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For almost five decades, the US Supreme Court had protected the right to abortion care in the United States. However, the Court's decision in 'Dobbs versus Jackson Women's Health Organization' in 2022 established that the US Constitution does not confer a right to abortion, effectively overturning the Court's own previous judgment in 'Roe versus Wade' from 1973. How could a decision that overturns the precedent for nationwide access to abortion affect women, children, and physicians? How will state laws impact healthcare equity regarding reproductive rights going forward? How will geography affect who can access care financially, and how will this shape the conditions that unwanted children are born into? This work is a systematic analysis of the impact of overturning 'Roe versus Wade' considering the scientific and medical evidence as well as the conflicting political and moral viewpoints regarding abortion. Furthermore, we make constructive recommendations with a view to detoxifying the inflammatory rhetoric surrounding this topic and protecting key stakeholders such as patients seeking abortion and their physicians. The moment 'Roe v. Wade' was overturned, several US states began to enact laws, both protecting and restricting abortion. California and New York, for example, have since enacted laws that extend protection to both patients seeking abortion and the physicians who provide it. Oklahoma and Texas, on the other hand, have enacted laws that make it more difficult for patients to have abortion access, even after fetal death or when the birthing individual's life is in danger. These differences are likely to exacerbate the healthcare access divide across the country and increase the financial burden for those who can become pregnant. As differences in healthcare access and quality of care increase across the nation, an unmatched demand for maternity care, especially in the most restrictive states, could precipitate increased maternal and fetal morbidity and mortality while physician shortages are expected to worsen. It will be up to the US Congress to address these differences while weighing competing stakeholder interests. Currently, the nation is at the center of a seismic shift surrounding health policy with laws changing rapidly. This systematic health policy analysis paper will explore what the long-term consequences of this recent Supreme Court decision might look like while considering some of the most recently reported short-term consequences after the landslide decision.

The microbiota in the lumen of patients with Crohn's disease (CD) is characterized by reduced diversity, particularly Firmicutes and Bacteroidetes. It is unknown whether the introduction of the intestinal microbiota from healthy individuals could correct this dysbiosis and reverse mucosal inflammation. We investigated the response to fecal microbial transplantation (FMT) from healthy individuals to subjects with active CD.MethodsWe performed a prospective open-label study (uncontrolled) of FMT from healthy donors to subjects with active CD. A single FMT was performed by colonoscopy. Recipients' microbial diversity, mucosal T-cell phenotypes, and clinical and inflammatory parameters were measured over 12 weeks, and safety over 26 weeks.ResultsNineteen subjects were treated with FMT and completed the study follow-up. Fifty-eight percent (11/19) demonstrated a clinical response (Harvey–Bradshaw Index decrease >3) following FMT. Fifteen subjects had sufficient pre/postfecal samples for analysis. A significant increase in microbial diversity occurred after FMT (P = 0.02). This was greater in clinical responders than nonresponders. Patients who experienced a clinical response demonstrated a significant shift in fecal microbial composition toward their donor's profile as assessed by the Bray–Curtis index at 4 weeks (P = 0.003). An increase in regulatory T cells (CD4+CD25+CD127lo) was also noted in recipients' lamina propria following FMT. No serious adverse events were noted over the 26-week study period.ConclusionsIn this open-label study, FMT led to an expansion in microbial bacterial diversity in patients with active CD. FMT was overall safe, although the clinical response was variable. Determining donor microbial factors that influence clinical response is needed before randomized clinical trials of FMT in CD.

