Intraocular pressure-lowering effect of Cordyceps cicadae mycelia extract in a glaucoma rat model.

Glaucoma is a leading cause of irreversible blindness worldwide. This study evaluates the reduction of intraocular pressure (IOP) induced by C. cicadae mycelia extract in a steroid-induced rat model of glaucoma. Cordyceps cicadae mycelia is a well-known and valued traditional Chinese herbal medicine. C. cicadae mycelia were cultured using a liquid fermentation technique. The harvested C. cicadae mycelia were then lyophilized and extracted with two solvents, water and ethanol. The aqueous extract (CCM-DW) and ethanolic extract (CCM-EtOH) of the mycelia were obtained through lyophilization. Sprague Dawley rats were randomly divided into four groups (n = 6 in each group): a normal group, a control group, and experimental groups treated with CCM-DW, or CCM-EtOH (both at 50 mg/kg/body weight). Except for those in the normal group, all rats received a subconjunctival injection of betamethasone to induce high IOP. The rats in the experimental groups received a daily administration of CCM by oral gavage for four consecutive weeks. IOP reduction is the known treatment for glaucoma. The results revealed that steroid treatment caused a significant increase in the animals' IOP (control group). Elevated IOP decreased significantly after treatment with CCM-DW and CCM-EtOH (p < 0.01), and CCM-DW was more effective than CCM-EtOH. CCM-DW and CCM-EtOH were capable of causing significant decreases in high IOP-induced lesions in pathological studies in which it was shown that the efficacy of CCM-DW surpassed that of CCM-EtOH. After CCM-DW administration for 28 days, there were significant decreases in malondialdehyde and lactate dehydrogenase levels and significant increases in catalase, superoxide dismutase, and glutathione peroxidase levels. In summary, C. cicadae mycelia may be beneficial for preventing or treating glaucoma due to its significant IOP-lowering and antioxidant activities.

Cinnamomum Cassia Extracts Suppress Human Lung Cancer Cells Invasion by Reducing u-PA/MMP Expression through the FAK to ERK Pathways.

Cinnamomum cassia exhibits antioxidative, apoptotic, and cytostatic properties. These activities have been attributed to the modulation of several biological processes and are beneficial for possible pharmaceutical applications. However, the potential of C. cassia in retarding lung adenocarcinoma cells metastasis remains ambiguous. We determined whether C. cassia extract (CCE) reduces metastasis of human lung adenocarcinoma cells. The results showed that CCE treatment (up to 60 µg/mL) for 24 h exhibited no cytotoxicity on the A549 and H1299 cell lines but inhibited the motility, invasiveness, and migration of these cells by repressing matrix metalloproteinase (MMP)-2 and urokinase-type plasminogen activator (u-PA). CCE also impaired cell adhesion to collagen. CCE significantly reduced p-focal adhesion kinase (FAK) Tyr397, p-FAK Tyr925, p-extracellular signal-regulated kinases (ERK)1/2, and Ras homolog gene family (Rho)A expression. CCE showed anti-metastatic activity of A549 and H1299 cells by repressing u-PA/MMP-2 via FAK to ERK1/2 pathways. These findings may facilitate future clinical trials of lung adenocarcinoma chemotherapy to confirm the promising results.

Response of Myeloid Leukemia Cells to Luteolin is Modulated by Differentially Expressed Pituitary Tumor-Transforming Gene 1 (PTTG1) Oncoprotein.

