TASK DEFINITION: In this task, you're given a paragraph and title from the research paper. Your task is to classify whether the given title is suitable or not for the research paper based on the given paragraph. Return "True" if title is proper according to paragraph else "False".
PROBLEM: Paragraph: So far, there has been scarce information about the status of immunoglobulins (Ig) and the gene expression of inflammatory cytokines in buffaloes showing digestive troubles. The purpose of the present study was to explore the modulation of gene expression of some immuneinflammatory markers in buffaloes suffered from various digestive disorders. For this reason, 50 native breed water buffaloes were studied. Forty of these buffaloes showed various symptoms of digestive disorders and were allocated into 4 groups of equal sizes (group 1: uncategorized stomatitis; group 2: acute traumatic reticuloperitonitis [TRR]; group 3: acute rumen impaction; and group 4: undifferentiated enteritis). Ten apparently healthy buffaloes were randomly selected and considered as a control group. RNA was firstly extracted from the whole blood then a reverse transcription kits was used to convert the RNA to cDNA. Real-time PCR was used to measure the expression of mRNAs of interleukin (IL)-1β, IL-6, IL-10, and tumor necrosis factor (TNF)-α, IgG, and IgA, while glyceraldehyde-3-phosphate dehydrogenase (GAPDH) used as an internal reference. The results of realtime PCR revealed a significant (P ≤ 0.05) upregulation of the gene expression of IL-1β, IL-6, IL-10, and TNF-α in blood of diseased buffaloes compared with those of controls. Animals showing acute TRP had peak values of both IL-6 and IL-10; while those exhibiting enteritis and rumen impaction had the highest values of IL-1β and TNF-α, respectively. The results of qPCR also revealed a significant (P ≤ 0.05) downregulation of both IgG and IgA gene expression in blood of all diseased buffaloes compared with controls. The lowest values of both genes were recorded in buffaloes showing acute TRP. The results herein suggest that the tested genes could have a pivotal role in the pathophysiologic mechanism of the underlying diseases. 
 Title: Modulation of immunity and inflammatory gene expression in buffalo (Bubalus bubalis) with some digestive disorders

SOLUTION: True

PROBLEM: Paragraph: Respiratory virus infection (RVI) in pediatric solid organ transplant (SOT) recipients poses a significant risk; however, the epidemiology and effects of an RVI after pediatric SOT in the era of current molecular diagnostic assays are unclear. Methods. A retrospective observational cohort of pediatric SOT recipients (January 2010 to June 2013) was assembled from 9 US pediatric transplant centers. Charts were reviewed for RVI events associated with hospitalization within 1 year after the transplant. An RVI diagnosis required respiratory symptoms and detection of a virus (ie, human rhinovirus/enterovirus, human metapneumovirus, influenza virus, parainfluenza virus, coronavirus, and/or respiratory syncytial virus). The incidence of RVI was calculated, and the association of baseline SOT factors with subsequent pulmonary complications and death was assessed. Results. Of 1096 pediatric SOT recipients (448 liver, 289 kidney, 251 heart, 66 lung, 42 intestine/multivisceral), 159 (14.5%) developed RVI associated with hospitalization within 12 months after their transplant. RVI occurred at the highest rates in intestine/ abdominal multivisceral (38%), thoracic (heart/lung) (18.6%), and liver (15.6%) transplant recipients and a lower rate in kidney (5.5%) transplant recipients. RVI was associated with younger median age at transplant (1.72 vs 7.89 years; P < .001) and among liver or kidney transplant recipients with the receipt of a deceased-donor graft compared to a living donor (P = .01). The all-cause and attributable case-fatality rates within 3 months of RVI onset were 4% and 0%, respectively. Multivariable logistic regression models revealed that age was independently associated with increased risk for a pulmonary complication (odds ratio, 1.24 [95% confidence interval, 1.02-1.51]) and that receipt of an intestine/multivisceral transplant was associated with increased risk of all-cause death (odds ratio, 24.54 [95% confidence interval, 1.69-327.96]). Conclusions. In this study, hospital-associated RVI was common in the first year after pediatric SOT and associated with younger age at transplant. All-cause death after RVI was rare, and no definitive attributable death occurred. 
 Title: A Multicenter Consortium to Define the Epidemiology and Outcomes of Pediatric Solid Organ Transplant Recipients With Inpatient Respiratory Virus Infection

