Examining the role of community resilience and social capital on mental health in public health emergency and disaster response: a scoping review.

The ability of the public to remain psychologically resilient in the face of public health emergencies and disasters (such as the COVID-19 pandemic) is a key factor in the effectiveness of a national response to such events. Community resilience and social capital are often perceived as beneficial and ensuring that a community is socially and psychologically resilient may aid emergency response and recovery. This review presents a synthesis of literature which answers the following research questions: How are community resilience and social capital quantified in research?; What is the impact of community resilience on mental wellbeing?; What is the impact of infectious disease outbreaks, disasters and emergencies on community resilience and social capital?; and, What types of interventions enhance community resilience and social capital?A scoping review procedure was followed. Searches were run across Medline, PsycInfo, and EMBASE, with search terms covering both community resilience and social capital, public health emergencies, and mental health. 26 papers met the inclusion criteria.The majority of retained papers originated in the USA, used a survey methodology to collect data, and involved a natural disaster. There was no common method for measuring community resilience or social capital. The association between community resilience and social capital with mental health was regarded as positive in most cases. However, we found that community resilience, and social capital, were initially negatively impacted by public health emergencies and enhanced by social group activities.Several key recommendations are proposed based on the outcomes from the review, which include: the need for a standardised and validated approach to measuring both community resilience and social capital; that there should be enhanced effort to improve preparedness to public health emergencies in communities by gauging current levels of community resilience and social capital; that community resilience and social capital should be bolstered if areas are at risk of disasters or public health emergencies; the need to ensure that suitable short-term support is provided to communities with high resilience in the immediate aftermath of a public health emergency or disaster; the importance of conducting robust evaluation of community resilience initiatives deployed during the COVID-19 pandemic.

Clinical trial design in the neurocritical care unit.

Clinical trials provide a robust mechanism to advance science and change clinical practice across the widest possible spectrum. Fundamental in the Neurocritical Care Society's mission is to promote Quality Patient Care by identifying and implementing best medical practices for acute neurological disorders that are consistent with the current scientific knowledge. The next logical step will be to foster rapid growth of our scientific body of evidence, to establish and disseminate these best practices. In this manuscript, five invited experts were impaneled to address questions, identified by the conference organizing committee as fundamental issues for the design of clinical trials in the neurological intensive care unit setting.

Benign and malignant hypertension after adrenal enucleation in the rat. Relationship to salt intake, response to hydrochlorothiazide, and similarity to essential hypertension.

Adrenal-enucleated, mononephrectomized rats given a high salt diet rapidly develop malignant hypertension, characterized by the presence of necrotizing vascular lesions in a number of organs and tissues. If a normal salt intake is provided, or if hydrochlorothiazide is given together with a high salt diet, there is, instead, the delayed onset of benign hypertension which either stabilizes or increases in intensity extremely slowly; Such animals display few, if any, pathologic vascular changes other than occasional focal glomerular hyalinization, show insignificant cardiac enlargement, and do not exhibit alterations in the serum sodium or potassium. Occasional animals behave atypically and develop malignant hypertension despite normal salt consumption, demonstrating that in susceptible rats excess salt is not essential to this disorder. Hydrochlorothiazide given to rats that imbibed distilled water postoperatively prevented hypertension entirely for 97 days, when one of eight rats developed mild hypertension and some others reached what is regarded as a prehypertensive range. It is concluded that adrenal regeneration provides a physiological milieu favorable to the development of benign hypertension, which is not, as a rule, manifest until regeneration is complete. Salt excess converts the response into one in which malignant hypertension begins during regeneration and worsens rapidly thereafter until death. The course and findings are compared with those of the benign and malignant phases of clinical essential hypertension, and the implications of the similarities are discussed.

Acute Budd-Chiari syndrome caused by inferior vena cava compression from a congenital diaphragmatic hernia.

Acute Budd-Chiari syndrome is a rare condition characterised by obstruction of hepatic venous outflow. We describe the case of a 52-year-old man, with a congenital Morgagni diaphragmatic hernia, who presented with acute onset abdominal pain, shortness of breath, lactic acidosis, hyperbilirubinaemia and transaminasaemia. Computed tomography revealed strangulation of the diaphragmatic hernia and extrinsic compression of the inferior vena cava from the herniated viscera. Emergency surgery was carried out to repair the hernia with a biosynthetic mesh, with complete resolution of the Budd-Chiari syndrome.

