[Prospects in the treatment of pulmonary hypertension with nitric oxide].
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Humans↗
Biomedical subjects
R Yu
Publications and source records attributed to R Yu.
[Relationship between lung function and nocturnal hypoxemia in patients with obstructive sleep apnea syndrome].
OBJECTIVE: To explore the relationship between the changes of lung function resulted from position changes and obesity, and nocturnal hypoxemia in patients with obstructive sleep apnea syndrome. METHOD: 34 patients with obstructive sleep apnea syndrome were detected by polysomnography with lung function and blood gas analysis in sitting and supine positions during wake, and the relationship between results of lung function and blood gas analysis, IBW% to the AI, and < 90% T (percentage of the duration of SaO2 below 90% to total sleep time) was analyzed. RESULT: The mean age of the patients was 44 +/- 13 years. The AI was 36 +/- 22 time.hour-1. On changing from sitting to supine position, PaO2, VC%, ERV, FRC, FRC%, RV%, TLC% decreased significantly, especially ERV and FRC%, which decreased 47% and 29% respectively. AI had positive correlation with VC% (r = 0.477, P < 0.01) and TLC% (r = 0.443, P < 0.01) in supine position, < 90% T had negative correlation with PaO2(r = -0.479, P < 0.01) and ERV (r = -0.416, P < 0.05) in sitting position. The IBW% had negative correlation with VC% in sitting (r = -0.547, P < 0.01) and supine position (r = -0.491, P < 0.01). IBW% also had negative correlation with ERV in sitting (r = -0.523, P < 0.01) and supine (r = -0.413, P < 0.01) position and FRC (r = -0.402, P < 0.05) in sitting position. The IBW% had positive correlation with the < 90% T(r = 0.514, P < 0.01). CONCLUSION: These results suggest that positional changes and obesity have effects on lung function in patients with OSAS, and lead to the deterioration of hypoxemia during apnea.
Adult↗
[Gliosis: follow-up and pathological study of 34 cases].
OBJECTIVE: To discuss the etiology, clinical characteristics, pathology and canceration in gliosis. METHOD: 34 cases of gliosis were analyzed retrospectively follow-up for a long period. Their pathologic slices were restudied. RESULT: The causes of gliosis included cranial infection, specially infection caused by virus without distinct symptoms cerebral ischemia, brain injury, radiological treatment of brain. most cases showed symptoms of intracranial hypertension, 55.9% of the patients accompanied with epilepsy. Pathological examination revealed proliferation of small gliosis in all cases, lligodendrogliosis in 79.4% of the cases. The cases with proliferation had better rehabilitation. Canceration was noted in 11.8% of all cases. CONCLUSION: Gliosis is a nonmalignant disease, however, it has the possibility of canceration.
Adolescent↗
[In vitro sensitivity of oral gram-negative bacteria to the bactericidal activity of defensins].
Oral gram-negative bacteria, including Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, Capnocytophaga sputigena, Provotella intermedius, Provotella melaninogenicus, have been associated with destructive periodontal infection. An ultrasensitive antibacterial assay was applied to determine the sensitivity of a battery of oral gram-negative bacteria to the bactericidal effects of the isolated human neutrophil defensins (HNP) and two kinds of rabbit defensins NP1 and NP2. All species tested were killed by HNP, NP1 and NP2 except that porphyromonas gingivalis was resistant to HNP. However, there was strain-to-strain variation in sensitivity. It was concluded that the oral gram-negative bacteria were sensitive to the cidal mechanism involved in defensinmediated bacterial killing.
Aggregatibacter actinomycetemcomitans↗
[The processing of Gekko gecko and the pharmacological action of its different parts].
Both pharmacologic and toxic experiments are made on different parts of Gekko gecko Linnaeus. The results show that Gekko gecko Linnaeus' heads and its feet have obvious pharmacological action without any toxic or side effects, which provides a sound basis for the increase in its clinical utilization and the expansion of its medicinal parts as well as guarantee of safety and effectiveness after taking the medicine.
Adjuvants, Immunologic↗
Differential activation of MAPK and ICE/Ced-3 protease in chemical-induced apoptosis. The role of oxidative stress in the regulation of mitogen-activated protein kinases (MAPKs) leading to gene expression and survival or activation of caspases leading to apoptosis.
