Reduction In Microvasculature Research Articles

Evaluation of glaucomatous macular and optic nerve vascular damage by optical coherence tomography angiography

Purpose The aim of this study was to compare the macular and optic nerve head vessel perfusion density in mild primary open-angle glaucoma (POAG) and moderate–severe POAG patients to normal eyes as a control cohort. Patients and methods This is a retrospective comparative case–control study that included 80 eyes of 46 participants. The study included 60 eyes of 36 POAG patients and 20 eyes of 10 healthy participants (control group). The patients underwent 3.0×3.0 mm optical coherence tomography angiography (OCTA) scans centered on the macula and 4.5×4.5 mm scans on the optic disc. Results The OCTA scans of the glaucomatous eyes revealed a reduction in microvasculature in the peripapillary area, which was absent in the control cohort. The whole disc vessel density (VD) was significantly less in the glaucomatous eyes (mean=38.02±8.74) compared to the control cohort (mean=50.41±2.58, P<0.001). The severity of glaucoma was linked to a decrease in macular VD percentage, with a mean superficial VD of 36.09±5.67 in the glaucoma cohorts and 46.64±5.53 in the control cohort (P<0.001), which was more pronounced than in the deep layer (P<0.008). There was no statistically significant difference in the foveal avascular zone size between the control and glaucoma cohorts at any stage (P=0.999). Conclusion The OCTA vascular density accurately distinguished the glaucoma from healthy eyes, with superior performance in the peripapillary region. The foveal avascular zone size did not indicate glaucoma severity. The OCTA noninvasive assessment of the capillary networks showed a potential for managing the glaucoma patients by characterizing the retinal vascular changes.

Wide-field swept-source optical coherence tomography angiography in the assessment of retinal microvasculature and choroidal thickness in patients with myopia

Background/aimsPathological myopia (PM) is a leading cause of blindness worldwide. We aimed to evaluate microvascular and chorioretinal changes in different stages of myopia with wide-field (WF) swept-source (SS) optical coherence...

The impact of intensity-modulated radiation treatment on dento-alveolar microvasculature in pharyngeal cancer implant patients.

Dental rehabilitation post-radiotherapy often requires the consideration of dental implants. However, these are tentatively prescribed due to the concern of hypovascularisation and possible osteoradionecrosis. Hence, the current study assessed the microvasculature of the dento-alveolar bone at implant sites taking into consideration the exact radiotherapy dose received to the region. Bone cores were taken from nine patients during implant treatment and compared to nine control patients. Specimens were stained using CD31 and digitalised using a high-resolution scanner for qualitative and quantitative assessment of the microvasculature. Monaco® treatment planning system was used to volume the implant site providing mean dose (Dmean ) and maximum dose (Dmax ). A total of 23 bone cores were retrieved for analysis. The cohort had a Dmean of 38.4Gy (59.6-24.3Gy). Qualitative analysis identified a clear reduction in the miniscule terminal capillaries and high incidence of obliterated lumens with increasing radiotherapy. Microvasculature density of irradiated patients was markedly reduced (P=.0034) compared to the control group with an inverse correlation to RT doses (P<.0001). Specifically, doses up to 30Gy appear to preserve sufficient vascularisation (~77% in comparison with control) and tissue architecture. By contrast, exposure to higher doses 40%-61% of the micro-vessels were lost. Intensity-modulated radiotherapy doses above 30Gy identified reduction in microvasculature which is a lower threshold than previously accepted. In pharyngeal cancer patients' doses to the jaw bones often exceed this threshold. Coupled with favourable survival in certain oropharyngeal and nasopharyngeal cancer, dental rehabilitation via implants provides a significant clinical challenge.

Photoacoustic microscopy for evaluating a lipopolysaccharide-induced inflammation model in mice.

Photoacoustic microscopy (PAM) is a noninvasive imaging technique and is excellent to study structural and functional changes in the microcirculation. In this work, a lipopolysaccharide (LPS)-induced inflammation model in mice is noninvasively evaluated by PAM. PAM is used to image the microvascular structural changes in mice for 8 hours after the LPS with different concentrations is applied. Quantitative analysis of five vessel parameters is conducted, which shows that the rate of reduction in microvasculature is highly dependent on the applied LPS concentrations. For low-concentration LPS, changes in the microvasculature are not obvious over the observation period, whereas for high-concentration LPS, quick and marked reduction in the microvasculature is observed. In addition, changes in capillaries are more significant than those in relatively large vessels. The results show that PAM is able to evaluate the inflammation mouse model by studying structural (and potentially functional) changes in the microcirculation. Furthermore, PAM may have potential for early intervention and treatment plan optimization of sepsis by monitoring the microcirculation and inflammatory response.

Enhancement of paclitaxel-mediated cytotoxicity in lung cancer cells by 17-allylamino geldanamycin: in vitro and in vivo analysis

Background. It has previously been demonstrated that 17-allylamino geldanamycin (17-AAG) enhances paclitaxel-mediated cytotoxicity and downregulates vascular endothelial factor expression in non-small cell lung cancer. This project was designed to evaluate the tumoricidal and antiangiogeneic effects of 17-AAG and paclitaxel in H358 non-small cell lung cancer cells grown as xenografts in nude mice. Methods. In vitro cytotoxic drug combination effects were evaluated by (4, 5-dimethylthiazo-2-yl)-2, 5-diphenyl tetrazolium bromide-based proliferation assays. The combinations of 17-AAG and paclitaxel were administered intraperitoneally in nude mice bearing H358 tumor xenografts. Tumor volumes were measured weekly. Tumor expression of erbB2, vascular endothelial cell growth factor, von Willebrand factor (tumor microvasculature), and activated caspase 3 (apoptosis) were determined by immunohistochemistry. Results. Five- to 22-fold enhancement of paclitaxel cytotoxicity was achieved by paclitaxel + 17-AAG combination that was paralleled with marked induction of apoptosis. This combination treatment profoundly suppressed tumor growth and significantly prolonged survival of mice bearing H358 xenografts. Immunohistochemical staining of tumor tissues indicated profound reduction of vascular endothelial cell growth factor expression associated with reduction of microvasculature in tumors treated with 17-AAG. Apoptotic cells were more abundant in tumors treated with 17-AAG + paclitaxel than in those treated with 17-AAG or paclitaxel alone. Conclusions. Concurrent exposure of H358 cells to 17-AAG and paclitaxel resulted in supraadditive growth inhibition effects in vitro and in vivo. Analysis of molecular markers of tumor tissues indicated that therapeutic drug levels could be achieved with this chemotherapy regimen leading to significant biological responses. Moreover, 17-AAG-mediated suppression of vascular endothelial cell growth factor production by tumor cells may contribute to the antitumor effects of this drug combination in vivo.