Ischemic stroke remains a leading cause of death and long-term disability, yet effective treatments that promote recovery beyond the acute phase are lacking. Neuregulin-1 (NRG-1) has shown potent neuroprotective and anti-inflammatory properties in preclinical stroke models, with evidence of enhanced neuronal regeneration when administered after injury. To investigate the spatial mechanisms underlying its neuroregenerative therapeutic effects, we examined brain proteomic responses to post-ischemic NRG-1 treatment in mice using NanoString Digital Spatial Profiling (DSP). Adult C57BL/6 mice were subjected to photothrombotic middle cerebral artery occlusion (MCAO) and treated with NRG-1β (5 μg/kg/day) or vehicle at 24- and 48-h post-stroke. Brains were collected at 3 days post-ischemia for spatial proteomic analysis of 68 neural proteins across the ischemic core, peri-infarct tissue, and peri-infarct normal tissue (PiNT). While NRG-1 did not significantly alter overall neuronal death, it markedly reshaped the neuroregenerative milieu, upregulating myelin basic protein (MBP) and synaptophysin and attenuating inflammatory mediators (SPP1, P2RX7, and CD39). NRG-1 also enhanced expression of autophagy and mitophagy markers (ULK1, LC3B, ATG5, PINK1, and Park7), suggesting restoration of cellular clearance and mitochondrial quality control. Pathway and network analyses revealed activation of neuroregeneration, autophagy, and lysosomal biogenesis pathways, while suppressing neuroinflammatory signaling. These findings demonstrate that delayed NRG-1 therapy, even when initiated 24 h after stroke, induces early molecular programs that prime an anti-inflammatory and neuroregenerative environment. The results support further development of NRG-1 as a clinically translatable, multimodal therapy for extending the post-stroke treatment window and promoting functional recovery.

The US Family Smoking Prevention and Tobacco Control Act requires the government to disseminate information about the toxic chemicals in cigarette smoke. We sought to understand how the descriptors \"organic,\" \"natural,\" or \"additive-free\" affect smokers' interest in cigarettes in the context of information about chemicals in cigarette smoke. Participants were a national probability sample of 1,101 US adult (ages ≥18) smokers recruited in 2014-2015. A between-subjects experiment randomized participants in a telephone survey to 1 of 4 cigarette descriptors: \"organic,\" \"natural,\" \"additive-free,\" or \"ultra-light\" (control). The outcome was expected interest in cigarettes with the experimentally assigned descriptor, after learning that 2 chemicals (hydrogen cyanide and lead) are in cigarette smoke. Experimental data analysis was conducted in 2016-2017. Smokers indicated greater expected interest in \"organic,\" \"natural,\" and \"additive-free\" cigarettes than \"ultra-light\" cigarettes (all p <.001) after learning that hydrogen cyanide and lead were in cigarette smoke. Smokers who intended to quit in the next 6 months expressed greater expected interest in the 4 types of cigarettes (\"organic,\" \"natural,\" \"additive-free,\" and \"ultra-light\") compared to smokers not intending to quit (p <.001). Smokers, especially those intending to quit, may be more inclined towards cigarettes described as \"organic,\" \"natural,\" and \"additive-free\" in the context of chemical information. An accumulating body of evidence shows that the US should fully restrict use of \"organic\" and \"natural\" descriptors for tobacco products as it has done for \"additive-free\" and \"light\" descriptors.

Stroke is ranked as the fifth leading cause of death and the leading cause of adult disability in the USA. The progression of neuronal damage after stroke is recognized to be a complex integration of glia, neurons, and the surrounding extracellular matrix, therefore potential treatments must target the detrimental effects created by these interactions. In this study, we examined the spatial cellular and neuroinflammatory mechanisms occurring early after ischemic stroke utilizing Nanostring Digital Spatial Profiling (DSP) technology. Male C57bl/6 mice were subjected to photothrombotic middle cerebral artery occlusion (MCAO) and sacrificed at 3 days post-ischemia. Spatial distinction of the ipsilateral hemisphere was studied according to the regions of interest: the ischemic core, peri-infarct tissues, and peri-infarct normal tissue (PiNT) in comparison to the contralateral hemisphere. We demonstrated that the ipsilateral hemisphere initiates distinct spatial regulatory proteomic profiles with DSP technology that can be identified consistently with the immunohistochemical markers, FJB, GFAP, and Iba-1. The core border profile demonstrated an induction of neuronal death, apoptosis, autophagy, immunoreactivity, and early degenerative proteins. Most notably, the core border resulted in a decrease of the neuronal proteins Map2 and NeuN; an increase in the autophagy proteins BAG3 and CTSD; an increase in the microglial and peripheral immune invasion proteins Iba1, CD45, CD11b, and CD39; and an increase in the neurodegenerative proteins BACE1, APP, amyloid β 1–42, ApoE, and hyperphosphorylated tau protein S-199. The peri-infarct region demonstrated increased astrocytic, immunoreactivity, apoptotic, and neurodegenerative proteomic profiles, with an increase in BAG3, GFAP, and hyperphosphorylated tau protein S-199. The PiNT region displayed minimal changes compared to the contralateral cortex with only an increase in GFAP. In this study, we showed that mechanisms known to be associated with stroke, such as apoptosis and inflammation, occur in distinct spatial domains of the injured brain following ischemia. We also demonstrated the dysregulation of specific autophagic pathways that may lead to neurodegeneration in peri-infarct brain tissues. Taken together, these data suggest that identifying post-ischemic mechanisms occurring in a spatiotemporal manner may lead to more precise targets for successful therapeutic interventions to treat stroke.

