Block Blood Supply Research Articles

Silent Stroke -a Drag on Quality of Life

A stroke is a condition because of something blocking blood supply to part of the brain or when a blood vessel in the brain bursts disrupting the blood supply to a particular portion of the brain. In either case, parts of the brain become damaged or die, manifesting as lasting brain damage, long-term disability, or even death. Symptoms include dizziness, numbness, weakness on one side of the body, and problems with talking, writing, or understanding language. Most of us have heard or seen of a case of a stroke, with symptoms like slurred speech, loss of balance, difficulty speaking, and so on - but not many know that one can have a stroke without even knowing it? known as a silent stroke or Mini-stroke or asymptomatic cerebral infarction. A silent stroke refers to a stroke that doesn't cause any noticeable symptoms. It is recognized by a brain (CT scan or an MRI) imaging that will show white spots or lesions where your brain cells have stopped functioning. Brain scans can detect one or multiple silent strokes. Most silent strokes are caused by a clot that blocks a blood vessel in the brain. The blockage prevents blood and oxygen from reaching that area, causing nearby brain cells to die. While in the middle-aged people with no apparent signs of stroke about 10% have brain damage from one and this rate increases to 25% among people over 80 years. The damage that happens is permanent, but therapy might help stimulate other parts of the brain so you regain abilities that may have weakened. Common Silent Stroke Symptoms include sudden lack of balance, temporary loss of basic muscle movement slight memory loss and sudden changes in mood or personality and issues with cognitive skills and ability. As different parts of our brain control different parts of our body, our symptoms will depend on the part of our brain affected and the extent of the damage but usually begin suddenly. Therefore, it is critical to seek diagnosis and treatment as soon as possible. The chances of getting a stroke go up among elderly, diabetes, hypertensives, persons with heart disease, vascular disease, or atrial fibrillation. The management of silent strokes involves prescribing medications for blood thinning, to lower blood pressure, blood sugar, and serum cholesterol medications to lower low-density lipoprotein (LDL) cholesterol. The significant burden of stroke on the mortality rates in India, is well-documented, but robust data regarding the aggregates of evidence on the quality of life (QOL) of stroke survivors is limited. Therefore, it is critical to seek diagnosis and treatment as soon as possible. Material & Methods: This manuscript is based on a real case study in last 15 months. Chidambar a male of 70 years with history of Diabetes for over 15 years and Hypertension for 10 years, both poorly controlled. He had left sided hemiparesis following a stroke in January 2022, that resulted in left sided hemiparesis, speech, and cognitive signs. Since early 2023 he is suffering frequent falls, vomiting, urinary incontinence, changing moods and worsening memory and dementia indicative recurrent silent strokes, that have worsened his quality of life. Review of literature and published articles have added value to this article.

Smart "Thrombus": Self-Localizing UCST-Type Microcage.

Embolization is often used to block blood supply for controlling the growth of fibroids and malignant tumors, but limited by embolic agents lacking spontaneous targeting and post-treatment removal. So we first adopted nonionic poly(acrylamide-co-acrylonitrile) with an upper critical solution temperature (UCST) to build up self-localizing microcages by inverse emulsification. The results showed that these UCST-type microcages behaved with the appropriate phase-transition threshold value around 40 °C, and spontaneously underwent an expansion-fusion-fission cycle under the stimulus of mild temperature hyperthermia. Given the simultaneous local release of cargoes, this simple but smart microcage is expected to act as a multifunctional embolic agent for tumorous starving therapy, tumor chemotherapy, and imaging.

One-step fabrication of lidocaine/CalliSpheres® composites for painless transcatheter arterial embolization

