Protective Effects of the Postbiotic Lactobacillus plantarum MD35 on Bone Loss in an Ovariectomized Mice Model.

Postmenopausal osteoporosis is caused by estrogen deficiency, which impairs bone homeostasis, resulting in increased osteoclastic resorption without a corresponding increase in osteoblastic activity. Postbiotics have several therapeutic properties, including anti-obesity, anti-diabetic, anti-inflammatory, and anti-osteoporotic effects. However, the beneficial effects of the postbiotic MD35 of Lactobacillus plantarum on bone have not been studied. In this study, we demonstrated that the postbiotic L. plantarum MD35, isolated from young radish water kimchi, influences osteoclast differentiation in mouse bone marrow-derived macrophage (BMM) culture. In addition, it was effective protecting against estrogen deficiency-induced bone loss in ovariectomized (OVX) mice, an animal model of postmenopausal osteoporosis. In BMM cells, postbiotic MD35 inhibited the receptor activator of nuclear factor-kappa B of NF-κB ligand (RANKL)-induced osteoclast differentiation by attenuating the phosphorylation of extracellular signal-related kinase, significantly suppressing the resorption activity and down-regulating the expression of RANKL-mediated osteoclast-related genes. In the animal model, the oral administration of postbiotic MD35 remarkably improved OVX-induced trabecular bone loss and alleviated the destruction of femoral plate growth. Therefore, postbiotic MD35 could be a potential therapeutic candidate for postmenopausal osteoporosis by suppressing osteoclastogenesis through the regulation of osteoclast-related molecular mechanisms.

Relationship Between Alcohol Consumption and Risky Sexual Behaviors Among Adolescents and Young Adults: A Meta-Analysis.

Objectives: Adolescents exposed to alcohol have increased risky sexual behaviors (RSBs); however, the association between alcohol consumption and RSBs has to be systematically and quantitatively reviewed. We conducted a meta-analysis of the literature to systematically and quantitatively review the association between alcohol consumption and RSBs in adolescents and young adults. Methods: We searched for qualified articles published from 2000 to 2020 and calculated pooled odds ratios (ORs) using the random-effect model. We also conducted meta-regression and sensitivity analyses to identify potential heterogeneity moderators. Results: The meta-analysis of 50 studies involving 465,595 adolescents and young adults indicated that alcohol consumption was significantly associated with early sexual initiation (OR = 1.958, 95% confidence interval (CI) = 1.635-2.346), inconsistent condom use (OR = 1.228, 95% CI = 1.114-1.354), and having multiple sexual partners (OR = 1.722, 95% CI = 1.525-1.945). Conclusion: Alcohol consumption is strongly associated with RSBs, including early sexual initiation, inconsistent condom use, and multiple sexual partners among adolescents and young adults. To prevent the adverse consequences of alcohol consumption, drinking prevention programs should be initiated at an early age and supported by homes, schools, and communities.

ANGPTL4 stabilizes atherosclerotic plaques and modulates the phenotypic transition of vascular smooth muscle cells through KLF4 downregulation.

Atherosclerosis, the leading cause of death, is a vascular disease of chronic inflammation. We recently showed that angiopoietin-like 4 (ANGPTL4) promotes cardiac repair by suppressing pathological inflammation. Given the fundamental contribution of inflammation to atherosclerosis, we assessed the role of ANGPTL4 in the development of atherosclerosis and determined whether ANGPTL4 regulates atherosclerotic plaque stability. We injected ANGPTL4 protein twice a week into atherosclerotic Apoe-/- mice and analyzed the atherosclerotic lesion size, inflammation, and plaque stability. In atherosclerotic mice, ANGPTL4 reduced atherosclerotic plaque size and vascular inflammation. In the atherosclerotic lesions and fibrous caps, the number of α-SMA(+), SM22α(+), and SM-MHC(+) cells was higher, while the number of CD68(+) and Mac2(+) cells was lower in the ANGPTL4 group. Most importantly, the fibrous cap was significantly thicker in the ANGPTL4 group than in the control group. Smooth muscle cells (SMCs) isolated from atherosclerotic aortas showed significantly increased expression of CD68 and Krüppel-like factor 4 (KLF4), a modulator of the vascular SMC phenotype, along with downregulation of α-SMA, and these changes were attenuated by ANGPTL4 treatment. Furthermore, ANGPTL4 reduced TNFα-induced NADPH oxidase 1 (NOX1), a major source of reactive oxygen species, resulting in the attenuation of KLF4-mediated SMC phenotypic changes. We showed that acute myocardial infarction (AMI) patients with higher levels of ANGPTL4 had fewer vascular events than AMI patients with lower levels of ANGPTL4 (p < 0.05). Our results reveal that ANGPTL4 treatment inhibits atherogenesis and suggest that targeting vascular stability and inflammation may serve as a novel therapeutic strategy to prevent and treat atherosclerosis. Even more importantly, ANGPTL4 treatment inhibited the phenotypic changes of SMCs into macrophage-like cells by downregulating NOX1 activation of KLF4, leading to the formation of more stable plaques.

