A retrospective analysis of social media posts pertaining to COVID-19 vaccination side effects

ObjectivesWith an uprising influence of social media platforms like Twitter and Instagram a multitude of worldwide accessible information is available. Since the beginning of COVID-19 pandemic the exchange of medical information about several topics related to this infectious disease and its vaccination has increased rapidly. The purpose of this investigation was to assess the content associated with COVID-19 vaccination and its side effects and evaluate its educational quality.MethodsWe conducted this retrospective study to investigate 600 Twitter and Instagram posts by #covidvaccinesideeffects due to number of ‘likes’, comments, type of post, language, its purpose and source. In addition, posts were evaluated due to educational quality by three examiners of different educational levels.ResultsThe majority of posts showed 0 to 50 “likes” and 0 to 5 comments in English language. A comparison between Twitter and Instagram by the influence of application showed significant differences in number of posts and “likes” or comments (p < 0.05). The major post type were texts for Twitter (251; 83.7%) and videos for Instagram (104; 34.7%). While a majority of posts by #covidvaccinesideeffects report about the occurrence of side effects, the majority of them were mild and general COVID-19 vaccination feedback during the first 4 months was positive. But, only 3 to 7% were rated by “excellent” educational and validatable content. Interrater reliability between all three examiners presented a high concordance with 89% (p = 0.001).ConclusionsThis study presents an analysis of quantity and quality of social media content according to COVID-19 vaccinations and its side effects. It supports the deduction that most of the content on Twitter and Instagram is shared by patients and unclear sources and thus is limited informative. Nevertheless, influence of social media on medical information especially during COVID-19 pandemic is increasing and practitioners have to face its effect on their patients.     

大鼠颈总动脉与脑膜中动脉粘弹性测试

以生物力学的观点研究大鼠颈总动脉与脑膜中动脉应力松弛和蠕变粘弹性行为,为临床提供生物力学参数。对大鼠颈总动脉与脑膜中动脉进行拉伸应力松弛、蠕变实验。得出了颈总动脉与脑膜中动脉拉伸应力松弛、蠕变实验数据和曲线,以一元线性回归分析的方法处理实验数据,得出了大鼠颈总动脉与脑膜中动脉归一化应力松弛函数、蠕变函数数据和曲线及两组试样实验数据的回归系数c、d和ab、值。结果表明:脑膜中动脉应力松弛、蠕变7200s应力松弛量、蠕变量显著大于颈总动脉(P<0.05)。     

Role for macrophage migration inhibitory factor in acute respiratory distress syndrome

The critical role of macrophage migration inhibitory factor (MIF) in mediating inflammatory lung injury in acute respiratory distress syndrome (ARDS) has been raised recently. The present study has identified enhanced MIF protein expression in alveolar capillary endothelium and infiltrating macrophages in lung tissues from ARDS patients. The possibility that MIF up-regulates its synthesis in an autocrine fashion in ARDS was tested using cultured endothelial cells stimulated with MIF and a murine model of lipopolysaccharide (LPS)-induced acute lung injury. MIF induced significant MIF and tumour necrosis factor (TNF)-alpha synthesis in cultured endothelial cells and the effect was blocked by neutralizing anti-MIF antibody. A similar blocking effect was observed when MIF-stimulated endothelial cells were pretreated with neutralizing anti-TNF-alpha antibody or glucocorticoid, supporting the notion that MIF induced TNF-alpha production via an amplifying pro-inflammatory loop. Treatment with anti-MIF or glucocorticoid effectively attenuated pulmonary pathology and the synthesis of MIF or TNF-alpha in mice with LPS-induced acute lung injury. Mildly augmented expression of aquaporin 1 (AQP1) was also detected in alveolar capillary endothelium in ARDS. In vitro studies revealed that both MIF and TNF-alpha induced a small increase of AQP1 synthesis in cultured endothelial cells. These findings suggest that MIF plays a crucial pathological role leading to alveolar inflammation in ARDS. Anti-MIF and early glucocorticoid therapy may represent a novel therapeutic approach for reducing alveolar inflammation in ARDS.     

