Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 34,148 posts. Searching is done in the search box in upper left corner. I blog on anything to do with stroke. DO NOT DO ANYTHING SUGGESTED HERE AS I AM NOT MEDICALLY TRAINED, YOUR DOCTOR IS, LISTEN TO THEM. BUT I BET THEY DON'T KNOW HOW TO GET YOU 100% RECOVERED. I DON'T EITHER BUT HAVE PLENTY OF QUESTIONS FOR YOUR DOCTOR TO ANSWER.
Changing stroke rehab and research worldwide now.Time is Brain!trillions and trillions of neuronsthatDIEeach day because there areNOeffective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.
What this blog is for:
My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.
Showing posts with label intracranial atherosclerotic stenosis. Show all posts
Showing posts with label intracranial atherosclerotic stenosis. Show all posts
Why do 'association' research instead of EXACTLY PREVENTING this problem from occurring? Your mentors and senior researchers incompetently didn't tell you that stroke research is supposed to solve survivors problems?
1. No. 971 Hospital of the People's Liberation Army Navy, Qingdao, China
2. Department of Neurology, The 960(th) Hospital of Joint Logistics Support, PLA, Jinan, China
Abstract
Background and aim:
Intracranial arterial stenosis (ICAS) is a major cause of ischemic stroke in older adults and is associated with substantial risk of recurrent cerebrovascular events. Whether increasing ICAS severity confers incremental recurrence risk in medically treated elderly patients in routine clinical practice remains incompletely characterized. This study aimed to investigate the association between intracranial arterial stenosis severity and 12-month recurrent stroke risk in elderly patients with ischemic stroke.
Methods:
This single-center retrospective cohort study screened 614 consecutive patients aged 65 years or older who were admitted with acute ischemic stroke between January 2022 and December 2023. After predefined exclusions, 527 patients were included in the final analysis. Intracranial arterial stenosis was assessed using computed tomography angiography or magnetic resonance angiography and categorized as none-to-mild (<50%; including no stenosis), moderate (50–69%), or severe (≥70%) according to the highest-grade lesion. The primary outcome was recurrent ischemic stroke within 12 months. Univariable and multivariable logistic regression models were used to evaluate independent predictors of recurrence.
Results:
Among the 527 included patients, recurrent ischemic stroke occurred in 86 (16.3%) during 12-month follow-up. Recurrence rates increased stepwise across stenosis categories, occurring in 18/214 (8.4%) patients with none-to-mild stenosis, 29/173 (16.8%) with moderate stenosis, and 39/140 (27.9%) with severe stenosis (p < 0.001). After adjustment for age, sex, vascular risk factors, stroke subtype, baseline NIHSS score, and medication use, severe ICAS remained independently associated with recurrent stroke (adjusted OR 3.12, 95% CI 1.85–5.26, p < 0.001); moderate stenosis was also independently associated with recurrence (adjusted OR 1.96, 95% CI 1.04–3.69, p = 0.037).
Conclusion:
In elderly patients with ischemic stroke, greater intracranial arterial stenosis severity is independently associated with higher 12-month recurrence risk despite contemporary medical management. These findings support early vascular imaging and risk stratification in elderly patients with ischemic stroke.
1Department of Neurology, Zhongnan Hospital Affiliated to Wuhan University, Wuhan, Hubei, China
2Department of Neurology, Yiling Hospital of Yichang City, Yichang, Hubei, China
Objective: Moderate-to-severe stenosis has been identified as a significant risk factor for stroke recently. This study aims to investigate the relationship between non-traditional lipid parameters and the location and distribution of stenosis, as well as symptomatic events, in patients with moderate-to-severe intracranial atherosclerotic stenosis (ICAS) and extracranial atherosclerotic stenosis (ECAS).
Methods: This study analyzed correlation between non-traditional lipid parameters and moderate-to-severe ICAS and ECAS concerning stenosis location, distribution, and the presence or absence of symptoms. Logistic models and restricted spline analysis were utilized to explore the relationship between Castelli's risk index-II (CRI-II) and the occurrence of stroke events.