Luteolin, a flavonoid nutraceutical abundant in vegetables and fruits, exhibits a wide range of bioactive properties, including antioxidant, anti-inflammatory and anti-cancer activities. Pituitary tumor-transforming gene 1 (PTTG1), an oncoprotein that regulates cell proliferation, is highly expressed in several types of cancer cells including leukemia. In this study, we aim to investigate the anti-cancer effects of luteolin on cells with differential PTTG1 expression and their underlying mechanisms in human myeloid leukemia cells. Methyl thiazolyl tetrazolium (MTT) assay data showed that luteolin (25-100 µM) significantly reduced cell viability in THP-1, HL-60 and K562 cells but did not affect normal peripheral blood mononuclear cells (PBMCs). Flow cytometric analysis and Western blot data demonstrated that luteolin induced a stronger apoptosis on undifferentiated myeloid leukemia cells with higher PTTG1 protein levels than on 12-myristate 13-acetate (PMA)- or all-trans-retinoic acid (ATRA)-differentiated cells with lower PTTG1 expression. Furthermore, PTTG1 knockdown by shRNA in leukemia cells suppressed cell proliferation, arrested cell-cycle progression and impaired the effectiveness of luteolin on cell-cycle regulation. Moreover, PTTG1-knockdown cells with luteolin exposure presented a reduction of the apoptotic proteins and maintained higher levels of the anti-apoptotic proteins such as Mcl-1, Bcl-2 and p21, which exhibited greater resistance to apoptosis. Finally, microarray analysis showed that 20 genes associated with cell proliferation, such as CXCL10, VEGFA, TNF, TP63 and FGFR1, were dramatically down-regulated in PTTG1-knockdown cells. Our current findings clearly demonstrate that luteolin-triggered leukemic cell apoptosis is modulated by the differential expression of the PTTG1. PTTG1 oncoprotein overexpression may modulate cell proliferation-related regulators and enhance the response of myeloid leukemia cells to luteolin. Luteolin is beneficial for the treatment of cancer cells with highly expressed PTTG1 oncoprotein.

Koelreuteria Formosana Extract Induces Growth Inhibition and Cell Death in Human Colon Carcinoma Cells via G2/M Arrest and LC3-II Activation-Dependent Autophagy.

Autophagy is a self-destructive process that degrades cytoplasmic constituents. In our previous study, Koelreuteria formosana ethanolic extract (KFEE), which is obtained from natural plants endemic to Taiwan, has inhibited cell metastasis in renal carcinoma cells. However, the anticancer effects of KFEE on colon cancer remain unclear. In this study, KFEE exerted a strong cytotoxic effect on DLD-1 and COLO 205 human colorectal cancer cell lines. KFEE effectively inhibited cancer cell proliferation, induced G2/M-phase arrest associated with downregulaton of cyclin E, cyclin B and cdc25C and upregulation of p21, and induced cell death by activating autophagy but did not cause apoptotic cell death. Exposed KFEE cells showed increased levels of acridine orange, autophagic vacuoles, and LC3-II proteins, which are specific autophagic markers. Bcl-2, p-Akt, and p-mTOR levels, which have been implicated in autophagic downregulation, were decreased after KFEE treatment. Autophagy inhibitor 3-methyladenosine and bafilomycin-A1 and genetic silencing of LC3 attenuated KFEE-induced growth inhibition. These findings suggested that KFEE causes cytostatic effect through autophagy. In xenograft studies, oral administration of KFEE had significantly inhibited the tumor growth in nude mice that had received subcutaneous injection of DLD-1 cells. KFEE is a promising candidate in phytochemical-based, mechanistic, and pathway-targeted cancer prevention strategies.

Nelumbo nucifera leaf extract treatment attenuated preneoplastic lesions and oxidative stress in the livers of diethylnitrosamine-treated rats.

