text:
Molecular Epidemiology and Evolution of European Bat Lyssavirus 2
LHCSR Expression under HSP70/RBCS2 Promoter as a Strategy to Increase Productivity in Microalgae
Metabolic Epilepsies—Commemorative Issue in Honor of Professor Uwe Heinemann
IJMS
Daci, A.
Bozalija, A.
Jashari, F.
Krasniqi, S.
Open AccessReview
Individualizing Treatment Approaches for Epileptic Patients with Glucose Transporter Type1 (GLUT-1) Deficiency
Armond Daci
1,2,
Adnan Bozalija
Fisnik Jashari
Shaip Krasniqi
2,*
Department of Pharmacy, Faculty of Medicine, University of Prishtina, Prishtina 10000, Kosovo
Institute of Pharmacology and Toxicology, Faculty of Medicine, University of Prishtina, Prishtina 10000, Kosovo
Department of Neurology, University Clinical Center of Kosovo, Prishtina 10000, Kosovo
Int. J. Mol. Sci. 2018, 19(1), 122; https://doi.org/10.3390/ijms19010122
Received: 8 December 2017 / Revised: 27 December 2017 / Accepted: 30 December 2017 / Published: 5 January 2018
(This article belongs to the Special Issue Commemorative Issue in Honor of Professor Uwe Heinemann: Metabolic Epilepsies)
Browse Figure
Monogenic and polygenic mutations are important contributors in patients suffering from epilepsy, including metabolic epilepsies which are inborn errors of metabolism with a good respond to specific dietetic treatments. Heterozygous variation in solute carrier family 2, facilitated glucose transporter member 1 (SLC2A1) and mutations of the GLUT1/SLC2A2 gene results in the failure of glucose transport, which is related with a glucose type-1 transporter (GLUT1) deficiency syndrome (GLUT1DS). GLUT1 deficiency syndrome is a treatable disorder of glucose transport into the brain caused by a variety of mutations in the SLC2A1 gene which are the cause of different neurological disorders also with different types of epilepsy and related clinical phenotypes. Since patients continue to experience seizures due to a pharmacoresistance, an early clinical diagnosis associated with specific genetic testing in SLC2A1 pathogenic variants in clinical phenotypes could predict pure drug response and might improve safety and efficacy of treatment with the initiation of an alternative energy source including ketogenic or analog diets in such patients providing individualized strategy approaches.
glucose transporter type-1 deficiency; SLC2A1; epilepsy; pharmacogenomic; diet
Epilepsy is a disease that cannot be described by only a single condition, but rather represents a family of diverse disorders having in common an abnormally increased predisposition to seizures, which occur due to abnormal, excessive, or synchronous brain neuronal activity [1]. It affects 65 million people worldwide and it is most common chronic and serious neurological disease [2]. Although different epileptic syndrome pathophysiologies can be identified, their appearance shares common characteristics such as increased and persistent neuron excitability and synchronicity, as well as misbalance between inhibitory and excitatory neurons in the brain [3].
Moreover, genetic background contributes in 40% of patients suffering from epilepsy; this includes monogenic and polygenic mutations. Based on this background, genetic basis is the second approach to be detected further with promising indications [4]. Despite molecular mechanisms of actions not being completely understood, there are a number of classes of therapeutics that are currently used in epilepsy [5].
Metabolic epilepsies are inborn errors of metabolism which respond to specific treatments based on a diet or supplementation alone or in combination with conventional treatment [6].
The ketogenic diet (KD) is a high-fat, low protein, and low-carbohydrate diet (4 g of fat to every 1 g of carbohydrate and protein combined (4:1 ratio) and classic (3:1 ratio). It reduces consumption of glucose from the brain and provides ketone bodies as alternative sources, which have a mechanism of action through GABA synthesis and reception, resulting in a neuroprotective effect and antiepileptogenesis.
The KD is used in drug-resistant epilepsy, young epileptic patients and infants, epilepsy syndromes, absence seizures, rett syndrome, tuberous sclerosis, refractory and secondary generalized epilepsy. Moreover, the other diet type including the modified atkins diet (MAD) contains unlimited proteins and provides carbohydrates amounts in lower amounts for children (10 g/day) compared to adults (15 g/day) with a 1:1 fat-to-nonfat ratio and is less restrictive alternative compared to the classic KD in terms of discipline and maintaining the compliance. However, using the MAD in the GLUT1 DS patients were shown to have comparable efficacy with KD with a lower ketosis, improved taste, easier daily management, and better selection of dietary foods [7,8,9]. Differences exist also in the indications of this diet corresponding to clinical phenotypes and age groups as follows: the classic ketogenic diet 4:1 carbohydrate is indicated in severe phenotypes in infants; the classic ketogenic diet 3:1 carbohydrate is indicated more in mild phenotypes in infants, both phenotypes in pre-school age, school age, adolescent, adults; and MAD is indicated in mild phenotypes in school age, adolescents, and adults [9,10].