BackgroundTranscatheter arterial embolization (TAE) is one of the first-line treatments for advanced hepatocellular cancer. The pain caused by TAE is a stark complication, which remains to be prevented by biomedical engineering methods.MethodsHerein, a commercial embolic agent CalliSpheres® bead (CB) was functionally modified with lidocaine (Lid) using an electrostatic self-assembly technique. The products were coded as CB/Lid-n (n = 0, 5, 10, corresponding to the relative content of Lid). The chemical compositions, morphology, drug-loading, and drug-releasing ability of CB/Lid-n were comprehensively investigated. The biocompatibility was determined by hemolysis assay, live/dead cell staining assay, CCK8 assay, immunofluorescence (IHC) staining assay and quantitative real-time PCR. The thermal withdrawal latency (TWL) and edema ratio (ER) were performed to evaluate the analgesia of CB/Lid-n using a plantar inflammation model. A series of histological staining, including immunohistochemistry (IL-6, IL-10, TGF-β and Navi1.7) and TUNEL were conducted to reveal the underlying mechanism of anti-tumor effect of CB/Lid-n on a VX2-tumor bearing model.ResultsLid was successfully loaded onto the surface of CalliSpheres® bead, and the average diameter of CalliSpheres® bead increased along with the dosage of Lid. CB/Lid-n exhibited desirable drug-loading ratio, drug-embedding ratio, and sustained drug-release capability. CB/Lid-n had mild toxicity towards L929 cells, while triggered no obvious hemolysis. Furthermore, CB/Lid-n could improve the carrageenan-induced inflammation response micro-environment in vivo and in vitro. We found that CB/Lid-10 could selectively kill tumor by blocking blood supply, inhibiting cell proliferation, and promoting cell apoptosis. CB/Lid-10 could also release Lid to relieve post-operative pain, mainly by remodeling the harsh inflammation micro-environment (IME).ConclusionsIn summary, CB/Lid-10 has relatively good biocompatibility and bioactivity, and it can serve as a promising candidate for painless transcatheter arterial embolization.

Investigation of Changes in Dental Pulp Tissue in Rats with Bilateral Ovariectomy by Histopathological Methods

In this study, we aimed to investigate the histopathological changes on 14th and 28th days in the dental pulp of ovariectomized rats. Twenty 12-week-old 21 female Sprague Dawleys were divided into 3 groups. Group 1: No procedure was applied to the animals. All teeth were excised at the end of the experiment (at the 14th day of experiment). Group 2: The abdomen was opened and the ovary tied with 3/0 silk sutures to block blood supply. The ovaries were placed in its original position. Teeth of ovariectomized rats were excised at the 14th day of experiment. Group 3: Similar procedure was applied as in Group 2. The teeth were removed on 28th days of experiment. The dental tissues taken after the experiment were processed for routine paraffin wax tissue preparation. Hematoxylin-Eosin staining was applied to sections of 4 μm thickness. As a result, when compared to the dental pulp of control group, degenerated dental pulp tissue, vascular dilatation and pyknotic osteoblast cells were observed in ovariectomized rats, however the pathological intesity was higher in ovariectomized rats for 28 days than ovariectomized rats for 14 days.

Circular suture of the uterine serosa and myometrium layer around placental attachment site for refractory postpartum hemorrhage.

The aim of the study was to analyze the clinical outcomes of circular suture at placental attachment site for refractory postpartum hemorrhage (PPH), which could block blood supply of the serosa and myometrium layer. Eighty cases of refractory PPH were enrolled and retrospective analyzed in this study for further analysis from a consecutive single center database between 2010 and 2018. After undergoing circular suture of the uterine serosa and myometrium layer around placental attachment site, surgical and perioperative outcomes were recorded and analyzed. Among all the patients enrolled, 28 cases (35.0%) of refractory PPH were mainly caused by uterine inertia, 36 cases (45.0%) caused by ectopic placenta, and 2 cases (2.5%) caused by coagulation disorders. After circular suture of the uterine serosa and myometrium layer at placental attachment site, all the uterine active bleeding was controlled below 40 ml without recurrence. The perioperative results were similar between the vaginal and cesarean sections groups. Circular suture of the uterine serosa and myometrium at the placental attachment site could control refractory PPH with few postoperative complications. Circular suture around placenta site could be applied in time to protect the endometrium even in primary hospital.

Studying of cyp2c19*2, *3 and *17 polymorphism in Vietnamese patients with coronary artery disease

Coronary artery disease is the most common type of cardiovascular disease, due to the accumulation of atherosclerotic plaque inside the arterial wall which leads to block blood supply to the heart muscle. A number of clinical trials have demonstrated that Clopidogrel is able to inhibit platelet aggregation in patients with acute coronary syndromes, reduce mortality and cardiovascular events. However, the antiplatelet effectiveness of Clopidogrel significantly depends on CYP2C19 genotypes. Therefore, the aim of this study was to identify the CYP2C19*2, *3 and allele frequencies in Vietnamese coronary artery patients by using PCR-RFLP method. Total genomic DNA were extracted from peripheral blood of 96 patients diagnosed with coronary artery disease. Thereafter, single nucleotide polymorphism sites in the CYP2C19 gene were identified by PCR with specific primers. The amplified products were then digested by restriction enzymes SmaI, BamHI, and MnlI, respectively. The results showed that the proportion of heterozygous individuals for CYP2C19*2 (c. 681G>A, rs4244285), CYP2C19*3 (c. 636G>A, rs4986893), and CYP2C19*17 (g. -3402C>T, rs11188072) accounted for 39.58%, 6.25%, and 2.08%, respectively. Among 96 subjects, 41.67% of patients were predicted for intermediate metabolic phenotype CYP2C19*1/*2 (37.50%) and CYP2C19*1/*3 (4.17%). Approximately 10.42% of total patients represented poor metabolizers in which 8.34% had two copies of the same allele *2/*2 and 2.08% had *2/*3 genotype. Particularly, two individuals (2.08%) detected with CYP2C19*1/*17 genotype were able to increase CYP2C19 activity (ultrarapid metabolizers). The results of this study generate a foundation for introducing individualized antiplatelet therapy in Vietnam based on genetic testing.

