Arteries - Science topic

Dr. He, the metabolism of the biomarkers of neurodegeneration and the impact of hepatic and renal dysfunctions seem to have been little explored. What about

Suhocki PV, Doraiswamy PM. Cerebral venous biomarkers and veno-arterial gradients: untapped resources in Alzheimer’s disease. Front Neurol 04 January 2023; 14.  https://doi.org/10.3389/fneur.2023.1295122 ...

or exploring diagnostic links to

Herndon RM, Johnson M. A method for the electron microscopic study of cerebrospinal fluid sediment. J Neuropathol Exp Neurol. 1970 Apr;29(2):320-30?

Rica Ederim. İyi günler

Ahmed G. Rahma Can you share your .stl file?

I'm interested in research that complements yours, looking at the mechanism of vessel ageing as a function of the force exerted by the stent. This involves characterising the ageing of the vessel and taking into account the characteristics of the blood: pH, viscosity, etc. We would then have a physico-chemical method to calculate the characteristics of the stent adapted to the vessel. This calculation has not yet been validated for biomaterials. IF you are interested in this idea, please contact me.

thanks

an alternative explanation as to effectively treat the systemic arterial hypertension , specially in regards to RITA grafted to RCA

Damini Singh

you are welcome,

Also try to post a snapshoot of the mechanical mesh, because sometime, it's better to modify the surfaces using the virtual topology before performing the meshing, which sometime in the interacted surfaces the lowest quality elements.

Dear Nimra Saleem

I feel you should go for organoids as it is one of the upcoming areas since it holds great potential as a tool to study a wide range of subjects, including developmental biology, disease pathology, cell biology, regenerative mechanisms, precision medicine, drug toxicity and efficacy testing. Patient-derived organoid cultures can serve as valuable diagnostic tools in precision medicine applications.

Organoids derived from patient samples can be used to screen patient drug responses in vitro before administering treatment to direct care and predict therapeutic outcomes.

You may grow patient-derived organoid in the laboratory and subject them to different types of treatments. The response of patient-derived organoids to treatment could predict the response of the corresponding patient. You may make use of such test to select the best drug for individual patient.

Wish you success, and have a great and exciting journey!

Regards,

Malcolm Nobre

Con el ejercicio físico (principalmente de tipo aeróbico), se logra aumentar la concentración de glóbulos rojos en sangre (eritropoyesis), a causa de una elevada producción de triyodotironina, la cual estimula la liberación de eritropoyetina (EPO) por parte de los riñones, estimulando a su vez esta a la médula ósea roja del tejido óseo trabecular a crear glóbulos rojos (eritropoyesis) (Wilmore & Costill 2004), (Ciloglu et. al. 2005), (Haff & Triplett 2015), (Prieto-Macías et al. 2016), (Herrera 2017) y (Aguilar Chasipanta et. al. 2017). También la hipoxia tanto en tejidos (tisular) como en la sangre (fenómenos evidenciados durante el ejercicio), estimulan la liberación de EPO por parte de los riñones, provocando el mismo efecto (Fernández-Tresguerres Hernández et. al. 2005), (Bonilla Briceño 2005), (Morici et al. 2005), (Calderón 2007), (García & Rubio 2014) y (Trompetero-González et al. 2015). Finalmente, el ejercicio provoca liberación de catecolaminas, las cuales también estimulan a los riñones a producir EPO (Wilmore & Costill 2004) y (Saba et. al. 2017).

This question reflects the disastrous distortion of medical theory and practice that presently prevails due to the powerful influence of corrupt corporations that dominate all aspects of health care.

There is only one reason that justifies the Whipple procedure, and that is cancer of the pancreas. How can it be that mutilating surgery, harmful radiation, and toxic chemicals can hope to cure cancer when all of these so-called “treatments” are known to cause cancer???? These stressful “treatments” exacerbate the hyperactivity of the mammalian stress mechanism that causes cancer to begin with. Cancer is self-sustaining tissue repair hyperactivity that occasionally subsides and resolves spontaneously, in which case doctors proclaim “victory” on behalf of their “heroic” efforts, but most often the “treatments” only grease the skids to armageddon, and doctors bury their mistakes.

