Coating of Chlorophylls a and b Enhanced Photoelectrochemical Capacitor Reaction of TiO2/MnO2 Composite Electrode.

We prepared composite electrodes using TiO2 coated with chlorophylls a and b as photoelectric conversion material and MnO2 as energy storage material and investigated their photoelectrochemical capacitor properties. The coating with the combination of chlorophylls a and b improved the photoelectric conversion function of TiO2, compared with the coating with each alone. Na+ adsorption on MnO2 was enhanced with increasing the chlorophyll coating amount. The reason is that more chlorophylls a and b absorb visible light in different wavelengths to promote an easier photoexcited electron transfer to MnO2, just as they improve the efficiency of photosynthesis reactions in nature.

Effects of percutaneous cryoablation for renal tumor on overall and split renal function.

PURPOSE: To evaluate retrospectively the influence of percutaneous cryoablation for small renal tumors on total and affected kidney function and risk factors associated with worsening function of the affected kidney. MATERIALS AND METHODS: Between April 2016 and March 2022, 27 patients who underwent cryoablation for small renal tumors at our institution participated in this study, which investigated time-dependent changes in postoperative renal function. We evaluated estimated glomerular filtration rates (eGFRs) and split renal function revealed by scintigraphy using 99 m technetium-mercaptoacetyltriglycine (99mTc-MAG3) before cryoablation and at 1 week, 1 month, and 6 months after cryoablation. Numerous variables were analyzed to assess risk factors for worsening renal function. RESULTS: Baseline eGFR (mean ± standard deviation) was 56.5 ± 23.7 mL/min/1.73 m2 (mean ± SD; range, 20.5-112.5). Mean eGFRs at 1 week, 1 month, and 6 months after cryoablation were 57.4 ± 24.5 (19.1-114.9), 57.1 ± 25.1 (21.5-114.9), and 53.8 ± 23.9 mL/min/1.73 m2 (20.0-107.5), respectively. Changes were statistically insignificant (p = 1.0000, = 0.6749, and = 0.0761, respectively). Regarding split renal function, mean baseline contribution of the affected kidney determined by 99mTc-MAG3 was 49.7% ± 6.0% (38.8-63.3%); these rates at 1 week, 1 month, and 6 months after cryoablation were 43.7% ± 8.8 (29.1-70.6%), 46.2% ± 7.7% (32.6-70.3%), and 46.0% ± 8.5% (32.5-67.6%), respectively. Differences from baseline were significant for all periods (p < 0001, < 0001, = 0.0001, respectively). Serum C reactive protein and lactate dehydrogenase at 1 day following cryoablation, tumor's nearness to the collecting system or sinus, and volume of ablated normal renal parenchyma were significantly correlated with decreased contributions of the affected kidney by > 10% after cryoablation. CONCLUSION: Unlike total renal function, affected kidney function could worsen after cryoablation.

Difference in arterial FDG accumulation in healthy study participants between digital PET/CT and standard PET/CT.

OBJECTIVE: To evaluate the differences in FDG accumulation in arteries throughout the body between digital and standard PET/CT. METHODS: Forty-six people who had FDG-PET examinations with a digital PET/CT scanner for health screening between April 2020 and March 2021 and had previous examinations with a standard PET/CT scanner were the study participants. FDG accumulation in arteries throughout the body was visually assessed in each segment. Scan was considered positive when arterial FDG accumulation was equal to or greater than that of the liver. The positivity rates for general arteries and each arterial segment were compared between the two kinds of scanners. If any one of the arterial segments was considered positive, the general arteries were classified as positive. Moreover, the rate of change in results from the standard PET/CT to the digital scanner in the same individual (negative to positive, positive to negative) was examined. RESULTS: In the evaluation of general arteries, the positivity rates were 21.7% (10 cases) for the standard PET/CT, whereas positive rates were 97.8% (45 cases) for the digital PET/CT (p < 0.001). In all arterial segments, the positivity rate was significantly higher with the digital PET/CT compared to the standard PET/CT; those with the digital PET/CT were, respectively, 95.7%, 87.0%, 73.9%, 37.0%, 34.8%, and 21.7% in the femoral, brachial, aortic, subclavian, iliac, and carotid arteries. On the other hand, those with the standard PET/CT were 13.0%, 13.0%, 19.6%, 2.2%, 0%, and 4.4% in segments in the above order. Changes from negative to positive were shown in many cases; 35 cases (76.0%) of general arteries, 38 cases (82.6%) for the femoral artery, and 34 cases (73.9%) for the brachial artery. The exception was one case in which a change from positive to negative was confirmed in the carotid artery. In all arteries considered to be positive, FDG accumulation was not greater than but was equal to that in the liver with both scanners. CONCLUSIONS: Arterial FDG accumulation was significantly higher with digital PET/CT compared to conventional PET/CT. With digital PET/CT, an arterial FDG accumulation equal to the liver may not to be considered as abnormal accumulation.

