Rothmcknight8119
Male sexual dysfunction negatively affects an individual's quality of life and thus its of prime public concern, hence the need to boost reproductive abilities in such individuals. This study assessed the effect of hydroethanolic root extracts of
(CBRE),
(SJRE), and
(PPRE), commonly used as aphrodisiacs in Ghana, using male Sprague-Dawley rats.
Plasma testosterone, follicle-stimulating hormone, and luteinizing hormone were assayed in grouped rats treated orally with 1 mL/kg normal saline, 50 mg/kg monosodium glutamate (MSG), and 100, 300, or 1000 mg/kg CBRE, SJRE, and PPRE, respectively, for 60 days. Epididymis and testis weights were determined. Semen was assessed on spermatozoa count, motility, and morphology. Malonyladehyde formation in lipid-peroxidation assay and histological examinations were performed to assess pathological changes in testes. Testicular testosterone was also assayed.
While MSG, CBRE, SJRE, and PPRE treatments did not result in significant reduction (
>0.05) in plasma testosterone, there was significant reduction (
≤0.05 -0.0001) in plasma luteinizing hormone, and follicle-stimulating hormone. The combined mean wet weights of epididymides and testes of all treated groups did not vary significantly (
>0.05) from the control. There was significant reduction (
≤0.0001) in sperm motility and count, with significant morphological changes (
≤0.05-0.001), ie, bent necks, tails, and midpieces, and multiple anomalies in the spermatozoa in extract and MSG-treated groups. There was also significant (
≤0.0001) reduction in testicular testosterone among all treatment groups.
Hydroethanolic CBRE, SJRE, and PPRE were found to have detrimental effects on reproductive function with prolonged usage and thus may not be safe to use in healthy males who intend to reproduce.
Hydroethanolic CBRE, SJRE, and PPRE were found to have detrimental effects on reproductive function with prolonged usage and thus may not be safe to use in healthy males who intend to reproduce.
The ability of statins to reduce LDL-c plays an important role in both primary and secondary prevention of atherosclerotic cardiovascular diseases. Such treatment can often be costly, but using generic atorvastatin may reduce cost by up to US$2635. In addition, a previous 8-week study found that it exhibited comparable efficacy to the brand-name medication. This study aimed to evaluate the efficacy of generic atorvastatin over a longer period of six months in a real-world setting.
This was a retrospective cohort study in adult patients who had received brand-name atorvastatin for at least three months and then had switched to generic atorvastatin for at least six months. Lipid and safety profiles were evaluated at six months after switching. Adjusted analyses for age, sex, co-morbid disease, dosage, and indications for statin therapy were also performed.
During the study period, there were 488 patients who met the study criteria. The mean (SD) age of the patients was 60.97 (12.26) years, and 48.36% were male (236 patients). At six months, average total cholesterol, HDL-c, and LDL-c were all lower, from 174.43 to 166.15 mg/dL, from 51.64 to 49.51 mg/dL, and from 110.08 to 100.78 mg/dL (p < 0.001), respectively. There were no significant differences in terms of any other laboratory test results. UNC 3230 manufacturer LDL-c exhibited the highest significant reduction at 9.30 mg/dL. Stratified analyses by age, sex, co-morbid disease, dose, and indications for statin therapy revealed similar decreases in HDL-c and LDL-c as in the study population as a whole.
Generic atorvastatin resulted in significantly lower LDL-c than name-brand atorvastatin but less of an increase in HDL-c.
Generic atorvastatin resulted in significantly lower LDL-c than name-brand atorvastatin but less of an increase in HDL-c.
Esophageal squamous cell carcinoma (ESCC) is the predominant histological type of esophageal cancer in China and has an extremely poor prognosis. Circulating free DNA (cfDNA) and plasma heat shock protein 90alpha (Hsp90a) are two novel noninvasive biomarkers for diagnosis and prognostic prediction of several types of cancer. However, to the best of our knowledge, the roles of the two biomarkers in ESCC are still unknown.
Here, we recruited 93 primary ESCC patients and detected plasma concentrations of the two markers at different time points, including 1-3 days pre-chemotherapy, 1-7 days pre-surgery and 7-14 days post-surgery. Baseline concentrations of the two markers were associated with main characteristics of ESCC patients which were collected at first diagnosis. Correlation between the two markers and traditional serum biomarkers at baseline was also examined. Furthermore, dynamic changes of the cfDNA and Hsp90α concentrations among different time points and the potential clinical significance were assessed.
Consequently, there was no significant association between baseline concentrations of the two markers and clinical features. Especially, cfDNA demonstrated stronger correlation with other circulating biomarkers than Hsp90α at baseline level. Importantly, both cfDNA and Hsp90α concentrations were significantly increased after surgery. Kaplan-Meier survival analysis showed that a change in concentration of cfDNA (ΔcfDNA) but not Hsp90α (ΔHSP90ɑ) between pre-surgery and post-surgery had significant effect on the overall survival of surgical patients with ESCC.
Thus, ΔcfDNA evaluation could be a promising prognostic marker for surgical ESCC patients. Our findings may improve the understanding of the function of cfDNA and Hsp90α in ESCC.
Thus, ΔcfDNA evaluation could be a promising prognostic marker for surgical ESCC patients. Our findings may improve the understanding of the function of cfDNA and Hsp90α in ESCC.
Lung adenocarcinoma (LUAD) is the primary subtype of human lung cancer. The effectiveness of treatment and long-term survival of patients with LUAD are current suboptimal. Tripartite motif containing 56 (TRIM56) is a member of the TRIM protein family that have functions predominantly in immunity and cancer.
To investigate the expression of TRIM56 in LUAD, and explore the potential regulatory role of TRIM56 in the invasion and migration of LUAD cells.
The Gene Expression Omnibus datasets and The Cancer Genome Atlas-LUAD cohort were used to analyze the mRNA expression of TRIM56 in LUAD. The differential expression profiles of miRNAs associated with TRIM56 were obtained from The Cancer Genome Atlas-LUAD cohort. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses were performed to determine the principal functions of miRNAs and interacting proteins. Transwell and wound healing were used to detect the effect of overexpression of TRIM56 on the invasion and migration of LUAD cells.