HEM0RRHE0L0GY AND KETANSERIN

1987 ◽  
Author(s):  
J De Crée ◽  
H Geukens ◽  
H Demoen ◽  
H Verhaegen
Keyword(s):  
Platelet Rich Plasma ◽  
White Blood Cells ◽  
Vascular Diseases ◽  
Control Group ◽  
Clinical Value ◽  
Constant Amount ◽  
Double Blind ◽  
Mediated Effects ◽  
Different Levels

Red blood cell (RBC) filtration in platelet rich plasma (PRP) and platelet poor plasma (PPP) was equally decreased (p < 0.0001) in 120 patients with acute myocardial infarction (AMI) as compared to a control group. In a double-blind experiment 2 groups of 30 patients with AMI received an acute oral dose of 60 mg of ketanserin, a serotonin (5-HT) antagonist at 5-HT2-receptors, or placebo. Ketanserin treatment improved RBC filtration in PRP with an average increase of 30%. A similar experiment using PPP showed a significant increase of 10%. Filtration of plasma improved after ketanserin treatment in PRP, but not in PPP. Cross-exchange experiments showed the ketanserin-induced improvement of RBC filtration in PRP and PPP to be also plasmadependent. 5-HT in vitro at 10−9M deteriorated RBC filtration in PPP (p < 0.05), and ketanserin in vitro at 10−7M counteracted this phenomenon (p < 0.001). Finally we found that the effect of a subacute treatment with ketanserin on the filtration of RBC Suspensions, enriched with a constant amount of white blood cells (WBC), was more pronounced than on control RBC suspensions of patients with AMI.These results indicate that the impaired RBC filtration, reported in vascular diseases may be dependent on a subtle interaction between platelets, WBC, RBC and plasma. Treatment with ketanserin is capable to interrupt this vicious circle of rheological disturbances at different levels, first of all, by improving RBC deformability, but also by counteracting the platelet mediated effects on RBC and by favourably influencing the physical properties of WBC and so preventing clogging phenomena. Serotonin probably plays a pivotal role in these cascade of events and therapy with ketanserin might be of clinical value in diseases where microcirculatory flow is compromised.

The Effect of Warfarin Sodium on the Duration of Platelet Aggregation

1967 ◽  
Vol 18 (03/04) ◽  
pp. 766-778 ◽  
Author(s):  
H. J Knieriem ◽  
A. B Chandler
Keyword(s):  
Platelet Count ◽  
Placebo Group ◽  
Platelet Aggregation ◽  
Prothrombin Time ◽  
Platelet Rich Plasma ◽  
Healthy Adults ◽  
Double Blind Study ◽  
Double Blind ◽  
Warfarin Sodium

SummaryThe effect of the administration of warfarin sodium (Coumadin®) on the duration of platelet aggregation in vitro was studied. Coumadin was given for 4 consecutive days to 10 healthy adults who were followed over a period of 9 days. The duration of adenosine diphosphate-induced platelet aggregation in platelet-rich plasma, the prothrombin time, and the platelet count of platelet-rich plasma were measured. Four other healthy adults received placebos and participated in a double-blind study with those receiving Coumadin.Although administration of Coumadin caused a prolongation of the prothrombin time to 2 or 21/2 times the normal value, a decrease in the duration of platelet aggregation was not observed. In most individuals who received Coumadin an increase in the duration of platelet aggregation occurred. The effect of Coumadin on platelet aggregation was not consistently related to the prothrombin time or to the platelet count. In the placebo group there was a distinct relation between the duration of platelet aggregation and the platelet count in platelet-rich plasma.The mean increase in the duration of platelet aggregation when compared to the control value before medication with Coumadin was 37.7%. In the placebo group there was a mean increase of 8.4%. The difference between the two groups is significant (p <0.001). Increased duration of platelet aggregation also occurred in two individuals who received Coumadin over a period of 10 and 16 days respectively.

