E. Pender, Liana Kostak, Kelsey Sutton, Cody Naccarato, A. Tsai, T. Chung, Stacey B. Daughters
Substance Use Disorder (SUD) is understood as the persistent use of substances to the detriment of the individual's livelihood and wellness. SUD can have serious mental, physical, and social ramifications if not properly addressed. Though SUD can develop at any age, it is especially important to address in adolescents, given the rising prevalence of certain substances (e.g. cannabis) in that age group and the poor prognosis associated with early-onset SUD[1][2]. Data from the National Survey on Drug Use and Health show the lifetime use of illicit drugs in people ages 12-17 is 20.9%[3] The same survey found the rate of Substance Use Disorder in the past year for people ages 12-17 who used illicit drugs or alcohol to be 6.3% in 2020[3]. This paper is intended for clinicians and laypeople to gain a deeper understanding of SUD in adolescents, particularly relating to alcohol, cannabis, nicotine, and opioids. Though alcohol, cannabis, and nicotine are the substances most commonly used by this age demographic nationally[4], opioid use – and resulting deaths – have been on the rise. According to the Centers for Disease Control and Prevention (CDC), opioids were connected to about 75% of the nearly 92,000 drug deaths in 2020[5]. Beyond significant death rates in the general population, recent spikes in adolescent death rates tied to the synthetic opioid fentanyl – which held a relatively stable death rate from 2010 to 2019 until seeing a 94% increase from 2019 to 2020 and an additional 20% increase to 2021 - warrants inquiry into opioids for this population[6]. Each of these substances can have adverse, long-lasting effects on health if not managed properly, resulting in seriously compromised lifelong well-being [7]. This article explores SUD prevalence and reviews diagnostic criteria in relation to adolescence, including a synopsis of changes in SUD classification between the DSM-IV and DSM-5 and a discussion of ICD-11 and the Research Domain Criteria (RDoC) as a basis for research related to substance use. Effective assessment and consideration of co-occurring disorders are covered as well. Although the prognosis of SUD varies by an individual's environment and circumstances, a modal developmental course for SUD is discussed. Finally, a curated list of nationally recognized resources including hotlines, treatment locators, informational sites, and support groups are provided, along with tools to compile local resources. By addressing these aspects of adolescent SUD, the research team offers a broader view of its prevalence in the United States, key warning signs and comorbidities, and possible assessments and treatments for adolescents with SUD.
{"title":"Resources for the Assessment and Treatment of Substance Use Disorder in Adolescents","authors":"E. Pender, Liana Kostak, Kelsey Sutton, Cody Naccarato, A. Tsai, T. Chung, Stacey B. Daughters","doi":"10.15347/wjx/2023.yyy","DOIUrl":"https://doi.org/10.15347/wjx/2023.yyy","url":null,"abstract":"Substance Use Disorder (SUD) is understood as the persistent use of substances to the detriment of the individual's livelihood and wellness. SUD can have serious mental, physical, and social ramifications if not properly addressed. Though SUD can develop at any age, it is especially important to address in adolescents, given the rising prevalence of certain substances (e.g. cannabis) in that age group and the poor prognosis associated with early-onset SUD[1][2]. Data from the National Survey on Drug Use and Health show the lifetime use of illicit drugs in people ages 12-17 is 20.9%[3] The same survey found the rate of Substance Use Disorder in the past year for people ages 12-17 who used illicit drugs or alcohol to be 6.3% in 2020[3]. This paper is intended for clinicians and laypeople to gain a deeper understanding of SUD in adolescents, particularly relating to alcohol, cannabis, nicotine, and opioids. Though alcohol, cannabis, and nicotine are the substances most commonly used by this age demographic nationally[4], opioid use – and resulting deaths – have been on the rise. According to the Centers for Disease Control and Prevention (CDC), opioids were connected to about 75% of the nearly 92,000 drug deaths in 2020[5]. Beyond significant death rates in the general population, recent spikes in adolescent death rates tied to the synthetic opioid fentanyl – which held a relatively stable death rate from 2010 to 2019 until seeing a 94% increase from 2019 to 2020 and an additional 20% increase to 2021 - warrants inquiry into opioids for this population[6]. Each of these substances can have adverse, long-lasting effects on health if not managed properly, resulting in seriously compromised lifelong well-being [7]. This article explores SUD prevalence and reviews diagnostic criteria in relation to adolescence, including a synopsis of changes in SUD classification between the DSM-IV and DSM-5 and a discussion of ICD-11 and the Research Domain Criteria (RDoC) as a basis for research related to substance use. Effective assessment and consideration of co-occurring disorders are covered as well. Although the prognosis of SUD varies by an individual's environment and circumstances, a modal developmental course for SUD is discussed. Finally, a curated list of nationally recognized resources including hotlines, treatment locators, informational sites, and support groups are provided, along with tools to compile local resources. By addressing these aspects of adolescent SUD, the research team offers a broader view of its prevalence in the United States, key warning signs and comorbidities, and possible assessments and treatments for adolescents with SUD.","PeriodicalId":36272,"journal":{"name":"WikiJournal of Medicine","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85900722","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The following paper advances our understanding of online volunteering in the medical context, through the study of Wikipedia volunteers who edit medical topics. It employs the Volunteer Functions Inventory (VFI) model to study volunteers' motivations through a survey carried out in 2021 (N=74). It highlights the importance of the non-traditional VFI dimensions of "fun" and "ideology" which have not been adequately discussed in the context of medical volunteering. The findings also show that Wikipedia volunteers who edit medical topics are older, more gender-balanced, and better educated than typical Wikipedia volunteers from a decade ago. Many are medical professionals, and their significant involvement helps to explain the above-average quality of Wikipedia medical topics. Conversely, the study reveals the need for more experts to engage with Wikipedia. Lack of volunteers, in particular, experts, and inadequate support from professional institutions, are identified as main reasons for problems in Wikipedia's quality.