Test, test, test - a complication of testing for coronavirus disease 2019 with nasal swabs.

BACKGROUND: Coronavirus disease 2019, a highly transmissible respiratory infection, has created a public health crisis of global magnitude. The mainstay of diagnostic testing for coronavirus disease 2019 is molecular polymerase chain reaction testing of a respiratory specimen, obtained with a viral swab. As the incidence of new cases of coronavirus disease 2019 increases exponentially, the use of viral swabs to collect nasopharyngeal specimens is anticipated to increase drastically. CASE REPORT: This paper draws attention to a complication of viral swab testing in the nasopharynx and describes the premature engagement of a viral swab breakpoint, resulting in impaction in the nasal cavity. CONCLUSION: This case highlights a possible design flaw of the viral swab when used to collect nasopharyngeal specimens, which then requires an aerosol-generating procedure in a high-risk patient to be performed. The paper outlines a safe technique of nasal foreign body removal in a suspected coronavirus disease 2019 patient and suggests alternative testing materials.

Management of airway obstruction with nebulised adrenaline resulting in takotsubo cardiomyopathy: case report.

BACKGROUND: Takotsubo cardiomyopathy has been associated with the use of catecholamines; however, its development after the use of nebulised adrenaline for the management of acute airway obstruction has not previously been described. CASE REPORT: A 66-year-old man with squamous cell carcinoma of the larynx, with tumour-node-metastasis staging of T3N2cM0, confirmed by biopsy and computed tomography, presented to the emergency department with acute airway obstruction. He was treated twice with nebulised adrenaline and intravenous dexamethasone. After a period of 24 hours, cardiac rhythm changes were noted on telemetry. A 12-lead electrocardiogram showed widespread T-wave inversion and QT prolongation suggestive of an acute coronary syndrome. Coronary angiography demonstrated no coronary artery disease, but left ventricular angiography showed marked apical ballooning and apical wall akinesia consistent with a diagnosis of takotsubo cardiomyopathy. CONCLUSION: Takotsubo cardiomyopathy can mimic true ischaemic heart disease and the diagnosis requires a high index of suspicion in patients managed with nebulised adrenaline.

Evolution of adrenal-regeneration hypertension in blinded rats.

The influence of blinding upon the blood pressure and adrenal regeneration of monoephrectomized but otherwise normal and mononephrectomized adrenal-enucleate rats on a high Na intake was evaluated. Blinding had no effect on control blood pressure, or upon the incidence, course and severity of adrenal-regeneration hypertension. Similarly there was no discernible effect on the regeneration of enucleate adrenal glands. The adrenal glandsands of otherwise normal blinded rats showed some enlargement in proportion to body weight, a finding which is probably attributable to loss of body weight in several animals.

Influence of 19-nor-deoxycorticosterone on blood pressure, saline consumption, and serum electrolytes, corticosterone, and renin activity.

Young, unilaterally nephrectomized, female Sprague-Dawley rats were given daily sc injections of 19-nor-deoxycorticosterone acetate (19-nor-DOCA) in oil at a dosage of 100 micrograms/day for 21 days and twice that amount for a further 11 days. One group drank distilled water and another drank 1% NaCl solution. Comparable control groups received oil injections. Another group received DOCA at the same steroid dosage and drank saline. Both 19-nor-DOCA-treated groups rapidly became hypertensive and developed cardiac hypertrophy, as did those given DOCA and saline. Saline consumption was greater in rats receiving 19-nor-DOCA, than in those given DOCA. Rats injected with 19-nor-DOCA and given water to drink showed enhanced growth and developed thymus enlargement and displayed hypokalemia and a reduction in both serum renin activity and corticosterone concentration. Plasma sodium concentration was not affected by any form of treatment. Clearly, 19-nor-DOCA is a potent mineralocorticoid and hypertensogenic agent. Since the parent steroid is known to be present abundantly in the urine of rats with regenerating adrenal glands, although circulating amounts have not yet been ascertained in that circumstance, it may be etiologically involved in adrenal regeneration hypertension, which such rats are prone to develop.

Experimental hypertension and other responses to 18-hydroxy-deoxycorticosterone treatment in the rat.

