Σφακιανάκης Αλέξανδρος
ΩτοΡινοΛαρυγγολόγος
Αναπαύσεως 5 Άγιος Νικόλαος
Κρήτη 72100
00302841026182
00306932607174
alsfakia@gmail.com

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Δευτέρα 10 Μαΐου 2021

Apoptosis in HUVECs induced by microRNA-616-3p via X-linked inhibitor of apoptosis protein targeting

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Exp Ther Med. 2021 Jun;21(6):661. doi: 10.3892/etm.2021.10093. Epub 2021 Apr 21.

ABSTRACT

Atherosclerosis causes stroke and coronary heart disease and is associated with a high mortality rate worldwide. However, the pathogenesis of atherosclerosis remains unclear. Endothelial cell apoptosis is one of the early changes observed in atherosclerosis. Previous studies have found that microRNA (miR)-616-3p may be involved in the development of atherosclerosis, but the specific mechanism is not clear. The present study aimed to investigate whether miR-616-3p is involved in endothelial cell apoptosis and its underlying mechanism. The present study demonstrated that compared with normal HUVECs, HUVECs treated with oxidized low-density lipoprotein expressed higher miR-616-3p and lower X-linked inhibitor of apoptosis protein (XIAP) levels. In the present study, HUVECs were transfected with miR-616-3p mimic and Cell Counting Kit-8 (CCK-8), flow cy tometry and TUNEL staining assays demonstrated that compared with miR-616-3p mimic control, the miR-616-3p mimic promoted HUVEC apoptosis. In addition, using StarBase 3.0 for bioinformatics analysis it was predicted that miR-616-3p may bind to the 3'untranslated region (UTR) of XIAP mRNA. The present study performed the CCK-8, flow cytometry, TUNEL staining and dual-luciferase reporter assays and demonstrated that miR-616-3p binds to the 3'UTR of the XIAP mRNA and inhibits its expression and that this further promotes apoptosis in HUVECs. In addition, western blotting demonstrated that compared with miR-616-3p mimic control, the miR-616-3p mimic increases the level of cleaved caspase-3 in HUVECs. In summary, the present study demonstrated that miR-616-3p can directly inhibit the expression of XIAP mRNA by targeting its 3'UTR which promoted apoptosis in HUVECs. miR-616-3p and XIAP may be used as therapeutic targets of atherosclerosis in the future.

PMID:33968191 | PMC:PMC8097190 | DOI:10.3892/etm.2021.10093

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Effects of leukocyte- and platelet-rich plasma on tendon disorders based on in vitro and in vivo studies (Review)

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Exp Ther Med. 2021 Jun;21(6):639. doi: 10.3892/etm.2021.10071. Epub 2021 Apr 16.

ABSTRACT

Tendon-related disorders are common musculoskeletal system disorders in clinical practice, accounting for 30-50% of all sports-related injuries, and they are difficult to treat due to the hypovascular structure of the tendons. Platelet-rich plasma (PRP), including pure PRP and leukocyte- and platelet-rich plasma (L-PRP), has been attracting increasing attention, as it may stimulate tissue regeneration through the release of growth factors and cytokines. The aim of the present review was to provide a summary of the effects of L-PRP on tendon disorders and the underlying mechanisms through a comprehensive examination of the published literature, including in vitro, animal and clinical studies. It has been demonstrated that L-PRP results in comparatively greater pain relief and improved function in patients suffering from tendon disorders. Fur thermore, L-PRP may exert its effects through a diverse range of mechanisms, such as neovascularization, cell proliferation and differentiation of tendon/progenitor stem cells into tenocytes, as well as extracellular matrix reorganization by transforming type III to type I collagen fibers. It has also been indicated that the effects of leukocytes in L-PRP depend on the biological state of the injured tissue and its surrounding microenvironment. L-PRP is beneficial and promotes tendon healing at the early stage, whereas it is likely detrimental to the repair of tendon at a later stage because of the risk of excessive catabolic and inflammatory responses. Overall, the application of L-PRP in tendon disorders appears to be a promising field that is worthy of further research.

PMID:33968170 | PMC:PMC8097231 | DOI:10.3892/etm.2021.10071

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Effects of hypothermia on inflammatory cytokine expression in rat liver following asphyxial cardiac arrest

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Exp Ther Med. 2021 Jun;21(6):626. doi: 10.3892/etm.2021.10058. Epub 2021 Apr 15.

