Notes

Real-world results within treatments for remarkably calcified coronary lesions together with intravascular shockwave lithotripsy.
We investigated whether DHEA supplementation had an impact on ovarian reserve parameters and pregnancy rates in patients with poor ovarian response (POR) and primary ovarian insufficiency (POI).

A total of 34 people, 6 patients with POI and 28 patients with POR, were included in the study. The patients in the POR group consisted of two different groups diminished ovarian reserve (DOR) and premature ovarian failure (PMOF). Patients in the POI and POR group were given 50 mg DHEA supplementation daily for 5 months. The primary outcome was to determine spontaneous clinical pregnancy rates. The monthly changes in the serum hormone levels and AFC were recorded for five months. AMH levels were also measured before and after treatment.

The total follow-up time was 152 cycles. The number of pregnancies during the follow-up period was 9. The ratio of pregnancies to the number of patients was 26.5% and the rate per cycle was 5.9%. While 8 of 9 pregnancies resulted in a live birth, one resulted in a miscarriage. The rate of abortion was 11.1%. The mean AFC was 0 to 5 before treatment. Following DHEA administration, a significant increase was detected in 30.8% of the patients. There was an increase in AMH levels after DHEA, but this was not significant. The live birth rate and pregnancy rate per cycle were significantly higher in POR patients than those in POF. Patients with POF had no pregnancy. Although the PMOF patients were younger than the DOR patients, the rate of pregnancy (36% vs. CAY10603 cell line 29%), and pregnancy rates per cycle (8.5% vs. 6.35%) were higher in the DOR group. The rates of live birth were the same in the PMOF and DOR groups (29% vs. 29%).

Oral DHEA supplementation improves both ovarian reserve and pregnancy rates in women with POR.
Oral DHEA supplementation improves both ovarian reserve and pregnancy rates in women with POR.
Bisphosphonate related osteonecrosis of the jaw (BRONJ) is progressive bone destruction in the maxillofacial region of patients under current or previous treatment with Bisphosphonates. The present case series study aimed to evaluate if ozone/oxygen therapy and debridement with piezoelectric surgery may improve the treatment of BRONJ.

The treatment modality of the patients included ozone/oxygen mixture from medical oxygen. The protocol for ozone/oxygen mixture therapy appointments was set as twice a week for 10 weeks, for a total of 20 applications for each patient. The evaluation of the lesions was based on the clinical and radiologic parameters. The primary outcome was the necrotic lesion reduction during ozone/oxygen therapy sessions and up to the end of follow up periods. The healing of the lesion was taken as a positive result. The level of significance was taken as p <0.05.

A total of 14 patients affected by osteonecrosis were included. The mean follow-up of the patients was 14.3 months. The overall success rate after treatment was 64.2%.

According to the results, ozone/oxygen therapy and debridement with Piezoelectric surgery for BRONJ treatment is a safe procedure with successful outcomes.
According to the results, ozone/oxygen therapy and debridement with Piezoelectric surgery for BRONJ treatment is a safe procedure with successful outcomes.
The therapeutic application of ozone and its derivatives in the dental field has been used for many purposes. However, there has yet to be a consistent evaluation of the outcomes, due to the lack of standardization of the treatment operating procedures.

The keywords "ozone", "ozonated", "ozonation" "ozonized", "ozonization", "dentistry", "periodontology", "oral surgery", "oxygen-ozone therapy" were used to perform a literature review using PubMed, Cochrane, Google Scholar, Zotero databases with the temporal restriction for manuscripts published between 2010 and 2020. Clinical trials and case reports of good, neutral, as well as negative results related to ozone treatment specifications were evaluated.

A better understanding of the mechanisms of action of this bio-oxidative therapy could open new horizons related to the personalization of treatments and the quality of dental care. The critical condition to achieve these goals is an improved knowledge of the qualitative/quantitative characteristics of ozone and its derivatives.
A better understanding of the mechanisms of action of this bio-oxidative therapy could open new horizons related to the personalization of treatments and the quality of dental care. The critical condition to achieve these goals is an improved knowledge of the qualitative/quantitative characteristics of ozone and its derivatives.
Prior cardiovascular event and kidney dysfunction are both strong risk factors for coronary artery disease. The aim of this study is to assess coronary atherosclerotic burden in a large population of patients undergoing coronary angiography, according to prior cardiovascular event or chronic kidney disease.

We evaluated 700 consecutive patients who underwent coronary angiography (CA). Serum creatinine to estimate glomerular filtration rate (eGFR) was measured. Clinically significant coronary artery disease (CAD) was defined by the presence of a coronary lesion resulting in a luminal stenosis >50%. For the purpose of the study, the whole population was divided into 4 subgroups according to the presence/absence of eGFR <60 ml/min/1.73 m2 or prior cardiovascular event eGFR≥60/no event (Group A), eGFR≥60/yes event (Group B), eGFR<60/no event (Group C), eGFR<60/yes event (Group D).

As expected, patients in group D had the worst clinical and biochemical profile. These patients also presented the highest values of urinary albumin creatinine ratio (ACR, p<0.001) and the lowest values of eGFR (p<0.01). One-hundred-ninety-six patients had three-vessel disease. Patients who had undergone PCI procedure showed a lower eGFR as compared to patients who had not (p=0.009). Considering group A as reference, the risk of having three-vessel disease was increased in group B (OR= 2.09; 95% CI 1.37-3.19), in group C, (OR= 1.80; 95% CI 1.04-3.14), and finally in group D (OR= 3.35; 95% CI 2.01-5.58). The risk carried by group C was not significantly different from that carried by Group B OR= 0.86; 95% CI 0.5-1.5.

