Sang Jin Kim

Bio: Sang Jin Kim is an academic researcher from Samsung Medical Center. The author has contributed to research in topics: Medicine & Macular degeneration. The author has an hindex of 23, co-authored 192 publications receiving 1705 citations. Previous affiliations of Sang Jin Kim include Inje University & Soonchunhyang University Hospital.

Clipping vs coiling of posterior communicating artery aneurysms with third nerve palsy

Abstract: The authors investigated the evolution of third nerve palsy in patients with posterior communicating artery aneurysms who underwent coiling vs clipping. There was no statistical difference of complete third nerve palsy recovery in both treatments. Both techniques were of clinical benefit. Older age, diabetes, delayed interventions, and complete third nerve palsy at presentation indicated a poor prognosis for recovery.

Increased expression of focal adhesion kinase in thyroid cancer: immunohistochemical study.

Abstract: Focal adhesion kinase (FAK) is a tyrosine kinase that is found in cellular structures called focal adhesions. FAK appears to be a key element in signal transduction pathways involved in cell adhesion and locomotion. FAK is overexpressed in various tumors, including tumors derived from regions of the head and neck, colon, breast, prostate, and liver. In this study, we investigated immunohistochemically whether FAK expression was increased in thyroid cancers. FAK staining was not seen in any of the 20 normal thyroid tissues or the 6 nodular hyperplasia specimens. In contrast, FAK staining was observed in all of 17 papillary carcinomas, 9 follicular carcinomas, 8 medullary carcinomas, and 2 anaplastic carcinomas. Nine of 17 follicular adenomas showed FAK immunoreactivity. FAK was not expressed in normal tissue and nodular hyperplasia, but was expressed in some of the follicular adenoma, and all of the follicular, papillary, medullary and anaplastic thyroid carcinoma. This result indicates that the up-regulation of FAK may play a role in the development of thyroid carcinogenesis.

Mutations in PCYT1A, Encoding a Key Regulator of Phosphatidylcholine Metabolism, Cause Spondylometaphyseal Dysplasia with Cone-Rod Dystrophy

Abstract: The spondylometaphyseal dysplasias (SMDs) are a group of about a dozen rare disorders characterized by short stature, irregular, flat vertebrae, and metaphyseal abnormalities. Aside from spondylometaphyseal dysplasia Kozlowski type (MIM 184252) caused by mutations in TRPV4 (MIM 605427) and spondyloenchondrodysplasia (MIM 607944) resulting from mutations in ACP5 (MIM 171640), the genetic etiologies of SMDs are unknown. 1 Two of these unexplained SMDs have ophthalmologic manifestations: SMD with cone-rod dystrophy (SMD-CRD [MIM 608940]) and axial SMD with retinal degeneration (MIM 602271). Delineated clinically a decade ago, SMD-CRD is a presumed autosomal-recessive disorder with postnatal growth deficiency leading to profound short stature; rhizomelia with bowing of the lower extremities; platyspondyly with anterior vertebral protrusions; progressive metaphyseal irregularity and cupping with shortened tubular bones; and early-onset, progressive visual impairment associated with a pigmentary maculopathy and electroretinographic evidence of cone-rod dysfunction. 2‐5 In contrast to retinitis pigmentosa, the CRDs have early involvement of cone photoreceptors. 6

Outcomes after laser versus combined laser and bevacizumab treatment for type 1 retinopathy of prematurity in zone i.

Abstract: PURPOSE To investigate the anatomical and refractive outcomes in patients with Type 1 retinopathy of prematurity in Zone I. METHODS The medical records of 101 eyes of 51 consecutive infants with Type 1 retinopathy of prematurity in Zone I were analyzed. Infants were treated by conventional laser photocoagulation (Group I), combined intravitreal bevacizumab injection and Zone I sparing laser (Group II), or intravitreal bevacizumab with deferred laser treatment (Group III). The proportion of unfavorable anatomical outcomes including retinal fold, disc dragging, retrolental tissue obscuring the view of the posterior pole, retinal detachment, and early refractive errors were compared among the three groups. RESULTS The mean gestational age at birth and the birth weight of all 51 infants were 24.3 ± 1.1 weeks and 646 ± 143 g, respectively. In Group I, an unfavorable anatomical outcome was observed in 10 of 44 eyes (22.7%). In contrast, in Groups II and III, all eyes showed favorable anatomical outcomes without reactivation or retreatment. The refractive error was less myopic in Group III than in Groups I and II (spherical equivalent of -4.62 ± 4.00 D in Group I, -5.53 ± 2.21 D in Group II, and -1.40 ± 2.19 D in Group III; P < 0.001). CONCLUSION In Type 1 retinopathy of prematurity in Zone I, intravitreal bevacizumab with concomitant or deferred laser therapy yielded a better anatomical outcome than conventional laser therapy alone. Moreover, intravitreal bevacizumab with deferred laser treatment resulted in less myopic refractive error.