Chemical-induced oxidative stress to a cell can signal many cellular responses which include proliferation, differentiation, hemeostasis, apoptosis or necrosis. To better understand the underlying molecular mechanisms after exposure to chemicals, we investigated the signal transduction pathways, in particular the mitogen-activated protein kinase (MAPK) pathway and the ICE/Ced-3 protease (caspase) pathway, activated by different agents. Butylated hydroxyanisol (BHA) and its metabolite, t-butyl-hydroquinone (tBHQ), both are well known phenolic antioxidants used in food preservatives, strongly activated c-Jun N-terminal kinase 1 (JNK1) and/or extracellular signal-regulated protein kinase 2 (ERK2) in a dose- and time-dependent fashion. Pretreatment with free radical scavengers N-acetyl-L-cysteine (NAC), glutathione (GSH), or vitamin E, inhibited ERK2 activation and, to a much lesser extent, JNK 1 activation by BHA and tBHQ, implicating the role of oxidative stress. Under conditions where JNK1 and ERK2 were activated, BHA also activated transcription factors nuclear factor kappa B (NF-kappaB), activated-protein-1 (AP-1), and anti-oxidant response element (ARE), leading to induction of genes such as c-jun, and c-fos. At relatively high concentrations, BHA and tBHQ stimulated proteolytic activity of ICE/Ced3 cysteine proteases, and caused apoptosis, which was blocked by pretreatment with NAC. Further increase in concentrations lead to rapid cell death predominantly occurred via necrosis. Some naturally occurring phytochemicals, such as phenylethyl isothiocyanate (PEITC), green tea polyphenols (GTP), and sulfarophane, which have been shown to be potent inducers of Phase II enzymes, also differentially regulated the activities of JNK, ERK, or CPP-32, in a time- and dose-dependent manner. Our data, together with the work of others, enable us to propose a model in which low concentrations of these chemicals (e.g., BHA, PEITC) activate MAPKs leading to induction of gene expression (e.g., c-jun, c-fos, GSI) which may protect the cells against toxic insults and enhance cell survival. At relatively high concentrations, these agents activated both MAPKS, and the ICE/Ced-3 caspase pathway, leading to apoptosis. The exact mechanisms by which MAPK and caspases are activated by these agents are currently unknown, but may involve oxidative modification of glutathione (GSH) and/or protein thiols, and/or generation of secondary messengers, ceramide and calcium, which further activate downstream events. Taken together, our results suggest that chemicals including phenolic antioxidants activate MAPK pathways which may lead to the induction of genes producing protection and survival mechanisms, as well as the ICE/Ced-3 protease pathway, leading to apoptosis. The balancing amongst these pathways may dictate the fate of the cells upon exposure to chemicals.
Journal Article↗
Modulation of select immune responses by dietary capsaicin.
Capsaicin (CAP) is the spicy principle of hot peppers that has been used as a food additive, preservative, and medicine. In this study, we investigated the effect of dietary CAP on immune status and selected immune responses. BALB/c mice were divided into 5 groups and fed diets with either 0, 5, 20, 50 or 100 ppm CAP for 3 weeks. The parameters measured with lymphocytes included mitogen-induced proliferation, plaque-forming cell number, and total serum immunoglobulin levels. In spleen cells of mice fed 20 ppm CAP there was a greater T-cell mitogen induced, lymphocyte proliferative response. In addition, the number of antibody-producing B cells and serum IgG and IgM levels increased in mice fed 20 ppm CAP as compared to the control with no CAP. The effect of dietary CAP on macrophage activity was assessed by phagocytosis and tumor necrosis factor-alpha (TNF alpha) production. Dietary CAP had no effect on phagocytic activity by peritoneal macrophages, but the levels of secreted TNF alpha increased in the groups fed 20 ppm CAP compared to the control. These results suggest that dietary CAP may differentially enhance immune status as well as select immune functions. That is in contrast with previous studies that show immunosuppression observed after CAP injection.
Animals↗
Expression of heterogeneous nuclear ribonucleoprotein A2/B1 in bronchial epithelium of chronic smokers.
