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Sdata Tool 64 & 128 GB New 2021+ Serial Key Free Download

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Toyota C-HR Space & Room

Find out the dimensions of the Toyota C-HR.

Toyota C-HR
  • Exterior length (mm)

    4390 mm
  • Exterior pdf creator - Free Activators (mm)

    1795 mm
  • Exterior height (mm)

    1555 mm
  • Front Tread (mm)

    1540 mm
  • Rear Tread (mm)

    1560 mm
  • Overhang Front (mm)

    935 mm
  • Overhang Rear (mm)

    815 mm
  • Wheelbase (mm)

    2640 mm
Toyota Toyota C-HR - GR SPORT - 5 Door Crossover
Toyota Toyota C-HR - GR SPORT - 5 Door Crossover
  • Luggage Capacity (laden to tonneau cover) l

    377 litres
  • 5 seat mode (laden to tonneau cover)

    377 litres
  • 5 seat mode (laden to roof)

    443 litres
  • 2 seat mode (laden to tonneau cover)

    924 litres
  • 2 seat mode (laden to roof)

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Contents

Download Now Betternet Crack VPN Premium 5.3.0 With Latest Crack Version

Betternet Crack VPN reviews look at paid “premium” services and free VPNs. You will find there the differences between the two services. I also found Sdata Tool 64 & 128 GB New 2021+ Serial Key Free Download free version useful despite the ads. Conversely, not all features need to be considered “premium” and are a bit slow.

This is one of the reasons Propriety.com regularly reminds customers about the difference between a paid VPN and a free VPN. Running a VPN is not easy – or cheap. So it is customary to earn services by advertising free VPN services. Is BetterNet guilty of this? Is this worse than the other 75% free VPN? Well, with 14 libraries tracked for advertising, that may not be a bad thing, but it’s definitely better than that.

Betternet claims to be a “super-fast VPN” because of the optimal location feature, which automatically connects you to the nearest server. Unfortunately, we were unable to connect when we tried to use this feature. Each time, the app displays a loading screen for about 30 seconds before it is disconnected. We had no problem when we finally decided to connect to the server manually instead. This time, the VPN made the connection in a few seconds.

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You’ve never heard of BetterNet Windows Crack, just because they’re new to VPN viewing; They have only been there since 2015. Since then, however, they have been growing rapidly and gaining a lot of users (especially on Android). The main draw of this VPN is of course that it is completely free.

You can use their iOS, Android, Windows and Mac apps as well as Chrome and Firefox extensions without paying a cent. You do not even need to register, so they will not Mcafee total protection 2020 crack + Activation Key Free Download your name or email address.

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There is a VPN for Windows that has no notifications and no registration. Sdata Tool 64 & 128 GB New 2021+ Serial Key Free Download allows you to surf the web anonymously without any worries of being tracked by the 360 total security premium license key 2019 - Activators Patch or your ISP. Your IP will change, and no one on the Internet will be able to track your activity. Betternet Crack gives you access to a website that is completely blocked in your country, school or work. You can unlock Facebook, Twitter, YouTube and other social networks and bypass government censorship.

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Betternet Crack Refund Policy

Betternet offers a 30-day money-back guarantee to let you test the premium service. However, you will only be refunded if you have used less than 50 MB of data. Similarly, you will need to call back within 30 days with as little use as possible. The 50 MB usage allowance is a very small amount. This makes it very difficult to actually qualify for a refund. What this really means: This is the worst 30 day money back guarantee I have ever seen from a VPN.

Apps

Betternet VPN Cracked Lacks all the VPN features that can commonly be called a “premium” service. There is no kill switch, no DNS leak protection, no fencing, no cloak and no “stilt” technology. Or with no port shipping options. Nothing. Because this is a paid service, it is completely invasive.

To select a server location, click ‘Select a virtual location.’ You get a choice from ten countries and seven cities in the United States. This option is in the right proportions. However, there are many VPNs in the market that consider that more than 50 of these countries have people in their market.

Cookies

BetterNet Terms of Service (TOS) allows third-party advertisers to deliver cookies to your device. TOS explains that this is to enable advertisers to measure the effectiveness of their campaigns. Betternet also says it has no control over those third-party practices. Ultimately, Betternet does not accept any liability for any damages or losses incurred by third parties. This is annoying, especially when you notice that it is not clear whether this is just happening on the free version.

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Solid privacy and Security Options

It is not easy to get information about the technology that BetterNet VPN uses to protect its users. I would like to present the information so far, where it is easy to see. After digging a bit, I found some information.

For example, a blog post from 201 says that Betternet VPN offers 256-bit AES encryption over OpenVPN protocol and 128-bit encryption over IPsec.

More visible VPNs offer more protocol options, but generally, you don’t need them. OpenVPN is the safest out there and when you can’t use it, ipsack is a solid second choice. Other than that, there is absolutely nothing about betternet security. Everything is very simple as there are not as many features as other VPNs.

If you are concerned about government surveillance, you may want to know that Betternet PC Crack is in Canada, a country that gathers intelligence and collaborates with other members of the Five Eyes Agreement. Their servers are worldwide, but the company is headquartered in Canadian jurisdiction.

This is not a shortcoming, but I know that some people are afraid to work with companies in five – eye countries.
Unfortunately, there are other issues that may prevent the use of their solid security technology. We will get to them in a minute.

No Log Files

Aside from the price tag, Betternet’s non-logging strategy is perhaps its greatest uncertainty. The help file simply states: “BetterNet Cracked does not collect, log, store or share any user data log.”
If you dig into their privacy policy, you can find a little more information.

Customer Support

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  • While customer support questions are usually redirected to the standard system, the Betternet team is very active on Twitter.
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Potential Security Threat

There is no doubt that it is popular, but BetterNet may not be as secure as it seems. In 201 In, several outlets reported the results of educational studies on VPN apps and said that they may be injecting malware or malware or may not provide the security they announced.

So far, I have not been able to find any Sdata Tool 64 & 128 GB New 2021+ Serial Key Free Download that BetterNet injected malware or anything else. But it is of great concern to us that they have been identified as suspects according to academic studies.

As you can see, Betternet Crack has more downloads than all the other free VPN apps, which gives it a bit of reliability. However, we prefer that her AV degree should be much higher than 13.

Vague Documentation

At one point, they say, Betternet uses 256-bit encryption. In the latter, it is called 128-bit. And at first it was hard to dig in that place. If you want to know more than the basics about the app, you need to do some research. And you might find some weird answers. Zenmate 7.7.0.0 Crack+ License Key 2021 - Free Activators user experience on the Betternet website is not good. The app is simple, but if you want anything more than that, you will have a little trouble.

If you are a heavy tormentor like me, Betternet is not the right choice for you. Betternet does not allow torrent on their servers, but warns that they will comply if warrants or other valid court orders are obtained. And also
It’s too late. I tried to download various files via eTorrent and failed to get the download speed worth waiting for.
Another big problem with my book is that it doesn’t work with Netflix. So far, Netflix has managed to block all Betternet Crack servers and IPs, so you have no way of streaming Netflix (or later) using their software. If you need a VPN that works with Netflix.

Betternet Paid Crack Offer the following Features:

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  • RAM, 32-bit: 2GB, 64-bit: 4GB
  • Disk space: 4.0 GB
  • 1360 x 768 display resolution with True Color

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Integated Diagnostic Software (IDS) - The factory Ford Motor Company vehicle diagnostic software provides complete dealership level vehicle diagnostic coverage for all 1996 to present Ford, Lincoln and Mercury vehicles. IDS is a flexible diagnostic tool that utilizes standard computing platforms to work with Ford's VCM, VCM II, VCMM and VMM devices. The IDS software license includes time based access to the IDS software, software udpates and calibration files.

Ford J2534 Reason 10 crack mac - Crack Key For U Software (FJDS) - The factory Ford Motor Company vehicle diagnostic tool designed for use with J2534 compatible Vehicle Communications Interfaces (VCI). FJDS software provides module reprogramming software (FMP) that covers 1996 to present Ford, Lincoln and Mercury module reprogramming functions, plus complete dealership level diagnostic software for all 2018 to present Ford and Lincoln vehicles. FJDS is a Acme CAD Converter For Windows diagnostic tool that utilizes standard computing platforms to work with Ford's VCM II or J2534 audacity full version crack download - Crack Key For U devices. The FJDS software license includes time based access to the FJDS software, software updates and calibration files.

Ford Diagnostic & Repair System (FDRS) - The next generation factory Ford Motor Company vehicle diagnostic Software designed for use with VCM II, VCMM and J2534 compatible Vehicle Communications Interfaces (VCI). FDRS provides complete dealership level vehicle diagnostic coverage for some 2018 and forward vehicles. FDRS provides superior capabilities, is more user-friendly and provides more diagnostic tools than IDS. The cloud-based system ensures the technician is provided the latest software every time FDRS logs into the Ford network.


Diagnostic Software Licensing

A software license is required to use IDS/FDRS software with a VCM, VCM II, or VCMM or FJDS/FDRS software with a VCM II or J2534 compatible device.

Purchase: Upon purchase of a Software License, a user will receive a 20-digit licensing activation code (key). The user can activate the key using the “Activate a License” feature in the software. Activating a key binds the key to the PC on which it is entered in. Users can release this tie to the PC or transfer the licensing key to another PC using the “Return a License” feature. Since the Software License binds to the PC and not the diagnostic hardware, a single Software License will on one PC at a time. Each PC running the software will require it’s own license or the transfer of a license, since each license binds to the PC.

