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1.
Int J Disaster Risk Reduct ; 93: 103776, 2023 Jul.
Article in English | MEDLINE | ID: mdl-37303828

ABSTRACT

Introduction: Individual and community characteristics predictive of knowledge, perception, and attitude on COVID-19, specifically on gender, have not been adequately explored. Objective: To examine the gender differences in COVID-19 knowledge, self-risk perception and public stigma among the general community and to understand other socio-demographic factors which were predictive of them. Method: A nationally representative cross-sectional multi-centric survey was conducted among adult individuals(≥18 yrs) from the community member (N = 1978) from six states and one union territory of India between August 2020 to February 2021. The participants were selected using systematic random sampling. The data were collected telephonically using pilot-tested structured questionnaires and were analyzed using STATA. Gender-segregated multivariable analysis was conducted to identify statistically significant predictors (p < 0.05) of COVID-19-related knowledge, risk perception, and public stigma in the community. Results: Study identified significant differences between males and females in their self-risk perception (22.0% & 18.2% respectively) and stigmatizing attitude (55.3% & 47.1% respectively). Highly educated males and females had higher odds of having COVID-19 knowledge (aOR: 16.83: p < 0.05) than illiterates. Highly educated women had higher odds of having self-risk perception (aOR: 2.6; p < 0.05) but lower public stigma [aOR: 0.57; p < 0.05]. Male rural residents had lower odds of having self-risk perception and knowledge [aOR: 0.55; p < 0.05 & aOR: 0.72; p < 0.05] and female rural residents had higher odds of having public stigma [aOR: 1.36; p < 0.05]. Conclusion: Our study findings suggest the importance of considering thegender differentials and their background, education status and residential status in designing effective interventions to improve knowledge and reduce risk perception and stigma in the community about COVID-19.

2.
Front Public Health ; 10: 992046, 2022.
Article in English | MEDLINE | ID: mdl-36311615

ABSTRACT

Objective: To assess factors associated with COVID-19 stigmatizing attitudes in the community and stigma experiences of COVID-19 recovered individuals during first wave of COVID-19 pandemic in India. Methods: A cross-sectional study was conducted in 18 districts located in 7 States in India during September 2020 to January 2021 among adults > 18 years of age selected through systematic random sampling. Data on socio demographic and COVID-19 knowledge were collected from 303 COVID-19 recovered and 1,976 non-COVID-19 infected individuals from community using a survey questionnaire. Stigma was assessed using COVID-19 Stigma Scale and Community COVID-19 Stigma Scale developed for the study. Informed consent was sought from the participants. Univariate and multivariate binary logistic regression analysis were conducted. Results: Half of the participants (51.3%) from the community reported prevalence of severe stigmatizing attitudes toward COVID-19 infected while 38.6% of COVID-19 recovered participants reported experiencing severe stigma. Participants from the community were more likely to report stigmatizing attitudes toward COVID-19 infected if they were residents of high prevalent COVID-19 zone (AOR: 1.5; CI: 1.2-1.9), staying in rural areas (AOR: 1.5; CI:1.1-1.9), belonged to the age group of 18-30 years (AOR: 1.6; CI 1.2-2.0), were male (AOR: 1.6; CI: 1.3-1.9), illiterate (AOR: 2.7; CI: 1.8-4.2), or living in Maharashtra (AOR: 7.4; CI: 4.8-11.3). COVID-19 recovered participants had higher odds of experiencing stigma if they had poor knowledge about COVID-19 transmission (AOR: 2.8; CI: 1.3-6.3), were staying for 6-15 years (AOR: 3.24; CI: 1.1-9.4) in the current place of residence or belonged to Delhi (AOR: 5.3; CI: 1.04-26.7). Conclusion: Findings indicated presence of stigmatizing attitudes in the community as well as experienced stigma among COVID-19 recovered across selected study sites in India during the first wave of COVID-19 pandemic. Study recommends timely dissemination of factual information to populations vulnerable to misinformation and psychosocial interventions for individuals affected by stigma.