The adipokine Retnla deficiency increases responsiveness to cardiac repair through adiponectin-rich bone marrow cells.

Resistin-like alpha (Retnla) is a member of the resistin family and known to modulate fibrosis and inflammation. Here, we investigated the role of Retnla in the cardiac injury model. Myocardial infarction (MI) was induced in wild type (WT), Retnla knockout (KO), and Retnla transgenic (TG) mice. Cardiac function was assessed by echocardiography and was significantly preserved in the KO mice, while worsened in the TG group. Angiogenesis was substantially increased in the KO mice, and cardiomyocyte apoptosis was markedly suppressed in the KO mice. By Retnla treatment, the expression of p21 and the ratio of Bax to Bcl2 were increased in cardiomyocytes, while decreased in cardiac fibroblasts. Interestingly, the numbers of cardiac macrophages and unsorted bone marrow cells (UBCs) were higher in the KO mice than in the WT mice. Besides, phosphorylated histone H3(+) cells were more frequent in bone marrow of KO mice. Moreover, adiponectin in UBCs was notably higher in the KO mice compared with WT mice. In an adoptive transfer study, UBCs were isolated from KO mice to transplant to the WT infarcted heart. Cardiac function was better in the KO-UBCs transplanted group in the WT-UBCs transplanted group. Taken together, proliferative and adiponectin-rich bone marrow niche was associated with substantial cardiac recovery by suppression of cardiac apoptosis and proliferation of cardiac fibroblast.

Synergistic Anti-cancer Activity of MH-30 in a Murine Melanoma Model Treated With Cisplatin and its Alleviated Effects Against Cisplatin-induced Toxicity in Mice.

BACKGROUND/AIM: Although cisplatin is an effective anticancer drug, its toxic effects on normal tissues limit its use. We developed a herbal formula, MH-30, with increased fat-soluble polyphenols by improving the manufacturing method of HemoHIM. In this study, we examined whether the combination of MH-30 with cisplatin exerts synergistic antitumor effect while it reduces cisplatin-induced toxicities. MATERIALS AND METHODS: MH-30 was produced by adding the ethanol-insoluble fraction to its extract after decocting herbs in 30% ethanol and water. We used a melanoma-bearing mice model to investigate synergistic anticancer effects. The NK cell activity and cytokine levels were measured by Cr51-release assay and ELISA. The AST, ALT, BUN, and creatinine levels were estimated in the serum. RESULTS: MH-30 effectively inhibited melanoma growth in vitro. Furthermore, MH-30 had a synergistic effect in combination with cisplatin on melanoma growth inhibition in vitro and in vivo. In melanoma-bearing mice, cisplatin alone decreased the activity of NK cells and the levels of IL-2 and IFN-γ, which were effectively restored by the combination of MH-30 with cisplatin. Combined treatment with MH-30 and cisplatin significantly inhibited the cisplatin-induced increase in the levels of AST, ALT, BUN, and creatinine. CONCLUSION: Combination of MH-30 with cisplatin may be a beneficial anticancer treatment with reduced adverse effects.

Korean Immigrant Women's Postpartum Experiences in the United States.

