chlorine has been researched along with Apoplexy in 21 studies
chloride : A halide anion formed when chlorine picks up an electron to form an an anion.
Excerpt | Relevance | Reference |
---|---|---|
"Ferric chloride-induced distal middle cerebral artery occlusion (MCAO) model of stroke was described in mice several years ago, however it lacked in-depth evaluation of the post-stroke functional outcomes in the animals." | 7.96 | Motor deficit in the mouse ferric chloride-induced distal middle cerebral artery occlusion model of stroke. ( Alamri, FF; Arumugam, TV; Jayaraman, S; Karamyan, ST; Karamyan, VT; Lee, P; Syeara, N, 2020) |
"0) had significantly higher odds of death within 90 days after adjustment for age, race and ethnicity, National Institutes of Health Stroke Scale score strata, hematoma volume, presence or absence of intraventricular hemorrhage, cigarette smoking, previous stroke, and maximum hourly dose of nicardipine." | 4.12 | Early Hyperchloremia is Independently Associated with Death or Disability in Patients with Intracerebral Hemorrhage. ( Hanley, DF; Hsu, CY; Huang, W; Malhotra, K; Martin, RH; Qureshi, AI; Steiner, T; Suarez, JI; Toyoda, K; Yamamoto, H, 2022) |
"Ferric chloride-induced distal middle cerebral artery occlusion (MCAO) model of stroke was described in mice several years ago, however it lacked in-depth evaluation of the post-stroke functional outcomes in the animals." | 3.96 | Motor deficit in the mouse ferric chloride-induced distal middle cerebral artery occlusion model of stroke. ( Alamri, FF; Arumugam, TV; Jayaraman, S; Karamyan, ST; Karamyan, VT; Lee, P; Syeara, N, 2020) |
"Stroke is one of the major causes of death and disability worldwide." | 2.55 | Chloride co-transporters as possible therapeutic targets for stroke. ( Darlison, MG; Martín-Aragón Baudel, MA; Poole, AV, 2017) |
"SLC26A11 inhibition ameliorates infarct formation and improves functional recovery." | 1.91 | SLC26A11 Inhibition Reduces Oncotic Neuronal Death and Attenuates Stroke Reperfusion Injury. ( Chen, B; Gao, Y; Liao, P; Low, SW; Nilius, B; Poore, CP; Wei, S, 2023) |
"Ischaemic stroke is very rarely reported in osteopetrosis, resulting from vascular impingement." | 1.72 | Haemodynamic stroke in a rare adult presentation of osteopetrosis. ( Benjamin, RN; Jasper, A; Lionel, SA; Ninan, GA, 2022) |
"Dual treatment with aspirin (5 mg kg(-1) ) and clopidogel (0." | 1.43 | A rabbit model of cerebral microembolic signals for translational research: preclinical validation for aspirin and clopidogrel. ( Chu, L; Desai, K; Gutstein, DE; Kurowski, S; Seiffert, D; Wang, X; Wu, W; Zhou, X, 2016) |
Timeframe | Studies, this research(%) | All Research% |
---|---|---|
pre-1990 | 1 (4.76) | 18.7374 |
1990's | 0 (0.00) | 18.2507 |
2000's | 7 (33.33) | 29.6817 |
2010's | 7 (33.33) | 24.3611 |
2020's | 6 (28.57) | 2.80 |
Authors | Studies |
---|---|
Qureshi, AI | 1 |
Huang, W | 1 |
Hanley, DF | 1 |
Hsu, CY | 1 |
Martin, RH | 1 |
Malhotra, K | 1 |
Steiner, T | 1 |
Suarez, JI | 1 |
Yamamoto, H | 1 |
Toyoda, K | 1 |
Wang, L | 1 |
Sheng, G | 1 |
Cui, J | 1 |
Yao, Y | 1 |
Bai, X | 1 |
Chen, F | 1 |
Yu, W | 1 |
Ninan, GA | 1 |
Benjamin, RN | 1 |
Jasper, A | 1 |