Cancer exaggerates the shedding of tissue factor from extravascular tissues into circulating blood, where it stabilizes and activates coagulation factor VII, which “triggers” the enzymatic interaction of factors VII, VIII, IX, and X that generates thrombin, soluble fibrin, and insoluble fibrin. The thrombin energizes systemic inflammation, and the insoluble fibrin exaggerates blood coagulability. This explains why all forms of cancer cause “Trousseau’s Syndrome” (hypercoagulability of blood. This, in turn, explains why most cancer victims die of myocardial infarction, stroke, and pulmonary embolus and spontaneous bleeding is rare. Cancer often culminates in severe stress mechanism hyperactivity that manifests as “critical illnesses” including ARDS, MOFS, ARF, DIC, and so forth.

Stress theory indicates that the most promising approach to curing cancer would be a combination of treatments that control and reduce stress mechanism hyperactivity to the point that the “vicious cycle” of malignant tissue disruption, nociception, and tissue factor release is disrupted. In theory this would allow spontaneous apoptosis and resolution of the tissue repair process. This would theoretically require sustained combinations of general anesthesia and opioid analgesia to control harmful nervous hyperactivity, plus magnesium sulphate and hypercarbia to control harmful thrombin activity. A better alternative to magnesium sulphate would be a safe antidote to tissue factor that could prevent factor VII activation in flowing blood, but no such treatment is presently available for clinical use.

Insofar as anticoagulants are concerned, the best choice would be warfarin and its congeners that disrupt the interaction of factor VII with tissue factor and factor X, because this inhibits the malignant process. Heparin and its congeners can palliate hypercoagulability, but they have no direct effect on the malignant process.

I think it is not possible to calculate a function of plaque grow taking into account foam cells and LDL disregarding the many other factors involved.

Blood pressure is the force that blood exerts on the walls of the blood vessels as it flows through them. It is generated by the heart pumping blood into the blood vessels and the resistance of the blood vessels to this flow.

When the heart beats, it generates a pressure wave that travels through the arteries, causing them to expand and contract. This wave of pressure is known as a pulse. The pressure generated by the heart during each beat is known as systolic pressure, while the pressure in the arteries when the heart is at rest between beats is known as diastolic pressure. The difference between these two pressures is called pulse pressure.

The vessels also play a role in generating blood pressure. The resistance of the blood vessels to the flow of blood creates a pressure gradient that helps to maintain blood flow and generate blood pressure. The diameter of the blood vessels, the thickness of their walls, and the viscosity of the blood all contribute to this resistance.

When the central artery stiffness rises, the pulse pressure increases. This is because the artery walls become less elastic and more rigid, which reduces their ability to expand and contract in response to the pressure wave generated by the heart. As a result, the pressure wave is reflected back to the heart more quickly, causing an increase in systolic pressure and a decrease in diastolic pressure, leading to an increase in pulse pressure. This increase in pulse pressure can put additional strain on the heart and increase the risk of cardiovascular disease.

All good points mentioned so far. I’m not sure I completely understand the question. I think there are perhaps two questions at hand: one about kidney blood flow and one about impacts of living with one kidney.

Kidney transplantation and Living kidney donation provide a nice model to describe both. In living kidney donation, an open or laparoscopic nephrectomy is performed. The renal arteries/veins are ligated in the donor and they are left with one kidney.

The recipient of a kidney transplant ends up with a surgically created anastomosis of the donor renal arteries and veins to the iliac system. This is typically performed on the right side but can be on the left. Either way you could have a donated left kidney with left renal arteries and veins connected to the recipients iliac system on the right. Point being laterally doesn’t really matter: it’s more about the patency of the vessels and surgical technique.

These are generalities/always exceptions to the rules/I’m not a transplant surgeon.

To summarize- laterality is less important in kidney blood flow compared to vessel/anastomosis characteristics.

