scholarly journals A Histological Evaluation of Artificial Dermal Scaffold Used in Micrograft Treatment: A Case Study of Micrograft and NPWT Performed on a Postoperative Ulcer Formation after Tumor Resection

Medicina ◽  
2022 ◽  
Vol 58 (1) ◽  
pp. 73
Author(s):  
Yuta Niimi ◽  
Kyoko Baba ◽  
Masako Tsuchida ◽  
Akira Takeda

Background and Objectives: Wound healing (WH) is a complex natural process: the achieving of a proper WH with standard therapies sometimes is not fulfilled and it is often observed in aged and diabetic patients, leading to intractable ulcers. In recent years, autologous micrograft (AMG) therapies have become a new, effective, and affordable wound care strategy among both researchers and clinicians. In this study, a 72-year-old female patient underwent a combination of treatments using micrograft and negative pressure wound therapy (NPWT) on a postoperative skin ulcer after a benign tumor resection on the back with the aim to present an innovative method to treat skin ulceration using AMG combined with an artificial dermal scaffold and NPWT. Materials and Methods: A section of the artificial dermal scaffold, infused with micrografts, was sampled prior to transplant, and sections were collected postoperatively on days 3 and 7. Hematoxylin-eosin (HE) and immunohistochemical stains were employed for the evaluation of Cytokeratin AE1/AE3, desmin, and Factor VIII. Additionally, on postoperative day 3, NPWT dressing was evaluated using HE stains, as well. The resulting HE and immunostaining analysis revealed red blood cells and tissue fragments within the collagen layers of the artificial dermis prior to transplant. On postoperative day 3, collagen layers of the artificial dermis revealed red blood cells and neutrophils based on HE stains, and scattering of cytokeratin AE1/AE3-positive cells were detected by immunostaining. The HE stains on postoperative day 7 showed more red blood cells and neutrophils within the collagen layers of the artificial dermis than on day 3, an increase in cytokeratin AE1/AE3-positive cells, and tissue stained positively with desmin and Factor VIII. Results: Results suggest that the effects of both micrografts and migratory cells have likely accelerated the wound healing process. Furthermore, the NPWT dressing on day 3 showed almost no cells within the dressing. This indicated that restarting NPWT therapy immediately after micrograft transplant did not draw out cells within the scaffold. Conclusions: Micrograft treatment and NPWT may serve to be a useful combination therapy for complex processes of wound healing.

Diagnostics ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 76
Author(s):  
Anastasia Maslianitsyna ◽  
Petr Ermolinskiy ◽  
Andrei Lugovtsov ◽  
Alexandra Pigurenko ◽  
Maria Sasonko ◽  
...  

Coronary heart disease (CHD) has serious implications for human health and needs to be diagnosed as early as possible. In this article in vivo and in vitro optical methods are used to study blood properties related to the aggregation of red blood cells in patients with CHD and comorbidities such as type 2 diabetes mellitus (T2DM). The results show not only a significant difference of the aggregation in patients compared to healthy people, but also a correspondence between in vivo and in vitro parameters. Red blood cells aggregate in CHD patients faster and more numerously; in particular the aggregation index increases by 20 ± 7%. The presence of T2DM also significantly elevates aggregation in CHD patients. This work demonstrates multimodal diagnostics and monitoring of patients with socially significant pathologies.


2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Henna Roshini Alexander ◽  
Sharifah Sakinah Syed Alwi ◽  
Latifah Saiful Yazan ◽  
Fatin Hanani Zakarial Ansar ◽  
Yong Sze Ong