A critical assessment of published guidelines and other decision-support systems for the antibiotic treatment of community-acquired respiratory tract infections

Guidelines are an important means by which professional associations and governments have sought to improve the quality and cost-effectiveness of disease management for infectious diseases. Prescribing of initial antibiotic therapy for community-acquired respiratory tract infections (RTIs) is primarily empiric and physicians may often have a limited appreciation of bacterial resistance. Recent guidelines for managing RTIs have adopted a more evidence-based approach. This process has highlighted important gaps in the existing knowledge base, e.g. concerning the impact of resistance on the effectiveness of oral antibiotics for outpatient community-acquired pneumonia and the level of resistance that should prompt a change in empiric prescribing. In upper RTIs, the challenge is to identify patients in whom antibiotic therapy is warranted. Concentrated, sustained efforts are needed to secure physicians' use of guidelines. The information should be distilled into a simple format available at the point of prescribing and supported by other behavioral change techniques (e.g. educational outreach visits). Advances in information technology offer the promise of more dynamic, computer-assisted forms of guidance. Thus, RTI prescribing guidelines and other prescribing support systems should help control bacterial resistance in the community. However, their effect on resistance patterns is largely unknown and there is an urgent need for collaborative research in this area. Rapid, cost-effective diagnostic techniques are also required and new antibiotics will continue to have a role in disease management.     

Effects of tri-iodothyronine (T3), insulin, insulin-like growth factor I (IGF-I) and transforming growth factor beta1 (TGFβ1) on the proportion of insulin cells in cultured embryonic chick pancreas

 With a view to ultimately identifying factors involved in the development of pancreatic insulin cells, we have cultured dorsal pancreatic buds from 5-day chick embryos on a basement membrane matrix (Matrigel) in a serum-free medium supplemented with selected factors. The endodermal components of the buds were freed of almost all the mesenchyme so as to eradicate as much as possible of this source of some such factors. In 7-day cultures, insulin and glucagon cells were demonstrated immunocytochemically; numbers of insulin cells were expressed as a percentage of insulin plus glucagon cell counts. Our standard medium contained insulin. Addition of tri-iodothyronine to this medium did not increase the proportion of insulin cells, but in combination with raised concentrations of glucose and essential amino acids it improved somewhat the marked increase previously recorded for these nutrient conditions. Omission of insulin from the standard medium greatly reduced the proportion of these cells; substitution of insulin by insulin-like growth factor I increased the proportion considerably more than did insulin. To test for an overall effect of growth factors, explants were cultured in standard medium on Matrigel containing reduced amounts of growth factors: the proportion of insulin cells proved to be increased over that reached on normal Matrigel. The suspicion that transforming growth factor β1, a component of Matrigel, might act to reduce the proportion of insulin cells was tested and found to be correct. It is suggested that the different factors studied here may affect either or both of proliferation and determination in the differentiation pathway of insulin vis-à-vis glucagon cells. Accepted: 13 March 1998     

The Ki-67 protein interacts with members of the heterochromatin protein 1 (HP1) family: a potential role in the regulation of higher-order chromatin structure.

The expression of the nuclear protein Ki-67 (pKi-67) is strictly correlated with cell proliferation. Because of this, anti-Ki-67 antibodies can be used as operational markers to estimate the growth fraction of human neoplasia in situ. For a variety of tumours, the assessment of pKi-67 expression has repeatedly been proven to be of prognostic value for survival and tumour recurrence, but no cellular function has yet been ascribed to the Ki-67 protein. This study shows that a C-terminal domain of pKi-67 (Kon21) is able to bind to all three members of the mammalian heterochromatin protein 1 (HP1) family in vitro and in vivo. This interaction can be manipulated in living cells, as evidenced by ectopic expression of GFP-tagged HP1 proteins in HeLa cells, which results in a dramatic relocalization of endogenous pKi-67. Taken together, the data presented in this study suggest a role for pKi-67 in the control of higher-order chromatin structure.