Young female unilaterally nephrectomized, salt-loaded, Sprague-Dawley rats were treated with 200 microgram or 1 mg 18-hydroxy-deoxycorticosterone-21-acetate (18-OH-DOCA) in oil daily, and a group of kidney-intact animals on a normal salt intake was given 2 mg/day. The hormone was not found to increase saline consumption, increase urinary potassium or kallikrein excretion, or depress serum renin activity or potassium concentration. Slight hypertension did develop at 3 weeks in salt-loaded rats on the lowest dose, but this was neither increased by higher dosage or longer treatment, nor reflected by increased heart or kidney weight. The effect of 40-mg pellet implantation of DOCA and 18-OH-DOCA was then compared in unilaterally nephrectomized, salt-loaded, female Fischer 344 rats. The former caused increased saline consumption, hypertension, hypokalemia, and heart and kidney enlargement, whereas 18-OH-DOCA did not. Thus, the hypertensogenic potency of 18-OH-DOCA is, at best, a reflection of its known, very weak, mineralocorticoid activity.

Mineralocorticoid and hypertensive effects of 19-nor-progesterone.

The mineralocorticoid potency of 19-nor-progesterone was evaluated by both its effect on electrolyte excretion in adrenalectomized animals and its ability to cause hypertension and electrolyte changes in mononephrectomized, salt-loaded rats. The mineralocorticoid activity, measured using an adrenalectomized rat bioassay, indicated that 19-nor-progesterone was 2.5% as potent as aldosterone but did not antagonize the effect of aldosterone when both were administered. In mononephrectomized rats, the daily administration of 1 mg/day quickly caused an enhanced consumption of 1% saline and induced severe hypertension within 3-4 weeks. Some severely hypertensive animals had marked anemia, but other did not; as a group they were found to have hypernatremia and hypokalemia. Hypertensive animals were found during life to display a relative hypothermia and, at necropsy, to have heart and kidney enlargement with severe and extensive vascular lesions in both organs, but not adrenal hypertrophy. It is concluded that 19-nor-progesterone has the characteristics of a potent mineralocorticoid and, as such, is capable of causing hypertension. It is not yet clear why this should be accompanied by hypothermia.

Hypertensive potency of 18-oxocortisol in the rat.

The hypertensogenic effect of 18-oxocortisol, an aldosterone analogue possessing both mineralocorticoid and glucocorticoid properties, was studied at the same dosage but under different experimental conditions in two experiments. Under experimental conditions conducive to the development of mineralocorticoid hypertension (i.e., rats with a single kidney on a high NaCl intake), there was an extremely rapid onset of saline polydipsia and hypertension accompanied by cardiac and renal enlargement, marked thymic involution without adrenal atrophy, cardiovascular lesions, and hypokalemia. With the exception of the thymic changes, the same changes occurred in rats given the biologically equivalent dose of deoxycorticosterone acetate. Under circumstances favoring the development of glucocorticoid hypertension (i.e., intact rats on a normal sodium intake), the same dose had only a transient blood pressure-elevating effect, attaining prehypertensive levels at most, and caused neither chronic hypertension nor hypokalemia. The biologically equivalent glucocorticoid dosage of cortisol was similarly ineffective. Under these circumstances, both steroids caused thymus involution but only 18-oxocortisol caused kidney enlargement.

Aldosterone binding sites in aortic cell cultures from spontaneously hypertensive rats.

Spontaneously hypertensive rats and rats made hypertensive by deoxycorticosterone-salt treatment have in common increased Na+ and K+ permeability and transport in their aortic cells. These changes may be important factors in the development of the hypertensive state and may be mediated by mineralocorticoid binding to intracellular sites in the aorta. Therefore, we examined 3H-aldosterone binding in aortic cell cultures from spontaneously hypertensive rats and normotensive Wistar-Kyoto rats. Vascular corticoid binding sites in the two strains were compared by Scatchard analysis of Kd and Bmax, pH and temperature stability, and subcellular binding. By all of these criteria normotensive rats. These results indicate that the underlying genetic defect in spontaneous hypertension is not an intrinsic cellular defect which alters mineralocorticoid binding in the aorta.

Decreased aldosterone receptor affinity in aortic cells from the Fischer 344 rat.

