Physiopathological Mechanism and Assessment of Fetal Asphyxia

Tsikouras, Panagiotis; Bothou, Anastasia; Koukouli, Zacharoula; Manav, Bachar; Bouschanetzis, Constantinos; Deuteraiou, Dorelia; Anthoulaki, Xanthoula; Chalkidou, Anna; Iatrakis, Georgios; Zervoudis, Stefanos; Galazios, G

doi:10.4236/ojog.2017.76064

Cited by 4 publications

(5 citation statements)

References 12 publications

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“…In the previous literature, CA125 combined with a variety of clinicopathological factors was also suggested to increase the accuracy of clinical diagnosis, such as MRI, 19 Mesothelin 20 and HE4. At present, HE4 and CA125 are clinically approved tumor markers for the diagnosis and prognosis of EC.…”

Section: Discussionmentioning

confidence: 99%

Preoperative serum CA125 level and age at diagnosis: An effective prognosis prediction tool for patients with early‐stage endometrial cancer

Sun

Wei

Zou

et al. 2022

Asia-Pac J Clncl Oncology

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To investigate the combined predictive value of the preoperative serum cancer antigen 125 (CA125) level and age at diagnosis among patients with early-stage endometrial cancer(EC) after initial treatment. MethodsWe retrospectively analyzed data from patients with early-stage EC from January 1999 to December 2015 in multiple institutions in China.All patients received primary hysterectomy± bilateral salpingo-oopho rectomy and adjuvant radiotherapy for pathology-con rmed stage I and II EC (FIGO 2009 staging). In total, 447 patients with complete data on preoperative serum CA125 levels were included. All patients were divided into low-risk, intermediate-risk, high-intermediate-risk and high-risk groups according to the ESMO-ESGO-ESTRO risk classi cation. Binary logistic regression was used to calculate the predictive probability of 5-year overall survival (OS) for each patient, and the receiver operating characteristic (ROC) curve was used to calculate the sensitivity and speci city of variables, as well as the combined predictive value of CA125 and age. ResultsThe median follow-up time was 59 months (3-201 months). The 5-year OS and disease-free survival (DFS) rates were 94.4% and 89.1%, respectively. Multivariate analysis showed that the preoperative CA125 level and age at diagnosis were independent prognostic factors for 5year OS. The best cutoff value forage at diagnosis was 61 years. The cutoff values of CA125 for patients aged ≤61 years and > 61 years were 37.7 U/mL and 39.35 U/mL, respectively. Patients aged >61years with CA125 > 39.35 U/ml and patients aged ≤61years with CA125 > 37.7 U/ml were classi ed as theCA125-positive group; the remaining patients constituted the CA125-negative group. The area under the curve (AUC) for CA125 combined with age at diagnosis was 0.692, and the corresponding sensitivity and speci city were 68.2% and 68.2% (P<0.002), respectively, which were signi cantly better than the corresponding values for CA125 or age alone. ConclusionsAlthough preoperative CA125 had limited sensitivity in predicting the prognosis for early-stage EC after initial treatment, it remains a useful serum marker for risk assessment of early-stage EC. Combining CA125 with age may increase its predictive sensitivity.

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Section: Discussionmentioning

confidence: 99%

Preoperative serum CA125 level and age at diagnosis: An effective prognosis prediction tool for patients with early‐stage endometrial cancer

Sun

Wei

Zou

et al. 2022

Asia-Pac J Clncl Oncology

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“…Type 2) Hypoxia, which results from a significant reduction of oxygen in the inhalation of air and, consequently, in the tissues. Therefore, the oxygen (O 2 ) supply is inadequate for the oxygen requirements of the tissues and the aerobic metabolism is completed with the anaerobic metabolism to maintain the energy balance (Tsikouras et al 2017), and Type 3) asphyxiation, in which hypoxia spreads to the central organs and can lead to metabolic acidosis (Sanchez-Salcedo et al 2019a) because, when hypoxia is prolonged, blood is redistributed from the non-vital organs (liver, kidney) to the brain and anaerobic metabolism produces lactic acid (hence, metabolic acidosis). Since oxygen deficiency is accompanied by acidosis, the energy balance can no longer be maintained which leads to reduction in organ function eventually resulting in permanent tissue damage (Tsikouras et al 2017).…”

Section: Classification and Importance Of Perinatal Asphyxiamentioning

confidence: 99%

Treatments and therapeutic protocols for the recovery of an asphyxiated new-born: A review of pre-clinical and clinical studies in human neonates and in different animal models