Regular Validation: IDS and FJDS must communicate with the License Server on a regular basis to validate the license. A validation automatically occurs at each start-up when IDS is connected to the internet. When not connected to the internet a validation cannot occur. Therefore, any PC needs to be connected to the internet at least every 29 days. Failure to validate every 30 days will cause the license to become invalid and functionality will be disabled within the software.

Renewal: Software Licenses expire based on the term purchased. Users can renew licenses up to 30 days prior to the expiration date by returning to their account and providing payment for the renewal. Renewal terms are based on the subscription length originally purchased. If a change in license term is desired a new license should be purchased.

PATS Ford Dealer Login Account Ford IDS FDRS Activation of latest version

Remote Activation for Ford IDS of latest version

Install Latest Version of Teamviewer

This is not a virtual machine solution and runs natively on your laptop and more stable than virtual machine options for programming modules

Leave login info in notes at order payment time

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Why use the old software when you can be using the latest version Online

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Option 1

Latest version Official Ford IDS  FJDS  Licence for 1 PC

12 Month Licence

Cannot be used on multiple computers

if your pc fails you will lose licence and best to install only on SSD Hard disks and good laptops

Ford IDS licence is a twelve month licence paid upfront allowing access to Ford diagnostic network. This give the ability to update software, add keys, adaptation like EGR or injector when parts are replaced. This will not allow full security related re-programming without a product key/token for the specific models from Ford which has to purchased separately when required.

Latest Version Remote Install + Activate for DTC Clearing up to 2020

 Key / Module Programming up to 2020 But need Buy Remote Login from us each time when need  to Do security Programming for each car from FORD

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Option    2 

Includes option 3 Plus Special Dealer Login that Support Lost Spare Keys to 2020 

Latest version Official Ford IDS  FJDS  Licence for 1 PC

12 Month Licence

Cannot be used on multiple computers

Ford IDS licence is a twelve month licence paid upfront allowing access to Ford diagnostic network. This give the ability to update software, add keys, adaptation like EGR or injector when parts are replaced. This will  Allow security related re-programming without a product key/token for the specific models from Ford which has to purchased separately when required.

Latest Version Remote Install + Activate for DTC Clearing up to 2020

 Key / Module Programming up to 2020 and can use Dealer Login to Do security Programming Online PATS

Ford_IDS_FDRS_ONE_TIME_Online_access_Programming__Configuration_via_Teamviewer

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2K/4MP Smart Video Doorbell that works w AC24V transformer Google Home/Alexa Echo

Introducing you the latest smart video doorbell that supports 2K resolution and works with both DC and AC power supply. The product enables you to upgrade your conventional doorbell system easily by wiring it to the existing 24V AC transformer. Morever, it adopts an ultra wide lens to provide nearly 166 degree field of view that helps to have a super wide viewing angle. Comparing other smart video doorbell, the product comes with an angle mount bracket that enables it to be mounted on the wall without compromising the field of view. Lastly, it works with Tuyasmart/Smart Life app that works with your Google Home Hub and Alexa Echo Show 2.

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Discussion

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Oxidative Stress in Neurodegenerative Diseases

Abstract

The pathophysiologies of neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS), Parkinson’s disease (PD), and Alzheimer’s disease (AD), are far from being fully explained. Oxidative stress (OS) has been proposed as one factor that plays a potential role in the pathogenesis of neurodegenerative disorders. Clinical and preclinical studies indicate that neurodegenerative diseases are characterized by higher levels of OS biomarkers and by lower levels of antioxidant defense biomarkers in the brain and peripheral tissues. In this article, we review the current knowledge regarding the involvement of OS in neurodegenerative diseases, based on clinical trials and animal studies. In addition, we analyze the effects of the drug-induced modulation of oxidative balance, and we explore pharmacotherapeutic strategies for OS reduction.

Introduction

Identifying factors that contribute to neurodegenerative processes in the brain is one of the major goals of modern medicine. Currently, there are several hypotheses concerning the mechanisms that lead to the damage and death of brain cells in neurodegenerative diseases, such as excitotoxic effects by excitatory amino acids, disturbed cellular energy metabolism, and oxidative stress (OS), which is caused by free radicals or other reactive molecules.

The excessive production of reactive species and insufficient activity of antioxidant defense mechanisms have been implicated in the pathogenesis of many neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS), Parkinson’s disease (PD), Alzheimer’s disease (AD), and Huntington disease (HD) [1].

Reactive Species, Sources, and Cellular Pro-/Antioxidant Balance

It is thought that the biological oxidants that cause oxidative damage comprise the products of endogenous and exogenous processes that involve oxygen and nitrogen. Reactive species that contain oxygen are produced during aerobic respiration, cellular metabolism, and defense against pathogens [2]. The chemical potential of the oxygen molecule relies on its electron structure (two unpaired electrons in its basic triplet state). It promotes one-electron reactions that form the basis for respiration (reduction of oxygen molecules in four single-electron reactions), microsomal electron transport chains (ETC) (via cytochrome P-450 (CYP 450)), and oxidative burst activity in macrophages [3].

The high dynamics of the chemical processes that are achieved in elementary single-electron reactions are desirable and are the source of reactive molecules, which are either undesirable side products (respiration and metabolism) or in excess of the established requirements (defense process). These reactive molecules are known as reactive oxygen species (ROS) and reactive nitrogen species (RNS). Among them, the best known are singlet oxygen (1O2), superoxide anion radicals (O2−•), hydroxyl radicals (HO), hydrogen peroxide (H2O2), nitric oxide (NO), and peroxynitrite anions (ONOO) [4, 5].

At physiological concentrations, ROS/RNS play important regulatory and mediator functions, but an uncontrolled increase in ROS/RNS concentrations leads to a chain of radical reactions that increases the risk of damage to biological molecules in a living organism. This is caused by the high reactivity of ROS and RNS with lipids, proteins, carbohydrates, and nucleic acids. Hence, establishing an antioxidant barrier is required to limit the amount of ROS/RNS to a level that is not threatening to the integrity of biological systems. Excessive formation of ROS/RNS that exceeds the maximum capacity of the antioxidant barrier leads to a disturbance in the pro-/antioxidant equilibrium and, finally, to the development of the state known as OS.

OS can be triggered by radicals produced by either exogenous processes (e.g., xenobiotics, cold, viral and bacterial infections, ionizing radiation, ultrasound or photo-oxidation, poor diet, alcohol consumption, and smoking) or endogenous processes, which are the basic biochemical reactions in the body mentioned earlier (Fig. 1).

Generation of reactive species (based on [280–283])

Full size image

ROS production as a side effect of aerobic respiration occurs on the inner membrane of the mitochondrion [6] (Fig. 2). The respiratory chain (mitochondrial ETC) consists of a series of membrane-bound complexes, such as complex I (reduced form of nicotinamide adenine dinucleotide (NADH)/ubiquinone reductase), complex II (succinate ubiquinone reductase), complex III (ubiquinol cytochrome c reductase), complex IV (cytochrome c oxidase), and complex V (adenosine triphosphate (ATP) synthase) [7]. The final acceptor of electrons and protons, an oxygen molecule, undergoes four-electron reduction, which can lead to the production of water molecules. During ETC, single electrons leak to reduce molecular oxygen and to form O2−• and, later, H2O2 and HO [8] (Fig. 1).

Source of radical and OS biomarkers. 8-OHA 2,8-hydroxyadenine, HNE 4-hydroxynonenal, 5-OHC 5-hydroxycytosine, 5-OHU 5-hydroxyuracil, 8-OHdG 8-hydroxy-2′-deoxyguanosine, 8-OH-Gua 8-hydroxyguanine, AGEs advanced glycation end products, ALES advanced lipid peroxidation end products, AOPP advanced oxidation products, CTL creatol, COX cyclooxygenases, CYP cytochrome P450, ETC electron transport chain, F2-isoPs F2-isoprostanes, F4-NPs F 4-neuroprostanes, HETE hydroxyeicosatetraenoic acids, HODE hydroxyoctadecadienoic acid, HIF-1a hypoxia-inducible factor-1a, IsoF isofuran, LF lipofuscin, LOX lipoxygenases, Lyso PC lysophosphatidylcholines, MPO myeloperoxidase, NOX NADPH oxidases, NFS neurofuran, Opht A ophthalmic acid, GSSG oxidized glutathione, ox-LDL oxidized LDL, GSSG/GSH oxidized/reduced glutathione, Prxs peroxiredoxins, PC protein carbonyl, TBARS thiobarbituric acid reactive substances, TQ/TQH2 tocopherylquinone/tocopheryl hydroquinone, TAC total antioxidant capacity, Tyr tyrosines, UQ/UQH2 ubiquinone/ubiquinol, XO xanthine oxidase

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Because of its high consumption of oxygen and its high lipid content, the brain is particularly vulnerable to damage caused by ROS and RNS. The extent of the damage varies, depending on, among other factors, the source and type of the reactive species. More active molecules, such as HO and ONOO, interfere with other molecules at the site of their production, while less active ones, such as 1O2 and O2−•, can diffuse over longer distances and produce effects in more specific locations [9]. They can also react with each other and form more active forms, as in the case of the reaction of O2−• with NO, which creates ONOO [10].

In mitochondria, NO is produced from l-arginine and l-citrulline in a reaction that is catalyzed by nitric oxide synthase (NOS), which has three isoforms with different tissue localizations. Cellular Ca2+-dependent neuronal NOS (nNOS) is expressed in astrocytes, microglia, and macrophages, and endothelial NOS (eNOS) is expressed in the vascular endothelium and Ca2+-independent inducible NOS (iNOS). NO is involved in many important processes within the central nervous system, such as the regulation of cerebral blood flow and memory. In addition, it plays a significant role in the regulation of the immune system, including the modulation of cytokine production. The released NO acts on neighboring cells, leading to somatic mutations and affecting cell cycle regulatory proteins, apoptosis, and DNA repair [11].