{"title":"Where experts and amateurs meet: the ideological hobby of medical volunteering on Wikipedia","authors":"Piotr Konieczny","doi":"10.15347/wjm/2023.005","DOIUrl":"https://doi.org/10.15347/wjm/2023.005","url":null,"abstract":"The following paper advances our understanding of online volunteering in the medical context, through the study of Wikipedia volunteers who edit medical topics. It employs the Volunteer Functions Inventory (VFI) model to study volunteers' motivations through a survey carried out in 2021 (N=74). It highlights the importance of the non-traditional VFI dimensions of \"fun\" and \"ideology\" which have not been adequately discussed in the context of medical volunteering. The findings also show that Wikipedia volunteers who edit medical topics are older, more gender-balanced, and better educated than typical Wikipedia volunteers from a decade ago. Many are medical professionals, and their significant involvement helps to explain the above-average quality of Wikipedia medical topics. Conversely, the study reveals the need for more experts to engage with Wikipedia. Lack of volunteers, in particular, experts, and inadequate support from professional institutions, are identified as main reasons for problems in Wikipedia's quality.","PeriodicalId":36272,"journal":{"name":"WikiJournal of Medicine","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79902983","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Inflammatory bowel diseases (IBD), including Crohn's disease and ulcerative colitis, are classified as chronic inflammatory disorders and typically require anti-inflammatory drug therapies, such as glucocorticoid regimens, non-steroidal anti-inflammatory drugs, and biologics, aimed at reducing inflammation in the bowel wall. However, each of these therapies is accompanied by a list of possible serious side effects. Because of this, there remains an urgent need to identify new pharmacologic options to reduce or prevent the pro-inflammatory events of IBD while minimizing adverse side effects and making available more cost-effective treatment modalities. We have previously identified several herbal extracts that demonstrate the potent bio-inhibitory activity of the innate immune response. In particular, Laurus nobilis (LN), or more commonly called bay laurel, demonstrated significant anti-inflammatory function by inhibiting nuclear factor-κB activation. Based upon our original in vitro findings, we have now examined the effects of this herbal extract on a murine dextran sodium sulfate (DSS) model of IBD. Hematoxylin and eosin-stained paraffin sections prepared from DSS-treated animals show clear epithelial damage, including ulcerations, extensive neutrophil infiltration into the mucosal layer, and granuloma formation. Tissue from DSS-treated animals that also received LN extract showed improved tissue morphology more closely resembling that from control animals. In addition, DSS-treated mice with co-administration of LN extract showed a significant reduction in CD4+ antibody staining within the mucosal layer in colonic sections indicating reduced lymphocyte infiltration. Based on these findings, we believe that the administration of LN extracts may be effective in reducing the intestinal epithelial damage seen in human IBD and warrants further investigation through clinical trials. Lay Summary: Inflammatory bowel diseases (IBD), such as Crohn's disease (CD) and ulcerative colitis (UC), manifest as chronic inflammation and ulceration of tissues lining the digestive tract. CD involves inflammation of the deeper layers of the digestive tract, including both the small and large intestines, and less commonly, the upper digestive tract. UC involves inflammation along the lining of the colon and rectum. Steroid or biological treatments for IBD are common, however, they are limited due to significant side effects and/or prohibitive costs. In the present study, we provide evidence for use of the natural product, Laurus nobilis (bay leaf), as a safe and effective anti-inflammatory therapy for IBD.
