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Objective: Stress increases CRH level in the blood, which then affects the mast cell's number and function. This study aims to determine whether there is a correlation between the lengths of exposure and changes in the level of CRH and the existence and the activity of the mast cells in the area of amygdale, thalamus and hippocampus in rats exposed to acute stress. Methods: Sixteen rats were divided randomly; 4 in the control group and 12 in the exploratory group. The latter were then equally divided into 3 experimental groups, each consisting of 4 subjects. Each of the 12 rats that belonged to the 3 experimental groups was exposed to stress using the psychological stress device for three different lengths of time; 30, 60, and 90 minutes. The CRH plasma was then examined using enzyme-linked immunosorbent assay (ELISA), mast cells in amygdale, thalamus and hippocampus using the light microscope. Results: There was no significant difference in the number of mast cells, but the ones in the thalamus tended to increase (p = 0.092), compared to the amygdale (p = 0.269) and hippocampus (p = 0.117), in line with the length of the treatment, amygdale (r=0,291, P=0,274), hippocampus (r=-0.250, p=0.350), thalamus (r=0.619, p=0.11) in the response to stress level. Conclusions: There was a significant correlation between the lengths of exposure, the level of CRH with the number of mast cells in the thalamus, but there was no correlation both in amygdale or hippocampus. [ABSTRACT FROM AUTHOR]

Objective: Stress triggers and causes psychiatric disorders. This study compared stress generated by different stressors: a cat as the predator of rats and a Psychological Stress Device (PSD) which was developed and modified by the researchers based on the model by Xu and Rocher. Methods: Twenty-eight Wistar rats were simple randomly divided into one control group and six treatment groups, each consisting of 4 rats. Each treatment group was individually exposed to stressor for 30, 60, and 90 minutes. The first three treatment groups were treated using the PSD while the other three treatment groups were treated exposed to the cat. Plasma CRH level was measured using the ELISA (Cusabio) method. Result: Plasma CRH levels in the rat exposed to stressor using the PSD ranged from 9.89 to 50.22 ng/mL, higher than plasma CRH level in the groups exposed to cat ranged from 0.22 to 23.44 ng/mL with significance level (p<0,05). The average of plasma CRH level in the rats exposed to the PSD for 30, 60, and 90 minutes were 14.83, 28.19, and 36 respectively. 14 ng/mL while in the groups exposed to cats were 11.53, 7.81, and 4.97 ng/mL respectively. The increase of plasma CRH level had positive correlation with the length of exposure to stressor in the group treated with the PSD (r=0.895, p of <0.05) while plasma CRH level in the group exposed to cat did not correlate with the length of exposure (r=-0.043, p>0.05). Conclusion: Plasma CRH level of the rats exposed to stressor using the PSD was higher and positively correlate with the length of exposure compared to those exposed to cat. [ABSTRACT FROM AUTHOR]

Aim: Find upregulation markers (i.e., mRNA expression, protein kinase C [PKC]-alpha enzyme level, prostate calcium level, and prostate contractility) in benign prostatic hyperplasia (BPH) patients with a history of long-term alpha-1 blocker (tamsulosin) therapy. Materials and Methods: Samples were taken from prostate chips in 30 BPH patients, which were divided into three groups: Without therapy, history of tamsulosin 0.4 mg therapy for 1 month, and >6 months, respectively. This study used organ baths to measure the prostate smooth muscle isometrical contractility and real-time polymerase chain reaction to count the number of mRNA a1-adrenergic receptors. Calcium levels were measured using confocal laser scanning; PKC-alpha enzymes were measured using ELISA. Results: Tamsulosin 0.4 mg therapy for 1 month decrease mRNA expression, PKC-alpha enzyme, prostate calcium level, and prostate contractility (significant in mRNA expression and PKC-alpha enzyme) compared to no therapy. Meanwhile, usage of tamsulosin 0.4 for >6 months significantly increased mRNA expression, PKC-alpha enzyme, prostate calcium level, and prostate contractility compared to therapy with tamsulosin 0.4 mg for a month. There were no significant differences in mRNA expression, PKC-alpha enzyme, prostate calcium level, and prostate contractility in the group using tamsulosin therapy for >6 months compared to the group without therapy. Conclusions: Tamsulosin 0.4 mg therapy for >6 months cause upregulation, shown by significant increases in mRNA expression, PKC-alpha enzyme, prostate calcium level, and prostate contractility. [ABSTRACT FROM AUTHOR]

Background: Benign prostate hyperplasia (BPH) is the most common degenerative disease in elderly men, with the alpha-1 blocker as the primary treatment. Long-term use of alpha-1 blocker, however, commonly leads to upregulation of alpha receptors and reduces the efficacy of treatment. Aim: This study aimed to find mRNA expression markers of upregulation and prostate contractility in BPH patients with a history of long-term alpha-1 blocker therapy. Methods: Prostate chips were obtained from 30 BPH patients with either no history of tamsulosin therapy, a history of tamsulosin 0.4 mg treatment therapy for 1 month and a history of tamsulosin 0.4 mg treatment therapy for >6 months with a histopathology result showing BPH. Organ bath instruments were used to measure isometric contractions of prostate smooth muscle, and real-time polymerase chain reaction was used to assess the number of adrenergic-a1 receptors. Results: Tamsulosin 0.4 mg therapy for 1 month decreased prostate smooth muscle contractility and significantly decreased mRNA expression compared to the group with no therapy. Tamsulosin 0.4 mg therapy for >6 months significantly increased mRNA expression and prostate smooth muscle contractility compared to the group with tamsulosin 0.4 mg therapy for 1 month. There were no significant differences in mRNA expression and prostate contractility in a group with 6 months of tamsulosin therapy compared to the group without tamsulosin therapy. Conclusion: Tamsulosin 0.4 mg therapy for >6 months led to upregulation marked by significantly increased in mRNA expression and prostate smooth muscle contractility. [ABSTRACT FROM AUTHOR]

Intra-abdominal adhesion (IAA) is the most significant complication after surgery. This study explores the active compound from Eleutherine americana Merr. as a regulator of mitochondrial calcium homeostasis in IAA. This study aimed to evaluate computationally the potential of E. americana Merr. extract as a mitochondrial calcium activator in IAA cases. Materials and Methods: The sample was 14 active compounds from E. americana Merr. extract that was collected from the PubChem database. Prediction as a calcium channel activator was conducted using Prediction of Activity Spectra for Substances SERVER. Human intestinal absorption (HIA) and lethal dose 50 (LD50) were evaluated using SERVER. Protein target and pathway were evaluated using STITCH, and computational analysis was done using Cytoscape. Results: The results showed that 10 bioactives from E. americana Merr. extract have potential as calcium activators (Pa >0.3). The active compound of E. americana Merr. can be easily absorbed in the intestine based on its HIA+ score (HIA >0.9). Conclusion: The application of this extract was possible due to LD50 evaluation that showed that it was less toxic (LD50 <3 mol/kg-BW). E. americana Merr. extract regulates mitochondrial calcium homeostasis, by modulation of two types of the mitochondrial calcium channels, VDAC1 and MARCK (mRyR). [ABSTRACT FROM AUTHOR]