Computational simulations of thrombolysis in acute stroke: Effect of clot size and location on recanalisation

Acute ischaemic stroke can be treated by intravenous thrombolysis whereby tissue plasminogen activator (tPA) is infused to dissolve clots that block blood supply to the brain. In this study, we aim to examine the influence of clot location and size on lysis pattern and recanalisation by using a recently developed computational modelling framework for thrombolysis under physiological flow conditions. An image-based patient-specific model is reconstructed which consists of the internal carotid bifurcation with the A1 segment of anterior cerebral arteries and M1 segment of middle cerebral arteries, and the M1 bifurcation containing the M2 segments. By varying the clot size and location, 7 scenarios are simulated mimicking thrombolysis of M1 and M2 occlusions. Our results show that initial breakthrough always occurs along the inner curvature of the occluded cerebral artery, due to prolonged tPA residence time in the recirculation zone. For a given occlusion site, lysis completion time appears to increase almost quadratically with the initial clot volume; whereas for a given clot volume, the simulated M2 occlusions take up to 30% longer for complete lysis compared to the corresponding M1 occlusions.

Giant Left Atrial Myxoma Masquerading as Cough-Syncope Syndrome.

Left atrial myxomas are the most common type of benign primary cardiac tumor. Patients can present with generalized symptoms, such as fatigue, symptoms from obstruction of the myxoma, or even embolization of the myxoma causing distal thrombosis. We describe a case with several-month duration of syncopal episodes that occurred after coughing and with exertion. Computed tomography of the chest showed a 6.1 cm by 4.5 cm mass in the left atrium, later evaluated with an echocardiogram. Cardiothoracic surgery removed the mass, and it was determined to be an atrial myxoma. It is important for an internist to be able to diagnose an atrial myxoma because of the risks associated with embolization and even sudden death as myxoma can block blood supply from atrium to ventricle.

Water-Borne Endovascular Embolics Inspired by the Undersea Adhesive of Marine Sandcastle Worms.

Transcatheter embolization is used to treat vascular malformations and defects, to control bleeding, and to selectively block blood supply to tissues. Liquid embolics are used for small vessel embolization that require distal penetration. Current liquid embolic agents have serious drawbacks, mostly centered around poor handling characteristics and toxicity. In this work, a water-borne in situ setting liquid embolic agent is described that is based on electrostatically condensed, oppositely charged polyelectrolytes-complex coacervates. At high ionic strengths, the embolic coacervates are injectable fluids that can be delivered through long narrow microcatheters. At physiological ionic strength, the embolic coacervates transition into a nonflowing solid morphology. Transcatheter embolization of rabbit renal arteries demonstrated capillary level penetration, homogeneous occlusion, and 100% devascularization of the kidney, without the embolic crossing into venous circulation. The benign water-borne composition and setting mechanism avoids many of the problems of current liquid embolics, and provides precise temporal and spatial control during endovascular embolization.

Protective role of Ursodeoxycholyl Lysophosphatidylethanolamide during hepatic ischemia and reperfusion injury in mice

