Significant improvement of a nevus spilus-type congenital melanocytic nevus with oral selumetinib.

Giant congenital melanocytic nevi (GCMN) can be cosmetically significant and can lead to melanoma. There is no standard pharmacologic treatment for GCMN. We present the case of an 8-year-old female with kaposiform lymphangiomatosis caused by an NRAS mutation whose nevus spilus-type GCMN improved on oral selumetinib.

Analysis of ultrasonographic images using a deep learning-based model as ancillary diagnostic tool for diagnosing gallbladder polyps.

BACKGROUND: Accurately diagnosing gallbladder polyps (GBPs) is important to avoid misdiagnosis and overtreatment. AIMS: To evaluate the efficacy of a deep learning model and the accuracy of a computer-aided diagnosis by physicians for diagnosing GBPs. METHODS: This retrospective cohort study was conducted from January 2006 to September 2021, and 3,754 images from 263 patients were analyzed. The outcome of this study was the efficacy of the developed deep learning model in discriminating neoplastic GBPs (NGBPs) from non-NGBPs and to evaluate the accuracy of a computer-aided diagnosis with that made by physicians. RESULTS: The efficacy of discriminating NGBPs from non- NGBPs using deep learning was 0.944 (accuracy, 0.858; sensitivity, 0.856; specificity, 0.861). The accuracy of an unassisted diagnosis of GBP was 0.634, and that of a computer-aided diagnosis was 0.785 (p<0.001). There were no significant differences in the accuracy of a computer-aided diagnosis between experienced (0.835) and inexperienced (0.772) physicians (p = 0.251). A computer-aided diagnosis significantly assisted inexperienced physicians (0.772 vs. 0.614; p < 0.001) but not experienced physicians. CONCLUSIONS: Deep learning-based models discriminate NGBPs from non- NGBPs with excellent accuracy. As ancillary diagnostic tools, they may assist inexperienced physicians in improving their diagnostic accuracy.

C-reactive protein binds to integrin α2 and Fcγ receptor I, leading to breast cell adhesion and breast cancer progression.

C-reactive protein (CRP) is an acute phase protein synthesized upon the inflammatory responses, associated with breast cancer. The process of tumor cell invasion and metastasis involves the adherence of cells to the extracellular matrix via integrin as a receptor for matrix molecules. The present study investigated the role of CRP in the adhesive phenotype of breast cells and the underlying mechanisms. Here, we first showed that CRP induces adhesion of MCF10A human breast epithelial cells through the activation of integrin α2 signaling. Expression of integrin α2 was induced by CRP in which transcription factors c-fos and SP1 may be involved. Binding of CRP with integrin α2 leads to the activation of focal adhesion kinase (FAK), paxillin and ERKs. CRP also binds to an Fcγ receptor Fcγ receptor I (FcγRI), and induces activation of paxillin, FAK and ERKs. Integrin α2 and FAK have crucial roles in the adhesive and invasive phenotypes as well as MMP-9 upregulation induced by CRP in MCF10A cells. Treatment with an inflammatory lipid sphingosine-1-phosphate induced CRP, which may be secreted and exert an autocrine effect by binding to FcγRI and integrin α2. Involvement of CRP in adhesion, invasion, anchorage-independent growth and upregulation of integrin α2, paxillin and FAK was observed in MDA-MB-231 triple-negative human breast cancer (TNBC) cells. Using an in vivo invasion model and an orthotopic mouse tumor model with MDA-MB-231 cells, we showed that CRP has an important role in intravasation and tumor growth in vivo, demonstrating the in vivo relevance of our in vitro results. The present study elucidates a critical molecular basis between CRP, integrin α2 and FcγRI pathways in MCF10A breast cells and MDA-MB-231 TNBC cells, thereby providing useful information on CRP-induced aggressiveness of breast cells in the inflammatory microenvironment.

Transformation of hepatitis C antiviral treatment in a national healthcare system following the introduction of direct antiviral agents.

