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자동차보험 승낙피보험자와 운전피보험자에 관한 연구 - 대법원 판례를 중심으로 -
김영길 ( Youngkil Kim ) 한국손해사정학회 2016 손해사정연구 Vol.14 No.-
자동차보험의 경우 피보험자의 범위를 기명피보험자 외에도 친족피보험자, 승낙피보험자, 사용피보험자, 운전피보험자 등으로 그 범위를 확대하여 인정하고 있다. 그런데 이들 피보험자 개념이 난해하여 손해사정실무 및 소송실무에서 해석상 다툼이 빈발하고 있다. 예컨대 손해사정실무에서는 렌터카회사(기명피보험자)로부터 렌터카(피보험자동차)를 빌려간 뒤 렌터카회사(기명피보험자)의 의사에 명백히 반하여 렌터카를 제3자에게 재차 빌려주거나 운전케 한 임차인을 승낙피 보험자로 보고 있으나 정작 이에 대한 관련 판례나 연구문헌은 나와 있지 않은 실정이다.또 피보험자동차를 운전기사와 함께 임차하여 작업중 임차인 본인이 사상한 경우 그 임차인이 승낙피보험자에 해당하는지 여부, 피보험자동차를 무단으로 운전한 고용운전자가 운전피보험자에 해당하는지 여부에 대하여는 보험이론에 반하는 판례로 인해 논란이 가중되고 있다. 이에 본 논문에서는 렌터카회사로부터 렌터카를 빌려간 뒤 렌터카회사의 의사에 명백히 반하여 그 자동차를 제3자에게 재차 빌려주거나 운전케 한 임차인과 피보험자동차를 운전기사와 함께 임차하여 작업 중 임차인 본인이 사상한 경우 그 임차인은 승낙피보험자 해당되지 않는다는 점, 운전피보험자는 통상 기명피보험자에 고용되어 피보험자동차를 운전하는 고용운전자(=자배법상 운전자)를 뜻 하지만 반드시 고용운전자에 국한하지는 않으며 고용운전자라 하더라도 무단으로 운전한 경우에는 비록 기명피보험자 등을 위하여 운전한다는 의사로 운전하였다고 하더라도 운전피보험자에 해당하지 않는다는 점 등을 명확히 하고 승낙피보험자와 운전피보험자 조항의 바람직한 해석론 및 약관개정론을 제시해 보고자 한다. 본 연구를 계기로 향후 본 논문에서 제기한 의제에 대한 활발한 논의와 연구 및 합리적 방향으로의 약관개정이 있기를 기대해 본다. In case of automobile insurance, it expands the range of the insured other than named insured to relative insured, allowed insured, employer insured, driving insured. However, the concept of the insured is unexpectedly too complicated to be generally acceptable, so many disputes occur for interpretation of the insured on claim adjustment field and lawsuit field. For example, in case of claim adjustment field recognizes the lessee who let a third party to drive or re-lease the insured car that lessee rented from the rental car company be allowed insured, however, there is not any judicial precedent or research case. Additionally, the dispute continues to rise due to opposing verdicts in relation to a lessee should be recognized as allowed insured when the lessee was hurt or killed by a driver rented along with insured car and the employee driver who drove insured car without the named insured`s permission is the driving insured or not. This thesis will establish the lessee who let a third party to drive or re-lease the insured car that lessee rented from the rental car or the lessee was hurt or killed by a driver rented along with the insured car company should not be recognized as allowed insured; though the driving insured generally describes the employee driver who drives the insured car hired by named insured, does not always limit the employee driver, and even the employee driver is recognized as the driving insured, he or she should not be recognized as driving insured even the purpose of driving was for named insured, if the driving was unauthorized. This will be discussed based on verdicts of precedents and references and it will guide to set the desirable theory of interpretation and Revision of clause. With this as the research, it expects to lead active discussion and rational Revision of clause for the proposed subject on this thesis.
Yang, Inmyung,Park, Seungjoon,Woo, Jeontaek,KIm, Sungwoon,Kim, Jinwoo,Kim, Youngseol,Choi, Youngkil 경희대학교 유전공학연구소 1995 遺傳工學論文集 Vol.7 No.-
A great variability in the plasma GH response to a somatostatin (SRIH) analog, octreotide, was observed among acromegalic patients. A marked decrease in SRIH receptor (SSTR) density was postulated as a mechanism of resistance to native SRIH or octreotide. SSTR subtype 5 (SSTR5) is believed to be specific to the pituitary gland. Recently the possibility has been suggested that GH-secreting adenomas with gsp oncogene may have higher expression of SSTR than those without the oncogene. Therefore, we investigated the individual variation of SSTR5 expression in GH-secreting adenomas, and whether the SSTR5 gene expression is increased in gsp-positive adenomas. Genomic DNA and total RNA were prepared from the adenomas of 18 acromegalic patients. The point mutations at codon 201 and 227 of the stimulatory G protein alpha-subunit were examined by direct PCR sequencing. The expression of SSTR5 mRNA was determined by RT-PCR with in vitro transcription. gsp oncogene was found in 7 tumors (39%). In vitro transcript of SSTR5 cDNA was found in all the tumors. The amount of SSTR5 cDNA transcript, expressed as arbitary unit, was considerably variable from 19.6 to 220. 5 units. Relatively high expression of SSTR5 (≥100 units) was observed in 11 tumors (61%). The clinical characteristics of the patients with relatively high expression of SSTR5 did not differ from those of the patients with low expression. There was no correlation between the amount of SSTR5 cDNA transcript and the GH response to octreotide. The amount of SSTR5 cDNA transcript of the gsp-positive tumors did not differ from that of the gsp-negative tumors. These results suggest that SSTR5 expression is not a major determinant for the GH response to octreotide, and its expression is not increased in gsp-positive adenomas.
성장호르몬분비성 뇌하수체 선종의 성장호르몬 방출호르몬 수용체 유전자의 발현과 내분비적 양상과의 관계
류미숙,양인명,박승준,우정택,김성운,김진우,김영설,최영길 경희대학교 생명자원과학연구원 1997 遺傳工學論文集 Vol.9 No.-
Growth hormone-releasing hormone (GHRH) plays a key role in the regulation of the proliferation and differentiation of somatomammotroph cells as well as secretion of GH. The actions of GHRH are mediated through the GHRH receptor (GHRH-R) that is a G protein coupled receptor with seven transmembrane domains. It has been demonstrated that alternative splicing occurs in the third cytoplasmic domain of rat and human GHRH-R mRNA. However, the clinical significance of the alternative splicing remains to be unsolved. To find an insight into the clinical significance, we investigate the correlation between the GHRH-R gene expression and a variety of clinical clinical and endocrinological findings in 11 acromegalic patients. Three different sized cDNA fragments 250 bp, 700 bp and 810 bp, were found after RT-PCR. The amount of 250 bp fragment was higher than those of the other two fragments. The clinical findings (age, size, GH level, frequency of paradoxical response to TRH or GnRH. octreotide response, hypothalamc somatostatinergic activity of the group with high expression of the 250 bp fragment did not significantly differ from those of the group with low expression. The GHRH-R gene expression of tumors with gsp oncogene did not significantly differ from that of tumors without gsp oncogene. These results suggest that the expression of GHRH-R gene may not be an important determinant for tumor growth, and the lower GH response to GHRH of tumors with gsp oncogene may not be attributed to the lower expression of GHRH-R gene. The expression of GHRH-R is likely to be regulated by a certain property of tumors for GH secretion and growth.