Political factors, carbon footprints, and fertility of women in sub-Saharan Africa.

The study aims to investigate how political factors such as government policies and economic development impact carbon emissions and subsequently affect the fertility rates in sub-Saharan Africa (SSA). The study made use of the data sourced from the World Development Indicators (WDI) and World Governance Indications (WGI) covering 45 SSA countries for the period 2000 -2021. The study applied the Pooled Ordinary Least Squares, and control for endogeneity, and the Generalized Method of Moments (GMM). The results show that carbon footprints have the potential of reducing fertility rate in sub-Saharan Africa (SSA). This impact in the full sample was also reflected in most of the subregions. With respect to governance, the result shows that regulatory quality has the potential of improving fertility rate in SSA. On the other hand, government effectiveness has a reduction impact on fertility rate. The research highlights the need for sustainable development policies that take into consideration the impact of carbon footprints on fertility rates in SSA.

L'étude vise à étudier comment des facteurs politiques tels que les politiques gouvernementales et le développement économique ont un impact sur les émissions de carbone et affectent par la suite les taux de fécondité en Afrique subsaharienne (ASS). L'étude a utilisé les données provenant des Indicateurs de développement dans le monde (WDI) et des Indications de la gouvernance mondiale (WGI) couvrant 45 pays d'ASS pour la période 2000-2021. L'étude a appliqué la méthode des moindres carrés ordinaires groupés, le contrôle de l'endogénéité et la méthode des moments généralisés (GMM). Les résultats montrent que les empreintes carbone ont le potentiel de réduire le taux de fécondité en Afrique subsaharienne (ASS). Cet impact sur l'échantillon complet s'est également reflété dans la plupart des sous-régions. En ce qui concerne la gouvernance, le résultat montre que la qualité de la réglementation a le potentiel d'améliorer le taux de fécondité en ASS. D'un autre côté, l'efficacité du gouvernement a un impact réducteur sur le taux de fécondité. La recherche souligne la nécessité de politiques de développement durable qui prennent en compte l'impact de l'empreinte carbone sur les taux de fécondité en ASS.

Novel biochar@CoFe2O4/Ag3PO4 photocatalysts for highly efficient degradation of bisphenol a under visible-light irradiation.

In the study, a series of novel Z-scheme biochar@CoFe2O4/Ag3PO4 photocatalysts were synthesized and employed to degrade bisphenol A under visible light irradiation (λ ≥ 420 nm). The structural morphology, optical properties and physicochemical properties of composites were characterized by means of TEM, XRD, FT-IR, XPS, UV-Vis, BET, EIS and VSM analysis. The photocatalytic performances of the photocatalysts were evaluated systematically. The MBA-3 photocatalyst exhibited the highest photocatalytic and mineralization ability within 60 min among all photocatalysts, 91.12% and 80.23%, respectively. After four cycles, the degradation of BPA still kept the photocatalytic activity of 73.94%, and the removal rate of TOC remained 58.96%. Moreover, the active species in the photocatalytic process were evaluated, and we proposed the Z-scheme photocatalytic mechanism for highly efficient degradation of BPA. According to the GC-MS results, the photodegradation pathway of BPA is also suggested. The present study has provided a valuable way of using the magnetic biochar in the design of new and efficient system for the degradation of organic pollutions in waste water.

NF-kappaB/STAT3/PI3K signaling crosstalk in iMyc E mu B lymphoma.

BACKGROUND: Myc is a well known driver of lymphomagenesis, and Myc-activating chromosomal translocation is the recognized hallmark of Burkitt lymphoma, an aggressive form of non-Hodgkin's lymphoma. We developed a model that mimics this translocation event by inserting a mouse Myc cDNA gene into the immunoglobulin heavy chain locus, just upstream of the intronic Emu enhancer. These mice, designated iMyc E mu, readily develop B-cell lymphoma. To study the mechanism of Myc-induced lymphoma, we analyzed signaling pathways in lymphoblastic B-cell lymphomas (LBLs) from iMyc E mu mice, and an LBL-derived cell line, iMyc E mu-1. RESULTS: Nuclear factor-kappaB (NF-kappaB) and signal transducer and activator of transcription 3 (STAT3) were constitutively activated in iMyc E mu mice, not only in LBLs but also in the splenic B-lymphocytes of young animals months before tumors developed. Moreover, inhibition of either transcription factor in iMyc E mu-1 cells suppressed growth and caused apoptosis, and the abrogation of NF-kappaB activity reduced DNA binding by both STAT3 and Myc, as well as Myc expression. Inhibition of STAT3 signaling eliminated the activity of both NF-kappaB and Myc, and resulted in a corresponding decrease in the level of Myc. Thus, in iMyc E mu-1 cells NF-kappaB and STAT3 are co-dependent and can both regulate Myc. Consistent with this, NF-kappaB and phosphorylated STAT3 were physically associated with one another. In addition, LBLs and iMyc E mu-1 cells also showed constitutive AKT phosphorylation. Blocking AKT activation by inhibiting PI3K reduced iMyc E mu-1 cell proliferation and caused apoptosis, via downregulation of NF-kappaB and STAT3 activity and a reduction of Myc levels. Co-treatment with NF-kappaB, STAT3 or/and PI3K inhibitors led to additive inhibition of iMyc E mu-1 cell proliferation, suggesting that these signaling pathways converge. CONCLUSIONS: Our findings support the notion that constitutive activation of NF-kappaB and STAT3 depends on upstream signaling through PI3K, and that this activation is important for cell survival and proliferation, as well as for maintaining the level of Myc. Together, these data implicate crosstalk among NF-kappaB, STAT3 and PI3K in the development of iMyc E mu B-cell lymphomas.