BACKGROUND: Highly effective direct antiviral agents (DAAs) for hepatitis C virus (HCV) were introduced recently. Their utilisation has been limited by high cost and low access to care. AIM: To describe the effect of DAAs on HCV treatment and cure rates in the United States Veterans Affairs (VA) national healthcare system. METHODS: We identified all HCV antiviral treatment regimens initiated from 1 January 1999 to 31 December 2015 (n = 105 369) in the VA national healthcare system, and determined if they resulted in sustained virological response (SVR). RESULTS: HCV antiviral treatment rates were low (1981-6679 treatments/year) in the interferon era (1999-2010). The introduction of simeprevir and sofosbuvir in 2013 and ledipasvir/sofosbuvir and paritaprevir/ombitasvir/ritonavir/dasabuvir in 2014 were followed by increases in annual treatment rates to 9180 in 2014 and 31 028 in 2015. The number of patients achieving SVR was 1313 in 2010, the last year of the interferon era, and increased 5.6-fold to 7377 in 2014 and 21-fold to 28 084 in 2015. The proportion of treated patients who achieved SVR increased from 19.2% in 1999 and 36.0% in 2010 to 90.5% in 2015. Within 2015, monthly treatment rates ranged from 727 in July to 6868 in September correlating with the availability of funds for DAAs. CONCLUSIONS: DAAs resulted in a 21-fold increase in the number of patients achieving HCV cure. Treatment rates in 2015 were limited primarily by the availability of funds. Further increases in funding and cost reductions of DAAs in 2016 suggest that the VA could cure the majority of HCV-infected Veterans in VA care within the next few years.

Reduced tissue osmolarity increases TRPV4 expression and pro-inflammatory cytokines in intervertebral disc cells.

The mechanical behaviour and cellular metabolism of intervertebral discs (IVDs) and articular cartilage are strongly influenced by their proteoglycan content and associated osmotic properties. This osmotic environment is a biophysical signal that changes with disease and may contribute to the elevated matrix breakdown and altered biologic response to loading observed in IVD degeneration and osteoarthritis. This study tested the hypothesis that changes in osmo-sensation by the transient receptor potential vallinoid-4 (TRPV4) ion channel occur with disease and contribute to the inflammatory environment found during degeneration. Immunohistochemistry on bovine IVDs from an inflammatory organ culture model were used to investigate if TRPV4 is expressed in the IVD and how expression changes with degeneration. Western blot, live-cell calcium imaging, and qRT-PCR were used to investigate whether osmolarity changes or tumour necrosis factor α (TNFα) regulate TRPV4 expression, and how altered TRPV4 expression influences calcium signalling and pro-inflammatory cytokine expression. TRPV4 expression correlated with TNFα expression, and was increased when cultured in reduced medium osmolarity and unaltered with TNFα-stimulation. Increased TRPV4 expression increased the calcium flux following TRPV4 activation and increased interleukin-1ß (IL-1ß) and IL-6 gene expression in IVD cells. TRPV4 expression was qualitatively elevated in regions of aggrecan depletion in degenerated human IVDs. Collectively, results suggest that reduced tissue osmolarity, likely following proteoglycan degradation, can increase TRPV4 signalling and enhance pro-inflammatory cytokine production, suggesting changes in TRPV4 mediated osmo-sensation may contribute to the progressive matrix breakdown in disease.

Renal Cell Cancer in a European Regional Renal Transplant Population: Is There a Role for Immediate Native Renal Radiological Surveillance Before and After Transplantation?

BACKGROUND: The risk of the development of renal cell cancer (RCC) in renal transplant recipients is several times higher than the general population. There can often be a delay between initial radiological imaging and patients undergoing renal transplantation. We present and evaluate the prevalence and clinical characteristics of RCC in renal transplant recipients at a single UK transplant center, with particular focus on tumors diagnosed in the immediate post-operative period, that is, likely present before transplantation. METHODS: This is a retrospective cohort study examining all renal transplant recipients with the diagnosis of RCC of native and/or graft kidneys followed up in a single UK transplant center. RESULTS: Between January 2002 and April 2014, 1386 patients underwent renal transplantation. 19 of 1386 patients had development of RCC (1.4%): 17 native and 2 graft tumors. The mean interval between pre-operative native renal imaging and transplantation was 3.5 years in 13 of 19 patients (range, 1-10 years). Six patients had no documented renal imaging before their renal transplant. The median time from transplantation to diagnosis of RCC was 5 years (range, 1 month to 30 years). In 5 patients (26.3%), RSS developed within 6 months of undergoing renal transplantation. CONCLUSIONS: In our study, we identified several patients with RCC diagnosed shortly after surgery, which raised the possibility that this was present before transplantation. With transplant recipients at increased risk of development of RCC and early detection key in the management of RCC, there appears to be a role for native renal radiological screening for patients undergoing renal transplantation.