Lotus (Nelumbo nucifera Gaertn) possesses antioxidant, hepatoprotective, and anticancer potential. This study determined the protective role of aqueous extract from Nelumbo nucifera leaves (NLE) against N-diethylnitrosamine (DEN)-induced oxidative stress and hepatocellular carcinogenesis in a sample of Sprague-Dawley rats. NLE was fed orally to rats in which hepatic carcinoma was induced with DEN for 12 weeks. Five groups of 12 rats each were used for the study: Group I (control group) rats received distilled water; Group II rats were induced with DEN; Group III rats were induced with DEN and cotreated with 0.5% NLE; Group IV rats were induced with DEN and cotreated with 1.0% NLE; and Group V rats were induced with DEN and cotreated with 2.0% NLE. Clinical chemistry, organ weight, inflammatory marker, protein expression, enzyme, and antioxidant analyses were conducted. NLE administration to rats resulted in significantly decreased levels of serum alanine aminotransferase, aspartate aminotransferase, and albumin, which is indicative of hepatocellular damage, compared with the control group. DEN-induced oxidative stress was inhibited by NLE and this inhibition was paralleled by decreased lipid peroxides and increased glutathione transferase, superoxide dismutase, catalase, and glutathione peroxidase activity in liver tissues. The status of nonenzymatic antioxidants, such as reduced glutathione, was also found to be increased in NLE-administered rats. Furthermore, NLE decreased tumor size, hepatic Rac1, PKCα, and GSTπ expressions compared with the DEN-only group. Thus, supplementation of NLE reduced the adverse changes that occur because of liver cancer. These results prove that NLE protects against liver carcinogenesis induced because of treatment with DEN through blocking lipid peroxidation, hepatic cell damage, and enhancing the antioxidant defense system.

Epigallocatechin gallate sensitizes cisplatin-resistant oral cancer CAR cell apoptosis and autophagy through stimulating AKT/STAT3 pathway and suppressing multidrug resistance 1 signaling.

Epigallocatechin gallate (EGCG) is a green tea polyphenol that presents anticancer activities in multiple cancer cells, but no available report was addressed for the underling molecular mechanism of cytotoxic impacts on drug-resistant oral squamous cell carcinoma cells. In the present study, the inhibitory effects of EGCG were experienced on cisplatin-resistant oral cancer CAR cells. EGCG inhibited cell viability in a time- and concentration-dependent manner by a sulforhodamine B (SRB) assay. EGCG induced CAR cell apoptosis and autophagy by 4',6-diamidino-2-phenylindole (DAPI) dye, acridine orange (AO) staining and green fluorescent protein (GFP)-tagged LC3B assay, respectively. EGCG also significantly enhanced caspase-9 and caspase-3 activities by caspase activity assay. EGCG markedly increased the protein levels of Bax, cleaved caspase-9, cleaved caspase-3, Atg5, Atg7, Atg12, Beclin-1, and LC3B-II, as well as significantly decreased the expression of Bcl-2, phosphorylated AKT (Ser473) and phosphorylation of STAT3 on Tyr705 by western blotting in CAR cells. Importantly, the protein and gene expression of multidrug resistance 1 (MDR1) were dose-dependently inhibited by EGCG. Overall, downregulation of MDR1 levels and alterations of AKT/STAT3 signaling contributed to EGCG-induced apoptosis and autophagy in CAR cells. Based on these results, EGCG has the potential for therapeutic effect on oral cancer and may be useful for long-term oral cancer prevention in the future. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 845-855, 2017.

Effect of Carvacrol on Ca²âº Movement and Viability in PC3 Human Prostate Cancer Cells.

Carvacrol, a monoterpenic phenol compound, has been shown to possess various biological effects in different models. However, the effect of carvacrol on intracellular Ca²âº and its related physiology in human prostate cancer is unknown. This study explored the effect of carvacrol on cytosolic free Ca²âº levels ([Ca²âº]i) and viability in PC3 human prostate cancer cells. Fura-2, a Ca²âº- sensitive fluorescent dye, was used to assess [Ca²âº]i. Cell viability was measured by the detecting reagent WST-1. Carvacrol at concentrations of 200-800 µM caused [Ca²âº]i rises in a concentration-dependent manner. Removal of extracellular Ca²âº reduced carvacrol's effect by approximately 60%. Carvacrol-induced Ca²âº entry was confirmed by Mn²âº entry-induced quench of fura-2 fluorescence, and was inhibited by approximately 30% by nifedipine, econazole, SKF96365, and the protein kinase C (PKC) inhibitor GF109203X. In Ca²âº-free medium, treatment with the endoplasmic reticulum Ca²âº pump inhibitor thapsigargin (TG) abolished carvacrol-induced [Ca²âº]i rises. Treatment with carvacrol also abolished TG-induced [Ca²âº]i rises. Carvacrol-induced Ca²âº release from the endoplasmic reticulum was abolished by inhibition of phospholipase C (PLC). Carvacrol killed cells at concentrations of 200-600 µM in a concentration-dependent fashion. Chelating cytosolic Ca²âº with BAPTA/AM did not prevent carvacrol's cytotoxicity. Together, in PC3 cells, carvacrol induced [Ca²âº]i rises by inducing PLC-dependent Ca²âº release from the endoplasmic reticulum and Ca²âº entry via PKC-sensitive store-operated Ca²âº channels and other unknown channels. Carvacrol also induced Ca²âº-dissociated cell death.