Subject(s)
COVID-19 , Pandemics , Adult , Male , Humans , Adolescent , Young Adult , Female , Cross-Sectional Studies , COVID-19/epidemiology , India/epidemiology , Social Stigma
3.
Indian J Med Res ; 155(1): 156-164, 2022 01.
Article in English | MEDLINE | ID: mdl-35859441

ABSTRACT

Background & objectives: COVID-19 pandemic has triggered social stigma towards individuals affected and their families. This study describes the process undertaken for the development and validation of scales to assess stigmatizing attitudes and experiences among COVID-19 and non-COVID-19 participants from the community. Methods: COVID-19 Stigma Scale and Community COVID-19 Stigma Scale constituting 13 and six items, respectively, were developed based on review of literature and news reports, expert committee evaluation and participants' interviews through telephone for a multicentric study in India. For content validity, 61 (30 COVID-19-recovered and 31 non-COVID-19 participants from the community) were recruited. Test-retest reliability of the scales was assessed among 99 participants (41 COVID-19 recovered and 58 non-COVID-19). Participants were administered the scale at two-time points after a gap of 7-12 days. Cronbach's alpha, overall percentage agreement and kappa statistics were used to assess internal consistency and test-retest reliability. Results: Items in the scales were relevant and comprehensible. Both the scales had Cronbach's α above 0.6 indicating moderate-to-good internal consistency. Test-retest reliability assessed using kappa statistics indicated that for the COVID-19 Stigma Scale, seven items had a moderate agreement (0.4-0.6). For the Community COVID-19 Stigma Scale, four items had a moderate agreement. Interpretation & conclusions: Validity and reliability of the two stigma scales indicated that the scales were comprehensible and had moderate internal consistency. These scales could be used to assess COVID-19 stigma and help in the development of appropriate stigma reduction interventions for COVID-19 infected, and mitigation of stigmatizing attitudes in the community.


Subject(s)
COVID-19 , Social Stigma , Humans , India/epidemiology , Pandemics , Psychometrics , Reproducibility of Results , Surveys and Questionnaires
4.
PLoS One ; 17(3): e0264956, 2022.
Article in English | MEDLINE | ID: mdl-35271652

ABSTRACT

BACKGROUND: COVID-19 has inundated the entire world disrupting the lives of millions of people. The pandemic has stressed the healthcare system of India impacting the psychological status and functioning of health care workers. The aim of this study is to determine the burnout levels and factors associated with the risk of psychological distress among healthcare workers (HCW) engaged in the management of COVID 19 in India. METHODS: A cross-sectional study was conducted from 1 September 2020 to 30 November 2020 by telephonic interviews using a web-based Google form. Health facilities and community centres from 12 cities located in 10 states were selected for data collection. Data on socio-demographic and occupation-related variables like age, sex, type of family, income, type of occupation, hours of work and income were obtained was obtained from 967 participants, including doctors, nurses, ambulance drivers, emergency response teams, lab personnel, and others directly involved in COVID 19 patient care. Levels of psychological distress was assessed by the General health Questionnaire -GHQ-5 and levels of burnout was assessed using the ICMR-NIOH Burnout questionnaire. Multivariable logistic regression analysis was performed to identify factors associated with the risk of psychological distress. The third quartile values of the three subscales of burnout viz EE, DP and PA were used to identify burnout profiles of the healthcare workers. RESULTS: Overall, 52.9% of the participants had the risk of psychological distress that needed further evaluation. Risk of psychological distress was significantly associated with longer hours of work (≥ 8 hours a day) (AOR = 2.38, 95% CI(1.66-3.41), income≥20000(AOR = 1.74, 95% CI, (1.16-2.6); screening of COVID-19 patients (AOR = 1.63 95% CI (1.09-2.46), contact tracing (AOR = 2.05, 95% CI (1.1-3.81), High Emotional exhaustion score (EE ≥16) (AOR = 4.41 95% CI (3.14-6.28) and High Depersonalisation score (DP≥7) (AOR = 1.79, 95% CI (1.28-2.51)). About 4.7% of the HCWs were overextended (EE>18); 6.5% were disengaged (DP>8) and 9.7% HCWs were showing signs of burnout (high on all three dimensions). CONCLUSION: The study has identified key factors that could have been likely triggers for psychological distress among healthcare workers who were engaged in management of COVID cases in India. The study also demonstrates the use of GHQ-5 and ICMR-NIOH Burnout questionnaire as important tools to identify persons at risk of psychological distress and occurrence of burnout symptoms respectively. The findings provide useful guide to planning interventions to mitigate mental health problems among HCW in future epidemic/pandemic scenarios in the country.


