We identify the need to increase access and use of mHealth services for sexual health, as it provides an innovative platform to bridge the health communication gaps in sexual health for Bangladeshi women.Background The risk of cancer patients to develop COVID19 infection is unclear. We aimed to prospectively study cancer patients and oncology healthcare workers for COVID19 serology. In IgG+ cases, immune profile was determined to portray the pattern of immune response to SARS-CoV2. Methods Cancer patients on active treatment and healthcare workers were enrolled. During the study period (3/2020-6/2020), demographic data and blood were collected at three time points. Expression of IgG, IgM, and IgA were assessed. In SARS-CoV-2 IgG+ cases and matched negative cases, we performed mass cytometry time of flight (CyTOF) analysis on the basis of the expression of surface markers. Results The study included 164 cancer patients on active intravenous treatment and 107 healthcare workers at the cancer center. No symptomatic cases were reported during the study period. Serology analysis revealed four IgG+ patients (2.4%) and two IgG+ healthcare workers (1.9%)-all were asymptomatic. CyTOF analysis demonstrated substantial reduction in myeloid cells in healthcare workers who were SARS-CoV-2 IgG+ compared to those who were SARS-CoV-2 IgG-, whereas in cancer patients, the reduction was relatively milder (≈50% reduction in SARS-CoV-2 IgG+ cancer patients compared with ≈90% reduction in SARS-CoV-2 IgG+ workers). Conclusion Our results indicate a similar rate of asymptomatic COVID19 infection in cancer patients and healthcare workers in a longitudinal study throughout the pandemic time. Due to differential immune cell profiles of cancer patients who are treated with immunomodulatory agents, the host response to the SARS-COV2 may play a role in COVID19 course and representation. The immunological perspective of cancer treatments on the risk for COVID19 infection should be further explored.Fouling is one of the major problems in electrodialysis. The aim of the present work was to investigate the effect of five different solution flow rates (corresponding to Reynolds numbers of 162, 242, 323, 404 and 485) combined with the use of pulsed electric field (PEF) current mode on protein fouling of bipolar membrane (BPM) during electrodialysis with bipolar membranes (EDBM) of skim milk. The application of PEF prevented the fouling formation by proteins on the cationic interface of the BPM almost completely, regardless of the flow rate or Reynolds number. Indeed, under PEF mode of current the weight of protein fouling was negligible in comparison with CC current mode (0.07 ± 0.08 mg/cm2 versus 5.56 ± 2.40 mg/cm2). When a continuous current (CC) mode was applied, Reynolds number equals or higher than 323 corresponded to a minimal value of protein fouling of BPM. This positive effect of both increasing the flow rate and using PEF is due to the facts that during pauses, the solution flow flushes the accumulated protein from the membrane while in the same time there is a decrease in concentration polarization (CP) and consequently decrease in H+ generation at the cationic interface of the BPM, minimizing fouling formation and accumulation.Lacripep is a therapeutic peptide derived from the human tear protein, Lacritin. Lacripep interacts with syndecan-1 and induces mitogenesis upon the removal of heparan sulfates (HS) that are attached at the extracellular domain of syndecan-1. https://www.selleckchem.com/products/art0380.html The presence of HS is a prerequisite for the syndecan-1 clustering that stimulates exosome biogenesis and release. Therefore, syndecan-1-mediated mitogenesis versus HS-mediated exosome biogenesis are assumed to be mutually exclusive. This study introduces a biosynthesized fusion between Lacripep and an elastin-like polypeptide named LP-A96, and evaluates its activity on cell motility enhancement versus exosome biogenesis. LP-A96 activates both downstream pathways in a dose-dependent manner. HCE-T cells at high confluence treated with 1 μM LP-A96 enhanced cell motility equipotent to Lacripep. However, cells at low density treated with 1 μM LP-A96 generated a 210-fold higher number of exosomes compared to those treated at low density with Lacripep. As monovalent Lacripep is capable of enhancing cell motility but not exosome biogenesis, activation of exosome biogenesis by LP-A96 not only suggests its utility as a novel molecular tool to study the Lacritin biology in the corneal epithelium but also implies activity as a potential therapeutic peptide that can further improve ocular surface health through the induction of exosomes.The retinal pigment epithelium (RPE) maintains visual function and preserves structural integrity of the retina. Chronic dysfunction of the RPE is associated with retinal degeneration, including age-related macular degeneration (AMD). The AMD pathogenesis includes both increased oxidative stress and complement dysregulation. Physiological sources of oxidative stress in the retina are well known, while complement sources and regulation are still under debate. Using human primary RPE (hpRPE) cells, we have established a model to investigate complement component expression on transcript and protein level in AMD-risk and non-risk hpRPE cells. We evaluated the effect of properdin, a complement stabilizer, on the hpRPE cell-dependent complement profile exposed to oxidative stress. hpRPE cells expressed complement components, receptors and regulators. Complement proteins were also stored and secreted by hpRPE cells. We associated AMD-risk single nucleotide polymorphisms with an increased secretion of complement factors D (CFD) and I (CFI). Furthermore, we detected hpRPE cell-associated complement activation products (C3a, C5a) independent of any extracellularly added complement system. Exogenous properdin increased the mRNA expression of CFI and CFD, but decreased levels of complement components (C1Q, C3), receptors (C3AR, C5AR1, CD11B) and inflammation-associated transcripts (NLRP3, IL1B) in hpRPE cells exposed to oxidative stress. This properdin effect was time-dependently counter regulated. In conclusion, our data unveiled a local, genotype-associated complement component production in hpRPE cells, regulated by exogenous properdin. The local complement production and activation via blood-independent mechanisms can be a new therapeutic target for AMD.