Progressive rear-view mirror for motorcycles.

In this work, we present the design and fabrication of a progressive rear-view mirror for motorcycles. In the context of physiological and physical background knowledge, we first analyze the geometric relationships among the profile of the mirror, the blind spot, the field of view, and the reflected image size. On the basis of Walker's eye model, the binocular disparity is further calculated according to the image size on each retina. We present the polynomial expansion that specifies our progressive mirror's profile, as well as the fused deposition modeling process for fabricating physical mirrors. Compared with a conventional aspheric or flat mirror, this progressive mirror can achieve a wider horizontal viewing angle and shows a more stable image, thus enhancing riding safety.

Rutin improves endotoxin-induced acute lung injury via inhibition of iNOS and VCAM-1 expression.

Endotoxins exist anywhere including in water pools, dust, humidifier systems, and machining fluids. The major causal factor is endotoxins in many serious diseases, such as fever, sepsis, multi-organ failure, meningococcemia, and severe morbidities like neurologic disability, or hearing loss. Endotoxins are also called lipopolysaccharide (LPS) and are important pathogens of acute lung injury (ALI). Rutin has potential beneficial effects including anti-inflammation, antioxidation, anti-hyperlipidemia, and anti-platelet aggregation. Pre-treatment with rutin inhibited LPS-induced neutrophil infiltration in the lungs. LPS-induced expression of vascular cell adhesion molecule (VCAM)-1 and inducible nitric oxide synthase (iNOS) was suppressed by rutin, but there was no influence on expression of intercellular adhesion molecule-1 and cyclooxygenase-2. In addition, activation of the nuclear factor (NF)κB was reduced by rutin. Furthermore, we found that the inhibitory concentration of rutin on expression of VCAM-1 and iNOS was similar to NFκB activation. In conclusion, rutin is a potential protective agent for ALI via inhibition of neutrophil infiltration, expression of VCAM-1 and iNOS, and NFκB activation.

Performance evolution of color cone lasing emissions in dye-doped cholesteric liquid crystals at different fabrication conditions.

This work investigates the performance evolution of color cone lasing emissions (CCLEs) based on dye-doped cholesteric liquid crystal (DDCLC) cells at different fabrication conditions. Experimental results show that the energy threshold (E(th)) and relative slope efficiency (η(s)) of the lasing signal emitted at each cone angle (0°-35°) in the CCLE decreases and increases, respectively, when the waiting time in a homogenously rubbed aligned DDCLC cell is increased from 0 hr to 216 hr (9 days). This result occurs because defect lines gradually shrink with the anchoring of the surface alignment when the waiting time is increased. Hence, the scattering loss decreases, and the dwelling time of the fluorescence photons in the resonator increases, which in turn enhances the CCLE performance. With the aligned cell given the pretreatment of a rapid annealing processing (RAP), the waiting time for obtaining an optimum CCLE can markedly be reduced sixfold. The surface alignment of the DDCLC cell also plays a necessary role in generating the CCLE. This work provides an insight into the temporal evolution of the performance for the CCLE laser and offers a method (RAP) of significantly speeding up the formation of a CCLE laser with optimum performance.