Gα12 gep oncogene deregulation of p53-responsive microRNAs promotes epithelial-mesenchymal transition of hepatocellular carcinoma.

Hepatocellular carcinoma (HCC) has a poor prognosis owing to aggressive phenotype. Gα12 gep oncogene product couples to G-protein-coupled receptors, whose ligand levels are frequently increased in tumor microenvironments. Here, we report Gα12 overexpression in human HCC and the resultant induction of zinc-finger E-box-binding homeobox 1 (ZEB1) as mediated by microRNA deregulation. Gα12 expression was higher in HCC than surrounding non-tumorous tissue. Transfection of Huh7 cell with an activated mutant of Gα12 (Gα12QL) deregulated microRNA (miRNA or miR)-200b/a/429, -194-2/192 and -194-1/215 clusters in the miRNome. cDNA microarray analyses disclosed the targets affected by Gα12 gene knockout. An integrative network of miRNAs and mRNA changes enabled us to predict ZEB1 as a key molecule governed by Gα12. Decreases of miR-200a/b, -192 and -215 by Gα12 caused ZEB1 induction. The ability of Gα12 to decrease p53 levels, as a result of activating protein-1 (AP-1)/c-Jun-mediated mouse double minute 2 homolog induction, contributed to transcriptional deregulation of the miRNAs. Gα12QL induced ZEB1 and other epithelial-mesenchymal transition markers with fibroblastoid phenotype change. Consistently, transfection with miR-200b, -192 or -215 mimic prevented the ability of Gα12QL to increase tumor cell migration/invasion. In xenograft studies, sustained knockdown of Gα12 decreased the overall growth rate and average volume of tumors derived from SK-Hep1 cell (mesenchymal-typed). In HCC patients, miR-192, -215 and/or -200a were deregulated with microvascular invasion or growth advantage. In the HCC samples with higher Gα12 level, a correlation existed in the comparison of relative changes of Gα12 and ZEB1. In conclusion, Gα12 overexpressed in HCC causes ZEB1 induction by deregulating p53-responsive miRNAs, which may facilitate epithelial-mesenchymal transition and growth of liver tumor. These findings highlight the significance of Gα12 upregulation in liver tumor progression, implicating Gα12 as an attractive therapeutic target.

Wafer-scale surface roughening for enhanced light extraction of high power AlGaInP-based light-emitting diodes.

A new approach to surface roughening was established and optimized in this paper for enhancing the light extraction of high power AlGaInP-based LEDs, by combining ultraviolet (UV) assisted imprinting with dry etching techniques. In this approach, hexagonal arrays of cone-shaped etch pits are fabricated on the surface of LEDs, forming gradient effective-refractive-index that can mitigate the emission loss due to total internal reflection and therefore increase the light extraction efficiency. For comparison, wafer-scale FLAT-LEDs without any surface roughening, WET-LEDs with surface roughened by wet etching, and DRY-LEDs with surface roughened by varying the dry etching time of the AlGaInP layer, were fabricated and characterized. The average output power for wafer-scale FLAT-LEDs, WET-LEDs, and DRY3-LEDs (optimal) at 350 mA was found to be 102, 140, and 172 mW, respectively, and there was no noticeable electrical degradation with the WET-LEDs and DRY-LEDs. The light output was increased by 37.3% with wet etching, and 68.6% with dry etching surface roughening, respectively, without compromising the electrical performance of LEDs. A total number of 1600 LED chips were tested for each type of LEDs. The yield of chips with an optical output power of 120 mW and above was 0.3% (4 chips), 42.8% (684 chips), and 90.1% (1441 chips) for FLAT-LEDs, WET-LEDs, and DRY3-LEDs, respectively. The dry etching surface roughening approach developed here is potentially useful for the industrial mass production of wafer-scale high power LEDs.

Inflammatory lipid sphingosine-1-phosphate upregulates C-reactive protein via C/EBPß and potentiates breast cancer progression.