Wound healing is a regulated biological event that involves several processes including infiltrating leukocyte subtypes and resident cells. Impaired wound healing is one of the major problems in diabetic patients due to the abnormal physiological changes of tissues and cells in major processes. Thymoquinone, a bioactive compound found in Nigella sativa has been demonstrated to possess antidiabetic, anti-inflammatory, and antioxidant effects. Today, the rapidly progressing nanotechnology sets a new alternative carrier to enhance and favour the speed of healing process. In order to overcome its low bioavailability, TQ is loaded into a colloidal drug carrier known as a nanostructured lipid carrier (NLC). This study aimed to determine the effect of TQ-NLC and TQ on cell proliferation and migration, mode of cell death, and the antioxidant levels in normal and diabetic cell models, 3T3 and 3T3-L1. Cytotoxicity of TQ-NLC and TQ was determined by MTT assay. The IC10 values obtained for 3T3-L1 treated with TQ-NLC and TQ for 24 hours were 4.7 ± 3.3 and 5.3 ± 0.6 μM, respectively. As for 3T3, the IC10 values obtained for TQ-NLC and TQ at 24 hours were 4.3 ± 0.17 and 3.9 ± 2.05 μM, respectively. TQ-NLC was observed to increase the number of 3T3 and 3T3-L1 healthy cells (87–95%) and gradually decrease early apoptotic cells in time- and dose-dependant manner compared with TQ. In the proliferation and migration assay, 3T3-L1 treated with TQ-NLC showed higher proliferation and migration rate (p<0.05) compared with TQ. TQ-NLC also acted as an antioxidant by reducing the ROS levels in both cells after injury at concentration as low as 3 μM. Thus, this study demonstrated that TQ-NLC has better proliferation and migration as well as antioxidant effect compared with TQ especially on 3T3-L1 which confirms its ability as a good antidiabetic and antioxidant agent.


Genes ◽  
2020 ◽  
Vol 12 (1) ◽  
pp. 47
Author(s):  
Carlos León ◽  
Francisco García-García ◽  
Sara Llames ◽  
Eva García-Pérez ◽  
Marta Carretero ◽  
...  

Defective healing leading to cutaneous ulcer formation is one of the most feared complications of diabetes due to its consequences on patients’ quality of life and on the healthcare system. A more in-depth analysis of the underlying molecular pathophysiology is required to develop effective healing-promoting therapies for those patients. Major architectural and functional differences with human epidermis limit extrapolation of results coming from rodents and other small mammal-healing models. Therefore, the search for reliable humanized models has become mandatory. Previously, we developed a diabetes-induced delayed humanized wound healing model that faithfully recapitulated the major histological features of such skin repair-deficient condition. Herein, we present the results of a transcriptomic and functional enrichment analysis followed by a mechanistic analysis performed in such humanized wound healing model. The deregulation of genes implicated in functions such as angiogenesis, apoptosis, and inflammatory signaling processes were evidenced, confirming published data in diabetic patients that in fact might also underlie some of the histological features previously reported in the delayed skin-humanized healing model. Altogether, these molecular findings support the utility of such preclinical model as a valuable tool to gain insight into the molecular basis of the delayed diabetic healing with potential impact in the translational medicine field.


Biorheology ◽  
1995 ◽  
Vol 32 (2-3) ◽  
pp. 388-388
Author(s):  
C BUCHERER ◽  
C ZEITOUN ◽  
C LACOMBE ◽  
J LELIEVRE ◽  
M FONFREDE ◽  
...  

Metabolism ◽  
1999 ◽  
Vol 48 (12) ◽  
pp. 1481-1484 ◽  
Author(s):  
Dildar Konukoğlu ◽  
Tülay Akçay ◽  
Yıldız Dinçer ◽  
Hüsrev Hatemi

Author(s):  
Swathi Balaji ◽  
Abdul Q. Sheikh ◽  
Lee Morris ◽  
Foong Y. Lim ◽  
Timothy M. Crombleholme ◽  
...  

Chronic ulcers are a leading cause of morbidity in diabetic patients. Diabetes is associated with major changes in the wound microenvironment and disruption of normal wound healing process, characterized by a prolonged inflammatory phase with elevated levels of wound proteases and increased degradation of extracellular matrix (ECM) components [1]. This impedes wound healing due to a lack of provisional matrix, impaired recruitment and survival of endothelial (EC) and endothelial precursor (EPC) cells, and insufficient neovascularization, resulting in delayed healing. Therefore, strategies focused on restoring the diabetic wound microenvironment by decreasing ECM degradation and promoting neovascularization are promising for development of new therapies to treat chronic diabetic ulcers.


2020 ◽  
Vol 26 (3) ◽  
pp. 329-336 ◽  
Author(s):  
Gengfan Ye ◽  
Qun Gao ◽  
Peng Qi ◽  
Junjie Wang ◽  
Shen Hu ◽  
...  