[Human esophageal carcinoma antigens screened by serologic analysis of recombinant cDNA expression libraries (SEREX)].

BACKGROUND & OBJECTIVE: In malignant transformation, mutant gene products and dysregulated proteins can become tumor antigens and activate immunoreactions. Therefore, auto-antibodies exist in sera of cancer patients. Serologic analysis of recombinant cDNA expression libraries (SEREX) using autologous and allogenic patient sera provides a powerful approach to identify tumor antigens. This study was to identify esophageal cancer antigens with SEREX for serologic diagnosis, gene therapy, and immune therapy. METHODS: Expression library of cDNA from esophageal squamous cell carcinoma was constructed. SEREX screened out 21 positive clones from the 1.6x10(6) clones in the established library. The 21 positive clones were subcloned to monoclonality and submitted to in vivo excision of pBluescript phagemids. The nucleotide sequences of cDNA inserts were analyzed with DNASIS and BLAST software on EMBL and GenBank. According to the bioinformatics analyses, serologic immunoreactions of 4 colons in 10 samples of esophageal cancer serum and 10 samples of normal control serum were further detected by SADA. RESULTS: Of the 21 positive clones, 4 had no homology to any known genes, 17 were known fragments which were defined as antigens of esophageal cancer for the first time. The serologic immunoreaction rates of 4 selected antigens, including Ribosomal protein S4, and so on, were 40%, 60%, 70%, and 30%, respectively, in cancer sera, and 0%, 10%, 20%, and 20%, respectively, in normal sera. CONCLUSIONS: Antigens, such as Ribosomal protein S4, are frequently involved in serologic immunoreactions of esophageal cancer. The 21 antigens identified by the present study can be used as potential targets for gene therapy and serologic biomarkers of esophageal cancer.

CDDO-Imidazolide inhibits growth and survival of c-Myc-induced mouse B cell and plasma cell neoplasms.

BACKGROUND: Gene-targeted iMycEmu mice that carry a His6-tagged mouse Myc(c-myc)cDNA, MycHis, just 5' of the immunoglobulin heavy-chain enhancer, Emu, are prone to B cell and plasma cell neoplasms, such as lymphoblastic B-cell lymphoma (LBL) and plasmacytoma (PCT). Cell lines derived from Myc-induced neoplasms of this sort may provide a good model system for the design and testing of new approaches to prevent and treat MYC-driven B cell and plasma cell neoplasms in human beings. To test this hypothesis, we used the LBL-derived cell line, iMycEmu-1, and the newly established PCT-derived cell line, iMycEmu-2, to evaluate the growth inhibitory and death inducing potency of the cancer drug candidate, CDDO-imidazolide (CDDO-Im). METHODS: Morphological features and surface marker expression of iMycEmu-2 cells were evaluated using cytological methods and FACS, respectively. mRNA expression levels of the inserted MycHis and normal Myc genes were determined by allele-specific RT-PCR and qPCR. Myc protein was detected by immunoblotting. Cell cycle progression and apoptosis were analyzed by FACS. The expression of 384 "pathway" genes was assessed with the help of Superarray cDNA macroarrays and verified, in part, by RT-PCR. RESULTS: Sub-micromolar concentrations of CDDO-Im caused growth arrest and apoptosis in iMycEmu-1 and iMycEmu-2 cells. CDDO-Im-dependent growth inhibition and apoptosis were associated in both cell lines with the up-regulation of 30 genes involved in apoptosis, cell cycling, NFkappaB signaling, and stress and toxicity responses. Strongly induced (> or = 10 fold) were genes encoding caspase 14, heme oxygenase 1 (Hmox1), flavin-containing monooxygenase 4 (Fmo4), and three members of the cytochrome P450 subfamily 2 of mixed-function oxygenases (Cyp2a4, Cyp2b9, Cyp2c29). CDDO-Im-dependent gene induction coincided with a decrease in Myc protein. CONCLUSION: Growth arrest and killing of neoplastic mouse B cells and plasma cells by CDDO-Im, a closely related derivative of the synthetic triterpenoid 2-cyano-3,12-dioxooleana-1,9-dien-28-oic acid, appears to be caused, in part, by drug-induced stress responses and reduction of Myc.