Recently, there have been significant improvements in genetic testing, including gene variations that could predict drug response and also improve safety and efficacy of antiepileptic drugs. There are different genes that have been identified can affect drug response by influencing pharmacokinetics—such as transporters and its systems, metabolism, and elimination—drug targets which are involved in the brain excitability. This also provides molecules and enzyme expressions in the pathogenesis of adverse reactions [11].
Since patients continue to experience seizures due to pharmacoresistance [12], there are different efforts and few examples when pharmacogenomic testing can be recommended in clinical practice, which provides better drug response or may predict the effective dose. However, currently, there is no identified biomarker with broadly applicable importance.
Recently, there is a tendency to focus on the personalization of therapy in the development of more applicable biomarkers and also an application of treatments or drugs which therapeutically could reverse molecular defects in epilepsy causes from genetic defects. It has also been shown that some antiepileptic treatments exacerbate seizures. Because of this, selection of appropriate antiepileptic therapy plays an important role in the personalization of therapy in responding to epilepsy genetic defects [13,14].
2. Glut1 Deficiency Syndrome Treatment Individualizing Approaches
Individualized treatment is based on the individual variability of genes by identification of underlying genetic etiology. Several strategies that could achieve this, including detection of causative genetic alterations, determination of functional alterations of the physiological system that are caused by the genetic mutation with an impact on reversing or inhibiting that functional alteration, and improvement of epilepsy treatment by targeting the biological mechanisms responsible for epilepsy in each individual [15].
Heterozygous variation in solute carrier family 2, facilitated glucose transporter member 1 (SLC2A1) and mutations of the GLUT1/SLC2A2 gene results in the failure of glucose transport, which is related with a glucose type-1 transporter (GLUT1) deficiency syndrome (GLUT1DS); this affects the transport of glucose across the blood–brain barrier and its availability in the brain [16,17]. This mutation is a result of haploinsufficiency of the SLC2A gene and a reduced expression of its translated products, including GLUT1 [18]. The affected patients display low glucose levels in the cerebrospinal fluid (CSF) and hypoglycorrhachia [19]. This is more common in young age and is manifested with infantile seizures that are resistant to conventional antiepileptic drugs, non-convulsive status epilepticus predominantly in fasting state, myoclonic-astatic epilepsy, paroxysmal exercise-induced dyskinesia, severe psychomotor retardation, dystonic features, ataxia, developmental delay, acquired microcephaly, hypotonia, spasticity and movement disorder, and also wide phenotypic pleiotropy, including intellectual disability, movement disorder, and drug-resistant epilepsy. There are rare conditions in generalized genetic epilepsies in the mutations of SLC2A1 which are found in early-onset absence seizures (EOAE) before the age of four and rarely classical juvenile absence epilepsy [20,21,22].
This can manifest with a variety of phenotypes including early-onset epileptic encephalopathy and early childhood-onset refractory absence epilepsy [23].
Although the generalized forms of epilepsy were not related to SLC2A1 mutations in some studies, there are reports that SLC2A1 mutations in combination with associated movement disorders, motor, and/or speech difficulties may be reflected in generalized epilepsy [24,25]. Similarly, in an additional study, a 2.1% SCL2A1 mutation had generalized epilepsy and movement disorders, abnormal movements, and family history of seizures [26].
Despite the tendency to include detection of other transporters with polymerase chain reaction and Sanger sequencing, GLUT1 remains the only metabolism transporter associated with generalized epilepsy. However, certain types of pathogenic variants may exist in these genes, which could not be detected with Sanger sequencing [27].
When this metabolic error is corrected, the brain functions may be almost completely restored, which is makes it essential to diagnose early and start with the ketogenic diet as soon as possible [28].
Epilepsy-related with GLUT-1 deficiency is associated with a poor response to a standard antiepileptic medication therapy [15]. In the therapeutically difficult patients with SLC2A1 mutations, the benefit from the ketogenic diet should also be considered in genetic generalized epilepsies.
In early infantile epileptic encephalopathies (EIEE) and severe epilepsies of infancy, SLCA1 mutations are rare and the identifications for these patients for specific therapy including ketogenic diet is an important strategy to be implemented [20]. The milder forms of epilepsy due to GLUT1 deficiency may respond to standard antiepileptic drugs even though there are currently no approved medicines for Glut1 DS; however, when unresponsive to medications or seizures that are typically refractory to medical treatments, the general gold standard treatment of these patients includes the ketogenic diet, which contributes to treating the symptoms of neuroglycopenia through bypasses in the defective glucose transport and alternative energy supply to the brain. Based on this, an early intervention is crucial for seizure control [14,29].
