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Tolerability and adequate therapeutic dosage of oral clomipramine for the treatment of premature ejaculation: A randomized, double-blind, placebo-controlled, fixed-dose, parallel-grouped clinical study
<P>To evaluate the adequate therapeutic dosage of clomipramine 15 mg/day and clomipramine 30 mg/day in male patients with premature ejaculation (PE), this study enrolled men aged 20-65 years who met diagnostic criteria for PE including Intravaginal Ejaculation Latency Time (IELT) less than 2 min for at least 75% of their sexual intercourses. Subjects received placebo, clomipramine 15 mg, or clomipramine 30 mg prn (2 similar to 6 h before intercourse) for 4 weeks. Efficacy was assessed using fold change, percentile change, and mean change of IELT, as well as Drug Coitus Interval Time (DCIT). A total of 101 patients were randomized into the placebo group, clomipramine 15 mg group, and clomipramine 30 mg group. Analyses of fold changes of IELT in each group revealed that the IELT of both the clomipramine 15 mg group and clomipramine 30 mg group was significantly increased 4 weeks after administration than the placebo group. Adverse events were reported by 11.76, 32.35, and 57.57% of patients in the placebo group, clomipramine 15 mg group, and clomipramine 30 mg group, respectively. Most common adverse events in the clomipramine treatment groups were gastrointestinal disorders and psychiatric disorders of mild to moderate severity. On-demand regimen of clomipramine 15 mg resulted in a significant improvement in IELT and was superior to a regimen of clomipramine 30 mg in terms of risk-to-benefit ratio.</P>
<▼1><P>Bone marrow-derived mesenchymal stem cells (BMMSCs) are used extensively for cardiac repair and interact with immune cells in the damaged heart. Macrophages are known to be modulated by stem cells, and we hypothesized that priming macrophages with BMMSCs would enhance their therapeutic efficacy. Rat bone marrow-derived macrophages (BMDMs) were stimulated by lipopolysaccharide (LPS) with or without coculture with rat BMCs. In the LPS-stimulated BMDMs, induction of the inflammatory marker iNOS was attenuated, and the anti-inflammatory marker Arg1 was markedly upregulated by coculture with BMMSCs. Myocardial infarction (MI) was induced in rats. One group was injected with BMMSCs, and a second group was injected with MIX (a mixture of BMMSCs and BMDMs after coculture). The reduction in cardiac fibrosis was greater in the MIX group than in the BMC group. Cardiac function was improved in the BMMSC group and was substantially improved in the MIX group. Angiogenesis was better in the MIX group, and anti-inflammatory macrophages were more abundant in the MIX group than in the BMMSC group. In the BMMSCs, interferon regulatory factor 5 (IRF5) was exclusively induced by coculture with macrophages. IRF5 knockdown in BMMSCs failed to suppress inflammatory marker induction in the macrophages. In this study, we demonstrated the successful application of BMDMs primed with BMMSCs as an adjuvant to cell therapy for cardiac repair.</P></▼1><▼2><P><B>Heart attacks: mixed cell therapy for heart regeneration</B></P><P>A tailored technique involving stem cells and anti-inflammatory immune cells shows promise for repairing heart tissue damage. Immune cells called anti-inflammatory macrophages are vital for healing of the heart following a heart attack. Youngkeun Ahn, Yong Sook Kim and co-workers at Chonnam National University Hospital in Gwangju, South Korea trialed a novel stem cell therapy on rats to improve cardiac repair. They took bone marrow-derived macrophages and stem cells from each rat and incubated the two cell types together to create individualized treatments. Following induced heart attacks, they injected one group of rats with both cell types, and another group with stem cells only. While heart function improved in both groups, the group treated with both cell types showed significant improvements with a greater reduction in cardiac fibrosis and increased the reparative activity of macrophages.</P></▼2>
Kim, Jin Won,Lee, Yun-Gyoo,Hwang, In Gyu,Song, Hong Suk,Koh, Su Jin,Ko, Yoon Ho,Shin, Seong Hoon,Woo, In Sook,Hong, Soojung,Kim, Tae-Yong,Kim, Sun Young,Nam, Byung-Ho,Kim, Hyun Jung,Kim, Hyo Jung,Lee, Nature Publishing Group UK 2018 The British journal of cancer Vol.118 No.9