BACKGROUND: Postpartum depression (PPD) affects one in seven women in the United States. Korean Americans are one of the six largest Asian American (AA) subgroups, representing 9% of the AA population in the United States. Women of Asian descent have not always been represented in studies of PPD. PURPOSE: The purpose of this study was to understand postpartum experiences, perceptions of PPD, and mental health help-seeking among Korean women living in the United States. METHODS: Individual, face-to-face, semistructured interviews of Korean immigrant women, over age 18, who were able to read, write, and speak English or Korean, and who had given birth to a live infant within the past 12 months, were conducted using a qualitative exploratory design. Thematic analysis approach was used to analyze qualitative data The Edinburgh Postnatal Depression Screening Scale (EPDS) was used to assess frequency of depressive symptoms over the past week. RESULTS: Eleven women participated. Total EPDS scores ranged from 2 to 17 (mean 6.5, SD = 3.2); three women had scores indicating a high risk for developing PPD. Two overall themes, postpartum experiences and perceptions of PPD and professional help-seeking, along with several subthemes were identified. They included postpartum challenges, importance of keeping Korean postpartum traditions, desire for professional Korean postpartum care, "Sanhoo-Joeri" postpartum support and social networking, normalization of PPD symptoms, family first for health seeking attitude and behavior, and stigma attached to mental health care. CLINICAL IMPLICATIONS: Nurses working with Korean women during postpartum can provide culturally competent care by assessing postpartum care needs, respecting cultural practices, and providing resources such as Korean postpartum care centers Sanhoo-Joeriwon, which can be found in major U.S. cities with large Korean communities (e.g., Los Angeles), and in-home postpartum care providers, Sanhoo-Joerisa. Nurses should be comfortable educating women about normal signs and symptoms of PPD and those requiring immediate medical follow-up.

Antiinflammatory activity of ANGPTL4 facilitates macrophage polarization to induce cardiac repair.

Mesenchymal stem cells (MSCs) can suppress pathological inflammation. However, the mechanisms underlying the association between MSCs and inflammation remain unclear. Under coculture conditions with macrophages, MSCs highly expressed angiopoietin-like 4 (ANGPTL4) to blunt the polarization of macrophages toward the proinflammatory phenotype. ANGPTL4-deficient MSCs failed to inhibit the inflammatory macrophage phenotype. In inflammation-related animal models, the injection of coculture medium or ANGPTL4 protein increased the antiinflammatory macrophages in both peritonitis and myocardial infarction. In particular, cardiac function and pathology were markedly improved by ANGPTL4 treatment. We found that retinoic acid-related orphan receptor α (RORα) was increased by inflammatory mediators, such as IL-1ß, and bound to ANGPTL4 promoter in MSCs. Collectively, RORα-mediated ANGPTL4 induction was shown to contribute to the antiinflammatory activity of MSCs against macrophages under pathological conditions. This study suggests that the capability of ANGPTL4 to induce tissue repair is a promising opportunity for safe stem cell-free regeneration therapy from a translational perspective.

Anti-bacterial effects of enzymatically-isolated sialic acid from glycomacropeptide in a Helicobacter pylori-infected murine model.

BACKGROUND/OBJECTIVES: Helicobacter pylori (H. pylori) colonization of the stomach mucosa and duodenum is the major cause of acute and chronic gastroduodenal pathology in humans. Efforts to find effective anti-bacterial strategies against H. pylori for the non-antibiotic control of H. pylori infection are urgently required. In this study, we used whey to prepare glycomacropeptide (GMP), from which sialic acid (G-SA) was enzymatically isolated. We investigated the anti-bacterial effects of G-SA against H. pylori in vitro and in an H. pylori-infected murine model. MATERIALS/METHODS: The anti-bacterial activity of G-SA was measured in vitro using the macrodilution method, and interleukin-8 (IL-8) production was measured in H. pylori and AGS cell co-cultures by ELISA. For in vivo study, G-SA 5 g/kg body weight (bw)/day and H. pylori were administered to mice three times over one week. After one week, G-SA 5 g/kg bw/day alone was administered every day for one week. Tumor necrosis factor-α (TNF-α), IL-1ß, IL-6, and IL-10 levels were measured by ELISA to determine the anti-inflammatory effects of G-SA. In addition, real-time PCR was performed to measure the genetic expression of cytotoxin-associated gene A (cagA). RESULTS: G-SA inhibited the growth of H. pylori and suppressed IL-8 production in H. pylori and in AGS cell co-cultures in vitro. In the in vivo assay, administration of G-SA reduced levels of IL-1ß and IL-6 pro-inflammatory cytokines whereas IL-10 level increased. Also, G-SA suppressed the expression of cagA in the stomach of H. pylori-infected mice. CONCLUSION: G-SA possesses anti-H. pylori activity as well as an anti-H. pylori-induced gastric inflammatory effect in an experimental H. pylori-infected murine model. G-SA has potential as an alternative to antibiotics for the prevention of H. pylori infection and H. pylori-induced gastric disease prevention.