The monoclonal antibody 703D4, which binds heterogeneous nuclear ribonucleoprotein A2/B1 (hnRNP A2/B1), has been reported to detect lung cancer more than a year earlier than routine chest X-ray or cytomorphology. To explore the biological basis of this detection, we studied the expression of this antigen in the central airways of smokers with evidence of bronchial metaplasia using specimens from a previously reported, randomized retinoid chemoprevention trial. By analyzing 1078 available biopsy specimens from 147 individuals at baseline and 68 individuals who completed the intervention, we frequently detected overexpression of hnRNP A2/B1 in normal and abnormal bronchial epithelium (i.e., in 41% of normal and 37% of squamous metaplasia samples). There was no correlation between hnRNP A2/B1 overexpression and the different histological changes. In cases with hnRNP A2/B1 overexpression, immunoreactivity was homogeneously expressed in all biopsied sites. For the 68 cases with serial biopsies, there was no significant modulation of hnRNP expression by retinoid intervention or smoking status. With lung cancer cell lines, 0.5-4 microM concentrations of 13-cis-retinoic acid reduced hnRNP A2/B1 overexpression by immunocytochemistry. We conclude that hnRNP A2/B1 overexpression is frequently found in central airways of chronic smokers, consistent with the pattern of expression that we reported previously in airways surrounding resected primary lung cancers. Oral 13-cis-retinoic acid at a dose of 1 mg/kg has no demonstrable effects on modulating hnRNP A2/B1 expression in proximal bronchial epithelium.
Biomarkers, Tumor↗
Characterization of the polymorphonuclear leukocyte-induced vasoconstriction in isolated human umbilical veins.
We investigated the contractile effects of both activated and unactivated polymorphonuclear leukocytes (PMNs) on human vascular tissue to characterize the influence of human PMNs on vascular tone. PMNs were added either unactivated or after f-met-leu-phe (fMLP) activation (10(-8) M), into tissue chambers containing human umbilical vein segments under either control or cytokine-treated conditions. The activation state of different PMN preparations was measured by immunofluorescence staining of the adhesion glycoproteins Mac-1 and L-selectin. Both unactivated and activated PMNs induced a cell number-dependent (1.5 x 10(5) to 2 x 10(6) cells/ml) vasoconstriction in human umbilical vein segments. This PMN-induced response was not inhibited by treatment with indomethacin (10(-5) M), superoxide dismutase (2 x 10(-7) M) or L-nitro-monomethyl arginine (10(-4) M). However, treatment of PMNs with the leukotriene biosynthesis inhibitor BIRM-270 partially inhibited (-61 +/- 19%, P <.05) the contraction induced only by unactivated PMNs. Moreover, the supernatant from unactivated, but not that from activated, PMNs elicited a contractile response comparable to that from the addition of cells. We observed a significant correlation between the Mac-1/L-selectin ratio of activated PMNs and the contractile response they generated (r = 0.77, P <.05). The activated PMN response had an endothelium-dependent component, whereas the unactivated PMN response was endothelium-independent. These results suggest that human PMNs of varying activation states have the capacity to modulate vascular smooth muscle tone via distinct mechanisms. Unactivated PMNs appear to modulate tone via a secreted product, whereas the more activated phenotype modulates vascular tone via a cognate interaction with the endothelium.
Flow Cytometry↗
Capsaicin can alter the expression of tumor forming-related genes which might be followed by induction of apoptosis of a Korean stomach cancer cell line, SNU-1.
Capsaicin (CAP) has been known to inhibit some tumor development in vivo (J.J. Jang, S.H. Kim, T.K. Yun, Inhibitory effect of capsaicin on mouse lung tumor development, in vivo, J. Korean Med. Sci. 3 (1989) 49-53; J.J. Jang, K.J. Cho, Y.S. Lee, J.H. Bae, Different modifying responses of capsaicin in a wide-spectrum initiation model of F344 rat, J. Korean Med. 6 (1991) 31-36) [1,2] even though its mechanism of action is not well understood. The objectives of this study were to examine the effect of CAP on expression of tumor forming-related genes in a Korean stomach tumor cell, SNU-1. We used slot blot hybridization to investigate its effect on a wide spectrum of proto-oncogenes. It was found that CAP enhanced the transcripts of two proto-oncogenes (c-myc and c-Ha-ras) and tumor suppressor gene p53. While a low concentration of CAP (0.01 microM) did not significantly increase the level of p53 transcript in SNU-1, it did increase it by a factor of 3.5 at a 10 microM dose of CAP. Consequently, SNU-1 cells are sensitive to CAP in the overexpression of tumor suppressor gene, p53 and proto-oncogenes, c-myc and c-Ha-ras, but not those of c-erbB-2, c-jun and bcl-2 genes. Both cell death and DNA fragmentation were shown in SNU-1 cells with treatment of CAP. Our results suggest that CAP induces apoptotic cell death in human gastric cancer cells (SNU-1) in vitro which may be possibly mediated by the overexpression of p53 and/or c-myc genes. Because cell suicide is arguably the most potent natural defense against cancer, the correlation between the induction of apoptosis and the change of tumor forming-related gene expression after CAP treatment should be further studied in detail.