Subject(s)
Burnout, Professional/psychology , COVID-19/psychology , Health Personnel/psychology , Adult , Aged , Burnout, Professional/epidemiology , Burnout, Psychological/epidemiology , Cross-Sectional Studies , Depression/epidemiology , Female , Humans , India/epidemiology , Interviews as Topic , Male , Mental Health/trends , Middle Aged , Pandemics , Psychological Distress , SARS-CoV-2/pathogenicity , Surveys and Questionnaires
5.
J Health Pollut ; 9(22): 190608, 2019 Jun.
Article in English | MEDLINE | ID: mdl-31259084

ABSTRACT

BACKGROUND: Evidence from various epidemiological studies has shown an association between particulate matter 2.5 (PM2.5) and diabetes mellitus. A prospective study from the United States reported that exposure to PM2.5 alters endothelial function, and leads to insulin resistance and reduction in peripheral glucose uptake. There is a paucity of data on the relation between air pollution and diabetes in low- and middle-income countries. OBJECTIVES: To estimate the prevalence of type 2 diabetes among people living in areas with higher exposures of suspended PM2.5 compared to people living in areas with lower exposures in Chennai, Tamil Nadu, India. METHODS: A cross-sectional study was carried out in two areas of Chennai city. The PM2.5 affecting vulnerable areas were stratified from a list of air quality monitoring stations in Tamil Nadu Pollution Control Board and Central Pollution Control Board. The highest and lowest areas of exposure were selected from the list. Households were randomly selected for the study. A total of 201 (67 male, 134 female) individuals from a high exposure area (HEA) and 209 (76 male 133 female) individuals from a low exposure area (LEA) were recruited for the study. Adults over 18 years of age were screened for random capillary blood glucose (RCBG) by glucometer (OneTouch Ultra). RESULTS: The prevalence of diabetes (34.8% vs 19.6% p =0.001) was 77.5% higher among people living in areas of high particulate matter exposure compared to people living in less exposed areas. Multivariable logistic regression analysis showed that age, gender, residential area, and family history of diabetes were significantly associated with the prevalence of diabetes (p<0.05). CONCLUSIONS: The present study indicates a link between high levels of exposure to PM2.5 and diabetes mellitus. Further prospective studies on populations exposed to elevated pollution are needed to establish whether this association has a causative link. PARTICIPANT CONSENT: Obtained. ETHICS APPROVAL: The study was approved by the Ethics Committee of the Prof. M Viswanathan Diabetes Research Centre, Chennai, India. COMPETING INTERESTS: The authors declare no competing financial interests.

6.
J Lifestyle Med ; 9(1): 44-51, 2019 Jan.
Article in English | MEDLINE | ID: mdl-30918833

ABSTRACT

BACKGROUND: MetS is one of the emerging health problems of the world with prevalence higher among Asians, including Indians, and is rising especially in the rural area. Hence, the objectives were to estimate the prevalence of MetS and its association with life style risk factors among adult men. METHODS: Cross-Sectional based study conducted in the rural area of Kancheepuram District recruiting 360 participants at the age group of 20-40 years by PPS from 9 villages and from each village participants were selected by simple random sampling. Using modified NCEP-ATP III guidelines, criteria for MetS were defined and the prevalence and its associated lifestyle risk factors were evaluated. RESULTS: The prevalence of MetS was found to be 16.7%. Higher prevalence was observed among the older age group 31-40 years with 32.4%. Among the five components of MetS, most observed component was Hypertriglyceridemia followed by high WC, abnormal DBP with 31%, 14% and 7% respectively. In Logistic Regression analysis, variables like Increased age, alcohol intake, high WC, raised TG level, raised FBS level and high average DBP were strongly associated with MetS as it was statistically significant. CONCLUSION: The present study showed a high prevalence of MetS amongst men 31-40 years and strong association between MetS and lifestyle risk factors could be a major health problem in rural area, indicating that it was not necessarily a result of modernization. These findings make it critical to plan further healthcare interventions to prevent the adverse consequences of the disease.