In terms of living with one kidney, it depends. Like others have mentioned, if congenitally absent or atrophies early in life, more likely that glomerular hypertrophy and secondary FSGS develop.

For people who are living donors, typically their remaining kidney compensates without developing secondary FSGS and their kidney function can end up being around 75% of their pre-donation GFR.

In conclusion- 1) Kidney blood flow is typically fine after nephrectomy and as transplant shows laterality of vessels is less important. 2) How someone does with one kidney is complicated and depends on timing/circumstances, but in the best of cases (living donation), people live relatively normal lives with kidney function that can be 75% of their pre-donation kidney function.

You may want to check my post elsewhere at this forum ― as a case study related to transient mass balance analysis:

Only abstract available: https://atcmeetingabstracts.com/abstract/impact-and-consequences-of-recipient-gastroduodenal-artery-gda-ligation-prior-to-hepatic-artery-ha-anastomosis-during-orthotopic-liver-transplantation-olt/

I would ask this specific question on Twitter involving the transplant community

At that moment the heart contracts isometrically.

Isometric: A muscular contraction in which the length of the muscle does not change. (This leads to incomplete evacuation of the blood).

You should at least really be running a URANS (Unsteady RANS) simulation. Then time-averaging the results if the flow is indeed statistically steady (the time average will be the same as the ensemble if turbulence is statistically steady by ergodic theorem).

Hello Camilla Romagnoli

You could make use of Human Coronary Artery Endothelial Cells (HCAEC). Please refer to the attached article.

Also, human aortic endothelial cells (HAECs) could be used as an alternative. Please refer to the article below.

Best.

Compared to arterial blood, there was a significant increase of erythrocyte count (2.7%) and haematocrit (3.1%) in the venous blood. The total and large leucocyte counts were significantly higher (9.2% and 12.6%, respectively) in the fingertip blood than in the venous blood.

Reference

Comparison of blood counts in venous, fingertip and arterial blood and their measurement variation

Z W Yang et al. Clin Lab Haematol. 2001 Jun.

Show details

Display options

doi: 10.1046/j.1365-2257.2001.00388.x.. 2001 Jun;23(3):155-9.Clin Lab Haematol

Authors

Z W Yang 1 , S H Yang, L Chen, J Qu, J Zhu, Z Tang

Affiliation

Thank you Mr. Daniel Galeazzi for your answer. I will try this out.

You are absolutery right when consider the obtaining pletismographic wave form is much easier than pulse wave contour. However these are two different proceses: pletismography describes blood flow and pulse wave contour depicts arterial wall motions. They look quite similar but are not the same. That is why we prefer pulse wave form analysis to pletismographic data.

Sir, i am also wandering same but in general angle should be less than 60 and close to 20, this is what came to know from reading some literatures.

even i wish to know wether angle is auto adjusted once set in the machine even after movement of probe.

thank you

Dear Benzaid,

if you are not getting the data set openly, kindly find the article related to this work and sent a request to the corresponding author. Mostly they wrote it like the datasets used and/or analyzed during the current study are available from the corresponding author on reasonable request.

The whole data set during stress Echocardiography can include the volumes of the left ventricular so that. Ejection fraction is derived from end diastolic and the end Systolic volumes. In normal person with excercise end Systolic volume decreases and hence we get increase ejection fraction. But in some normal person who gets hypertensive responses show no changes or increased end Systolic volumes and eventually decrease ejection fraction during excercise. This happens because of increase peripheral vascular resistance ehich causes decrease cardizc out put despite increase cardiac contraction.

Thanks, dear Mahesh Golla for your kind suggestion.

Apple cider vinegar will not unclog your arteries or cure atherosclerosis on its own. Making long-term lifestyle adjustments, such as stopping smoking, decreasing weight, and keeping physically active, is crucial.

Please visit the following RG link for insights.

You can put function with time by inputting equation in f(x) Analytic (an1) [arguments: time]. You can also use Gaussian pulse (gp1) to make your function smoother in order to prevent convergent problem. Hope this can help!

