and response to antineoplastic treatments, eventually leading to clinical conditions that are not compatible with survival. Among the mechanisms underlying cachexia, protein and energy dysmetabolism play a major role. In this regard, several potential treatments have been proposed, mainly on the basis of promising results obtained in preclinical models. However, at present, no treatment yet reached validation to be used in the clinical practice, although several drugs are currently tested in clinical trials for their ability to improve muscle metabolism in cancer patients. Along this line, the results obtained in both experimental and clinical studies clearly show that cachexia can be effectively approached by a multidirectional strategy targeting nutrition, inflammation, catabolism, and inactivity at the same time. In the present study, approaches aimed to modulate muscle metabolism in cachexia will be reviewed.

A: Modulating Metabolism to Improve Cancer-Induced Muscle Wasting
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Q: The purpose of this study was to compare the biochemical and biological properties of nonstructural protein (nsp) 15 among mouse hepatitis virus (MHV), severe acute respiratory syndrome coronavirus (SARS-CoV) and transmissible gastroenteritis virus (TGEV) in virus-infected and ectopically expressed cells. In virus-infected cells, MHV nsp15 distributed unevenly throughout the cytoplasm but predominantly in the perinuclear region. When expressed as N-terminal enhanced green fluorescence protein (EGFP) fusion, it predominantly formed speckles in the cytoplasm. In contrast, SARS-CoV and TGEV EGFP-nsp15s distributed smoothly in the whole cell and did not form speckles. Deletion mapping experiments identified two domains responsible for the speckle formation in MHV EGFP-nsp15: Domain I (aa101-150) and Domain III (aa301-374). Interestingly, Domain II (aa151-250) had an inhibitory effect on Domain IIIbut not on Domain I-mediated speckle formation. Expression of a small (35aa) sequence in Domain III alone was sufficient to form speckles for all 3 viral nsp15s. However, addition of surrounding sequences in Domain III abolished the speckle formation for TGEV nsp15 but not for MHV and SARS-CoV nsp15s. Further domain swapping experiments uncovered additional speckle-inducing and -suppressive elements in nsp15s of SARS-CoV and TGEV. Homotypic interaction involving Domain III of MHV nsp15 was further demonstrated biochemically. Moreover, the biological functions of the expressed nsp15s were assessed in MHV-infected cells. It was found that the effects of EGFP-nsp15s on MHV replication were both virus species-and nsp15 domain-dependent. Collectively these results thus underscore the differential biochemical and biological functions among the nsp15s of MHV, TGEV and SARS-CoV in host cells.

A: Comparative in vivo analysis of the nsp15 endoribonuclease of murine, porcine and severe acute respiratory syndrome coronaviruses
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Q: The present study describes the association between inflammatory cell types and feline infectious peritonitis virus (FIPV) antigen in the brain of 4 cats diagnosed as feline infectious peritonitis (FIP). Immunohistochemically, FIPV antigens were detected in the inflammatory foci of the leptomeninges, choroid plexus and ventricles in 3 of the 4 cats. In 3 cases, inflammatory foci mainly consisted of CD204-and Iba1-positive macrophages, and the FIPV antigens were found in the macrophages. In the other case which was negative for FIPV antigen, severe inflammation predominantly consisting of CD20-positive B lymphocytes was observed in the leptomeninges and subventricles, accompanied with diffuse proliferation of gemistocytic astrocytes. The difference in histopathology may reflect the inflammatory process or the strain variation of FIP virus. Feline infectious peritonitis (FIP) is a widely distributed infectious disease caused by feline coronavirus (FCoV) in domestic and wild cat species [1, 2, 11, 13] . FCoV consists of two biotypes including feline enteric coronavirus (FECV) and FIP virus (FIPV). FECV infection is asymptomatic or exclusively causes mild gastrointestinal clinical symptons, while FIPV causes fatal symptoms such as fever, anorexia, weight loss, abdominal distention and neurological symptoms in young cats [2, 13] . The clinical symptoms differ depending on the form and organ distribution of the lesion, and in cases with lesions in central nervous system, neurological symptoms such as depression, ataxia and seizures appear in 85% of cases [15] . It was assumed that FIPV originating from FECV acquired its monocyte-or macrophage-tropism responsible for viral dissemination and developed specific FIP lesions due to vasculitis [17, 18] . The FIP lesions are characterized by localized or disseminated fibrinous, pyogranulomatous, or granulomatous inflammation with protein-rich effusion in the body cavities [9, 10]. These lesions are often accompanied with granulomatous or necrotizing phlebitis and/or periphlebitis, which have been considered as a typical hallmark of FIP [3, 10] . Lesions in the central nervous system (CNS) are frequently observed mainly in the leptomeninges, ventricles, choroid plexus and sometimes neuroparenchyma [5, 12, 16] . Although histopathological features of FIP lesions in the CNS have been well documented [6, 14, 15] , the association between inflammatory cell types and the distribution of viral antigens remains to be clarified. The present study describes the inflammatory cell types and viral antigen distribution in the brain lesions of 4 cats diagnosed as FIP. Also, considering that the FIPV has monocyte and macrophage tropism, immunohistochemical examinations were performed using two kinds of macrophage markers: CD204 (monocyte and macrophage marker) and Iba-1 (microglia and macrophage marker). Four necropsy cases of cats diagnosed as FIP were obtained from the specimen archives of the Laboratory of Veterinary Pathology, Graduate School of Agricultural and Life Sciences, the University of Tokyo. Diagnoses of FIP were mainly based on clinical history, physical examination findings, general blood chemistry and antibody titer for FCoV antigen. Final diagnoses were based on gross findings at necropsy and histopathological findings. Information of the 4 cases, including age, sex, major clinical signs, the antibody titer of FCoV and organs with histologically severe inflammatory lesions is summarized in Table 1. 

A:
NOTE Immunohistochemical studies on meningoencephalitis in feline infectious peritonitis (FIP)
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