RNS are important for the generation of OS. ONOO is rapidly decomposed into HO, nitrogen dioxide radical (NO2), and nitryl cation (NO2+). All of these can damage nerve cells [12].

These highly reactive compounds induce changes in the structure and function of cell membranes, proteins, lipoproteins, enzymes, hormones, and genetic material. In particular, membranes are a primary target for ROS. Conversion products of lipid peroxidation lead to the decomposition of polyunsaturated fatty acids and the formation of the final products, i.e., the reactive aldehydes, such as malondialdehyde (MDA) and 4-hydroxynonenal (HNE). These compounds react with DNA or protein molecules and modify their structure and functions [13, 14].

There are several mechanisms designed to protect the organism from the harmful effects of ROS and RNS. The ultimate amount of ROS/RNS is under strict control in the body as a result of enzymatic and non-enzymatic defense mechanisms. The production of ROS- and RNS-induced damage (the final effect of OS) in tissue can be confirmed by the presence of tissue-specific and non-specific biomarkers [15–20]. Several markers of OS and antioxidant activity are presented in Fig. 2. Recent technical advances used to detect and identify ROS/RNS biomarkers and free radical metabolism are electron spin resonance (ESR), the immuno-spin trapping technique (IST), and radioimmunoassay (RIA) [21, 22].

The cellular antioxidant system, designed to prevent damage to tissue, is composed of antioxidant enzymes and other non-enzymatic compounds that have the ability to reduce different chemical structures [21]. These compounds are responsible for maintaining the balance between pro- and antioxidant agents and alleviating OS (see Table 1). The essential components of the enzymatic antioxidant defense are superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and glutathione reductase (GR), while the non-enzymatic antioxidants include glutathione (GSH), thioredoxin (Trx), vitamins A, E, and C, flavonoids, trace elements, and proteins, e.g., albumin, ceruloplasmin, and metallothionein.

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A large body of evidence confirms a relationship between OS and the development of neurodegenerative diseases. The increased neuronal ROS production and accumulation of oxidative damage that occurs with age correlate well with the extent of neurodegeneration. In the following sections of this article, we present the current knowledge on the relationships between the intensity of OS and the initiation and progression of the major neurodegenerative diseases AD, PD, and ALS. The assessment of these relationships is based on biomarkers of OS and indicators of the pro-/antioxidant balance in nervous tissue that are correlated with the typical characteristics of neurodegenerative processes.

Amyotrophic lateral sclerosis (ICD-10 G12.21)

ALS (also known also as Charcot’s or Lou Gehrig’s disease) is a severe neurodegenerative disease that is characterized by progressive upper motor neuron loss in the cerebral cortex and lower motor neuron loss in the brainstem and spinal cord [23, 24]. This results in spasticity, muscle wasting, and weakness, leading finally to paralysis and difficulties with speech, swallowing, and breathing. ALS may have either a limb onset (80 % cases) or a bulbar onset (20 % cases) [24, 25]. There is currently no cure for ALS and only riluzole, which acts on glutamate signaling, has been registered for the treatment of the disease. Riluzole was shown to slow disease progression and to improve limb function; however, the survival of patients was prolonged by only 2–3 months and death due to respiratory failure occurred in most cases within 3–5 years of the diagnosis [26].

The main pathological hallmark of ALS is the formation of cytoplasmic aggregates in degenerating motor neurons and surrounding oligodendrocytes, but those inclusions are also present in the frontal and temporal cortices, hippocampus, and cerebellum [27].

Only 5–10 % of ALS cases are inherited (familial ALS (FALS)); the remaining cases have no clear genetic background (sporadic ALS (SALS)) [24], and their pathogenesis is still poorly understood. Studies concerning the mechanisms of ALS development indicate that many factors, including excitotoxicity, mitochondrial dysfunction, endoplasmic reticulum stress, neuroinflammation, and OS, can be involved in this process. The two forms of the disease are clinically indistinguishable because the symptoms and pathological changes in SALS and FALS are similar. FALS is caused by mutations in some genes, such as those coding for SOD1, FUS RNA binding protein, TAR DNA binding protein, vesicle-associated membrane protein B, valosin-containing protein, optineurin, alsin, senataxin, spatascin, angiogenin, or ubiquilin-2 [24, 26]. Some of these gene mutations have also been found in SALS patients [28, 29].

The most common known genetic mutation for ALS is the recently described expanded GGGGCC hexanucleotide repeat in the non-coding region of the C9Orf72 gene, on chromosome 9p21 [30]. Another common mutation is localized in SOD1. SOD1 in its native state metabolizes O2−• to molecular misfolding [31]. Pathogenic mutations of SOD1 enzyme can be present in different regions of the enzyme, e.g., G93A (glycine 93 changed to alanine), H46R (histidine at codon 46 changed to arginine), or A4V (alanine at codon 4 changed to valine). Mutated SOD1 can form cytotoxic protein aggregates alone or with other proteins what possibly leads to loss of the enzymatic function or to acquiring the toxic properties [32, 33]. As SOD1 plays a crucial role in O2−• clearance, its functional loss can lead to increased levels of OS. Then, the remaining wild-type SOD1 may become itself a target of oxidative modification after which it dissociates from dimers to monomers and further forms aggregates with toxic properties of mutant forms of SOD1. That was shown in in vitro studies [34, 35]. Accumulation of abnormal SOD1 was also confirmed in the spinal cord [34] in animal studies [36, 37] as well as in ALS patients [38].

Clinical Studies

OS Biomarkers

Post-mortem studies on tissue samples from SALS and FALS patients support the hypothesis of oxidative damage of proteins, lipids, and DNA. For instance, HNE and 3-nitrotyrosine (3-NT) levels were increased in CSF in SALS patients [39, 40], while a rise in 8-hydroxy-2′-deoxyguanosine (8-OHdG) has been described in both SALS and FALS patients [41, 42]. However, no correlation between these markers and the severity or duration of the disease has been found [43].

Raised levels of thiobarbituric acid reactive substances (TBARS) and advanced oxidation protein products (AOPP) and decreased ferric-reducing ability of plasma (FRAP) were detected in the plasma or erythrocytes of SALS patients [44–46], but plasma protein carbonyl (PC) levels surprisingly did not differ between SALS patients and control subjects [16]. More conclusive results came from a study where urine from SALS patients contained a higher level of isoprostanoids (IsoPs) and 8-OHdG compared to a control group [16, 47], suggesting that IsoPs and 8-OHdG could be considered markers of OS in ALS. These studies included only 50 participants with SALS compared to 46 control subjects. Thus, these results should be confirmed in larger cohorts.

The presence of OS biomarkers in regions of the CNS that are critical for ALS suggests that they are implicated in motor neuron degeneration. This fact is supported by very recent positron emission tomography (PET) imaging data in humans, which confirmed that OS were enhanced in the motor cortex in ALS patients compared with controls. Moreover, the observed OS increase in the mild stage of the disease led to the conclusion that OS may be an important factor associated with the development of neurodegeneration in ALS patients [48].

Antioxidant Defense Biomarkers

Most studies concerning antioxidant defense biomarkers in ALS patients have shown changes in peripheral tissues or in CSF but rarely in the brain. For example, GSH levels were reduced in erythrocytes in ALS patients [45]. In contrast, an earlier study demonstrated a lower GSSG/GSH ratio with a concomitant rise in NO in the CSF of SALS patients [49]. According to the latter study, the lower GSSG/GSH level was caused by the decreased production of O2−•-oxidizing GSH because of the shift of oxidation to NO production or oxidation [49]. Very recent in vivo imaging studies have shown decreased GSH levels in the motor cortex of ALS patients by using the J-editing technique or 62copper-diacetyl-bis(N4-methylthiosemicarbazone (62CU-ATSM)) PET technique [25, 48].

The activity of SOD decreased in red blood cells and the CSF of FALS- and SALS-diagnosed patients [42, 50–52]. Interestingly, the reduction in the SOD1 protein concentration in erythrocytes of FALS patients correlated with SOD1 gene mutations [42]. However, SALS patients displayed enhanced activity of SOD1 in CSF [53], indicating that this different outcome may depend on either the ALS type, the disease duration, or the sampling time [54].

Apart from SOD, the activity of CAT, another antioxidant defense enzyme, was also found to be diminished in red blood cells in FALS [51] and SALS [51, 52] patients. Another study revealed that CAT activity decreased in erythrocytes with disease progression, which may suggest a link between this parameter and ALS duration [45].

Results regarding GPx or GR activity in ALS patients are controversial. GPx type 3 (also known as plasma GPx) and GR levels were lower in the serum or in red blood cells, respectively, in ALS patients [45, 55]. In contrast, another study showed enhanced GPx in the serum and CSF of ALS patients [56], while GR activity was elevated in the erythrocytes in both SALS and FALS patients [51, 52]. One study reported no change in GR activity in red blood cells in SALS patients [57].

In ALS patients, the plasma and/or CSF levels of other antioxidants (i.e., vitamin E, β-carotene, vitamin C, uric acid, and thiol group-containing molecules, such as ubiquinol-10) were either elevated [53] or not changed [44, 58, 59].

