This document provides a brief summary of the current scientific evidence for the adjuvant use of the COC Protocol medications in glioma, including glioblastoma and other high-grade gliomas. A table of all currently ongoing or recently finished clinical trials related to the use of these medications in glioma and other brain tumours is provided in Table 1, which you can find at the end of this article.
For more information regarding your own personal situation, please contact the Care Oncology Clinic on 800-392-1353 or fill out the Patient Eligibility Form.
Glioma tumours grow from glial cells in the brain and are the most common type of brain tumour. Low-grade benign gliomas are slower growing and less dangerous than high-grade, aggressive (malignant) gliomas. Glioblastoma multiforme (GBM), a type of malignant astrocytoma, is the most common high-grade brain tumour in adults.
The standard treatment for high-grade glioma is usually surgery, followed by courses of chemotherapy (i.e. temozolomide) and radiation. Much current glioma research is focussed on adding extra (adjuvant) treatments alongside this standard regime in the hope of improving results for patients.
Scientific interest is growing in the use of treatments which target the metabolic pathways of cancer cells (i.e. the processes used by cells to generate energy) to slow or stop the growth of cancers. Care Oncology specialises in using already-licensed (off-label) medications with known anti-metabolic activity to help treat and control cancer. We have developed an adjuvant treatment called the COC Protocol, which combines what we believe to be the most effective metabolically-targeted offlabel medications available.
This section summarises briefly the existing evidence for effective use of COC Protocol medications in glioma, and of the current clinical trials in this area.
High-grade gliomas like GBM are thought to be very dependent on the cell processes primarily targeted by statins for survival, and fat-soluble 'lipophilic' statins like atorvastatin can cross the human BBB relatively easily (1). These qualities, along with the demonstrated ability of statins to slow and suppress glioma cancer cell growth in the lab and in preclinical mouse models makes atorvastatin a good candidate as a repurposed glioma treatment (2).
Several studies show that statins can target and damage glioma cells in a number of different ways, including by increasing programmed and unprogrammed cell death (eg apoptosis and necrosis) (3–5), and reducing cancer cell growth, division, and movement (proliferation and migration)(5–8).
Other lab studies have also shown that statins can help to reduce tumour resistance to other glioma treatments (9–11). One lab study using pitavastatin, a statin similar in profile to atorvastatin, showed that MDR-1, a molecule which is excessively produced in glioma cells in response to treatment and which helps these cells become resistant, is blocked by statins. In this study, statins helped to improve the effectiveness of chemotherapy (12). In a separate lab study, combining statins with an additional metabolically-targeted drug also appeared to increase potency on glioblastoma cells (13).
Most clinical studies for statin use in glioma patients are still ongoing or awaiting results (see Table 1). But completed clinical studies show promise. Early-phase studies from the 1990s, where adult and child patients with solid central nervous system (i.e. brain) tumours and high-grade gliomas took lovastatin or fluvastatin in 3 or 4 weekly cycles, showed that statins were well tolerated. Promising tumour responses were noted in patients with GBM and anaplastic astrocytoma, and study investigators suggested a less cyclical and more constant treatment regime could be more effective (14,15). Patient population studies monitoring survival in large numbers of people who took statins before and during glioblastoma diagnosis and treatment have had inconclusive results, possible due to different study designs (16–18).
Scientific interest in mebendazole as a potential anticancer treatment is relatively new and is mostly based on promising mechanistic studies and compelling reports from case studies in cancer patients (19, 20).
Emerging evidence also suggests that mebendazole may have particularly high levels of activity against cancers of the brain. This is partly because mebendazole is a small, fat-soluble molecule which can easily cross the BBB. It is also thought to work in a similar way to vincristine, a chemotherapy drug currently used for treatment of some types of cancer, including some gliomas (18). Mebendazole is thought to kill cancer cells partly by disrupting special structures inside the cell, called microtubules (21). It can inhibit glioma tumour cell growth in the lab and has been shown to improve survival in preclinical mouse models of glioblastoma (22). In addition, some forms of mebendazole (including the form which is prescribed as part of the COC Protocol) are thought to cross the BBB more readily than vincristine (23), which has led to suggestions that mebendazole should replace vincristine in the treatment of brain tumours (24). In a computer modelling study which looked at 51 different drugs including all chemotherapies used or previously used for treatment of a childhood glioma called DIPG, mebendazole was one of just 8 drugs which was predicted to reach effective concentrations in the brain following systemic (i.e. by mouth or injection) administration (25). Evidence from lab studies also suggests that simultaneous use of microtubule disruptors like mebendazole can help to improve the effectiveness of radiotherapy and temozolomide, two standard glioma treatments (26,27). Numerous clinical trials are now underway to investigate this possibility (see Table 1).
Metformin is not fat soluble but is predicted to cross the BBB using special transporter molecules (28–30). An impressive number of lab studies show metformin can block glioma and glioblastoma cell and tumour growth via a number of different mechanisms, including supressing growth, division and movement of glioma cells (31–33), increasing programmed glioma cell death (34, 35), and blocking growth of new blood vessels (angiogenesis) to glioma tumours (36).
Within the last 5 years scientists have also discovered that metformin can target and disrupt glioblastoma stem cells (37–39). This is important, because these cells are believed to be the initiating cells of a tumour. They can be less responsive to radio- and chemotherapies and are thought to be responsible for tumour regrowth following treatment. Scientists believe control of these cells is key for ensuring long-term survival for patients with glioblastoma (39,40).
Metformin's real potential in glioma is revealed when metformin is tested in combination with standard therapies or newly-developed anticancer medications. These studies repeatedly show that metformin's multi-targeted activity against cancer cells and cancer stem cells can potentially improve potency of a combinatorial anticancer treatment regimen. In lab studies, improved anticancer activity (33,41–43) and/or resistance of glioma cells and glioma stem cells to standard therapies such as temozolomide has been overcome using metformin in combination with other drugs (33, 44, 45).
Numerous clinical trials are now underway investigating metformin in combination with other therapies in the treatment of advanced glioblastoma in both adults and children.
Doxycycline is an antibiotic with other extremely valuable properties, including anti-inflammatory and anticancer activity. This gives doxycycline real therapeutic potential in treating a range of other diseases, including cancer (46).
In glioma, a 2007 lab study has shown that doxycycline helps to block tumour cell growth and division and reduces glioma cells' potential to move and invade other areas of the body (47). Importantly, doxycycline appears to be particularly good at targeting tumour stem cells. Doxycycline can block a process called 'mitochondrial biogenesis', which stem cells need to use to make energy for survival and growth. Lab studies show that doxycycline treatment could make glioma stem cells more susceptible to other treatments like radiotherapy (48), and less able to regrow after temozolomide treatment (49). The results of these lab studies are now starting to be replicated in patients- a very recent study has just reported that doxycycline was able to effectively reduce cancer stem cells in patients with early-stage breast cancer (50).
Doxycycline is also well absorbed by the body and is known to cross the BBB effectively (51). These qualities combine to make doxycycline a potentially very powerful anticancer treatment for brain tumours such as glioma (48).
Table 1 summarises current ongoing or recently completed clinical trials investigating individual metabolically targeted off-label COC Protocol medications in the treatment of brain tumours, including gliomas of all types, glioblastoma, and childhood brain tumours such as medulloblastoma.
It's notable that whereas most studies are testing just 1 or 2 of these medications in combination with standard treatments, Care Oncology's own METRICS study (NCT02201381) is currently the only study to investigate the tolerability and effectiveness of a combination of four off-label metabolic treatments (i.e. atorvastatin, mebendazole, metformin, and doxycycline) alongside standard treatments in glioma and other cancers. You can find out more about our study by contacting us.
NB: Table accurate according to www.Clinicaltrials.gov website as of October 2018.
This article is an overview of some of the scientific and medical published literature concerning the medications which comprise the patented Care Oncology protocol. Care has been taken to select relevant articles supporting the off-label use of these medicines in a clinical setting for the adjunct treatment of cancer. This article does not purport to be a comprehensive review of all the evidence, nor does it capture all of the potential side-effects of such treatment.
This article is for information purposes only and it does NOT constitute medical advice. The medicines discussed herein are available on prescription-only and should not be taken without consultation with your doctor or other professional healthcare provider. Care Oncology doctors will discuss the suitability of these medicines with you and will liaise with your doctor or oncologist to discuss their suitability for you.
You must NOT rely on the information in this article as an alternative to medical advice from your doctor or other professional healthcare provider. If you have any specific questions about any medical matter you should consult your doctor or other professional healthcare provider. If you think you may be suffering from any medical condition you should seek immediate medical attention. You should never delay seeking medical advice, disregard medical advice, or discontinue medical treatment because of information contained in this article.
The copyright in this article is owned by Health Clinics LLC and its licensors.
The Care Oncology ("COC") Protocol is protected by United States patent US9622982B2 and by various additional international patents.
2. Rundle-Thiele D, Head R, Cosgrove L, Martin JH. Repurposing some older drugs that cross the blood-brain barrier and have potential anticancer activity to provide new treatment options for glioblastoma. Br J Clin Pharmacol. 2016 Feb;81(2):199–209.
3. Bababeygy SR, Polevaya NV, Youssef S, Sun A, Xiong A, Prugpichailers T, et al. HMG-CoA reductase inhibition causes increased necrosis and apoptosis in an in vivo mouse glioblastoma multiforme model. Anticancer Res. 2009 Dec;29(12):4901–8.
4. Bayat N, Ebrahimi-Barough S, Norouzi-Javidan A, Saberi H, Tajerian R, Ardakan MMM, et al. Apoptotic effect of atorvastatin in glioblastoma spheroids tumor cultured in fibrin gel. Biomed Pharmacother. 2016 Dec;84:1959–66.
5. Yanae M, Tsubaki M, Satou T, Itoh T, Imano M, Yamazoe Y, et al. Statin-induced apoptosis via the suppression of ERK1/2 and Akt activation by inhibition of the geranylgeranyl-pyrophosphate biosynthesis in glioblastoma. J Exp Clin Cancer Res. 2011 Aug 10;30:74.
6. Bouterfa HL, Sattelmeyer V, Czub S, Vordermark D, Roosen K, Tonn JC. Inhibition of Ras farnesylation by lovastatin leads to downregulation of proliferation and migration in primary cultured human glioblastoma cells. Anticancer Res. 2000 Aug;20(4):2761–71.
7. Oliveira KA, Dal-Cim T, Lopes FG, Ludka FK, Nedel CB, Tasca CI. Atorvastatin Promotes Cytotoxicity and Reduces Migration and Proliferation of Human A172 Glioma Cells. Mol Neurobiol. 2018 Feb;55(2):1509–23.
8. Yongjun Y, Shuyun H, Lei C, Xiangrong C, Zhilin Y, Yiquan K. Atorvastatin suppresses glioma invasion and migration by reducing microglial MT1-MMP expression. J Neuroimmunol. 2013 Jul 15;260(1–2):1–8.
9. Cemeus C, Zhao TT, Barrett GM, Lorimer IA, Dimitroulakos J. Lovastatin enhances gefitinib activity in glioblastoma cells irrespective of EGFRvIII and PTEN status. J Neurooncol. 2008 Oct;90(1):9–17.
10. Chang Y-L, Huang L-C, Chen Y-C, Wang Y-W, Hueng D-Y, Huang S-M. The synergistic effects of valproic acid and fluvastatin on apoptosis induction in glioblastoma multiforme cell lines. Int J Biochem Cell Biol. 2017;92:155–63.
11. Hamm R, Zeino M, Frewert S, Efferth T. Up-regulation of cholesterol associated genes as novel resistance mechanism in glioblastoma cells in response to archazolid B. Toxicol Appl Pharmacol. 2014 15;281(1):78–86.
12. Jiang P, Mukthavaram R, Mukthavavam R, Chao Y, Bharati IS, Fogal V, et al. Novel anti-glioblastoma agents and therapeutic combinations identified from a collection of FDA approved drugs. J Transl Med. 2014 Jan 17;12:13.
13. Tapia-Pérez JH, Preininger R, Kirches E, Reinhold A, Butzmann J, Prilloff S, et al. Simultaneous Administration of Statins and Pioglitazone Limits Tumor Growth in a Rat Model of Malignant Glioma. Anticancer Res. 2016;36(12):6357–65.
14. Larner J, Jane J, Laws E, Packer R, Myers C, Shaffrey M. A phase I-II trial of lovastatin for anaplastic astrocytoma and glioblastoma multiforme. Am J Clin Oncol. 1998 Dec;21(6):579–83.
16. Bhavsar S, Hagan K, Arunkumar R, Potylchansky Y, Grasu R, Dang A, et al. Preoperative statin use is not associated with improvement in survival after glioblastoma surgery. J Clin Neurosci. 2016 Sep;31:176–80.
17. Gaist D, Andersen L, Hallas J, Sørensen HT, Schrøder HD, Friis S. Use of statins and risk of glioma: a nationwide case-control study in Denmark. Br J Cancer. 2013 Feb 19;108(3):715–20.
21. Lai SR, Castello SA, Robinson AC, Koehler JW. In vitro anti-tubulin effects of mebendazole and fenbendazole on canine glioma cells. Vet Comp Oncol. 2017 Dec;15(4):1445–54.
22. Bai R-Y, Staedtke V, Aprhys CM, Gallia GL, Riggins GJ. Antiparasitic mebendazole shows survival benefit in 2 preclinical models of glioblastoma multiforme. Neuro-oncology. 2011 Sep;13(9):974–82.
23. Bai R-Y, Staedtke V, Wanjiku T, Rudek MA, Joshi A, Gallia GL, et al. Brain Penetration and Efficacy of Different Mebendazole Polymorphs in a Mouse Brain Tumor Model. Clin Cancer Res. 2015 Aug 1;21(15):3462–70.
25. El-Khouly FE, van Vuurden DG, Stroink T, Hulleman E, Kaspers GJL, Hendrikse NH, et al. Effective Drug Delivery in Diffuse Intrinsic Pontine Glioma: A Theoretical Model to Identify Potential Candidates. Front Oncol. 2017;7:254.
26. Kipper FC, Silva AO, Marc AL, Confortin G, Junqueira AV, Neto EP, et al. Vinblastine and antihelmintic mebendazole potentiate temozolomide in resistant gliomas. Invest New Drugs. 2018 Apr;36(2):323–31.
27. Markowitz D, Ha G, Ruggieri R, Symons M. Microtubule-targeting agents can sensitize cancer cells to ionizing radiation by an interphase-based mechanism. Onco Targets Ther. 2017;10:5633–42.
30. Molenaar RJ, Coelen RJS, Khurshed M, Roos E, Caan MWA, van Linde ME, et al. Study protocol of a phase IB/II clinical trial of metformin and chloroquine in patients with IDH1-mutated or IDH2-mutated solid tumours. BMJ Open. 2017 10;7(6):e014961.
32. Seliger C, Meyer A-L, Renner K, Leidgens V, Moeckel S, Jachnik B, et al. Metformin inhibits proliferation and migration of glioblastoma cells independently of TGF-β2. Cell Cycle. 2016 Jul 2;15(13):1755–66.
34. Isakovic A, Harhaji L, Stevanovic D, Markovic Z, Sumarac-Dumanovic M, Starcevic V, et al. Dual antiglioma action of metformin: cell cycle arrest and mitochondria-dependent apoptosis. Cell Mol Life Sci. 2007 May;64(10):1290–302.
35. Songthaveesin C, Sa-Nongdej W, Limboonreung T, Chongthammakun S. Combination of metformin and 9-cis retinoic acid increases apoptosis in C6 glioma stem-like cells. Heliyon. 2018 May;4(5):e00638.
36. Elmaci İ, Altinoz MA. A Metabolic Inhibitory Cocktail for Grave Cancers: Metformin, Pioglitazone and Lithium Combination in Treatment of Pancreatic Cancer and Glioblastoma Multiforme. Biochem Genet. 2016 Oct;54(5):573–618.
37. Gritti M, Würth R, Angelini M, Barbieri F, Peretti M, Pizzi E, et al. Metformin repositioning as antitumoral agent: selective antiproliferative effects in human glioblastoma stem cells, via inhibition of CLIC1-mediated ion current. Oncotarget. 2014 Nov 30;5(22):11252–68.
38. Würth R, Pattarozzi A, Gatti M, Bajetto A, Corsaro A, Parodi A, et al. Metformin selectively affects human glioblastoma tumor-initiating cell viability: A role for metformin-induced inhibition of Akt. Cell Cycle. 2013 Jan 1;12(1):145–56.
39. Würth R, Barbieri F, Florio T. New molecules and old drugs as emerging approaches to selectively target human glioblastoma cancer stem cells. Biomed Res Int. 2014;2014:126586.
40. Najbauer J, Kraljik N, Németh P. Glioma stem cells: markers, hallmarks and therapeutic targeting by metformin. Pathol Oncol Res. 2014 Oct;20(4):789–97.
41. Aldea MD, Petrushev B, Soritau O, Tomuleasa CI, Berindan-Neagoe I, Filip AG, et al. Metformin plus sorafenib highly impacts temozolomide resistant glioblastoma stem-like cells. J BUON. 2014 Jun;19(2):502–11.
43. Valtorta S, Dico AL, Raccagni I, Gaglio D, Belloli S, Politi LS, et al. Metformin and temozolomide, a synergic option to overcome resistance in glioblastoma multiforme models. Oncotarget. 2017 Dec 22;8(68):113090–104.
44. Yang SH, Li S, Lu G, Xue H, Kim DH, Zhu J-J, et al. Metformin treatment reduces temozolomide resistance of glioblastoma cells. Oncotarget. 2016 Nov 29;7(48):78787–803.
45. Yu Z, Zhao G, Xie G, Zhao L, Chen Y, Yu H, et al. Metformin and temozolomide act synergistically to inhibit growth of glioma cells and glioma stem cells in vitro and in vivo. Oncotarget. 2015 Oct 20;6(32):32930–43.
46. Bahrami F, Morris DL, Pourgholami MH. Tetracyclines: drugs with huge therapeutic potential. Mini Rev Med Chem. 2012 Jan;12(1):44–52.
47. Wang-Gillam A, Siegel E, Mayes DA, Hutchins LF, Zhou Y-H. Anti-Tumor Effect of Doxycycline on Glioblastoma Cells. 2007;8.
COC Protocol is offered as an adjunctive therapy for conventional cancer therapies. COC Protocol may enhance the efficacy of conventional cancer therapies. It is not intended to replace conventional cancer therapies.
"May halve the risk of dying from cancer" Statement is quoted from findings that were presented during the American Society of Clinical Oncology (ASCO) 2015 Annual Meeting. Context: Statin use was associated with a 22% reduction in deaths from various cancer types in women and a 55% reduction in deaths from bone/connective tissue cancers. The study in men looked at statin use together with metformin and found a 40% reduction in prostate cancer mortality, with the effect more pronounced in men with obesity/metabolic syndrome.
"COC Protocol" and "Care Oncology" and the "flame" icon are registered trademarks by Care Oncology LLC. COC Protocol is protected by United States patent US9622982B2 and by various additional international patents.