ABSTRACT

Hypothermic treatment is known to protect against cardiac arrest (CA) and improve survival rate. However, few studies have evaluated the CA-induced liver damage and the effects of hypothermia on this damage. Therefore, the aim of the present study was to determine possible protective effects of hypothermia on the liver after asphyxial CA. Rats were subjected to a 5-min asphyxial CA followed by return of spontaneous circulation (ROSC). The body temperature was controlled at 37±0.5˚C (normothermia group) or 33±0.5˚C (hypothermia group) for 4 h after ROSC. Livers were examined at 6, 12 h, 1 and 2 days after ROSC. Histopathological examination was performed by H&E staining. Alterations in the expression levels of pro-inflammatory (TNF-α and interleukin IL-2) and anti-inflammatory cytokines (IL-4 and IL-13) were investigated by immunohistochem istry. Sinusoidal dilatation and vacuolization were observed after asphyxial CA by histopathological examination. However, these CA-induced structural alterations were prevented by hypothermia. In immunohistochemical examination, the expression levels of pro-inflammatory cytokines were reduced in the hypothermia group compared with those in the normothermia group while the expression levels of anti-inflammatory cytokines were increased in the hypothermia group compared with those in the normothermia group. In conclusion, hypothermic treatment for 4 h following asphyxial CA in rats inhibited the increase of pro-inflammatory cytokines and stimulated the expression of anti-inflammatory cytokines compared with the normothermic group. The results of the present study suggested that hypothermic treatment after asphyxial CA reduced liver damage via the regulation of inflammation.

PMID:33968162 | PMC:PMC8097226 | DOI:10.3892/etm.2021.10058

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Effects of Supine and Prone Positions on Nasal Patency in Healthy Individuals

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Ear Nose Throat J. 2021 May 10:1455613211015437. doi: 10.1177/01455613211015437. Online ahead of print.

ABSTRACT

OBJECTIVES: Supine position reduces nasal patency compared with that in the sitting position; however, data on the effects of prone position on nasal patency is lacking.

METHODS: We assessed the nasal patency of 30 healthy individuals without upper respiratory tract disorders by using visual analog scale (VAS) score and acoustic rhinometry in 7 positions: si tting; frontal, right, and left supine; and frontal, right, and left prone.

RESULTS: According to the VAS scores, compared with that in the sitting position, both the supine and prone positions significantly increased subjective nasal obstruction (P < .001). The prone position had a more significant effect than did the supine position (P = .017). The results of minimal cross-sectional area measured through acoustic rhinometry demonstrated that both the supine and prone positions reduced the nasal patency significantly, but without significant differences between the effects of prone and supine positions (P = .794).

CONCLUSION: This is the first study to elucidate that the prone position can significantly reduce the nasal patency in healthy individuals through subjective and objective assessments.

LEVEL OF EVIDENCE: IV.

PMID:33970694 | DOI:10.1177/01455613211015437

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Role of Bilateral Inferior Turbinoplasty as an Adjunct to Septoplasty in Improving Nasal Obstruction and Subjective Performance in Patients With Deviated Nasal Septum Associated With Allergic Rhinitis: An Interventional, Prospective Study

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Ear Nose Throat J. 2021 May 10:1455613211015440. doi: 10.1177/01455613211015440. Online ahead of print.

ABSTRACT

BACKGROUND: Patients with nasal obstruction due to deviated nasal septum (DNS) often have allergic rhinitis (AR) as contributing factor. When optimal medical therapy for AR fails, septoplasty alone may not adequately treat nasal obstruction. Therefore, with bilateral inferior turbinate hypertrophy representing long-standing AR, adding bilateral inferior turbinopla sty (BIT) to septoplasty might be beneficial.

OBJECTIVE: To assess whether septoplasty with/without BIT alleviates nasal obstruction in the above patient cohort and whether adding BIT to septoplasty brings significant benefit.

METHODOLOGY: In this interventional, prospective study, patients with nasal obstruction due to DNS and persistent, moderate-severe AR refractory to optimal medication were randomly allocated into group A (septoplasty alone) and group B (septoplasty with BIT). Nasal Obstruction and Symptom Evaluation (NOSE) score, along with Subjective Performance parameters (days-off/month; number of outdoor visits/month; overall satisfaction score [OSS]) were used to assess the symptom and quality of life, respectively, at follow-up.