Abstract Significance The public incorrectly believes very low nicotine content (VLNC) cigarettes are less carcinogenic than current cigarettes, a belief associated with lower motivation to quit under a VLNC standard. We examined how different descriptions of the nicotine level in VLNC cigarettes affect the accuracy of the public’s perceptions about nicotine content, addictiveness, and cancer risk. Methods Participants were a national convenience sample of 1353 US adults (22% smokers). In an online experiment, we randomized participants to a VLNC description using (1) concise language; (2) a percentage; (3) an interpretation; (4) a percentage and interpretation; (5) a percentage and a pictograph; or (6) a percentage, interpretation, and pictograph; or to a control description using (7) FDA's “minimally or nonaddictive” phrasing. We assessed accuracy of perceived nicotine content, addictiveness, and cancer risk compared to current cigarettes. Results Compared to control, the percentage description resulted in more accurate perceptions about nicotine content (76% vs. 49% accuracy) and addictiveness (44% vs. 34%), but less accurate perceptions about cancer risk (56% vs. 68%; all ps < .05). Adding interpretation or pictographs to the percentage description did not increase accuracy. The concise language description reduced accuracy of perceived nicotine content and addictiveness but increased accuracy of cancer risk (all ps < .05). Conclusions Stating that 95% of nicotine would be removed more accurately conveyed the nicotine content and addictiveness of VLNC cigarettes. However, descriptions that better conveyed nicotine content and addictiveness misled people about cancer risk. Implications Implementation of a VLNC standard should include plans for a communication campaign that conveys that VLNC cigarettes will be less addictive but equally toxic to smoke. Stating the percent reduction in nicotine is likely to more clearly communicate reduced addictiveness but may also exacerbate risk misperceptions. VLNC communication requires further study to ensure the public accurately understands a VLNC standard.

The American seaweed industry is growing, primarily into the edible sector, and more seaweed products are available for human consumption. It is necessary to evaluate the safety of industry’s current post-harvest storage and processing methods to ensure the risk of foodborne pathogens on edible seaweed remains low. We evaluated the pathogen load of edible kelp post-harvest under three different storage temperatures (4˚C, 10˚C, 20˚C) and two different drying methods (air- and freeze-drying). The focal pathogens for this research included: Listeria monocytogenes, Salmonella enterica, Staphylococcus aureus, pathogenic Escherichia coli, Vibrio vulnificus and Vibrio parahaemolyticus. We tested all six pathogens under each treatment condition on both sugar kelp (Saccharina latissima) and rockweed (Ascophyllum nodosum) as these are the most commonly farmed and wild-harvested species in Maine, respectively. We inoculated a known concentration of pathogen onto freshly harvested kelp, treated it under a storage temperature or drying method, and sampled it over time to determine the impact of treatment on pathogen load. Our results showed that storage at 20˚C can lead to replication while storage at 4˚C and 10˚C halted the replication of focal pathogens. Both air-drying and freeze-drying produced significant log scale reductions in surface pathogen load for all focal pathogens. Additionally, air-drying reduced pathogen load more than freeze-drying for a majority of pathogens and storing dried kelp for 6-weeks further reduced pathogen load across all cases. These results are promising for industry as they corroborate historical evidence that current post-harvest storage and processing conditions are producing products safe for human consumption.