These divergent results could be explained by the heterogeneity of ALS [60]. In fact, ALS-diagnosed patients vary in their rate of disease progression and may differ in the number of years of survival. The median survival from onset to death in ALS varies from 20 to 48 months; however, many studies have reported a survival time of longer than 10 years in 10–20 % of patients [60]. Moreover, a study from Cova et al. [57] showed that the activity of GPx, GR, and CuZn SOD in erythrocytes was decreased in patients who had a faster disease progression rate and that SOD1 activity significantly decreased along the disease course in subjects with a more impaired functional status. All of these results support the hypothesis that ALS has many variants or mimic syndromes that differ in their pathogenic mechanisms and in their profile of enzymatic and non-enzymatic antioxidant responses [57].

Pharmacological Strategies to Reduce OS

Several pharmacotherapeutic agents with antioxidant properties have been attempted to slow ALS progression; however, most of them failed to do so (Table 2). Vitamin E, when combined with riluzole, diminished TBARS levels, enhanced GPx activity in the plasma, and prolonged the milder stages of the ALS Health State scale, but it did not affect survival and motor function [61].

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Another study investigated a very high dose of vitamin E as an add-on therapy to riluzole for ALS treatment; however, this treatment with vitamin E, at a dose of 5,000 mg/day for 18 months, failed to slow disease progression [62]. On the other hand, another study showed that intake of a combination of polyunsaturated fatty acids and vitamin E reduced the risk of developing ALS [63].

Edavarone (MCI-186) is another free radical scavenger that is already approved to treat cerebral infarction and to investigate ALS. It eliminates lipid peroxide and hydroxyl radicals by transferring an electron to the radical and thereby exerting a protective effect on neurons. In ALS patients, edavarone was shown to diminish nitrosative stress (NS) in CSF [64] and is now being tested in a phase III clinical trial in Japan for ALS treatment [65]. Coenzyme Q10 was administered for 9 months in a dose of 2,700 mg/day to ALS patients in a multicenter trial that unfortunately showed a lack of compound efficacy for ALS treatment [66]. This study also determined 8-OHdG levels in the plasma; however, according to the authors, the results for this measure will only be available later [66].

Other antioxidant medications, i.e., acetylcysteine, creatine, or selegiline, had no significant effect on survival or the rate of clinical progression of ALS [67–69]. In these studies, the influence on antioxidant defense biomarkers and oxidant damage was not evaluated. In another study, melatonin was used as a potential neuroprotective compound and, when normalized to control values, was found to elevate the level of PC in the serum of 31 SALS patients [70].

The novel antioxidant AEOL 10150, which is a small molecule that catalytically consumes ROS and RNS, is considered to be the most promising compound under evaluation in a clinical trial [71]. In a small, open-label study in ALS patients, AEOL 10150 was shown to be a safe and well-tolerated drug [71]. However, neither efficacy nor measurement of oxidative biomarkers in ALS patients who were on AEOL 10150 has been published.

The antioxidant medications used in ALS clinical trials have so far been unable to slow the progression of the disease. Moreover, a limited number of clinical studies have investigated oxidative damage or changes in the antioxidant defense status after antioxidant therapy.

Anti-ALS Drugs that Modulate the Oxidative Balance

No data.

Animal Studies

OS Biomarkers

The most popular animal models of ALS are based on SOD1 mutant transgenic mice (for example: SOD1 G93A, SOD1 H46R, SOD1 H46R/H48Q, SOD1 A4V, etc. (for more details, see [72])). Other ALS models include Wobbler mice and rodent models with genetic mutations in TAR DNA binding protein of 43 kDa (TDP-43), VAMP-associated protein B, dynactin or FUS/TLS, or C9Orf72 [73].

Changes in oxidative biomarkers have been detected in ALS models in rodents (Table 3). For example, free radical levels were elevated in the spinal cord of SOD1 G93A mice post-mortem [74, 75], and trapped radical adducts were also recently detected in the spinal cord of these mice in vivo [76]. In line with this latter observation, increased levels of PC in the spinal cord and in the motor cortex [77, 78], MDA and 4-HDA in the brain and CSF [79], and HNE, HNE-adducts, and 8-OHdG in the spinal cord [80, 81] have been observed in several ALS animal models (see Table 3).

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It has been established that enhanced nitration processes are also present in animal models of ALS. For example, 3-NT was found in the spinal cords of aged SOD1 G93A mice together with the presence of overnitrated proteins (actin or ATPase) in the spinal cord [82], in the motor and sensory cortices [78], and in the peripheral blood mononuclear cells [83] in transgenic mouse models of ALS and that these were observed even before the onset of the disease.

OS and NS are widely present in ALS, and in vitro studies suggest that this mechanism can facilitate the formation of protein aggregates [84]. In support of this conclusion, recent studies have revealed that a selective nNOS inhibitor increased survival in SOD1 transgenic mice [85].

Antioxidant Defense Biomarkers

In general, transgenic mouse models overexpressing mutant human SOD1 showed increased activity by the enzyme [32]. However, in the end stage of the disease, SOD1 activity in SOD1 G93A mice remained at the same level as wild-type SOD in non-transgenic mice [86]. What is interesting is that SOD1 knockout mice did not show an ALS-like phenotype [32].

Other antioxidant biomarkers, including GSH, GPx, and GR, are also changed during the course of ALS. The levels of GSH differed in mice carrying different SOD1 mutations. For example, in SOD1 G93A mutant mice, the GSH level decreased and the level of GSSG rose in the lumbar spinal cord [87], while in the same tissue in SOD1 mice with the H46R/H48Q mutations, the GSH level was not changed [88]. A recent study by Vargas et al. [88] showed that decreased GSH content accelerated neurological deficits in the SOD1 G93A mouse model. The mechanism of GSH reduction is linked to the nuclear transcription factor Nrf2 because its transfection into the SOD G93A mouse brain led to the up-regulation of GSH synthesis in astrocytes and reduced the most apparent neurological and biochemical symptoms of the disease [89].

In animal models of ALS, motor neurons have displayed overexpression of Prx2 and glutathione peroxidase-1 (GPx1). The number of neurons containing Prx2 and GPx1 decreased in the terminal stage of ALS [90], suggesting a breakdown of this redox system at the advanced stages of the disease. As discussed by Kato et al. [91], a possible reason for Prx2 and GPx1 breakdown might be related to the co-aggregation of these enzymes with mutant SOD1 and the exacerbation of mutant SOD1-mediated toxicity in neuronal Lewy body-like hyaline inclusions (LBHIs), which was shown in the spinal cords of transgenic rats [91]. Similarly, GPx3 protein levels in the serum of SOD1 H46R rats were increased in the pre-symptomatic stage and decreased gradually with disease progression [55]. However, another study did not reveal significance for the role of GPx in ALS [92], and further investigation is therefore necessary to clarify this problem.

Because enhanced SOD activity in ALS animal models remains enhanced in most of the disease stages and decreases only to the control level of non-transgenic mice in the end stage of the disease, this raises the question of whether these ALS animal models are suitable to study ALS antioxidant defense biomarkers because an ALS key enzyme, SOD, is decreased in ALS patients. These contradictory results, obtained in animals and humans, do not allow researchers to draw conclusions regarding the significance of these biomarkers in animal ALS models.

Pharmacotherapeutic Strategy to Reduce OS

Many substances possessing antioxidant properties have been proposed as ALS treatment strategies (Table 4). For example, coenzyme Q10 was shown recently to be unable to prolong survival when given after ALS onset [93]. As coenzyme Q10 is characterized by rather poor CNS availability (which possibly explains its small pharmacological effects), its reduced form, ubiquinol-10, has better bioavailability and antioxidant properties and was also investigated. However, similar to its parent drug, ubiquinol-10 did not prolong lifespan. Nevertheless, it was noted that poor CNS availability after oral dosing was observed in this study, which possibly explains the lack of pharmacological effects, similar to the case with its parent drug [93].

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Creatine was the next drug that extended survival, but not age of onset, in ALS animals [94–96]. It has neuroprotective properties and buffers against ATP depletion in mitochondria. Its dysfunction can lead to ATP decreases, which may contribute to cell death [97]. Because mitochondrial swelling and vacuolization are among the earliest pathological features in ALS mice with the SOD mutations [98], creatine could be useful for protecting mitochondria and for disease treatment in such a preclinical model. In most studies, creatine was delivered in the diet as a 1 or 2 % food supplementation. In addition to its effect of prolonging the lifespan in a mouse ALS model, creatine also improved motor performance [96] and provided protection from motor neuron loss at 120 days of age in these mice [98]. Moreover, creatine was shown to prevent the rise of 3-NT in the spinal cord and ROS production in the dialysate from microdialysis in ALS animals [98], and it also had a positive effect on weight retention [99]. However, one study found that creatine administration had no effect on the disturbed muscle function [100]. Moreover, co-administration of creatine with the cyclooxygenase-2 inhibitors rofecoxib and celecoxib or of creatine with minocycline (a tetracycline antibiotic with neuroprotective and anti-inflammatory effects) [101] may be even more beneficial for extending survival (even by 30 %) [94, 96].

Other antioxidants that extended survival in ALS mice include EUK-8 and EUK-134. In preclinical studies, these two synthetic SOD/CAT mimetics reduced the levels of OS, as measured by MDA, PC, and prolonged survival, but not disease onset, in ALS mice [102]. On the other hand, treatment with vitamin E significantly delayed ALS onset with no effect on survival but with a diminishing effect on 8-hydroxyguanine (8-OHG) levels in the spinal cord [103]. Drugs that shared both effects (ALS onset delay and lifespan extension) were melatonin, ammonium tetrathiomolybdate (a copper-chelating drug), and resveratrol (a substance that originates in plants and is found in highest amounts in red wine and the skin of red grapes) [86, 104–106]. However, in case of melatonin, the data were not clear as it was given in a dose range of 2.5–50 mg/kg intraperitoneal (i.p.) (in the same animal model) and also produced a surprisingly shortened survival, accelerated disease onset, enhanced lipid peroxidation in the spinal cord, and increased spinal motoneuron loss [107]. A possible reason for these results might be due, according to authors, to melatonin’s effect on upregulating the gene expression of human toxic SOD1, which presumably overrides any of the anti-oxidant properties of melatonin. Such a hypothesis needs to be tested in future studies.