Results: The present study comprised 1,030 participants, of whom 143 were non-stenotic and 887 were patients with moderate-to-severe stenosis. The study focuses on the latter and indicated statistically significant differences in AIP, LCI, RC, AC, CRI-I, and CRI-II among the three groups of ICAS, ECAS, and combined ICAS and ECAS (P = 0.012, 0.005, 0.013, 0.009, 0.009, 0.032, respectively). Lipid parameters for ICAS were generally higher than those for ECAS. Remnant cholesterol (RC) exhibited a discrepancy among the anterior, posterior, and combined anterior and posterior circulation stenosis groups (P = 0.047). Logistic regression analysis revealed that CRI-II (Odds ratio [OR] = 1.20, Confidence interval [CI] 1.03–1.40, P = 0.009) and low-density lipoprotein cholesterol (LDL-c) (OR = 1.21, CI 1.03–1.42, P = 0.011) demonstrated remarkable elevations in symptomatic stenosis patients compared to patients without symptoms. After adjusting for potential confounding factors, CRI-II remained an independent risk factor for symptomatic stenosis. Furthermore, multivariate spline regression modeling elucidated that an augmented risk of stroke events in moderate-to-severe stenosis was associated with an elevated CRI-II. As CRI-II elevated, the risk of stroke events increased progressively.
Hemodynamic
impairment of blood pressure may play a crucial role in determining the
mechanisms of stroke in symptomatic intracranial atherosclerotic
stenosis). We aimed to elucidate this issue and assess the impacts of
modifications to blood pressure on hemodynamic impairment.
METHODS:
From
the Third China National Stroke Registry III, computed fluid dynamics
modeling was performed using the Newton-Krylov-Schwarz method in 339
patients with symptomatic intracranial atherosclerotic stenosis during
2015 to 2018. The major exposures were translesional systolic blood
pressure (SBP) drop and poststenotic mean arterial pressure (MAP), and
the major study outcomes were cortex-involved infarcts and
borderzone-involved infarcts, respectively. Multivariate logistic
regression models and the bootstrap resampling method were utilized,
adjusting for demographics and medical histories.
RESULTS:
In
all, 184 (54.3%) cortex-involved infarcts and 70 (20.6%)
borderzone-involved infarcts were identified. In multivariate logistic
model, the upper quartile of SBP drop correlated with increased
cortex-involved infarcts (odds ratio, 1.92 [95% CI, 1.03–3.57];
bootstrap analysis odds ratio, 2.07 [95% CI, 1.09–3.93]), and the lower
quartile of poststenotic MAP may correlate with increased
borderzone-involved infarcts (odds ratio, 2.07 [95% CI, 0.95–4.51];
bootstrap analysis odds ratio, 2.38 [95% CI, 1.04–5.45]). Restricted
cubic spline analysis revealed a consistent upward trajectory of the
relationship between translesional SBP drop and cortex-involved
infarcts, while a downward trajectory between poststenotic MAP and
borderzone-involved infarcts. SBP drop correlated with poststenotic MAP
negatively (rs=−0.765; P<0.001). In generating
hemodynamic impairment, simulating blood pressure modifications
suggested that ensuring adequate blood pressure to maintain sufficient
poststenotic MAP appears preferable to the reverse approach, due to the
prolonged plateau period in the association between the translesional
SBP drop and cortex-involved infarcts and the relatively short plateau
period characterizing the correlation between poststenotic MAP and
borderzone-involved infarcts.
CONCLUSIONS:
This
research elucidates the role of hemodynamic impairment of blood
pressure in symptomatic intracranial atherosclerotic stenosis-related
stroke mechanisms, underscoring the necessity to conduct hemodynamic
assessments when managing blood pressure in symptomatic intracranial
atherosclerotic stenosis.
See if your doctor is up-to-date on this, it has already been two months, easily long enough to know about new research in their specialty. Or, don't you have a functioning stroke doctor?