Spontaneous regression of small cell lung cancer associated with Lambert-Eaton Myasthenic Syndrome: Case report.

Spontaneous regression (SR) of cancer is very rare, especially of small cell lung cancer (SCLC). Recently, an association of paraneoplastic neurological syndrome (PNS) has been reported as a cause of SR of cancer, and onconeural antibodies are a possible factor in the SR of cancer associated with PNS. We herein report the first case of SR of SCLC combined with anti-P/Q-type of voltage-gated calcium channel (VGCC) antibody-positive Lambert-Eaton myasthenic syndrome (LEMS), a subtype of PNS. This case report suggests that SCLC may be spontaneously reduced by an autoimmune response induced by VGCC antibodies associated with LEMS. Our finding may help elucidate the mechanisms that inhibit tumor growth and cause the regression of tumors.

A case of pulmonary pleomorphic carcinoma associated with cystic airspace.

Lung cancer associated with a cystic airspace is frequently misdiagnosed or overlooked. Adenocarcinoma, followed by squamous cell carcinoma, is the most typical histologic type of lung cancer connected to a cystic airspace. Here we present the rare case of lung pleomorphic carcinoma associated with a cystic airspace. We encountered a 74-year-old Japanese man diagnosed by computed tomography (CT) as having a nodule outside a cystic airspace in the lung. Several previous CT images showed that the cystic airspace preceded the nodule. Postsurgery, pathology indicated a diagnosis of pleomorphic carcinoma. Since pulmonary pleomorphic carcinomas pursue an aggressive clinical course, their early detection may contribute to an improved prognosis. Our case demonstrated that pleomorphic carcinoma can arise with cystic airspaces. For early diagnosis of those aggressive lung cancers, chest physicians should carefully examine the walls of cystic airspaces on CT.

Predicting the pathological invasiveness of early lung adenocarcinoma prior to surgery using Deauville criteria: reliability and validity.

PURPOSE: This retrospective study aimed to investigate the validity and reliability of FDG-PET/CT visual assessment using Deauville criteria to predict pathological invasiveness of early lung adenocarcinoma prior to surgery. MATERIALS AND METHODS: Between April 2020 and January 2022, 51 patients who underwent surgery for pathological stage 0/I lung adenocarcinoma were enrolled. The pulmonary lesions were divided into two groups according to pathological invasiveness: less invasive (including adenocarcinoma in situ and minimally invasive adenocarcinoma and invasive adenocarcinoma. We compared CT size (total and solid size), SUVmax, and Deauville score between the two groups. Furthermore, we investigated inter-rater and intra-rater agreements regarding the Deauville score. Receiver operating characteristic (ROC) curve analysis was performed to identify the diagnostic performance of each method. RESULTS: Based on pathologic diagnoses, 51 lesions in the 51 patients were divided into 6 less invasive and 45 invasive adenocarcinoma lesions. According to quadratic-weighted Kappa statistics, inter-rater (k = 0.93) and intra-rater (k = 0.97) agreements among all five components of the Deauville score indicated high agreement. There was a statistically significant difference in CT solid size, SUVmax, and Deauville score between the two groups. There were no significant differences between CT solid size and FDG-PET/CT assessments (AUC = 0.93 for Deauville score and SUVmax, AUC = 0.84 for CT solid size). CONCLUSION: FDG-PET/CT visual assessment using the Deauville score could assist in deciding upon minimally invasive surgery for early lung adenocarcinoma.

Involvement of GLCCI1 in mouse spermatogenesis.

