Empowering the affected: Informing community-based solutions through interviews with survivors of interpersonal firearm violence-Perspectives of survivors of firearm injuries.

Proceedings from the Second Medical Summit on Firearm Injury Prevention, 2022: Creating a Sustainable Healthcare Coalition to Advance a Multidisciplinary Public Health Approach.

The author proposes the addition of narrative and existential therapies to current empirically based treatments for victims of interpersonal violence who are experiencing posttraumatic stress disorder (PTSD). A brief history of PTSD, current diagnostic criteria, and cultural influences in relation to this disorder are addressed. ********** The breadth of interpersonal violence is continuously expanding. According to Broman-Fulks et al. (2006), epidemiological studies estimated that between 50% and 70% of individuals in the United States have experienced some form of interpersonal violence during their lifetime. Interpersonal violence and trauma are exceedingly complex phenomena that have cultural, social, political, and psychological implications (Carlson, 2005; De Silva, 1993; Goto & Wilson, 2003). One constant commonly associated with interpersonal violence is the prevalence of posttraumatic stress disorder (PTSD) among survivors of such violence (Phillips, Rosen, Zoellner, & Feeny, 2006). The complexity of working with survivors of interpersonal violence who are experiencing PTSD makes it imperative for clinicians to provide holistic treatment that attends to all of these layers. In this article, I propose an integration of existential and narrative therapies with current evidence-supported approaches to treating the aforementioned population. First, I briefly define interpersonal violence, then provide a history and review of the diagnostic criteria for PTSD, which frequently results from such crimes. I then address cultural influences that could have an impact on diagnosis and treatment, followed by current treatments within the mental health field. Finally, I review the essential components of existential and narrative approaches and conclude with a discussion of how a combination of these treatment modalities could be beneficial for counselors in their work with survivors of interpersonal violence. INTERPERSONAL VIOLENCE Interpersonal violence is defined here as an encounter that threatens or manifests bodily or emotional harm (Gore-Felton, Gill, Koopman, & Spiegel, 1999, p. 294). There are various forms of interpersonal violence, for example, sexual assault, domestic violence, executions, emotional abuse of children and spouses, terrorist attacks, mass shootings, torture, and other forms of homicide. The diffusion of impact can range from a single victim of assault to thousands affected by a mass shooting. Unfortunately, interpersonal violence is becoming a more common occurrence across the United States (Gore-Felton et al., 1999). In 2002, an estimated 1.6 million people across the globe died from self-inflicted, interpersonal, or communal violence. Of these, one third were homicide victims, and about 170,000 died as a direct result of mass violence (World Health Organization, 2007). The disruptive effects of interpersonal violence can be a determinant of mental health (Satcher, Friel, & Bell, 2007). Because of the growing evidence of such violence, it is important to understand the psychological consequences of it (Gore-Felton et al., 1999). PTSD History PTSD is a relatively new diagnostic category, although pathological responses to stressful events have been acknowledged in various contexts for decades (De Silva, 1993). The study of psychological trauma has been chronically forgotten because it provokes powerful controversy and requires one to encounter the essence of human vulnerability and villainy (J. Herman, 1997). It has been postulated that the conception of this disorder was in the late 19th century and was originally referred to as hysteria. At the time, most physicians considered hysteria to be a disease proper to women and originating in the uterus (Sgroi, as cited in J. Herman, 1997, p. 10). French neurologist Jean-Martin Charcot was one of the founding scientists to study the controversial disorder. Through various case studies, Charcot was able to demonstrate that the root of hysterical symptoms was psychological (J. …

BackgroundResearch on interpersonal violence towards women has commonly focused on individual or proximate-level determinants associated with violent acts ignores the roles of larger structural systems that shape interpersonal violence. Though this research has contributed to an understanding of the prevalence and consequences of violence towards women, it ignores how patterns of violence are connected to social systems and social institutions.MethodsIn this paper, we discuss the findings from a scoping review that examined: 1) how structural and symbolic violence contributes to interpersonal violence against women; and 2) the relationships between the social determinants of health and interpersonal violence against women. We used concept mapping to identify what was reported on the relationships among individual-level characteristics and population-level influence on gender-based violence against women and the consequences for women’s health. Institutional ethics review was not required for this scoping review since there was no involvement or contact with human subjects.ResultsThe different forms of violence—symbolic, structural and interpersonal—are not mutually exclusive, rather they relate to one another as they manifest in the lives of women. Structural violence is marked by deeply unequal access to the determinants of health (e.g., housing, good quality health care, and unemployment), which then create conditions where interpersonal violence can happen and which shape gendered forms of violence for women in vulnerable social positions. Our web of causation illustrates how structural factors can have negative impacts on the social determinants of health and increases the risk for interpersonal violence among women.ConclusionPublic health policy responses to violence against women should move beyond individual-level approaches to violence, to consider how structural and interpersonal level violence and power relations shape the ‘lived experiences’ of violence for women.Electronic supplementary materialThe online version of this article (doi:10.1186/s12905-015-0256-4) contains supplementary material, which is available to authorized users.