Introduction: Ischemia and reperfusion (I/R) injury of the liver which may occur during liver transplantation can cause severe complications leading to transplantation failure. We have designed cytoprotective agent ursodeoxycholyl lysophosphatidylethanolamide (UDCA-LPE), which has been shown to be protective in ameliorating apoptosis and inflammation in acute and chronic liver injury models, such as, endotoxic shock and feeding with high-fat diet. This study is aimed to explore whether UDCA-LPE can also serve as a protective agent against hepatic I/R injury in mice. Methods: Ischemia in C57/BL6 mice was introduced by blocking blood supply to middle and left liver lobes for 90 min, and reperfusion was allowed for 2h causing I/R injury in 75% of the liver. Four groups were studied, i.e., sham, I/R for 2h (IR), UDCA-LPE1 and UDCA-LPE2. UDCA-LPE1 represented intraperitoneal (i.p.) injection with 100 mg/kg UDCA-LPE 30 min prior to ischemia induction. UDCA-LPE2 represented two i.p. injections of 50 mg/kg UDCA-LPE at 30 min prior to ischemia and just prior to reperfusion. Liver injury was assessed by liver enzyme activities, hepatic mRNA expression of inflammatory genes, apoptosis protein expression by Western Blot, and histological evaluation. Results: I/R under our experimental protocol caused significant liver injury compared with sham. I/R increased serum transaminase activities (ALT, AST, LDH) which were decreased by UDCA-LPE treatment (ALT: 215.2 ± 40.5 U/L for IR; 130.3 ± 22.4 U/L for UDCA-LPE1; 91.3 ± 37.1 U/L for UDCA-LPE2, n = 9). I/R caused increased hepatic expression of inflammatory TNF-α, IL-6, IL-1β, MCP-1 mRNA as well as apoptosis cleaved caspase-3 and PARP-1 proteins. This elevation was inhibited by UDCA-LPE treatment with UDCA-LPE2 being better than UDCA-LPE1. Histology revealed that I/R caused significant hepatic necrosis, and increased immunohistochemical staining of MCP-1 receptor (CCR2) and cleaved caspase-3. UDCA-LPE treatment, particularly UDCA-LPE2, significantly improved these histological abnormalities to the sham levels. Conclusions: UDCA-LPE was a hepatoprotectant in attenuating liver injury induced by I/R in mice. Multiple dosages of UDCA-LPE given during I/R were more effective than a single pre-I/R dose. Thus, UDCA-LPE may be of therapeutic use in a liver transplantation setting.

Pretreatment with interleukin-33 reduces warm hepatic ischemia/reperfusion injury in mice

Background Interleukin (IL)-33 is a recently identified member of the IL-1 family that binds to the receptor, ST2L. This study examined IL-33 production in mouse liver and investigated its role in hepatic ischemia/reperfusion (I/R) injury. Methods Male BALB/c mice ((22±3) g) were subjected to 90 minutes partial hepatic ischemia, followed by 6 hours reperfusion. First, mice were randomized into two groups: control group (laparotomy only, without blocking blood supply) and ischemia model group. IL-33 mRNA and serum protein levels were measured at 30, 60, 90 minutes after ischemia and 2 and 6 hours after reperfusion. Second, mice were randomized into four groups: control, model (injection of rabbit IgG polyclonal antibody), recombinant IL-33 intervention and anti-ST2L antibody intervention group. Mice were sacrificed 6 hours after reperfusion. Liver pathology was observed via transmission electron microscopy. Serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), IL-4, IL-5, IL-13, interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α) levels were measured. Results Levels of IL-33 mRNA and protein did not change during ischemia (P >0.05) but increased significantly during reperfusion (P <0.05). After reperfusion for 6 hours, serum levels of ALT, AST, IL-4, IL-5, IL-13, IFN-γ and TNF-α were significantly increased (P <0.05), and hepatocellular ultrastructure was damaged. Pretreatment with IL-33 attenuated severity of liver damage compared with controls, but pretreatment with anti-ST2L antibody increased severity. Serum levels of IL-4, IL-5 and IL-13 protein increased whereas IFN-γ decreased following IL-33 pretreatment. Pretreatment with anti-ST2L antibody significantly decreased serum IL-4, IL-5, IL-13 levels and increased serum IFN-γ levels compared with controls (P <0.05). There was no change in the level of TNF-α. Conclusion IL-33 is produced systematically and locally in liver during I/R injury. Pretreatment with IL-33 is therapeutic for hepatic I/R injury, possibly via inducing a Th1 to Th2 shift.

Density of microvessels positive for CD105 (endoglin) is related to prognosis in meningiomas