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Video Game Review
Horror And Sons
Horror, Classic Sci-Fi, + B-Movie Reviews, And A Few Other Things
70's, Movie Review
Foes (1977) – Movie Review
Date: March 9, 2020Author: Horror And Sons 1 Comment
Foes is a 1977 "alien encounter" film written and directed by John Coats, who also co-stars in the film. Coats also handled the visual effects for this film. While Foes would prove to be his only directorial effort, Coats (sometimes credited as John Coates) would go on to have a long career as a visual effects artist on a vast array of well known films, such as Weird Al Yankovic's UHF (one of the funniest movies ever), Wes Craven's New Nightmare, and 2 of the 3 Austin Powers movies.
As I've previously mentioned more than a few times on this site, my love for horror originally started as a love for science fiction. Growing up on a steady diet of Tom Baker's "Doctor", Star Trek reruns (long before TNG was a "thing"), and the original Star Wars trilogy, I was enamored and captivated by each new alien species I was introduced to. This, in turn, lead to a fascination with monsters, which lead to….. Well, you can assume the rest.
This new fondness for aliens also created an early obsession with reading as much as I could about UFO sightings, alien encounters, and abductions. Thanks to the box-office successes of Close Encounters of the Third Kind in 1977, Alien in 1979, and E.T. in 1982, extraterrestrials (whether malevolent or benevolent) weren't leaving the public consciousness any time soon. This provided young, impressionable me (and all of you as well) with endless films and books dealing with the subject to consume.
Foes was one of those films that I had first heard about sometime in the early 1980s. I believe I first discovered the film while digging through the latest issue of TV Guide. I was pretty OCD about reading the ENTIRE TV Guide when we received each new issue, so I knew when EVERYTHING was on and on which station/channel!. So, I feel fairly certain that I saw airings of Foes listed in those pages many times, and 6 or 7-year old me couldn't wait to watch this film!
Unfortunately, that viewing never happened. I usually didn't receive whatever station it was airing on or it was showing well after I had been put to bed for the night.
While I can't sit here and tell you that Foes stayed at the forefront of my thoughts for years to come, it was most certainly a film that would make me say, "Oh, yeah! I remember wanting to watch that when I was a kid.", whenever I read about it or heard it mentioned, which admittedly wasn't much. To be very honest, which I try to be with each review, I had pretty much forgotten about the film, which is understandable as it did not receive a release on VHS or DVD, until a blu-ray was released in 2019 by Garagehouse Pictures.
Having finally watched the film, what would 7-year old me have thought of this film? Would he have been terrified? Would he have be mesmerized? Or would he just get bored, go to his bedroom, and read back issues of "ROM"?
In the most basic of terms, Foes deals with an encounter with an alien spacecraft. While that plot description really tells you nothing about Foes, the less that is said about the events of the film, the more enjoyable it may be for first time viewers. However, as this is a review, I guess I'm kinda obligated to give a few more details, as well as my opinions of the finished product.
Two people try to escape from a small island that has become the subject of reconnaissance by a large flying saucer, while also helping the survivor of a violently brutal abduction. Macdonald Carey of Days of Our Lives fame and well-traveled character actor Jerry Hardin (Honkytonk Man, "Deep Throat" on The X-Files) star as the scientist and military general (respectively) who must find answers for what to do about the UFO and how to rescue the people stranded on the island. Making both of these tasks much more difficult is a magnetic field encircling the island which shorts out the engines of any aircraft or sea vessel that attempt to approach it.
Foes was made on a very small budget, which is mostly revealed in the film's sometimes impressive, sometimes hokey visual effects. Granted, the effects may have been more impressive had I first witnessed them 40+ years ago. In other aspects, the limited budget may actually benefit the film as it is then forced to rely on its use of tone, pacing, landscape photography, and (albeit sparsely used) music.
Foes moves along at a fairly solid pace, although there is still fair argument that not much is happening at any given time. This is because the film is focused on continuously building a sense of anxious dread, making the characters (and hopefully the audience) just as curious to what the alien craft will do next as they are frightened by the possibilities. This means that the characters spend quite a bit of time spectating, naturally intrigued and perplexed by the situation at hand.
While music is generally used quite sparingly in Foes, it may actually be one of the film's strongest assets. The film features a dark, electro-ambient soundtrack that helps create an atmosphere of cosmic horror, but is used infrequently, so as to truly intensify key moments. Also of note are the sound effects used for the UFO's various actions, as they feel quite in line with the score.
For me, Foes was an exemplary example of making a lot out of nothing. The film takes a rather thin premise and limited budget and milks it for as much as it will give. It's insanely ambitious, but smart enough to know its limitations. However, undoubtedly the film's biggest achievement is that it gives the viewer ample time to use their imagination as to what they would do or how they would react if they found themselves in a similar situation. Unfortunately, the fact that what we imagine is presumably much more fascinating or horrifying than what is actually shown may serve as the film's ultimate flaw for many.
As mentioned prior, Foes received a blu-ray release courtesy of Garagehouse Pictures in 2019. For many, this release may be a mixed bag. The transfer appears to be sourced from a 35mm print, presumably one of few in existence, although parts of the film were shot in 16mm. As such, the picture quality on the blu-ray tends to fluctuate frequently. Simply put, some scenes look like crap, grain heavy and none too clear. This is due more to the quality of the print and the budgetary issues while shooting. Other times, the image is surprising crisp and detailed. All in all, it's a safe assumption that this release is still the best the film has ever looked.
It is also worth noting that the film gets quite dark at times. This is due to a lack of lighting on the shoot and not any fault of the transfer. Sure, some additional lighting may have made things easier to see, but the lack thereof also helps ground the film in realism, as most witnesses of unidentified flying saucer encounters generally aren't carrying lighting rigs with them.
Too many years may have passed to truly be sure of what I would have thought had I watched this film all those years ago, but I like to think that 7-year old me may have had a few nightmares after watching Foes for the first time. However, I assure you, he'd want to watch it again the next night!
Foes (Blu-ray) is, of course, available on Amazon at the following link. https://amzn.to/2wBzaIy (Any purchases made after clicking on the link do help H&S earn a commission, so this way helps support the site!)
That said, you can also find it at www.DiabolikDVD.com
AliensClose Encounters of the Third KindFoesGaragehouse PicturesJohn CoatsMacdonald CareyROMStar TrekThe X-FilesUFOsWeird AlWes Craven
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One thought on "Foes (1977) – Movie Review"
rdfranciswriter says:
Wow. I never heard of hits. Never. Never seen it UHF TV or on the VHS shelves. I have to seek this out. It reminds me of Ed Hunt's Starship Invasions, but more accurately, his early film from 1976, Point of No Return, with its UFO conspiracy storyline. Great review.
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Ending the 'war on drugs' requires justice for the impoverished communities who grow them
The drugs trade is often portrayed as populated by wealthy individuals. The reality is poor communities targeted for repression, criminalisation and even the death penalty.
Lauren Tapp
12 June 2019, 4.05pm
A plane sprays aerial fumigations on Colombian mountains to eradicate coca plantations
Motte Jules/ABACA/PA Images
Amidst media furore over illicit drug use, Tory leadership favourite Boris Johnson dodged questions today over past drug use, whilst the wheels of Michael Gove's campaign for the premiership are careering to a halt. Eight of the eleven candidates have admitted to some form of drug consumption, from Hunt's cannabis infused lassi, to Rory Stewart's opium smoking in Iran.
Quite rightly, Gove has been taken to task for advocating policies which saw teachers banned from their profession for taking class A drugs while he was education secretary and for upholding a justice system which incarcerates people for up to seven years for the very behaviour he previously engaged in. Despite the political elite's refusal to deviate from the party line that prohibition is essential to create a 'drug free world', the evidence from around the world is clear - more people now produce, sell and consume illicit drugs than ever before.
Undoubtedly, the scandal has shone light on the hypocrisy of the so called 'war on drugs' in the United Kingdom, particularly, the highly racialised and class based dimensions of its application. It is clear this is not a war on illicit substances, but on racialised and working class people.
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Yet the scope of drug policy discourse rarely turns to the people whose livelihoods depend on the production of plants which go on to be consumed by the political elite as illicit drugs. Indeed only Rory Stewart made passing reference to this when he referred to the communities he smoked with in Iran, saying "the family may have been so poor that they put very little opium into the pipe."
Despite the dominant narrative of the drugs trade painting a picture of assumed wealth, violence and organised crime, the majority of people involved tend to be poor and otherwise marginalised due to their race, gender, indigenous status and/or lack of formal land rights. The global commitment to prohibit drugs at all costs means that rural and indigenous communities involved in the cultivation of prohibited plants such as cannabis, coca leaf and opium poppy are routinely targets for repression and suffer from discrimination, stigmatisation, criminalisation, imprisonment, and the destruction of their livelihoods.
While political actors from the UN and state governments argue that prohibition can coexist with a human rights approach, the evidence remains that focusing on eradication and punitive responses creates and reinforces cycles of impoverishment that can be hard to get out of. For instance, when producers' crops are eradicated, farmers can lose all of their (small) income, making it harder for them to access healthcare or buy food. This can create a vicious cycle where illicit crop producers become increasingly dependent on cultivating prohibited plants to counter the poverty forced on them by eradication. Both at home and abroad, people who receive criminal convictions for supplying or possessing drugs can often find it harder to access jobs, which makes it harder for them to stop engaging in the drug trade and consigns them to a lifetime of poverty.
In the case of Michael Gove's cocaine, prohibition has been a recipe for human rights violations against coca growers in the Andean region. Indiscriminate aerial crop spraying of the herbicide glyphosate (more commonly known as Monsanto's RoundUp) to destroy illicit crops was the foremost strategy employed by the US backed "Plan Colombia" between 1999 and 2015. During this time, around 1,800,000 hectares of coca fields were sprayed across rural areas of Colombia. As a result, the Colombian Ombudsman's Office received many thousands of complaints about the effects of glyphosate including reports of polluted drinking water, destruction of food crops and health problems to communities and livestock (skin rashes, diarrhoea, headaches and respiratory problems), severely impacting on the right to food, water and health of those exposed.
In addition, violent repression of the coca growing community by military and police forces has been reported across Latin America. In 2017, six coca growers were shot dead and 21 others injured during a protest against coca eradication in Colombia. In Peru two farmers were killed as recently as April this year during a similar dispute over eradication.
In terms of opium, the situation is similar. While farmers in countries like Mexico and Afghanistan battle eradication, criminalisation and violence, the fate of those caught up in the transportation and supply of the raw opium and heroin is stark, with numerous governments around the world continuing to use the death penalty for drug related offences. As reported by Harm Reduction International in their recent report, a number of these people are engaged in the lowest levels of the drug trade, socio-economically vulnerable, are tried without due process and/or have inadequate legal representation – which means that the death penalty is in reality reserved for the most marginalised in society.
Turning to cannabis, it could be argued that things start to look a little bit brighter given the recent developments in legal regulation of recreational and medicinal markets within a number of US states, including Canada, Uruguay and others. Portugal decriminalised personal use of all drugs in 2001, leading to a sharp decline in drug related deaths, new HIV infections and drug related crime. Clearly, prohibition is not working. We must commit to exploring the alternatives, but we must not forget that legal regulation and decriminalisation are not panaceas.
We can see the tide is turning towards legalisation, in part because there is a great deal of profit to be made by transnational corporations. Producing cannabis in a country of the Global South country where land can be cheap, labour law is lax and the tax system provides plenty of leeway for foreign investment, and is leading to the so called 'green rush'. We cannot allow the interests of capital to erase the rights and needs of traditional growers of these plants nor the communities who have been most affected by the violence of prohibition.
Legalisation, combined with robust and social justice focused regulation could provide a real opportunity to begin repairing some of the harms of prohibition, reinvesting in communities which have suffered from police harassment, criminalisation and incarceration should be a critical priority. Diverting the nearly $100 billion currently spent on funding prohibition towards public health systems, education and the structural causes of poverty which drive people towards the drugs trade in the first place.
But this can only be done by foregrounding social justice within legal regulation and putting the health and rights of those who are currently marginalised under prohibition at the centre.
What will be left of the BBC in 2028?
The UK's culture secretary wants to appease right-wingers by abolishing the licence fee. Will the market now rule all broadcasting? And would that be that a bad thing? Join us for this free live event on Thursday 27 January at 5pm UK time.
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Kazakh leader's grandson under McMafia order was mystery client at collapsed London 'golden visa' firm
If Tory whips are blackmailing MPs, that's corruption. We should call it that
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text:
Retardation and repair of fatigue cracks in a microcapsule toughened epoxy composite -- Part II: In situ self-healing
Dept. of Theoretical and Applied Mechanics (1926-2006)
Technical Reports - Theoretical and Applied Mechanics (TAM)
Brown, Eric N.; White, Scott R.; Sottos, Nancy R.
http://hdl.handle.net/2142/319
1061.pdf (4MB) (no description provided) PDF
Title: Retardation and repair of fatigue cracks in a microcapsule toughened epoxy composite -- Part II: In situ self-healing
Author(s): Brown, Eric N.; White, Scott R.; Sottos, Nancy R.
Subject(s): Fatigue cracks
Abstract: Successful arrest and retardation of fatigue cracks is achieved with an in situ self-healing epoxy matrix composite that incorporates microencapsulated dicyclopentadiene (DCPD) healing agent and Grubbs' first generation Ru catalyst. Healing agent is released into the crack plane by the propagating crack, where it polymerizes to form a polymer wedge, generating a crack tip shielding mechanism. Due to the complex kinetics of healing a growing crack, the resulting in situ retardation and arrest of fatigue cracks exhibit a strong dependence on the applied range of cyclic stress intensity DKI. Significant crack arrest and life extension result when the in situ healing rate is faster than the crack growth rate. In loading cases where the crack grows too rapidly (maximum applied stress intensity factor is a significant percentage of the mode-I fracture toughness value), a carefully timed rest period can be used to prolong fatigue life up to 118%. At moderate DKI, in situ healing extends fatigue life by as much as 213%. Further improvements in fatigue life-extension are achieved by employing a rest period, which leads to permanent arrest at this moderate DKI. At lower values of applied stress intensity factor, self-healing yields complete arrest of fatigue cracks providing infinite fatigue life-extension.
Issue Date: 2005-01
Publisher: Department of Theoretical and Applied Mechanics (UIUC)
Series/Report: TAM Reports 1061, (2005)
Genre: Technical Report
URI: http://hdl.handle.net/2142/319
Publication Status: published or submitted for publication
Peer Reviewed: is peer reviewed
Is Version Of: Published as: Eric N. Brown, Scott R White, Nancy R. Sottos. Composites Science and Technology, Vol. 65, No. 15-16, 2005, pp. 2474-2480. DOI: 10.1016/j.compscitech.2005.04.053. Copyright 2005 Elsevier.
TAM technical reports include manuscripts intended for publication, theses judged to have general interest, notes prepared for short courses, symposia compiled from outstanding undergraduate projects, and reports prepared for research-sponsoring agencies.