Guanosine 5'-monophosphate-chelated calcium and iron feed additives maintains egg production and prevents Salmonella Gallinarum in experimentally infected layers.

We evaluated the effects of guanosine 5'-monophosphate (GMP)-chelated calcium and iron (CaFe-GMP) on health and egg quality in layers experimentally infected with Salmonella Gallinarum. In this study, a CaFe-GMP feed additive was added to a commercial layer feed and fed to layers over a four-week period. All were inoculated with Salmonella Gallinarum. Body weight, mortality, clinical symptoms, and poultry production including feed intake, egg production, egg loss, and feed conversion rate were observed, and Salmonella Gallinarum was re-isolated from the liver, spleen, and cecum of the layers. All tested internal organs for the CaFe-GMP additive group exhibited significantly lower re-isolation numbers of Salmonella Gallinarum and less severe pathological changes than those in the control group, indicating that the CaFe-GMP feed supplement induced bacterial clearance and increased resistance to Salmonella Gallinarum. Additionally, due to the inhibitory action of CaFe-GMP on the growth of Salmonella Gallinarum, the CaFe-GMP additive group exhibited better egg production, including a higher laying rate and fewer broken eggs. The results suggest that a 0.16% CaFe-GMP additive may help prevent salmonellosis in the poultry industry.

Anti-Helicobacter pylori effect of CaG-NANA, a new sialic acid derivative.

AIM: To investigate the bactericidal effects of calcium chelated N-acetylneuraminic acid-glycomacropeptide (CaG-NANA) against Helicobacter pylori (H. pylori). METHODS: For manufacture of CaG-NANA, calcium (Ca) was combined with glycomacropeptide (GMP) by chelating, and N-acetylneuraminic acid (NANA) was produced with Ca-GMP substrate by an enzymatic method. The final concentration of each component was 5% Ca, 7% NANA, 85% GMP, and 3% water. For in vitro study, various concentrations of CaG-NANA were investigated under the minimal inhibitory concentration (MIC). For in vivo study, CaG-NANA was administered orally for 3 wk after H. pylori infection. The levels of inflammatory cytokines in blood were analyzed by enzyme-linked immunosorbent assay and eradication of H. pylori was assessed by histological observation. RESULTS: The time-kill curves showed a persistent decrease in cell numbers, which depended on the dose of CaG-NANA, and MIC of CaG-NANA against H. pylori was 0.5% in vitro. Histopathologic observation revealed no obvious inflammation or pathologic changes in the gastric mucosa in the CaG-NANA treatment group in vivo. The colonization of H. pylori was reduced after CaG-NANA treatment. The levels of interleukin (IL)-6, IL-1ß, tumor necrosis factor-α, and IL-10 were also decreased by CaG-NANA. CONCLUSION: CaG-NANA demonstrates effective anti-bactericidal activity against H. pylori both in vitro and in vivo.

Naïve CD8(+) T cell derived tumor-specific cytotoxic effectors as a potential remedy for overcoming TGF-ß immunosuppression in the tumor microenvironment.