In my opinion, although not perfectly, the I profile curve corresponds to the velocity profile in the iliac artery. It is certainly the best representation of those you have presented. Remember in addition the period of the function, which is most often taken in the literature as 0.8 s, which corresponds to 72 heartbeats per minute or 1 s - 60 beats per minute.

I wish you luck in implementation,

Damian

Dear Navid Freidoonimehr

These links might be useful, have a lok:

1. https://github.com/ArsoVukicevic

2. https://github.com/ucuapps/CoronaryArteryStenosisScoreClassification

3. https://github.com/zgongkuang/IterativeCNN

4. https://github.com/syshin1014/VGN

Kind Regards

Faheem Ejaz add line/plane?? Yes, i used same to draw above shown yellow line but my question is about exact center of fluid volume or at mid of axis i want to draw a line. I know ur options , those are also not workout.\ Thanks

Regards,

Is there any way to couple ABAQUS and Ansys(fluent)?

As we know that Fat , cholesterol and other substances like Calcium , are the building block for the formation of plaque inside the lumen of coronary arteries , partially or totally block the blood flow to heart , leads to Ishaemia or infarction. There is no specific novel biomarkers to assess the progression of atherosclerosis. Besides the usual novel biomarkers like BNP , NT-Pro BNP , tropinin HDL-c , HDL function ,now researcher are eager to find out the novel biomarkers( produced by cardiac tissues) like miRNA , protein , fat by use of new technologies like Mass spectroscopy ,pcR bases array and MS based lipidomics

Abdul Gaphur as the image provided is 2D, I understand your concern. However, it's not attached to any surface (according to the 3d view). Thank you.

Selective angio of the celiac trunk or better superselective angio of the liver artery (a. hepatica propria) to identify suspicious av fistula. Therapy (embolisation/stentgrafting) can be done I same session, but only if there is a medical indication.

María Martín-Grau I hope you find these answers helpful.

Friends,

I have no definite answer to my own question

But I did a small trial. For my patients in ICU (most were intubated), I increased the FiO2 to 100% and did the ABG as well as a VBG (from the CVP line in the neck)

Let me give you the paired readings of 7 patients (ABG Po2/ CVP Po2)

Pao2 315/ Pvo2 63

349/<40

355/<40

287/54

407/<40

149/49

194/<40

So it looks like in some cases, the Pvo2 can go upto levels of 60

All the cases where the Pvo2 was > 40 were cases of shock (septic) on inotropes

And all the others with Pvo2< 40 were not needing inotropes

This may confirm the theory that in sepsis, the O2 uptake by tissues may be impaired (? mitochondrial dysfunction) and the hence the O2 content in the venous blood may be elevated

dear Pooyan Barati

hi pooyan. how are you?!

i suggest to visit the grab cad website and search for Artery.

i hope you find what you are looking for.

Unless there's a powerful reason for not using other arteries, I would use the PA (pulmonary artery) but all other big arteries as well (aorta, carotid, femoral) in the first experiment to maximize the use of one animal life. - In the same experiment I'd measure the length of the PA as well as other arteries (take a picture of the dissection). In the second experiment, you are better positioned to focus on the PA artery rings, assuming all other rings are not useful. Besides pressure, are there other variables that make the PA unique for your investigation?

"...The typical Reynolds number range of blood flow in the body varies from 1 in small arterioles to approximately 4000 in the largest artery, the aorta..." Ku DN. BLOOD FLOW IN ARTERIES. Annu. Rev. Fluid Mech. 1997. 29:399–434

Clasical pulse wave velocity (PWV) estimation in the elastic arteries is a measuring of the wave propagation alongside of aorta: from carotid to femoral artery. When you evaluate PWV in muscular-type arteries you use a sector from the carotid to the radial artery. In Sphygmocor device the software evaluates the delay of the pulse wave onset in each site of investigation (carotid, femoral and radial artery) to R wave on ECG. If the heart rate is the same (constant) the software calculates PWV. The main problem of this device is the requirement of constant heart rate. In other type of devices (Complior, etc.) you can record pulse wave from two or three sites simultaneously and it could be more accurate PWV estimation in comparison with Sphygmocor. However, all these devices are recommended for PWV evaluation.