{"title":"Extract of Laurus nobilis attenuates inflammation and epithelial ulcerations in an experimental model of inflammatory bowel disease","authors":"Natalie S. Correa, R. Orlando","doi":"10.15347/wjm/2023.xxx","DOIUrl":"https://doi.org/10.15347/wjm/2023.xxx","url":null,"abstract":"Inflammatory bowel diseases (IBD), including Crohn's disease and ulcerative colitis, are classified as chronic inflammatory disorders and typically require anti-inflammatory drug therapies, such as glucocorticoid regimens, non-steroidal anti-inflammatory drugs, and biologics, aimed at reducing inflammation in the bowel wall. However, each of these therapies is accompanied by a list of possible serious side effects. Because of this, there remains an urgent need to identify new pharmacologic options to reduce or prevent the pro-inflammatory events of IBD while minimizing adverse side effects and making available more cost-effective treatment modalities. We have previously identified several herbal extracts that demonstrate the potent bio-inhibitory activity of the innate immune response. In particular, Laurus nobilis (LN), or more commonly called bay laurel, demonstrated significant anti-inflammatory function by inhibiting nuclear factor-κB activation. Based upon our original in vitro findings, we have now examined the effects of this herbal extract on a murine dextran sodium sulfate (DSS) model of IBD. Hematoxylin and eosin-stained paraffin sections prepared from DSS-treated animals show clear epithelial damage, including ulcerations, extensive neutrophil infiltration into the mucosal layer, and granuloma formation. Tissue from DSS-treated animals that also received LN extract showed improved tissue morphology more closely resembling that from control animals. In addition, DSS-treated mice with co-administration of LN extract showed a significant reduction in CD4+ antibody staining within the mucosal layer in colonic sections indicating reduced lymphocyte infiltration. Based on these findings, we believe that the administration of LN extracts may be effective in reducing the intestinal epithelial damage seen in human IBD and warrants further investigation through clinical trials. Lay Summary: Inflammatory bowel diseases (IBD), such as Crohn's disease (CD) and ulcerative colitis (UC), manifest as chronic inflammation and ulceration of tissues lining the digestive tract. CD involves inflammation of the deeper layers of the digestive tract, including both the small and large intestines, and less commonly, the upper digestive tract. UC involves inflammation along the lining of the colon and rectum. Steroid or biological treatments for IBD are common, however, they are limited due to significant side effects and/or prohibitive costs. In the present study, we provide evidence for use of the natural product, Laurus nobilis (bay leaf), as a safe and effective anti-inflammatory therapy for IBD.","PeriodicalId":36272,"journal":{"name":"WikiJournal of Medicine","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79030215","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Steroidogenic routes to androgens have been discovered and characterized over the last two decades that fall outside the Δ4 and Δ5 "classical androgen pathways" to testosterone and 5α-dihydrotestosterone. There has been considerable investigation into these routes that has come with natural inconsistencies and overlap in naming that can make it difficult to discover information about them as might be needed in a clinical context. This expository review uses "alternative androgen pathways" to include what has been called the "backdoor" pathway to 5α-dihydrotestosterone, the 5α-dione pathway and pathways to 11-oxygenated steroids. A brief history of what led to the discovery of these pathways, basic information about the steroids and proteins involved in their biosynthesis as well as a summary of clinically significant findings is provided. PubChem CIDs for all steroids have been compiled to help authors avoid naming errors in their work. Modest suggestions for future work in these pathways are also given at the end. Patient comprehension and the clinical diagnosis of relevant conditions such as hyperandrogenism can be impaired by the lack of clear and consistent knowledge of alternative androgen pathways; the authors hope this review will accurately disseminate such knowledge to facilitate the beneficial treatment of such patients.