Other substances used in preclinical ALS models, i.e., resveratrol, which, when given before disease onset, decreased MDA levels [106], and ammonium tetrathiomolybdate, which decreased spinal SOD activity [86]. The latter compound also ameliorated ALS-like symptoms in SOD1 G93A mice, probably by chelating the copper ions from the Cys111 site in the SOD-1 enzyme, which is important because various SOD-1 mutations affect Cu and Zn metal-binding, thereby promoting toxic protein aggregation [86]. Moreover, successful effects were achieved from treatment with ammonium tetrathiomolybdate when it was given after disease onset, which is satisfactory because this regime of administration closely reflects clinical practice.

Edaravone and AEOL 10150 are recently studied drugs for ALS that were administered at ALS onset. Although edaravone did not prolong survival in an ALS mouse model, it diminished SOD1 deposition in the anterior horn of the spinal cord and slowed disease progression and motor neuron degeneration [36]. Another substance that gave more promising results is AEOL 10150, which, when administered to ALS mice, decreased 3-NT and MDA levels in the spinal cord, extended animal survival [108], provided better preservation of motor neuron architecture, and diminished the level of astrogliosis [108].

In conclusion, according to animal studies, antioxidants may become putative ALS therapies because many of them extend the lifespan and diminish OS in ALS animals. However, it must be remembered that many of them, when tested in humans, have not yet shown benefits for survival time and motor function amelioration.

Anti-ALS Drugs that Modulate Oxidative Balance

Riluzole was shown to extend the lifespan in mice in the SOD1 G93A ALS animal model, but it did not change the disease onset [109] or have a satisfactory effect on the latter parameter [110]. No studies concerning oxidative defense or oxidative damage biomarkers were conducted; however, in vitro studies showed that riluzole had antioxidant properties in cultured cortical neurons [111].

Parkinson’s Disease (ICD-10 G20)

PD is a progressive degenerative disorder that is characterized by the loss of dopamine-producing neurons in the substantia nigra (SN) and by the presence of Lewy bodies in the SN and locus coeruleus. Clinical manifestations of PD include resting tremor, muscle rigidity, slowing of voluntary movements (bradykinesia), a tendency to fall (postural instability), and a mask-like facial expression [112]. The pathological hallmarks of PD, Lewy bodies, contain various proteins, including α-synuclein, ubiquitin, Parkin, and neurofilaments.

PD occurs in sporadic (non-inherited; 90–95 % cases) and familial (inherited; 5–10 % cases) forms. Mutations in the α-synuclein gene cause one of the familial forms of PD via autosomal dominant inheritance [113]. Recently, it was suggested that OS and imbalances between ROS/RNS and antioxidant defense mechanisms are linked to the etiology of PD.

Clinical Studies

Oxidative Biomarkers

Many studies have demonstrated the presence of OS and its markers in the brain and CSF in PD patients. Cholesterol lipid hydroperoxide and MDA were found to be up to 10-fold higher in SN in post-mortem brains of PD patients compared with other brain regions and age-matched controls [114]. In contrast, a recent paper demonstrated lower levels of MDA in the caudate nucleus and putamen and increased MDA levels in the frontal cortex in the post-mortem analyses of PD brains compared to healthy age-matched controls. Those results suggested that the non-SN regions, such as the caudate nucleus or the putamen, may have different compensatory mechanisms against OS could protect them from oxidative damage [115]. Moreover, HNE and acrolein-modified proteins were found in the neocortex and brainstem and in the SN, respectively, of PD patients [116–118]. According to in vitro studies, HNE modification of α-synuclein has been shown to trigger oligomerization and fibrillization of unmodified α-synuclein in the nervous system, which might lead to dopaminergic neuron injury. A recent observation suggests that HNE-modified proteins should be considered to be important players in PD pathophysiology [119].

Despite a number of studies supporting lipid peroxidation in the brains of PD patients, the levels of F2-isoprostanes were not elevated in the SN of PD patients [120], and the reason for this observed difference needs to be explained.

PCs were also found in PD patients’ brains compared to age-matched controls [121]. PCs are present not only in the brain regions specific for PD (the SN, caudate nucleus, and putamen) but also in other brain areas not directly linked with PD. Because most PD patients are treated with l-DOPA, this observation may suggest that l-DOPA, the “gold standard” for PD therapy, may contribute to carbonyl formation because it was shown to have pro-oxidant properties in vitro [122]. Interestingly, brain regions from individuals with putative presymptomatic PD (incidental Lewy body disease) showed no PC rise. This information suggests that in PD, oxidative protein damage occurs late during disease progression and/or that l-DOPA treatment contributes to carbonyl formation [121]. Oxidative damage to proteins in PD also occurred through nitration, and 3-NT was found to be increased within Lewy bodies in the SN pars compacta (SNpc) of PD patients [123].

Another pathology found in PD brains is DNA and RNA damage [124, 125]. The factors 8-OHG and 8-OHdG were elevated in various parts of the PD brain compared to controls; however, the most striking rise was detected in the SN [124, 125]. Similarly, increased levels of 8-OHG and 8-OHdG were observed in CSF [126, 127]. However, these studies came to opposite conclusions with respect for the correlation between 8-OHG levels and disease duration.

In the CSF of living PD patients, enhanced levels of HNE and MDA have been shown as well [128–130], but different results were obtained by Shukla et al. [131]. Moreover, markers of oxidative damage in PD patients were also detected in the serum and urine [132–135], but their use as indicators of the course of the disease is far from being useful for clinical practice because the existing data are contradictory [136–138]. As has been suggested [136–138], these differences may be due to the variability in methods used to measure OS markers.

The results of many studies have demonstrated the presence of OS in the brain, CSF, serum, and urine of PD patients; however, none of the OS markers has been established as a specific biomarker for PD disease or as a marker for PD disease progression.

Antioxidant Defense Biomarkers

PD is characterized by a selective loss of GSH in the SN (40 % compared to control subjects) but not in other parts of the brain [139]. This decrease is one of the earliest biochemical changes that has been observed in the disease [140–143], and it results in a selective drop in mitochondrial complex I activity, another hallmark of PD [144]. On the other hand, a substantial rise in SOD levels has been observed in the SN and basal ganglia in PD patients [145], while no change in activities of CAT, GPx, and GR was found compared to age-matched controls [145]. Another study showed some deficiency in GPx in the SN in Parkinsonian patients [146], but the weak (ca. 19 %) reduction in such a small number of patients (n = 11) cannot be considered to be conclusive. Another small pilot study in PD patients (n = 8) indicated a peripheral (in blood) increase in GSH/GSSG [147] when the patients went off of PD medications (dopamine receptor agonists) for 12 h in comparison to GSH/GSSG levels when they were on medications. This suggests that PD medications may play a disadvantageous role that leads to enhanced peripheral oxidative stress; however, the small sample size excludes a final conclusion [147].

Pharmacological Strategies to Reduce OS

Because there is an overwhelming amount of evidence showing that OS and NS in PD patients leads to an increase in pathological damage in the SN, many approaches have been attempted to reduce ROS/RNS production. One of the possible strategies was to supplement GSH. As shown by Sechi et al. [148], in nine patients in the early stage of the disease [148], GSH (600 mg twice daily) administered intravenously for 30 days reduced (by 42 %) the clinical disability of PD patients, and this effect lasted for 2–4 months. Furthermore, a recent study of N-acetylcysteine (150 mg/kg), which is a GSH precursor, revealed an elevation in brain GSH levels and the blood GSH/GSSG ratio after 1-h of intravenous (i.v.) infusion [149]. Unfortunately, no results concerning the clinical status of PD patients have been described. However, N-acetylcysteine, in a smaller dose (70 mg/kg p.o., every 12 h over 2 days), produced negligible changes in GSH levels in the CSF and no immediate improvement to symptoms (according to the Unified Parkinson’s Disease Rating Scale and the Montreal Cognitive Assessment) [150].

Magnetic resonance imaging (MRI) studies showed a rise in iron concentrations in the SN in PD patients [151]. Because iron can lead to ROS production in PD patients, an iron-binding compound, deferiprone, has been tested in a pilot study in PD patients (FAIRPARK trial, registered as ClinicalTrials.gov NCT00943748). Patients in early-stage PD who were on a stabilized dopamine regimen received deferiprone (30 mg/kg/day) for 12 months (early-start paradigm, n = 19), while the other group received the drug for only 6 months, with the latter, shorter therapy starting 6 months later than the early-start paradigm (delayed-start paradigm, n = 18) [152]. The earlier therapy start diminished SN iron deposits to a greater extent than the delayed-start paradigm and improved motor performance vs. placebo and vs. the delayed-start paradigm, according to the Unified Parkinson’s Disease Rating Scale [152]. Moreover, in deferiprone-treated patients, GPx and SOD activity in the CSF increased, which supports the connection between the chelator treatment and the antioxidant response.

Vitamin E (α-tocopherol) was also suggested as a way to diminish the OS and to reduce clinical symptoms in PD. However, the clinical trial The Deprenyl and Tocopherol Antioxidant Therapy of Parkinsonism study (DATATOP study) revealed no evidence of any beneficial effect for α-tocopherol (2,000 IU/day) in either slowing functional declines or ameliorating the clinical features of Parkinson’s disease. It is of note that no analysis of OS biomarkers was performed in that trial [153, 154]. Since DATATOP, no clinical trials using vitamin E as a potential PD medication have been conducted. In fact, vitamin E was only used in PD clinical trials as a supplement for coenzyme Q10 or as a placebo [155] or a control [156].