A crucial role of the inflammatory lipid sphingosine-1-phosphate (S1P) in breast cancer aggressiveness has been reported. Recent clinical studies have suggested that C-reactive protein (CRP) has a role in breast cancer development. However, limited information is available on the molecular basis for the expression of CRP and its functional significance in breast cell invasion. The present study aimed to elucidate the molecular link between S1P and CRP during the invasive process of breast epithelial cells. This is the first report showing that transcription of CRP was markedly activated by S1P in breast cells. Our data suggest that not only S1P treatment but also the endogenously produced S1P may upregulate CRP in breast carcinoma cells. Transcription factors CCAAT/enhancer-binding protein beta and c-fos were required for S1P-induced CRP expression. Coupling of S1P3 to heterotrimeric Gαq triggered the expression of CRP, utilizing signaling pathways involving reactive oxygen species (ROS), Ca(2+) and extracellular signal-related kinases (ERKs). S1P-induced CRP expression was crucial for the transcriptional activation of matrix metalloproteinase-9 through ERKs, ROS and c-fos, leading to breast cell invasion. Using a xenograft mice tumor model, we demonstrated that S1P induced CRP expression both in vitro and in vivo. Taken together, our findings have revealed a molecular basis for S1P-induced transcriptional activation of CRP and its functional significance in the acquisition of the invasive phenotype of human breast epithelial cells under inflammatory conditions. Our findings may provide useful information on the identification of useful therapeutic targets for inflammatory breast cancer.

Anal sphincter fibrillation: is this a new finding that identifies resistant chronic anal fissures that respond to botulinum toxin?

AIM: Anal fissures can be resistant to treatment and some patients may undergo several trials of medical therapy before definitive surgery. It would be useful to identify predictors of poor response to medical therapy. This study assesses the role of anorectal physiological criteria to identify patients with anal fissure predicted to fail botulinum toxin (BT) treatment. METHOD: A retrospective analysis of anorectal physiological data collected for patients with resistant chronic anal fissures, referred to one consultant surgeon between 2007 and 2011, was undertaken. These were correlated with treatment plans and healing rates. RESULTS: Twenty-five patients with idiopathic chronic anal fissures underwent anorectal physiology studies and were subsequently treated with BT injection. Eleven had a characteristic high-frequency low-amplitude 'saw tooth' waveform or anal sphincter fibrillation (ASF) and higher anal sphincter pressures. Nine (82%) of these patients had resolution of their anal fissure symptoms following treatment with BT. Of 14 patients with no evidence of ASF and a greater range of anal sphincter pressures, only one (7%) had resolution following BT. CONCLUSION: ASF appears to be an anorectal physiological criterion that helps predict response of anal fissures to BT injection. This could help streamline fissure management.

Ossification variants of the femoral condyles are not associated with osteochondritis dissecans.

PURPOSE: To determine if ossification variants of the femoral condyles involving the subchondral bone plate are associated with osteochondritis dissecans (OCD). MATERIALS AND METHODS: The prevalence of ossification variants of the unaffected femoral condyle in 116 patients (aged 9-14 years) with unicondylar OCD on MRI (magnetic resonance imaging) of the knee was compared to a control group of 579 patients (aged 9-14 years) without OCD. The evolution of the ossification variants in both groups was studied by reviewing follow-up MR imaging side by side with the baseline study. RESULTS: The prevalence of ossification variants in the unaffected condyle in patients with OCD (12.9%) and in the control group of patients without OCD (12.6%) was similar (p=0.88). Evolution of ossification variants to OCD was not seen on follow-up MRI examinations. All variants had decreased in size or were no longer visible. CONCLUSION: Ossification variants of the femoral condyle that involve the subchondral bone plate are not associated with OCD. CLINICAL RELEVANCE STATEMENT: Ossification variants are not associated with OCD, indicating that routine MRI follow-up in affected children is not mandatory.

Challenging pyogenic cerebral abscess complicated by subdural empyema. A case report.

Brain abscesses develop in response to a parenchymal infection with pyogenic bacteria, beginning as a localized area of cerebritis and evolving into a suppurative lesion surrounded by a well-vascularized fibrotic capsule. The leading etiologic agents of brain abscess are the streptococcal strains and S. aureus. Abscesses may also be secondary to fungal or parasitic organisms. Brain abscess represents a significant medical problem, accounting for one in every 10,000 hospital admissions in the United States, and remains a serious situation despite recent advances made in detection and therapy. These lesions often produce complex clinical and radiologic findings and require prompt recognition and treatment to avoid a fatal neurologic outcome. Subdural empyema represents an important type of intracranial suppurative infectious-inflammatory disorder. Clinically, these patients initially have signs and symptoms of meningitis, but this course might be complicated later by the development of seizures and focal neurologic signs.

Ara h 2: crystal structure and IgE binding distinguish two subpopulations of peanut allergic patients by epitope diversity.