RESULTS: Each group had 40 age/sex-matched patients. Friedman test, and subsequent pair-wise comparison within groups without Bonferroni correction, revealed that septoplasty with/without BIT elicited significant reductio n in NOSE scores and in the Subjective Performance parameters (days-off/month; number of outdoor visits/month) at 3 and 6 months. Wilcoxon Signed Rank test revealed that the OSS within groups also improved significantly with time. Further, comparison between groups revealed significant improvement in NOSE scores at all levels of follow-up when BIT was included. However, there were no significant differences between groups in the Subjective Performance parameters at any level of follow-up. Improvement in OSS between groups was significant only at 3 months but not subsequently.

CONCLUSION: Septoplasty with/without BIT is helpful in treating patients with DNS and refractory AR. However, although adding BIT brings significant benefit in decreasing nasal obstruction, it does not significantly improve the Subjective Performance parameters during follow-up, except for OSS at the third month.

PMID:33970700 | DOI:10.1177/01455613211015440

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Κυριακή 9 Μαΐου 2021

Tension pneumoventricle: Reversible cause for aphasia

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Qatar Med J. 2021 Apr 23;2021(1):15. doi: 10.5339/qmj.2021.15. eCollection 2021.

ABSTRACT

Pneumocephalus is air in the cranium commonly seen in postcraniotomy and in head injury patients. When this air causes an increase in intracranial pressure leading to neurological deterioration, it is called tension pneumocephalus. Similarly, intraventricular air causing compression on vital centers and increasing intracranial pressure is called tension pneumoventricle, and this causes expressive aphasia, which is rarely described in the literature. This study reported a case of a traumatic cerebrospinal fluid (CSF) leak leading to tension pneumoventricle and aphasia. Case: A young male patient sustained severe head injury and had extradural hematoma (EDH) and multiple skull and skull base fractures. EDH was drained, and he recovered and was discharged with a Glasgow coma scale score of 15. He presented to neurosurgical outpatient with CSF leak, aphasia, and loss of bowel and bladder control for a duration of three days. Computed tomography brain scan showed tension pneumoventricles, and he was started on conservative management. His general condition deteriorated, and the next day, his pupils became unequal, and Glasgow coma scale (GCS) dropped to 8/15. He was immediately taken to theater, and the air was aspirated from the ventricles, and an external ventricular drain was inserted. The patient woke up in the immediate postoperative period and started talking normally by day four. Conclusion: Tension pneumoventricles should be considered a cause of aphasia. Immediate intervention and reduction of intracranial pressure are crucial to reverse neurological abnormality and improve patient's outcome.

PMID:33959489 | PMC:PMC8067619 | DOI:10.5339/qmj.2021.15

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Increased risk of secondary lung cancer in patients with tuberculosis: A nationwide, population-based cohort study

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by Li-Ju Ho, Hung-Yi Yang, Chi-Hsiang Chung, Wei-Chin Chang, Sung-Sen Yang, Chien-An Sun, Wu-Chien Chien, Ruei-Yu Su

Background

Tuberculosis (TB) presents a global threat in the world and the lung is the frequent site of metastatic focus. A previous study demonstrated that TB might increase primary lung cancer risk by two-fold for more than 20 years after the TB diagnosis. However, no large-scale study has evaluated the risk of TB and secondary lung cancer. Thus, we evaluated the risk of secondary lung cancer in patients with or without tuberculosis (TB) using a nationwide population-based dataset.

Methods

In a cohort study of 1,936,512 individuals, we selected 6934 patients among patients with primary cancer and TB infection, based on the International Classification of Disease (ICD-p-CM) codes 010–011 from 2000 to 2015. The control cohort comprised 13,868 randomly selected, propensity-matched patients (by age, gender, and index date) without TB exposure. Using this adjusted date, a possible association between TB and the risk of developing secondary lung cancer was estimated using a C ox proportional hazards regression model.

Results

During the follow-up period, secondary lung cancer was diagnosed in 761 (10.97%) patients with TB and 1263 (9.11%) patients without TB. After adjusting for covariates, the risk of secondary lung cancer was 1.67 times greater among primary cancer in the cohort with TB than in the cohort without TB. Stratification revealed that every comorbidity (including diabetes, hypertension, cirrhosis, congestive heart failure, cardiovascular accident, chronic kidney disease, chronic obstructive pulmonary disease) significantly increased the risk of secondary lung cancer when comparing the TB cohort with the non-TB cohort. Moreover, the primary cancer types (including head and neck, colorectal cancer, soft tissue sarcoma, breast, kidney, and thyroid cancer) had a more significant risk of becoming secondary lung cancer.

Conclusion

A significant association exists between TB and the subsequent risk for metastasis among primary cancers and comorbidities. Therefore, TB patients should be evaluated for the subsequent risk of secondary lung cancer.

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