Despite of the potential implications for cancer immunotherapy, conventional approaches using in vitro expanded CD8(+) T cells have suboptimal outcomes, mostly due to loss of functionality from cellular exhaustion. We therefore investigated the phenotypic and functional differences among in vitro activated CD8(+) T cells of three different sources, namely naïve (NTeff), memory (MTeff) and tumor-infiltrating lymphocytes (TILeff) from human and mice, to better understand mechanisms behind potent effector functions and potential for overcoming current limitations. In line with the greater proliferation activity and longer telomere lengths of NTeff populations, cells of naïve origin exhibited significantly less amounts of T cell exhaustion markers than those of MTeff and TILeff, and moreover, acquired distinct expression patterns of memory-promoting transcription factors, T-bet and Eomes, induced in a rapid and sustainable manner. NTeff cells appeared to have lower expression of Foxp1 and were refractory to apoptosis upon TGF-ß conditioning, implying better survival potential and resistance to tumor-induced immune suppression. Of CD8(+) T cell pools activated to tumor-specific CTLs, naïve cell generated effectors possessed the most potent cytotoxic activity, validating implications for use in rational design of adoptive immunotherapy.

Regulation of MMP/TIMP by HUVEC transplantation attenuates ventricular remodeling in response to myocardial infarction.

AIMS: We elucidated the therapeutic potential of human umbilical vein endothelial cells (HUVECs) for ameliorating progressive heart failure in a myocardial infarction (MI) rat model. MAIN METHODS: MI was induced by ligation of left anterior descending artery, and HUVEC was transplanted 1week after MI. Cardiac function was evaluated by echocardiography, and histological analyses were performed. KEY FINDINGS: Phosphate-buffered saline (MI-V, n=5) or HUVEC (MI-HV, n=5) were injected into the border zone and infarcted area 7days after ligation of the left coronary artery in rats. The MI-HV group showed attenuation of left ventricular (LV) remodeling compared with the MI-V group. In the infarcted myocardium, a few of injected HUVEC was retained up to 28days. The ratios of matrix metalloproteinase (MMP)-2 or MMP-9 to tissue inhibitor of metalloproteinase (TIMP)-1 or TIMP-3 were decreased in the MI-HV group compared with the MI-V group. In vivo zymography analysis showed that HUVEC transplantation decreased the activities of MMP-2 and MMP-9. In immunohistochemistry, decreased MMP-2 and increased TIMP-1 and TIMP-3 expression were observed at 48h after HUVEC transplantation. These effects on MMP/TIMP balance were inhibited by L-NAME administration (an eNOS inhibitor, 10mg/kg). NOS inhibition decreased the protein expressions of TIMP-1 and TIMP-3 but did not change the protein expressions of MMP-2 and MMP-9. SIGNIFICANCE: Our data suggest that altered balance between MMP and TIMP by HUVEC transplantation contributed to attenuation of ventricular remodeling after MI via eNOS.

Cilostazol protects vessels against hyperglycemic injury and accelerates healing after implantation of drug-eluting stent in a type 1 diabetes mellitus rat aorta stent model.

OBJECTIVE: Cilostazol, a selective phosphodiesterase-3 (PDE-3) inhibitor, can effectively suppress platelet activation and attenuate the increase in carotid intima-media thickness in diabetes mellitus (DM) patients. Therefore, we investigated whether cilostazol had effects on the healing process after implantation of a drug-eluting stent (DES) in a rat model of type 1 DM. METHODS AND RESULTS: Streptozotocin-induced DM rats were divided into 2 groups in which cilostazol (30 mg/kg/day; DM-Cilostazol) or vehicle (DM-Vehicle) was orally administered. Age-matched rats treated with the vehicle were used as a control group (NDM-Vehicle). After 4 weeks, cilostazol changed the expression of vascular cell adhesion molecule and intercellular adhesion molecule and the apoptotic cell ratio of the media (DM-Vehicle: 53.5 ± 9.8%, DM-Cilostazol: 26.4 ± 8.3%, p < 0.05) in the aortic wall. Also, in a modified aortic ring test, cilostazol preserved the angiogenic potential of the aorta ([height of the sprouting tubes] DM-Vehicle: 0 ± 0 µm, DM-Cilostazol: 344.6 ± 236.8 µm, p < 0.05). After implantation of paclitaxel-eluting stents (PES) in rats treated with cilostazol or vehicle, thrombus formation, deposition of fibrin, and infiltration of inflammatory cells were attenuated by cilostazol. In particular, the re-endothelialization by von Willebrand factor expression in the DM-PES-Cilostazol group was enhanced compared with that in the DM-PES-Vehicle group. CONCLUSION: Cilostazol has potential for protecting vessels against hyperglycemic injury and for accelerating the healing process after implantation of DES.