A super quick and tasty lunch.
Beat together the eggs, 1 tbsp of parmesan cheese and the herbs.
Heat up a frying pan and melt the butter.
Pour in your omelette mixture and cooking for a minute or two until firm on the bottom.
Flip the omelette over and spread with the pesto and sprinkle on the rest of the parmesan.
Cook for another minute, fold over and serve. Enjoy!
i fell in love with pesto when i had it with baked chiken, now i crave it on everything but i have yet to try this omelette but im sure its delightful thanks for sharing the idea!
Oh my gosh -- this looks DELICIOUS!


text:
El navegado, vino navegado o candola es una bebida alcohólica, popular en el sur de Chile, que se prepara a partir de una mezcla de vino tinto, rodajas de naranja, azúcar y especias. Se le llama "navegado" por la analogía entre el vino con trozos flotantes de naranja y el mar cuando es atravesado por una embarcación.

Para prepararlo se debe calentar el vino tinto y mientras tanto se le añaden rodajas de naranja, azúcar y canela, a veces también clavo de olor. La mezcla se revuelve y se mantiene en el fuego hasta que esté a punto de hervir, de lo contrario quedará amargo. Justo al momento de hervir hay quienes prenden fuego a la mezcla, eliminando así parte del alcohol del vino (apagando la flama con un soplido) o todo eliminando todo su alcohol (dejando que la flama extinga sola); con esto último se logra del navegado una bebida no alcohólica. Servir caliente.

En el imaginario chileno esta bebida se asocia con el invierno y con la juventud de los años sesenta, por lo que es habitual que se venda en peñas folclóricas y encuentros costumbristas del sur del país. En Concepción principalmente se conoce como candola.

Etimología
Si bien su nombre se debe probablemente al hecho de que las rodajas de naranja flotan o "navegan" en el vino, en la época de los barcos a vela se creía que el vino transportado por mar mejoraba su calidad, idea que en Chile perduró incluso después de la llegada de los barcos a vapor. Ya en el siglo XX, existe una anécdota de un partida de exportación de vino chileno que fue rechazada por las autoridades estadounidenses luego de que se detectara una pequeña cantidad de vidrio molido en su interior, por lo que fue devuelta al país. A fin de recuperar parte de la inversión, en Chile se vendió el vino rechazado como un producto especial que había mejorado su sabor al "navegarse" y haber cruzado dos veces el trópico. Por lo mismo, "vino navegado" quedó como sinónimo de un vino con gran aroma y sabor, características que habría adquirido luego el vino calentado con especias.

