Given a passage classify if the passage has a definite objective/aim/goal or not. Output '1' if the passage has a defininte objective/aim/goal and output '0' if the passage does not have a definite objective/aim/goal.

Input: Consider Input: To test the hypothesis that hyporesponsiveness to ghrelin due to reduced growth hormone (GH) contributes to the aging-related hyperinflammatory state in sepsis.', 'Sepsis and septic shock are a serious problem, particularly in the geriatric population. Ghrelin is an endogenous ligand for the GH secretagogue receptor 1a (GHSR1a, ie, ghrelin receptor). The decline in GH with age is directly associated with many adverse changes that occur with aging. However, the role of GH, ghrelin, and GHSR1a in the age-associated vulnerability to sepsis remains unknown.', 'Male Fischer 344 rats (young: 3 months; aged: 24 months) were used. Plasma GH levels, ghrelin receptor expression, and neuronal activity in the parasympathostimulatory nuclei of the brain stem in normal young and aged animals were measured. Endotoxemia was induced by intravenous injection of lipopolysaccharide (LPS, 15 mg/kg BW).', 'While LPS-induced release of proinflammatory cytokines from macrophages isolated from aged rats decreased, LPS injection resulted in an in vivo hyperinflammatory state. GH levels were lower in aged rats, which was associated with lower expression of GHSR1a in the dorsal vagal complex and a decrease in parasympathostimulatory neuronal activity. GHSR1a antagonist elevated LPS-induced cytokine release in young rats. GH increased GHSR-1a expression in the dorsal vagal complex in aged rats. Coadministration of ghrelin and GH, but not ghrelin alone or GH alone, markedly reduced cytokine levels and organ injury after endotoxemia in aged rats, which was associated with significantly elevated parasympathostimulatory neuronal activity.

Output: 1


Input: Consider Input: Syndromic forms of osteosarcoma (OS) account for less than 10% of all recorded cases of this malignancy. An individual OS predisposition is also possible by the inheritance of low penetrance alleles of tumor susceptibility genes, usually without evidence of a syndromic condition. Genetic variants involved in such a non-syndromic form of tumor predisposition are difficult to identify, given the low incidence of osteosarcoma cases and the genetic heterogeneity of patients. We recently mapped a major OS susceptibility QTL to mouse chromosome 14 by comparing alpha-radiation induced osteosarcoma in mouse strains which differ in their tumor susceptibility.', 'Tumor-specific allelic losses in murine osteosacoma were mapped along chromosome 14 using microsatellite markers and SNP allelotyping. Candidate gene search in the mapped interval was refined using PosMed data mining and mRNA expression analysis in normal osteoblasts. A strain-specific promoter variant in Rb1 was tested for its influence on mRNA expression using reporter assay.', 'A common Rb1 allele derived from the BALB/cHeNhg strain was identified as the major determinant of radiation-induced OS risk at this locus. Increased OS-risk is linked with a hexanucleotide deletion in the promoter region which is predicted to change WT1 and SP1 transcription factor-binding sites. Both in-vitro reporter and in-vivo expression assays confirmed an approx. 1.5 fold reduced gene expression by this promoter variant. Concordantly, the 50% reduction in Rb1 expression in mice bearing a conditional hemizygous Rb1 deletion causes a significant rise of OS incidence following alpha-irradiation.

Output: 0


Input: Consider Input: The presence of echolucent artery plaques is associated with increased risk of cardiovascular events as compared to echogenic plaques. Whether inflammatory markers are associated with carotid plaque morphology is questioned.', '5,341 individuals were examined with ultrasonography of the right carotid artery. Of these, 3,205 had carotid plaque(s), in whom plaque area (mm(2)) and plaque echogenicity, expressed as the computer-assisted gray scale median (GSM), were determined. White blood cell count (WBC), fibrinogen and C-reactive protein (CRP) were analyzed, as well as other cardiovascular risk factors. In multiple linear and logistic regression models, we determined the relationship between plaque area and echogenicity, and inflammatory markers.', 'Women and men with carotid plaque(s) had significantly elevated levels of WBC and fibrinogen, but not CRP, as compared to subjects without plaques. All inflammatory markers were significantly associated with plaque area in men. WBC was significantly associated with plaque echogenicity in women, whereas no association was found between fibrinogen and CRP and plaque echogenicity in either gender.


Output: 0