Interpersonal Violence: Global Impact and Paths to Prevention

In urban, large metropolitan trauma centers, we are accustomed to seeing the most gruesome morbidity and mortality in medicine. By far, the most devastating morbidity and mortality to observe are those inflicted on one human being to another. Gun violence is pervasive in this industrialized country, and it impacts us all. Staff, residents, and faculty in trauma centers bear the brunt of this trauma, second only to the families and communities that suffer the loss of loved ones. This burden is especially heavy for health care workers who share the same ethnic background of those who are disproportionately affected by interpersonal gun violence. Survivors of gun violence exist on a spectrum of chronic illness that ranges in physical and mental morbidity and social disruption in loss of wages and capabilities. This disease not only infects those wounded or killed but also transmits through communities and generations. Urban violence exists because of historic and systematic racism. It continues to persist because racism creates inequities in the quality of education, housing, and investment in urban environments, exacerbated by residential segregation. For two providers, a trainee and a faculty member of African descent, conscious of the determinants that create gun violence, it is overwhelming. We, as health care providers, must tell our stories and the stories of those whose voices are not empowered. We can hope that, by sharing these experiences, we stimulate action and change by raising the moral consciousness of those unaware of the tragedies we witness every day.

BackgroundViolence is a global public health concern leading to injuries, long-term physical, sexual or mental health problems and even mortality. The burden of violence-related injuries on hospital systems remains understudied in the Arabian Gulf region. The present study aimed to describe the epidemiology of hospitalized violence-related injuries in a rapidly developing Middle Eastern country.MethodsA retrospective analysis from a level 1 trauma center, in the state of Qatar, was conducted. Data were retrieved from the Qatar national trauma registry for all patients who were admitted with violence-related injuries between June 2010 and June 2017. Analyzed data were used to compare hospitalized interpersonal and self-inflicted violence groups.ResultsThe hospitalization rate of violence-related injuries was 4.6 per 100,000 population per year; it was significantly higher in males (5.5/100,000 males/year vs. 1.8/100,000 females/year) and younger persons, particularly in the 25–34 years old population (41%). South Asians constituted 55% of the affected study population. Interpersonal violence (76.7%) was the most common mechanism of injury. Significant differences between interpersonal and self-inflicted violence groups were evident, especially for the type of trauma (i.e. blunt or penetrating), injured body regions, alcohol use, injury severity, need for intubation and psychiatric referral (p < 0.05). Overall, in-hospital mortality was 6.4%; with a significantly higher rate in females (16% vs.5%, p = 0.001). Outcomes, including length of hospital stay and mortality, were comparable between the two study groups. Multivariate analysis showed that male gender and alcohol use were predictors for interpersonal violence whereas high Injury Severity Score (ISS) and low Glasgow Coma Scale (GCS) were predictors of hospital mortality.ConclusionsThe rate of hospitalization for violence-related injuries in Qatar is low; however, its burden on the trauma system is of concern. Although it comprised only 9.6% of the study population, females are more likely to get hospitalized following self-inflicted injuries when compared to interpersonal violence. The disproportionate burden of violence among South Asian and young populations warrants an evidence-based public health approach to appropriately address the risk factors and set prevention programs.

Penetrating head & neck trauma – Epidemiology and injury characteristics in terror-related violence, interpersonal violence and deliberate self-harm at a level 1 trauma centre