7.
Article in English | MEDLINE | ID: mdl-27213179

ABSTRACT

Virulence gene regulation in Vibrio cholerae is under the control of the ToxR-ToxT regulatory cascade. Chemotaxis and net motility have been shown to influence the infectivity of Vibrio cholerae. V. cholerae toxR mutants do not synthesize proteins required for chemotaxis towards mucus. The inability of the toxR mutant strain to recognize and swim towards mucus is due to their failure to synthesize AcfB, a methyl-accepting chemotaxis protein. AcfB has previously been shown to be involved in intestinal colonization using the infant mouse model of cholera infection. Wild type V. cholerae recognizes galactose-6-sulfate in the capillary tube assay whereas V. cholerae acfB mutants fail to migrate into the capillary tubes. Vibrio strains carrying a mutation in tcpI, a ToxR regulated gene found within the Vibrio Pathogenicity Island (VPI), which encodes a methyl accepting chemotaxis protein are fully chemotactic towards mucus and galactose-6-sulfate.

8.
Basic Res Cardiol ; 108(5): 377, 2013 Sep.
Article in English | MEDLINE | ID: mdl-23917520

ABSTRACT

Ischaemic preconditioning is one of the most potent experimental modalities known to decrease infarct size after ischaemia and reperfusion. Much interest has been stimulated by the phenomenon of remote ischaemic conditioning (RIC), in which the preconditioning stimulus is applied to a limb remote from the heart to stimulate cardioprotection via an unidentified humoral factor, believed to be a protein between 3.5 and 15 kDa. Stromal cell-derived factor-1 (SDF-1α or CXCL12) is a chemokine of 10 kDa that is induced by hypoxia and recruits stem cells, but also exerts direct, acute, cardioprotection via its receptor, CXCR4. The serum dipeptidase DPPIV cleaves and inactivates SDF-1α. We measured SDF-1α in rat plasma and found it was significantly increased by RIC. DPPIV activity was unchanged after RIC, suggesting that increased synthesis or release or SDF-1α caused the increase in plasma levels. AMD3100, a highly specific inhibitor of CXCR4, was used to investigate the hypothesis that SDF-1α is involved in RIC. RIC in rats, which decreased infarct size from 53 ± 3 % to 27 ± 3 % (n = 6, P < 0.05), was blocked in rats treated with AMD3100 (40 ± 4 %). RIC also improved functional recovery of cardiac papillary muscle, and this, too, was blocked by AMD3100. Direct application of SDF-1α was confirmed to be protective in this model and was blocked by AMD3100. RIC stimulates SDF-1α release, and this 10-kDa peptide appears to be required for the mechanism of RIC.


Subject(s)
Chemokine CXCL12/metabolism , Ischemic Preconditioning, Myocardial , Myocardial Reperfusion Injury/metabolism , Signal Transduction/physiology , Animals , Blotting, Western , Enzyme-Linked Immunosorbent Assay , Male , Rats , Rats, Sprague-Dawley , Receptors, CXCR4/metabolism
10.
Exp Neurol ; 221(1): 107-14, 2010 Jan.
Article in English | MEDLINE | ID: mdl-19837065

ABSTRACT

beta1 integrin is a cell surface molecule that is critical for endothelial cell adhesion, migration and survival during angiogenesis. In the present study we employed in vivo and in vitro models to elucidate the role of beta1 integrin in vascular remodelling and stroke outcomes. At 24 h after cerebral ischemia and reperfusion (I/R), the ischemic cortex (ipsilateral area) exhibited modest beta1 integrin immunoreactivity and a robust increase was observed at 72 h. Double-label immunohistochemical analysis for beta1 integrin with neuronal (NeuN), microglial (Iba-1), astrocyte (GFAP), progenitor cell (Ng2) and blood vessel (collagen 4) markers showed that beta1 integrin expression only localized to blood vessels. In vitro studies using cultured endothelial cells and a beta1 integrin blocking antibody confirmed that beta1 integrin is required for endothelial cell migration, proliferation and blood vessel formation. In vivo studies in the cerebral I/R model using the beta1 integrin blocking antibody further confirmed that beta1 integrin signaling is involved in vascular formation and recovery following ischemic stroke. Finally, we found that beta1 integrin is critically involved in functional deficits and survival after a stroke. These results suggest that beta1 integrin plays important roles in neurovascular remodelling and functional outcomes following stroke, and that targeting the beta1 integrin signalling may provide a novel strategy for modulating angiogenesis in ischemic stroke and other pathological conditions.