The novel role of mast cells in the microenvironment of acute myocardial infarction.

Mast cells are multifunctional cells containing various mediators, such as cytokines, tryptase, and histamine, and they have been identified in infarct myocardium. Here, we elucidated the roles of mast cells in a myocardial infarction (MI) rat model. We studied the physiological and functional roles of mast cell granules (MCGs), isolated from rat peritoneal fluid, on endothelial cells, neonatal cardiomyocytes, and infarct heart (1-hour occlusion of left coronary artery followed by reperfusion). The number of mast cells had two peak time points of appearance in the infarct region at 1day and 21days after MI induction in rats (p<0.05 in each compared with sham-operated heart). Simultaneous injection of an optimal dose of MCGs modulated the microenvironment and resulted in the increased infiltration of macrophages and decreased apoptosis of cardiomyocytes without change in the mast cell number in infarct myocardium. Moreover, MCG injection attenuated the progression of MI through angiogenesis and preserved left ventricular function after MI. MCG-treated cardiomyocytes were more resistant to hypoxic injury through phosphorylation of Akt, and MCG-treated endothelial cells showed enhanced migration and tube formation. We have shown that MCGs have novel cardioprotective roles in MI via the prolonged survival of cardiomyocytes and the induction of angiogenesis.

Palmitate induces insulin resistance without significant intracellular triglyceride accumulation in HepG2 cells.

Previous studies showed that increased release of free fatty acids from adipocytes leads to insulin resistance and triglyceride (TG) accumulation in the liver, which may progress into hepatic steatohepatitis. We and other investigators have previously reported that palmitate induces endoplasmic reticulum stress-mediated toxicity in several tissues. This work investigated whether palmitate could induce insulin resistance and steatosis in HepG2 cells. We treated cells with either saturated fatty acid (palmitate) or unsaturated fatty acid (oleate), and observed that palmitate significantly activated c-jun N-terminal kinase and inactivated protein kinase B. Both 4-phenylbutyric acid and glycerol significantly activated protein kinase B, confirming the involvement of endoplasmic reticulum stress in palmitate-mediated insulin resistance. Oleate, but not palmitate, significantly induced intracellular TG deposition and activated sterol regulatory element binding protein-1. Instead, diacylglycerol level and protein kinase C epsilon activity were significantly increased by palmitate, suggesting the possible role of diacylglycerol in palmitate-mediated lipotoxicity. Therefore, the present study clearly showed that palmitate impairs insulin resistance, but does not induce significant TG accumulation in HepG2 cells.

Synergistic induction of ER stress by homocysteine and beta-amyloid in SH-SY5Y cells.

Clinical studies have raised the possibility that elevated plasma levels of homocysteine increase the risk of atherosclerosis, stroke and possibly neurodegenerative diseases such as Alzheimer's disease (AD); however, the direct impact of homocysteine on neuron cells and the mechanism by which it could induce neurodegeneration have yet to be clearly demonstrated. Here, we investigated the effect of homocysteine on endoplasmic reticulum (ER) stress, the suggested mechanism of neurotoxicity, in human neuroblastoma SH-SY5Y cells. The effect of homocysteine on amyloid-beta (Abeta)-induced neurotoxicity and the protective activity of folate were also investigated. Homocysteine led to increased expressions of the binding protein (BiP) and the spliced form of X-box-protein (XBP)-1 mRNAs, suggesting activation of the unfolded-protein response and an increase in apoptosis. When cells were cotreated with homocysteine and Abeta, caspase-3 activity was significantly increased, and expressions of BiP and the spliced form of XBP-1 mRNAs were significantly induced. The neurotoxicity of homocysteine was attenuated by the treatment of cells with folate, as determined by caspase-3 activity and apoptotic body staining. These findings indicate that homocysteine induces ER stress and, ultimately, apoptosis and sensitizes neurons to amyloid toxicity via the synergistic induction of ER stress. Furthermore, a neuroprotective effect of folate against homocysteine-induced toxicity was also observed. Therefore, the findings of our study suggest that ER stress-induced homocysteine toxicity may play an important physiological role in enhancing the pathogenesis of Abeta-induced neuronal degeneration.