The Fischer 344 rat strain represents a uniform population that is immune to salt induced hypertension and resistant to mineralocorticoid hypertension. We have compared aldosterone binding in aortic cells cultured from salt-resistant Fischer 344 rats to that from salt-sensitive Wistar-Kyoto controls for aldosterone binding. Aortic smooth muscle cells of both strains contain two classes of aldosterone binding sites: corticoid receptor I with high affinity and low capacity and corticoid receptor II with low affinity and high capacity. The corticoid receptor I of Fischer 344 rats has a significantly (P less than 0.001) lower affinity than that of age and sex-matched Wistar-Kyoto controls, but the binding capacity was the same. There was no difference between the strains in the affinity or binding capacity of corticoid receptor II. These results indicate that mineralocorticoid binding may be important in susceptibility and resistance to hypertension and support the contention that mineralocorticoids regulate blood pressure in part by direct action on vascular smooth muscle cells.

Influenza surveillance in the Pacific Northwest 1976-1980.

Between June 1976 and June 1980 active year-round surveillance for influenza was carried out in Seattle in order to establish an early warning system. This report compares yield by different community groups and age. Waves of influenza virus infection appearing in three successive springs were followed in each instance by epidemics with the same subtype virus(es) in the following winter. These included two co-circulating A/H3N2 variants (A/Victoria/75 and A/Texas/77) in spring 1977 and winter 1977-1978, A/H1N1 (A/USSR) in spring 1978 and H1N1 (A/Brazil) winter 1978-1979, and type B influenza in spring 1979 and winter 1979-1980. Despite intensive surveillance through the summer and fall, the first isolate was not obtained until early December each year. Young adults (18-30) were as good sources for influenza viruses as children (less than 18).

Effect of pregnancy on the immune response of cattle to a Brucella vaccine.

An experiment was performed to determine whether humoral- or cell-mediated immune responses of cattle to a Brucella abortus vaccine were influenced by the stage of gestation. Heifers were vaccinated 2 mth before and 2 mth after breeding with cell envelopes of B. abortus in an oil adjuvant containing trehalose dimycolate and muramyl dipeptide. Control groups received adjuvant alone or no vaccine. Following breeding, vaccinated animals were divided into pregnant and nonpregnant subgroups. Immune responses to two outer membrane proteins were measured at monthly intervals by ELISA and lymphocyte blastogenesis tests. Skin tests were performed during the ninth month of gestation. Vaccination induced sustained immune responses, but few differences were detected between pregnant and non-pregnant animals. The relative increase in IgA antibodies to group 3 protein in nonpregnant heifers exceeded that in pregnant heifers during months 4 and 6 of gestation (P less than 0.05). Dermal hypersensitivity, measured by changes in double skin thickness, was significantly greater in nonpregnant heifers to porin (P less than 0.01) and group 3 (P less than 0.05) antigens at 24 h post-injection, but no significant differences in skin thicknesses or in the nature of the lesions were observed at 48 h. Animals which received adjuvant alone demonstrated negligible responses. Pregnancy had no significant effect on the responses of lymphocytes to phytohemagglutinin (PHA) or Concanavalin A (Con A). However, plasmas from nonvaccinated pregnant heifers taken during the sixth and seventh (but not eight or ninth) months of pregnancy decreased responses of normal donor cells to PHA and Con A when compared with those in autologous plasma (P less than 0.05).

Structural, functional and hypertensive effects of 19-oxo-11-deoxycorticosterone acetate (19-oxo-DOCA) in the rat.

Mononephrectomized rats were given 1% NaCl solution to drink; half of them received 1 mg/day of 19-oxo-11 deoxycorticosterone acetate (19-oxo-DOCA) in sesame oil subcutaneously and half received only the oil for a period of four weeks. The steroid had no effect upon saline intake, systolic blood pressure, growth or the size of adrenals, hearts or kidneys, although it did produce hypernatremia and hypokalemia. The discrepancy between a demonstrable mineralocorticoid effect without blood pressure elevation awaits elucidation.

Prevention of spontaneous and glucocorticoid hypertension in rats by nisoldipine.