Interactions between cells and the extracellular matrix, mediated by integrin adhesion complexes, play key roles in fundamental cellular processes, including the sensing and transduction of mechanical cues. Here, we investigate systems-level changes in the integrin adhesome in patient-derived cutaneous squamous cell carcinoma cells and identify the actin regulatory protein Mena as a key node in the adhesion complex network. Mena is connected within a subnetwork of actin-binding proteins to the LINC complex component nesprin-2, with which it interacts and co-localises at the nuclear envelope. Moreover, Mena potentiates the interactions of nesprin-2 with the actin cytoskeleton and the nuclear lamina. CRISPR-mediated Mena depletion causes altered nuclear morphology, reduces tyrosine phosphorylation of the nuclear membrane protein emerin and downregulates expression of the immunomodulatory gene PTX3 via the recruitment of its enhancer to the nuclear periphery. We uncover an unexpected role for Mena at the nuclear membrane, where it controls nuclear architecture, chromatin repositioning and gene expression. Our findings identify an adhesion protein that regulates gene transcription via direct signalling across the nuclear envelope. Cells transmit mechanical force to the nucleus via the cytoskeleton. Here, the authors reveal a role for the actin regulator Mena in force transmission at the nuclear envelope, where it regulates nuclear architecture, chromatin organization and gene expression.

Background Pictorial cigarette pack warnings discourage smoking, but most evidence comes from studies of adults. Our qualitative study explored adolescents’ reactions to pictorial warnings on their parents’ cigarette packs. Methods We interviewed 24 adolescents whose parents received pictorial warnings on their cigarette packs as part of a randomized clinical trial. We conducted a thematic content analysis of the interview transcripts. Results Pictorial cigarette pack warnings led adolescents to imagine the depicted health effects happening to their parents, which elicited negative emotions. The warnings inspired adolescents to initiate conversations with their parents and others about quitting smoking. Adolescents believed the warnings would help smokers quit and prevent youth from starting smoking. Some current smokers said the warnings made them consider quitting. Conclusions Conversations about the pictorial warnings may amplify their effectiveness for smokers, their adolescent children, and friends of the adolescent children. Cigarette pack warnings may reach a broad audience that includes adolescent children of smokers.

Identifying novel neuroprotectants that can halt or reverse the neurological effects of stroke is of interest to both clinicians and scientists. We and others previously showed the pre-clinical neuroprotective efficacy of neuregulin-1 (NRG-1) in rats following focal brain ischemia. In this study, we examined neuroprotection by exogenous and endogenous NRG-1 using a mouse model of ischemic stroke. C57BL6 mice were subjected to middle cerebral artery occlusion (MCAO) followed by reperfusion. NRG-1 or vehicle was infused intra-arterially (i.a.) or intravenously (i.v.) after MCAO and before the onset of reperfusion. NRG-1 treatment (16 μg/kg; i.a.) reduced cerebral cortical infarct volume by 72% in mice when delivered post-ischemia. NRG-1 also inhibited neuronal injury as measured by Fluoro Jade B labeling and rescued NeuN immunoreactivity in neurons. Neuroprotection by NRG-1 was also observed in mice when administered i.v. (100 μg/kg) in both male and female mice. We investigated whether endogenous NRG-1 was neuroprotective using male and female heterozygous NRG-1 knockout mice (NRG-1+/−) compared with wild-type mice (WT) littermates. NRG-1+/− and WT mice were subjected to MCAO for 45 min, and infarct size was measured 24 h following MCAO. NRG-1+/− mice displayed a sixfold increase in cortical infarct size compared with WT mice. These results demonstrate that NRG-1 treatment mitigates neuronal damage following cerebral ischemia. We further showed that reduced endogenous NRG-1 results in exacerbated neuronal injury in vivo. These findings suggest that NRG-1 represents a promising therapy to treat stroke in human patients.