Another potent antioxidant, coenzyme Q10 (1200 mg a day), in the first reported multicenter, randomized, placebo-controlled, and double-blind trial slowed functional declines compared to placebo [157]. Lower doses or different formulations of coenzyme Q10 displayed no symptomatic effects on midstage PD [158]. Recent clinical trial did not show a benefit for coenzyme Q10 (1,200 or 2,400 mg/day) in 600 patients in early-stage PD [155].

An early clinical study on creatine monohydrate (10 g/day for 12 months) in 67 subjects who were within 5 years of a PD diagnosis showed some positive results for treating behavioral difficulties [159], and an additional 18-month follow-up study confirmed this finding [160]. On the other hand, a smaller (n = 31 creatine PD group, n = 17 placebo PD group), but longer, 2-year clinical trial demonstrated that creatine had no effect on PD scores or dopamine transporter imaging [161]. In September 2013, the NINDS discontinued the NET-PD LS-1 study (phase III clinical trial with a total of 1,720 planned participants, ClinicalTrials.gov identifier: NCT00449865) that started in 2007 because the results obtained from a study of creatine used for the treatment of early stage PD did not demonstrate a statistically significant difference between the active substance and placebo [162].

In conclusion, although evidence for the link between OS and damage in PD is overwhelming, suggesting the potential efficacy of antioxidant drugs, most clinical trials have so far failed to support this statement.

Anti-Parkinsonian Strategies to Restore Oxidative Balance

Administration of zonisamide, an anticonvulsant drug prescribed to treat resting tremor in PD, inhibited the rise of 8-OHdG levels in the urine of PD patients. As the 8-OHdG rise correlates with disease progression and aging, it can be presumed that zonisamide could be helpful in defending against OS-evoked DNA modifications in PD patients. Other drugs used for treatment of PD (i.e., l-DOPA, monoamine oxidase B (MAO-B) inhibitors, catechol-O-methyltransferase (COMT) inhibitors, and the dopamine receptor agonists ropinirole and pramipexole) have not shown such properties [163].

Interesting findings were reported in a study that measured GSH levels in venous blood in PD subjects who were on- and off-medication while performing acute physical exercises, because we know that this type of physical activity leads to GSH depletion and GSSG rise [164]. Surprisingly, the off-medication patients had a lower drop in GSH level than the on-medication group. This finding suggests that patients in the off-medication state handled acute stress better than those in the on-medication state, indicating that medication may impede the ability to tolerate acute OS [165]. Similar conclusions were obtained in a very recent study by Nikolova et al. [166], who observed a greater rise in PC and 8-OHdG levels in the blood of PD patients who were treated with l-DOPA in comparison to untreated PD patients, demonstrating that administration of l-DOPA may cause greater OS than PD itself [166].

Animal Studies

Oxidative Biomarkers

The most popular animal models of PD include pharmacological (6-hydroxydopamine (6-OHDA), 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), rotenone, and paraquat) as well as several genetic (with mutations in the α-synuclein, PINK1, Parkin, or LRRK2 genes) models [167].

The 6-OHDA model (Table 5), wherein the toxin is injected directly into the SNpc, medial forebrain bundle, or striatum, was the first animal model of PD associated with dopaminergic neuronal death within the SNpc [168].

Full size table

Another PD model utilizes MPTP, a highly lipophilic molecule that rapidly crosses the blood–brain barrier, leading to an irreversible and selective loss of dopaminergic neurons in the SN in non-human primates [169, 170] and in rodents [162, 171], although the latter species was less sensitive to MPTP than primates [172]. Other chemical models are based on an insecticide, rotenone, or paraquat, an herbicide. Rotenone, when given i.v. in a low dose to rats, produces selective degeneration of SN dopaminergic neurons that is accompanied by α synuclein-positive LB-like inclusions [173]. Paraquat is used less widely than MPTP, rotenone, or 6-OHDA models and is used instead as an addition to other toxic agents, such as the fungicide maneb [174]. It was reported to cause selective degeneration of nigrostriatal dopaminergic neurons in mice [175]. The mechanism of action of MPTP (a precursor form of the reactive metabolite MPP+), rotenone, or paraquat is based on the inhibition of mitochondrial complex I, which leads to ROS production [167, 174, 175].

As has been demonstrated in numerous studies, OS is widely present in all of these toxin-based models (see Table 5). 6-OHDA, when injected into the striatum, increased MDA, HNE, PC, and 3-NT levels in this structure and increased TBARS in SN [176–179]. Similarly, in the MPTP and in the rotenone models, elevated levels of lipid peroxidation products [180–185] and oxidatively modified proteins [185, 186] were observed in various parts of the brain (striatum, cortex, SN, hippocampus, cerebellum, and midbrain). In addition to lipid damage, increased 3-NT levels were also detected following the use of MPTP in the SN, striatum, and ventral midbrain [181, 187]. MPTP or rotenone-treated animals also showed oxidatively modified RNA or DNA in the SN or striatum [185, 188, 189]. In the paraquat and maneb PD models, enhanced lipid peroxidation in the nigrostriatal areas of animal brains was also shown [190] (Table 5). A very recent report from Kumar et al. [175] demonstrated for the first time that α-synuclein radical is formed in the midbrain in paraquat- and maneb-treated mice, indicating that radical formation is mediated by peroxynitrite and depends on both NADPH oxidase and iNOS. This interesting result regarding α-synuclein radical formation was obtained by using the immuno-spin trapping method in combination with immunoprecipitation [175]. Moreover, it was noted that protein radicals such as α-synuclein radical may trigger protein aggregation, which plays a causal role in dopaminergic neuronal death [175].

For review of genetic models and OS, see the excellent paper [167].

All toxin-based models share common characteristics, including the ability to produce ROS and further oxidative damage, which causes death in dopaminergic neurons and reflects part of the pathology observed in PD. Although all of those models have drawbacks, they are useful for testing neuroprotective therapies.

Antioxidant Defense Biomarkers

A characteristic shared feature observed in all toxin-based models is a drop in GSH level in key PD structures [177, 183–187, 191–196] (Table 5). Importantly, lower GSH levels make nigrostriatal neurons more susceptible to oxidative damage and further degeneration.

Studies using 6-OHDA also showed a reduction in activity by SOD, CAT, and glutathione S-transferase (GST) in striatum and SN [177, 178, 191]. On the other hand, results from the MPTP model are inconclusive regarding SOD and CAT activity. Moreover, some of the MPTP studies showed increased SOD activity in the SN [192] and striatum [183], while others reported diminished SOD activity in these regions [180, 197]. These differences may have resulted from the use of different doses of the toxin, varied routes of drug administration (intracranial versus i.p. or s.c.), and different use of rodent species in the studies (see Table 5).

Similar to SOD activity, CAT activity cannot be considered a biomarker of OS in rodent PD models as its activity was both diminished [182, 191, 193, 194, 196, 197] and enhanced [184]. Moreover, GPx activity was diminished in striatum in an MPTP model [197], while GST activity was found to be elevated in a maneb and paraquat PD animal model [190] (Table 5).

All of these reports on the enhanced activities of SOD, CAT, and GST suggest the presence of mechanisms in brain areas that defend against exposure to PD toxin models. On the other hand, diminished activities or levels of antioxidant enzymes may indicate that these defense mechanisms were overcome and that the degeneration process had begun.

Pharmacotherapeutic Strategy to Reduce OS

Several agents, such as valproic acid [178] and melatonin [198], effectively reversed changes in antioxidant defense biomarkers and oxidative damage in the 6-OHDA rat model of PD (Table 6).

Full size table

There are also data in the literature showing that other agents and drugs have antioxidant activity (i.e., ceftriaxone [182] and N-acetylcysteine [199], which decreased oxidative damage and/or enhanced antioxidant defense biomarkers in the striatum, cortex or SN in rodent MPTP models).

Ibuprofen (a non-steroidal anti-inflammatory drug [193]), acetyl-l-carnitine (a natural compound reported to prevent mitochondrial injury deriving from oxidative damage in vivo), α-lipoic acid (given alone or in combination with acetyl-l-carnitine [185]), and centrophenoxine (a potent nootropic agent that acts as an antioxidant) [184] were demonstrated to enhance GSH levels and CAT and SOD activity and to decrease lipid peroxidation in investigated brain regions in a rat rotenone model (Table 6).

Prevention of oxidative damage and the presence of antioxidant defense biomarkers have been documented following treatment with natural compounds, such as lycopene [195], aqueous extract of tomato seeds (TSE) [186], and melatonin [190].

Many different agents may improve antioxidant brain status in different PD models. However, it should be noted that most of these agents were given before or concomitantly with rotenone, MPTP, or other PD-causing toxins. To definitively answer whether these agents can also show efficacy in reducing the consequences of exposure to prior administration of PD-inducing toxins, further studies are required. This is especially true because the latter type of drug administration would be a better model for evaluating any pharmacological strategy for reducing OS in PD patients.

Anti-Parkinsonian Drugs that Modulate Oxidative Balance

Most anti-parkinsonian drugs may improve brain antioxidant status in PD preclinical tests (Table 7). Ropinirole, a second-generation, non-ergoline dopamine receptor agonist with D2-like receptor selectivity and a chemical structure similar to that of dopamine was found to enhance GSH levels and CAT [182] activity and to diminish nitrate levels [182] in the striatum in MPTP-lesioned animals.