{"title":"Alternative androgen pathways","authors":"Maxim G Masiutin, Maneesh K Yadav","doi":"10.15347/wjm/2023.003","DOIUrl":"https://doi.org/10.15347/wjm/2023.003","url":null,"abstract":"Steroidogenic routes to androgens have been discovered and characterized over the last two decades that fall outside the Δ4 and Δ5 \"classical androgen pathways\" to testosterone and 5α-dihydrotestosterone. There has been considerable investigation into these routes that has come with natural inconsistencies and overlap in naming that can make it difficult to discover information about them as might be needed in a clinical context. This expository review uses \"alternative androgen pathways\" to include what has been called the \"backdoor\" pathway to 5α-dihydrotestosterone, the 5α-dione pathway and pathways to 11-oxygenated steroids. A brief history of what led to the discovery of these pathways, basic information about the steroids and proteins involved in their biosynthesis as well as a summary of clinically significant findings is provided. PubChem CIDs for all steroids have been compiled to help authors avoid naming errors in their work. Modest suggestions for future work in these pathways are also given at the end. Patient comprehension and the clinical diagnosis of relevant conditions such as hyperandrogenism can be impaired by the lack of clear and consistent knowledge of alternative androgen pathways; the authors hope this review will accurately disseminate such knowledge to facilitate the beneficial treatment of such patients.","PeriodicalId":36272,"journal":{"name":"WikiJournal of Medicine","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85892730","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Vitalii Moskalov, O. Koshova, Sabina Ali, N. Filimonova, I. Tishchenko
Objective. To determine such parameters of humoral immunity as the number of antibody-forming cells and the titer of antibodies in the blood under the action of the whole fraction of the secretome of xenogenic mesenchymal stem cells in mice with a normal immune status and mice with secondary immunodeficiency caused by the hydrocortisone acetate. Methods. The following methods were used in the study: isolation of mesenchymal stem cells from the bone marrow of cattle; culturing of isolated cells and obtaining a conditioned medium containing exometabolites with subsequent purification; modeling of secondary immunodeficiency in mice; setting up a test on mice to determine the number of antibody-forming cells in the spleen and hemagglutinin titers in blood serum; statistical data analysis. Results. A study of the impact of the secretome of xenogenic mesenchymal stem cells (MSCs) on the humoral arm of immunity in mice with a normal immune status showed a significant increase in the antibody-forming cells count compared with the control by 3.4-8.8 times when administered intramuscularly and by 4.2-5.4 times when administered subcutaneously (at the same time, in the group of the reference drug, the increase was four times), as well as an increase in the titer of hemagglutinins concerning the control by 25-95% when administered intramuscularly and 32-52% when administered subcutaneously (the reference drug Thymalin was at the control level). With intramuscular administration, a clear relationship was observed between the concentration of MSC secretome and the biological effect (high significant positive correlation: ρ = 0.99, p ≤ 0.05 for calculating AFC; ρ = 0.97, p ≤ 0.05 for HA titer). Lethality in the group of animals what administered only hydrocortisone acetate (HCA, positive control) was 100%. The use of the mesenchymal stem cells secretome increased the survival of animals by 50% by stimulating the formation of the required number of antibody-forming cells and antibody titer, except for the subcutaneous route of administration (at the level of immunized control, animals with a normal immune status). The reference drug showed a result at a level significantly lower than the immunized control. The antibody titer with the subcutaneous route of administration of secretion of MSCs was significantly lower than the immunized control but significantly higher concerning the reference drug. Conclusion. The administration of the secretome of xenogenic mesenchymal stem cells stimulated the humoral arm of immunity as same in mice with normal immune status as in mice with secondary immunodeficiency. The data obtained supplement the information on the introduction of live mesenchymal stem cells. Live allogeneic MSCs have a suppressive effect on B cells, while xenogenic MSCs cause a response on themselves. The secretome of xenogenic MSCs does not contain surface immunogenic molecules that are carried by living cells, but nevertheless increases the activity of the
{"title":"Impact of xenogenic mesenchimal stem cells secretome on a humoral component of the immune system","authors":"Vitalii Moskalov, O. Koshova, Sabina Ali, N. Filimonova, I. Tishchenko","doi":"10.15347/wjm/2023.004","DOIUrl":"https://doi.org/10.15347/wjm/2023.004","url":null,"abstract":"Objective. To determine such parameters of humoral immunity as the number of antibody-forming cells and the titer of antibodies in the blood under the action of the whole fraction of the secretome of xenogenic mesenchymal stem cells in mice with a normal immune status and mice with secondary immunodeficiency caused by the hydrocortisone acetate. Methods. The following methods were used in the study: isolation of mesenchymal stem cells from the bone marrow of cattle; culturing of isolated cells and obtaining a conditioned medium containing exometabolites