Spermatid production is a complex regulatory process in which coordination between hormonal control and apoptosis plays a pivotal role in maintaining a balanced number of sperm cells. Apoptosis in spermatogenesis is controlled by pro-apoptotic and anti-apoptotic molecules. Hormones involved in the apoptotic process during spermatogenesis include gonadotrophins, sex hormones, and glucocorticoid (GC). GC acts broadly as an apoptosis inducer by binding to its receptor (glucocorticoid receptor: GR) during organ development processes, such as spermatogenesis. However, the downstream pathway induced in GC-GR signaling and the apoptotic process during spermatogenesis remains poorly understood. We reported previously that GC induces full-length glucocorticoid-induced transcript 1 (GLCCI1-long), which functions as an anti-apoptotic mediator in thymic T cell development. Here, we demonstrate that mature murine testis expresses a novel isoform of GLCCI1 protein (GLCCI1-short) in addition to GLCCI1-long. We demonstrate that GLCCI1-long is expressed in spermatocytes along with GR. In contrast, GLCCI1-short is primarily expressed in spermatids where GR is absent; instead, the estrogen receptor is expressed. GLCCI1-short also binds to LC8, which is a known mediator of the anti-apoptotic effect of GLCCI1-long. A luciferase reporter assay revealed that ß-estradiol treatment synergistically increased Glcci1-short promotor-driven luciferase activity in Erα-overexpressing cells. Together with the evidence that the conversion of testosterone to estrogen is preceded by aromatase expression in spermatids, we hypothesize that estrogen induces GLCCI1-short, which, in turn, may function as a novel anti-apoptotic mediator in mature murine testis.

A Novel Mouse Model of Idiopathic Nephrotic Syndrome Induced by Immunization with the Podocyte Protein Crb2.

BACKGROUND: The cause of podocyte injury in idiopathic nephrotic syndrome (INS) remains unknown. Although recent evidence points to the role of B cells and autoimmunity, the lack of animal models mediated by autoimmunity limits further research. We aimed to establish a mouse model mimicking human INS by immunizing mice with Crb2, a transmembrane protein expressed at the podocyte foot process. METHODS: C3H/HeN mice were immunized with the recombinant extracellular domain of mouse Crb2. Serum anti-Crb2 antibody, urine protein-to-creatinine ratio, and kidney histology were studied. For signaling studies, a Crb2-expressing mouse podocyte line was incubated with anti-Crb2 antibody. RESULTS: Serum anti-Crb2 autoantibodies and significant proteinuria were detected 4 weeks after the first immunization. The proteinuria reached nephrotic range at 9-13 weeks and persisted up to 29 weeks. Initial kidney histology resembled minimal change disease in humans, and immunofluorescence staining showed delicate punctate IgG staining in the glomerulus, which colocalized with Crb2 at the podocyte foot process. A subset of mice developed features resembling FSGS after 18 weeks. In glomeruli of immunized mice and in Crb2-expressing podocytes incubated with anti-Crb2 antibody, phosphorylation of ezrin, which connects Crb2 to the cytoskeleton, increased, accompanied by altered Crb2 localization and actin distribution. CONCLUSION: The results highlight the causative role of anti-Crb2 autoantibody in podocyte injury in mice. Crb2 immunization could be a useful model to study the immunologic pathogenesis of human INS, and may support the role of autoimmunity against podocyte proteins in INS.

18F FDG-PET/CT analysis of spread through air spaces (STAS) in clinical stage I lung adenocarcinoma.

OBJECTIVE: The purpose of this retrospective study was to investigate the utility of F-18 fluorodeoxyglucose positron emission tomography/computed tomography (18F FDG-PET/CT) to predict spread through air spaces (STAS) in clinical stage I lung adenocarcinoma. METHODS: Between April 2020 and January 2022, 52 patients (55 lesions) who underwent surgery for clinical stage I lung adenocarcinoma were enrolled. The lesions were divided into two groups according to the presence of STAS. 18F FDG-PET/CT parameters, specifically the maximum standardized uptake value (SUVmax), metabolic tumor volume (MTV), and total lesion glycolysis (TLG), were calculated. The SUVmax, MTV, and TLG were compared between the two groups upon surgical pathological examination. Receiver operating characteristic (ROC) curve analysis was performed to identify a cut-off value. RESULTS: Nineteen lesions (35%) were positive for STAS and 36 lesions were negative for STAS. According to the presence of STAS, significant differences were detected in the SUVmax (5.21 [range 1.52-16.50] vs. 2.42 [range 0.74-11.80], p = 0.0040) but not MTV (3.44 [range 0.65-24.36] vs. 2.95 [0.00-20.07], p = 0.20) and TLG (7.92 [range 0.93-47.82] vs. 5.63 [0.00-58.66], p = 0.14). SUVmax had an AUC value of 0.74 (95% CI 0.61-0.87) with a sensitivity of 89.5% and specificity of 52.8% at a cut-off of 2.48. CONCLUSIONS: SUVmax rather than MTV and TLG were shown to be valuable indices for the prediction of STAS in clinical stage I lung adenocarcinoma.