<P><B>Background</B></P><P>Older patients have increased risk of toxicity from chemotherapy. Current prediction tools do not provide information on cumulative risk.</P><P><B>Methods</B></P><P>Patients aged ≥ 70 years with solid cancer were prospectively enrolled. A prediction model was developed for adverse events (AEs) ≥ Grade 3 (G3), based on geriatric assessment (GA), laboratory, and clinical variables.</P><P><B>Results</B></P><P>301 patients were enrolled (median age, 75 years). Median number of chemotherapy cycles was 4. During first-line chemotherapy, 53.8% of patients experienced AEs ≥ G3. Serum protein < 6.7 g/dL, initial full-dose chemotherapy, psychological stress or acute disease in the past 3 months, water consumption < 3 cups/day, unable to obey a simple command, and self-perception of poor health were significantly related with AEs ≥ G3. A predicting model with these six variables ranging 0–8 points was selected with the highest discriminatory ability (c-statistic= 0.646), which could classify patients into four risk groups. Predicted cumulative incidence of AEs ≥ G3 was discriminated according to risk groups.</P><P><B>Conclusions</B></P><P>This prediction tool could identify the risk of AEs ≥ G3 after chemotherapy and provide information on the cumulative incidence of AEs in each cycle.</P><P><B>Clinical Trial Id</B></P><P>WHO ICTRP number, KCT0001071</P>
<P>Spintronic and nanomagnetic devices often derive their functionality from layers of different materials and the interfaces between them. We discuss the opportunities that arise from synthetic antiferromagnets consisting of two or more ferromagnetic layers that are separated by metallic spacers or tunnel barriers and have antiparallel magnetizations.</P>
Translation, the mRNA-templated synthesis of peptides by the ribosome, can be manipulated to incorporate variants of the 20 cognate amino acids. Such approaches for expanding the range of chemical entities that can be produced by the ribosome may accelerate the discovery of molecules that can perform functions for which poorly folded, short peptidic sequences are ill suited. Here, we show that the ribosome tolerates some artificial helical aromatic oligomers, so-called foldamers. Using a flexible tRNA-acylation ribozyme—flexizyme—foldamers were attached to tRNA, and the resulting acylated tRNAs were delivered to the ribosome to initiate the synthesis of non-cyclic and cyclic foldamer–peptide hybrid molecules. Passing through the ribosome exit tunnel requires the foldamers to unfold. Yet foldamers encode sufficient folding information to influence the peptide structure once translation is completed. We also show that in cyclic hybrids, the foldamer portion can fold into a helix and force the peptide segment to adopt a constrained and stretched conformation.
Yoo, Ki-Chun,Suh, Yongjoon,An, Yoojeong,Lee, Hae-June,Jeong, Ye Ji,Uddin, Nizam,Cui, Yan-Hong,Roh, Tae-Hoon,Shim, Jin-Kyoung,Chang, Jong Hee,Park, Jong Bae,Kim, Min-Jung,Kim, In-Gyu,Kang, Seok-Gu,Lee, Nature Publishing Group UK 2018 Oncogene Vol.37 No.24
<P>Ionizing radiation is widely used for patient with glioblastoma (GBM). However, the effect of radiation on patient survival is marginal and upon recurrence tumors frequently shift toward mesenchymal subtype adopting invasiveness. Here, we show that ionizing radiation affects biomechanical tension in GBM microenvironment and provides proinvasive extracellular signaling cue, hyaluronic acid (HA)-rich condition. In response to radiation, HA production was increased in GBM cells by HA synthase-2 (HAS2) that was transcriptionally upregulated by NF-kappa B. Notably, NF-kappa B was persistently activated by IL-1 alpha-feedback loop, making HA abundance in tumor microenvironment after radiation. Radiation-induced HA abundance causally has been linked to invasiveness of GBM cells by generating movement track as an extracellular matrix, and by acting as a signaling ligand for CD44 receptor, leading to SRC activation, which is sufficient for mesenchymal shift of GBM cells. Collectively, our findings provide an explanation for the frequent brain tumor relapse after radiotherapy, and potential therapeutic targets to block mesenchymal shift upon relapse.</P>