Véase también
 Jote (bebida alcohólica)
 Vino caliente

Referencias

Bibliografía

Enlaces externos
 Navegado.cl - Promoviendo vinos naturales y agricultura
 Receta para preparar el Vino Navegado con más detalle

Cócteles con vino
Bebidas alcohólicas de Chile
Bebidas alcohólicas calientes

redpajama_set_name: RedPajamaWikipedia


Thank you to everyone who has already taken advantage of my book available FREE on Kindle, now through Thursday, June 14, 2018.
I pray God uses it to bless you.
Paperback also available on Amazon with interior illustrations accompanying most stories.
I was suddenly woken by an impressionable thought. It was a Sunday. The thought, not my own, said, "Your God stories are not yours, they are Mine, and they are meant to be shared." I knew it was God speaking to me.
This is a collection of sixty-two true stories from personal experience that will inspire the believer, as well as show a doubting world that God exists. Stories tell how God rescues from danger, clears a storm for safe travel, makes money miraculously appear, sends angels to help, and answers prayer. You'll discover the various ways God protects, provides, redeems, encourages, communicates, and delights those who are looking for Him. If that's you, these stories will help you identify God's miraculous presence in your own life.
If you are seeking stories on specific topics, a list in the back of the book groups stories in categories. Topics include protection, provision, guidance, healing, answered prayer, angels, and small miracles.
There is nothing special about me. I am only ordinary person. The only One who is truly amazing is the Almighty God, His Son and Savior Jesus, and the Holy Spirit who comforts and guides us. He is the One I wish to point you to. He is the only One who can do the miraculous. I trust He will use these stories to draw you closer to Him, to prove His great power, and reveal His deep love for you.
I can't predict what God intends to do with these stories. I know He's going to use them; otherwise He wouldn't have been so persistent in getting me to share them. Nor would He allow me to experience Him in these events in the first place. A part of me struggled with publishing this book. Sharing some of these personal stories means I had to be vulnerable. Yet God constantly reminded me that when I gave my life to Him I also became His vessel to be used for His purposes. These stories aren't about me; they are about Him. They are His stories, and like He said, they are meant to be shared.


The country of one thousand hills is one of the most beautiful places on earth. It is the perfect setting to trek to see the mountain gorillas in the misty Virunga Mountains, probably the greatest wildlife experience in the world. There are also other safari options, particularly for primates in Nyungwe Forest as well as the ideal relaxation spot of Lake Kivu. Rwanda�s public perception may still be blighted by the 1994 genocide but that shouldn�t stop you exploring this beautiful country and a friendly and resilient people. Explore in depth highlights of Rwanda.
For help planning your trip to Rwanda including visas, vaccinations, currency exchange, flights, accomodation and insurance, see our Rwanda trip planning page.
Discover more about Rwanda - the country's geogrpahy and natural features, an assessment of its status on freedom and rights and data on the country's population and economy.
Climate: Temperate climate with two rainy seasons (February to April and November to January).
Summary status and rankings for Rwanda from classifications of different organisations measuring political and economic freedom, democracy and civil rights. See more details of these rankings.


Background: The literature is inconsistent and inconclusive on the relationship between bone mineral density (BMD) and muscular strength in postmenopausal women.
Objective: To evaluate the relationship between isokinetically and isometrically determined muscle strength and BMD in postmenopausal women of different age groups.
Methods: Healthy postmenopausal women (n = 293; mean age, 54.22 ± 3.85 years) were enrolled in this study. They were grouped by age according to World Health Organization life expectancy: 45–50 years, 51–53 years, 54–56 years, 57–59 years, and 60–64 years. Total BMD, L2–4 BMD, and femoral neck BMD were measured by dual-energy X-ray bone densitometry; isokinetic and isometric muscle strength of the right hip and trunk muscles were measured during contractile exercise. Stepwise regression analysis was used to examine the relationships between BMD and strength measures, controlling for subject age and years since menopause.
Results: Results of stepwise regression showed that hip extensor and flexor strength at 120°/second and back extend strength at 30°/second accounted for 26% total BMD variance among menopausal subjects, 19% L2–4 BMD variance, and 15% femoral neck BMD variance; in postmenopausal women of different age groups, hip extensor and flexor strength at 120°/second and back extend strength at 30°/second accounted for 25%–35% total BMD variance.
Conclusion: Different optimal strength measurements were identified for different age groups. Age-appropriate testing mode can improve detection of osteoporotic fracture risk in early menopause by determining muscular strength reduction related to BMD loss. This may enable early initiation of preventative therapies.