Effect of methoxychlor on Ca²âº homeostasis and apoptosis in HA59T human hepatoma cells.

Methoxychlor, an organochlorine pesticide, is thought to be an endocrine disrupter that affects Ca²âº homeostasis and cell viability in different cell models. This study explored the action of methoxychlor on cytosolic free Ca²âº concentrations ([Ca²âº]i) and apoptosis in HA59T human hepatoma cells. Fura-2, a Ca²âº-sensitive fluorescent dye, was applied to measure [Ca²âº]i. Methoxychlor at concentrations of 0.1-1 µM caused a [Ca²âº]i rise in a concentration-dependent manner. Removal of external Ca²âº abolished methoxychlor's effect. Methoxychlor-induced Ca²âº influx was confirmed by Mn²âº-induced quench of fura-2 fluorescence. Methoxychlor-induced Ca²âº entry was inhibited by nifedipine, econazole, SK&F96365, and protein kinase C modulators. Methoxychlor killed cells at concentrations of 10-130 µM in a concentration-dependent fashion. Chelation of cytosolic Ca²âº with 1,2-bis(2-aminophenoxy) ethane-N,N,N',N'-tetraacetic acid/AM (BAPTA/AM) did not prevent methoxychlor's cytotoxicity. Methoxychlor (10 and 50 µM) induced apoptosis concentration-dependently as determined by using Annexin V/propidium iodide staining. Together, in HA59T cells, methoxychlor induced a [Ca²âº]i rise by inducing Ca²âº entry via protein kinase C-sensitive Ca²âº-permeable channels, without causing Ca²âº release from stores. Methoxychlor also induced apoptosis that was independent of [Ca²âº]i rises.

Spatially tunable photonic bandgap of wide spectral range and lasing emission based on a blue phase wedge cell.

This study demonstrates for the first time a continuously tunable photonic bandgap (PBG) of wide spectral range based on a blue phase (BP) wedge cell. A continuously shifting PBG of the BP wedge cell occurs due to the thickness gradient of the wedge cell at a fixed temperature. The wedge cell provides a gradient of boundary force on the LCs and thus forms a distribution of BP crystal structure with a gradient lattice. Additionally, a spatially tunable lasing emission based on a dye-doped BP (DDBP) wedge cell is also demonstrated. The tunable band of the PBG and lasing emission is about 130 nm and 70 nm, respectively, which tuning spectral ranges are significantly wider than those of CLC and DDCLC wedge cells, respectively. Such a BP device has a significant potential in applications of tunable photonic devices and displays.

Paeonol suppresses chondrosarcoma metastasis through up-regulation of miR-141 by modulating PKCδ and c-Src signaling pathway.

Chondrosarcoma, a primary malignant bone cancer, has potential for local invasion and distant metastasis, especially to the lungs. Patients diagnosed with it show poor prognosis. Paeonol (2'-hydroxy-4'-methoxyacetophenone), the main active compound of traditional Chinese remedy Paeonia lactiflora Pallas, exhibits anti-inflammatory and anti-tumor activity; whether paeonol regulates metastatic chondrosarcoma is largely unknown. Here, we find paeonol do not increase apoptosis. By contrast, at non-cytotoxic concentrations, paeonol suppresses migration and invasion of chondrosarcoma cells. We also demonstrate paeonol enhancing miR-141 expression and miR-141 inhibitor reversing paeonol-inhibited cell motility; paeonol also reduces protein kinase C (PKC)d and c-Src kinase activity. Since paeonol inhibits migration and invasion of human chondrosarcoma via up-regulation of miR-141 via PKCd and c-Src pathways, it thus might be a novel anti-metastasis agent for treatment of metastatic chondrosarcoma.

Effect of clotrimazole on cytosolic Ca(2+) rise and viability in HA59T human hepatoma cells.

