Comfort with having sexual orientation recorded on official databases among a community and online sample of gay and bisexual men in Aotearoa New Zealand.

Introduction Sexual orientation minorities have worse health outcomes than the heterosexual majority. In 2023, Aotearoa New Zealand (NZ) added sexual and gender identity items to the Census, offering actionable data for improving sexual identity and gender identity (SOGI) community health. However, this also raises questions about individuals' willingness to provide such information to Government and their comfort with data privacy and governance. Methods Using data from gay, bisexual, and other men who have sex with men (GBM) participants of the Gay Auckland Periodic Sex Survey and Gay Men's Online Sex Survey 2014 cross-sectional surveys, the study question examined comfort having their sexual orientation recorded in official databases. A logistic regression model was used to identify independent predictors of comfort, including sociodemographic and behavioural variables. Results Of 3173 participants who completed the question, 63.1% were comfortable with recording sexual orientation. Adjusted odds ratios showed less comfort among those identifying with an 'Other' ethnicity (AOR: 0.64, 95% CI: 0.43-0.96), identifying as bisexual (AOR: 0.45, 95% CI: 0.35-0.56), and those who did not believe their GP to be aware of their sexuality (AOR: 0.32, 95% CI: 0.26-0.40). No sexual behaviours were independently associated with comfort. Discussion The majority of GBM participants reported comfort with having their sexual orientation recorded on official databases, but some are not, and this is patterned by sociodemographic variables. Officials should improve the safety and perceived relevance of sexual orientation data collection efforts to increase their representativeness and utility for sexual minority populations.

The effect of citalopram treatment on amyloid-ß precursor protein processing and oxidative stress in human hNSC-derived neurons.

Selective Serotonin Reuptake Inhibitors (SSRIs) may hold therapeutic benefits for people with Alzheimer's disease (AD). SSRIs may perturb AD progression, or the conversion from MCI to AD, via increased neurogenesis, reduced oxidative stress and/or favourable Amyloid-ß Precursor Protein (AßPP) processing. This study used iPSC derived cortical neuronal cells carrying 3 different PSEN1 mutations, to investigate the effect of treatment with the SSRI, Citalopram on AßPP processing and oxidative stress. Control and PSEN1 mutation (L286V, A246E, M146L) iPSC-derived neurons were treated with Citalopram for 45 days. ADAM10 activity, AßPP processing and Aß generation was measured in addition to cellular redox status. Citalopram treatment reduced the Aß1-42:40 ratio in control but not in fAD PSEN1 cells. ADAM10 activity was increased with Citalopram treatments in fAD PSEN1 cell lines, which was also seen for sAßPPα secretion. Lower superoxide generation in fAD PSEN1 cells following Citalopram treatment was identified, although there was no effect on end markers of oxidative stress. Treatment with Citalopram appears to have little effect on Aß generation in fADPSEN1 cells, but our findings suggest that treatment can significantly increase non-amyloidogenic AßPP processing and reduce oxidative stress. These changes may explain why SSRIs appear most effective in the prodromal period of the disease progression, as opposed to reducing established AD pathology. Further investigation of specific pathways conferring the beneficial effects of SSRIs treatment are warranted.

Essential amino acids of Escherichia coli DnaC protein in an N-terminal domain interact with DnaB helicase.

Escherichia coli DnaC protein bound to ATP forms a complex with DnaB protein. To identify the domain of DnaC that interacts with DnaB, a genetic selection was used based on the lethal effect of induced dnaC expression and a model that inviability arises by the binding of DnaC to DnaB to inhibit replication fork movement. The analysis of dnaC alleles that preserved viability under elevated expression revealed an N-terminal domain of DnaC involved in binding to DnaB. Mutant proteins bearing single amino acid substitutions (R10P, L11Q, L29Q, S41P, W32G, and L44P) that reside in regions of predicted secondary structure were inert in DNA replication activity because of their inability to bind to DnaB, but they retained ATP binding activity, as indicated by UV cross-linking to [alpha-(32)P]ATP. These alleles also failed to complement a dnaC28 mutant. Other selected mutations that map to regions carrying Walker A and B boxes are expected to be defective in ATP binding, a required step in DnaB-DnaC complex formation. Lastly, we found that the sixth codon from the N terminus encodes aspartate, resolving a reported discrepancy between the predicted amino acid sequence based on DNA sequencing data and the results from N-terminal amino acid sequencing (Nakayama, N., Bond, M. W., Miyajima, A., Kobori, J., and Arai, K. (1987) J. Biol. Chem. 262, 10475-10480).

Relapse of maternal thyrotoxicosis presenting as a second-trimester fetal goiter.

A large fetal goiter was detected at 22 weeks of gestation during an antenatal ultrasound scan of a woman with a previous history of Graves' disease treated by partial thyroidectomy. This unsuspected finding initiated maternal investigations and treatment. In untreated cases poor fetal outcome is common and unfortunately fetal thyrotoxicosis/thyroid enlargement frequently remains unrecognized in the first pregnancy. We report the case and its management and discuss the literature emphasizing the importance of screening for antibodies in the 'at-risk' women and the increasing importance of ultrasound in the evaluation and follow-up of these patients. Reports of thyrotoxic fetal goiters are extremely rare and, to our knowledge, there have been no previous reports of this in the second trimester.