Project description:Quantitative survey findings are important in measuring health-related phenomena, including on sensitive topics such as respectful maternity care (RMC). But how well do survey results truly capture respondent experiences and opinions? Quantitative tool development and piloting often involve translating questions from other settings and assessing the mechanics of implementation, which fails to deeply explore how respondents understand survey questions and response options. To address this gap, we conducted cognitive interviews on survey questions (n = 88) adapted from validated RMC instruments used in Ethiopia, Kenya and elsewhere in India. Cognitive interviews with rural women (n = 21) in Madhya Pradesh, India involved asking the respondent the survey question, recording her response, then interviewing her about what the question and response options meant to her. We analysed the interviews to revise the tool and identify question failures, which we grouped into six areas: issues with sequencing, length and sensitivity; problematic response options; inappropriate vocabulary; temporal and spatial confusion; accessing different cognitive domains; and failure to resonate with the respondent's worldview and reality. Although women tended to provide initial answers to the survey questions, cognitive interviews revealed widespread mismatch between respondent interpretation and question intent. Likert scale response options were generally incomprehensible and questions involving hypothetical scenarios could be interpreted in unexpected ways. Many key terms and concepts from the international RMC literature did not translate well and showed low resonance with respondents, including consent and being involved in decisions about one's care. This study highlights the threat to data quality and the validity of findings when translating quantitative surveys between languages and cultures and showcases the value of cognitive interviews in identifying question failures. While survey tool revision can address many of these issues, further critical discussion is needed on the use of standardized questions to assess the same domains across contexts.

Project description:Steroids are currently being used in sepsis, particularly in septic shock. However, clinical trials to date have shown contradictory results. This could be attributed to the different patient endotypes and steroid doses, which have also contributed to the inconclusive results. We investigated the effects of glucocorticoid therapy on sepsis in a polymicrobial sepsis model in a variety of settings, such as steroid dose, severity, and sepsis phase. We used a rat model of fecal slurry polymicrobial sepsis. First, we investigated the optimum dose of steroids in a sepsis model. We administered different doses of dexamethasone after sepsis induction (0.1DEX; 0.1 mg/kg, 0.2DEX; 0.2 mg/kg, 5DEX; 5 mg/kg). Second, we used two different severities of the fecal slurry polymicrobial sepsis rat model to examine the effects of the steroids. A moderate or severe model was defined as a survival rate of approximately 70% and 30%, respectively. Third, we administered steroids in an early (1 h after sepsis induction) or late phase (25 h after sepsis). In all the experiments, we investigated the survival rates. In the determined optimal model and settings, we measured serum lactate, alanine transferase (ALT), creatinine, tumor necrosis factor-α (TNF-α), interleukin (IL)-6, IL-10, and arterial blood gas. We evaluated the bacterial burden in the blood and spleen. Endotoxin tolerance of peripheral blood mononuclear cells (PBMCs) and splenocytes was also investigated to determine the level of immune suppression 24 h after sepsis by measuring TNF-α production after stimulation with lipopolysaccharide (LPS) in an ex vivo model. Early treatment of 0.2 mg/kg dexamethasone in a severe sepsis model showed the best beneficial effects. In moderate- or late-phase sepsis, there was no survival gain with steroid treatment. DEX0.2 group showed less acute kidney injury manifested by serum creatinine and blood urea nitrogen. DEX decreased the levels of cytokines, including IL-6, IL-10, and TNF-α. Colony-forming units were significantly decreased in the blood when administered with dexamethasone. Endotoxin tolerance was not significantly different between the DEX0.2 and control groups. In conclusion, early treatment of 0.2 mg/kg dexamethasone improved the outcomes of rats in a severe sepsis model.

Project description:My father was diagnosed with stomach cancer recently. Luckily, it was still at an early stage, and endoscopic surgery successfully took care of it. My father was fortunate; since people with stomach cancer do not show clear symptoms in the early stages, the disease is often not diagnosed until it becomes advanced. In his case, the diagnosis started from a suggestion by his doctor to check whether he had a gastric infection with Helicobacter pylori, a bacterial species found in the digestive tract. In Japan, where he lives, a majority of gastric cancer patients (more than 99%) have been infected with H. pylori [1], and the causative role of this bacterial species in promoting gastric cancer is very well established. Now, scientific understanding connecting gastric cancer to H. pylori is saving the lives of many people, including my father. Thinking about this recent personal experience, I wonder if the connection between bacteria and cancer might have been considered a crazy idea decades ago. Research makes it possible to connect seemingly unrelated matters. My laboratory works on seemingly unrelated research topics, such as fungal infections and autoimmunity. However, my question is the same whatever the topic: How do leukocytes elicit and regulate inflammation when they detect infections or endogenous signals? In fact, host receptors detecting pathogens can induce autoimmunity, and autoimmunity alters host sensitivity to pathogens due to the imbalance in the immune system. We are beginning to gain some insight into this question, as revealed by some of our recent studies. For example, the NLR family, pyrin domain containing 3 (NLRP3) inflammasome, which is known to sense a wide variety of pathogens, can also change the course of experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS). In particular, our study suggested that disease treatment approaches need to be changed based on the activation status of the NLRP3 inflammasome [2]. Another recent study from our laboratory demonstrated that a protein, termed osteopontin (OPN), skews the balance of population sizes between myeloid cells (i.e., innate immunity) and lymphoid cells (i.e., adaptive immunity) during infections and other biological insults [3]. An intracellular isoform of OPN (iOPN) negatively regulates emergency myelopoiesis. Thus, OPN attenuates host resistance by limiting neutrophil supply at the early stage of systemic Candida infection. In contrast, a secreted OPN (sOPN) isoform positively regulates the expansion of T lymphocytes and ends up triggering autoimmune colitis. I am an immunologist but obtained my PhD in mycology. Nevertheless, it took some time for me to appreciate that research enables us to connect the dots placed far apart. This is a truly exciting time to connect seemingly unrelated biological phenomena, because scientists are exponentially increasing our understanding of nature. This is particularly true in innate immunity, which is not only the central alarming system in host-microbe interactions but also relates to almost any human disease we can imagine. However, we are facing a dark age for science and research, in which certain interests wrongfully discredit some research fields. There are things that can be achieved only by research. I am always ready to tell anyone, "Yes, research matters!".

Dataset Information

Steroids for sepsis: yes, no or maybe.

Publications

Steroids for sepsis: yes, no or maybe.

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