Early Platelet-Collagen Interactions in Whole Blood and Their Modifications by Aspirin and Dipyridamole Evaluated by a New Method (Basic Wave)

1985 ◽  
Vol 54 (04) ◽  
pp. 799-803 ◽  
Author(s):  
José Luís Pérez-Requejo ◽  
Justo Aznar ◽  
M Teresa Santos ◽  
Juana Vallés
Keyword(s):  
Whole Blood ◽  
Ex Vivo ◽  
Platelet Rich Plasma ◽  
White Blood Cells ◽  
Reversible Aggregation ◽  
Inhibitory Compounds ◽  
Rapid Generation ◽  
Stimulation Of ◽  
Collagen Stimulation

SummaryIt is shown that the supernatant of unstirred whole blood at 37° C, stimulated by 1 μg/ml of collagen for 10 sec, produces a rapid generation of pro and antiaggregatory compounds with a final proaggregatory activity which can be detected for more than 60 min on a platelet rich plasma (PRP) by turbidometric aggregometry. A reversible aggregation wave that we have called BASIC wave (for Blood Aggregation Stimulatory and Inhibitory Compounds) is recorded. The collagen stimulation of unstirred PRP produces a similar but smaller BASIC wave. BASIC’s intensity increases if erythrocytes are added to PRP but decreases if white blood cells are added instead. Aspirin abolishes “ex vivo” the ability of whole blood and PRP to generate BASIC waves and dipyridamole “in vitro” significantly reduces BASIC’s intensity in whole blood in every tested sample, but shows little effect in PRP.

Allogenic Pure Platelet-Rich Plasma Therapy for Adhesive Capsulitis: A Bed-to-Bench Study With Propensity Score Matching Using a Corticosteroid Control Group

2021 ◽  
pp. 036354652110186
Author(s):  
Min Ji Lee ◽  
Kang Sup Yoon ◽  
Sohee Oh ◽  
Sue Shin ◽  
Chris Hyunchul Jo
Keyword(s):  
Muscle Strength ◽  
Propensity Score ◽  
Inflammatory Cytokines ◽  
Platelet Rich Plasma ◽  
Corticosteroid Injection ◽  
Adhesive Capsulitis ◽  
Shoulder Function ◽  
Control Group ◽  
Inflammatory Condition

Background: While platelet-rich plasma (PRP) has been widely studied for musculoskeletal disorders, few studies to date have reported its use for adhesive capsulitis (AC). Fully characterized and standardized allogenic PRP may provide clues to solve the underlying mechanism of PRP with respect to synovial inflammation and thus may clarify its clinical indications. Purpose: To clinically evaluate the safety and efficacy of a fully characterized pure PRP injection in patients with AC and to assess the effects of pure PRP on synoviocytes with or without inflammation in vitro. Study Design: Controlled laboratory study and cohort study; Level of evidence, 3. Methods: For the clinical analysis, a total of 15 patients with AC received an ultrasonography-guided intra-articular PRP injection and were observed for 6 months. Pain, range of motion (ROM), muscle strength, shoulder function, and overall satisfaction in the patients were evaluated using questionnaires at 1 week as well as at 1, 3, and 6 months after the PRP injection and results were compared with the results of a propensity score−matched control group that received a corticosteroid injection (40 mg triamcinolone acetonide). For the in vitro analysis, synoviocytes were cultured with or without interleukin-1β (IL-1β) and PRP. The gene expression of proinflammatory and anti-inflammatory cytokines as well as matrix enzymes and their inhibitors was evaluated. Results: At 6-month follow-up, pure PRP significantly decreased pain and improved ROM, muscle strength, and shoulder function to levels comparable with those after a corticosteroid injection. All pain values, strength measurements, and functional scores significantly improved up to 6 months in the PRP group, but these measures improved up to 3 months and then were decreased at 6 months in the corticosteroid group. ROM was significantly improved in the 2 groups at 6 months compared with baseline. Allogenic PRP did not cause adverse events. For the in vitro findings, PRP induced inflammation but significantly improved the IL 1β−induced synovial inflammatory condition by decreasing proinflammatory cytokines such as IL-1β, tumor necrosis factor−α, IL-6, cyclooxygenase-2, and microsomal prostaglandin E synthase−1 and decreased matrix enzymes (matrix metalloproteinase−1, −3, and −13 as well as a disintegrin and metalloproteinase with thrombospondin motifs−4 and −5) and further increasing anti-inflammatory cytokines such as vasoactive intestinal peptide. Conclusion: This study showed that PRP decreased pain and improved shoulder ROM and function to an extent comparable with that of a corticosteroid in patients with AC. Allogenic pure PRP acted in a pleiotropic manner and decreased proinflammatory cytokines only in the inflammatory condition. Clinical Relevance: Allogenic PRP could be a treatment option for the inflammatory stage of AC.