Apoptosis↗
Butylated hydroxyanisole and its metabolite tert-butylhydroquinone differentially regulate mitogen-activated protein kinases. The role of oxidative stress in the activation of mitogen-activated protein kinases by phenolic antioxidants.
Phenolic antioxidant butylated hydroxyanisole (BHA) is a commonly used food preservative with broad biological activities, including protection against acute toxicity of chemicals, modulation of macromolecule synthesis and immune response, induction of phase II detoxifying enzymes, and especially its potential tumor-promoting activities. Understanding the molecular basis underlying these diverse biological actions of BHA is thus of great importance. Here we demonstrate that BHA is capable of activating distinct mitogen-activated protein kinases (MAPKs), extracellular signal-regulated protein kinase 2 (ERK2), and c-Jun N-terminal kinase 1 (JNK1). Activation of ERK2 by BHA was rapid and transient, whereas the JNK1 activation was relatively delayed and persistent. A major metabolite of BHA, tert-butylhydroquinone (tBHQ), also activated ERK2 but weakly stimulated JNK1 activity. Furthermore, tBHQ activation of ERK2 was late and prolonged, showing a kinetics different from that induced by BHA. ERK2 activation by both compounds required the involvement of an upstream signaling kinase MAPK/ERK kinase (MEK), as evidenced by the inhibitory effect of a MEK inhibitor, PD98059. Pretreatment with N-acetyl-L-cysteine, glutathione, or vitamin E attenuated ERK2 but not JNK1 activation by BHA and tBHQ. Modulation of intracellular H2O2 levels by direct addition of catalase or pretreatment with a catalase inhibitor, aminotriazole, also affected BHA- and tBHQ-stimulated ERK2 activity but not JNK1, indicating the involvement of oxidative stress in the ERK2 activation by these two compounds. However, we did not observe any generation of H2O2 after exposure of cells to BHA or tBHQ using a H2O2-sensitive fluorescent probe, 2',7'-dichlorofluorescein diacetate. Instead, BHA and tBHQ substantially reduced the amount of intracellular H2O2. Furthermore, BHA and tBHQ activation of ERK2 was strongly inhibited by ascorbic acid and a peroxidase inhibitor, sodium azide, suggesting the potential role of phenoxyl radicals and/or their derivatives. Taken together, our results indicate that (i) BHA and its metabolite tBHQ differentially regulate MAPK pathways, and (ii) oxidative stress due to the generation of reactive intermediates, possibly phenoxyl radicals but not H2O2, is responsible for the ERK2 activation by BHA and tBHQ, whereas the JNK1 activation may require a distinct yet unknown mechanism.
Amitrole↗
Desensitization of thyrotropin-releasing hormone receptor-mediated responses involves multiple steps.
Desensitization and recovery of the inositol 1,4,5-trisphosphate (IP3) and intracellular free calcium concentration ([Ca2+]i) responses to thyrotropin-releasing hormone (TRH) were measured in HEK293 cells stably expressing the G protein-coupled TRH receptor. TRH caused a large, rapid, and transient increase in IP3 and a biphasic increase in [Ca2+]i. Desensitization of the TRH response was measured by exposing cells to TRH, washing, and then incubating the cells in hormone-free medium before reintroducing TRH and measuring IP3, [Ca2+]i, and intracellular Ca2+ pool size. When cells were incubated with 1 microM TRH for 10 s or 10 min and reexposed to TRH, there was almost no IP3 or [Ca2+]i increase. The IP3 response recovered first, followed by the [Ca2+]i response. The ionomycin-releasable intracellular Ca2+ pool was almost completely depleted by TRH, and pool refilling was slow. Thrombin, endothelin, and carbachol, when combined, stimulated large increases in IP3 and [Ca2+]i, but did not block the IP3 or [Ca2+]i responses to TRH measured 10 min later. In contrast, cells exposed to TRH first responded to combined agonists with a nearly normal increase in IP3, but no rise in [Ca2+]i. Thus, the IP3 response to TRH displays homologous desensitization, whereas the [Ca2+]i response displays heterologous desensitization because depletion of intracellular Ca2+ pools prevents responses to other hormones.