Symptomatic
intracranial atherosclerotic stenosis (sICAS), typically defined as an
ischemic stroke or transient ischemic attack associated with a proximal
50% to 99% stenosis of a relevant intracranial artery, is one of the
most common causes of ischemic stroke in the world.1 Non-ICAS strokes have a first-year recurrence rate of 5%,2 which is similar to the 1-year stroke rate in patients with asymptomatic severe ICAS.3 In clinical trials of sICAS, the 1-year recurrence rate has been ≈15%4,5 and varies based on patient features such as degree of stenosis or history of prior stroke.6,7 In real-world or enriched cohorts, it is even higher at 20% to 30% in the first year.8
Due to the high risk of recurrence, the randomized clinical trials
(RCTs) in ICAS populations have focused on secondary prevention. In this
article, we will review major RCTs in sICAS patients (Figure).
Figure.Timeline
of major randomized trials studying secondary prevention in individuals
with symptomatic intracranial atherosclerotic stenosis.
CAPTIVA indicates Comparison of Anti-Coagulation and Anti-Platelet
Therapies for Intracranial Vascular Atherostenosis; EC/DC,
extracranial/intracranial artery; RICA, Remote Ischemic Conditioning for
Avoiding Recurrence of Symptomatic Intracranial Atherosclerotic
Stenosis; SAMMPRIS, Stenting and Aggressive Medical Management for
Preventing Recurrent Stroke in Intracranial Stenosis; and WASID,
Warfarin Aspirin Symptomatic Intracranial Disease.
The
first RCT to include sICAS patients was the EC/IC Bypass Study
([International Cooperative Study of Extracranial/Intracranial
Anastomosis]; n=1377), which tested surgical anastomosis from the
superficial temporal artery to the middle cerebral artery among patients
with stroke due to extracranial carotid occlusion or ICAS.9
One-quarter of the cohort qualified for enrollment with proximal middle
cerebral artery stenosis or occlusion and, among those with ICAS, post
hoc analyses showed an excessive periprocedural risk of stroke and death
in the bypass group compared with the medical group, similar to the
trial as a whole. Over a decade later, the WASID (Warfarin Aspirin
Symptomatic Intracranial Disease; n=569) and subsequent SAMMPRIS
(Stenting and Aggressive Medical Management for Preventing Recurrent
Stroke in Intracranial Stenosis; n=451) RCTs studied therapeutic
approaches used in practice (warfarin anticoagulation in WASID and
angioplasty plus stenting in SAMMPRIS). Both studies changed the
practice by identifying excessive adverse events due to these
therapeutic approaches—hemorrhagic events in WASID and periprocedural
stroke in SAMMPRIS.4,5
Furthermore, in SAMMPRIS, even beyond the periprocedural period, there
was no benefit of stenting over medical therapy after a mean follow-up
of almost 3 years.10
SAMMPRIS was followed by 2 more angioplasty and stenting RCTs, VAST (Vertebral Artery Stenting Trial; n=115)11 and VISSIT ([Vitesse Intracranial Stent Study for Ischemic Stroke Therapy]; n=112).12
They also showed no benefit and, despite different stenting technology,
the same harmful periprocedural risk. Almost a decade later, the
results of another RCT, CASSIS ([China Angioplasty and Stenting for
Symptomatic Intracranial Severe Stenosis]; n=358), again showed no
benefit from stenting in a sICAS population selected to be at lower
procedural risk.13
The result of these RCTs is that intracranial stenting for stroke
prevention in sICAS is recommended only as an option of last resort in
treatment-refractory patients.14–16 The treatment of sICAS with angioplasty alone is still an active area of investigation.
Yet,
SAMMPRIS did establish a new paradigm for sICAS medical management.