Molecular and cytological features of the mouse B-cell lymphoma line iMycEmu-1.

BACKGROUND: Myc-induced lymphoblastic B-cell lymphoma (LBL) in iMycEmu mice may provide a model system for the study of the mechanism by which human MYC facilitates the initiation and progression of B cell and plasma cell neoplasms in human beings. We have recently shown that gene-targeted iMycEmu mice that carry a His6-tagged mouse Myc cDNA, MycHis, just 5' of the immunoglobulin heavy-chain enhancer, Emu, are prone to B cell and plasma cell tumors. The predominant tumor (approximately 50%) that arose in the iMycEmu mice on the mixed genetic background of segregating C57BL/6 and 129/SvJ alleles was LBL. The purpose of this study was to establish and characterize a cell line, designated iMycEmu-1, for the in-depth evaluation of LBL in vitro. METHODS: The morphological features and the surface marker expression profile of the iMycEmu-1 cells were evaluated using cytological methods and FACS, respectively. The cytogenetic make-up of the iMycEmu-1 cells was assessed by spectral karyotyping (SKY). The expression of the inserted MycHis gene was determined using RT-PCR and qPCR. Clonotypic immunoglobulin gene arrangements were detected by Southern blotting. The global gene expression program of the iMycEmu-1 cells and the expression of 768 "pathway" genes were determined with the help of the Mouse Lymphochip(c) and Superarray(c) cDNA micro- and macroarrays, respectively. Array results were verified, in part, by RT-PCR and qPCR. RESULTS: Consistent with their derivation from LBL, the iMycEmu-1 cells were found to be neoplastic IgMhighIgDlow lymphoblasts that expressed typical B-cell surface markers including CD40, CD54 (ICAM-1), CD80 (B7-1) and CD86 (B7-2). The iMycEmu-1 cells harbored a reciprocal T(9;11) and three non-reciprocal chromosomal translocations, over-expressed MycHis at the expense of normal Myc, and exhibited gene expression changes on Mouse Lymphochip microarrays that were consistent with MycHis-driven B-cell neoplasia. Upon comparison to normal B cells using eight different Superarray cDNA macroarrays, the iMycEmu-1 cells showed the highest number of changes on the NFkappaB array. CONCLUSION: The iMycEmu-1 cells may provide a uniquely useful model system to study the growth and survival requirements of Myc-driven mouse LBL in vitro.

Insertion of c-Myc into Igh induces B-cell and plasma-cell neoplasms in mice.

We used gene targeting in mice to insert a His(6)-tagged mouse c-Myc cDNA, Myc(His), head to head into the mouse immunoglobulin heavy-chain locus, Igh, just 5' of the intronic enhancer, Emu. The insertion of Myc(His) mimicked both the human t(8;14)(q24;q32) translocation that results in the activation of MYC in human endemic Burkitt lymphomas and the homologous mouse T(12;15) translocation that deregulates Myc in certain mouse plasmacytomas. Beginning at the age of 6 months, Myc(His) transgenic mice developed B-cell and plasma neoplasms, such as IgM(+) lymphoblastic B-cell lymphomas, Bcl-6(+) diffuse large B-cell lymphomas, and CD138(+) plasmacytomas, with an overall incidence of 68% by 21 months. Molecular studies of lymphoblastic B-cell lymphoma, the most prevalent neoplasm (50% of all tumors), showed that the lymphomas were clonal, overexpressed Myc(His), and exhibited the P2 to P1 promoter shift in Myc expression, a hallmark of MYC/Myc deregulation in human endemic Burkitt lymphoma and mouse plasmacytoma. Only 1 (6.3%) of 16 lymphoblastic B-cell lymphomas contained a BL-typical point mutation in the amino-terminal transactivation domain of Myc(His), suggesting that most of these tumors are derived from naive, pregerminal center B cells. Twelve (46%) of 26 lymphoblastic B-cell lymphomas exhibited changes in the p19(Arf)-Mdm2-p53 tumor suppressor axis, an important pathway for Myc-dependent apoptosis. We conclude that Myc(His) insertion into Igh predictably induces B-cell and plasma-cell tumors in mice, providing a valuable mouse model for understanding the transformation-inducing consequences of the MYC/Myc-activating endemic Burkitt lymphoma t(8;14)/plasmacytoma T(12;15) translocation.

