Secondary School Athletic Trainers' Clinical Management Decisions of Low Socioeconomic Status Patients.

CONTEXT: Evidence suggests that negative social determinants of health (SDOH) and lower socioeconomic status (SES) contribute to health care disparities. Due to their accessibility in the high school setting, secondary school athletic trainers (SSATs) may encounter patients that are historically underserved in health care such as low SES patients. However, there is a significant gap in knowledge regarding how SES and SDOH may influence SSATs' clinical management decisions. OBJECTIVE: The purpose of this study was to describe SSATs' perceptions of how patient SDOH and SES influence clinical management decisions and to identify barriers to athletic healthcare. DESIGN: Cross-sectional study. SETTING: Online survey. PARTICIPANTS: NATA SSATs (6.7% response rate). MAIN OUTCOME MEASURE(S): SSATs were asked about their perceptions of patient SES and the SDOH (CVI = 0.83 for relevancy). Questions were ranked on a 4-point Liker scale on level of relevance and agreement. Data were summarized by means and standard deviations (SD), frequencies and proportions (%), and median scores. RESULTS: A total of 380 SSATs participated (years of experience mean=14.9±11.7 years). When providing care, most (71.3%) SSATs believed that their patient's health/health care access SDOH to be the most relevant of the 5 SDOH whereas the other 4 SDOH were less than 60% relevant. Most SSATs agreed/strongly agreed that patient SES impacts referral (67.4%) and the reliance on conservative treatment before referral (71.2%). SSATs identified patient/guardian compliance (70.2%) and type of health insurance (61.5%) as barriers to providing care to low SES patients. CONCLUSIONS: SSATs perceived health/health care access as the most relevant SDOH when providing care to low SES patients. When SSATs further considered the SES of patients, they identified all SDOHs as barriers to providing health care they were ill equipped to navigate as they delivered care and engaged in patient referral.

Reduced-order modeling and analysis of dynamic cerebral autoregulation via diffusion maps.

Objective.A data-driven technique for parsimonious modeling and analysis of dynamic cerebral autoregulation (DCA) is developed based on the concept of diffusion maps. Specifically, first, a state-space description of DCA dynamics is considered based on arterial blood pressure, cerebral blood flow velocity, and their time derivatives. Next, an eigenvalue analysis of the Markov matrix of a random walk on a graph over the dataset domain yields a low-dimensional representation of the intrinsic dynamics. Further dimension reduction is made possible by accounting only for the two most significant eigenvalues. The value of their ratio indicates whether the underlying system is governed by active or hypoactive dynamics, indicating healthy or impaired DCA function, respectively. We assessed the reliability of the technique by considering healthy individuals and patients with unilateral internal carotid artery (ICA) stenosis or occlusion. We computed the sensitivity of the technique to detect the presumed side-to-side difference in the DCA function of the second group (assuming hypoactive dynamics on the occluded or stenotic side), using McNemar's chi square test. The results were compared with transfer function analysis (TFA). The performance of the two methods was also compared under the assumption of missing data.Main results.Both diffusion maps and TFA suggested a physiological side-to-side difference in the DCA of ICA stenosis or occlusion patients with a sensitivity of 81% and 71%, respectively. Further, both two methods suggested the difference between the occluded or stenotic side and any two sides of the healthy group. However, the diffusion maps captured additional difference between the unoccluded side and the healthy group, that TFA did not. Furthermore, compared to TFA, diffusion maps exhibited superior performance when subject to missing data.Significance.The eigenvalues ratio derived using the diffusion maps technique can be potentially used as a reliable and robust biomarker for assessing how active the intrinsic dynamics of the autoregulation is and for indicating healthy versus impaired DCA function.

Point-of-care ultrasound use in emergencies: what every anaesthetist should know.