scholarly journals Azithromycin and hydroxychloroquine in hospitalised patients with confirmed COVID-19–a randomised double-blinded placebo-controlled trial

2021 ◽  
pp. 2100752
Author(s):  
Pradeesh Sivapalan ◽  
Charlotte Suppli Ulrik ◽  
Therese Sophie Lapperre ◽  
Rasmus Dahlin Bojesen ◽  
Josefin Eklöf ◽  
...  
Keyword(s):  
Primary Outcome ◽  
Controlled Trial ◽  
Intervention Group ◽  
Control Group ◽  
Double Blind ◽  
Safety Outcome ◽  
Hospitalised Patients ◽  
Double Blinded ◽  
Combined Intervention

BackgroundCombining the antibiotic azithromycin and hydroxychloroquine induces airway immunomodulatory effects, with the latter also having in vitro antiviral properties. This may improve outcomes in patients hospitalised for COVID-19.MethodsPlacebo-controlled double-blind randomised multicentre trial. Patients ≥18 years, admitted to hospital for≤48 h (not intensive care) with a positive SARS-CoV-2 RT-PCR test, were recruited. The intervention was 500 mg daily azithromycin for 3 days followed by 250 mg daily azithromycin for 12 days combined with 200 mg twice daily hydroxychloroquine for all 15 days. The control group received placebo/placebo. The primary outcome was days alive and discharged from hospital within 14 days (DAOH14).ResultsAfter randomisation of 117 patients, at the first planned interim analysis, the data and safety monitoring board recommended stopping enrolment due to futility, based on pre-specified criteria. Consequently, the trial was terminated on February 1, 2021. A total of 61 patients received the combined intervention and 56 patients received placebo. In the intervention group, patients had a median of 9.0 DAOH14 (IQR, 3–11) versus. 9.0 DAOH14 (IQR, 7–10) in the placebo group (p=0.90). The primary safety outcome, death from all causes on day 30, occurred for 1 patient in the intervention group versus. 2 patients receiving placebo (p=0.52), and readmittance or death within 30 days occurred for 9 patients in the intervention group versus. 6 patients receiving placebo (p=0.57).ConclusionsThe combination of azithromycin and hydroxychloroquine did not improve survival or length of hospitalisation in patients with COVID-19.

Platelet inhibition by aspirin is diminished in patients during carotid surgery: a form of transient aspirin resistance?

2004 ◽  
Vol 92 (07) ◽  
pp. 89-96 ◽  
Author(s):  
David Payne ◽  
Chris Jones ◽  
Paul Hayes ◽  
Sally Webster ◽  
A. Naylor ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Platelet Rich Plasma ◽  
Platelet Inhibition ◽  
Aspirin Resistance ◽  
Arachidonic Acid Metabolism ◽  
Significant Rise ◽  
Control Group

SummaryThe majority of patients who suffer peri-operative thromboembolic complication while undergoing vascular procedures do so despite taking aspirin. This study examined the antiplatelet effect of aspirin during surgery in patients undergoing carotid endarterectomy (CEA). Fifty patients undergoing CEA were standardised to 150 mg aspirin daily for ≥2 weeks. Platelet aggregation in response to arachidonic acid (AA) was measured in platelet rich plasma prepared from blood taken prior to, during, and at the end of surgery. Spontaneous platelet aggregation was also studied, as was the role of physiological agonists (ADP, collagen, thrombin, and epinephrine) in mediating the in vivo and in vitro responses to AA. Eighteen patients undergoing leg angioplasty, also on 150 mg aspirin, without general anaesthesia, served as a control group. In the CEA patients aggregation induced by AA (5 mM) increased significantly from 7.6 ± 5.5% pre-surgery to 50.8 ± 29.5% at the end of surgery (p <0.0001). Aggregation to AA was even greater in samples taken mid-surgery from a sub-set of patients (73.8 ± 7.2%; p = 0.0001), but fell to 45.9 ± 7.4% by the end of surgery. The increased aggregation in response to AA was not due to intra-operative release of physiological platelet agonists since addition of agents that block/neutralise the effects of ADP (apyrase; 4 µg/ml), thrombin (hirudin; 10 units/ml), or epinephrine (yohimbine; 10 µM/l) to the samples taken at the end of surgery did not block the increased aggregation.The patients undergoing angioplasty also showed a significant rise in the response to AA (5 mM), from 5.6 ± 5.5% pre-angioplasty to 32.4 ± 24.9% at the end of the procedure (p <0.0001), which fell significantly to 11.0 ± 8.1% 4 hours later. The antiplatelet activity of aspirin, mediated by blockade of platelet arachidonic acid metabolism, diminished significantly during surgery, but was partially restored by the end of the procedure without additional aspirin treatment.This rapidly inducible and transient effect may explain why some patients undergoing cardiovascular surgery remain at risk of peri-operative stroke and myocardial infarction.