Dual antiplatelet therapy (DAPT) with aspirin and clopidogrel was
required for the first 90 days in SAMMPRIS. While this DAPT combination
had demonstrated bleeding complications without clear benefit in the
SPS3 (Secondary Prevention of Small Subcortical Strokes) and MATCH
(Management of Atherothrombosis with Clopidogrel in High-Risk Patients)
trials,17,18
the lower than expected stroke rate in SAMMPRIS medical participants
receiving DAPT led to guideline endorsement for DAPT for at least 90
days in sICAS.14–16
SAMMPRIS also changed practice as the first stroke prevention trial to
implement multimodal, protocol-driven intensive risk factor management
and healthy lifestyle coaching. The impact from the vascular risk factor
management approach used in SAMMPRIS, including targeted blood pressure
and cholesterol management and lifestyle counseling, along with
findings from other risk factor analyses of trials that included sICAS
patients, demonstrated the importance of thinking beyond antithrombotic
medications for stroke prevention.14–16,19
Preliminary studies of remote ischemic conditioning suggested benefit in sICAS patients for stroke prevention,20 potentially mediated by improved distal organ perfusion and lowering of systemic inflammation.21
This led to the RICA (Remote Ischemic Conditioning for Avoiding
Recurrence of Symptomatic Intracranial Atherosclerotic Stenosis) RCT
(n=3033),22
the largest sICAS secondary prevention trial to date. RICA was a
sham-controlled RCT of a remote ischemic conditioning device placed on
the upper arm for 45 min a day for over a year. Unfortunately, in both
study groups of RICA, over 50% of participants had low compliance with
the study protocol. The intervention appeared to numerically reduce
recurrent strokes, particularly in the per-protocol analysis, but the
results were not consistent with a meaningful treatment effect.
The
largest current ongoing RCT in sICAS patients is CAPTIVA (Comparison of
Anti-Coagulation and Anti-Platelet Therapies for Intracranial Vascular
Atherostenosis),23
which is a 3-arm, double-blind phase III trial comparing different
antithrombotic combinations. CAPTIVA will randomize up to 1683 subjects
with severe sICAS and recent stroke to 1 year of aspirin 81 mg combined
with (1) ticagrelor (90 mg BID), (2) low-dose rivaroxaban (2.5 mg BID),
or (3) clopidogrel (75 mg daily). All subjects will receive aggressive
vascular risk factor management and the superior CAPTIVA arm at the end
of the trial will likely set the new standard for sICAS secondary
prevention.
Despite some progress in sICAS medical treatment over
the years, the risk of stroke recurrence remains excessively high for
symptomatic patients with severe stenosis. Prior studies have shown that
the selection of low-risk patients with sICAS for therapeutic trials
can improve adverse outcome rates but does not result in the
practice-changing studies that are urgently needed.24
Prioritized research areas for sICAS include exploring novel
lipid-lowering therapies; anti-inflammatory medications; better
understanding the interplay between plaque morphology, local and distal
perfusion, and the success of treatment strategies; identifying genetic
variants and surrogate markers that can inform new treatments and refine
patient selection for future trials; improved revascularization
technologies or techniques; and implementation science trials to
pragmatically increase adherence to risk factor control. Although there
is a wealth of research opportunities on the horizon, sICAS therapeutic
trials must remain rigorous and focused on selecting patients at the
highest risk of recurrent stroke who most need these novel treatments.
Predictors
of recurrent stroke after endovascular treatment for symptomatic
intracranial atherosclerotic stenosis (ICAS) remain uncertain.
Objectives:
Among
baseline characteristics, lesion features, and cerebral perfusion
changes, we try to explore which factors are associated with the risk of
recurrent stroke in symptomatic ICAS after endovascular treatment.
Design:
Consecutive
patients with symptomatic ICAS of 70–99% receiving endovascular
treatment were enrolled. All patients underwent whole-brain computer
tomography perfusion (CTP) within 3 days before and 3 days after the
endovascular treatment. Baseline characteristics, lesion features, and
cerebral perfusion changes were collected.
Methods:
Cerebral
perfusion changes were evaluated with RAPID software and calculated as
preprocedural cerebral blood flow (CBF) < 30%, time to maximum of the
residue function (Tmax) > 6 s, and Tmax > 4 s volumes minus
postprocedural. Cerebral perfusion changes were divided into
periprocedural perfusion improvement (>0 ml) and non-improvement
(⩽ 0 ml). Recurrent stroke within 180 days was collected. The Cox
proportional hazards analysis analyses were performed to evaluate
factors associated with recurrent stroke.
Results:
From
March 2021 to December 2021, 107 patients with symptomatic ICAS were
enrolled. Of the 107 enrolled patients, 30 (28.0%) patients underwent
balloon angioplasty alone and 77 patients (72.0%) underwent stenting.
