Policies enacted during COVID-19 came with unintended health benefits: why go back?

OBJECTIVES: To explore the impact of COVID-19 on the implementation of bundled interventions to improve the engagement and retention of Black women in HIV care. METHODS: Pre-implementation interviews conducted between January and April 202 L with 12 demonstration sites implementing bundled interventions for Black women with HIV. Directed content analysis was employed to examine the site interview transcripts. RESULTS: The pandemic intensified barriers to care and harmful social conditions. However, COVID-19 also forced pivots in health care and social service delivery and some of these changes benefited Black women living with HIV. CONCLUSIONS: The continuation of policies that support the material needs of Black women with HIV and ease access to care is critical. Racial capitalism impedes the enactment of these policies and thus threatens public health.

The long road. Interview by Lynne Pearce.

In the fifth aticle on the management of change, Joy Jones describes how she improved services for people with eating disorders, while Stephen Wright explores the skills she brought to the work.

Discovering the research priorities of people with diabetes in a multicultural community: a focus group study.

BACKGROUND: Usually experts decide on which research is worthwhile, yet it is government policy to involve service users in research. There has been a lack of published research about involving patients from minority ethnic groups and people from deprived areas in setting research agendas. In this study we wanted to hear the voices of patients that are not often heard. AIM: To find out the research priorities of people with diabetes from an inner city community and compare these with current expert-led research priorities in diabetes. DESIGN OF STUDY: A qualitative study using a participatory approach with consumer groups. SETTING: Primary care within inner city Nottingham, UK. METHOD: Thirty-nine adult patients with diabetes with varying ethnic backgrounds recruited from three general practices. Six focus groups carried out in participants' preferred language, analysed using the constant comparative method. RESULTS: Nine main themes equating to research priorities were identified. Within these themes, information and awareness, service delivery and primary prevention of diabetes emerged as the main factors. There were no science-based topics and there was more emphasis on culturally influenced research questions, which differed from recent Department of Health priorities. There were several themes about service delivery, patient self-management and screening and prevention of diabetes that overlapped. CONCLUSIONS: There is some divergence between expert-led and patient-led agendas in research about diabetes. Patient perspectives have a significant influence on research priorities, and there are likely to be several different patient perspectives.

Ferritin heavy chain upregulation by NF-kappaB inhibits TNFalpha-induced apoptosis by suppressing reactive oxygen species.

During inflammation, NF-kappaB transcription factors antagonize apoptosis induced by tumor necrosis factor (TNF)alpha. This antiapoptotic activity of NF-kappaB involves suppressing the accumulation of reactive oxygen species (ROS) and controlling the activation of the c-Jun N-terminal kinase (JNK) cascade. However, the mechanism(s) by which NF-kappaB inhibits ROS accumulation is unclear. We identify ferritin heavy chain (FHC)--the primary iron storage factor--as an essential mediator of the antioxidant and protective activities of NF-kappaB. FHC is induced downstream of NF-kappaB and is required to prevent sustained JNK activation and, thereby, apoptosis triggered by TNFalpha. FHC-mediated inhibition of JNK signaling depends on suppressing ROS accumulation and is achieved through iron sequestration. These findings establish a basis for the NF-kappaB-mediated control of ROS induction and identify a mechanism by which NF-kappaB suppresses proapoptotic JNK signaling. Our results suggest modulation of FHC or, more broadly, of iron metabolism as a potential approach for anti-inflammatory therapy.

Short stature with normal growth hormone stimulation testing: lack of evidence for partial growth hormone deficiency or insensitivity.

OBJECTIVES: To test the hypothesis that children with short stature and peak stimulated GH (pGH) of 7-10 microg/l have partial GH deficiency and to test the hypothesis that short children with normal pGH but low IGF-I levels have partial GH deficiency or partial GH insensitivity. DESIGN AND PATIENTS: Retrospective analysis of the clinical and biochemical profiles of 76 children who underwent an evaluation for short stature (height < 5th percentile) that included two, sex steroid-primed GH stimulation tests. RESULTS: Patients with pGH < 7 microg/l (n = 14) differed significantly from those with pGH > 7 microg/l (n = 62), having greater midparental height (MPH) SDS, a greater disparity between height SDS and MPH SDS, and lower IGF-I SDS. Patients with pGH of 7-10 microg/l (n = 12) did not have characteristics intermediate between those with pGH < 7 microg/l and those with pGH > or = 10 microg/l, but instead resembled those with pGH > or = 10 microg/l. Patients with pGH > or = 7 microg/l, but low IGF-I (< -2 SDS) (n = 5), did not show characteristics intermediate between those with pGH < 7 microg/l and those with pGH > or = 7 microg/l and normal IGF-I. CONCLUSIONS: These data do not support either the hypothesis that children with pGH of 7-10 microg/l have partial GH deficiency or the hypothesis that children with normal pGH but subnormal IGF-I levels have partial GH deficiency or insensitivity.

Regulation of the gadd45beta promoter by NF-kappaB.

In addition to coordinating immune and inflammatory responses, NF-kappaB/Rel transcription factors control cell survival. The NF-kappaB antiapoptotic function is crucial to oncogenesis, cancer chemoresistance, and to antagonize tumor necrosis factor (TNF) receptor-induced killing. Recently, we have shown that the suppression of the c-Jun-N-terminal kinase (JNK) cascade is a pivotal protective mechanism by NF-kappaB, and that this suppression involves the upregulation of gadd45beta/myd118. Induction of gadd45beta by stress and cytokines requires NF-kappaB; however, the regulatory mechanisms underlying this induction are not known. Here, we report that, in HeLa cells, the NF-kappaB subunit RelA is sufficient to activate gadd45beta expression, whereas Rel and p50 are not. Activation of gadd45beta by RelA depends on three kappaB elements at positions -447/-438 (kappaB-1), -426/-417 (kappaB-2), and -377/-368 (kappaB-3) of the gadd45beta promoter. Each of these sites binds to NF-kappaB complexes in vitro, and is required for optimal promoter transactivation. The data establish the direct participation of NF-kappaB in the regulation of Gadd45beta, thereby providing important mechanistic insights into the control of apoptosis by the transcription factor.