Cervical Cancer Prevention on Instagram: Content and Social Interaction Analysis of Brazilian Accounts

Abstract: Objective: The aim of the present study was to analyse the content of posts on Instagram about cervical cancer. Methods: It was conducted a qualitative analysis using the 50 most popular publicly available Portuguese-language Instagram posts, containing the hashtags #cervicalcancer, #papsmear, #hpv, #papillomavirus, and #hpvvac-cine, during the Brazilian national cervical cancer prevention campaign in March 2018. Results: Posts recruited using #cervicalcancer provided 60% of posts with contents related to secondary prevention; the #papsmear provided 46% of posts with irrelevant contents; the #hpv and #papillomavirus provided 50% and 64% of posts with informative content, respectively; and the #hpvvaccine provided 58% of posts with content related to primary prevention. The posts that received the highest number of likes were those from the hashtags #hpv and #papillomavirus with 151.33 and 78.00 likes/post, respectively. The majority of posts presented less than 05 comments/post, except for the #hpv, which had 64.76 comments/post. According to the users’ profiles, the majority of the posts, regardless of the hashtag used, were made by health professionals. Conclusion: The focus of Instagram posts about cervical cancer is on secondary prevention, which can contribute to the promotion of health behaviours not directed to aspects of primary prevention of the disease.     

European legislation impedes critical care research and fails to protect patients' rights

The European Clinical Trials Directive requires an informed consent from the patient or a proxy in drug trials. Although informed consent is a valuable tool to protect patients' rights in clinical trials, this requirement largely impedes research in critical care settings, and if pursued in this context, it does not provide the patient with adequate protection. Instead of insisting on informed consent, we suggest that the focus should be shifted towards two other ethically relevant elements in human experimentation: risk assessment and selection of research subjects. When reviewing protocols in which a waiver of consent is deemed necessary, the Ethical Review Board should ensure that non-therapeutic risks are minimal, that the research is specifically designed to benefit critically ill patients, and that it cannot be conducted under circumstances where an informed consent can be obtained. If the European Directive is changed accordingly, this permits clinical trials in critical care settings, while adequate protection from risky non-therapeutic procedures is ensured and exploitation of the patient as an easily accessible research subject is prevented.     

Clinical differences between children and adults with pulmonary hypertension and sickle cell disease

Pulmonary hypertension (PHT) is an important co-morbidity in sickle cell disease (SCD). Despite increasing research in adults, the prevalence and implication of this condition in children is unknown. Charts of 362 SCD patients followed at the Children's Hospital & Research Center Oakland were reviewed to determine clinical variables associated with obtaining echocardiographic screening for PHT, clinical associations of PHT, and associated mortality following diagnosis in adults and children with SCD. In this cohort, patients with underlying lung abnormalities or those on chronic transfusions were more likely to have echocardiograms, however the diagnosis of PHT was often unrecognized. A different clinical phenotype for PHT in adults versus children was identified. Associations with PHT for adults included age, renal and lung disease, hepatitis C, chronic transfusions, and a history of acute chest syndrome (ACS), with ACS being protective. Surprisingly, for children, a history of sepsis, along with a history of ACS, or obstructive lung disease were associated with PHT. Survival analysis found significant mortality for PHT, with a hazard ratio of 17·3 (95% confidence interval 4·9–60·4). The divergent clinical spectrum for PHT between adults and children may point to different age-specific mechanisms or biological expression of PHT.     

Point mutations in the conserved box 1 region inactivate the human granulocyte colony-stimulating factor receptor for growth signal transduction and tyrosine phosphorylation of p75c-rel

The human granulocyte colony-stimulating factor receptor (hG-CSFR) belongs to the cytokine receptor superfamily. As with other members of this family, the cytoplasmic domain of hG-CSFR lacks intrinsic tyrosine kinase activity. To identify critical regions mediating growth signal transduction by hG-CSFR, deletions or site-directed amino acid substitutions were introduced into the cytoplasmic domain of hG-CSFR, and the mutant cDNAs were transfected into the murine interleukin-3 (IL- 3)-dependent Ba/F3 and FDCP cell lines. Truncation of the carboxy- terminal end of the receptor to the membrane-proximal 53 amino acids of the cytoplasmic domain, which retained the conserved Box 1 and Box 2 sequence motifs, decreased the ability of hG-CSFR to transduce G-CSF- mediated growth signals without an associated loss in receptor binding affinity. Substitution of proline by alanine at amino acid positions 639 and 641 within Box 1 completely abolished the G-CSF-mediated growth signal. Rapid induction of tyrosine phosphorylation of several cellular proteins, including a 75-kD protein (p75) identified as c-rel, was an early event associated with transduction of proliferative signals by hG- CSFR in Ba/F3 transfectants. Mutant receptors containing Pro-to-Ala substitutions that inactivated the receptor for mitogenic activity also inactivated the receptor for tyrosine-specific phosphorylation of p75. These results show that the conserved Box 1 sequence motif (amino acids 634 to 641) is critical for mitogenesis and activation of cellular tyrosine kinases by hG-CSFR.     

Immunolocalization of beta 1 integrins in platelets and platelet- derived microvesicles

Human platelets contain several adhesion receptors belonging to the integrin superfamily. At least three beta 1 integrins are present on platelets and have been shown to mediate platelet adhesion to collagen, fibronectin, and laminin. To study the cellular localization of the beta 1 integrins in platelets, we produced a polyclonal antibody by immunization of goat 172 with purified beta 1 subunit from HPB-ALL cells. Antibody 172 (Ab172) specifically immunoblotted a 135-Kd protein in a lysate of whole platelets. The reactivity of Ab172 with platelet membrane proteins was further determined by immunoprecipitation of lysates of surface-radioiodinated platelets. Ab172 immunoprecipitates, resolved by nonreducing/reducing two-dimensional sodium dodecyl sulfate- polyacrylamide gel electrophoresis consisted of three labeled proteins with migrational properties of platelet glycoprotein (GP)Ia, GPIc and GPIIa. Neither GPIIb/IIIa nor the vitronectin receptor were immunoprecipitated by Ab172, confirming a lack of cross-reactivity with the beta 3 integrins in platelets. Immunofluorescence studies using Ab172 were performed to investigate the cellular distribution of beta 1 integrins in platelets. Fluorescent labeling of intact cells demonstrated the presence of beta 1 antigen on the surface of resting cells. Permeabilization of platelets with Triton X-100 showed the presence of an intracellular pool of beta 1 antigen. Double-label experiments using Ab172 and AP-2 (anti-GPIIb/IIIa) showed identical labeling patterns, suggesting a similar subcellular distribution for these integrins. Following thrombin stimulation, permeabilized cells showed a centralized clearing of both beta 1 antigen and GPIIb/IIIa as well as an intensification of surface labeling for beta 1 antigen. These findings suggest the translocation of intracellular beta 1 antigen to the platelet surface as a result of thrombin stimulation. Because platelet-derived microvesicles have been reported to contain GPIIb/IIIa, we investigated the possible distribution of beta 1 integrins in these structures. Microvesicles, produced as a result of platelet activation, were labeled with Ab172, suggesting the distribution of beta 1 integrins in these structures as well as in intact cells.