The effect of daily treatment (sometimes interrupted) with the calcium blocker nisoldipine at two different dose levels, one double the other, on the development of spontaneous hypertension in the rat was evaluated. Both doses prevented development of the disorder during daily administration, but when treatment was stopped the same degree of hypertension as in controls quickly developed. Resumption of treatment caused blood pressure to fall to or towards normal again. The higher dose caused a more rapid and greater fall than the lower, and allowed a lesser pressor response when it was discontinued. The drug had no effect on growth, and the only consistent hematological effect was a slight thrombocytosis. Daily treatment at a single dose level slightly reduced normal blood pressure and prevented cortisone hypertension. Serum renin activity was unaffected by nisoldipine but was elevated by cortisone treatment: nisoldipine increased aldosterone levels, but not when cortisone was also given.

Effects of the protein kinase C stimulant bryostatin 1 on the proliferation and colony formation of irradiated human T-lymphocytes.

The protein kinase C stimulant bryostatin 1 (Bryo) was used in examining human peripheral blood T-lymphocyte radiosensitivities in proliferation assays. Bryo was similar to PMA in inducing T-cell proliferation by the CD3, CD28 and CD69 pathways. No difference in radiosensitivities was observed in T-cells stimulated by the three independent surface antigen-mediated activation pathways. CD3 was chosen as the second signal for comparing the potencies of the three different first signals Bryo, phorbol 12-myristate, 13-acetate (PMA), and interleukin 2 (IL-2) in stimulating T-cell proliferation and in maintaining this response after radiation. Though there were radioresponse differences among various individuals, the irradiated lymphocytes consistently showed significantly greater proliferation when treated with Bryo or PMA than with IL-2 (p < 0.05- < 0.005). No difference in proliferative responses was observed in T-cells irradiated between 4 h before and 15 h after the addition of stimulants. Colony forming assays showed higher colony survival for irradiated T-cells stimulated with Bryo than with PMA. These results support the important role of protein kinase C in T-cell radiation responses, and suggest a potential role for Bryo in enhancing T-lymphocyte survival during radiation therapy.

DNA repair in the genomic region containing the beta-actin gene in xeroderma pigmentosum complementation group C and normal human cells.

The limited DNA excision repair in UV-irradiated fibroblasts from xeroderma pigmentosum complementation group C (XP-C) occurs in selected chromatin regions. The small beta-actin gene (3.5 kb) is one of these and is repaired as part of a large region (about 50 kb). We show here that only one of the DNA strands is repaired through this extended region. Several genomic fragments spanning about 70 kb in the beta-actin region have been cloned and mapped and some have been examined for repair activity. Both strands of one fragment (14 kb) in the immediate vicinity of the gene are repaired. Transcripts associated with both strands are detected. In normal cells, both strands of the same fragment are preferentially repaired relative to the genome overall and also associated with transcription. The repair activity in XP-C cells associated with other defined DNA fragments indicates that termini for the repaired regions in either strand can be located. Results are consistent with those of others indicating that transcription promotes repair in XP-C cells and that several levels of repair activity, at least one coupled to transcription, occur in normal cells. We conclude that the beta-actin repair domain, defined in XP-C cells, comprises both strands of a small region (about 14 kb) in the vicinity of the beta-actin gene and a single strand extending through a larger region of about 50 kb. We suggest that a similar genomic organization for repair exists in normal cells.

Augmented depression and reduced excitability of the central nervous system (CNS) by cadmium in the rat.

Reports indicating that low doses of cadmium caused vasodilation, but that larger quantities elicited a pressor response, apparently mediated by a CNS reflex, prompted an examination of cadmium-induced changes in CNS responsiveness and activity. Rats were injected intraperitoneally with either 2 mg/kg or 4 mg/kg of CdCl2 solution, after which the CNS was either depressed by pentobarbital or excited by strychnine at different dose levels. Cadmium treatment, administered before pentobarbital, decreased the time required for sleep induction and prolonged sleep duration at doses of either 20 mg/kg or 30 mg/kg: at 40 mg/kg only induction was affected and at 60 mg/kg neither was influenced. At a dosage of 60 micrograms/kg, strychnine caused convulsions in all control animals, but in none pretreated with CdCl2. When either 75 or 120 micrograms/kg of strychnine was used, cadmium at either dosage failed to prevent convulsions, although the onset was delayed and duration curtailed. The rapidity with which Cd modified CNS activity indicated that the effect can not depend upon cadmium-induced synthesis of metallothionine, but represents a direct effect of Cd on the CNS. Cadmium treatment did not substantially improve the survival of rats that convulsed when treated with strychnine.