Novel targeted deregulation of c-Myc cooperates with Bcl-X(L) to cause plasma cell neoplasms in mice.

Deregulated expression of both Myc and Bcl-X(L) are consistent features of human plasma cell neoplasms (PCNs). To investigate whether targeted expression of Myc and Bcl-X(L) in mouse plasma cells might lead to an improved model of human PCN, we generated Myc transgenics by inserting a single-copy histidine-tagged mouse Myc gene, Myc(His), into the mouse Ig heavy-chain Calpha locus. We also generated Bcl-X(L) transgenic mice that contain a multicopy Flag-tagged mouse Bcl-x(Flag) transgene driven by the mouse Ig kappa light-chain 3' enhancer. Single-transgenic Bcl-X(L) mice remained tumor free by 380 days of age, whereas single-transgenic Myc mice developed B cell tumors infrequently (4 of 43, 9.3%). In contrast, double-transgenic Myc/Bcl-X(L) mice developed plasma cell tumors with short onset (135 days on average) and full penetrance (100% tumor incidence). These tumors produced monoclonal Ig, infiltrated the bone marrow, and contained elevated amounts of Myc(His) and Bcl-X(L)(Flag) proteins compared with the plasma cells that accumulated in large numbers in young tumor-free Myc/Bcl-X(L) mice. Our findings demonstrate that the enforced expression of Myc and Bcl-X(L) by Ig enhancers with peak activity in plasma cells generates a mouse model of human PCN that recapitulates some features of human multiple myeloma.

[Expression of NY-ESO-1 gene in human esophageal carcinoma and its cloning].

BACKGROUND & OBJECTIVE: NY-ESO-1 is a tumor antigen from cDNA library of esophageal carcinoma. However, there was no report about its expression in the tissue of esophageal carcinoma. In the current study, the authors examined the frequency of the NY-ESO-1 gene expression in esophageal carcinoma in order to determine whether NY-ESO-1 antigen-based vaccine therapy be available for the patients with esophageal carcinoma. METHODS: Reverse transcriptase and polymerase chain reaction amplification techniques were utilized to assay 30 esophageal carcinoma tissues and the matched adjacent normal esophageal tissues for expression of NY-ESO-1 gene. And the cDNA sequence of NY-ESO-1 was cloned from esophageal carcinoma tissues by molecular cloning techniques. RESULTS: Out of 30 esophageal carcinoma tissues, 50% expressed NY-ESO-1 gene while no expressed in the matched adjacent normal esophageal tissues. The sequence of NY-ESO-1 cloned was identical to the sequence of that from GenBank. CONCLUSIONS: NY-ESO-1 gene is expressed highly in esophageal carcinoma and NY-ESO-1 antigen can be recognized by cytolytic T lymphocytes when presented by HLA-class-I molecular.

[Screening and identification of human lung cancer-related antigens].

One of the cardinal questions in tumor immunology is the identification of antigenic structures in human tumors that are recognized by host immune system. A powerful new methodology for identifying human tumor antigens eliciting humoral immune response is SEREX (serological identification of antigen by recombinant cDNA expression cloning). Here, by using this method, a recombinant cDNA expression library from lung cancer was analysed and several new tumor antigens were isolated. Using the lambda-ZAP vector, cDNA expression library was constructed from lung cancer tissues of three patients including a moderately differentiated lung adenocarcinoma, a highly differentiated lung squamous cell carcinoma and a moderately differentiated lung adeno-squamous carcinoma. The primary library consisted of 0.8 x 10(6) recombinants. 33 positive clones encoding antigen genes were obtained after immunoscreening, and the nucleotide sequences of cDNA inserts were determined and analysed with DNASIS and BLAST softwares in EMBL and GenBank. These antigen genes included known genes, such as MAGE (melanoma antigen gene), vitiligo-associated protein VIT-1, fibronectin, Na-K-ATPase et al and unknown genes or ESTs. To characterize expression profile of these genes, antibodies in sera from 48 lung cancer patients and 48 health donors were assayed with three antigens (L-8, L-19, L-51) to screen specific and relative serum markers for lung cancer. The results show that positive rates in lung cancer patients are higher than in health donors. Our research indicates that some of these antigens may be related to lung cancer and may be valuable tumor markers in diagnosis of lung cancer.