Subject(s)
Blood Vessels/metabolism , Gene Expression Regulation/physiology , Infarction, Middle Cerebral Artery/metabolism , Infarction, Middle Cerebral Artery/physiopathology , Interferon-beta/metabolism , Neovascularization, Pathologic/metabolism , Animals , Antibodies/pharmacology , Antibodies/therapeutic use , Antigens/metabolism , Brain/pathology , Calcium-Binding Proteins/metabolism , Cell Line , Cell Movement/drug effects , Cell Movement/physiology , Cell Proliferation/drug effects , Cell Proliferation/ethics , Collagen/metabolism , Disease Models, Animal , Endothelial Cells/drug effects , Endothelial Cells/physiology , Glial Fibrillary Acidic Protein/metabolism , Infarction, Middle Cerebral Artery/drug therapy , Infarction, Middle Cerebral Artery/pathology , Interferon-beta/immunology , Male , Mice , Mice, Inbred C57BL , Microfilament Proteins , Neovascularization, Pathologic/drug therapy , Phosphopyruvate Hydratase/metabolism , Proteoglycans/metabolism , Reperfusion Injury/drug therapy , Reperfusion Injury/metabolism , Statistics, Nonparametric
11.
J Pharmacol Exp Ther ; 332(2): 371-9, 2010 Feb.
Article in English | MEDLINE | ID: mdl-19889792

ABSTRACT

We have previously shown that nicotine, the addictive component of tobacco products, alters the blood-brain barrier (BBB) Na(+),K(+),2Cl(-) cotransporter (NKCC) during in vitro hypoxia-aglycemia exposure. Attenuation of abluminal NKCC suggests that accumulation of ions in the brain extracellular fluid would result in an increase of fluid or cytotoxic edema in the brain during hypoxia-aglycemia or stroke conditions. To further investigate whether nicotine products have the potential to worsen stroke outcome by increasing edema formation, two separate models to mimic stroke conditions were utilized to decipher the effects of short-term and long-term administrations of nicotine products on brain edema following stroke. Oxygen glucose deprivation (OGD) was studied in rat hippocampal slices with short-term or long-term exposure to nicotine and cigarette smoke constituents. During short-term exposure, the presence of nicotine at a concentration mimicking heavy smokers increased water content of hippocampal slices during OGD. Furthermore, long-term 1-week administration of nicotine increased water content in hippocampal slices that could be attenuated with nicotine acetylcholine receptor (nAChR) antagonists, suggesting nicotine increase edema during OGD via nAChRs. A second model of focal ischemia, middle cerebral artery occlusion, showed an increase of infarct size during short-term exposure to nicotine and an increase of edema during both short-term and long-term administration of nicotine, compared with saline controls. These findings support the paradigm that nicotine products not only increase the incidence of stroke but also have the potential to worsen stroke outcome by increased edema formation.


Subject(s)
Brain Edema/pathology , Brain/drug effects , Hippocampus/drug effects , Hypoxia-Ischemia, Brain/pathology , Nicotine/adverse effects , Animals , Blood Gas Analysis , Body Temperature/drug effects , Brain/pathology , Brain Edema/blood , Brain Infarction/blood , Brain Infarction/pathology , Drug Administration Schedule , Female , Hippocampus/pathology , Hypoglycemia/pathology , Hypoxia-Ischemia, Brain/blood , Mice , Mice, Inbred Strains , Motor Activity/drug effects , Nicotine/administration & dosage , Rats , Rats, Sprague-Dawley , Smoke/adverse effects , Nicotiana/adverse effects
12.
J Neurosci ; 28(51): 13978-84, 2008 Dec 17.
Article in English | MEDLINE | ID: mdl-19091986

ABSTRACT

Toll-like receptors (TLRs) play important roles in innate immunity. Several TLR family members have recently been shown to be expressed by neurons and glial cells in the adult brain, and may mediate responses of these cells to injury and infection. To address the possibility that TLRs play a functional role in development of the nervous system, we analyzed the expression of TLRs during different stages of mouse brain development and assessed the role of TLRs in cell proliferation. TLR3 protein is present in brain cells in early embryonic stages of development, and in cultured neural stem/progenitor cells (NPC). NPC from TLR3-deficient embryos formed greater numbers of neurospheres compared with neurospheres from wild-type embryos. Numbers of proliferating cells, as assessed by phospho histone H3 and proliferating cell nuclear antigen labeling, were also increased in the developing cortex of TLR3-deficient mice compared with wild-type mice in vivo. Treatment of cultured embryonic cortical neurospheres with a TLR3 ligand (polyIC) significantly reduced proliferating (BrdU-labeled) cells and neurosphere formation in wild type but not TLR3(-/-)-derived NPCs. Our findings reveal a novel role for TLR3 in the negative regulation of NPC proliferation in the developing brain.