scholarly journals Short-Term Outcomes of Percutaneous Trephination with a Platelet Rich Plasma Intrameniscal Injection for the Repair of Degenerative Meniscal Lesions. A Prospective, Randomized, Double-Blind, Parallel-Group, Placebo-Controlled Study

2019 ◽  
Vol 20 (4) ◽  
pp. 856 ◽  
Author(s):  
Rafal Kaminski ◽  
Marta Maksymowicz-Wleklik ◽  
Krzysztof Kulinski ◽  
Katarzyna Kozar-Kaminska ◽  
Agnieszka Dabrowska-Thing ◽  
...  
Keyword(s):  
Platelet Rich Plasma ◽  
Meniscal Tear ◽  
Controlled Study ◽  
Control Group ◽  
Double Blind ◽  
Non Union ◽  
Parallel Group ◽  
Significant Difference ◽  
Clinically Significant ◽  
Patient Related Outcome

Meniscal tears are the most common orthopaedic injuries, with chronic lesions comprising up to 56% of cases. In these situations, no benefit with surgical treatment is observed. Thus, the purpose of this study was to investigate the effectiveness and safety of percutaneous intrameniscal platelet rich plasma (PRP) application to complement repair of a chronic meniscal lesion. This single centre, prospective, randomized, double-blind, placebo-controlled study included 72 patients. All subjects underwent meniscal trephination with or without concomitant PRP injection. Meniscal non-union observed in magnetic resonance arthrography or arthroscopy were considered as failures. Patient related outcome measures (PROMs) were assessed. The failure rate was significantly higher in the control group than in the PRP augmented group (70% vs. 48%, P = 0.04). Kaplan-Meyer analysis for arthroscopy-free survival showed significant reduction in the number of performed arthroscopies in the PRP augmented group. A notably higher percentage of patients treated with PRP achieved minimal clinically significant difference in visual analogue scale (VAS) and Knee injury and Osteoarthritis Outcome Score (KOOS) symptom scores. Our trial indicates that percutaneous meniscal trephination augmented with PRP results in a significant improvement in the rate of chronic meniscal tear healing and this procedure decreases the necessity for arthroscopy in the future (8% vs. 28%, P = 0.032).

scholarly journals Rat duodenal motility in vitro: Prokinetic effects of DL-homocysteine thiolactone and modulation of nitric oxide mediated inhibition

2013 ◽  
Vol 65 (4) ◽  
pp. 1323-1330
Author(s):  
Marija Stojanovic ◽  
Lj. Scepanovic ◽  
D. Mitrovic ◽  
V. Scepanovic ◽  
T. Stojanovic ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Hypertrophic Pyloric Stenosis ◽  
Vascular Diseases ◽  
Cholinergic Innervation ◽  
Control Group ◽  
Infantile Hypertrophic Pyloric Stenosis ◽  
Homocysteine Thiolactone ◽  
Spontaneous Movements ◽  
Rat Duodenum