text:
A 15-month evaluation of bond failures of orthodontic brackets bonded with direct versus indirect bonding technique: a clinical trial
Anna Menini1,
Mauro Cozzani2,
Maria Francesca Sfondrini1,
Andrea Scribante1,
Paolo Cozzani3 &
Paola Gandini1
The purpose of this clinical longitudinal study was to investigate the effectiveness of indirect bonding technique evaluating the number of bond failures which occurred during treatment.
Fifty-two patients were selected and divided into two groups: group A (33 patients) bonded with the direct technique and group B (19 patients) bonded with the indirect technique. The number and date of bracket failure were recorded for over 15 months. Moreover, also the effect of crowding level on bracket failures was calculated. Statistical analysis was performed by means of t-test, Kaplan-Meier survival estimates and chi-squared test.
No statistically significant differences were found in the total bond failure rate between direct and indirect techniques, also when comparing the upper and lower arches. The only significant difference was found comparing the posterior segment of the lower arches, in which a higher percentage of detachments were recorded in group B, bonded with the indirect technique. Moreover, no significant differences between direct and indirect bonding were found when evaluating crowding level.
Orthodontic practitioners can safely use the indirect bonding technique, even in patients with severe crowding, because it does not influence the adhesive quality and the bracket survival rate.
In orthodontics, indirect bonding technique offers numerous advantages over direct bonding [1], such as chair time saving, a more precise bracket placement [2]–[4] and removal of flash to the bracket bases [5],[6] which can promote plaque and calculus formation [7].
Indirect bonding technique involves a two-stage procedure. The first stage is carried out in a laboratory, where brackets are positioned and attached to a plaster model of the patient's teeth. The second stage is clinical: when the brackets are transferred from the cast model to the patient's mouth with a tray and bonded to the etched enamel.
Indirect bonding has become increasingly popular since the method was first described in detail by Silverman and Cohen [8],[9] in 1972. Different indirect bonding techniques have been proposed, with different preparations of the bracket base (standard or customized), transfer mask type (single jigs or full arch) and transfer tray material (acrylic resin, silicone, thermo-printed material) [10]–[12].
Many studies have been conducted in order to test the indirect technique effectiveness. In fact, only few reports evaluated the clinical reliability of the indirect bonding technique compared with the conventional bonding technique.
Accordingly, the purpose of the present study is to test the efficacy of indirect bonding compared with conventional direct bonding, evaluating the number of bond failures which occurred during treatment; the observation period was 15 months for both groups. The null hypothesis of the study was that there is no significant difference in bracket failure rates between the two bonding techniques, also when comparing the upper and lower arches and the anterior and posterior segments.
A total of 52 patients treated with fixed orthodontic appliance were included in this study. All of them had to satisfy the following inclusion criteria:
permanent dentition
no dental morphogenesis anomalies
no enamel anomalies
no presence of vestibular reconstruction
no genetic syndromes connected with oral cavity anomalies
no need of adjunctive orthodontic device (facial mask, forsus, etc.)
No restriction was applied in respect of age, gender, type of malocclusion and grade of crowding.
For each patient, the following were recorded: the date of bonding, age at the start of treatment, gender, value of irregularity index [13] (calculated on the initial model cast) and type of malocclusion. A formal sample size calculation was not undertaken.
Fifty-two patients agreed to participate and were divided into two groups: 33 patients in group A (18 females and 15 males, mean age = 20.75 years) bonded with the direct technique and 19 patients in group B (9 females and 10 males, mean age = 25 years) bonded with the indirect technique. Informed consent was obtained from all the patients before starting the therapy, and the study was conducted in accordance with the Declaration of Helsinki. Data analysts were blinded; however, blinding of the operators was not possible.
Stainless steel brackets and molar tubes 0.018″ × 0.025″ and 0.022″ × 0.028″ (AO, 1714 Cambridge Avenue, Sheboygan, WI, USA) and the same adhesive system (Transbond XT, 3M, Monrovia, CA, USA) were used for both groups.
All patients had professional oral hygiene 3 days before bonding, and then both arches were bonded, including the first molars.
All patients were provided with oral instruction for maintenance of their fixed appliance. Checkup was carried out every 4 weeks. The patients were recommended to inform the dentist immediately if suspecting a detachment. Detachment date was registered, and the bracket was replaced with a new one; in group B, a section of the transfer tray used for the initial bonding has been used for repositioning when necessary.
A total of 1,248 brackets were positioned: 792 attachments were fixed with the direct technique while the remaining 456 with the indirect technique. The observation period was 15 months.
Direct technique
All teeth were cleaned with water and fluoride-free pumice for at least 30 s and then dried with an oil-free air syringe. The enamel was then etched for 30 s with 37% orthophosphoric acid (etching gel, 3M, Monrovia, CA, USA), and the Primer (Transbond XT, 3M, Monrovia, CA, USA) was applied with a small brush and spread with oil-free compressed air. The composite (Transbond XT, 3M, Monrovia, CA, USA) was applied on the bracket base, and the attachment was positioned on the tooth surface. Composite excess was removed with a probe before polymerization. The composite was polymerized with a LED lamp (Opticore L3; Marslev Byvej, Denmark) for 80 s per bracket (20 s for side: mesial, distal, occlusal and gingival).
Indirect technique
For indirect bonding, the modified Fantozzi technique [5],[14] was used, which consists of two transparent trays: one for etching and one for bracket transfer. Each tray is divided into three sections: one anterior (incisors and canines) and two posterior (premolars and first molars). The transfer tray is made of two layers: the inner one is soft and thin and holds the bracket completely, while the extern is rigid and assures a precise position during the trays transfer from the cast to the oral cavity (Figure 1). The composite is positioned on the bracket base during the laboratory phase [14].
Soft tray extending buccally to cover the entire bracket and rigid tray extending only to the bracket slot. The soft tray (yellow) extends buccally to cover the entire bracket, holding it in place while covering half of the clinical crown on the lingual side. The rigid tray (pink) extends only to the bracket slot to retain the bracket without impeding tray removal during the clinical phase.
The clinical phase was carried out as follows: the etching mask was placed over the cleaned facial surface of the appropriate teeth. The etchant was applied for 30 s. The mask was removed, the teeth rinsed thoroughly for about 10 s and then dried. A layer of primer (Transbond XT) was applied both on the etched surface and the bracket base inside the transfer tray; the trays were fitted in the mouth and light-cured for 20 s each on the buccal, distal, mesial and occlusal sides, for a total of 80 s per bracket. The transfer trays were removed using a probe.
The statistical analysis was performed using the Software Stata 9 (Stata, College Station, TX, USA).
Differences in bond failure frequency in groups A and B were analysed using a Fisher exact test. To evaluate the time of detachment, Kaplan-Meier survival curves were obtained using a log-rank test.
Chi-squared test was used to analyse the detachment in the upper jaw compared to the lower jaw, and when considered, each arch splits into anterior and posterior sections.
To analyse irregularity index, samples were divided into two groups (irregularity index <4 mm and irregularity index >4 mm) and chi-squared test was applied. Significance level was set at P < 0.05.
In group A, of 33 patients, 792 brackets were bonded using the direct technique. Nine patients presented a class I malocclusion, 18 a class II and 6 a class III. The mean value of irregularity index was 2.58 mm (DS 2.57 mm); 28 detachments were reported.
In group B, of 19 patients, 456 brackets were bonded using the indirect technique. Nine patients presented a class I malocclusion, 8 a class II and 2 a class III. The mean value of irregularity index was 3.58 mm (DS 2.52 mm); 26 detachments occurred.
Bond failure
No significant differences were found between direct and indirect bonding (P < 0.05) (Table 1).
Table 1 The number and percentage of detachments in groups A and B
Kaplan-Meier survival plots showed no significant differences during the observation period between group A and group B (Figure 2) (hazard ratio: 0.61; confidence interval 95%: 0.34 to 1.04; log-rank test: P = 0.0699).
Kaplan-Meier survival plots. A: Direct Bonding, B: Indirect bonding.
Bond failure comparing the upper and lower arches was also investigated (Tables 2 and 3). No differences in the upper jaws were found between two techniques, while a significantly greater number of detachment occurred in the lower arch (9.64% of the total bonded bracket).
Table 2 Comparison between groups A and B of detachment number in the upper arch
Table 3 Comparison between groups A and B of detachment number in the lower arch
The number of detachments in the anterior (including incisors and canines) and posterior (including molars and bicuspids) sections was also investigated for both upper and lower arches (Tables 2 and 3). No significant differences were found in the upper jaws neither for the anterior nor for the posterior segments in group A as compared with group B. As regards the lower jaws, in the posterior section, chi-squared test showed that the percentage of detachments was greater in group B (17.54%), bonded with the indirect technique, than in group A (5.56%) (P < 0.01).
Irregularity index
t-test revealed that the two groups were homogeneous as regards the irregularity index (I.I.) value.
It was also decided to subdivide the sample on the strength of the I.I. value, in order to investigate the differences of bond failure in patients with various crowding levels.
Patients with severe crowding level were considered if the I.I. values were ≥4 mm and light crowding level when the I.I. values were <4 mm. Chi-squared test showed no significant differences in the number of bond failure between the two groups (Table 4).
Table 4 Comparison of detachment number in groups A and B with a high/low value of I.I.
As reported in the results, the null hypothesis of the study was partially accepted. In fact, the present investigation demonstrated that when using the indirect technique, the bond failure rate is not significantly different than when the direct technique is used.