Point-of-care ultrasound has been embraced by anaesthetists as an invaluable tool for rapid diagnosis of haemodynamic instability, to ensure procedural safety and monitor response to treatments. Increasingly available, affordable and portable, with emerging evidence of improved patient outcomes, point-of-care ultrasound has become a valuable tool in the emergency setting. This state-of-the-art review describes the feasibility of point-of-care ultrasound practice, training and maintenance of competence. It also describes the many uses of point-of-care ultrasound for the anaesthetist and describes the most salient point-of-care ultrasound views for anaesthetic emergencies including: undifferentiated shock; hypoxemia; and trauma. Procedural safety is also discussed in addition to relevant important governance aspects. Cardiac function should be assessed using the parasternal long axis, parasternal short basal/mid-papillary/apical, apical four chamber and subcostal four chamber views, and should include a visual estimation of global left ventricular ejection fraction. Other cardiovascular conditions that can be identified using point-of-care ultrasound include: pericardial effusion; cardiac tamponade; and pulmonary embolism. Pulmonary emergency conditions that can be diagnosed using point-of-care ultrasound include pneumothorax; pleural effusion; and interstitial syndrome. The extended focused assessment with sonography for trauma examination may of value in patients who are hypotensive in order to identify intra-abdominal haemorrhage, pneumothoraces and haemothoraces.

Cardiometabolic health after first pregnancy: Associations with social determinants of health. A nuMoM2b-HHS study.

Study objective: This study sought to evaluate the associations between social determinants of health (SDOH) at the time of first pregnancy and subsequent cardiometabolic health, defined as the development of metabolic syndrome. Design: nuMoM2b-HHS (Nulliparous Pregnancy Outcomes Study- Monitoring Mothers-to-Be-Heart Health Study) is an ongoing prospective cohort study. Setting: Eight academic medical centers enrolled and continue to follow participants. Participants: 4484 participants followed a mean of 3.2 years from the time of their first pregnancy. Interventions: N/a. Main outcome measure: Unadjusted and adjusted Poisson regression models with robust standard errors were used to obtain relative risks and 95% confidence intervals estimating the risk of metabolic syndrome for each baseline SDOH. In secondary analyses we examined the associations between SDOH and incident hypertension, obesity, and diabetes mellitus. Results: Metabolic syndrome developed in 13.6% of participants. Higher socioeconomic position at the time of pregnancy was associated with lower rates of metabolic syndrome [income > 200% poverty level aRR 0.55 (95% CI, 0.42-0.71), attainment of a bachelor's degree aRR 0.62 (0.46-0.84) or higher aRR 0.50 (0.35-0.71)], while being single [aRR 1.45 (95% CI, 1.18-1.77)] and having low health literacy were associated with a greater risk of metabolic syndrome [aRR 1.98 (95% CI, 1.28-3.07)]. Conclusions: Over a short interval following first pregnancy, participants accumulated high proportions of cardiovascular risk factors and metabolic syndrome, with some risk associated with SDOH. The impact of interventions addressing SDOH in pregnant people on cardiometabolic health should be tested as a means of reducing health inequities at the population level.

Joint time-frequency analysis of dynamic cerebral autoregulation using generalized harmonic wavelets.