The perioperative complications occurred in three patients. Among
CBF < 30%, Tmax > 6 s, and Tmax > 4 s volumes, Tmax > 4 s
volume was available to evaluate cerebral perfusion changes.
Periprocedural perfusion improvement was found in 77 patients (72.0%)
and non-improvement in 30 patients (28.0%). Nine patients (8.4%)
suffered from recurrent stroke in 180-day follow-up. In Cox proportional
hazards analysis adjusted for age and sex, perfusion non-improvement
was associated with recurrent stroke [hazards ratio (HR): 4.472; 95% CI:
1.069–18.718; p = 0.040].
Conclusion:
In
patients with symptomatic ICAS treated with endovascular treatment,
recurrent stroke may be related to periprocedural cerebral perfusion
non-improvement.
Intracranial atherosclerotic stenosis (ICAS) is one of the most common causes of ischemic stroke worldwide.1–3
Patients with 70–99% symptomatic ICAS are at high risk of recurrent
stroke (12.2%) at 1 year despite aggressive medical management (AMM),4 and especially higher (37%) in those patients with impaired hemodynamics.5 Endovascular treatment remains an alternative therapy for patients with symptomatic ICAS refractory to AMM.6–8
In two recent multiple registries focusing on endovascular treatment
for symptomatic ICAS, the 1-year recurrent stroke declined to 6.3% and
8.5% compared with 20% in Stenting Versus Aggressive Medical Therapy for
Intracranial Atherosclerosis (SAMMPRIS) trial.9,10
So
far, the predictors of the risk of recurrent stroke after endovascular
treatment for symptomatic ICAS remain uncertain. We hypothesize that
some baseline characteristics, lesion features, or cerebral perfusion
parameters (preprocedural, postprocedural, or periprocedural changes)
might be related to the risk of recurrent stroke after endovascular
treatment. As for the evaluation of cerebral perfusion parameters, RAPID
software (iSchemia View) which is an automatic software for
post-processing computer tomography perfusion (CTP) images can
quantitatively evaluate cerebral perfusion parameters, and it had been
used to identify potential beneficiary with acute large vessel occlusion
through endovascular thrombectomy.11,12 Furthermore, RAPID software was used to assess impaired perfusion for patients with ICAS.13
In
this study, we collected baseline characteristics, lesion features, and
preprocedural and postprocedural cerebral perfusion parameters of
patients with symptomatic ICAS treated with endovascular therapy in a
high-volume stroke center and evaluated which factors were associated
with the 180-day outcome of recurrent stroke.
Intracranial atherosclerotic stenosis (ICAS) is one of the most frequent causes of
stroke worldwide and confers one of the greatest risks of recurrent stroke compared
with other causes of stroke. Asymptomatic ICAS is increasingly recognised as a risk
factor for silent brain infarctions and dementia, magnifying the global burden of
ICAS. Although ICAS is a lumen-based diagnosis, newer diagnostic imaging techniques,
such as high-resolution MRI, might help to identify high-risk population subgroups
to test interventions that might reduce the risk of stroke recurrence. Secondary stroke
prevention in patients with ICAS currently consists of intensive management of modifiable
risk factors and dual antiplatelet therapy, which is subsequently reduced to aspirin
alone. Despite these therapies, the risk of recurrent stroke in patients presenting
with stroke related to 70–99% ICAS exceeds 20% at 1 year; as such, better therapies
are urgently needed. The optimal duration and combination of dual antiplatelet therapy
in patients with ICAS is uncertain and is being investigated in addition to low-dose
anticoagulation and aspirin. Other ongoing or planned studies will provide high-quality
observational data on the role of transluminal angioplasty and stenting, submaximal
balloon angioplasty alone, direct or indirect arterial bypass, and ischaemic conditioning
for prevention of stroke in patients with ICAS.
Department of Interventional Neuroradiology, Beijing Tiantan Hospital, Capital Medical University, Beijing, China
Background: For patients with
symptomatic intracranial artery stenosis (sICAS), endovascular treatment
has been shown to be feasible and safe in recent studies. However,
in-stent restenosis (ISR) risks the recurrence of ischemic stroke. We
attempt to elucidate the risk factors for ISR.