Full size table

Other anti-parkinsonian drugs, such as selegiline (a selective irreversible MAO-B inhibitor) [196], deferoxamine [177], and pramipexole (a non-ergoline dopamine agonist) [200], increased GSH levels in the striatum, SN, or cortex. Deferoxamine also decreased a protein oxidative damage biomarker [177] and enhanced SOD activity in the striatum, while selegiline reduced superoxide anion generation (SAG) and increased CAT activity in midbrain regions and the cortex [196]. Interestingly, l-DOPA, the most commonly used drug in PD treatment, did not restore the reduced GSH levels in the SN in the MPTP mouse model [200].

The above studies suggest that antiparkinsonian drugs, with the exception of l-DOPA, display some antioxidant properties, which may be considered as part of their mode of action and efficacy in PD treatment.

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AD is the most common neurodegenerative disease and is characterized by memory loss, dysfunctions in cognitive abilities (e.g., executive function, attention, language, and visuospatial skills), confusion, aggression, and mood swings [113, 201

Источник: https://link.springer.com/article/10.1007/s12035-015-9337-5

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  • Connect Yoosee cameras to Wi-Fi and access it from your smartphone, tablet or laptop. Feel reassured by watching your baby or sick loved one in the other room. or maybe you want to keep tabs on your pet’s well-being when you’re not there? Well, with Yoosee, you can restore your peace of mind to know that your baby, family or businesses are all ok in your absence.

  • The monitoring capabilities of the Yoosee will greatly improve the lives of you and your loved ones. Mothers who tend to check on their sleeping children at night will be able to do so conveniently from their phones instead of having to physically walk into their children’s bedrooms, which runs the risk of disturbing their children’s sleep.

  • Yoosee’s two-way audio function, you will be able to communicate with people on the camera’s side. You can watch,hear and talk back to the camera makes you feel like you're right there with them. Yoosee is also smart, as it can detect motion and sound. With this detection feature, Yoosee camera will automatically capture any suspicious motions or sounds and send an alert to you.

Additional Features

Advanced features enable it can be deployed in professional applications.

Privacy Protection

Press "Privacy" key on remote control can stop video streaming to protect the privacy.

Alarm Monitoring

Support up to 64 wireless security detectors, the real deterrent to burglars.

CMSClient

Free video management software (Windows OS), managing multiple cameras simultaneously.

ONVIF Compliant

Compliant with ONVIF standard, can be integrated with third-party NVR/VMS, and other systems.

Yoosee Smart 1080p/720p WiFi Cameras

Demo Video

Watch the Yoosee demo video here!

Yoosee Products

WiFi cameras and WiFi NVR kits, WiFi video door-phone

720p WiFi Pan/Tilt Yoosee Camera

D1800

2MP Mini PTZ Bullet IR Camera

Pan/Tilt Rotation, 4x Optical Zoom, 2.4G Wi-Fi, up to 64G microSD Card Slot, ONVIF/RTSP
Discover More

Full HD 1080p Yoosee Camera

D1000G

Full HD 1080p Cube Camera

Built-in a PIR motion sensor, FHD 1080p resolution, up to 32GB TF card storage.
Discover More

Outdoor Smart WiFi Camera Yoosee

D1400

Outdoor 1080p WiFi Bullet Camera

IP67 weatherproof, 1080p HD video, 128GB TF card video storage, 30 meters IR range
Discover More

1.3MP 960P 360° VR Camera

D1101VR

360°1.3MP Panoramic VR Camera

New Fisheye lens panoramic camera,WiFi and Ethernet connection, 64G TF card video storage.
Discover More

720p HD WiFi Pan/Tilt Camera Yoosee

D1001

1080P WiFi Pan/Tilt Camera

Remote pan/tilt, thermometer sensor adapter, up to 64 wireless security detectors.
Discover More

Yoosee Smart Wi-Fi Doorbell

SD-M2

Smart Wi-Fi Doorbell

Yoosee Smart Wi-Fi Video Doorbell 1080p HD PIR Motion Detection
Discover More

Yoosee's News

Yoosee releases regular updates giving you access to the latest features and improving the user experience.

Yoosee iOS App has upgraded to 2.2 version (00.46.02.02)

We have optimized the things as below:

  • Optimized add device procedures;
  • Optimized manually add connected device function;
  • Optimized the account login, register, forgot password UI;
  • Changed the appearance of photo album;
  • Optimized the display of device info;
  • Added the reminding in playback list page if there is no SD card;
  • Changed the device list UI;

Yoosee App will support HD panoramic/VR cameras

Yoosee App can not only work with smart WiFi NVR kits and 433MHz/868MHz security sensors, soon it can support the latest panoramic/VR cameras. Panoramic cameras can provide you 360 degree surround view by using panoramic algorithm, tapping on motion objects can achieve fast auto-track. Gravity sensor function, can automatically rotate the image right and left according to your smartphone’s position.

Yoosee can support hotspot WiFi cameras

Yoosee released AP network cameras, the AP network cameras can connect to Smartphone without Internet access. Users are able to config the WiFi setting directly on Smartphone's WiFI hot-spot, the camera's hot-spot default password is 12345678.

Grain Media firmware upgraded to 14.00.00.57

The new firmware fixed some bugs and added some new functions. 1. Fix wrong reset reminding sound. 2. Add network connection through sound. 3. Support FTP function. 4. Support SC1145 CMOS image sensor. 5. Updating SC2035, to optimize the image quality. 6. Remind users if users want to format the SD card, but camera is still recording. 7. Fixed email picture wrong time&date problem. 8. Changed the list reading & writing method, minimize the frequency of reading/writing. 9. Increased the video recording redundant space to prevent Disk fragmentation problem. 10. Fixed SC2035 horizontal stripes problem.

Yoosee camera's firmware version upgraded to 13.0.0.96

Optimized and fixed some bugs: 1. After network disconnection, the recording end time can precisely show the power cut/restore time. 2. Add Fahrenheit degree support. 3. Fixed 163 mailbox can't send Email. 4. Add watchdog timer (requiring hardware to support). 5. Fixed binded user push notification bug 6. Fixed the bug, the camera will lose WiFi connection, when plug in/out Ethernet cable. 7. Add snapshot folder path and alarm mute function. 8. Optimized TF card video recording and storage.

Yoosee now supports WiFi NVRs

Yoosee NVRs leveraging the Broadcom WiFi module, NVR's WiFi coverage can reach up to 300 meters outdoor, indoor coverage also reaches up to 400㎡, the WiFi cameras can connect to the NVR by using Yoosee G1 protocol. Smart Qos algorithm to adjust bitrate and frame rate to provide smooth video streaming experience under different bandwidth condition. One key Wi-Fi pairing, no wired cable, plug-and-play, built-in Gview P2P connection engine, easy to connect.

4K H.265 smart doorbell for office/home

Yoosee SD-M5 is the best selling smart doorbell employs 2-megapixel CMOS image sensor and high-performance SoC can achieve 1080p/FHD video resolution. The product still adopts the mature H.264 video compression technology, which has been widely supported by almost all smartphone and computers. In addition to 1080p and H.264, the product supports both Wi-Fi and Ethernet (RJ45) wired network connection, it supports wide range voltage input (AC 8-24V, DC 9-36V), so can provide great flexibility to different applications.

2K/4MP Smart Video Doorbell that works w AC24V transformer Google Home/Alexa Echo

Introducing you the latest smart video doorbell that supports 2K resolution and works with both DC and AC power supply. The product enables you to upgrade your conventional doorbell system easily by wiring it to the existing 24V AC transformer. Morever, it adopts an ultra wide lens to provide nearly 166 degree field of view that helps to have a super wide viewing angle. Comparing other smart video doorbell, the product comes with an angle mount bracket that enables it to be mounted on the wall without compromising the field of view. Lastly, it works with Tuyasmart/Smart Life app that works with your Google Home Hub and Alexa Echo Show 2.

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Discussion

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Copyright 2010~2021 Yoosee All Rights Reserved.

Источник: https://www.yooseecamera.com/

Adobe flash player pro

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Flash Player Pro 6.0 Download TechSpot


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8 hours agoFlash Player Pro is a handy flash tool kit designed as Adobe Flash player and manager. It has several powerful flash tools download flash movies, preview and …

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9 hours agoAdobe Flash Player is the standard for delivering high-impact, rich Web content. Designs, animation, and application user interfaces are deployed immediately across all browsers and platforms, attracting and engaging users with a rich Web experience. The table …

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2 hours ago However, until that happens, you will still need to either download or enable Adobe Flash Player when you visit a site, watch a video, or play a game that uses Flash. Chrome Users: Adobe Flash is built-in to your browser. Click here for instructions on how to enable it. Microsoft Edge Users: Adobe Flash is built-in to your browser.

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6 hours agoAdobe Flash Player is a freeware flasher player software download filed under media players and made available by Adobe for Windows. The review for Adobe Flash Player has not been completed yet, but it was tested by an editor here on a PC and a list of features has been compiled; see below. Macromedia flash is an internet media player.

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2 hours agoAdobe Flash Player for when you need it. 1/2. Adobe Flash Player is software used to view multimedia content on computers or other supported devices first released in 1996. Users looking for an application to play audio and video would download Flash Player

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9 hours ago Add new flash file: - navigate to the webpage with some flashes files - click to icon of extension Flash Player + - select on top menu "Add flash from actual page" - click to blue icon "add" - if you want can change flash name Play saves flashes: - click to icon of Flash Player + - select on top menu "My Flash Playlist" - click to blue icon

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6 hours ago Download free trials and updates for Adobe products including Creative Cloud, Photoshop, InDesign, Illustrator, Acrobat Pro DC, and many more. Adobe Premiere Pro. Adobe Flash Player. Adobe AIR. 7-day free trial of Creative Cloud. 7-day free trial of Creative Cloud.