Evaluation of pleural lesions after pleurodesis with OK-432 by fluorodeoxyglucose-positron emission tomography/CT.

OBJECTIVE: This study aimed to determine changes in FDG-PET/CT after pleurodesis with OK-432 and to investigate differences in the changes between non-malignant and malignant lesions. METHODS: Study participants were 17 patients with a history of malignant chest disease who underwent FDG-PET/CT after pleurodesis using OK-432 and in whom pleural lesions were determined to be non-malignant (n = 8) or malignant (n = 9). FDG uptake (SUVmax) was counted on all pleural lesions. CT findings (CT attenuation, shape) of pleural lesions with increased FDG uptake were evaluated. RESULTS: The number of patients with increased FDG uptake in the pleura differed significantly between the non-malignant group (3/8) and malignant group (9/9) (p < 0.01) The mean SUVmax of non-malignant lesions with increased FDG uptake was 2.3 ± 0.7 vs. 6.2 ± 2.2 in malignant lesions, for a significant difference (p < 0.01). The mean CT attenuation of lesions was 36 ± 11 HU in the non-malignant group and 34 ± 14 HU in the malignant group, a difference that was not significant (p = 0.91). There was a significant difference in nodular and linear shapes between non-malignant and malignant lesions (p < 0.01). All non-malignant lesions were linear. CONCLUSIONS: Positive FDG uptake was shown in non-malignant pleural lesions as well as in malignant pleural lesions after pleurodesis using OK-432. Combined analysis of FDG accumulation and CT morphology is helpful to distinguish between benign and malignant lesions.

GLCCI1 is a novel protector against glucocorticoid-induced apoptosis in T cells.

Glucocorticoids (GCs) potently induce T-cell apoptosis in a GC receptor (GR)-dependent manner and are used to control lymphocyte function in clinical practice. However, its downstream pathways remain controversial. Here, we showed that GC-induced transcript 1 (GLCCI1) is a novel downstream molecule of the GC-GR cascade that acts as an antiapoptotic mediator in thymic T cells. GLCCI1 was highly phosphorylated and colocalized with microtubules in GLCCI1-transfected human embryonic kidney QBI293A cells. GR-dependent up-regulation of GLCCI1 was associated with GC-induced proapoptotic events in a cultured thymocyte cell line. However, GLCCI1 knockdown in a thymocyte cell line led to apoptosis. Consistently, transgenic mice overexpressing human GLCCI1 displayed enlarged thymi that consisted of larger numbers of thymocytes. Further molecular characterization showed that GLCCI1 bound to both dynein light chain LC8-type 1 (LC8) and its functional kinase, p21-protein activated kinase 1 (PAK1), thereby inhibiting the kinase activity of PAK1 toward LC8 phosphorylation, a crucial event in apoptotic signaling. GLCCI1 induction facilitated LC8 dimer formation and reduced Bim expression. Thus, GLCCI1 is a candidate factor involved in apoptosis regulation of thymic T cells.-Kiuchi, Z., Nishibori, Y., Kutsuna, S., Kotani, M., Hada, I., Kimura, T., Fukutomi, T., Fukuhara, D., Ito-Nitta, N., Kudo, A., Takata, T., Ishigaki, Y., Tomosugi, N., Tanaka, H., Matsushima, S., Ogasawara, S., Hirayama, Y., Takematsu, H., Yan, K. GLCCI1 is a novel protector against glucocorticoid-induced apoptosis in T cells.

Association of crumbs homolog-2 with mTORC1 in developing podocyte.

The evidence that gene mutations in the polarity determinant Crumbs homologs-2 (CRB2) cause congenital nephrotic syndrome suggests the functional importance of this gene product in podocyte development. Because another isoform, CRB3, was reported to repress the mechanistic/mammalian target of the rapamycin complex 1 (mTORC1) pathway, we examined the role of CRB2 function in developing podocytes in relation to mTORC1. In HEK-293 and MDCK cells constitutively expressing CRB2, we found that the protein localized to the apicolateral side of the cell plasma membrane and that this plasma membrane assembly required N-glycosylation. Confocal microscopy of the neonate mouse kidney revealed that both the tyrosine-phosphorylated form and non-phosphorylated form of CRB2 commence at the S-shaped body stage at the apicolateral side of podocyte precursor cells and move to foot processes in a capillary tuft pattern. The pattern of phosphorylated mTOR in developing podocytes was similar to that of CRB2 tyrosine phosphorylation. Additionally, the lack of a tyrosine phosphorylation site on CRB2 led to the reduced sensitivity of mTORC1 activation in response to energy starvation. CRB2 may play an important role in the mechanistic pathway of developing podocytes through tyrosine phosphorylation by associating with mTORC1 activation.