Abstract Clotrimazole is an antimycotic imidazole derivative that interferes with cellular Ca(2+) homeostasis. This study examined the effect of clotrimazole on cytosolic Ca(2+) concentrations ([Ca(2+)](i)) and viability in HA59T human hepatoma cells. The Ca(2+)-sensitive fluorescent dye fura-2 was applied to measure [Ca(2+)](i). Clotrimazole induced [Ca(2+)](i) rises in a concentration-dependent manner. The response was reduced by removing extracellular Ca(2+). Clotrimazole-evoked Ca(2+) entry was suppressed by store-operated channel inhibitors (nifedipine, econazole and SK&F96365) and protein kinase C modulators (GF109203X and phorbol, 12-myristate, 13-acetate). In Ca(2+)-free medium, incubation with the endoplasmic reticulum Ca(2+) pump inhibitor 2,5-di-tert-butylhydroquinone abolished clotrimazole-induced [Ca(2+)](i) rise. Inhibition of phospholipase C with U73122 abolished clotrimazole-induced [Ca(2+)](i) rise. At 10-40 µM, clotrimazole inhibited cell viability, which was not reversed by chelating cytosolic Ca(2+). Clotrimazole at 10 and 30 µM also induced apoptosis. Collectively, in HA59T cells, clotrimazole-induced [Ca(2+)](i) rises by evoking phospholipase C-dependent Ca(2+) release from the endoplasmic reticulum and Ca(2+) entry via store-operated Ca(2+) channels. Clotrimazole also caused apoptosis.

A New Pharmacological Vitreolysis through the Supplement of Mixed Fruit Enzymes for Patients with Ocular Floaters or Vitreous Hemorrhage-Induced Floaters.

Purpose: Ocular floaters caused by vitreous degeneration or blood clots may interfere with various visual functions. Our study investigated the pharmacologic effects of oral supplementation of mixed fruit enzymes (MFEs) for treating spontaneous symptomatic vitreous opacities (SVOs) and those secondary to vitreous hemorrhage (VH). Methods: 224 patients with monocular symptomatic vitreous opacities (SVOs) were recruited between September and December 2017 and received oral supplementation of MFEs (190 mg bromelain, 95 mg papain, and 95 mg ficin) for 3 months in a double-blind clinical trial. Participants were divided according to the etiology of the SVOs, spontaneous (experiment 1) versus VH (experiment 2), and then randomly assigned into four treatments groups: one group received oral vitamin C, as a placebo; and the other 3 groups received 1 capsule per day (low dose), 2 capsules per day (middle dose), or 3 capsules per day (high dose) of MFEs. The number of SVOs was determined at baseline and then 1, 2, and 3 months after initiating treatment. Further, in cases secondary to VH, the changes in corrected distance visual acuity (CDVA) were assessed after 3 months. Second, we compared the free radical scavenging capabilities of each substance: vitamin C, bromelain, papain, ficin, and MFEs (combination of bromelain, papain, and ficin) by DDPH assay. Finally, SVOs-related symptoms and satisfaction with the treatments were evaluated at the last follow-up visit Results: In experiment 1, the disappearance rate of SVOs was 55%, 62.5%, and 70% after taking 1, 2, and 3 capsules daily, respectively (total p < 0.001), in a dose-dependent manner. In experiment 2, the disappearance rate of VH-induced SVOs was 18%, 25%, and 56% (p < 0.001) after 1, 2, and 3 capsules of the supplement daily, respectively. Additionally, the patients' vision elevated from 0.63LogMAR to 0.19LogMAR (p = 0.008). Conclusions: A pharmacological approach using a high dose of oral supplementation with MFEs (bromelain, papain, and ficin) was effective in reducing vitreous opacities, even after intraocular hemorrhage. Furthermore, pharmacologic vitreolysis with MFEs supplementation showed high patient satisfaction, and also improved CDVA in patients with vitreous hemorrhage-induced floaters

Improvement of Presbyopia Using a Mixture of Traditional Chinese Herbal Medicines, Including Cassiae Semen, Wolfberry, and Dendrobium huoshanense.