Microvessel density (MVD) is considered to be a prognostic marker in many tumours. Nevertheless, conflicting results were achieved regarding its prognostic role in meningiomas when it was quantified through pan-endothelial markers such as CD34, CD31 or Factor VIII. In the present study, MVD was assessed in meningiomas through the specific marker for neo-angiogenesis CD105. Fifty-four formalin fixed, paraffin embedded, surgical cases of meningiomas (WHO 28 grade I and 26 grade II) as well as ten normal leptomeningeal samples were submitted to immunohistochemical analysis for CD105. CD34 immuno-expression was also evaluated on consecutive parallel sections. For each case, MVD was estimated in terms of number of vessels/mm(2). CD105 was not evidenced in normal samples, whereas it was demonstrated in the vessels within 14/28 WHO grade I cases and within 24/26 WHO grade II meningiomas. On the contrary, CD34 antibody stained blood vessels in both normal and neoplastic samples; moreover, in each case, it stained more microvessels than CD105 antibody (25.33 +/- 21.16 vs. 50.72 +/- 26.75). Higher CD105 counts were significantly correlated with higher histological grade and Ki-67 LI > 4%. No statistical significant correlations were encountered between MVD measured by either CD105 and CD34 and sex, age, site of tumour or extent of surgical resection. CD105-MVD, but not CD34-MVD, showed an inverse significant correlation with overall survival and recurrence-free survival. In conclusion, our study suggests the higher specificity of CD105 in comparison to pan-endothelial markers in the evaluation of meningioma neo-angiogenesis, and its higher prognostic significance. CD105 might serve as a target for therapeutic approaches blocking blood supply in meningiomas.

Polymer used to block blood supply to tumors

A synthetic rubber that can be deposited as minute particles in capillaries to block the blood supply—and thus the growth—of solid tumors has been developed by chemists at the Swiss Federal Institute of Technology, Zurich. The polyurethane resin is soluble in ethanol but insoluble in water. Physicians deliver the ethanolic solution of the resin through a catheter threaded along the patient's arteries to the site of the tumor. Tissue fluids then precipitate the elastomer as particles that are less than 10 μm in diameter. The particles lodge in the capillaries supplying the tumor with blood, thus starving it. Iodine atoms along the polymer chain make the resin visible in x-rays, so doctors can guide the solution-bearing catheter to the site. The resin hydrolyzes after a month, leaving no residue. Polymer science professor Ulrich W. Suter and organic chemistry professor Peter Neuenschwander make the polyurethane by reaction of 2,2,4-trimethylhexane 1,6-diisocyanate, tetramethylene glycol, and the 1-glyceryl ...

Human copper-zinc superoxide dismutase transgenic mice are highly resistant to reperfusion injury after focal cerebral ischemia.

We have demonstrated in a previous study that superoxide radicals play a role in the pathogenesis of cerebral infarction, using a transgenic mouse model of distal middle cerebral artery occlusion, permanent ipsilateral cerebral carotid artery occlusion, and 1-hour contralateral cerebral carotid artery occlusion that produced infarction only in the cortex. However, the role of superoxide radicals in reperfusion injury in transgenic mice overexpressing superoxide dismutase (SOD) is unknown. Using a mouse model of intraluminal blockade of middle cerebral artery that produced both cortical and striatal infarction, we now further examined the role of superoxide radicals in ischemic cerebral infarction after reperfusion in transgenic mice overexpressing human CuZn-SOD activity. Transgenic mice of strain Tg HS/SF-218, carrying human SOD-1 genes, and nontransgenic littermates were anesthetized with chloral hydrate (350 mg/kg IP) and xylazine (4 mg/kg IP). Physiological parameters were maintained at a normal range using a 30% O2/70% N2O gas mixture inserted via an inhalation mask. Body temperature was maintained at 37 +/- 0.5 degrees C by using a heating pad throughout the studies. The middle cerebral artery occlusion was achieved with a 5-0 rounded nylon suture placed within the internal cerebral artery for 3 hours followed by the removal of the suture to allow reperfusion for another 3 hours. Cerebral infarct size in brain slices and infarct volume, neurological deficit, cortical blood flow, and glutathione levels were measured in both transgenic and nontransgenic mice. Compared with the nontransgenic mice, the infarcted areas were significantly decreased in coronal slices from transgenic mice. The infarct volume (in cubic millimeters) was reduced by 26% in transgenic mice after ischemia and reperfusion. This decrease in the infarct volume in transgenic mice closely paralleled the reduced neurological deficits. Introduction of the suture to block blood supply to the middle cerebral artery territory produced a rapid decrease in the relative surface blood flow in the ipsilateral core and the peri-ischemic (penumbra) areas. There were no significant differences in the local cerebral blood flow in the ischemic core or the penumbra areas between the transgenic and nontransgenic groups. However, the level of reduced glutathione in the penumbra area was significantly higher in transgenic mice than in nontransgenic mice, whereas there was no difference in the reduced glutathione levels in the ischemic core between these two groups. Our study demonstrated that superoxide radicals play a major role in the pathogenesis of cerebral infarction in reperfusion injury after a focal stroke. The reduction in infarct volume and neurological deficits is not dependent on the changes in cerebral blood flow but rather correlate with reduced oxidative stress in the ischemic brain tissue, which was indicated by the relatively high levels of endogenous reduced glutathione in transgenic mice.