These results are in agreement with Deahl et al. [15] and Thiyagarajah et al. [16] that found no difference in detachment rate in the two techniques. Nevertheless, we can notice that the percentage of bond failure reported in the present study (3.54% for direct technique, 5.79% for indirect one) is higher for both techniques than the percentage reported by Deahl (1.17% ± 3.62% and 1.21% ± 3.81%, respectively) as well as those reported by Thiyagarajah (2.9% for direct technique, 2.2% for indirect one). The reasons of this difference can be found in the numerous differences in the study drawing: type of bracket and adhesive system, procedure used for the transfer tray confection, number of patients included in the sample and study design. It is important to consider that in our investigation, the first molar tubes were included in all statistical analysis and these attachments presented a great number of bond failure: on 28 total detachments in the direct technique, 13 were molar tubes, while 8 were the molar tube detachments on 26 of the total bond failure observed for the indirect technique.
The detachment rate obtained in our study for patient bonded with the indirect technique is similar to the findings of Read and O'Brien [17] that investigated the failure rate in patients bonded with the indirect technique using a new visible light-cured adhesive (Opalux, I.C.I. Dental, Macclesfield, UK). On the other hand, Read did not found any differences in comparing anterior and posterior sections. As regards the direct technique, the results are similar to others reported by various authors: Mirabella et al. [18] found a bond failure rate of 2.95%, thus showing a significant difference between the upper and lower arches (1.67% and 4.35%, respectively); Varlik and Demirbaş [19] reported a percentage of 3.7%; and Pasquale et al. [20] of 4.1%.
Romano et al. [21] recorded a lower percentage value (1.57%), even if it is proper to consider that he did not include the first molars in his study, and the observation period was 6 months.
Shear bond strength of brackets bonded with the indirect technique has been tested in vitro, and comparison with direct bonding shows no significant difference between the two techniques [22]–[24].
A direct comparison among the studies present in the literature is difficult, as numerous differences and variances among various investigations (type of bracket and adhesive [25],[26], observation period, sample size, etc.) are present.
Kaplan-Meier survival plots showed no statistically significant differences in failure rate between brackets bonded with direct or indirect technique. A longer period of examination could reveal if the discrepancy, actually not significant, between the two curves is going to increase over time, thus demonstrating a difference in survival rate of brackets bonded directly or indirectly, or if the results obtained in the present research are confirmed also after a longer observation time.
Moreover, in the present investigation, different results were found in the percentage of failure when comparing the upper and lower arches as well as the anterior and posterior segments.
In fact, as regards the upper jaw, no significant differences were found in groups A and B when considering full arch neither when considering sectors separately. Statistically significant results (P < 0.01) were observed in the posterior segment of the lower arch, with a higher failure rate in group B (17.54%) when compared to group A (5.56%).
Gender, age and type of malocclusion were not evaluated in the present work. Conflicting reports are present in the literature concerning these variables: some authors found significant differences in bond failure rate in patients with different malocclusions [27], age [28] and gender [29]. Others found the same results in male and female [27],[30],[31], patients with different age [30],[31] and malocclusion [29],[31].
To analyse the irregularity index, group A and group B were splitted in two subgroups: with high I.I. values (≥4 mm) or low I.I. values (<4 mm). No differences were found between direct and indirect techniques also when evaluating the irregularity index values. Crowding severity seems not to be a variance influencing risk of detachment. The increase of I.I. values does not correspond to an increased percentage of failure rates.
This suggests that the use of transfer trays offers a good adhesion quality also in the case of severe crowding, as much as the direct bonding technique.
Indirect technique does not seem to be less efficient than the direct one in terms of detachment percentage; neither bond failure seems to be influenced by crowding level. Therefore, the indirect technique can be used safely also in patients presenting crowding and rotations in the anterior segments or when malpositioned elements could seem an obstacle for a correct fitting of the trays.
In the present clinical study, there were no statistically significant differences in the total bond failure rate between direct and indirect techniques. No statistically significant differences in the percentage of detachment were recorded between the two different bonding techniques when comparing the upper and lower arches.
The only difference in bond failure rate was observed comparing the posterior segments of the lower arch, in respect of which was found a significantly greater number of detachment in group B, bonded with the indirect technique. No difference in bond failure can be associated to crowding level.
Kalange JT: Indirect bonding: a comprehensive review of the advantages. World J Orthod 2004, 4(5):301–307.
White LW: A new and improved indirect bonding technique. J Clin Orthod 1999, 33(1):17–23.
Fortini A, Giuntoli F, Franchi L: A simplified indirect bonding technique. J Clin Orthod 2007, 11: 680–683.
Hoge TM, Dhopatkar AA, Rock WP, Spary DJ: The Burton approach to indirect bonding. J. Orthod. 2001, 28: 267–270. 10.1093/ortho/28.4.267
Cozzani M, Menini A, Bertelli A. Etching masks for precise indirect bonding. J Clin Orthod. 44: 326–330. Cozzani M, Menini A, Bertelli A. Etching masks for precise indirect bonding.J Clin Orthod.44:326–330.
Kalange JT, Thomas RG: Indirect bonding: a comprehensive review of the literature. Semin. Orthod. 2007, 13: 3–10. 10.1053/j.sodo.2006.11.003
Sinha PK, Nanda RS, Ghosh J: A thermal-cured, fluoride-releasing indirect bonding system. J Clin Orthod 1995, 29: 97–100.
Silverman E, Cohen M: A universal direct bonding system for both metal and plastic brackets. Am. J. Orthod. 1972, 62: 236–244. 10.1016/S0002-9416(72)90264-3
Silverman E, Cohen M: A report on a major improvement in the indirect bonding technique. J Clin Orthod 1975, 9: 270–276.
Dalessandri D, Dalessandri M, Bonetti S, Visconti L, Paganelli C: Effectiveness of an indirect bonding technique in reducing plaque accumulation around braces. Angle Orthod. 2012, 82: 313–318. 10.2319/041811-273.1
Zachrisson B, Brobakkeen B: Clinical comparison of direct versus indirect bonding, with different bracket types adhesives. Am. J. Orthod. 1978, 74: 62–78. 10.1016/0002-9416(78)90046-5
Aguirre MJ, King GJ, Waldrom MJ: Assessment of bracket placement and bond strength when comparing direct bonding technique. Am. J. Orthod. 1982, 82: 269–276. 10.1016/0002-9416(82)90461-4
Little RM: The irregularity index: a quantitative score of mandibular anterior alignment. Am. J. Orthod. 1975, 6: 554–563. 10.1016/0002-9416(75)90086-X
Fantozzi F. Brackettaggio indiretto: fasi di laboratorio sulla costruzione personalizzata di trasbrackets e mascherine per la mordenzatura. Boll Inform Ortod. 1997; 56: 38–45. Fantozzi F. Brackettaggio indiretto: fasi di laboratorio sulla costruzione personalizzata di trasbrackets e mascherine per la mordenzatura.Boll Inform Ortod. 1997; 56:38–45.
Deahl ST, Salome N, Hatch JP, Rugh JD: Practice-based comparison of direct and indirect bonding. Am J Orthod Dentofacial Orthop 2007, 132: 738–742. 10.1016/j.ajodo.2006.01.037
Thiyagarajah S, Spary DJ, Rock WP: A clinical comparison of bracket bond failures in association with direct and indirect bonding. J. Orthod. 2006, 33: 198–204. 10.1179/146531205225021615
Read MJ, O'Brien KD: A clinical trial of an indirect bonding technique with a visible light-cured adhesive. Am J Orthod Dentofacial Orthop 1990, 98: 259–262. 10.1016/S0889-5406(05)81603-8
Mirabella D, Spena R, Scognamiglio G, Luca L, Gracco A, Siciliani G: LED vs halogen light-curing of adhesive-precoated brackets. Angle Orthod. 2008, 78: 935–940. 10.2319/042707-211.1
Varlik SK, Demirbaş E: Effect of light-cured filled sealant on the bond failure rate of orthodontic brackets in vivo. Am J Orthod Dentofacial Orthop 2009, 135: 144–145. 10.1016/j.ajodo.2008.10.003
Pasquale A, Weinstein M, Borislow AJ, Braitman LE: In-vivo prospective comparison of bond failure rates of 2 self-etching primer/adhesive systems. Am J Orthod Dentofacial Orthop 2007, 132: 671–674. 10.1016/j.ajodo.2006.12.008
Romano FL, Valério RA, Gomes-Silva JM, Ferreira JT, Faria G, Borsatto MC: Clinical evaluation of the failure rate of metallic brackets bonded with orthodontic composites. Braz Dental J 2012, 23: 399–402. 10.1590/S0103-64402012000400015
Yi GK, Dunn WJ, Taloumnis LJ: Shear bond strength comparison between direct and indirect bonded orthodontic brackets. Am J of Orthod and Dent Orthop 2003, 124: 577–581. 10.1016/S0889-5406(03)00503-1
Linn BJ, Berzins DW, Dhuru VB, Bradley TG: A comparison of bond strength between direct- and indirect-bonding methods. Angle Orthod. 2006, 76: 289–294.
Swetha M, Pai VS, Sanjay N, Nandini S: Indirect versus direct bonding - a shear bond strength comparison: an in vitro study. J. Contemp. Dent. Pract. 2011, 12: 232–238. 10.5005/jp-journals-10024-1040
Montasser MA, Taha M: Effect of enamel protective agents on shear bond strength of orthodontic brackets. Prog. Orthod. 2014, 18: 15–34.
Elsaka SE, Hammad SM, Ibrahim NF: Evaluation of stresses developed in different bracket-cement-enamel systems usig finite element analysis with in vitro bond strength tests. Prog. Orthod. 2014, 16: 15–33.
Millett DT, McCluskey LA, McAuley F, Creanor SL, Newell J, Love J: A comparative clinical trial of a compomer and a resin adhesive for orthodontic bonding. Angle Orthod. 2000, 70: 233–340.
Millett DT, Gordon PH: A 5-year clinical review of bond failure with a no-mix adhesive (Right on®). Europ J Orthod 1994, 16: 203–211. 10.1093/ejo/16.3.203
Shammaa I, Ngan P, Kim H, Kao E, Gladwin M, Gunel E, Brown C: Comparison of bracket debonding force between two conventional resin adhesive and a resin-reinforces glass ionomer cement: an in vitro an in vivo study. Angle Orthod. 1999, 69: 463–469.
Marcusson A, Norevall LI, Persson M: White spot reduction when using glass ionomer cement for bonding in orthodontics: a longitudinal and comparative study. Europ J Orthod 1997, 19: 233–242. 10.1093/ejo/19.3.233
Millett DT, Hallgren A, Cattanach D, McFadzean R, Pattison J, Robertson M, Love J: A 5-years clinical rewiew of bond failure with a light-cured resin adhesive. Angle Orthod. 1998, 68: 351–356.
Unit of Orthodontics and Paediatric Dentistry, Department of Clinical, Diagnostic and Paediatric Sciences, School of Dentistry, University of Pavia, Pavia, Italy
Anna Menini, Maria Francesca Sfondrini, Andrea Scribante & Paola Gandini
Department of Surgical Science, School of Dental Medicine, University of Cagliari, Cagliari, Italy
Mauro Cozzani
Private Practice, La Spezia, Italy
Paolo Cozzani
Anna Menini
Maria Francesca Sfondrini
Andrea Scribante
Paola Gandini
Correspondence to Anna Menini.
MA participated in the data acquisition and manuscript editing. CM participated in the design of the study, organized the clinical phase and manuscript correction. SMF participated in the design of the study and manuscript correction. SA carried out the data analysis and manuscript correction. CP organized the clinical phase. GP participated in the workflow supervision. All authors read and approved the final manuscript.
Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0), which permits use, duplication, adaptation, distribution, and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
Menini, A., Cozzani, M., Sfondrini, M.F. et al. A 15-month evaluation of bond failures of orthodontic brackets bonded with direct versus indirect bonding technique: a clinical trial. Prog Orthod. 15, 70 (2014). https://doi.org/10.1186/s40510-014-0070-9
Indirect bonding technique