BACKGROUND: Peanut allergy affects 1% of the population and causes the most fatal food-related anaphylactic reactions. The protein Ara h 2 is the most potent peanut allergen recognized by 80-90% of peanut allergic patients. METHODS: The crystal structure of the major peanut allergen Ara h 2 was determined for the first time at 2.7 Å resolution using a customized maltose-binding protein (MBP)-fusion system. IgE antibody binding to the MBP fusion construct vs the natural allergen was compared by ELISA using sera from peanut allergic patients. RESULTS: The structure of Ara h 2 is a five-helix bundle held together by four disulfide bonds and related to the prolamin protein superfamily. The fold is most similar to other amylase and trypsin inhibitors. The MBP--Ara h 2 fusion construct was positively recognized by IgE from 76% of allergic patients (25/33). Two populations of patients could be identified. Subpopulation 1 (n = 14) showed an excellent correlation of IgE antibody binding to natural vs recombinant Ara h 2. Subpopulation 2 (n = 15) showed significantly reduced IgE binding to the MBP fusion protein. Interestingly, about 20% of the IgE binding in subpopulation 2 could be recovered by increasing the distance between MBP and Ara h 2 in a second construct. DISCUSSION: The reduced IgE binding to the MBP--Ara h 2 of subpopulation 2 indicates that the MBP molecule protects an immunodominant epitope region near the first helix of Ara h 2. Residues involved in the epitope(s) are suggested by the crystal structure. The MBP--Ara h 2 fusion constructs will be useful to further elucidate the relevance of certain epitopes to peanut allergy.

An eight year audit before and after the introduction of modified early warning score (MEWS) charts, of patients admitted to a tertiary referral intensive care unit after CPR.

AIMS: To determine whether cardiac arrest calls, the proportion of adult patients admitted to intensive care after CPR and their associated mortalities were reduced, in a four year period after the introduction of a 24/7 Critical Care Outreach Service and MEWS (Modified Early Warning System) Charts. METHODS: A retrospective analysis of prospectively collected data during two four-year periods, (2002-05 and 2006-09) in a UK University Teaching Hospital Comparisons were via χ(2) test. A p value of ≤0.05 was regarded as being significant. RESULTS: In the second audit period, compared to the first one, the number of cardiac arrest calls relative to adult hospital admissions decreased significantly (0.2% vs. 0.4%; p<0.0001), the proportion of patients admitted to intensive care having undergone in-hospital CPR fell significantly (2% vs. 3%; p=0.004) as did the in-hospital mortality of these patients (42% vs. 52%; p=0.05). CONCLUSION: The four years following the introduction of a 24/7 Critical Care Outreach Service and MEWS Charts were associated with significant reductions in the incidence of cardiac arrest calls, the proportion of patients admitted to intensive care having undergone in-hospital CPR and their in-hospital mortality.

BAX inhibitor-1 enhances cancer metastasis by altering glucose metabolism and activating the sodium-hydrogen exchanger: the alteration of mitochondrial function.

The anti-apoptotic protein, BAX inhibitor-1 (BI-1), has a role in cancer/tumor progression. BI-1-overexpressing HT1080 and B16F10 cells produced higher lung weights and tumor volumes after injection into the tail veins of mice. Transfection of BI-1 siRNA into cells before injection blocked lung metastasis. in vitro, the overexpression of BI-1 increased cell mobility and invasiveness, with highly increased glucose consumption and cytosolic accumulation of lactate and pyruvate, but decreased mitochondrial O(2) consumption and ATP production. Glucose metabolism-associated extracellular pH also decreased as cells excreted more H(+), and sodium hydrogen exchanger (NHE) activity increased, probably as a homeostatic mechanism for intracellular pH. These alterations activated MMP 2/9 and cell mobility and invasiveness, which were reversed by the NHE inhibitor, 5-(N-ethyl-N-isopropyl) amiloride (EIPA), suggesting a role for NHE in cancer metastasis. In both in vitro and in vivo experiments, C-terminal deleted (CDeltaBI-1) cells showed similar results to control cells, suggesting that the C-terminal motif is required for BI-1-associated alterations of glucose metabolism, NHE activation and cancer metastasis. These findings strongly suggest that BI-1 reduces extracellular pH and regulates metastasis by altering glucose metabolism and activating NHE, with the C-terminal tail having a pivotal role in these processes.

Caspase-3 activation as a key factor for HBx-transformed cell death.