with subsequent purification; modeling of secondary immunodeficiency in mice; setting up a test on mice to determine the number of antibody-forming cells in the spleen and hemagglutinin titers in blood serum; statistical data analysis. Results. A study of the impact of the secretome of xenogenic mesenchymal stem cells (MSCs) on the humoral arm of immunity in mice with a normal immune status showed a significant increase in the antibody-forming cells count compared with the control by 3.4-8.8 times when administered intramuscularly and by 4.2-5.4 times when administered subcutaneously (at the same time, in the group of the reference drug, the increase was four times), as well as an increase in the titer of hemagglutinins concerning the control by 25-95% when administered intramuscularly and 32-52% when administered subcutaneously (the reference drug Thymalin was at the control level). With intramuscular administration, a clear relationship was observed between the concentration of MSC secretome and the biological effect (high significant positive correlation: ρ = 0.99, p ≤ 0.05 for calculating AFC; ρ = 0.97, p ≤ 0.05 for HA titer). Lethality in the group of animals what administered only hydrocortisone acetate (HCA, positive control) was 100%. The use of the mesenchymal stem cells secretome increased the survival of animals by 50% by stimulating the formation of the required number of antibody-forming cells and antibody titer, except for the subcutaneous route of administration (at the level of immunized control, animals with a normal immune status). The reference drug showed a result at a level significantly lower than the immunized control. The antibody titer with the subcutaneous route of administration of secretion of MSCs was significantly lower than the immunized control but significantly higher concerning the reference drug. Conclusion. The administration of the secretome of xenogenic mesenchymal stem cells stimulated the humoral arm of immunity as same in mice with normal immune status as in mice with secondary immunodeficiency. The data obtained supplement the information on the introduction of live mesenchymal stem cells. Live allogeneic MSCs have a suppressive effect on B cells, while xenogenic MSCs cause a response on themselves. The secretome of xenogenic MSCs does not contain surface immunogenic molecules that are carried by living cells, but nevertheless increases the activity of the","PeriodicalId":36272,"journal":{"name":"WikiJournal of Medicine","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81179005","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The Kivu Ebola epidemic[note 1] began on 1 August 2018, when four cases of Ebola virus disease (EVD) were confirmed in the eastern region of Kivu in the Democratic Republic of the Congo (DRC).[2][3][4] The disease affected the DRC, Uganda, and is suspected to have also affected Tanzania, though the Ministry of Health there never shared information with the WHO.[5] The outbreak was declared ended on 25 June 2020, with a total of 3,470 cases and 2,280 deaths.[6][7] Other locations in the DRC affected included the Ituri Province, where the first case was confirmed on 13 August 2018.[1] In November 2018, it became the biggest Ebola outbreak in the DRC's history,[8][9][10] and by November, it had become the second-largest Ebola outbreak in recorded history,[11][12] behind only the 2013–2016 Western Africa epidemic. On 3 May 2019, 9 months into the outbreak, the DRC death toll surpassed 1,000.[13][14] In June 2019, the virus reached Uganda, having infected a 5-year-old Congolese boy who entered with his family,[15] but this was contained. Since January 2015, the affected province and general area have been experiencing a military conflict, which hindered treatment and prevention efforts. The World Health Organization (WHO) has described the combination of military conflict and civilian distress as a potential "perfect storm" that could lead to a rapid worsening of the situation.[16][17] In May 2019, the WHO reported that, since January of that year, there had been 42 attacks on health facilities and 85 health workers had been wounded or killed. In some areas, aid organizations have had to stop their work due to violence.[18] Health workers also had to deal with misinformation spread by opposing politicians.[19] Due to the deteriorating security situation in North Kivu and surrounding areas, the WHO raised the risk assessment at the national and regional level from "high" to "very high" in September 2018.[20] In October, the United Nations Security Council stressed that all armed hostility in the DRC should come to a stop to address the ongoing outbreak better.[21][22][23] A confirmed case in Goma triggered the decision by the WHO to convene an emergency committee for the fourth time,[24][25] and on 17 July 2019, the WHO announced a Public Health Emergency of International Concern (PHEIC), the highest level of alarm the WHO can sound.[26] On 15 September 2019, some slowdown of cases was noted in the DRC.[27] However, contact tracing continued to be less than 100%; at the time, it was at 89%.[27] In mid-October the transmission of the virus had significantly reduced; by then it was confined to the Mandima region near where the outbreak began, and was only affecting 27 health zones in the DRC (down from a peak of 207).[28] New cases decreased to zero by 17 February 2020,[29] but after 52 days without a case, surveillance and response teams confirmed three new cases in mid-April.[30][31][32] As a new and separate outbreak, was reported on 1 June 2020 in Éq