Concerns have been raised as the ketogenic diet induces an increase in cholesterol levels, increases the risk of metabolic syndrome, transiently increases lipids in children, and increases cardiovascular risk factors in adults. Direct replenishment of energy substrates feeding into the TCA-cycle represents an alternative mechanism to decrease seizure activity. The rationale of treating patients with GLUT1-DS is that triheptanoin (anaplerotic substrate) with its metabolized products including heptanoate and C4 and C5 carbon compound ketone bodies easily cross the blood–brain barrier via monocarboxylate transporters and may enhance the effect of the regular ketones as an alternative fuel for the brain. Due to this, there are positive preclinical studies performed in epilepsy-related GLUT1-DS [30] with ongoing clinical trials [31]. A recent clinical report has shown that triheptanoin resulted in a 90% clinically improvement in GLUT-DS patients with nonepileptic paroxysmal manifestations previously objected to or intolerant in KD [32]. Similarly, another open-label study conducted in GLUT1-DS patients showed a reduction in spike waves on electroencephalogram after 90 min of treatment with triheptanoin [33]. Taking this into consideration, anaplerosis allows better carbohydrate intake and glucose levels relative to KD without exacerbation of the deficiency of glucose transport into the brain which further indicates promising therapeutic strategy in the future, even though there are larger controlled studies required to better establish a therapeutic approach in patients who object to KD or cannot comply with its constrictions [34,35].
However, the more flexible diets, including modified Atkins diet and carbonic anhydrase inhibitors such as acetazolamide or zonisamide can be effective in milder cases by reducing the seizure control, improvement of movement disorders, and dyskinesia [36,37]. These alternative energy sources are depicted in Figure 1.
Careful consideration must be given for adjunctive treatment in children on the ketogenic diet and adjunctive antiepileptic drugs—including phenobarbital, valproic acid (through inhibiting Glut1 transport), valproic acid (inhibition of beta-oxidation of fatty acids), acetazolamide, topiramate, and zonisamide (inhibition of carbonic anhydrase which potentiate metabolic acidosis and kidney stones)—and patients affected with Glut1-DS are advised to avoid barbiturates (especially in children with infantile-onset-seizures), caffeine, and valproic acid due to unpredicted clinical consequences of its use [38,39,40]. Lately, the gene therapy in mouse models produced exogenous GLUT1 in neural cells and also improved CSF glucose levels suggesting that this will be an effective human therapy in the future [41]. However, the summarizing of all the possible treatment options for GLUT1 deficiency syndrome related to epilepsy is shown in Table 1.
3. Genetic Testing in Glut1-DS
Diagnosis may go undetected if comprehensive laboratory investigations are not undertaken, including urine and CSF analysis, MR spectroscopy or detection of inborn errors of metabolism in the early onset refractory epilepsies with unclear etiology, especially with epilepsy phenotype including the seizures for suggestive of Glut-1 deficiency syndrome which also requires additional metabolic studies to provide a diagnosis rapidly that can impact the management [19].
Genetic testing has a pre-test probability of 1% for idiopathic generalized epilepsy (IGE) and 10% for early-onset absence epilepsy [15,20]. Glut1 defects are more common in IGE, featuring absence epilepsies with onset from early childhood to adult life [42].
Despite the clinical diagnosis, the genetic testing approaches in the SLC2A1 gene mutations are detected in 70–80% of patients with GLUT1DS and should be reserved for those patients with borderline clinical and investigational findings prior to initiation of diet [14].
In a study performed in Japanese patients with hypoglycorrhachia and typical clinical symptoms of Glut1-DS, there were 33% patients without mutations in exons and exon–intron boundaries of the SLC2A1 gene detected by direct sequencing, which potentially could be underdiagnosed in the promoter sequences and/or sequences deep with introns [43].
If the patients are negative in these mutations and there is still strong clinical suspicion present, they should also be treated with diet.
The GLUT-1 deficiency challenge also has a possible genetic diagnosis in epilepsy due to the pleiotropic manifestations of mutated genes. Based on these new sequencing technologies, exome sequencing may identify other genes responsible for the glucose transport across the blood–brain barrier, which may help to overcome this difficulty and suggest novel drug targets [14,28,44].