OBJECTIVE: To develop a joint time-frequency analysis technique based on generalized harmonic wavelets (GHWs) for dynamic cerebral autoregulation (DCA) performance quantification. APPROACH: We considered two groups of human subjects to develop and validate the method: 55 healthy volunteers and 35 stroke-free subjects with unilateral internal carotid artery stenosis (CAS). We determined the mean and coherence-weighted average of the phase shift (PS) of appropriately defined GHW-based transfer functions, based on data points over the joint time-frequency domain. We compared agreement of standard transfer function analysis (TFA) and GHW analyses in healthy subjects using Bland-Altman plots. We assessed sensitivity of each metric to detect the presumed side-to-side difference in DCA function in CAS subjects (with decreased PS on the occluded side), using McNemar's chi square test to compare each metric to the standard TFA approach. An alternative Morlet wavelet-based approach was also considered. MAIN RESULTS: The GHW and TFA methods exhibited strong agreement in healthy subjects. Among CAS subjects, GHW metrics outperformed TFA and Morlet wavelet-based approaches in identifying expected side-to-side differences: TFA sensitivity was 40.0% (95%CI 23.9-57.9), Morlet 60.0% (95%CI 42.1-76.1), and GHW >70% for both metrics (GHW mean PS sensitivity 74.3, 95%CI 56.7-87.5, p  = 0.0027 versus TFA; GHW coherence-weighted PS sensitivity 71.4, 95%CI 53.7-85.4, p  = 0.0009 versus TFA). SIGNIFICANCE: In comparison to the widely used stationary Fourier transform-based TFA and to Morlet wavelet-based analysis, our data suggest that the GHW-based analysis performs better in identifying DCA asymmetry between the two cerebral hemispheres in patients with high grade unilateral carotid stenosis. Our method may provide enhanced confidence in employing DCA metrics as a sensitive diagnostic tool for detecting impaired DCA function in a variety of pathological settings.

Nutrition and diet-related problems.

Adolescence is a period of remarkable change. Nutrient requirements increase to promote physical growth and development and adolescents begin to make lifelong diet choices. These choices are often influenced by family, peers, and individual nutrition beliefs. This article addresses typical problems and recommendations for normal adolescent nutrition as well as nutrient needs for special conditions such as obesity, athletics, and vegetarianism.

Utilizing clinical factors to reduce head CT scan ordering for minor head trauma patients.

Our study objective was to determine whether simple clinical criteria can be used to safely reduce the number of patients who require cranial computed tomography (CT) scan after sustaining minor head trauma. Awake patients (Glascow Coma Scale = 15) who presented to the emergency department with acute head injury associated with a loss of consciousness were evaluated for clinical predictors of head injury prior to CT scan. The studied risk factors included severe headache, nausea, vomiting, and depressed skull fracture on physical examination. Patients with no risk factors present were compared with patients with one or more risk factors with respect to abnormal CT rate and rate of operative intervention for head injury. Of the 2143 patients entered into the study, 1302 (61%) had no risk factor for head injury, whereas 841 (39%) had one or more risk factors present. A total of 138 (6.4%) of those studied had an abnormal CT scan. This number included 3.7% of those patients with no risk factors vs. 11% in patients with one or more risk factors. The CT scan abnormalities in the no-risk-factor group were not clinically significant. All 5 patients who required operative intervention had at least one of the risk factors present. The use of four simple clinical criteria in minor head trauma patients would allow a 61% reduction in the number of head CT scans performed and still identify all patients who require neurosurgical intervention and the majority of patients with an abnormal CT scan. This method could lead to a large savings in patient charges nationwide. Further studies may be helpful in confirming these findings.

Minor head trauma: Is computed tomography always necessary?

STUDY OBJECTIVE: To determine the clinical value of routine computed tomography (CT) of the head in patients with normal mental status after minor head trauma. METHODS: We carried out a prospective study of a consecutive series of patients of all ages who presented to our urban university Level I trauma center emergency department with a Glasgow Coma Scale score of 15 and underwent CT of the head after loss of consciousness (LOC) or amnesia to event. A data form was filled out for each patient before CT. Patients with abnormal CT results were followed to discharge. We analyzed data with the chi 2 and student t tests. RESULTS: Of 1,382 patients, traumatic intracranial abnormality was identified on CT of the head in 84 (6.1%). Three patients in this group (.2%) required surgery. The subgroup of patients with history of LOC/amnesia but no symptoms or signs of a depressed skull fracture had a rate of abnormal CT findings of only 3% (24 of 789), and no patient in this group required medical or surgical intervention. Nausea and vomiting and signs of head trauma were significantly more common in the group with abnormal CT findings. CONCLUSION: Routine CT of the head in patients with history of LOC/amnesia but no symptoms or signs of depressed skull fracture has minimal clinical value and is not warranted. Patients with symptoms of head injury or apparent depressed skull fracture should undergo head CT because a small number will require surgery.