{"title":"The Kivu Ebola epidemic","authors":"O. Anis","doi":"10.15347/wjm/2021.005","DOIUrl":"https://doi.org/10.15347/wjm/2021.005","url":null,"abstract":"The Kivu Ebola epidemic[note 1] began on 1 August 2018, when four cases of Ebola virus disease (EVD) were confirmed in the eastern region of Kivu in the Democratic Republic of the Congo (DRC).[2][3][4] The disease affected the DRC, Uganda, and is suspected to have also affected Tanzania, though the Ministry of Health there never shared information with the WHO.[5] The outbreak was declared ended on 25 June 2020, with a total of 3,470 cases and 2,280 deaths.[6][7] Other locations in the DRC affected included the Ituri Province, where the first case was confirmed on 13 August 2018.[1] In November 2018, it became the biggest Ebola outbreak in the DRC's history,[8][9][10] and by November, it had become the second-largest Ebola outbreak in recorded history,[11][12] behind only the 2013–2016 Western Africa epidemic. On 3 May 2019, 9 months into the outbreak, the DRC death toll surpassed 1,000.[13][14] In June 2019, the virus reached Uganda, having infected a 5-year-old Congolese boy who entered with his family,[15] but this was contained. Since January 2015, the affected province and general area have been experiencing a military conflict, which hindered treatment and prevention efforts. The World Health Organization (WHO) has described the combination of military conflict and civilian distress as a potential \"perfect storm\" that could lead to a rapid worsening of the situation.[16][17] In May 2019, the WHO reported that, since January of that year, there had been 42 attacks on health facilities and 85 health workers had been wounded or killed. In some areas, aid organizations have had to stop their work due to violence.[18] Health workers also had to deal with misinformation spread by opposing politicians.[19] Due to the deteriorating security situation in North Kivu and surrounding areas, the WHO raised the risk assessment at the national and regional level from \"high\" to \"very high\" in September 2018.[20] In October, the United Nations Security Council stressed that all armed hostility in the DRC should come to a stop to address the ongoing outbreak better.[21][22][23] A confirmed case in Goma triggered the decision by the WHO to convene an emergency committee for the fourth time,[24][25] and on 17 July 2019, the WHO announced a Public Health Emergency of International Concern (PHEIC), the highest level of alarm the WHO can sound.[26] On 15 September 2019, some slowdown of cases was noted in the DRC.[27] However, contact tracing continued to be less than 100%; at the time, it was at 89%.[27] In mid-October the transmission of the virus had significantly reduced; by then it was confined to the Mandima region near where the outbreak began, and was only affecting 27 health zones in the DRC (down from a peak of 207).[28] New cases decreased to zero by 17 February 2020,[29] but after 52 days without a case, surveillance and response teams confirmed three new cases in mid-April.[30][31][32] As a new and separate outbreak, was reported on 1 June 2020 in Éq","PeriodicalId":36272,"journal":{"name":"WikiJournal of Medicine","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82996679","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Leptospirosis is a blood infection caused by the bacterium Leptospira. Signs and symptoms can range from none to mild (headaches, muscle pains, and fevers) to severe (bleeding in the lungs or meningitis). Weil's disease, the acute, severe form of leptospirosis, causes the infected individual to become jaundiced (skin and eyes become yellow), develop kidney failure, and bleed. Pulmonary hemorrhage in association with leptospirosis is known as "severe pulmonary haemorrhage syndrome". More than ten genetic types of Leptospira, which are a type of a spirochaete, cause disease in humans. Both wild and domestic animals can spread the disease, most commonly rodents. The bacteria are spread to humans through animal urine, or water and soil contaminated with animal urine, coming into contact with the eyes, mouth, nose or breaks in the skin. In developing countries, the disease occurs most commonly in farmers and low-income people who live in areas with poor sanitation. In developed countries, it occurs during heavy downpours and can affect those involved in outdoor activities in warm and wet areas. Diagnosis is typically by testing for antibodies against the bacteria or finding bacterial DNA in the blood. Efforts to prevent the disease include protective equipment to block contact when working with potentially infected animals, washing after contact, and reducing rodents in areas where people live and work. The antibiotic doxycycline is effective in preventing leptospirosis infection. Human vaccines are of limited usefulness; vaccines for other animals are more widely available. Treatment when infected is with antibiotics such as doxycycline, penicillin, or ceftriaxone. The overall risk of death is 5–10%. However, when the lungs are involved, the risk of death increases to the range of 50–70%. It is estimated that one million people worldwide are infected by leptospirosis every year, causing approximately 58,900 deaths. The disease is most common in tropical areas of the world but may occur anywhere. Outbreaks may arise after heavy rainfall. The disease was first described by physician Adolf Weil in 1886 in Germany. Infected animals may have no, mild or severe symptoms. These may vary by the type of animal. In some animals Leptospira live in the reproductive tract, leading to transmission during mating.