Nanoporous Structure Formation on the Surface of InSb by Ion Beam Irradiation.

Nanoporous structures have a great potential for application in electronic and photonic materials, including field effect transistors, photonic crystals, and quantum dots. The control of size and shape is important for such applications. In this study, nanoporous structure formation on the indium antimonide (InSb) surface was investigated using controlled focused ion beam irradiation. Upon increasing the ion dose, the structures grew larger, and the shapes changed from voids to pillars. The structures also became larger when the ion flux (high-dose) and accelerating voltage were increased. The structure grew obliquely on the substrate by following the ion beam irradiation of 45°. The shapes of the structures formed by superimposed ion beam irradiation were affected by primary irradiation conditions. The nanostructural features on the InSb surface were easy to control by changing the ion beam conditions.

Nanoporous Structure Formation in GaSb, InSb, and Ge by Ion Beam Irradiation under Controlled Point Defect Creation Conditions.

Ion beam irradiation-induced nanoporous structure formation was investigated on GaSb, InSb, and Ge surfaces via controlled point defect creation using a focused ion beam (FIB). This paper compares the nanoporous structure formation under the same extent of point defect creation while changing the accelerating voltage and ion dose. Although the same number of point defects were created in each case, different structures were formed on the different surfaces. The depth direction density of the point defects was an important factor in this trend. The number of point defects required for nanoporous structure formation was 4 × 1022 vacancies/m² at a depth of 18 nm under the surface, based on a comparison of similar nanoporous structure features in GaSb. The nanoporous structure formation by ion beam irradiation on GaSb, InSb, and Ge surfaces was controlled by the number and areal distribution of the created point defects.

Reactivity of CA19-9 and CA125 in histological subtypes of epithelial ovarian tumors and ovarian endometriosis.

Previous reports have shown that some ovarian endometrioid adenocarcinomas and ovarian clear cell adenocarcinomas derive from ovarian endometriosis (OE), and that endocervical-like mucinous borderline ovarian tumors are associated with OE. We examined the relationship between the staging and histological subtypes of OE or epithelial ovarian tumors (EOT) and the serum levels of carbohydrate antigen 19-9 (CA19-9) and carbohydrate antigen 125 (CA125) to evaluate the potential of these markers for preoperative diagnosis. First, we analyzed the preoperative serum levels of CA19-9 and CA125 in 195 patients who were histopathologically diagnosed with OE or EOT. We then performed a case-control study in which 308 women were enrolled, the 195 women described above and 113 healthy women as control subjects. Serum CA19-9 and CA125 levels were found to be useful in differentiating between OE and serous adenocarcinoma, but not between OE and other EOT. Moreover, serum CA19-9 levels were useful for preoperative assessment between OE and stage I mucinous borderline ovarian tumors, with or without the interstitial infiltration. In addition, considering that the serum CA19-9 levels in stage I mucinous borderline ovarian tumors were elevated via the interstitial infiltration of leukocytes and that precancerous lesions are associated with a cancerous glycosylation disorder in the process of inflammatory carcinogenesis, the CA19-9 level may be considered a suitable biomarker for estimating drug susceptibility.

Controlled synthesis and luminescent properties of erbium silicate nanostructures.

Erbium silicate (Er2SiO5 and Er4Si3O12) nanostructures were successfully synthesized by a facile molten-salt approach in the presence of NaCI and surfactant. The synthesized products were structurally and morphologically characterized by X-ray diffraction (XRD), scanning electron microscopy (SEM), transmission electron microscopy (TEM), and high-resolution transmission electron microscopy (HRTEM), whereas the luminescent properties were characterized by temperature-dependent luminescence measurements. The results revealed that the composition, crystalline phase, and yield of the final products can be readily controlled by choosing suitable surfactant and tailoring the molar ratio of reactants used for the reactions. Moreover, the single-crystalline nature of Er2SiO5 and of Er4Si3O12 nanostructures results in sharp photoluminescence (PL) of Er3+, and both nanostructures are immunized from temperature quenching of PL. We suggest that the nanostructures developed in the present work are promising building blocks for Si-based optoelectronics nanodevices.