Familial hyperkalemic hypertension (FHHt) syndrome (1,2), also known as Gordon syndrome (3) or pseudohypoaldosteronism type 2 (4), is a rare inherited form of low-renin hypertension associated with hyperkalemia and hyperchloremic metabolic acidosis in patients with a normal GFR (OMIM no. 145260). This monogenic form of arterial hypertension has excited new interest since the discovery of a new, unsuspected molecular pathway that is responsible for both the biochemical abnormalities and the increase in BP observed. Genetic analysis has led to the identification of mutations in two genes that belong to a new family of kinases, the WNK family. Although the physiologic functions of these kinases and the pathophysiology of FHHt are not completely solved, these results have opened up major new avenues toward understanding the regulation of ion handling in the aldosterone-sensitive nephron. Chasing the Gene Phenotypic and Genetic Heterogeneity Since the first description of the disease by Paver and Pauline in 1964 (1), approximately 50 other cases and families have been reported (5,6). The original case was a 15-yr-old boy with severe hypertension (180/120 mmHg) and very high potassium levels (7.0 to 8.2 mmol/L). Detailed analyses using different diets and pharmacologic stimuli showed that the kidney was probably involved but that the renal tubule reacted normally to an acid load and to carbonic anhydrase inhibitor. Sensitivity to thiazide diuretics was reported a few years later in unrelated, affected individuals (2,7). Gordon's group reported their first case in 1970 (8) and helped to demonstrate the existence of a unifying syndrome (5). High levels of variability, in terms of age at diagnosis, which may vary from the first few weeks of life (9) until late in adulthood (10), have been reported in sporadic and familial cases. We observed a similarly high level of variability in the first 14 FHHt families studied at our center (6), with the age at diagnosis of index cases ranging from 7 mo to 39 yr. An analysis of the affected and unaffected individuals of our largest kindred showed no relationship between the severity of biochemical abnormalities and age or BP, which seemed to depend primarily on age in affected individuals (11). This phenotypic variability, associated with sensitivity to thiazides—which are widely used in hypertension—and with a low probability of this rare disease's being recognized by most doctors may have led to an underestimation of its frequency. The mode of inheritance of the disease is consistent with autosomal dominant transmission in most, if not all, of the pedigrees reported. However, we have identified two families in which the parents of the affected individuals were first cousins, suggesting possible autosomal recessive transmission. This would provide further evidence of the genetic heterogeneity of the disease. Indeed, three loci have already been implicated in this disease, and additional loci probably are responsible for the same apparent phenotype. Genomic analysis of kindreds with FHHt revealed no linkage with SLC12A3, encoding the thiazide-sensitive NaCl co-transporter (NCC) (12 and our own data). In 1997, Lifton's group at Yale University demonstrated locus heterogeneity of the trait, with a multilocus logarithm of odds score of 8.1 for linkage to two loci: a 20- to 33-cM interval on chromosome 1q31-q42 (PHA2A locus) and a 21- to 43-cM linkage interval on chromosome 17p11-q21 (PHA2B locus) (13). Our analysis of a large French pedigree led to the identification of a new locus on chromosome 12p13.3 (14). We were able to exclude linkage with the previously identified loci and with SLC12A3 in three other French kindreds, demonstrating the involvement of at least one other gene in the disease (15). Thus, at least four different genes are responsible for FHHt, suggesting that this syndrome is actually a set of related disorders (Table 1). Two of these genes were identified recently (16). Identification of the WNK1 and WNK4 Genes A fruitful collaboration with Lifton's group led to the identification of deletions and missense mutations in two genes encoding members of a novel family of serine/threonine kinases. These two genes, WNK1 and WNK4, were shown to be responsible for the disease in six families (16). One large genomic deletion (41 kb) was found in an American family, and a smaller deletion (22 kb) was found in a French family. Both of the deletions that were found in these unrelated kindreds were located in the same part of the first intron of the WNK1 gene. No mutation was identified in the coding sequence of the gene. WNK1 is located at the telomeric part of chromosome 12 (12p12.3). It contains 28 exons in a 156-kb segment. This segment is particularly large as a result, in part, of the large size (60 kb) of intron 1 (NM_018979.1). Several WNK1 isoforms have been identified (see below). An analysis of WNK1 transcript levels in leukocytes from affected and unaffected members of one of these FHHt families revealed that the intronic deletion was associated with five times higher levels of its expression (16). The identification of mutations in WNK1 and knowledge of the existence of a putative PHA2 locus on chromosomes 1 and 17 led to the identification of WNK4, located on 17q21-q22. This gene contains 18 exons in a 16-kb segment (NM_032387). WNK1 and WNK4 have similar sequences and intron-exon organizations, but the WNK4 mutations that were found in several FHHt kindreds differ considerably from the WNK1 mutations identified. The WNK4 mutations are missense mutations that affect short (approximately 10 amino acids) sequences that are highly conserved in the WNK family, immediately downstream from the first and second coiled-coil domains (Figure 1). They result in the substitution of a charged residue in these negatively and positively charged sequences (16,17). As coiled-coil domains are generally thought to be involved in protein–protein interactions, the mutations may affect the interaction of WNK4 with its partners. WNK Kinase Structure WNK (with no lysine [K] [18]) proteins form a small family of serine/threonine kinases that were identified by Xu et al. (19). They lack a conserved lysine that usually is found in subdomain II of the catalytic domain that is critical for ATP binding to the catalytic site and strictly conserved in all other serine/threonine kinases that have been identified to date. In WNK, this lysine is replaced by a cysteine, and the catalytic lysine is located in subdomain I. This new subfamily of protein kinases has been found only in multicellular organisms. Four members of the family have been identified in humans: WNK1, WNK2, WNK3, and WNK4, located on 12p13.3, 9q22.31, Xp11.22, and 17p11-q21, respectively (16,20,21). New insight recently has been provided into the structure and function of these kinases. The structure of the kinase domain of WNK1 has been resolved at a resolution of 