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5 hours agoAdobe Flash Player pro prohlížeč Internet Explorer (IE) nebo Edge. Možná se Vám už stalo že některé stránky se nechtěly zobrazit nebo v nich něco chybělo, obvykle jde i o online hry, stačí tak nainstalovat tento balíček Flash player(u) pro Váš prohlížeč.

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5 hours agoAdobe flash player free download for windows 7 64 bit - Note: On December 31st 2020, Adobe Systems will officially stop updating and distributing Adobe Flash: Adobe Flash Player Support is Coming to An End. Adobe does not recommend that you download Flash Player, and they recommend that you Uninstall Adobe

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Just Now Play Flash anytime, even in 2021 and beyond, using an emulator. Want to fix "This plug-in isn't supported" and "Adobe Flash Player is blocked" messages? This extension will remove those messages and allow you to play Flash in any website with a single click. It's easy to use: Click once and that's it! The extension does all the work for you.

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1 hours agoAdobe Animate (formerly Flash Professional) is an application for developing rich content, user interfaces, and web applications. Adobe Flash Player is a multiplatform client runtime. Web users must download and install Flash Player to view and interact with SWF content.

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7 hours agoAdobe has ended support for Flash Player at the end of 2020 and encourages content creators to migrate any existing Flash content to new open formats, such as HTML5, WebGL, and WebAssembly. For more information, see Flash Player end-of-life. Check out Adobe's detailed announcement: Flash and the Future of Interactive Content.

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6 hours agoFlash Player Pro is a handy flash tool kit designed as Adobe flash player and manager. It has several powerful flash tools: download flash movies, preview and browse flash movie, capture flash image and set it as wallpaper, create flash screensaver with ease, make conversion between SWF and EXE flash movies etc.

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7 hours ago The most common and most popular alternative to Adobe Flash Player is HTML5. Is Adobe Flash Professional free? macromedia flash 8 isn ‘t (legally) free. legal license holders can download it free. Animate CC (formerly Flash Pro) is only available by subscription to …

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5 hours ago In Site permissions, select Adobe Flash. Set the toggle on for the Ask before running Flash option. The Block and Allow lists will be available after you visit a site that uses Flash. The next time you visit a site the uses Flash, the browser will ask for your permission before allowing Flash to run. Note: This topic is for the new Microsoft Edge .

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3 hours agoAdobe Flash Player Pro Software Adobe Flash Player for Android v.11.0.1.152 Adobe® Flash® Player is a cross-platform browser-based application runtime that delivers uncompromised viewing of expressive applications, content, and videos across screens and browsers.

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1 hours agoAdobe Flash Player EOL General Information Page. Since Adobe no longer supports Flash Player after December 31, 2020 and blocked Flash content from running in Flash Player beginning January 12, 2021, Adobe strongly recommends all users immediately uninstall …

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5 hours ago Our website provides a free download of Adobe Flash Player 32.0.0.465 for Mac. The Adobe Flash Player installer is commonly called install_flash_player_osx.dmg. The bundle identifier for Adobe Flash Player for Mac is com.adobe.flashplayer.installmanager. Our antivirus scan shows that this Mac download is virus free.

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1 hours agoAdobe Flash will be going away soon, but for now, you can easily install and enable Adobe Flash Player on a Mac computer using a Safari browser. MacBook Pro (From $1,299 at Apple)

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6 hours agoAdobe enterprise product learning, documentation, communities and support are now in one place, Experience League.

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Please leave your comments here:

Frequently Asked Questions

How does one install adobe flash player?

Steps Go to Adobe.com. Using the browser you want to install Adobe Flash Player into, go to http://get.adobe.com/flashplayer/. Click the yellow "Download now" button. Save the file when prompted. Open the installer. Locate the "AdobeFlashPlayerInstaller_" file on your drive, and double-click to open it. Run the installer.

Do i have to install adobe flash player?

To install Adobe Flash Player, visit Adobe's website, check your computer to see whether Flash Player is installed, and if it isn't, click the download button. If you have issues with the installation process, check your web browser to make sure Flash is enabled.

How do you add adobe flash player?

Navigate to Adobe's website Open your web browser and go to adobe.com. At the top of the page, click on the Search icon. Type "Adobe Flash Player" into the box, and select the application from the list. Under the Help heading, click on the Help & Support link.

What is adobe flash player and what does it do?

Adobe Flash is a deprecated multimedia software platform used for production of animations, rich Internet applications, desktop applications, mobile applications, mobile games and embedded web browser video players. Flash displays text, vector graphics and raster graphics to provide animations, video games and applications.

Источник: https://convertf.com/adobe-flash-player-pro/

Diagnostic Software

Integated Diagnostic Software (IDS) - The factory Ford Motor Company vehicle diagnostic software provides complete dealership level vehicle diagnostic coverage for all 1996 to present Ford, Lincoln and Mercury vehicles. IDS is a flexible diagnostic tool that utilizes standard computing platforms to work with Ford's VCM, VCM II, VCMM and VMM devices. The IDS software license includes time based access to the IDS software, software udpates and calibration files.

Ford J2534 Diagnostic Software (FJDS) - The factory Ford Motor Company vehicle diagnostic tool designed for use with J2534 compatible Vehicle Communications Interfaces (VCI). FJDS software provides module reprogramming software (FMP) that covers 1996 to present Ford, Lincoln and Mercury module reprogramming functions, plus complete dealership level diagnostic software for all 2018 to present Ford and Lincoln vehicles. FJDS is a flexible diagnostic tool that utilizes standard computing platforms to work with Ford's VCM II or J2534 compatible devices. The FJDS software license includes time based access to the FJDS software, software updates and calibration files.

Ford Diagnostic & Repair System (FDRS) - The next generation factory Ford Motor Company vehicle diagnostic Software designed for use with VCM II, VCMM and J2534 compatible Vehicle Communications Interfaces (VCI). FDRS provides complete dealership level vehicle diagnostic coverage for some 2018 and forward vehicles. FDRS provides superior capabilities, is more user-friendly and provides more diagnostic tools than IDS. The cloud-based system ensures the technician is provided the latest software every time FDRS logs into the Ford network.


Diagnostic Software Licensing

A software license is required to use IDS/FDRS software with a VCM, VCM II, or VCMM or FJDS/FDRS software with a VCM II or J2534 compatible device.

Purchase: Upon purchase of a Software License, a user will receive a 20-digit licensing activation code (key). The user can activate the key using the “Activate a License” feature in the software. Activating a key binds the key to the PC on which it is entered in. Users can release this tie to the PC or transfer the licensing key to another PC using the “Return a License” feature. Since the Software License binds to the PC and not the diagnostic hardware, a single Software License will on one PC at a time. Each PC running the software will require it’s own license or the transfer of a license, since each license binds to the PC.

Regular Validation: IDS and FJDS must communicate with the License Server on a regular basis to validate the license. A validation automatically occurs at each start-up when IDS is connected to the internet. When not connected to the internet a validation cannot occur. Therefore, any PC needs to be connected to the internet at least every 29 days. Failure to validate every 30 days will cause the license to become invalid and functionality will be disabled within the software.

Renewal: Software Licenses expire based on the term purchased. Users can renew licenses up to 30 days prior to the expiration date by returning to their account and providing payment for the renewal. Renewal terms are based on the subscription length originally purchased. If a change in license term is desired a new license should be purchased.

PATS Ford Dealer Login Account Ford IDS FDRS Activation of latest version

Remote Activation for Ford IDS of latest version

Install Latest Version of Teamviewer

This is not a virtual machine solution and runs natively on your laptop and more stable than virtual machine options for programming modules

Leave login info in notes at order payment time

We can remotely login and Activate Latest Ford IDS on your pc and keep you up to date with current Versions.

No Physical product is shipped here

We Supply the Activation of the software Remotely via Teamviewer login info you supply at order time

Why use the old software when you can be using the latest version Online

-----------------------------------------------------------------------------------------------------------------------------------------------------

Option 1

Latest version Official Ford IDS  FJDS  Licence for 1 PC

12 Month Licence

Cannot be used on multiple computers

if your pc fails you will lose licence and best to install only on SSD Hard disks and good laptops

Ford IDS licence is a twelve month licence paid upfront allowing access to Ford diagnostic network. This give the ability to update software, add keys, adaptation like EGR or injector when parts are replaced. This will not allow full security related re-programming without a product key/token for the specific models from Ford which has to purchased separately when required.

Latest Version Remote Install + Activate for DTC Clearing up to 2020

 Key / Module Programming up to 2020 But need Buy Remote Login from us each time when need  to Do security Programming for each car from FORD

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Option    2 

Includes option 3 Plus Special Dealer Login that Support Lost Spare Keys to 2020 

Latest version Official Ford IDS  FJDS  Licence for 1 PC

12 Month Licence

Cannot be used on multiple computers

Ford IDS licence is a twelve month licence paid upfront allowing access to Ford diagnostic network. This give the ability to update software, add keys, adaptation like EGR or injector when parts are replaced. This will  Allow security related re-programming without a product key/token for the specific models from Ford which has to purchased separately when required.

Latest Version Remote Install + Activate for DTC Clearing up to 2020

 Key / Module Programming up to 2020 and can use Dealer Login to Do security Programming Online PATS

Ford_IDS_FDRS_ONE_TIME_Online_access_Programming__Configuration_via_Teamviewer

Источник: https://www.jlridssddmongoose.com/

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