Lionel, SA | 1 |
Hugues, N | 1 |
Pin-Barre, C | 1 |
Brioche, T | 1 |
Pellegrino, C | 1 |
Berton, E | 1 |
Rivera, C | 1 |
Laurin, J | 1 |
Wei, S | 1 |
Chen, B | 1 |
Low, SW | 1 |
Poore, CP | 1 |
Gao, Y | 1 |
Nilius, B | 1 |
Liao, P | 1 |
Syeara, N | 1 |
Alamri, FF | 1 |
Jayaraman, S | 1 |
Lee, P | 1 |
Karamyan, ST | 1 |
Arumugam, TV | 1 |
Karamyan, VT | 1 |
Bei, HZ | 1 |
You, SJ | 1 |
Zheng, D | 1 |
Zhong, CK | 1 |
Du, HP | 1 |
Zhang, Y | 1 |
Lu, TS | 1 |
Cao, LD | 1 |
Dong, XF | 1 |
Cao, YJ | 1 |
Liu, CF | 1 |
Yang, J | 1 |
Chen, J | 1 |
Del Carmen Vitery, M | 1 |
Osei-Owusu, J | 1 |
Chu, J | 1 |
Yu, H | 1 |
Sun, S | 1 |
Qiu, Z | 1 |
Pan, R | 1 |
Timmins, GS | 1 |
Liu, W | 1 |
Liu, KJ | 1 |
Zhou, X | 1 |
Kurowski, S | 1 |
Wu, W | 1 |
Desai, K | 1 |
Chu, L | 1 |
Gutstein, DE | 1 |
Seiffert, D | 1 |
Wang, X | 1 |
Martín-Aragón Baudel, MA | 1 |
Poole, AV | 1 |
Darlison, MG | 1 |
STENNING, JC | 1 |
Zhang, YP | 1 |
Zhang, H | 1 |
Duan, DD | 1 |
Alam, MN | 1 |
Uddin, MJ | 1 |
Rahman, KM | 1 |
Ahmed, S | 1 |
Akhter, M | 1 |
Nahar, N | 1 |
Swapan, MK | 1 |
Alam, MM | 2 |
Sultana, N | 1 |
Hallaz, MM | 1 |
Uddin, MM | 1 |
Bari, MS | 1 |
Israil, MA | 1 |
Limbrick, DD | 2 |
Sombati, S | 2 |
DeLorenzo, RJ | 2 |
Music, M | 1 |
Schmidlin, O | 2 |
Tanaka, M | 2 |
Bollen, AW | 1 |
Yi, SL | 2 |
Morris, RC | 2 |
Solini, A | 1 |
Zamboni, P | 1 |
Passaro, A | 1 |
Fellin, R | 1 |
Ferrannini, E | 1 |
Deshpande, LS | 1 |
Ahmad, S | 1 |
Olson, JL | 1 |
Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
---|---|---|---|---|---|---|---|
Antihypertensive Treatment of Acute Cerebral Hemorrhage (ATACH)-II: A Phase III Randomized Multicenter Clinical Trial of Blood Pressure Reduction for Hypertension in Acute Intracerebral Hemorrhage[NCT01176565] | Phase 3 | 1,000 participants (Actual) | Interventional | 2011-05-15 | Terminated (stopped due to Planned interim analysis: no significant outcome differences between groups) | ||
[information is prepared from clinicaltrials.gov, extracted Sep-2024] |
The complete count of all subjects who experienced any serious adverse events throughout their participation in the trial was included in this tabulation. Adverse events (AEs) and serious adverse events (SAEs) were assessed by the site investigators for all patients. Potential relatedness to the study treatment was a required reporting element for all adverse events but was not considered in this count. Terminology from the Medical Dictionary for Regulatory Activities (MedDRA) and severity criteria from the Common Terminology Criteria for Adverse Events (CTCAE v. 4.03) were used as a basis for reporting adverse events. Serious adverse events are defined as being fatal, life-threatening, resulting in hospitalization or prolonged hospitalization, resulting in disability or congenital anomaly, or requiring intervention to prevent permanent impairment or damage and were required to be reported promptly. An Independent Oversight Committee (IOC) reviewed and adjudicated adverse event data. (NCT01176565)
Timeframe: From randomization through the 90 day visit (90 ± 14 days per protocol window; up to ± 30 days data is used) or until known death, withdrawal, or loss to follow-up.