Involvement of Endoplasmic Reticulum Stress in Palmitate-induced Apoptosis in HepG2 Cells.

The results of recent studies indicate that high levels of free fatty acids (FFAs) and adipokines may be the main causes of non-alcoholic liver disease; however, the molecular mechanism that links FFAs to lipotoxicity remains unclear. In the present study, we treated HepG2 cells with FFA (either palmitate or oleate) to investigate the mechanisms involved in lipotoxicity in the liver cells. We also treated cells with palmitate in the presence of a chemical chaperone, 4-phenylbutyric acid (PBA), to confirm the involvement of ER stress in lipotoxicity. Palmitate significantly induced cytotoxicity in dose- and time-dependent manners. Apoptosis was also significantly induced by palmitate as measured by caspase-3 activity and DAPI staining. Palmitate led to increased expressions of the spliced form of X-box-protein (Xbp)-1 mRNA and C/EBP homologous transcription factor (CHOP) protein, suggesting activation of the unfolded-protein response. PBA co-incubation significantly attenuated apoptosis induced by palmitate. The above data demonstrate that high levels of palmitate induce apoptosis via the mediation of ER stress in the liver cells and that chemical chaperones act to modulate ER stress and accompanying apoptosis.

[Association between diverticulosis and colonic Neoplasm in Koreans].

BACKGROUND/AIMS: Although a few published studies have reported on the relationship between diverticulosis and neoplasia in the west, it is not yet examined in Korea. The aim of this study was to determine whether there is an association between diverticulosis and colonic neoplasia. METHODS: We retrospectely analysed the medical records of 3,007 patients (M:F=1.3:1) who underwent colonoscopic examinations from year 2002 to year 2004. Patients who had a history of previous polypectomy, colon resection, or inflammatory bowel diseases were excluded. The size, extent (none, few, or many), and location of diverticuli and polyps were analyzed. RESULTS: Of 2,377 patients, included 57% were male and the mean age was 50.8 year-old. Nine percent of the patient had diverticulosis, 29% had more than one neoplasm, and 6% had advanced neoplasia. Patients with diverticular diseases had higher risks of any neoplasia than those without diverticulum (p=0.03, 37.7% vs. 28.2%). There was no correlation between diverticular diseases and advanced neoplasia. Patients with proximal diverticular diseases had higher risk of any proximal neoplasia than other patients (p0.01 24.6% vs. 14.3%). Moreover, they had higher risk of proximal advanced neoplasia than others (p=0.01, 4.5% vs. 2%). In addition, comparison of multiple diverticular disease with few or no diverticuli revealed no difference in the risk of any neoplasia. CONCLUSIONS: These data show that the patients with diverticular diseases have more neoplasms than controls without diverticula.

Imaging findings of hepatic paragonimiasis : a case report.

Hepatic paragonimiasis is a rare form of ectopic infestation caused by Paragonimus. We experienced a case of hepatic paragonimiasis that showed characteristic imaging findings. CT and MR images showed a cluster of small cysts with rim enhancement in the subcapsular area of the liver. This finding seems to be characteristic for hepatic paragonimiasis, considering imaging findings in paragonimiasis involving other organs.

Primary health care for Korean immigrants: sustaining a culturally sensitive model.

This report describes a 4-year long bilingual interdisciplinary primary health care project that was designed to make culturally sensitive services available to underserved Korean immigrants in Chicago. It also describes some of the particular needs of this population and the strategies that the project staff adopted to identify and address the population's mental health needs. The project reflected the successful collaborative efforts of four participating principals: the Korean community, the University of Illinois at Chicago College of Nursing, the Chicago Department of Public Health, and the W. K. Kellogg Foundation. The model of service demonstrated in the project paired a bilingual advanced practice nurse, a certified family nurse practitioner, with a bilingual community advocate to conduct a program emphasizing community outreach and health promotion and prevention. A bilingual physician provided consultation for the nurse and attended to patients in need of medical care. Patients were referred to bilingual community social service agencies for assistance with a variety of other problems. A central goal of the project was for the services developed during its course to be assimilated into the regular programming of the Chicago Department of Public Health, a goal that was achieved. Finally, some of the challenges of introducing role change into an organization are discussed.