BACKGROUND: Presbyopia is a primary cause of a decline in near vision. In this study, we developed a new mixed herbal medicine to retard presbyopic progression and increase the amplitude of accommodation (AA), which is beneficial for near vision. METHODS: A total of 400 participants between the ages of 45 and 70 years were recruited. We designed the mixed herbal drug to include Cassiae Semen (200 mg), wolfberry (200 mg), and Dendrobium huoshanense (DD) (40 mg) in one capsule. In experiment 1, the recruited subjects were directed to perform a push-up test to measure their AA; this was then converted to the additional diopters of reading glasses. In experiment 2, 240 subjects took three capsules daily for six months and then stopped medical therapy for a six-month follow-up. In experiment 3, 160 subjects were randomly categorized into four groups: a placebo group, low-dose group (LDG) (1 capsule daily), middle-dose group (MDG) (two capsules daily), and high-dose group (HDG) (three capsules daily). The 160 volunteers took different doses for six months and then stopped treatment, accompanied by another six-month follow-up. In experiments 2 and 3, the change in AA, uncorrected far visual acuity (UFVA), and uncorrected near visual acuity (UNVA) were recorded each month for one year. RESULTS: In experiment 1, AA was found to decrease with age and a great deal of additional power was needed in older individuals. In experiment 2, the mean AA reached a maximum value of 2.1D (P < 0.05) after six months, while the UNVA improved by about two to three lines of a Jaeger chart in most of the subjects. At nine months, all the means decreased slightly to 2.0 D (P < 0.05). This meant that the mixed herbal medicine could still maintain AA for another three months because the herbal therapy was stopped at the seventh month. In experiment 3, the maximal AA was 2.8D, 2.9D, and 3.2D (P < 0.05) in the LDG, MDG, and HDG after six-month treatments, respectively. Experiment 3 showed that AA gain occurred in a dose-dependent manner; the higher the dose, the greater the AA value. CONCLUSION: Only two studies on the use of herbal drugs for presbyopia have been reported in PubMed. In our study, we found that taking a mixed herbal drug caused an excellent gain in AA. This is the first study to report that the characteristics of the new herbal regimen could retard and even ameliorate presbyopia.

Oral Treatment of Central Serous Chorioretinopathy Patients Using Propranolol Tablets.

PURPOSE: To evaluate the pharmacological effects of propranolol treatment of patients with central serous chorioretinopathy (CSCR) over 4 months. RESULTS: Among the 89 male and 31 female patients, the mean BCVA decreased to 0.42 ± 0.08 logMAR during CSCR attacks. Oral propranolol showed good effectiveness in reducing CSCR signs after at least 4 months of treatment. The final BCVA of the patients in groups 1 and 2 was 0.09 ± 0.01 and 0.19 ± 0.03 logMAR, respectively (p < 0.05). Moreover, the mean complete remission time in groups 1 and 2 was 1.9 and 3.5 months, respectively (p < 0.05), while the "success" rate in groups 1 and 2 was 95.0% (57/60) and 78.3% (47/60), respectively (p < 0.05). The recurrence rate in groups 1 and 2 was 5.3% (3/57) and 25.5% (12/47) after a further 5 months of follow-up, respectively (p < 0.05). MATERIALS AND METHODS: One hundred and twenty patients were enrolled and randomly divided into two groups that both underwent a visual acuity test and optical coherence tomography (OCT) scanning, between April and December 2017. The 60 patients in group 1 were requested to take propranolol for 4 months, while the other 60 subjects (group 2) received placebo therapy during the same period. The best-corrected visual acuity (BCVA) of every volunteer and an OCT image of each patient were checked and recorded at the beginning of the study and each week thereafter. If the signs of CSCR disappeared completely from the OCT scans, the case was considered a "success" and treatment stopped at once. However, the "success" subjects were further evaluated in follow-ups throughout the next 5 months to determine the rate of recurrence in groups 1 and 2. The time of total complete remission of CSCR from the OCT scans was also measured in groups 1 and 2. CONCLUSION: CSCR patients revealed an excellent prognosis and success rate of 95.0% after taking propranolol. The treatment was able to enhance subretinal fluid (SRF) absorption, shorten the time to total complete remission, and significantly decrease CSCR recurrence. As such, we suggest that taking propranolol may be an alternative and viable choice for CSCR patients, given that the new method was shown to be safe, cheap, effective, well tolerated and convenient.