Thank you for sharing this Question

NO!!!! Systolic pulse can be altered in many situation, not only in hyperthyroidism. Hashimoto's thyroiditis is most frequently associated with hypothyroidism, but we must not forget that "hashitoxicosis" does occur too.

Thanks

see the following paper

In this paper, a fractional relaxation model is studied to determine the effect of heat transfer and magnetic field on the blood flow. The flow is due to an oscillating periodic pressure gradient and body acceleration. We apply Laplace transform as well as finite Hankel transform to obtain the closed-form solutions of the velocity and temperature distributions of the fractional time partial differential equations. The effect of the fluid flow parameters is shown graphically with changes in the ordinary model as well as the fractional parameters. The analysis shows that a fractional derivative is an excellent tool that gives a remarkable change in controlling temperature and blood flow. The analysis depicts graphically, that the presence of a strong applied (exterior) magnetic field, reduces the temperature and blood flow velocities, which is appropriate to avoid tissue damage during treatment. Besides, it is seen that some of the aforementioned parameters influenced the fluid flow profiles in an increasing and decreasing fashion which is interpreted as useful to the study.

Have a look at these informative articles:

1.

2.

3.

the examinations are according on the type of analysis.

First enable boundary flux in physics settings~ then u can use the expression like stress dot product with boundary coordinate system (like nx t1x and t2x etc) manually putting in the variables to find the components of interface tractions (normal shear1 and shear2).

You can also plot in 5.5 to see the directions of each traction.

Also check the supplementary information of my paper (debonding mechanism in electrochemical society) I have calculated the normal and shear tractions and showed how their direction changes with respect to the charging time...

-Pterion is an important landmark for the anterior branch of the middle meningeal artery, which underlines this area on the inside of the skull. It is not a single point but an area where the frontal, parietal, squamous part of the temporal and greater wing of the sphenoid bone adjoin one another.

Hello Francisco,

If you are planning on monitoring NO generation real-time, then any grossly invasive procedures seem not very productive for your goals.

Given that NO is actually a diffusive gas, prolonged and elaborate procedures prior to detection add to possibilities of artificial outcomes. Therefore, the additional staining like DAPI is actually not advised, if NO staining itself is already challenging enough. It also concerns the magnification of info at which you want to show -- NO as detected by DAF-FM, for example, is best presented at the whole cell or cell population level (tissue sections), not at the subcellular level (thus, counter-staining with a nuclear DNA dye does not help much).

Probe incubation followed by prolonged PFA fixation and detection is not ideal, because these procedures tend disrupt cell membranes and alter permeability signficantly. DAF series probes are small molecules, and fixing will reduce the chance of their fluorescent products being detected (false negatives).

Please consult our paper on staining mouse vessels with a fluorescent probe for peroxynitrite (ONOO-), an RNS derived from NO, using a protocol involving live tissue probe staining by perfusion, brief PFA fixing, embedding, cryosectioning, and finally confocal imaging. (See details in SI). This method should work for other small-molecule fluorescent probes provided they are sufficiently retained and survive the fixation and wash steps performed by the experimenters.

pubs.acs.org/doi/suppl/10.1021/ja504624q/suppl_file/ja504624q_si_001.pdf

In general, if you are interested in test acute drug effects, the procedure would be:

- pre-loading the NO probe (to a final recommended conc.) into the cells or isolated/bathed tissue. Typically 30 min will do. Wash is usually not needed at this stage unless the commercial protocols state so, or you can test it out in imaging, to see how much fluorescence survive following washes.

- add the drug to simulate NO production. Allow sufficient time for build-up.

- terminate the incubation by a lavish wash (2x original volume for example) or directly proceeding to PFA fixation (5 min, on ice; 4% PFA in PBS).

- Wash lavish 1-2 times to remove residual PFA (when dried, or concentrated, this becomes autofluorescence or other artifacts).

- proceed to OCT embedding and normal cryostat sectioning (low temp.). Do not use paraffin embedding, which will invariably fail.

