Red ginseng extract blocks histamine-dependent itch by inhibition of H1R/TRPV1 pathway in sensory neurons

Background: Korean Red Ginseng—a steamed root of Panax ginseng Meyer—has long been used as a traditional medicine in Asian countries. Its antipruritic effect was recently found, but no molecular mechanisms were revealed. Thus, the current study focused on determining the underlying molecular mechanism of Korean Red Ginseng extract (RGE) against histamine-induced itch at the peripheral sensory neuronal level. Methods: To examine the antipruritic effect of RGE, we performed in vivo scratching behavior test in mice, as well as in vitro calcium imaging and whole-cell patch clamp experiments to elucidate underlying molecular mechanisms. Results: The results of our in vivo study confirmed that RGE indeed has an antipruritic effect on histamine-induced scratching in mice. In addition, RGE showed a significant inhibitory effect on histamine-induced responses in primary cultures of mouse dorsal root ganglia, suggesting that RGE has a direct inhibitory effect on sensory neuronal level. Results of further experiments showed that RGE inhibits histamine-induced responses on cells expressing both histamine receptor subtype 1 and TRPV1 ion channel, indicating that RGE blocks the histamine receptor type 1/TRPV1 pathway in sensory neurons, which is responsible for histamine-dependent itch sensation. Conclusion: The current study found for the first time that RGE effectively blocks histamine-induced itch in peripheral sensory neurons. We believe that the current results will provide an insight on itch transmission and will be helpful in understanding how RGE exerts its antipruritic effects

Laparoendoscopic Single-Site Surgery (LESS) for Excision of a Seminal Vesicle Cyst Associated with Ipsilateral Renal Agenesis

We report a case of laparoendoscopic single-site surgery (LESS) for a symptomatic left seminal vesicular cyst and ipsilateral renal agenesis. A 49-year-old man presented with a 1-year history of severe irritation upon voiding and intractable, recurrent hematospermia. A computed tomography scan showed a 68×41×38 mm sized left seminal vesicular cyst with ipsilateral renal agenesis. LESS was performed successfully to treat the seminal vesicle cyst. The total operative time was 125 minutes, and blood loss was minimal. The patient was discharged from the hospital on the second postoperative day

Amniotic fluid exerts a neurotrophic influence on fetal neurodevelopment via the ERK/GSK-3 pathway

Background: The fetus is surrounded by the amniotic fluid (AF) contained by the amniotic sac of the pregnant female. The AF is directly conveyed to the fetus during pregnancy. Although AF has recently been reported as an untapped resource containing various substances, it remains unclear whether the AF could influence fetal neurodevelopment. Results: We used AF that was extracted from embryos at 16 days in pregnant SD rat and exposed the AF to the neural cells derived from the embryos of same rat. We found that the treatment of AF to cortical neurons increased the phosphorylation in ERK1/2 that is necessary for fetal neurodevelopment, which was inhibited by the treatment of MEK inhibitors. Moreover, we found the subsequent inhibition of glycogen synthase kinase-3 (GSK-3), which is an important determinant of cell fate in neural cells. Indeed, AF increased the neural clustering of cortical neurons, which revealed that the clustered cells were proliferating neural progenitor cells. Accordingly, we confirmed the ability of AF to increase the neural progenitor cells through neurosphere formation. Furthermore, we showed that the ERK/GSK-3 pathway was involved in AF-mediated neurosphere enlargement. Conclusions: Although the placenta mainly supplies oxygenated blood, nutrient substances for fetal development, these findings further suggest that circulating-AF into the fetus could affect fetal neurodevelopment via MAP kinases-derived GSK-3 pathway during pregnancy. Moreover, we suggest that AF could be utilized as a valuable resource in the field of regenerative medicine

Power Limiter with PIN Diode Embedded in Cavity to Minimize Parasitic Inductance

This letter introduces a power limiter that limits the input power to protect the receiver when a large power enters the radio frequency receiver. When the power limiter receives a large power signal, a positive-intrinsic-negative (PIN) diode is turned on to limit the input power by lowering the impedance. We analyzed the characteristics of the power limiter according to the method of connecting the PIN diode in parallel with the input and output transmission lines of the power limiter. By embedding a PIN diode into the cavity and minimizing the length of the wire, a power limiter was designed and implemented to minimize parasitic inductance. In the S-band, the proposed power limiter’s insertion loss was below 0.5 dB, and the reflection loss characteristics were below 15 dB. Furthermore, it achieved an output P1dB of 21.8 dBm at 3.5 GHz

Acute Severe Symptomatic Hyponatremia Following Coronary Angiography

Hyponatremia is a relatively common electrolyte disorder. Although severe acute hyponatremia following coronary angiography is rare, potentially lethal neurologic manifestations may result. We describe a patient with severe, symptomatic hyponatremia, an unusual complication of coronary angiography. Lack of familiarity with contrast media-related hyponatremia caused a delay in diagnosis and therapy in our case. The diagnosis of acute hyponatremia should be considered in any patient who develops behavioral or neurologic manifestations following coronary angiography. Prompt diagnosis and treatment is essential to avoid permanent neurologic damage or death

Overexpression of USF increases TGF-beta1 protein levels, but G1 phase arrest was not induced in FRTL-5 cells

Transforming growth factor-beta1 (TGF-beta1) is a potent inhibitor of cellular growth and proliferation by G1 phase arrest or apoptosis. We investigated the association of TGF-beta1 with the anti-proliferative effect of upstream stimulatory factor (USF) in Fischer rat thyroid cell line (FRTL-5) cells. [methyl-(3)H] thymidine uptake was measured after treatment of FRTL-5 cells with TGF-beta1 to identify its anti-proliferative effect. USF-1 and USF-2 proteins were in vitro translated, and an electrophoretic mobility shift assay was performed to identify the interaction between USF and the TGF-beta1 promoter. FRTL-5 cells were transfected with USF cDNA, and then the expression of TGF-beta1 was examined with Northern and Western blotting. The cell cycle-regulating proteins associated with TGF-beta1 were also measured. TGF-beta1 significantly inhibited [methyl-(3)H] thymidine uptake in FRTL-5 cells. Two specific binding sites for USF were found in the TGF-beta1 promoter: -1,846 approximately -1,841 (CACATG) and -621 approximately -616 (CATGTG). Overexpression of USF increased both the mRNA levels and protein levels of TGF-beta1. However, the expression of cyclin D1, CDK4, cyclin E, and CDK2, and the phosphorylation of retinoblastoma protein remained unchanged. Overexpression of USF in FRTL-5 cells increased the expression of TGF-beta10 through specific binding to TGF-beta1 promoter. However, the USF-induced expression of TGF-beta1 did not cause G1 arrest