Recasting Florida's insanity defense. Two modest proposals.

Three states have established psychiatric security review boards mandated to primarily provide protection from the potentially destructive behavior of insanity acquitees. Each year in Florida there are 100 of these patients; 5% have been involved in capital offenses. These boards, as compared with the extant judiciary system, are more effective and parsimonious and serve the end of primary prevention. It is recommended that the plea, "not guilty by reason of insanity," be changed to "guilty but insane." The change is largely semantic but should result in greater prosecutorial and public acceptance of the insanity plea and be more in keeping with individual freedom for patients as provided under the Constitution.

7-Sulfooxymethyl-12-methylbenz[a]anthracene is an electrophilic mutagen, but does not appear to play a role in carcinogenesis by 7,12-dimethylbenz[a]anthracene or 7-hydroxymethyl-12-methylbenz[a]anthracene.

Although a bay-region dihydrodiolepoxide metabolite has been considered as a principal ultimate electrophilic and carcinogenic form of 7,12-dimethylbenz[a]anthracene (DMBA), other reactive metabolites might also play a role in the activation of this hydrocarbon in vivo. Earlier studies suggested the hydroxylation of a meso-anthracenic methyl group with subsequent formation of a benzylic ester bearing a good leaving group (e.g. sulfate) as a metabolic activation pathway for DMBA. In support of this hypothesis, the formation of an electrophilic and mutagenic sulfuric acid ester of 7-hydroxymethyl-12-methylbenz[a]anthracene (HMBA) by rat liver cytosolic sulfotransferase activity has previously been demonstrated, but no data have been reported on the carcinogenicity of this reactive ester. In the present study, we compared the carcinogenicity of chemically synthesized sodium 7-sulfooxymethyl-12-methylbenz[a]anthracene (SMBA) with that of the parent methyl and hydroxymethyl hydrocarbons. For this purpose, tests were made in several animal tumor models: induction of hepatomas in male B6C3F1 mice, lung adenoma induction in A/J mice, initiation of mouse skin tumors, development of sarcomas in rats at the injection sites, and initiation of preneoplastic enzyme-altered foci in rat liver. Data from all of these studies indicate that SMBA is not more carcinogenic than DMBA or HMBA. In addition, the carcinogenic activity of HMBA was not altered by dehydroepiandrosterone, a strong inhibitor of sulfotransferase activity for HMBA. DMBA produced only a low level of hepatic benzylic DNA adducts in rats when a relatively high dose was administered. These adducts constitute less than 5% of total DMBA residues bound to hepatic DNA. The rest of the adducts appear to be associated with other electrophilic intermediates including the dihydrodiol epoxide metabolites. Based on the results of our present study, it is unlikely that DMBA exerts its carcinogenic activity via metabolic activation to SMBA.

Age- and sex-related differences in activation of the carcinogen 7-hydroxymethyl-12-methylbenz[a]anthracene to an electrophilic sulfuric acid ester metabolite in rats. Possible involvement of hydroxysteroid sulfotransferase activity.