- mount sections onto a glass slide with coverslip (plus anti-fade Gold, Invitrogen), for imaging (confocal, magnification at 40x or 63x).

Good luck.

One has to make sure that the positions are changed to avoid causing another evil while managing COVID-19, the pressure sores.

Try LeMaitre Vascular: good quality.

I’m not familiar with the whole body MRA, as far as I know it’s been using in PAD patients. But it sounds like taking forever!

In other word there was no predictor for arterial thrmbosis

Put comments in your code! Doings so will help you finding the bug(s).

The pressure applied on an artery to close (rather than get stenosis) depends on which artery is concerned because there are medium sized artery that have a muscular wall eg radial artery and large elastic arteries (eg aorta) and on the pressure inside the said artery. On another note stenosis is most commonly caused by disease inside the artery disease such as atheroma. I hope this is helpful

"It takes a lot of malpractice to hit an artery instead of a vein identified by ultrasound Doppler. I believe this probability is close to zero"

Carlos don't be so sure. As a vascular surgeon I have put sutures many times on ruptured subclavian, femoral, iliac ..... (you name it) arteries after central venous line misplacement. :-D. Now seriuosly - the complication rate is estimated on 1% total, with US guidance it is said to be lower however there is no strong evidence (besides logical). … Read more

Dear Bacha Munir ,

I think the following links can help you. In the first case, ignore the electric field.

- https://www.comsol.com/model/separation-through-electrocoalescence-8592

- https://www.comsol.com/model/droplet-breakup-in-a-t-junction-1994

Posterior cerebral

Coronary angiography is a luminogram and that explains low sensitivity for diffuse disease

Unfamiliar with application here, but if you want to exclude regions from particle analysis, apply a mask. Duplicate image, add 1 to every pixel, draw a region, clear it out, turn into binary, and apply as mask (there's a plugin, or just multiply images) before doing particle analysis

The pressure at which stent is deployed has nothing to do with blood pressure. The nominal pressure for most of the stents as has been pointed out is 8 to 12 bar. But most stents require post dilatation with non compliant balloon at 18 to 20 bar. Some lesions rarely require post dilatation at even higher pressures . If the lesion and vascular bed are properly prepared, very high pressure post dilatation can be avoided, as it carries risk of vascular rupture.

You can start with wolf dynamics website. I learned with it and its free of cost. For more help take printout of manual.

Don't hesitate to perform wrong simulations. It will add up to your accuracy.

Very important findings by memory disorders, demnetias and schizophrenias!

Blood flow is an non-Newtonian fluid so you can use a fluid that near to blood properties and make numerical simulation representing the actual case study.So the mechanism including the non-Newtonian fluid case can be used in validating the actual case study.

Wow!

I don't think that any of the above answer would be nesecary.

Just freeze your biopsies in -20 or -70.

Try crushing the tissue into powder before adding TRIzol reagent. Arterial tissue should be easily crushed when it is frozen in liquid nitrogen.

Dear Dr. Kozlov:

I get the PDF file of Chapter 92, Portal Hypertension and Esophageal Bleeding,10th edition of Sleisenger and Fordtran's Textbook of Gastroneterology and read the hemodyanamic principle of portal hypertension. The pathophisiology of splanchnic hyperdynamics is still the same as what I have understood.

An mechanism of A-V shunting may exists between the splanchnic, intrahepatic or pulmonary vessels. Splenic A-V shunting is the most common type of splanchnic hyperdynamic state and your result can support this theory, better than my case report.

Is this position still vacant? Please let me know email ekram.aust08@gmail.com....thanks in advance

Try to solve the problem by using "System Coupling". I think this video tutorial can be helpful.

you can check the following links

Hi Sergio,

Thank you! I understood that the fluctuations in the brain and scalp are synchronised and your tip simplifies the things a bit for me, but I am more interested in the relation (of these fluctuations) to the heart cycle. I need to read the paper you suggest now.

Thanks.

thanks a lot Mr Emiliano Diez .I need a protocol to obtain rat ECG using an ExAO.CAN YOU HELP ME?