{"title":"Leptospirosis","authors":"Siang Ching Chieng Raymond","doi":"10.15347/wjm/2022.002","DOIUrl":"https://doi.org/10.15347/wjm/2022.002","url":null,"abstract":"Leptospirosis is a blood infection caused by the bacterium Leptospira. Signs and symptoms can range from none to mild (headaches, muscle pains, and fevers) to severe (bleeding in the lungs or meningitis). Weil's disease, the acute, severe form of leptospirosis, causes the infected individual to become jaundiced (skin and eyes become yellow), develop kidney failure, and bleed. Pulmonary hemorrhage in association with leptospirosis is known as \"severe pulmonary haemorrhage syndrome\". More than ten genetic types of Leptospira, which are a type of a spirochaete, cause disease in humans. Both wild and domestic animals can spread the disease, most commonly rodents. The bacteria are spread to humans through animal urine, or water and soil contaminated with animal urine, coming into contact with the eyes, mouth, nose or breaks in the skin. In developing countries, the disease occurs most commonly in farmers and low-income people who live in areas with poor sanitation. In developed countries, it occurs during heavy downpours and can affect those involved in outdoor activities in warm and wet areas. Diagnosis is typically by testing for antibodies against the bacteria or finding bacterial DNA in the blood. Efforts to prevent the disease include protective equipment to block contact when working with potentially infected animals, washing after contact, and reducing rodents in areas where people live and work. The antibiotic doxycycline is effective in preventing leptospirosis infection. Human vaccines are of limited usefulness; vaccines for other animals are more widely available. Treatment when infected is with antibiotics such as doxycycline, penicillin, or ceftriaxone. The overall risk of death is 5–10%. However, when the lungs are involved, the risk of death increases to the range of 50–70%. It is estimated that one million people worldwide are infected by leptospirosis every year, causing approximately 58,900 deaths. The disease is most common in tropical areas of the world but may occur anywhere. Outbreaks may arise after heavy rainfall. The disease was first described by physician Adolf Weil in 1886 in Germany. Infected animals may have no, mild or severe symptoms. These may vary by the type of animal. In some animals Leptospira live in the reproductive tract, leading to transmission during mating.","PeriodicalId":36272,"journal":{"name":"WikiJournal of Medicine","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74457235","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-01-01DOI: 10.1007/978-94-007-0753-5_102905
R. R. Abidin, Logan T. Smith, Hannah Kim, E. Youngstrom
{"title":"Parenting stress","authors":"R. R. Abidin, Logan T. Smith, Hannah Kim, E. Youngstrom","doi":"10.1007/978-94-007-0753-5_102905","DOIUrl":"https://doi.org/10.1007/978-94-007-0753-5_102905","url":null,"abstract":"","PeriodicalId":36272,"journal":{"name":"WikiJournal of Medicine","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72974697","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The history of coronaviruses is an account of the discovery of coronaviruses and the diseases they cause. It starts with a report of a new type of upper-respiratory tract disease among chickens in North Dakota, US, in 1931. The causative agent was identified as a virus in 1933. By 1936, the disease and the virus were recognised as unique from other viral diseases. The virus became known as infectious bronchitis virus (IBV), but later officially renamed as Avian coronavirus. A new brain disease of mice (murine encephalomyelitis) was discovered in 1947 at Harvard Medical School in Boston. The virus was called JHM (after Harvard pathologist John Howard Mueller). Three years later a new mouse hepatitis was reported from the National Institute for Medical Research in London. The causative virus was identified as mouse hepatitis virus (MHV), later renamed Murine coronavirus. In 1961, a virus was obtained from a school boy in Epsom, England, who was suffering from common cold. The sample, designated B814, was confirmed as novel virus in 1965. New common cold viruses (assigned 229E) collected from medical students at the University of Chicago were also reported in 1966. Structural analyses of IBV, MHV, B18 and 229E using transmission electron microscopy revealed that they all belong to the same group of viruses. Making a crucial comparison in 1967, June Almeida and David Tyrrell invented the collective name coronavirus, as all those viruses were characterised by solar corona-like projections (called spikes) on their surfaces. Other coronaviruses have been discovered from pigs, dogs, cats, rodents, cows, horses, camels, Beluga whales, birds and bats. As of 2022, 52 species are described. Bats are found to be the richest source of different species of coronaviruses. All coronaviruses originated from a common ancestor about 293 million years ago. Zoonotic species such as Severe acute respiratory syndrome-related coronavirus (SARS-CoV), Middle East respiratory syndrome-related coronavirus (MERS-CoV) and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a variant of SARS-CoV, emerged during the past two decades and caused the first pandemics of the 21st century.