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Applicability of VAT on Real Estate Transactions in Nigeria
The New Practice
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Nigeria September 18 2018
With its realisation of the futility of heavy reliance on oil revenue, Nigeria is taking giant strides to refocus its revenue generation strategy by in focusing more on non-oil revenue to alternative sources. This has led to an aggressive tax regime by the Federal Government to ensure that more revenue is derived from taxes. In encouraging tax compliance by tax payers, the Federal Government introduced the Voluntary Assets and Income Declaration Scheme (VAIDS).
There is however a fear of government ignoring the letter of the existing tax laws in its quest to generate more revenue to its coffers by bringing in more taxpayers into the tax net. This fear has in fact become a reality, especially when it comes to real estate.
Recently, a client of ours in the Real Estate Sector was in the process of acquiring a piece of property in the Lekki axis of Lagos. The purchase price had already been agreed, necessary due diligence investigations conducted at the land registry, and title over the property was certified to be unencumbered. The prospective seller of the property issued his invoice to our client for the sale of the land and included Value Added Tax (VAT) of 5% to the purchase price. Our Client was startled by the inclusion of VAT and requested to know the position of the law on VAT on property transactions.
Though Nigeria's VAT rate of 5% pales in comparison to other countries including the United Kingdom which charges 20%, it makes a difference on large transactions such as property and real estate. The Taxman's interest in these burgeoning property transactions is not surprising as he seeks to generate revenue for government. But the question that needs to be asked and answered is: is VAT applicable to property and real estate transactions, or are buyers being made to bear an unnecessary unlawful cost?
Understanding VAT vis-à-vis Property Transactions
VAT is a consumption tax that has been embraced by many countries all over the world. Since it is a consumption tax, it is relatively easy to administer and difficult to evade.
The Federal Government's will to diversify the economy is understandable in the face of the current economic situation of the country. With the fluctuating inflation rates, the single most important aim of Nigeria's tax policy would be to raise more revenue. Consequently, government through the Federal Inland Revenue Service ("FIRS") is taking steps to bring into the tax net, real estate and property transactions with a conviction that these transactions are subject to VAT.
But what does the VAT Act have to say about this?
What is VATable under the VAT Act?
As earlier pointed out, VAT is a consumption tax which applies solely to the supply of goods and services. It is a tax levied on value created at every stage of the production and distribution value chain. It must be pointed out however, that the burden of VAT is ultimately borne by the final consumers, as he has to pay higher sum for the goods purchased or services rendered.
The New Practice - Oladimeji Sarumi and Genevieve Henshaw
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Q: Powershell how to check if friday is the last day of the month , returning True from a Function I have tried to make a function in Powershell that produces a True if the last day of the month is friday.
function Get-LastFridayOfMonth([DateTime] $d) {
    $lastDay = new-object DateTime($d.Year, $d.Month,[DateTime]::DaysInMonth($d.Year, $d.Month))
    $diff = ([int] [DayOfWeek]::Friday) - ([int] $lastDay.DayOfWeek)
    if ($diff -gT 0) {
        return $lastDay.AddDays(- (7-$diff))
    } else {
        return $lastDay.AddDays($diff)
    }
}
$testdate = Get-LastFridayOfMonth (Get-Date)