Suppression of experimental uveitis by a recombinant adeno-associated virus vector encoding interleukin-1 receptor antagonist.

PURPOSE: To evaluate the potential of gene therapy with a recombinant adeno-associated virus vector encoding the interleukin-1 receptor antagonist gene (rAAV-IL-1Ra) in the treatment of experimental uveitis. METHODS: The vitreal cavity of New Zealand white rabbits was injected with rAAV-IL-1Ra (4x10(7) infectious units), and the contralateral eye was injected with the same amount of rAAV-LacZ or PBS as a control. Transgene expression was evaluated by immunohistochemistry, ELISA, and RT-PCR. To evaluate the therapeutic potential of rAAV-IL-1Ra, experimental uveitis was induced by intravitreal injection of IL-1alpha at 10 and 100 days after rAAV-IL-1Ra administration. The effects of rAAV-IL-1Ra on experimental uveitis were investigated using histological and aqueous analysis. RESULTS: Following intravitreal injection of rAAV-IL-1Ra, transgene expression was found in various cell types of the ocular tissues, such as ciliary epithelial cells, retinal ganglion cells, and retinal pigment epithelial cells. RT-PCR and ELISA showed that the IL-1Ra transgene persisted in the rabbit eye for at least 100 days. Compared with the control eyes, the transgene expression ameliorated experimental uveitis at 10 and 100 days after a single administration of rAAV-IL-1Ra. CONCLUSIONS: Intravitreal administration of rAAV-IL-1Ra led to sustained human IL-1Ra transgene expression in rabbit eyes for 100 days. The transgene expression suppressed uveitis episodes at 10 and 100 days after rAAV-IL-1Ra injection. Long-term suppression of experimental uveitis could be achieved by gene therapy with rAAV-IL-1Ra.

Changes in visual function during the Coriolis illusion.

BACKGROUND: The Coriolis illusion produces spatial disorientation and is, therefore, dangerous for pilots. It is not known whether it also affects visual function (visual acuity and stereopsis). METHODS: There were 18 subjects (15 men and 3 women, mean age 24.7 yr) enrolled in the study. A spatial disorientation simulator was used to produce Coriolis stimulation. The visual acuity of the subjects was evaluated with the Rosenbaum Vision Card before and during Coriolis stimulation. Stereopsis was measured with the Titmus stereo test. Throughout the experiments, eyeball movements were observed on a television monitor. Electrooculography (EOG) and electroencephalography (EEG) were also documented. RESULTS: Before Coriolis stimulation, the visual acuity and stereopsis of all subjects were 20/20 and 40 s of arc, respectively. During the Coriolis illusion, the visual acuity of nine subjects (50%) remained 20/20, whereas the visual acuity of the others (50%) dropped by two lines. The stereopsis of most subjects (77.8%) decreased to 800 arc-seconds or less. Rhythmic nystagmus was observed, while EOG amplitudes were significantly elevated compared with those at baseline (9.41 +/- 0.26 microv2 and 8.45 +/- 0.36 microv2, respectively). EEG activity (frequency) was also greater than at baseline (13.15 +/- 0.84 Hz and 11.94 +/- 1.20 Hz, respectively; P < 0.05). CONCLUSIONS: During Coriolis stimulation, the visual acuity of the subjects remained stable, but their stereopsis was reduced. Further study is warranted.