Islas-Fabila¹,

Orozco-Gregorio²,

Roldán-Santiago³

et al. 2022

Vet. Med. - Czech

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The objective of this review is to ascertain the advantages and disadvantages of several treatments and therapeutic protocols that have been used for the prevention and treatment of perinatal asphyxia in human neonates and in different animal models. Perinatal asphyxia is one of the main causes of mortality worldwide and is an important factor in triggering physio-metabolic disorders that result in serious neurological consequences and learning disorders not only in human foetuses and neonates, but also in animals. In recent years, the search for new pharmacological protocols to prevent and reverse physio-metabolic disorders and brain damage derived from perinatal asphyxia has been and continues to be the subject of intense research. Currently, within these pharmacological protocols, therapeutic strategies have been evaluated that use respiratory and hormonal stimulants, as well as hypothermic therapies in combination with other putative neuroprotective agents. Similarly, energy supplements have been evaluated with the objective of preventing perinatal asphyxia and treating new-borns with this condition, and to decrease the incidence of neonatal and foetal deaths associated with it. However, despite these promising advances, this pathology has persisted, since the administration of these therapies in low doses may not exert a neuroprotective effect or, in high doses, can trigger adverse effects (such as reduced cardiac contractility, reduced cerebral blood flow, poor perfusion, sympathetic and neuroendocrine stimulation, and increased blood viscosity) in human foetuses and neonates as well as in different animal models (rats, piglets, sheep and rabbits). Therefore, it is important to determine the minimum effective dose with which these therapies exert a neuroprotective effect, as well as the mode of administration, the duration of therapy, etc. Therefore, until a powerful strategy is found to improve the consequences of suffocation, this topic will continue to be the subject of intensive research in the future.

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“…Cervical cancer remains one of the main cancer in women, particularly in developing countries [1][2][3][4]. At present, cervical cancer is the main cause of mortality in women [2,5,6].…”

Section: Introductionmentioning

confidence: 99%

“…Cervical cancer remains one of the main cancer in women, particularly in developing countries [1][2][3][4]. At present, cervical cancer is the main cause of mortality in women [2,5,6]. Lymphatic metastasis has been identified as a risk factor for cervical cancer recurrence [7].…”

Section: Introductionmentioning

confidence: 99%

Tumor Necrosis Factor-α Promotes the Tumorigenesis, Lymphangiogenesis, and Lymphatic Metastasis in Cervical Cancer via Activating VEGFC-Mediated AKT and ERK Pathways

Xiao

Lin

et al. 2023

Mediators of Inflammation

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Background. Lymphatic metastasis is a common phenomenon of cervical cancer. Tumor necrosis factor-α (TNF-α) was found to be closely associated with lymphatic cancer metastasis. However, the mechanism through which TNF-α regulates lymphatic metastasis in cervical cancer remains unclear. Methods. In this study, cervical cancer cells were cultured in Dulbecco’s modified Eagle’s medium (DMEM) with or without TNF-α for 48 h, and then the corresponding conditional medium (CM-TNF-α or CM) was collected. The level of vascular endothelial growth factor (VEGFC) in the corresponding CM was then detected using an enzyme-linked immunosorbent assay (ELISA). Next, human lymphatic endothelial cells (HLECs) were cultured in CM-TNF-α or CM for 48 h. Cell viability was measured using the cell counting kit-8 (CCK-8) assay, and angiogenesis was detected using a tube formation assay. Subsequently, the expressions of AKT, p-AKT, ERK, and p-ERK in HLECs were detected using western blotting. In addition, to further investigate the effect of TNF-α on the progression of cervical cancer, a C33A subcutaneous xenograft model was established in vivo. Results. We found that TNF-α significantly stimulated cervical cancer cells to secrete VEGFC. Additionally, the CM collected from the TNF-α-treated cervical cancer cells notably promoted the proliferation, migration, and angiogenesis of HLECs; however, these changes were reversed by MAZ51, a VEGFR3 inhibitor. Moreover, TNF-α obviously elevated D2-40 and VEGFC protein expressions in tumor tissues, promoting lymphangiogenesis and lymphatic metastasis in vivo. Meanwhile, TNF-α markedly upregulated p-AKT and p-ERK expressions in tumor tissues, whereas these changes were reversed by MAZ51. Conclusion. Collectively, TNF-α could promote tumorigenesis, lymphangiogenesis, and lymphatic metastasis in vitro and in vivo in cervical cancer via activating VEGFC-mediated AKT and ERK pathways. These results may provide new directions for the treatment of cervical cancer.

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Physiopathological Mechanism and Assessment of Fetal Asphyxia

Cited by 4 publications

References 12 publications

Preoperative serum CA125 level and age at diagnosis: An effective prognosis prediction tool for patients with early‐stage endometrial cancer

Preoperative serum CA125 level and age at diagnosis: An effective prognosis prediction tool for patients with early‐stage endometrial cancer

Treatments and therapeutic protocols for the recovery of an asphyxiated new-born: A review of pre-clinical and clinical studies in human neonates and in different animal models

Tumor Necrosis Factor-α Promotes the Tumorigenesis, Lymphangiogenesis, and Lymphatic Metastasis in Cervical Cancer via Activating VEGFC-Mediated AKT and ERK Pathways

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