1.8 A (22). This structure has confirmed that the lysine residue that is responsible for kinase activity is located in strand β2 rather than in β3 as in other protein kinases and the precise conformation of the activation loop and has identified residues that contribute to substrate specificity. These findings should facilitate the design of WNK1 inhibitors. In addition to the catalytic domain located near the N-terminus, WNK1 and WNK4 contain an autoinhibitory domain, two predicted coiled-coil domains, and three proline-rich regions that may interact with the SH3 domains of other proteins, all of which are strongly conserved in WNK (23). Several in vitro studies have shown that WNK oligomerize and that WNK1 may act as a tetramer (24). WNK1 phosphorylates itself and a generic substrate (19,25). WNK1 activation requires the autophosphorylation of at least one serine residue, Ser-382, within the WNK1 activation loop, and is affected by extracellular ion concentration (19). Changes in NaCl concentration and other osmotic challenges activate the kinase in kidney epithelial cells and in a variety of cell lines, suggesting that WNK1 acts as an osmotic sensor (26). The autoinhibitory sequence is 55 residues long and is located just after the kinase domain. It regulates the kinase activity of WNK1 and probably also its interactions with substrates and/or partners. The WNK1 autoinhibitory domain was shown recently to inhibit the autophosphorylation of WNK4, suggesting that these two kinases may belong to the same cascade (26). WNK1 probably has many functions. It has been shown to be involved in the extracellular signal-regulated kinase 5 mitogen-activated protein kinase pathway, suggesting that it may be regulated by the growth factors and stress stimuli that control this cascade (26). WNK1 has also been demonstrated to be one of the numerous substrates of Akt/protein kinase B, a kinase involved in the metabolic and mitogenic functions of insulin (27). WNK1 interacts with and phosphorylates synaptotagmin 2 (Syt2) (28), whereas WNK4 does not. Synaptotagmins are involved in the regulation of membrane trafficking and vesicle fusion via a calcium-sensing mechanism (29). Both binding and phosphorylation are enhanced by Ca2+ binding to Syt2. As the phosphorylation of Syt2 inhibits the interaction of this protein with phospholipid vesicles, the binding of Syt2 to the membrane requires higher Ca2+ concentrations after phosphorylation by WNK1. Thus, WNK1 is thought to regulate the function of Syt2, depending on cellular Ca2+ concentration. Like Syt2, WNK1 is present in the cerebellum (C. Delaloy et al., unpublished observations) and in neuroendocrine cells, in which WNK1 and Syt2 co-localize with secretory granules (28). Synaptotagmins are involved in exocytosis, endocytosis, and regulating the membrane insertion of transporters and channels. WNK1 phosphorylation therefore may affect these processes. Much less is known about the determinants of WNK4 kinase activity. Comparisons of the WNK1 and WNK4 kinase domains showed differences in structure and function. Min et al. (22) looked at differences that might account for substrate specificity. They generated a homology-based structural model of WNK4, using the WNK1 coordinates. They identified two residues, at positions 318 and 448, that differed between the two enzymes and that seemed to mediate stable binding between WNK1 and Syt2. This may account for the poor phosphorylation of synaptotagmin 2 by WNK4 in their experiments. Wang et al. (25), using GST fusion constructs, confirmed the capacity of WNK1 constructs to autophosphorylate and to phosphorylate the generic substrate histone. Conversely, the WNK4 kinase domain displayed no kinase activity, either in vitro or in HEK 293 cells, suggesting that as-yet-unidentified factors are required for WNK4 kinase activation. In these experiments, the WNK4 autoinhibitory domain inhibited WNK1 kinase activity, consistent with the interaction demonstrated in experiments with Xenopus oocytes. Wilson et al. (30) demonstrated the co-immunoprecipitation of NCC and WNK4 in HEK 293 cells, but it is not known whether this interaction is direct or indirect. The partners of WNK4 therefore remain to be identified. Possible Physiological Functions of WNK1 and WNK4 WNK1 and WNK4 are produced in many different tissues. Northern blot analysis has shown that WNK1 is predominantly expressed in the kidney, heart, and skeletal muscle in humans, rats, and mice (16,19,20,31–33). Immunostaining in mice and humans has shown that WNK1 is present in the kidney and in various reabsorptive epithelia (31). WNK1 expression is either intracytoplasmic or restricted to the basolateral membrane, depending on the tissue. WNK4 is mostly produced in the kidney, where it is specifically present in the cytoplasm and tight junctions of the distal convoluted tubule (DCT) and cortical collecting duct (CCD) (16). WNK4 transcripts and protein are also present in several epithelial tissues, particularly in tight junctions (34). Only one isoform of WNK4 has been identified, whereas multiple isoforms are produced from the WNK1 gene as a result of the existence of three promoters, two polyadenylation sites, and three alternatively spliced exons (32) (Figure 2). The first two proximal promoters, P1 and P2, are located upstream from and within exon 1, respectively, and generate ubiquitous isoforms that contain the entire kinase domain. A third promoter, rP, is located in intron 4 and controls the production of a kidney-specific isoform, with transcription initiated from a specific exon (exon 4a). This isoform lacks most of the kinase domain and is produced in large amounts in the DCT and connecting tubule (CNT). The consequences of the identified intronic deletions on the pattern of production of the various WNK1 isoforms are unknown. Their characterization is crucial if we are to understand the precise mechanism of the disease. It is interesting that all epithelia that express WNK1 and WNK4 are involved in chloride transport. In Xenopus laevis oocytes, the activities of the basolateral isoform of the Na+-K+-2Cl− co-transporter (BSC2/NKCC1) and of the apical Cl−/HCO3− exchanger CFEX are reduced by WNK4 (34). Furthermore, in MDCK cells, WNK4 reduces transepithelial resistance by increasing chloride permeability but does not alter the flux of uncharged solutes (35,36). No such effect was observed in a mutant with an inactivated kinase. The linear current-voltage curve and the pharmacologic properties of these effects indicated that they were attributable to the paracellular pathway. Yamauchi et al. (35) showed that WNK4 phosphorylates claudins 1 to 4. These proteins are the major tight-junction membrane proteins involved in regulating paracellular ion permeability. As no effect on tight-junction structure was observed on electron microscopy, these findings suggest that WNK4 is involved in regulating the tight-junction