In our study, low eGFR seems to have the same excess risk of prior CV event.
In our study, low eGFR seems to have the same excess risk of prior CV event.
Oxidative stress is one of the main factors leading to myocardial cell damage, and the redox imbalance promotes apoptosis. Therefore, the purpose of this study was to explore the protective effect of PrxII on H2O2-induced H9c2 cell injury.

The overexpressed PrxII cell model was constructed by virus. The H9c2 cells were treated with H2O2, and the supernatant and cells were collected. Then, the chymotrypsin-like activity, caspase-like activity, and trypsin-like activity were detected by the kit, and the expressions of P21, P27, and P53 were detected by the ELISA method. Finally, the expressions of antioxidant factors, apoptosis-related factors, and AMPK/Sirt1 signaling pathway were detected by Western blot and Real-time polymerase chain reaction (PCR).

Overexpression of PrxII inhibited the decrease of enzyme activity induced by H2O2, promoted the expressions of anti-oxidation factors GPX1, GPX2, and GSX, and inhibited the expressions of apoptosis-related factors P21, P27, and P53, and activated AMPK/Sirt1 pathway.

Overexpression of PrxII can activate the AMPK/Sirt1 pathway, thereby inhibiting H2O2-induced oxidative stress and slowing apoptosis.
Overexpression of PrxII can activate the AMPK/Sirt1 pathway, thereby inhibiting H2O2-induced oxidative stress and slowing apoptosis.
Acute myocardial infarction (AMI) is a severe fatal disease throughout the world. Myocardial IR limits the recovery of impaired cardiac function in AMI patients. This study aims to elucidate the role of long non-coding RNA (lncRNA) HOTAIR in myocardial ischemia-reperfusion (IR) and the underlying mechanism, thus providing a novel therapy for AMI.

Myocardial IR model in mice was firstly constructed by LAD. Plasma levels of LDH, CK-MB, HOTAIR, and microRNA-126 in mice were detected. Subsequently, in vitro HR model was constructed in H9c2 cells. Regulatory effects of HOTAIR on proliferative ability, LDH release, and Caspase-3 activity in H2O2-induced H9c2 cells were determined. Relative levels of inflammatory factors in in vitro HR model were measured by enzyme-linked immunosorbent assay (ELISA). The regulatory loop HOTAIR/microRNA-126/SRSF1 was finally verified by Dual-Luciferase reporter assay.

LDH and CK-MB were significantly released in mice with myocardial IR. HOTAIR was upregulated, while microRNA-126 was downregulated in IR mice and H2O2-induced H9c2 cells. Overexpression of HOTAIR stimulated proliferative ability, LDH release, and Caspase-3 activity in H2O2-induced H9c2 cells. Besides, overexpression of microRNA-126 inhibited the release of inflammatory factors in H9c2 cells undergoing HR induction. The regulatory loop HOTAIR/microRNA-126/SRSF1 was identified to influence IR development.

HOTAIR aggravates myocardial IR by competitively binding SRSF1 with microRNA-126.
HOTAIR aggravates myocardial IR by competitively binding SRSF1 with microRNA-126.
To detect the potential of microRNA-492 (miR-492) as a diagnostic biomarker of acute myocardial infarction (AMI) in the acute phase.

A total of 100 AMI patients and 100 controls (non-AMI patients with chest pain) were retrospectively analyzed. Blood samples were collected at 0, 6, 12, and 24 h after admission, followed by detection of the serum miR-492 level. Serum levels of cTnI and creatine kinase-MB (CK-MB) in AMI patients were examined by enzyme-linked immunosorbent assay (ELISA). The potential relationship between miR-492 level with cTnI and CK-MB levels was analyzed by Pearson correlation test. Moreover, diagnostic value of miR-492 was assessed by depicting receiver operating characteristic (ROC) curves.

Serum level of miR-492 achieved the peak at 6 h after admission, which was time-dependently reduced at 12 h and 24 h. Serum levels of cTnI and CK-MB were higher in AMI patients than those of controls. However, miR-492 level achieved the peak before cTnI and CK-MB increased to the highest levels. MiR-492 level was positively correlated to cTnI and CK-MB levels. ROC curves verified the diagnostic value of miR-492 in AMI (AUC=0.8621, 95% CI=0.8129-0.9112, sensitivity=80%, specificity=75%).

Serum level of miR-492 remarkably increases in the acute phase of AMI, which may be used as an effective biomarker for diagnosing AMI.
Serum level of miR-492 remarkably increases in the acute phase of AMI, which may be used as an effective biomarker for diagnosing AMI.
Arterial stiffness may be an early marker for vascular changes associated with hypertension in young adults. Individuals with a family history of hypertension are at high risk of developing hypertension. We investigated whether arterial stiffness measured, such as mean arterial pressure (MAP) and brachial to ankle pulse wave velocity (baPWV), were increased in normotensive offspring with a parental history of hypertension.

We compared MAP and baPWV in a sample of 1953 non-hypertensive participants (974 men, mean age 42±3 years) recruited in the previous Hanzhong adolescent hypertension cohort study. Standardized questionnaires, physical examinations and laboratory tests were used to obtain information, with a particular focus on family hypertension history, anthropometric, hemodynamic, and biochemical factors.

A total of 1039, 759, 155 participants had 0, 1, and 2 parents with hypertension, respectively. Parental hypertension was associated with elevated offspring MAP (in multivariable-adjusted models, B=1.
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