Purpose Diabetes mellitus indicated poor clinical prognosis for patients with acute ischemic stroke. Furthermore, diabetes mellitus could also impact the hemostatic system, while its influence on the histological composition of thrombus is unclear. Methods Consecutive patients with retrieved clots were included. Histologic staining for thrombus included hematoxylin and eosin, Martius Scarlet Blue, immunohistochemistry for von Willebrand factor. The differences in clot composition were compared according to diabetes mellitus history or hyperglycemia (≥7.8 mmol/L) on admission. Results A total of 52 patients were included; half of them were diagnosed as diabetes mellitus previously. Diabetic patients showed higher serum glucose on admission (8.90 vs. 7.40, p = 0.012). The baseline characteristics (expect smoking history and thrombus location), procedural, and clinical outcomes were similar between diabetic patients and nondiabetic patients. As for histologic composition, thrombus in patients with diagnosed diabetes mellitus had more fibrin (44.2% vs. 28.3%, p = 0.004) and fewer red blood cells (26.0% vs. 42.9%, p = 0.013) and equivalent content of platelets (24.0% vs. 21.5%, p = 0.694) and von Willebrand factor (0.041 vs. 0.031, p = 0.234) than patients without diabetes mellitus. However, there was no statistical difference in the content of red blood cells (41.6% vs. 27.3%, p = 0.105), fibrin (37.6% vs. 34.3%, p = 0.627), platelets (21.2% vs. 24.2%, p = 0.498), and von Willebrand factor (0.038 vs. 0.034, p = 0.284) between patients with or without hyperglycemia on admission. Conclusion Clots in diabetic patients had more fibrin and fewer erythrocyte components compared with patients without diabetes mellitus, while hyperglycemia on admission did not show association with clot composition. Further studies are needed to confirm these results.


2017 ◽  
Vol 37 (suppl_1) ◽  
Author(s):  
Zhichao Zhou ◽  
Ali Mahdi ◽  
Yahor Tratsiakovich ◽  
Oskar Kövamees ◽  
Jiangning Yang ◽  
...  

We previously showed that increased arginase activity is a key mechanism for endothelial dysfunction in patients with type 2 diabetes mellitus (T2DM) thereby arginase inhibition improves endothelial function. Recently, we demonstrated a crucial role of red blood cells (RBCs) in control of cardiac function via an arginase-dependent regulation of nitric oxide export from RBCs, suggesting a direct interaction of RBCs with cardiovascular function. Considering an increase in arginase activity in T2DM, we hypothesized that RBCs induce endothelial dysfunction in T2DM via up-regulated arginase I. Healthy rat aortas were incubated with RBCs from patients with T2DM (T2DM-RBCs) and age-matched healthy subjects (H-RBCs) for 18 h in the absence and presence of the arginase inhibition or scavenging of reactive oxygen/nitrogen species (ROS/RNS). Following the incubation, endothelium-dependent and -independent relaxations (EDR and EIR) were determined using wire myograph. Human internal mammary arteries (IMAs) obtained from non-diabetic patients who underwent cardiac surgery were also incubated with RBCs for functional evaluation. Arginase activity and protein expression were determined in RBCs. EDR was impaired in vessels incubated with T2DM-RBCs (Emax: 43.2±3.0% in aortas, n=8; 32.3±2.7% in IMAs, n=3) but not H-RBCs (Emax: 74.3±3.4% in aortas; 71.5±5.1% in IMAs) in comparison with buffer (Emax: 74.4±2.3% in aortas; 73.1±5.0% in IMAs; P<0.01 vs. T2DM-RBCs). EIR was not affected by T2DM-RBCs. The impairment in EDR in rat aortas was fully reversed by inhibition of arginase, ROS and RNS in RBCs. Arginase activity was significantly elevated in T2DM-RBCs. The increased arginase activity was attributed to arginase I, as there was increased arginase I expression in RBCs, whereas no arginase II expression was detected. Moreover, high glucose and RNS stimulation increased arginase activity in H-RBCs, while ROS/RNS scavenging decreased arginase activity in T2DM-RBCs. This study demonstrates a novel mechanism behind endothelial dysfunction that T2DM-RBCs induce endothelial dysfunction via ROS/RNS-dependent up-regulation of arginase I. Targeting arginase I in RBCs may serve as a novel therapeutic tool for treatment of endothelial dysfunction in T2DM.


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