<P>Light is reflected at the interface between heterogeneous media due to the mismatch of impedance(1-3). Removing this mismatch using additional materials, a technique known as anti-reflection, has so far been restricted to specific frequencies and incidence angles(3-7). The anti-reflection of white light, which requires the simultaneous matching of impedance over extremely wide angular and spectral ranges, has until now been considered impossible. Here, we develop a theory of universal impedance matching and introduce a matching layer that enables the perfect transmission of white light. The ability of a matching layer to assist in omnidirectional and frequency-independent anti-reflection has been confirmed analytically and numerically. We explain the feasibility of a universal matching layer using metamaterials, and demonstrate a transmission rate of over 99% for white light in the visible range with a double-layered dielectric metamaterial. This is confirmed experimentally by demonstrating the omnidirectional anti-reflection of microwaves in heterogeneous media.</P>
<▼1><P><I>Streptococcus mutans (S. mutans)</I>, a major aetiologic agent of dental caries, is involved in systemic diseases, such as bacterial endocarditis, if it enters the bloodstream through temporary bacteraemia. Interleukin (IL)-1β, a proinflammatory cytokine, is related to the host defences against pathogens, and its synthesis, maturation, and secretion are tightly regulated by the activation of the inflammasome, an inflammatory signalling complex. This study examined the signalling mechanism of IL-1β secretion and the inflammasome pathway induced by <I>S. mutans</I> to explain the molecular mechanism through which systemic infection by oral streptococci can occur. After infection of THP-1 cells with <I>S. mutans</I>, the expression of inflammasome components was detected using various methods. <I>S. mutans</I> induced IL-1β secretion via caspase-1 activation, and <I>S. mutans</I>-induced IL-1β secretion required absent in melanoma (AIM2), NLR family pyrin domain-containing 3 (NLRP3) and NLR family CARD domain-containing 4 (NLRC4) inflammasome activation. In particular, the <I>S. mutans</I>-induced NLRP3 inflammasome was mediated by adenosine triphosphate (ATP) release, potassium depletion and lysosomal damage. Our study provides novel insight into the innate immune response against <I>S. mutans</I> infection.</P></▼1><▼2><P><B>Bacterial infection: The immune response to <I>Streptococcus mutans</I></B></P><P><I>Streptococcus mutans</I> triggers an early-stage immune response via a chain of events that leads to the activation of immune component, interleukin-1β. A group of academics from Korea’s Pusan National University, led by Jin Chung, tested the response of human immune cell cultures to infection with <I>S. mutans</I>—a common oral bacteria that can cause systemic disease if it enters the bloodstream. The group found that S. mutans infection leads to the activation of protein signaling complexes known as inflammasomes, which in turn activate an enzyme known as caspase-1. Caspase-1 then activates interleukin-1β, a pro-inflammatory molecule that forms part of a host’s defenses against pathogens. The team also identified that ATP release, ion depletion, and integrity of intracellular enzyme containers, also impacted inflammasome activation. This study offers insights into the immune response against <I>S. mutans</I> and may inform future investigations into systematic oral bacteria infections.</P></▼2>
<▼1><P>The opto-mechanical force response from light-illuminated nanoscale materials has been exploited in many tip-based imaging applications to characterize various heterogeneous nanostructures. Such a force can have two origins: thermal expansion and induced dipoles. The thermal expansion reflects the absorption of the material, which enables one to chemically characterize a material at the absorption resonance. The induced dipole interaction reflects the local refractive indices of the material underneath the tip, which is useful to characterize a material in the spectral region where no absorption resonance occurs, as in the infrared (IR)-inactive region. Unfortunately, the dipole force is relatively small, and the contrast is rarely discernible for most organic materials and biomaterials, which only show a small difference in refractive indices for their components. In this letter, we demonstrate that refractive index contrast can be greatly enhanced with the assistance of a functionalized tip. With the enhanced contrast, we can visualize the substructure of heterogeneous biomaterials, such as a polyacrylonitrile-nanocrystalline cellulose (PAN-NCC) nanofiber. From substructural visualization, we address the issue of the tensile strength of PAN-NCC fibers fabricated by several different mixing methods. Our understanding from the present study will open up a new opportunity to provide enhanced sensitivity for substructure mapping of nanobiomaterials, as well as local field mapping of photonic devices, such as surface polaritons on semiconductors, metals and van der Waals materials.