Metabolic activation of 7-hydroxymethyl-12-methylbenz[a]anthracene (HMBA) and related hydroxymethyl polycyclic aromatic hydrocarbons to electrophilic and mutagenic sulfuric acid esters has been demonstrated previously (Watabe et al., In: Xenobiotic Metabolism and Disposition (Eds. Kato R, Estabrook RW and Cayen MN), pp. 393-400. Taylor & Francis, London, 1989). In the present study, the rat hepatic sulfotransferase activity catalyzing the formation of such reactive sulfuric acid esters was inhibited strongly by dehydroepiandrosterone, a typical substrate hydroxysteroid sulfotransferases (HSSTs). Pentachlorophenol, a potent phenol sulfotransferase inhibitor, had little effect in this regard. A marked sex difference was observed for the hepatic cytosolic sulfotransferase activity for HMBA in rats. This sex difference was age-related; no significant difference was observed in preweanling rats, whereas in adult rats female rat liver showed a much higher enzyme activity. These age- and sex-related differences in the sulfonation of HMBA reflect the regulation of HMBA sulfotransferase activity by gonadal hormones as previously demonstrated with HSSTs. Thus, pretreatment with estradiol benzoate significantly enhanced the sulfotransferase activity for HMBA in both male and female rats, (P less than 0.01 and P less than 0.05 respectively), whereas testosterone propionate pretreatment decreased this activity. Castration of male rats increased the HMBA sulfotransferase activity 2- to 3-fold compared with that in control animals. By contrast, ovariectomy reduced the enzyme activity 38% in females. These results imply that rat liver HSST activity is responsible for the sulfonation of HMBA. Intraperitoneal injection of HMBA (0.25 mumol/g body wt) into infant rats produced benzylic DNA adducts in the liver which were chromatographically identical with those obtained from incubations of HMBA with deoxyguanosine and deoxyadenosine in the presence of hepatic cytosolic sulfotransferase activity. Intraperitoneal administration of sodium 7-sulfooxymethyl-12-methylbenz[a]anthracene resulted in much higher levels of these adducts and the deoxycytidine adduct in the liver DNA than did an equimolar amount of the parent hydroxymethyl hydrocarbon. The levels of hepatic benzylic DNA adducts formed from HMBA were reduced markedly by pretreatment of rats with dehydroepiandrosterone, a strong inhibitor of hepatic sulfotransferase activity for this hydrocarbon.

The strong hepatocarcinogenicity of the electrophilic and mutagenic metabolite 6-sulfooxymethylbenzo[a]pyrene and its formation of benzylic DNA adducts in the livers of infant male B6C3F1 mice.

6-Hydroxymethylbenzo[a]pyrene was activated to an electrophilic and mutagenic sulfuric acid ester metabolite by rat and mouse liver sulfotransferase activity. The intrinsic mutagenicity of this reactive ester, 6-sulfooxymethylbenzo[a]pyrene, was inhibited by glutathione and glutathione S-transferase. A single i.p. dose of 2.5 nmol/g body wt of 6-sulfooxymethylbenzo[a]pyrene in infant male B6C3F1 mice induced liver tumors in 35 of 36 mice at 10 months with an average multiplicity of 4.4. A comparable dose of the parent hydrocarbon, 6-hydroxymethylbenzo[a]pyrene, was only a tenth as active. The electrophilic sulfuric acid ester produced high levels of benzylic DNA adducts in the livers of these mice that accounted for about 80% of the total DNA adducts. These results strongly suggest that this sulfuric acid ester is an important ultimate electrophilic and carcinogenic metabolite in carcinogenesis by 6-hydroxymethylbenzo[a]pyrene and possibly even by 6-methylbenzo[a]pyrene and benzo[a]pyrene in mouse liver.

1,N6-ethenoadenosine formation, mutagenicity and murine tumor induction as indicators of the generation of an electrophilic epoxide metabolite of the closely related carcinogens ethyl carbamate (urethane) and vinyl carbamate.