pores that selectively drive paracellular chloride reabsorption in the distal nephron (36). Further studies in Xenopus laevis oocytes showed that the regulatory role of WNK4 is not restricted to chloride transport. Instead, it extends to the regulation of a wide range of transport systems expressed in the distal nephron (Figure 3). The injection of WNK4 into Xenopus oocytes decreases membrane expression of the distal Na-Cl co-transporter NCC (31) and of the renal apical K+ channel ROMK (37) and increases that of the renal epithelial calcium channel (ECaC) (38). WNK4 seems to regulate NCC and ECaC membrane expression in a kinase-dependent In ROMK is by and is of WNK4 kinase activity. However, two have studied the of NCC and have results the for the WNK4 kinase domain. Wilson et al. (30) showed that an mutation in the kinase domain the effect observed in Xenopus oocytes. et al. showed that the part of WNK4 was required for this whereas the kinase domain was not. These results the role of WNK4 in and paracellular NaCl reabsorption and K+ in the distal nephron The regulation of WNK4 in individuals with would ROMK activity increasing reabsorption K+ Conversely, in individuals with WNK4 regulation would inhibit NCC K+ The differences in the effects of WNK4 in of hyperkalemia and probably other One of these factors may be the kidney-specific WNK1 isoform, which has been shown to be by in vitro and may regulate the interaction between WNK1 and WNK4 (see below). the regulation of ECaC by WNK4 may it possible to regulate the of and calcium An relationship has been found between the of reabsorption of these two in the distal This might account for the observed in FHHt, as a result of WNK4 mutations (see It might also the increase in and that was observed recently in a large family with FHHt The physiologic functions of WNK1 are less Several studies in vitro have shown that it may act as an osmotic sensor in various cells (24). In kidney, it has been to a of the functions of WNK1 of expression of the long WNK1 isoform and expression of the short isoform in the distal In a cell that a physiologic concentrations of have been shown to the expression of the kidney-specific WNK1 isoform but not that of the long isoforms of this short isoform increases the cellular transport of the et al. that such might affect the or activity of the epithelial channel but not its The possible effect of WNK1 on was very recently confirmed by in vitro studies from WNK1 was shown to and activate the and protein kinase by increasing its In WNK1 in Xenopus oocytes via the pathway. These new findings suggest that WNK1 regulate in the late distal nephron by increasing the of in the membrane (Figure The second mechanism of of WNK1 in the distal nephron seems to be its interaction with Indeed, WNK4, WNK1 was found to have no effect on NCC activity in the Xenopus laevis expression However, if WNK4 and WNK1 are WNK1 the of This requires an interaction between the kinase domain of WNK1 and WNK4 and seems to be by the part of WNK4 These results therefore suggest that a WNK1 protein that lacks the kinase domain, such as the kidney-specific isoform, would not be able to regulate the of NCC activity. The precise mechanism of interaction between the two kinases is as results have been It is also to that is no evidence that WNK1 activity itself is regulated by (24). Thus, we not whether the production or activity of WNK1 is affected by other than the of in NaCl transport. the physiologic effect of WNK1 on BP by the et al. generated a mutant of WNK1 by gene in that were for the mutation in the first of whereas showed a in BP than that in However, no in concentrations were in that were a suggesting that the in BP was not to in the These that WNK1 is for and is a of BP as the of a of the gene led to a in of FHHt The mechanism of FHHt has been for many The high sensitivity of both hypertension and metabolic disorders to thiazide diuretics and the low levels have been as reabsorption via the thiazide-sensitive co-transporter NCC in the DCT This would the of to the and the flux the in potassium et al. an suggesting that the syndrome may result from high levels of chloride This would reabsorption via the potassium In both low-renin hypertension and hyperkalemic metabolic acidosis result primarily from with potassium These have to be to the knowledge of mutations at the WNK4 and WNK1 FHHt by WNK4 In Xenopus laevis oocytes, WNK4 expression decreases NCC production and expression at the membrane (Figure 3). No such are observed in the same with a WNK4 the mutation results were recently with a novel mutation that cell expression of NCC but reduced expression of ROMK the of these it has been that the mutations that are responsible for FHHt may be the physiologic of NCC by WNK4, in high levels of chloride reabsorption the thiazide-sensitive pathway. However, other mutations and have been shown to have as an effect on NCC activity as WNK4 This that the mechanism of the disease may not be the same in all FHHt kindreds, the existence of phenotypic However, this seems as all of these missense mutations in a highly conserved sequence and affect the of this negatively charged segment in a similar The consequences of the and mutations for the of ROMK in the membrane have also been studied in the Xenopus Both mutations further the of K+ and expression of the and mutations a effect on paracellular chloride permeability than WNK4 (35,36). It was further demonstrated that WNK4 phosphorylation of the tight-junction proteins claudins 1 to 4 and that mutant WNK4 further phosphorylation These suggest that mutations in WNK4 would as mutations for NCC but mutations for ROMK and WNK4 seems to have multiple of of which are kinase activity and of which are kinase WNK4 probably increases chloride reabsorption NCC by the physiologic of ROMK by WNK4 or should to potassium by increasing the chloride paracellular pathway, WNK4 further increases chloride concentration. These three effects major involved in reabsorption in the distal which a role in reabsorption and potassium They are also consistent with the and observed in patients with high BP, and with high sensitivity to thiazide Although these similar lines, it should be that the levels of provided by the various studies are not The in distal epithelial renal cell lines, by two that all FHHt mutations studied increase the paracellular pathway is consistent with the of WNK4 with the tight-junction protein in the DCT and with the chloride by than However, the from the Xenopus model should not be that not all of the FHHt mutations to NCC levels at the is a of also that the of WNK4 in renal epithelial cells the apical of NCC However, this effect not differ between and mutant Our understanding therefore and further studies of the WNK pathway are In that results in are of Lifton's group recently findings that that were for mutant WNK4 a higher thiazide-sensitive co-transporter protein