Calcium↗
Clonal genetic alterations in the lungs of current and former smokers.
BACKGROUND AND PURPOSE: Genetic damage has been identified at multiple chromosomal sites (i.e., loci) in lung cancer cells. We questioned whether similar damage could be detected in the bronchial epithelial cells of chronic smokers who do not have this disease. METHODS: Biopsy specimens from six different bronchial regions were obtained from 54 chronic smokers (40 current smokers and 14 former smokers). The presence of squamous metaplasia and dysplasia (abnormal histologic changes) in the specimens was documented by examination of hematoxylin-eosin-stained sections, and a metaplasia index ([number of biopsy specimens with metaplasia/total number of biopsy specimens] x 100%) was calculated for each subject. Loss of heterozygosity (i.e., loss of DNA sequences from one member of a chromosome pair) involving microsatellite DNA at three specific loci-chromosome 3p14, chromosome 9p21, and chromosome 17p13-was evaluated by means of the polymerase chain reaction. Fisher's exact test and logistic regression analysis were used to assess the data. Reported P values are two-sided. RESULTS: Data on microsatellite DNA status at chromosomes 3p14, 9p21, and 17p13 were available for 54, 50, and 44 subjects, respectively. The numbers of individuals who were actually informative (i.e., able to be evaluated for a loss of heterozygosity) at the three loci were 36 (67%), 37 (74%), and 34 (77%), respectively. DNA losses were detected in 27 (75%), 21 (57%), and six (18%) of the informative subjects at chromosomes 3p14, 9p21, and 17p13, respectively. Fifty-one subjects were informative for at least one of the three loci, and 39 (76%) exhibited a loss of heterozygosity. Forty-two subjects were informative for at least two of the loci, and 13 (31%) exhibited losses at a minimum of two loci. Loss of heterozygosity at chromosome 3p14 was more frequent in current smokers (22 [88%] of 25 informative) than in former smokers (five [45%] of 11 informative) (P = .01) and in subjects with a metaplasia index greater than or equal to 15% (21 [91%] of 23 informative) than in subjects with a metaplasia index of less than 15% (six [46%] of 13 informative) (P = .003). In five informative individuals among nine tested nonsmokers, a loss of heterozygosity was detected in only one subject at chromosome 3p14 (P = .03), and no losses were detected at chromosome 9p21 (P = .05). CONCLUSIONS: Genetic alterations at chromosomal sites containing putative tumor-suppressor genes (i.e., 3p14 and the FHIT gene, 9p21 and the p16 gene [also known as CDKN2], and 17p13 and the p53 gene [also known as TP53]) occur frequently in the histologically normal or minimally altered bronchial epithelium of chronic smokers.
Adult↗
Activation of signal transduction kinases by tamoxifen.
PURPOSE: To study the signal transduction mechanisms of tamoxifen via the activation of MAPKs, JNK and ERK in order to understand its regulation of gene expression. METHODS: The effects of tamoxifen (TAM) on the activation of serine/threonine mitogen-activated protein kinase (MAPK, p42/ERK2) and the stress-activated protein kinases (p46 SAPK or c-Jun N-terminal kinase, JNK1) were evaluated using a human cervical epitheloid carcinoma HeLa cell line. RESULTS: TAM activated both JNK1 and ERK2 activities in a time- and dose-dependent manner in HeLa cells. The activation of JNK1 was enhanced when the cells were pretreated with prooxidant H2O2. CONCLUSIONS: These studies show that TAM activates the signal transduction kinases, JNK1 and ERK2, which may play important roles in the regulation of gene expression by TAM.
Antineoplastic Agents, Hormonal↗
Activation of mitogen-activated protein kinases by green tea polyphenols: potential signaling pathways in the regulation of antioxidant-responsive element-mediated phase II enzyme gene expression.