Previous studies from this laboratory showed that (i) vinyl carbamate (VC) was much more carcinogenic than ethyl carbamate (EC) and that both carbamates induced the same spectrum of tumors in mice and rats, (ii) adducts of [14C]- or [3H]1,N6-ethenoadenosine and [14C]- or [3H]3,N4-ethenocytidine e were formed in the hepatic RNA of infant male B6C3F1 mice administered [1-14C]ethyl or [1,2-3H]ethyl EC and (iii) VC formed much more of the 1,N6-ethenoadenosine (epsilon Ado) adduct in the hepatic RNA and the 7-(2-oxoethyl)-guanine adduct in the hepatic DNA of mice than did EC. By analogy to the similar results of earlier studies by other investigators on the related carcinogen vinyl chloride, the above data suggested that VC epoxide was a reactive electrophilic metabolite of these carbamates. In the present studies, VC, but not EC, was found to be oxidized by 3-chloroperbenzoic acid to a derivative that reacted with adenosine to form epsilon Ado. Far more of this etheno nucleoside was formed from VC than from EC when these carbamates were metabolized by cofactor-fortified mouse liver microsomes in the presence of adenosine. Sodium diethyldithiocarbamate strongly inhibited these microsomal reactions and the formation of epsilon Ado in the hepatic RNA of mice administered either carbamate. Likewise, the i.p. preadministration of deithyldithiocarbamate markedly inhibited the induction of tumors by single i.p. doses of EC or VC in the livers of infant male B6C3F1 mice and in the livers, lungs and Harderian glands of infant female B6C3F1 mice. This inhibitor also considerably reduced lung tumor induction by VC in adult female A/Jax mice. 2-(2,4-Dichloro-6-phenyl) phenoxyethyl amine, a cytochrome P450 inhibitor, reduced the carcinogenicity of low doses of EC but appeared to increase the carcinogenicity of low doses of VC. The mutagenicity of VC for Salmonella typhimurium TA1535 in the presence of a hepatic activating system was greatly reduced by these inhibitors. The data from all these studies are consistent with the proposal that VC epoxide is an ultimate electrophilic and carcinogenic metabolite of EC and VC in the mouse.

Metabolic activation of the carcinogen 6-hydroxymethylbenzo[a]pyrene: formation of an electrophilic sulfuric acid ester and benzylic DNA adducts in rat liver in vivo and in reactions in vitro.

Hydroxylation of meso-methyl groups with subsequent formation of reactive electrophilic esters has been proposed as a possible activation pathway in the metabolism, DNA binding and carcinogenicity of some methyl-substituted polycyclic aromatic hydrocarbons. Some data in vitro have been reported in support of this concept. In this study, sulfotransferase activity for 6-hydroxymethylbenzo[a]pyrene (HMBP) in rat and mouse liver cytosols was demonstrated to mediate formation of benzylic adducts from this hydrocarbon with guanosine and with deoxyguanosine and deoxyadenosine in DNA. These benzylic adducts were also obtained from reactions of synthetic 6-sulfooxymethylbenzo[a]pyrene (SMBP) with individual (deoxy)ribonucleosides or DNA. The structure of the major DNA adduct formed from HMBP and SMBP was determined from NMR spectroscopy to be N2-(benzo[a]pyrene-6-methylenyl)-deoxyguanosine. Low levels of a deoxycytidine adduct were also obtained from DNA reacted with SMBP. Covalent modification of DNA by acetyl-CoA- and ATP-dependent activation of HMBP also produced the identical benzylic adducts, but the amounts were smaller than those obtained in the sulfotransferase-mediated reaction. The i.p. administration of HMBP to rats resulted in the formation of a hepatic DNA adduct. After enzymatic hydrolysis to the nucleoside level, this DNA adduct was chromatographically identical with the deoxyguanosine adduct formed in the above in vitro reactions. This adduct accounted for approximately 20-30% of total HMBP residues bound to hepatic DNA and its formation was significantly inhibited by pretreatment of rats with dehydroepiandrosterone, an inhibitor of the sulfotransferase activity for HMBP. The i.p. administration of comparable doses of SMBP to rats led to the formation of much larger amounts of the adducts with the guanine, adenine, and cytosine bases in the liver DNA. The data indicate that the sulfotransferase activity in the rat liver for HMBP plays a major role in the benzylic DNA adduct formation from this hydrocarbon in rat liver in vivo.