Subject(s)
Brain/cytology , Gene Expression Regulation, Developmental , Neurons/metabolism , Stem Cells/metabolism , Toll-Like Receptor 3/physiology , Animals , Brain/embryology , Cell Proliferation/drug effects , Cells, Cultured , Mice , Mice, Inbred C57BL , Mice, Knockout , Neurons/cytology , Poly I-C/pharmacology , Signal Transduction/drug effects , Signal Transduction/physiology , Spheroids, Cellular/cytology , Stem Cells/cytology , Stem Cells/drug effects , Toll-Like Receptor 3/drug effects , Toll-Like Receptor 3/genetics
13.
Exp Neurol ; 213(1): 114-21, 2008 Sep.
Article in English | MEDLINE | ID: mdl-18586243

ABSTRACT

The innate immune system senses the invasion of pathogenic microorganisms and tissue injury through Toll-like receptors (TLR), a mechanism thought to be limited to immune cells. We recently found that neurons express several TLRs, and that the levels of TLR2 and TLR4 are increased in neurons in response to energy deprivation. Here we report that TLR4 expression increases in neurons when exposed to amyloid beta-peptide (Abeta1-42) or the lipid peroxidation product 4-hydroxynonenal (HNE). Neuronal apoptosis triggered by Abeta and HNE was mediated by jun N-terminal kinase (JNK); neurons from TLR4 mutant mice exhibited reduced JNK and caspase-3 activation and were protected against apoptosis induced by Abeta and HNE. Levels of TLR4 were decreased in inferior parietal cortex tissue specimens from end-stage AD patients compared to aged-matched control subjects, possibly as the result of loss of neurons expressing TLR4. Our findings suggest that TLR4 signaling increases the vulnerability of neurons to Abeta and oxidative stress in AD, and identify TLR4 as a potential therapeutic target for AD.


Subject(s)
Alzheimer Disease/metabolism , Apoptosis , Lipid Peroxidation , Nerve Degeneration/metabolism , Oxidative Stress , Toll-Like Receptor 4/metabolism , Aged , Aged, 80 and over , Aldehydes/metabolism , Alzheimer Disease/drug therapy , Alzheimer Disease/pathology , Amyloid beta-Peptides/metabolism , Amyloid beta-Peptides/toxicity , Animals , Apoptosis/drug effects , Brain/metabolism , Brain/pathology , Caspase 3/drug effects , Caspase 3/metabolism , Female , Humans , JNK Mitogen-Activated Protein Kinases/drug effects , JNK Mitogen-Activated Protein Kinases/metabolism , Male , Membrane Lipids/metabolism , Mice , Mice, Knockout , Nerve Degeneration/chemically induced , Nerve Degeneration/pathology , Oxidative Stress/drug effects , Peptide Fragments/metabolism , Peptide Fragments/toxicity , Signal Transduction/drug effects , Toll-Like Receptor 4/genetics
14.
Expert Opin Ther Targets ; 12(1): 19-29, 2008 Jan.
Article in English | MEDLINE | ID: mdl-18076367

ABSTRACT

BACKGROUND: Intravenous immunoglobulin (IVIG) is a therapeutic modality approved for the treatment of autoimmune disorders. OBJECTIVE: This review discusses how IVIG can prevent brain damage following ischemic stroke and discuss the potential mechanisms of action. METHODS: Medline and the world wide web were searched and the relevant literature was classified under the following categories: IVIG, IVIG mechanism of action, and ischemic stroke injury mechanisms. RESULTS/CONCLUSION: Brain ischemia induces an inflammatory response that contributes to neuronal cell death. Because of its ability to block multiple molecular events, IVIG may have particularly strong neuroprotective action against ischemic brain injury. In light of the extensive clinical experience with IVIG for other indications, development of clinical trials to evaluate the use of IVIG in human stroke patients are warranted.


Subject(s)
Brain Ischemia/drug therapy , Drug Delivery Systems/methods , Immunoglobulins, Intravenous/administration & dosage , Animals , Brain Injuries/drug therapy , Brain Injuries/metabolism , Brain Ischemia/metabolism , Drug Delivery Systems/trends , Humans , Signal Transduction/drug effects , Signal Transduction/physiology
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