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- Ahmed, Anisuddin, et al.
(författare)
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Factors influencing delivery-related complications and their consequences in hard-to-reach areas of Bangladesh
- 2024
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Ingår i: Sexual & Reproductive HealthCare. - : Elsevier. - 1877-5756 .- 1877-5764. ; 40
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Tidskriftsartikel (refereegranskat)abstract
- Background and objectives: Bangladesh's high maternal mortality ratio is exacerbated by delivery-related complications, particularly in hard-to-reach (HtR) areas with limited healthcare access. Despite this, few studies have explored delivery-related complications and factors contributing to these complications among the disadvantaged population. This study aimed to investigate the factors contributing to delivery-related complications and their consequences among the mothers residing in the HtR areas of Bangladesh. Methods: Data were collected using a cross-sectional study design from 13 HtR sub-districts of Bangladesh between September 2019 and October 2019. Data from 1,290 recently delivered mothers were analysed. Results: Around 32% (95% CI: 29.7-34.8) of the mothers reported at least one delivery-related complication. Prolonged labour pain (21%) was the highest reported complication during the delivery, followed by obstructive labour (20%), fever (14%), severe headache (14%). Mothers with higher education, a higher number of antenatal care (ANC) visits, complications during ANC, employed, and first-time mothers had higher odds of reporting delivery-related complications. More than one-half (51%) of these mothers had normal vaginal delivery. Nearly one-fifth (20%) of mothers who reported delivery-related complications were delivered by unskilled health workers at homes. On the other hand, about one-fifth (19%) of the mothers without any complications during delivery had a caesarean delivery. Nine out of ten of these caesarean deliveries were done at the private facilities. Conclusion: Delivery-related complications are significantly related to a woman's reproductive history and other background characteristics. Unnecessary caesarean delivery is prominent at private facilities.
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| 4. |
- Pandya, Jayesh M., et al.
(författare)
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CD4+and CD8+CD28(null) T Cells Are Cytotoxic to Autologous Muscle Cells in Patients With Polymyositis
- 2016
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Ingår i: Arthritis & Rheumatology. - : John Wiley & Sons. - 2326-5191 .- 2326-5205. ; 68:8, s. 2016-2026
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Tidskriftsartikel (refereegranskat)abstract
- Objective. Inflammatory T cell infiltrates in the skeletal muscle tissue of patients with polymyositis are dominated by CD28-negative effector (CD28(null)) T cells of both the CD4 and CD8 lineage. These cells are potentially cytotoxic, and the aim of the present study was to develop a fully autologous cell culture system in which to investigate the functional contribution of such CD28(null) T cells to myotoxicity. Methods. In vitro cocultures of autologous skeletal muscle cells and T cell subsets obtained from 5 polymyositis patients were performed. Myotoxicity of T cells was quantified by calcein release and flow cytometric analyses. T cell degranulation was blocked with concanamycin A. Specific blocking of perforin, cytokines, and HLA was performed using antibodies. Results. Both CD4+CD28(null) and CD8+CD28(null) T cells induced more muscle cell death than did their CD28+ counterparts. Differentiated muscle cells (myotubes) were more sensitive to T cell-mediated cell death than were their precursors (myoblasts). Both CD8+ and CD4+ CD28(null) T cells displayed perforin polarization toward muscle cells and secreted higher levels of granzyme B and interferon-gamma (IFN gamma) in coculture than did CD28+ T cells. The myotoxic effects of CD28(null) T cells were reduced upon the blocking of perforin, cytokines, and HLA. Addition of IFN gamma or tumor necrosis factor did not induce skeletal muscle cell death in the absence of T cells; however, it did up-regulate HLA expression on muscle cells. Conclusion. Myotoxicity of CD4+ and CD8+ CD28(null) T cells is mediated by directed perforin-dependent killing and can be further influenced by IFN gamma-induced HLA expression on muscle cells. The data suggest that CD28(null) T cells are key effector cells that contribute to the muscle cell damage in polymyositis.
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