One-step synthesis and near-infrared luminescent properties of Er3+ and Ni2+ doped single-crystalline Al18B4O33 nanorods.

Er(3+) and Ni(2+) doped single-crystalline Al(18)B(4)O(33) nanorods were synthesized by a facile one-step toxic-free combustion method. The products were characterized by x-ray diffraction, transmission electron microscopy, selected area electron diffraction, and integrated and time-resolved photoluminescence (PL) measurements. The phase purity, morphology, and PL properties of Er(3+) and Ni(2+) doped Al(18)B(4)O(33) nanorods can be readily controlled by tailoring the annealing temperature. The mechanism for the formation of Al(18)B(4)O(33) nanorods with different aspect ratio is discussed. Er(3+) doped Al(18)B(4)O(33) nanorods show strong PL centered at 1531 nm, while Ni(2+) doped products show superwide PL with a full width at half maximum of up to 250 nm. These aluminum borate nanostructures are promising building blocks for optoelectronics nanodevices.

Cilostazol inhibits monocytic cell adhesion to vascular endothelium via upregulation of cAMP.

AIM: Cilostazol is clinically used as an inhibitor of platelet aggregation. Although several reports have demonstrated its anti-inflammatory effect, its effect on monocytes and their adhesive interaction to vascular endothelium remains unclear. We thus examined the potential role of cilostazol towards monocyte endothelial interaction under physiological flow conditions. METHODS: THP-1 cells, a monocytic cell line, were pretreated with cilostazol (5 microM) for 48 hours. The cells were then perfused over TNF-alpha (5 microg/mL for 4 hours)-stimulated monolayers of human umbilical vein endothelial cells (HUVECs) at shear stress of 1.0 dyen/cm(2). RESULTS: TNF-alpha-activated HUVECs supported significantly more monocyte adhesion to HUVECs (7.32+/-1.25/HPF) compared to inactivated HUVECs (0.74+/-0.15/HPF), and the amount of adhesion to TNF-alpha-activated HUVECs was markedly reduced (3.63+/-0.55/HPF) when THP-1 cells were incubated in the presence of cilostazol at 5 microM. Interestingly, surface expressions of integrins were not dramatically changed after cilostazol treatment. Intracellular concentration of cAMP was significantly increased after cilostazol treatment, and treatment with Forskolin and Dibutyryl-cAMP, potent inducers of cAMP, dramatically increased THP-1 adhesion to HUVECs. CONCLUSION: These data suggest that cilostazol has a potential anti-inflammatory effect on monocyte-endothelial interactions via the upregulation of intracellular cAMP.

Apolipoprotein CIII-induced THP-1 cell adhesion to endothelial cells involves pertussis toxin-sensitive G protein- and protein kinase C alpha-mediated nuclear factor-kappaB activation.

OBJECTIVE: Plasma apolipoprotein CIII (apoCIII) independently predicts risk for coronary heart disease (CHD). We recently reported that apoCIII directly enhances adhesion of human monocytes to endothelial cells (ECs), and identified the activation of PKC alpha as a necessary upstream event of enhanced monocyte adhesion. This study tested the hypothesis that apoCIII activates PKC alpha in human monocytic THP-1 cells, leading to NF-kappaB activation. METHODS AND RESULTS: Among inhibitors specific to PKC activators, phosphatidylcholine-specific phospholipase C (PC-PLC) inhibitor D609 limited apoCIII-induced PKC alpha activation and THP-1 cell adhesion. ApoCIII increased PC-PLC activity in THP-1 cells, resulting in PKC alpha activation. Pertussis toxin (PTX) inhibited apoCIII-induced PC-PLC activation and subsequent PKC alpha activation, implicating PTX-sensitive G protein pathway. ApoCIII further activated nuclear factor-kappaB (NF-kappaB) through PKC alpha in THP-1 cells and augmented beta1-integrin expression. The NF-kappaB inhibitor peptide SN50 partially inhibited apoCIII-induced beta1-integrin expression and THP-1 cell adhesion. ApoCIII-rich VLDL had similar effects to apoCIII alone. CONCLUSIONS: PTX-sensitive G protein pathway participates critically in PKC alpha stimulation in THP-1 cells exposed to apoCIII, activating NF-kappaB, and increasing beta1-integrin. This action causes monocytic cells to adhere to endothelial cells. Furthermore, because leukocyte NF-kappaB activation contributes to inflammatory aspects of atherogenesis, apoCIII may stimulate diverse inflammatory responses through monocyte activation.