But how to check if that friday is the last day of the month ?

A: @Theo's answer reframes your question and gives a nice all-in-one solution, but to address your specific question:

"how to check if [a date] is the last day of the month ?"

you can just add one day to the date and see if the month changes. If it does change then the original date must be the last one in the month…
$testdate = [datetime] "2023-01-31"
$isLastDayOfMonth = $testdate.AddDays(1).Month -ne $testdate.Month
$isLastDayOfMonth
# True

$testdate = [datetime] "2023-01-30"
$isLastDayOfMonth = $testdate.AddDays(1).Month -ne $testdate.Month
$isLastDayOfMonth
# False

$testdate = Get-LastFridayOfMonth (Get-Date)
$isLastDayOfMonth = $testdate.AddDays(1).Month -ne $testdate.Month
$isLastDayOfMonth
# depends on if the month ends on a friday

A: I would change that function to just return the last days weekday so after calling it you can decide what weekday you get for the given date.
function Get-LastWeekDayOfMonth {
    param (
        [datetime]$Date = (Get-Date)
    )
    # .AddDays(-$Date.Day+1) sets the given date to the 1st of that month
    $Date.AddDays(-$Date.Day+1).AddMonths(1).AddDays(-1).DayOfWeek
}

switch (Get-LastWeekDayOfMonth) {
    'Friday' { "It's a Friday !" }
    default  { $_ }
}

Using the current date (February 2023) it would yield Tuesday
If you specify for instance March 2023
$d = Get-Date -Year 2023 -Month 3 -Day 1
switch (Get-LastWeekDayOfMonth -Date $d) {
    'Friday' { "It's a Friday !" }
    default  { $_ }
}

The outcome will be It's a Friday !

If however you want a function to simply return $true or $false when the month end in a Friday or not, do this instead:
function Test-LastDayOfMonthIsFriday {
    param (
        [datetime]$Date = (Get-Date)
    )
    # .AddDays(-$Date.Day+1) sets the given date to the 1st of that month
    $Date.AddDays(-$Date.Day+1).AddMonths(1).AddDays(-1).DayOfWeek -eq 'Friday'
}

Test-LastDayOfMonthIsFriday                                              # --> $false
Test-LastDayOfMonthIsFriday -Date (Get-Date -Year 2023 -Month 3 -Day 1)  # --> $true

Special thanks to mklement0 for the $Date.AddDays(-$Date.Day+1) part which always sets the date to the first day of that month

redpajama_set_name: RedPajamaStackExchange


Kirin's 'Fuji Gotemba' Distillery, located at the base of Mount Fuji, produces three type of grain whisky in addition to malt: light - from a column still, medium - from a kettle and column, and heavy - from a beer column and doubler.
Chief Blender Jota Tanaka has favoured the medium and heavier grains along, of course with malts, to create the Fuji Sanroku 50. It is the first permanently available entry-level Japanese blended whisky which is not chill filtered.


Sherrard Roe Voigt & Harbison is pleased to announce that Tracy Powell has been recognized as a top health care transaction lawyer of 2015 according to The Ambulatory M&A Advisor. Individuals are nominated by clients, colleagues and other service professionals within the health care transaction field. Recipients of the Leading Lawyer award are employed full-time at a law firm, have partner status or above, have 10 or more years of experience with health care transactions and practice with a focus on M&A.


Monday, February 8th evening, MarShawn M. McCarrel II, a "Black Lives Matter" activist, stood on the statehouse steps in Ohio and committed suicide, according to a Columbus Dispatch report.
Reports are that he shot himself right on the front steps. There were no witnesses and that McCarrel was pronounced dead at the scene.
The "demons" McCarrell spoke of are many of the signs of someone who is seriously contemplating taking their life.
But one thing is for sure, when ANY of these signs are shown, please take them seriously and see k help for that person.
"If only he had known that HIS life mattered too," tweeted a friend earlier today.
McCarrel was involved in a mentorship program in Franklin Township and also helped launch a nonprofit group that fed the homeless.
McCarrel, who had recently worked with Black Lives Matter, helped organize protests in Ohio after a Missouri cop shot and killed unarmed black teenager Michael Brown in 2014.


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ACCEPTED

#### According to
International Plant Names Index

#### Published in
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#### Original name
Modecca celebica Koord.

### Remarks
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redpajama_set_name: RedPajamaGithub


Maralen of the Mornsong at StarCityGames.com!
Card Text: Players can't draw cards.
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More than 1 in 4 (26%) of UK consumers not confident about their finances post Covid-19, says CISI
by Lora Benson | Sep 24, 2020
Following the stresses and strains of the Covid-19 pandemic, 26% of UK consumers say they are not confident about their financial situation, according to a Chartered Institute for Securities & Investment (CISI) survey.
The survey of 1,965 UK adults over the age of 25, undertaken by YouGov for CISI, also showed 33% of 35-54 year olds and 27% of women were not confident about their finances post Covid-19. The picture across UK regions reflected a similar trend:
I am confident about my financial situation following the impact of Covid-19
Northern Ireland 36% 59% 5%
North East 30% 59% 12%
London 28% 64% 9%
East 28% 64% 8%
East Midlands 27% 66% 7%
Yorkshire and The Humber 26% 66% 7%
South West 26% 67% 8%
Wales 25% 67% 8%
South East 24% 71% 5%
North West 23% 71% 6%
West Midlands 23% 71% 6%
Scotland 23% 71% 6%
This most recent survey builds on past surveys the CISI has undertaken. In 2017, 30% of respondents said that they would not know how to seek financial advice if they wanted it. Now, with 33% of 35-54 year olds not feeling confident about controlling their own finances, it is more important than ever that the financial planning community come together to help allay anxieties.
The survey was undertaken in the run up to CISI Financial Planning Week 5-11 October when qualified financial planners and Certified Financial PlannerTM professionals will be offering free, one hour sessions, worth £500, to consumers throughout the UK.
Consumers were also asked whether they were confident that they had the knowledge to make the right financial choices in their lives. Of those who responded overall 15% disagreed. In Northern Ireland, 23% disagreed with this statement compared to 11% in the East Midlands. Of 25-34 year olds, 20% said they were not confident.
In addition, respondents were asked whether they were confident that they knew enough about money management to support their family long-term.
Overall, 16% disagreed with this statement, with 22% of 25-34 year olds and 21% in Northern Ireland disagreeing.
Jacqueline Lockie, CFP™ Chartered FCSI, CISI Head of Financial Planning said: "It's clear that many families across the nation will have had their lives turned upside down by the impact of this pandemic, perhaps through ill health, bereavement, furlough or business losses. The findings of this survey show the real impact on people's confidence in managing their future finances. Financial planners, this year more than any other, can offer a steadying hand to anyone worried about money and Financial Planning Week is an opportunity for the public to engage with financial planners for an hour's free financial help during these confidential guidance sessions."
All figures, unless otherwise stated, are from YouGov Plc. Total sample size was 2,116 adults, of which 1,965 were over the age of 25. Fieldwork was undertaken between 8th - 9th September 2020. The survey was carried out online. The figures have been weighted and are representative of all GB adults (aged 18+).
For further information on CISI's Financial Planning Week 5-9 October or to sign up to a session with a financial planner go to cisi.org/findaplanner or call 020 7645 0777.
CISI YouGov regional UK survey of consumers and confidence in money management Sept 2020


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