SOLUTION: True

PROBLEM: Paragraph: The aim of the present study was to investigate long-term outcomes of the offspring in a lipopolysaccharide (LPS)-induced maternal immune activation (MIA) model and the effect of maternal molecular hydrogen (H 2 ) administration. We have previously demonstrated in the MIA mouse model that maternal administration of H 2 attenuates oxidative damage and neuroinflammation, including induced pro-inflammatory cytokines and microglial activation, in the fetal brain. Short-term memory, sociability and social novelty, and sensorimotor gating were evaluated using the Y-maze, threechamber, and prepulse inhibition (PPI) tests, respectively, at postnatal 3 or 4 weeks. The number of neurons and oligodendrocytes was also analyzed at postnatal 5 weeks by immunohistochemical analysis. Offspring of the LPS-exposed dams showed deficits in short-term memory and social interaction, following neuronal and oligodendrocytic loss in the amygdala and cortex. Maternal H 2 administration markedly attenuated these LPS-induced abnormalities. Moreover, we evaluated the effect of H 2 on LPS-induced astrocytic activation, both in vivo and in vitro. The number of activated astrocytes with hypertrophic morphology was increased in LPS-exposed offspring, but decreased in the offspring of H 2 -administered dams. In primary cultured astrocytes, LPS-induced pro-inflammatory cytokines were attenuated by H 2 administration. Overall, these findings indicate that maternal H 2 administration exerts neuroprotective effects and ameliorates MIA-induced neurodevelopmental deficits of offspring later in life. Published: xx xx xxxx OPEN www.nature.com/scientificreports/ 2 ScIENtIfIc REPORTS | (2018) 8:9221 | lead to direct and indirect death or dysfunction of neuronal and oligodendrocyte cells 10 , which are considered to be the main targets of fetal brain injury 11 . We have previously suggested that the maternal administration of molecular hydrogen (H 2 ) plays a neuroprotective role in the fetal brain against injury caused by oxidative stress and inflammation 12-14 . Ohsawa et al. discovered that H 2 acts as an antioxidant that selectively neutralizes hydroxyl radicals (•OH) and protects the brain from injury 15 . H 2 reacts with strong oxidants, such as •OH, but remains mild enough to neither disturb the metabolic redox reactions nor affect ROS signaling. Several subsequent studies have explored the therapeutic and preventive effects of H 2 , and have indicated that H 2 has other properties as well, including anti-inflammatory and anti-apoptotic effects 16, 17 . The safety and some promising benefits of H 2 have already been demonstrated, not only in animal models but also in patients, including those with Parkinson's disease 18 , diabetes mellitus 19 and mild cognitive impairment 20 , although no large randomized controlled trials have been conducted to date. Recently, we demonstrated that the administration of H 2 to pregnant mouse dams significantly increased H 2 concentration in the fetal brain, through the maternal-fetal interface, in a mouse model of lipopolysaccharide (LPS)-induced MIA 12 . Fetal damage in this MIA model and the effect of maternal H 2 administration on this damage can be summarized as follows 12 : (1) high mortality rate of MIA fetuses, (2) brain injury associated with elevated levels of pro-inflammatory cytokines, aberrant microglial activation, and oxidative damage in the MIA fetal brains, and (3) attenuation of these adverse outcomes by maternal H 2 administration. Thus, the protective effect of maternal H 2 administration on short-term outcomes in the MIA offspring has been demonstrated. However, long-term outcomes of the surviving offspring are yet to be investigated. Therefore, the present study investigated long-term neurological outcomes in the MIA mouse model and the efficacy of H 2 administration in pregnant dams, using both histological and behavioral examinations. Astrocytes, which are the most abundant cell population in the CNS, play a key role in normal brain development 21, 22 . However, when astrocytes are exposed to maternally-derived cytokines in MIA models, they secrete various cytokines that lead to neurodevelopmental impairments 23 . Moreover, activation of astrocytes is known to be a factor in the prolongation of brain damage, and contributes to the formation of glial scars that limit neuronal plasticity 24 . Thus, in the present study, the MIA-related astrocytic activation and its modification by H 2 administration were also investigated, both in vivo and in vitro. Maternal H 2 administration restored offspring growth. We investigated postnatal growth, which could be related to neurologic outcome. From postnatal day (P) 6 to P10, offspring growth was significantly retarded in the LPS group than in the Control group (p < 0.05). Although significant differences were not observed between the LPS and LPS + HW group, maternal administration of Hydrogen water (HW) restored offspring growth to the control level (Fig. 1) . 
 Title: Administration of molecular hydrogen during pregnancy improves behavioral abnormalities of offspring in a maternal immune activation model OPEN

SOLUTION:
True