and a ROMK at the membrane, in oocytes. FHHt by WNK1 As previously two large genomic deletions (41 and in the first intron of WNK1 have been identified as being responsible for FHHt in two unrelated kindreds, with no mutation in the coding sequence (16). An analysis of WNK1 transcript levels in leukocytes from affected and unaffected members of one of these families revealed that the intronic deletion was associated with a increase in the levels of a WNK1 isoform, the of which has to be effect does the of WNK1 have in the renal WNK4 and WNK1 are in Xenopus oocytes, WNK1 completely the of NCC et al. recently confirmed that WNK1 the effect of WNK4 on NCC activity but that a WNK1 the kinase domain the effect of Thus, the kidney-specific isoform might not be able to inhibit WNK4, as it lacks the kinase domain WNK1 intronic mutations may increase production of the WNK1 isoform that is normally produced in only small This in would the of NCC by WNK4 and increase activity increasing NaCl reabsorption This requires in The second major mechanism by which in WNK1 expression might affect transport to its activity on as shown by Xu et al. and Thus, the consequences of WNK1 mutations in the kidney would not be their consequences on WNK4 but also a further increase in activity (Figure 3). such an an expression of the long WNK1 isoform would contribute to reabsorption and hypertension in An expression of the kidney-specific isoform would to hypertension of It to be in vitro and in whether the WNK1 intronic deletions to or in WNK1 transcripts We also to our understanding of the expression of the WNK1 isoform in the DCT and mice that or WNK genes are being by various and should to the of WNK physiologic functions and FHHt The identification of WNK1 and WNK4 has it possible to a few large FHHt and observed that affected individuals in an family the missense mutation displayed in addition to hyperkalemic metabolic This was associated with a in In in our WNK1 affected patients hyperkalemic metabolic acidosis of similar severity to that observed in the family but similar to unaffected (11). The of an increase in calcium and an increase in reabsorption in the distal nephron would not be the relationship between and calcium transport. However, this does not for WNK1 The between the two families may be related to a specific interaction between WNK4 and the However, et al. found no between WNK4 and Thus, these findings is not the phenotypic differences may be to WNK1 expression in and to and/or Thus, the two FHHt probably the pathophysiology of the two is probably not strictly the It is interesting that in both metabolic disorders In the French hypertension not until patients were in their The patients of the 17 the mutation were but displayed metabolic abnormalities of similar severity to of the were reported for the pedigree In this family, the between of hyperkalemia and of hypertension was yr. In both affected patients concentrations than unaffected but the of the was similar in and concentration that reabsorption to is to the disease, but that individuals remain until that reabsorption is less than in other of monogenic such as type 2 or and the to It is interesting that hypertension resolved two in previously of the whereas hyperkalemia and of the functions of WNK1 and WNK4 in the regulation of distal ion handling has opened up new and of that may our understanding of nephron However, the precise FHHt remain for both WNK1 and The effects on NCC and ROMK remain to be in as the possible effects of on WNK1 expression and activity. Furthermore, if WNK1 does result in the activation of and WNK4 missense mutations to reabsorption via by increasing paracellular chloride both of hypertension a mechanism with The of affected kindreds also the of metabolic disorders and patients with FHHt remain until adulthood may provide insight into the the of which with In terms of one of the findings of the few years is the that several loci are responsible for Two genes have already been and the involvement of locus is with a locus as (15). In addition to the identification of substrates and/or partners of WNK1 and WNK4 should to the genes it to the regulation of ion transport in the distal nephron. that is after the identification of genes that are responsible for a the that mutations might be responsible for of the disease. of the genes that are responsible for monogenic of hypertension have produced results in analyses of However, several of evidence WNK genes in individuals are to thiazide which are particularly in patients with The locus that contains WNK4 within the largest genetic linkage for BP observed in and in the This has also been to hypertension in a but has not been reported in other in large analysis of the coding sequence of WNK4 revealed no mutation in the with to the control In humans, a of genetic have been identified in of and No has been reported between WNK4 and but by of and In that a analysis of WNK1 in families recently showed a but between one located from the WNK1 and the severity of hypertension with the that expression of WNK1 might contribute to to Structure of the WNK4 gene and description of the familial hyperkalemic hypertension (FHHt) missense The WNK4 gene is long and contains The kinase domain is by exons 1 to the autoinhibitory domain is by exons to 7 and 17 the first and second coiled-coil domains, respectively, and the small where the FHHt missense mutations were These 10 and amino acid are conserved the WNK Structure of the WNK1 gene. The two proximal the renal and the two polyadenylation and are alternatively spliced exons and kidney exon (exon 4a). The large intronic deletions found in the American and French kindreds are by Structure and expression of WNK1 The and promoters, located upstream of and in exon 1, respectively, to long isoforms that contain the entire kinase domain. P1 isoforms are with a expression in the skeletal muscle and the heart, as shown in the Northern isoforms are The to a isoform, the major part of the kinase domain and specifically and strongly expressed in the kidney, as shown in the Northern with the exon specific to this isoform (exon WNK4 and transport in Xenopus laevis oocytes experiments. a and with the thiazide-sensitive NaCl co-transporter (NCC) in laevis oocytes, WNK4 inhibits reabsorption by the of NCC present at the A WNK4 has no effect on NCC in the all FHHt mutations only the mutation is to NCC in the increasing reabsorption with a and with the potassium channel WNK4 inhibits K+ by increasing ROMK of the This is kinase and is by a In to is with the and mutations to an of ROMK of the membrane, further K+ Possible effects of WNK1 on transport in the distal tubule of the nephron. Two major transcripts are to a long and kidney-specific In the distal is than The possible effects of these two isoforms on the are indicated (see for Genetic heterogeneity of familial hyperkalemic was by from the French of and et