Intervention | Participants (Count of Participants) |
---|---|
Standard SBP Reduction Arm | 100 |
Intensive SBP Reduction Arm | 128 |
Hematoma expansion as determined by serial CT scans: Hematoma expansion was defined as an increase in the volume of intraparenchymal hemorrhage of 33% or greater as measured by a central imaging analyst who was was unaware of the treatment assignments, clinical findings, and time points of image acquisition. The area of the hematoma was delineated by image analysis software with the use of density thresholds on each slice, followed by manual correction. To ensure accuracy and consistency of the readings, images were coded randomly and independently of subject numbers and manual correction was also done without awareness of treatment assignments, clinical findings, or time points of image acquisition. This data point is defined as being present (hematoma expansion of 33% or more was calculated between the baseline scan hematoma volume and the 24 +/- 6 hours hematoma volume measures at data analysis), meaning that hematoma expansion as defined must have occurred or it was not counted. (NCT01176565)
Timeframe: From the baseline head CT to the 24 +/- 6 hours from randomization head CT
Intervention | Participants (Count of Participants) |
---|---|
Standard SBP Reduction Arm | 104 |
Intensive SBP Reduction Arm | 85 |
Hypotension (abnormally low blood pressure) was the most likely adverse event that could be associated with the study treatment, and is the primary basis (risk) on which neurological deterioration or other untoward effects of the study treatment could occur. It is therefore examined as a numerically-measured occurrence in addition to monitoring patients closely for neurological deterioration or other symptoms. Hypotension, when named as an adverse event, was defined as the syndrome of low blood pressure with SBP < 85 mmHg. Instances of hypotension were to be avoided through close monitoring, and administration of fluid bolus for SBP < 110 mmHg. If hypotension did occur, it was to be reversed as quickly as possible through discontinuation of intravenous nicardipine and intravenous fluid administration, which can be accomplished readily in a variety of settings where patients with intracerebral hemorrhage are routinely housed during early hospitalization. (NCT01176565)
Timeframe: From randomization through 72 hours from randomization
Intervention | Participants (Count of Participants) |
---|---|
Standard SBP Reduction Arm | 3 |
Intensive SBP Reduction Arm | 6 |
Neurologic deterioration was measured using two scales. The Glasgow Coma Scale (GCS) score measures of level of consciousness in eye, motor, and verbal components. At least one point is given in each category. The scale ranges from 3 to 15, with 3 indicating deep unconsciousness and 15 indicating consciousness is not impaired. The National Institutes of Health Stroke Scale (NIHSS) quantifies neurologic deficits in 11 categories. Level of consciousness, horizontal eye movement, visual fields, facial palsy, movement in each limb, sensation, language & speech, and extinction or inattention on one side of the body are tested. Scores range from 0 to 42, with 0 indicating normal function and higher scores indicating greater deficit severity. Neurological status was checked per ICU standards through 24 hours, recommended as hourly GCS and full assessment every 2 hours. NIHSS assessment at baseline and 24 +/- 3 hours was pre-specified. Assessments were added for suspected neurological change. (NCT01176565)
Timeframe: From randomization through the 24-hour treatment period
Intervention | Participants (Count of Participants) |
---|---|
Standard SBP Reduction Arm | 40 |
Intensive SBP Reduction Arm | 55 |
Adverse events (AEs) and serious adverse events (SAEs) were assessed by the site investigators for all patients, including for their potential relatedness to the study treatment. An Independent Oversight Committee (IOC) reviewed and adjudicated all adverse event data. The 72-hours-from-randomization time window was considered the most likely time frame during which treatment-related adverse events or serious adverse events would be observed. Terminology from the Medical Dictionary for Regulatory Activities (MedDRA) and severity criteria from the Common Terminology Criteria for Adverse Events (CTCAE v. 4.03) were used as a basis for reporting adverse events. Serious adverse events are defined as being fatal, life-threatening, resulting in hospitalization or prolonged hospitalization, resulting in disability or congenital anomaly, or requiring intervention to prevent permanent impairment or damage and were required to be reported promptly. (NCT01176565)