{"title":"A history of coronaviruses","authors":"K. Lalchhandama","doi":"10.15347/wjm/2022.005","DOIUrl":"https://doi.org/10.15347/wjm/2022.005","url":null,"abstract":"The history of coronaviruses is an account of the discovery of coronaviruses and the diseases they cause. It starts with a report of a new type of upper-respiratory tract disease among chickens in North Dakota, US, in 1931. The causative agent was identified as a virus in 1933. By 1936, the disease and the virus were recognised as unique from other viral diseases. The virus became known as infectious bronchitis virus (IBV), but later officially renamed as Avian coronavirus. A new brain disease of mice (murine encephalomyelitis) was discovered in 1947 at Harvard Medical School in Boston. The virus was called JHM (after Harvard pathologist John Howard Mueller). Three years later a new mouse hepatitis was reported from the National Institute for Medical Research in London. The causative virus was identified as mouse hepatitis virus (MHV), later renamed Murine coronavirus. In 1961, a virus was obtained from a school boy in Epsom, England, who was suffering from common cold. The sample, designated B814, was confirmed as novel virus in 1965. New common cold viruses (assigned 229E) collected from medical students at the University of Chicago were also reported in 1966. Structural analyses of IBV, MHV, B18 and 229E using transmission electron microscopy revealed that they all belong to the same group of viruses. Making a crucial comparison in 1967, June Almeida and David Tyrrell invented the collective name coronavirus, as all those viruses were characterised by solar corona-like projections (called spikes) on their surfaces. Other coronaviruses have been discovered from pigs, dogs, cats, rodents, cows, horses, camels, Beluga whales, birds and bats. As of 2022, 52 species are described. Bats are found to be the richest source of different species of coronaviruses. All coronaviruses originated from a common ancestor about 293 million years ago. Zoonotic species such as Severe acute respiratory syndrome-related coronavirus (SARS-CoV), Middle East respiratory syndrome-related coronavirus (MERS-CoV) and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a variant of SARS-CoV, emerged during the past two decades and caused the first pandemics of the 21st century.","PeriodicalId":36272,"journal":{"name":"WikiJournal of Medicine","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74432889","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-01-01DOI: 10.1001/jama.1944.02850380032013
K. Lalchhandama
The history of penicillin was shaped by the contributions of numerous scientists. The ultimate result was the discovery of the mould Penicillium's antibacterial activity and the subsequent development of penicillins, the most widely used antibiotics. Following an accidental discovery of the mould, later identified as Penicillium rubens, as the source of the antibacterial principle (1928) and the production of a pure compound (1942), penicillin became the first naturally derived antibiotic. There is anecdotal evidence of ancient societies using moulds to treat infections and of awareness that various moulds inhibited bacterial growth. However, it is not clear if Penicillium species were the species traditionally used or if the antimicrobial substances produced were penicillin. In 1928, Alexander Fleming was the first to discover the antibacterial substance secreted by the Penicillium mould and concentrate the active substance involved, giving it the name penicillin. His success in treating Harry Lambert's streptococcal meningitis, an infection until then fatal, proved to be a critical moment in the medical use of penicillin. Many later scientists were involved in the stabilisation and mass production of penicillin and in the search for more productive strains of Penicillium. Among the most important were Ernst Chain and Howard Florey, who shared with Fleming the 1945 Nobel Prize in Physiology or Medicine.
{"title":"History of penicillin","authors":"K. Lalchhandama","doi":"10.1001/jama.1944.02850380032013","DOIUrl":"https://doi.org/10.1001/jama.1944.02850380032013","url":null,"abstract":"The history of penicillin was shaped by the contributions of numerous scientists. The ultimate result was the discovery of the mould Penicillium's antibacterial activity and the subsequent development of penicillins, the most widely used antibiotics. Following an accidental discovery of the mould, later identified as Penicillium rubens, as the source of the antibacterial principle (1928) and the production of a pure compound (1942), penicillin became the first naturally derived antibiotic. There is anecdotal evidence of ancient societies using moulds to treat infections and of awareness that various moulds inhibited bacterial growth. However, it is not clear if Penicillium species were the species traditionally used or if the antimicrobial substances produced were penicillin. In 1928, Alexander Fleming was the first to discover the antibacterial substance secreted by the Penicillium mould and concentrate the active substance involved, giving it the name penicillin. His success in treating Harry Lambert's streptococcal meningitis, an infection until then fatal, proved to be a critical moment in the medical use of penicillin. Many later scientists were involved in the stabilisation and mass production of penicillin and in the search for more productive strains of Penicillium. Among the most important were Ernst Chain and Howard Florey, who shared with Fleming the 1945 Nobel Prize in Physiology or Medicine.","PeriodicalId":36272,"journal":{"name":"WikiJournal of Medicine","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79914287","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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