Enhanced Depth Imaging Optical Coherence Tomography of the Choroid in Normal Eyes

Abstract: PURPOSE To measure macular choroidal thickness in normal eyes at different points using enhanced depth imaging (EDI) optical coherence tomography (OCT) and to evaluate the association of choroidal thickness and age. DESIGN Retrospective, observational case series. METHODS EDI OCT images were obtained in patients without significant retinal or choroidal pathologic features. The images were obtained by positioning a spectral-domain OCT device close enough to the eye to acquire an inverted image. Seven sections were obtained within a 5 x 30-degree area centered at the fovea, with 100 scans averaged for each section. The choroid was measured from the outer border of the retinal pigment epithelium to the inner scleral border at 500-microm intervals of a horizontal section from 3 mm temporal to the fovea to 3 mm nasal to the fovea. Statistical analysis was performed to evaluate variations of choroidal thickness at each location and to correlate choroidal thickness and patient age. RESULTS The mean age of the 30 patients (54 eyes) was 50.4 years (range, 19 to 85 years), and 14 patients (46.7%) were female. The choroid was thickest underneath the fovea (mean, 287 microm; standard deviation, +/- 76 microm). Choroidal thickness decreased rapidly in the nasal direction and averaged 145 microm (+/- 57 microm) at 3 mm nasal to the fovea. Increasing age was correlated significantly with decreasing choroidal thickness at all points measured. Regression analysis suggested that the subfoveal choroidal thickness decreased by 15.6 microm for each decade of life. CONCLUSIONS Choroidal thickness seems to vary topographically within the posterior pole. The thickness of the choroid showed a negative correlation with age. The decrease in the thickness of the choroid may play a role in the pathophysiologic features of various age-related ocular conditions.

Plasma phospholipids identify antecedent memory impairment in older adults

Abstract: Alzheimer's disease causes a progressive dementia that currently affects over 35 million individuals worldwide and is expected to affect 115 million by 2050 (ref. 1). There are no cures or disease-modifying therapies, and this may be due to our inability to detect the disease before it has progressed to produce evident memory loss and functional decline. Biomarkers of preclinical disease will be critical to the development of disease-modifying or even preventative therapies. Unfortunately, current biomarkers for early disease, including cerebrospinal fluid tau and amyloid-β levels, structural and functional magnetic resonance imaging and the recent use of brain amyloid imaging or inflammaging, are limited because they are either invasive, time-consuming or expensive. Blood-based biomarkers may be a more attractive option, but none can currently detect preclinical Alzheimer's disease with the required sensitivity and specificity. Herein, we describe our lipidomic approach to detecting preclinical Alzheimer's disease in a group of cognitively normal older adults. We discovered and validated a set of ten lipids from peripheral blood that predicted phenoconversion to either amnestic mild cognitive impairment or Alzheimer's disease within a 2-3 year timeframe with over 90% accuracy. This biomarker panel, reflecting cell membrane integrity, may be sensitive to early neurodegeneration of preclinical Alzheimer's disease.

Signal transduction by focal adhesion kinase in cancer

Abstract: Cellular interactions with extracellular matrix play essential roles in tumor initiation, progression and metastasis. Focal adhesion kinase (FAK) is a cytoplasmic tyrosine kinase identified as a key mediator of signaling by integrins, a major family of cell surface receptors for extracellular matrix, as well as other receptors in both normal and cancer cells. FAK is activated by integrins through disruption of an auto-inhibitory intra-molecular interaction between its kinase domain and the amino terminal FERM domain. The activated FAK forms a binary complex with Src family kinases which can phosphorylate other substrates and trigger multiple intracellular signaling pathways to regulate various cellular functions. Subcellular localization of FAK in focal adhesions is essential for FAK signaling, which is another distinguishing feature of the kinase. Integrin-FAK signaling has been shown to activate a number of signaling pathways through phosphorylation and protein-protein interactions to promote tumorigenesis. FAK also plays a prominent role in tumor progression and metastasis through its regulation of both cancer cells and their microenvironments including cancer cell migration, invasion, epithelial to mesenchymal transition, and angiogenesis. More recently, a role for FAK in tumor initiation and progression has been demonstrated directly using xenograft as well as conditional knockout mouse models. In agreement with these experimental data, overexpression and activation of FAK have been found in a variety of human cancers. A number of small molecule inhibitors for FAK have been developed and in various phases of testing for cancer treatments. Overall, the intensive research on FAK signaling in cancer have yielded a wealth of information on this pivotal kinase and these and future studies are leading to potentially novel therapies for cancer.