Timeframe: From randomization through 72 hours (3 days)
Intervention | Participants (Count of Participants) |
---|---|
Standard SBP Reduction Arm | 6 |
Intensive SBP Reduction Arm | 8 |
The primary outcome was death or disability, defined by modified Rankin scale (mRS) of 4-6 at 90 days following treatment. The modified Rankin Scale score ranges from 0, indicating no symptoms, to 6, indicating death. A score of 4 indicates moderately severe disability including the inability to walk or attend to one's own bodily needs. A score of 5 indicates severe disability; bedridden, incontinent, and requiring constant nursing care. To score a 3 or lower on the mRS, a person must at least be able to walk without the assistance of another person. We chose the mRS because of its high inter-observer reliability, superiority to other indices, and consistency with previous trials in patients with ICH. Reliability was further increased by use of a structured interview template and by requiring mRS assessors to pass a certification test. Persons conducting the 90-day mRS assessment were to be unaware of the treatment arm or clinical course of the patients they assessed. (NCT01176565)
Timeframe: 90 days (± 14 days per protocol window; up to ± 30 days data is used) from randomization
Intervention | Participants (Count of Participants) | |
---|---|---|
Death or disability at 90 days (mRS = 4 - 6) | Known death at or before 90 days | |
Intensive SBP Reduction Arm | 186 | 33 |
Standard SBP Reduction Arm | 181 | 34 |
Standardized scales developed by the EuroQol Research Foundation were used as a secondary outcome measure in addition to the mRS scale score. The EQ-5D is a simple, standardized non-disease-specific instrument for describing and valuating health-related quality of life. The EQ-5D-3L questionnaire consists of 5 questions in 5 different domains and allows for responses from 1 (the best outcome) to 3 (the worst outcome) in each of five categories (mobility, self-care, usual activities, pain/discomfort, and anxiety/depression). Total scores range from 5 to 15, with lower scores indicating better quality of life and a higher score indicating a worse quality of life. A second component of EuroQol outcome measurements is a printed 20 cm visual analogue scale (EQ VAS) that appears somewhat like a thermometer, on which a score from 0 (worst imaginable health state or death) to 100 (best imaginable health state) is marked by the patient (or, when necessary, their proxy) with the scale in view. (NCT01176565)
Timeframe: 90 days (± 14 days per protocol window; up to ± 30 days data is used) from randomization
Intervention | units on a scale (Median) | |
---|---|---|
EQ-5D utility scale questionnaire | EQ VAS (visual analog scale) | |
Intensive SBP Reduction Arm | 0.7 | 62.5 |
Standard SBP Reduction Arm | 0.7 | 70 |
2 reviews available for chlorine and Apoplexy
Article | Year |
---|---|
Chloride co-transporters as possible therapeutic targets for stroke.
Topics: Animals; Brain; Cell Death; Chlorides; Humans; Neuroprotective Agents; Stroke; Symporters | 2017 |
Chloride channels in stroke.
Topics: Animals; Chloride Channels; Chlorides; Humans; Muscle, Smooth, Vascular; Oxidative Stress; Stroke | 2013 |
19 other studies available for chlorine and Apoplexy
Article | Year |
---|---|
Early Hyperchloremia is Independently Associated with Death or Disability in Patients with Intracerebral Hemorrhage.
Topics: Antihypertensive Agents; Cerebral Hemorrhage; Chlorides; Humans; Nicardipine; Stroke | 2022 |
Electroacupuncture attenuates ischemic injury after stroke and promotes angiogenesis via activation of EPO mediated Src and VEGF signaling pathways.
Topics: Animals; Chlorides; Electroacupuncture; Endothelial Cells; Erythropoietin; Glucose; Ischemia; Oxygen | 2022 |
Haemodynamic stroke in a rare adult presentation of osteopetrosis.
Topics: Brain Ischemia; Chloride Channels; Chlorides; Female; Hemodynamics; Humans; Ischemic Stroke; Osteope | 2022 |
High-intensity training with short and long intervals regulate cortical neurotrophic factors, apoptosis markers and chloride homeostasis in rats with stroke.
