Investigating behaviours and attitudes regarding recommended vaccination in adults 50 years and above in Australia.

Background Vaccination is important for adults to reduce the morbidity and mortality associated with infectious diseases. In Australia, many vaccines are recommended and funded under the Australian National Immunisation Program. However, a number of vaccines are recommended for adults but not funded.

A 1,8-Naphthalimide-based Tripodal Fluorescent Chemosensor to Selectively Detect Copper Ions.

A 1,8-naphthalimide-based tripodal fluorescent ligand (L3) was synthesized through the copper (I) catalyzed Huisgen azide-alkyne cycloaddition reaction of 2-(2-azidoethyl)-6-morpholino-1 H-benzo[de]isoquinoline-1,3(2 H)-dione with triproparagylamine. Naphthalimide acts as the fluorophore while the triazole and amine nitrogens chelate the metal ion. L3 showed a selective fluorescence turn-off for Cu(II) over other metal ions in aqueous acetonitrile solution.

Public health management of pertussis in adults: Practical challenges and future strategies.

A panel of 24 international experts met in July 2022 to discuss challenges associated with pertussis detection, monitoring, and vaccination in adults; conclusions from this meeting are presented. There has been a shift in the epidemiology of pertussis toward older children and adults. This shift has been attributed to the waning of infection- or vaccine-induced immunity, newer detection techniques causing detection bias, and possibly the replacement of whole-cell pertussis with acellular vaccines in high-income countries, which may lead to immunity waning more quickly.

TDP-43 proteinopathy in ALS is triggered by loss of ASRGL1 and associated with HML-2 expression.

TAR DNA-binding protein 43 (TDP-43) proteinopathy in brain cells is the hallmark of amyotrophic lateral sclerosis (ALS) but its cause remains elusive. Asparaginase-like-1 protein (ASRGL1) cleaves isoaspartates, which alter protein folding and susceptibility to proteolysis. ASRGL1 gene harbors a copy of the human endogenous retrovirus HML-2, whose overexpression contributes to ALS pathogenesis.