The purpose of the present study was to examine the relationship between functional disability and fear of falling during daily activities. Also examined was the relationship between fear of falling and health-related Quality of Life (QOL). Health-related QOL concepts were measured using the Short Form 36 Health Survey (SF-36) within an elderly day services sample. Eligible subjects were elderly persons using Day Service (type B) who were capable of independently answering a questionnaire and had no memory problems. Forty-three males and 92 females were eligible for this study. Forty-nine (36.3%) subjects expressed no fear of falling, whereas 22 (16.3%) reported that they were very fearful of falling. Among females, walking and bathing had a highly significant relationship with the fear of falling. The fear of falling can contribute to psychological conditions such as depression, and also impacts on the health-related QOL of frail elderly people. Thus, it is critical to provide integrated health care activities for these individuals that address both psychological well-being and physical functioning.
The erythropoietin-producing hepatocellular (EPH)A2 receptor, tyrosine kinase, is overexpressed and phosphorylated in several types of human tumors and has been associated with malignant transformation. A recent report, however, indicated that stimulation of the EPHA2 receptor ligand, ephrinA1 (EFNA1), inhibits the growth of EPHA2-expressing breast cancer. The authors examined the expression of EPHA2 and EFNA1 using semiquantitative reverse transcription-polymerase chain reaction (RT-PCR) in four gastric cancer cell lines and 49 primary gastric cancer samples, as well as in normal gastric tissue. EPHA2 was more highly expressed in tumor tissue than in normal tissue in 27 cases (55%). EFNA1 was overexpressed in tumor tissue in 28 cases (57%). No significant correlation was detected between the expression levels and histologic features such as tumor size, age, vessel invasion, or lymph node involvement. However, EPHA2 overexpression was more prominent in macroscopic type 3 and 4 tumors than in type 1 or 2 advanced gastric cancer. The authors observed EPHA2 expression in three of the four gastric cancer cell lines (AGS, KATO3, and MKN74) that were examined. In one cell line, TMK1, EPHA2 expression was barely detectable using northern blotting, RT-PCR, and western blotting. In contrast, EFNA1 was detected in all cell lines. In the gastric cancer cell lines that endogenously expressed EPHA2, stimulation with ephrinA1-Fc led to decreased EPHA2 protein expression and increased EPHA2 phosphorylation. Finally, the growth of T he erythropoietin-producing hepatocellular (EPH ) receptors represent the largest known family of receptor tyrosine kinases and are activated by interaction with the cell-surface ligands, ephrins (EFN). There is evidence to suggest that some members of the EPH family and their EFN ligands are involved in angiogenesis and oncogenesis through cell adhesion, morphogenesis, capillary sprouting, and chemoattraction.(1−5) EPH receptors have been classified into two subfamilies, EPHA and EPHB. EPHA receptors bind mainly to glycosylphosphatidylinositolanchored EFNA ligands, and EPHB receptors bind to transmembrane EFNB ligands. The expression of EPH family transcripts has been documented in some melanomas and carcinomas.(6,7) Overexpression of EPHA2 is believed to be sufficient to confer malignant/tumorigenic potential on nontransformed mammary epithelial cells.(8) Esophageal squamous cell carcinomas that overexpress EFNA2 have a poorer prognosis than those that do not. (9)
Mutations in several genes encoding transcription factors of the hepatocyte nuclear factor (HNF) cascade are associated with maturity-onset diabetes of the young (MODY), a monogenic form of early-onset diabetes mellitus. The ability of the orphan nuclear receptor small heterodimer partner (SHP, NR0B2) to modulate the transcriptional activity of MODY1 protein, the nuclear receptor HNF-4␣, suggested SHP as a candidate MODY gene. We screened 173 unrelated Japanese subjects with earlyonset diabetes for mutations in this gene and found five different mutations (H53fsdel10, L98fsdel9insAC, R34X, A195S, and R213C) in 6 subjects as well as one apparent polymorphism (R216H), all present in the heterozygous state. Interestingly, all of the subjects with the mutations were mildly or moderately obese at onset of diabetes, and analysis of the lineages of these individuals indicated that the SHP mutations were associated with obesity rather than with diabetes. Therefore, an additional group of 101 unrelated nondiabetic subjects with early-onset obesity was screened for mutations in the SHP gene. Two of the previously observed mutations (R34X and A195S) and two additional mutations (R57W and G189E) were identified in 6 subjects, whereas no mutations were identified in 116 young nondiabetic lean controls (P ؍ 0.0094). Functional studies of the mutant proteins show that the mutations result in the loss of SHP activity. These results suggest that genetic variation in the SHP gene contributes to increased body weight and reveal a pathway leading to this common metabolic disorder in Japanese.nuclear receptor ͉ maturity-onset diabetes of the young ͉ insulin secretion ͉ body weight ͉ hepatocyte nuclear factor H eterozygous mutations in genes encoding transcription factors in the hepatocyte nuclear factor (HNF) regulatory cascade (1) are associated with an early-onset autosomal dominant form of diabetes mellitus, maturity-onset diabetes of the young (MODY) (2). To date, diabetes-associated mutations have been found in three members of this regulatory network, HNF-1␣, -1, and -4␣ (MODY3, 5, and 1, respectively) (3-6). These forms of MODY are characterized primarily by defective insulin secretion with normal body weight (7-9). In contrast, forms of early-onset autosomal-dominant type 2 diabetes that are not linked to known MODY genes are often characterized by insulin resistance with high body weight, rather than by pure pancreatic -cell defects (10). It is not known whether obesity-associated MODY genes or other common modifying factors are responsible for these phenotypic features.The protein small heterodimer partner (SHP; also called NROB2 for nuclear receptor subfamily 0, group B, member 2), an atypical orphan nuclear receptor that lacks a conventional DNA-binding domain, interacts with a number of other nuclear receptors, including HNF-4␣, and inhibits their transcriptional activity (11)(12)(13)(14)(15)(16)(17). SHP is expressed in the liver and has recently been suggested to regulate cholesterol homeostasis by an inhibitory e...
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