Topics: Animals; Apoptosis; Chlorides; High-Intensity Interval Training; Homeostasis; Humans; Nerve Growth F | 2023 |
SLC26A11 Inhibition Reduces Oncotic Neuronal Death and Attenuates Stroke Reperfusion Injury.
Topics: Animals; Brain Ischemia; Chlorides; Edema; Glucose; Hypoxia; Infarction; Rats; Reperfusion Injury; S | 2023 |
Motor deficit in the mouse ferric chloride-induced distal middle cerebral artery occlusion model of stroke.
Topics: Animals; Behavior, Animal; Cerebral Cortex; Cerebral Infarction; Chlorides; Disease Models, Animal; | 2020 |
Prognostic role of hypochloremia in acute ischemic stroke patients.
Topics: Aged; Biomarkers; Chlorides; Female; Humans; Hyponatremia; Male; Middle Aged; Prognosis; Sodium; Str | 2017 |
PAC, an evolutionarily conserved membrane protein, is a proton-activated chloride channel.
Topics: Animals; Calcium; Cell Death; Chloride Channels; Chlorides; Conserved Sequence; Evolution, Molecular | 2019 |
Autophagy Mediates Astrocyte Death During Zinc-Potentiated Ischemia--Reperfusion Injury.
Topics: Animals; Astrocytes; Autophagy; Blotting, Western; Cell Culture Techniques; Cell Hypoxia; Cell Line; | 2015 |
A rabbit model of cerebral microembolic signals for translational research: preclinical validation for aspirin and clopidogrel.
Topics: Animals; Aspirin; Carotid Artery Thrombosis; Chlorides; Clopidogrel; Disease Models, Animal; Drug Ev | 2016 |
Salt deficiency states in tropical climates.
Topics: Chlorides; Heat Stroke; Hot Temperature; Humans; Hygiene; Sodium; Sodium Chloride; Stroke; Tropical | 1945 |
Electrolyte changes in stroke.
Topics: Adult; Aged; Cerebral Hemorrhage; Cerebral Infarction; Chlorides; Electrolytes; Female; Humans; Male | 2012 |
Calcium influx constitutes the ionic basis for the maintenance of glutamate-induced extended neuronal depolarization associated with hippocampal neuronal death.
Topics: Animals; Animals, Newborn; Brain Injuries; Calcium; Calcium Channel Blockers; Calcium Signaling; Cel | 2003 |
Testing of potassium, sodium and chlorine in liquor at the patients with diabetes mellitus.
Topics: Blood-Brain Barrier; Chlorides; Diabetes Mellitus; Humans; Potassium; Sodium; Stroke | 2004 |
Chloride-dominant salt sensitivity in the stroke-prone spontaneously hypertensive rat.
Topics: Animals; Bicarbonates; Blood Pressure; Body Weight; Chlorides; Creatinine; Drug Combinations; Electr | 2005 |
Acute vascular events and electrolytes variations in elderly patients.
Topics: Aged; Aging; Calcium; Chlorides; Electrolytes; Female; Glucose Intolerance; Glucose Tolerance Test; | 2006 |
Activation of a novel injury-induced calcium-permeable channel that plays a key role in causing extended neuronal depolarization and initiating neuronal death in excitotoxic neuronal injury.
Topics: 6-Cyano-7-nitroquinoxaline-2,3-dione; Animals; Animals, Newborn; Apoptosis; Calcium; Calcium Channel | 2007 |
Acetazolamide and enalapril combination offers complete protection from nitric oxide-deficient stroke in stroke-prone spontaneously hypertensive rats.
Topics: Acetazolamide; Angiotensin-Converting Enzyme Inhibitors; Animals; Barium Compounds; Blood Pressure; | 2000 |
Chloride-sensitive renal microangiopathy in the stroke-prone spontaneously hypertensive rat.
Topics: Animals; Bicarbonates; Blood Pressure; Chlorides; Creatinine; Disease Susceptibility; Hypertension; | 2001 |