Homocysteine is a significant but modifiable risk factor for vascular diseases. As gastrointestinal smooth musculature is similar to blood vessel muscles, we investigated how elevated homocysteine levels affect nitric oxide-mediated neurotransmission in the gut. There is accumulated evidence that a dysfunction of NO neurons in the myenteric plexus may cause various diseases in the gastrointestinal tract such as achalasia, diabetic gastroparesis and infantile hypertrophic pyloric stenosis. In the present study, we aimed to assess the effects of homocysteine on NO-mediated responses in vitro, and to examine the effects of DL-homocysteine thiolactone on the spontaneous motility of rat duodenum and nitrergic neurotransmission. DL-homocysteine thiolactone concentration of 10 ?mol/L leads to the immediate increase in tone, amplitude and frequency of spontaneous movements in isolated rat duodenum. L-NAME (30 ?mol/L) leads to an increase in basal tone, amplitude and frequency of spontaneous contractions. The relaxations induced by EFS were significantly reduced in duodenal segments incubated in DL-homocysteine thiolactone compared with the control group. EFS-induced relaxations were inhibited by L-NAME in both experimental and control groups. These results suggest that a high level of homocysteine causes an important impairment of non-adrenergic non-cholinergic innervation of the rat duodenum.

scholarly journals Wound Healing: In Vitro and In Vivo Evaluation of a Bio-Functionalized Scaffold Based on Hyaluronic Acid and Platelet-Rich Plasma in Chronic Ulcers

2019 ◽  
Vol 8 (9) ◽  
pp. 1486 ◽  
Author(s):  
Barbara De Angelis ◽  
Margarida Fernandes Lopes Morais D’Autilio ◽  
Fabrizio Orlandi ◽  
Giampiero Pepe ◽  
Simone Garcovich ◽  
...  
Keyword(s):  
Wound Healing ◽  
Hyaluronic Acid ◽  
Platelet Rich Plasma ◽  
Combined Treatment ◽  
Skin Grafting ◽  
Control Group ◽  
In Vivo Evaluation ◽  
Chronic Ulcers

Chronic ulcers are characterized by loss of substance without a normal tendency towards spontaneous healing. The Wound Bed Preparation Guideline advises that after diagnosis, the expert should correct the biological state of the ulcer micro-environment based on TIME principles (Tissue, Infection, Moisture balance, Epidermal). There are many ways to treat such ulcers, for example through use of advanced dressings, negative pressure, surgical toilets, dermal substitutes, autologous skin grafting, and free or local flaps. In vitro and in vivo pre-clinical models hold widely acknowledged potential yet complex limitations. Tissue bioengineering could be an ideal approach to foster innovative strategies in wound healing. Our observational study reports on an in vitro and in vivo evaluation of a bio-functionalized scaffold composed of platelet-rich plasma (PRP) and hyaluronic acid (HA) used in 182 patients affected by chronic ulcers (diabetic and vascular), comparing the results with a control group of 182 patients treated with traditional dressings (HA alone). After 30 days the patients who had undergone the combined treatment (PRP + HA), showed 96.8% ± 1.5% re-epithelialization, as compared to 78.4% ± 4.4% in the control group (HA only). Within 80 days, they had 98.4% ± 1.3% re-epithelialization as compared to 87.8% ± 4.1% in the control group (HA only; p < 0.05). No local recurrence was observed during the follow-up period. PRP + HA treatment showed stronger regenerative potential in terms of epidermal proliferation and dermal renewal compared with HA alone.

Targeting Survivin Using ICG-001 May Overcome Drug Resistance in Primary B-Cell Acute Lymphoblastic Leukemia.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 3072-3072
Author(s):  
Enzi Jiang ◽  
Eugene Park ◽  
Carlton Scharman ◽  
Yao-Te Hsieh ◽  
Asha Kadavallore ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Blood Cells ◽  
Lymphoblastic Leukemia ◽  
White Blood Cells ◽  
Leukemia Cells ◽  
Control Group ◽  
Drug Resistant ◽  
Control Groups ◽  
Standard Chemotherapy