OBJECTIVES: Nuclear factor-kappa B (NF-kappaB) activation has been associated with the tumorigenic growth of hepatitis B virus X protein (HBx)-transformed cells. This study was aimed to find a key target for treatment of HBx-mediated cancers. MATERIALS AND METHODS: NF-kappaB activation, endoplasmic reticulum-stress (ER-stress), caspase-3 activation, and cell proliferation were evaluated after Chang/HBx cells permanently expressing HBx viral protein were treated with inhibitors of NF-kappaB, proteasome and DNA topoisomerase. RESULTS: Inhibition of NF-kappaB transcriptional activity by transient transfection with mutant plasmids encoding Akt1 and glycogen synthase kinase-3beta (GSK-3beta), or by treatment with chemical inhibitors, wortmannin and LY294002, showed little effect on the survival of Chang/HBx cells. Furthermore, IkappaBalpha (S32/36A) mutant plasmid or other NF-kappaB inhibitors, 1-pyrrolidinecarbonidithioic acid and sulphasalazine, were also shown to have little effect on the cell proliferation. By contrast, proteasome inhibitor-1 (Pro1) and MG132 enhanced the HBx-induced ER-stress response and the subsequent activation of caspase-12, -9 and -3 and reduced cell proliferation. Camptothecin (CPT), however, triggered activation of caspase-3 without induction of caspase-12, and reduced cell proliferation. In addition, CPT-induced cell death was reversed by pre-treatment with z-DEVD, a caspase-3-specific inhibitor. CONCLUSIONS: Detailed exploitation of the regulators of caspase-3 activation could open the gate for finding an efficient target for development of anticancer therapeutics against HBx-transformed hepatocellular carcinoma.

NF-kappaB inhibition enhances caspase-3 degradation of Akt1 and apoptosis in response to camptothecin.

DNA damaging agents, such as camptothecin, and ionizing radiation (IR), can induce both NF-kappaB activation and apoptosis, however, the mechanism of their inter-regulation is not yet clear. In the present study, we discovered that Akt1 is degraded when cells deficient in Ataxia Telangiectasia mutated (ATM) were treated to CPT for apoptosis induction. While CPT-induced NF-kappaB activation could not be detected in ATM-deficient AT5BIVA cells, caspase-3 activation occurred and was even further enhanced by pretreatment with proteasome inhibitor-1 (Pro1), a NF-kappaB inhibitor. In contrast, activation of NF-kappaB but not of caspase-3 by CPT could be found in normal MRC5CV1 cells. NF-kappaB inhibition by Pro1, dominant negative mutant IkappaBalpha (S32/36) or p65 (N250), however, induced the caspase-3 activation in the normal cells, indicating the role of ATM-mediated NF-kappaB activation against cell apoptosis. On the other hand, interestingly, CPT significantly reduced the level of Akt1, this effect further enhanced by Pro1 pretreatment in AT5BIVA cells. In MRC5CV1 cells, however, Akt1 level could be reduced only when CPT and NF-kappaB inhibitors were co-treated to the cells, and this reversed by DEVD-cho treatment, demonstrating the caspase-3-mediated Akt1 degradation. Moreover, although MRC5CV1 cells were much more resistant to CPT compared with AT5BIVA, wortmannin and LY294002 significantly increased the chemosensitivity of MRC5CV1 cells to CPT. Given the accumulating evidences demonstrating Akt as a promising anticancer therapeutic target, all these results suggest that DNA damage induced apoptosis could be regulated by ATM-mediated NF-kappaB activation, and that Akt1 degradation be necessarily required for this apoptotic process.

Determinants of psychological distress over time among older Korean immigrants and Non-Hispanic White elders: evidence from a two-wave panel study.

The purpose of this study is to examine racial/ethnic differences in the change of psychological distress as measured by CES-D over time and its associated factors between older Korean immigrants and non-Hispanic White elders, based on a social stress perspective. Data come from a two-wave panel survey of 172 older Korean immigrants and 157 non-Hispanic White elders, with a follow-up period of 12 to 15 months. The sample was drawn from a three-stage probability sampling method. Ordinary least square regressions in a hierarchical process and change score method were used to analyze the two-wave panel data. Older Korean immigrants reported higher levels of psychological distress than the non-Hispanic White elderly at both Time 1 and Time 2. Changes in self-assessed health status and functional limitations were significantly associated with change in psychological distress for both ethnic groups. Increased social support significantly decreased psychological distress at Time 2, for older Korean immigrants only. This study discusses practice and policy implications for service and interventions for older immigrants to assist their adjustment to a host society.