Green tea polyphenols, major constituents of green tea, are potent chemopreventive agents in a number of experimental models of cancer in animals. The mechanisms of cancer protection by these agents are not clear, but may involve modulation of the enzyme systems responsible for the detoxification of chemical carcinogens. The present studies show that a green tea polyphenol extract (GTP) induces chloramphenicol acetyltransferase (CAT) activity in human heptoma HepG2 cells transfected with a plasmid construct which contains an antioxidant-responsive element (ARE) and a minimal glutathione S-transferase Ya promoter linked to the CAT reporter gene. This indicates that GTP stimulates the transcription of Phase II detoxifying enzymes through the ARE. To explore the upstream signaling pathways leading to gene expression, we studied the involvement of the mitogen-activated protein kinases (MAPKs) extracellular signal-regulated kinase 2 (ERK2) and c-Jun N-terminal kinase 1 (JNK1). Potent activation of ERK2 was seen following treatment of HepG2 cells with different concentrations of GTP. Similar to ERK2, JNK1 was also strongly activated by treatment with GTP, although to a lesser extent and in a different dose-dependent fashion. Kinetic studies revealed that GTP activation of JNK1 was delayed and sustained, whereas ERK2 activation was rapid and transient. Furthermore, GTP treatment also increased mRNA levels of the immediate-early genes c-jun and c-fos, as determined by reverse transcriptase-coupled polymerase chain reaction. Taken together, these studies provide insights into the action of GTP and suggest that the stimulation MAPKs may be the potential signaling pathways utilized by GTP to activate ARE-dependent genes.
Calcium-Calmodulin-Dependent Protein Kinases↗
Calcium antagonist-induced photo-exposed telangiectasia.
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Aged↗
Ameliorating effect of erythromycin on bleomycin-induced pulmonary fibrosis: role of alveolar macrophage activation and cytokine release.
The objective of this study was to evaluate the effectiveness of erythromycin (EM) on bleomycin-induced pulmonary fibrosis in rats and its possible mechanisms. Seventy-five rats were divided into three groups. Alveolar macrophages (AM) were harvested through bronchalveolar lavage (BAL) and consecutive changes of tumour necrosis factor-alpha (TNF-alpha) and platelet-derived growth factor (PDGF) in AM supernatant and bronchoalveolar lavage fluid (BALF) were assayed with ELISA and bioassay, respectively. The AM-derived TNF-alpha was elevated on day 3, peaked day 7 and then decreased but remained at higher level until day 28. The AM-derived PDGF was increased on day 3, peaked on day 7 then decreased to non-statistically significant higher level. The TNF-alpha in BALF was increased significantly on day 3 then decreased to normal level; the peak preceded that of AM-derived TNF-alpha. The PDGF in BALF was increased on day 3, peaked on day 7, and then decreased to normal, which exhibited a consecutive change similar to that of AM-derived PDGF. The EM significantly suppressed TNF-alpha and PDGF release by AM, markedly decreased TNF-alpha and PDGF levels in BALF. The EM also lessened the collagen deposition, the lung hydroxyproline comprised 75.44%, 72.72% and 56.24% that of bleomycin-treated group on day 7, 14 and 28, respectively. In conclusion, EM can ameliorate bleomycin-induced pulmonary fibrosis possibly through suppression of TNF-alpha and PDGF as well as the inhibition on accumulation of inflammatory cells in the lung.
Animals↗
Characterisation of an outer membrane protein of Moraxella catarrhalis.
To elucidate potential vaccine antigens, Moraxella catarrhalis outer membrane proteins (OMPs) were studied. We have previously shown an OMP to be a target for human IgG and have now further characterised this OMP which appears to have a molecular mass of 84 kDa and to be distinct from the 81-kDa OMP, CopB. Human transferrin was shown to bind the 84-kDa OMP alone. N-terminal sequencing of this OMP and purified M. catarrhalis transferrin binding protein B (TbpB) revealed homology both with each other and with the TbpB of Haemophilus influenzae and Neisseria meningitidis. Adsorption of human anti-serum with purified TbpB from two M. catarrhalis strains abolished or reduced binding of IgG to the 84-kDa OMP from three M. catarrhalis isolates. IgG binding to CopB was unaffected. It is clear that the 84-kDa OMP is distinct from CopB and is a likely homologue of TbpB.
Adult↗