Abstract Abstract 3072 Poster Board III-9 Despite advances in chemotherapeutic treatment of acute lymphoblastic leukemia (ALL), 20% of children relapse with high death rates, highlighting the need for new treatment modalities. Recent population studies have demonstrated that Survivin, a member of the inhibitor of apoptosis (IAP) family proteins, is expressed in most cancerous cells but has also been implicated in normal erythropoiesis. It is upregulated in ALL of relapsed patients but not in drug-sensitive ALL. The expression of Survivin depends on the formation of a complex between β-catenin and its co-activator CBP. Selective suppression of CBP/β-catenin signaling using the novel small-molecule inhibitor ICG-001 offers a novel mechanism to target Survivin in the sensitization of leukemia cells to conventional drug treatment. We hypothesize that inhibition of CBP/β-catenin signaling by ICG-001 in combination with conventional therapy represents a promising therapeutic principle to eradicate drug resistant ALL while sparing normal hematopoiesis. An in vivo study utilized our bioluminescent model to non-invasively monitor leukemogenesis of a primary ALL, transduced with a lentiviral construct encoding firefly luciferase prior to xenotransplantation. NOD/SCIDIL2R gamma-/- mice were sublethally irradiated prior intravenous injection of 50,000 cells per animal. Leukemic animals were treated with a combination of intraperitoneally administered VDL and ICG-001 (100mg/kg/d) (n=3), which was delivered via subcutaneous osmotic pumps to ensure stable plasma levels, with VDL only (n=4), or PBS only (n=2) as a control for 4 weeks. Bioluminescent imaging on Day 42 post-injection showed a contrast in the containment of leukemia of ICG-001+VDL mice as compared to those of the VDL control group. The animals in the PBS control group and the VDL+PBS Pump control groups had Median Survival Times (MST) of 35 days and 66.5 days post-treatment, respectively. In marked contrast, the animals treated with a combination of VDL+ICG-001 had a significant 14% extension in MST of 76 days post-treatment (p=0.016 compared to VDL group). Survivin mRNA expression was found to be downregulated after VDL+ICG treatment compared to treatment with VDL only. Analysis of peripheral blood showed no effect of ICG-001 on leukocyte or red blood cells compared to control groups. Next, we determined in vitro the ability of ICG-001 to increase sensitivity of patient-derived ALL cells and ALL celllines including BEL-1, REH, 697 and SUPB15 to chemotherapy including VDL or Imatinib. After 4 days we observed significantly increased toxicity assessed by MTT assay and AnnexinV staining as well as downregulation of Survivin confirmed by real-time PCR and Western Blot. To determine if ICG-001 is non-toxic to normal hematopoiesis, we treated normalC57BL/6 mice for 3 weeks with ICG-001 only. At end of treatment, normal blood counts including red blood cell, white blood cells and platelets, normal histology and normal weight gain indicated that ICG-001 is not detrimental to the recipient. In vitro apoptotic studies using normal white blood cells isolated from peripheral blood and co-cultured with a stromal layer confirmed further the non-toxicity of ICG-001 to normal cells. In summary, the sustained survival of the mice treated with combination of standard chemotherapy and ICG-001 is compatible with our hypothesis that ICG-001 can sensitize drug resistant leukemia cells to treatment with standard chemotherapy while sparing normal hematopoiesis and may lead to novel therapeutic options to overcome drug resistance. Disclosures No relevant conflicts of interest to declare.

scholarly journals Role of White Blood Cells in Blood- and Bone Marrow-Based Autologous Therapies

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
William King ◽  
Krista Toler ◽  
Jennifer Woodell-May
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Growth Factors ◽  
Blood Cells ◽  
Platelet Rich Plasma ◽  
White Blood Cells ◽  
Complex Mixture ◽  
Negative Results

There has been significant debate over the role of white blood cells (WBCs) in autologous therapies, with several groups suggesting that WBCs are purely inflammatory. Misconceptions in the practice of biologic orthopedics result in the simplified principle that platelets deliver growth factors, WBCs cause inflammation, and the singular value of bone marrow is the stem cells. The aim of this review is to address these common misconceptions which will enable better development of future orthopedic medical devices. WBC behavior is adaptive in nature and, depending on their environment, WBCs can hinder or induce healing. Successful tissue repair occurs when platelets arrive at a wound site, degranulate, and release growth factors and cytokines which, in turn, recruit WBCs to the damaged tissue. Therefore, a key role of even pure platelet-rich plasma is to recruit WBCs to a wound. Bone marrow contains a complex mixture of vascular cells, white blood cells present at much greater concentrations than in blood, and a small number of progenitor cells and stem cells. The negative results observed for WBC-containing autologous therapies in vitro have not translated to human clinical studies. With an enhanced understanding of the complex WBC biology, the next generation of biologics will be more specific, likely resulting in improved effectiveness.

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