Objectives: This scoping review provides an overview of the current evidence base for trauma-informed yoga (TIY) for survivors of sexual, domestic, and interpersonal violence to document the spectrum of study designs, population and intervention characteristics, and associated results of TIY for trauma survivors. Methods: Authors utilized the scoping review methodology outlined by Arksey and O'Malley (2005). Pubmed and Scopus were searched initially conducted on August 16, 2022, and updated to include any new studies on March 25, 2025. Data extracted included study design, population characteristics, intervention specifics, and results. Authors devexbvgloped an innovative mnemonic to inform discussion of results: WELLNESS: Well-being; Empathy; Longevity (durability of therapeutic effect); Lessen trauma symptoms; Nurturing (self-compassion), Ease stress, Security, and Self-awareness). Results: The combined initial and updated literature searches yielded 4167 studies. Title and abstract screening netted 35 studies meeting review criteria. Full-text review netted 18 studies meeting criteria. Sexual, interpersonal, and domestic violence survivors who participated in TIY reported enhancement of physical and psychological function and well-being. Effects included increased sense of safety, self-compassion, personal growth, and self-regulation. Studies reported reduced depression, anxiety, negative thoughts, stress and trauma symptoms, and increased self-esteem; positive coping; improved relationships, better sleep and enhanced mindfulness; and sense of peace. Conclusion: TIY is beneficial to survivors of sexual, domestic, and interpersonal violence by promoting peaceful embodiment without retraumatization and enhancing affect regulation to decrease reactivity and agitation. The constellation of effects can improve the sequelae of trauma, and survivors may benefit from long-term TIY programming to ensure more robust improvement.