Methods: We retrospectively analyzed 97
patients with sICAS from a prospective registry trial that included 20
centers from September 2013 to January 2015. Cases were classified into
the ISR≥ 50% group or the ISR < 50% group. The baseline
characteristics and long-term follow-up were compared between the two
groups. Binary logistic regression analyses were identified as an
association between ISR and endovascular technique factors.
Results: According to whether ISR was detected by CT angiography, 97 patients were divided into the ISR group (n = 24) and the non-ISR group (n
= 73). The admission baseline features and lesion angiography
characteristics were similar, while plasma hs-CRP (mg/L) was higher in
the ISR≥ 50% group at admission (8.2 ± 11.4 vs. 2.8 ± 4.1, p = 0.032). Binary logistic regression analysis identified the longer stents (adjusted OR 0.816, 95% CI 0.699–0.953; p = 0.010), balloon-mounted stents (adjusted OR 5.748, 95% CI 1.533–21.546; p = 0.009), and local anesthesia (adjusted OR 6.000, 95% CI 1.693–21.262; p = 0.006) as predictors of ISR at the 1-year follow-up.
Conclusions: The longer stents,
balloon-mounted stents implanted in the intracranial vertebral or
basilar artery, and local anesthesia were significantly associated with
in-stent restenosis. Further studies are required to identify accurate
biomarkers or image markers associated with ISR in ICAS patients.
The prevalence of intracranial atherosclerotic stenosis
(ICAS) in Chinese patients was up to 46.6% in symptomatic ischemic
stroke patients (1). Symptomatic ICAS (sICAS) is associated with recurrent ischemic stroke (2).
SAMMPRIS and VISSIT trials have shown that aggressive medical
management has been more effective and safer than endovascular therapy
in the past decade (3, 4).
However, a recent Wingspan Stent System Post Market Surveillance Study
(WEAVE) indicated that the perioperative complication rate is quite low
for on-label patients (2.6%). Patients enrolled in this study, including
patients with symptomatic and severe ICAS lesions, had suffered at
least two ischemic strokes (5). It is obvious that patients with sICAS who failed the best medical treatment would benefit from endovascular therapy.
As we reported, the 30-days rate of primary endpoints,
including stroke, transient ischemic attack, and death, was 4.3% in a
multicenter prospective registry study of stenting for sICAS in China (6).
The incidence of the composite endpoint in this study at 1 year was
8.1%, and restenosis ≥50% was found in 27.6% of patients at the
12-months follow-up. Although the majority of patients (78.9%) were
asymptomatic (7),
restenosis would be a risk factor for ischemic stroke, causing acute
large vessel occlusion or transient ischemic attack (TIA) (2).
Therefore, in the present study, according to the inflammatory index
(hs-CRP), features of the lesion in angiography, and characteristics of
the stent in the operation procedure, we aimed to identify risk factors
for in-stent restenosis of endovascular treatment in intracranial
atherosclerotic stenosis in a 12-months follow-up.
Annals of Neurology — Leng X, et al. | April 11, 2019
Advertisement
Using a computational fluid dynamics
model, researchers ascertained if hemodynamic characteristics of
symptomatic intracranial atherosclerotic stenosis (sICAS) are correlated
with the risk of stroke relapse. The study sample consisted of 245
patients with acute ischemic stroke attributed to 50% to 99% ICAS, which
was confirmed by computed tomographic angiography. Investigators found
that the risk of recurrent ischemic stroke in the same territory was
significantly higher for patients with both low-pressure ratio
(PR=pressurepoststenotic/pressureprestenotic) and high wall shear stress ratio (WSSR=WSSstenotic − throat/WSSprestenotic)
vs those with normal PR and WSSR. This investigation represents a step
forward in the study of intracranial atherosclerotic disease through the
use of computational flow simulation techniques, showing a sICAS
hemodynamic pattern that is more susceptible to stroke relapse and
supporting hypoperfusion and artery-to-artery embolism as common
ischemic stroke mechanisms in such patients.
Yin Fei Huang
Zhen Xing Liu
Kuan Cen1
Ren Wei Zhang
Yu Xie
Yu Min Liu
Xu Guo
Ning Ma, 
Zhong-Rong Miao