</P></▼1><▼2><P><B>Photoinduced force microscopy: Enhanced sensitivity</B></P><P>Contamination of a scientific instrument is usually considered to be an undesirable outcome. However, researchers from Korea and Canada have now discovered that it can actually benefit an imaging technique called photoinduced force microscopy (PiFM). PiFM is a high-resolution scanning technique that is capable of mapping local refractive index contrast of a sample by measuring the light-induced force that arises between the sample and a closely-spaced tip. Junghoon Jang and coworkers from the Korea Research Institute of Standards and Science (KRISS) and the University of British Columbia have now discovered that the presence of a small amount of polydimethylsiloxane (PDMS) contaminant on the tip can serve to functionalize it and significantly increase the strength of the sample-tip interaction. The team has shown that the functionalized tip can map the substructure of nanofibres of a biomaterial called polyacrylonitrile-nanocrystalline cellulose.</P></▼2>
<▼1><P>Mesangial cell proliferation has been identified as a major factor contributing to glomerulosclerosis, which is a typical symptom of diabetic nephropathy (DN). Lysophosphatidic acid (LPA) levels are increased in the glomerulus of the kidney in diabetic mice. LPA is a critical regulator that induces mesangial cell proliferation; however, its effect and molecular mechanisms remain unknown. The proportion of α-SMA<SUP>+</SUP>/PCNA<SUP>+</SUP> cells was increased in the kidney cortex of <I>db/db</I> mice compared with control mice. Treatment with LPA concomitantly increased the proliferation of mouse mesangial cells (SV40 MES13) and the expression of cyclin D1 and CDK4. On the other hand, the expression of p27<SUP>Kip1</SUP> was decreased. The expression of Krüppel-like factor 5 (KLF5) was upregulated in the kidney cortex of <I>db/db</I> mice and LPA-treated SV40 MES13 cells. RNAi-mediated silencing of KLF5 reversed these effects and inhibited the proliferation of LPA-treated cells. Mitogen-activated protein kinases (MAPKs) were activated, and the expression of early growth response 1 (Egr1) was subsequently increased in LPA-treated SV40 MES13 cells and the kidney cortex of <I>db/db</I> mice. Moreover, LPA significantly increased the activity of the Ras-related C3 botulinum toxin substrate (Rac1) GTPase in SV40 MES13 cells, and the dominant-negative form of Rac1 partially inhibited the phosphorylation of p38 and upregulation of Egr1 and KLF5 induced by LPA. LPA-induced hyperproliferation was attenuated by the inhibition of Rac1 activity. Based on these results, the Rac1/MAPK/KLF5 signaling pathway was one of the mechanisms by which LPA induced mesangial cell proliferation in DN models.</P></▼1><▼2><P><B>Kidney disease: Mechanisms of diabetes-related damage</B></P><P>A potent molecular mediator of diabetic kidney disease induces its pathogenic effects via proteins that could be targeted with future drug therapies. Yoon Sin Oh from Eulji University in Seongnam-si and Hee-Sook Jun from Gachon University in Incheon, both in South Korea, and colleagues treated certain cells found in the kidney’s glomerulus, the organ’s filtering unit, with a signaling molecule called lysophosphatidic acid (LPA) that is elevated in the blood of diabetic mice. They showed that LPA stimulated cellular proliferation and boosted the expression of proteins involved in regulating the cell cycle and a multipurpose signaling pathway. They then inhibited the activity of these proteins to prevent the kidney cells’ hyperproliferation, both in cell culture and in diabetic mice. The results highlight the potential of blocking mediators of LPA signaling to treat kidney-related complications of diabetes.</P></▼2>