The emergency department (ED) serves as the main source of care for patients who are victims of interpersonal violence. As a result, emergency physicians across the nation are at the forefront of delivering care and determining dispositions for many at-risk patients in a dynamic healthcare environment. In the majority of cases, survivors of interpersonal violence are treated and discharged based on the physical implications of the injury without consideration for risk of reinjury and the structural drivers that may be at play. Some exceptions may exist at institutions with hospital-based violence intervention programs (HVIPs). At these institutions, disposition decisions often include consideration of a patient’s risk for repeat exposure to violence. Ideally, HVIP services would be available to all survivors of interpersonal violence, but a variety of current constraints limit availability. Here we offer a scoping review of HVIPs and our perspective on how risk-stratification could help emergency physicians determine which patients will benefit most from HVIP services and potentially reduce re-injury secondary to interpersonal violence.

Violence, Criminalization &amp; Punitive Excess

The global coronavirus disease 2019 (COVID-19) viral outbreak and the rise of the anti-Black racism movement have produced a dual pandemic over the past few years, which has been associated with a dramatic rise in gun violence across the United States. This comprehensive review was performed to examine the current levels of gun violence in the context of these dual pandemics, delineate factors which have synergistically produced this surge in interpersonal violence, and propose future directions. Dual pandemics have mutually contributed to a worsening in many social determinants of health and thereby have had a particularly dramatic impact on many of our most vulnerable patients, including patients of minority races and ethnicities, in terms of interpersonal violence. Firearm injuries are at their highest rate in decades. The challenges in the trauma care of these patients have been compounded by staffing and resource shortages related to the COVID-19 pandemic and attrition of medical workers related to burnout. Consequences of the COVID-19 pandemic and the anti-Black racism movement have produced a social environment in the United States in recent years where interpersonal violence, especially firearm injuries, have surged. Particularly, during a time of challenged patient care delivery, the medical system struggles to support the increase in trauma volume. A broad approach to improving social determinants of health should be pursued in order to decrease the risk of gun violence from the recent near-historical high levels.

Interpersonal violence occurs frequently and has devastating effects on the health of Hispanic trauma survivors. However, the incidence and risk factors associated with interpersonal violence remain understudied in U.S.-Mexico border communities. This study aims to identify the incidence and factors associated with interpersonal violence in trauma patients in a U.S.-Mexico border city. A single-center, retrospective cohort study design was used to explore interpersonal violence in patient records from the sexual assault nurse examiner trauma registry in a Southwestern Level I trauma center from 2017 to 2022. Inclusion criteria included all interpersonal violence trauma survivors seen by the sexual assault nurse examiner department. Exclusion criteria included specific data points in the trauma registry, such as types of injury, zip code of interpersonal violence survivor residency, and outreach services that could reidentify trauma survivors. Variables of interest included survivor and interpersonal violence incident characteristics. Of the total N =1,249 patients studied, the mean age was 23; 86% (N=1,077) were female, and 69.7% (N=870) were Hispanic/Latino/Spanish. Interpersonal violence events were more likely to occur in May, June, and October, on the weekends, and between 12a.m. and 6a.m. Significant associations were noted between age and gender, race and ethnicity, hearing status, and disability. This study demonstrates the importance of assessing regional patterns of interpersonal violence to identify local population trends that can inform staff training and community outreach efforts for targeted interpersonal violence prevention.

Gun violence, often characterized as a singular issue, is not one cohesive problem. Instead, it takes many forms resulting from the complex interplay of multiple factors. Outcomes of gun violence also vary significantly. They may be (a) physically non-injurious (a gun is brandished), (b) injurious but non-lethal, or (c) lethal. To understand and address gun violence effectively, it is essential to consider various risk factors for both non-lethal and lethal gun violence victimization, using a comprehensive, comparative framework. We present a novel comparative framework for better understanding gun violence, and for developing policy responses to this violence. We disaggregate gun violence into its various forms and propose a conceptualization of risk factors in discrete categories, each with important implications for policy intervention. While we emphasize the value of this framework for understanding and combatting interpersonal gun violence in America, the research and policy approaches discussed here should be equally applicable to other international contexts with gun violence as a serious public health issue as well.

Intentions Matter: Long-Term Patient Outcomes After Intentional, Interpersonal Injury.