The molecular genetic testing used in Glut1-DS include sequence analysis were reported in two studies to be 89% and 81% from total probands in the SCL2A1 pathogenic variant. Moreover, in (multi)exon or whole-gene deletions this varies with 11% and 14% and to increase this percentage the variety of methods that may be used are quantitative PCR, long-range PCR, multiplex ligation-dependent probe amplification (MLPA), and chromosomal microarray (CMA) that includes this gene/chromosome segment.
When the patients do not have a pathogenic variant in the tested gene through sequence analysis, the gene may be either at another locus which cannot be detected or covered by the laboratory's test including the sequence analysis [38].
There are alternative genetic testing strategies, including the multi-gene panel in case of failure with single-gene molecular genetic testing of SLC2A1 through the sequence and deletion/duplication analysis. Due to this, there was a recently reported study in childhood-onset epilepsy (COE) in which the detection rate is relatively small (2.8%) in patients who were clinically suspected to have GLUT1 DS.
To further enhance the genetic testing potential, the multi genes panel analysis is a promising approach [45]. However, exome sequencing, genome sequencing, and mitochondrial sequencing may also be considered.
Recently, developments in pharmacogenomic and precision medicine approaches are promising in the management of GLUT-1 deficiency [15,17]. A new era of precision medicine will continue to establish larger gene discovery consortia with progression to a whole genome sequencing, which will lead to improvements in patients with unexplained epilepsy in the clinic.
The availability of gene-specific patients to monitor the effects of drugs will be important in influencing therapy decisions and prognosis of the disease [23]. Moreover, it will enable and improve the outcomes in terms of predictions and genetic counseling for family planning and enhance the detection of therapeutic and unwanted effects [28].
4. Common Pathogenic Variants in GLUT-1 Deficiency
There are common selected pathogenic variants of SLC2A1 which are responsible for GLUT1 DS. The complete list of pathogenic variants responsible for the GLUT1 DS and respective clinical phenotypes was shown in Table 2 and Figure 1.
The absence of the pathogenic mutation in the SLC2A1 gene does not exclude the diagnosis of the GLUT-1 deficiency. There are case reports that described this phenomenon with sporadic mutation detected by Sanger sequencing with reporting of the novel heterozygous variant c.538T>A, p.Met180Lys in the exon 5 of SLC2A1 gene associated with epilepsy expression, paroxysmal dyskinesias provoked by infection, emotional stress, and fasting which were responding well to the ketogenic diet [46,47].
The SLC2A1 pathogenic mutation of the gene in heterozygosity (c.823G>A, p.Ala275Thr), detection should be suspected for the individualizing the KD treatment in absence seizures mainly in the early childhood associated with irregular ictal EEG discharges, mild mental retardation, migraine, microcephaly, drug resistance, and worsening during fasting [48].
Moreover, the SLC2A1 gene mutations studied in children have shown the presence of de novo and heritable paternal origin mutations including the point mutations c.388g>a, p.Gly132Ser, c.634T>T, p.Arg212Cys, and amino acid insertion c.(688-11G>A), Ser_Val227insValProPro [48].
Recently, a new identification method using whole-exome sequencing was developed, which included detection of rare homozygous missense variants (c.526C>T (p.Arg176Trp) and c.629C>T (p.Ala210Val)) in SLC45A1, encoding another cerebral glucose transporter which indicates that recessive mutation in SLC45A1 (second cerebral glucose transporter in addition to GLUT1) which cause intellectual disability and epilepsy. There was a lack of other clinical features associated with GLUT-1 and also hypoglycorrhachia was not documented in individuals tested in this cohort.
Regarding the potential treatment target, there is some promising indication for ketogenic diet in individuals with SLC45A1 mutations, however, further investigation is needed [49].
Attempts in continuing the identification of the new pathogenic variant spectrum in GLUT1DS are recently documented with a new variant the gene of SLC2A1, including c.734A>C, which could serve as a potential variant in the exploring the individualizing approaches in such patients [50].
GLUT1 deficiency syndrome is a treatable disorder of glucose transport into the brain caused by a variety of mutations in the SLC2A1 gene which are the cause of different neurological disorders including different types of epilepsy. Since the patients continue to experience seizures due to a pharmacoresistance, an early clinical diagnosis associated with specific genetic testing including SLC2A1 defect could predict drug response and improve safety and efficacy of treatment in the different clinical phenotypes.
Taking this into consideration, new pathogenic variants analyses, clinical phenotype investigations, and evidence are still developing in the improvement of this corresponding genetic detection, new therapeutic approaches which will influence the treatment, decisions, and prognosis of the disease.
The initiation of an alternative energy source with the introduction of a ketogenic diet in patients with GLUT1-DS is an important and promising individualizing strategy to prevent unnecessary anticonvulsant therapy trials, which are usually ineffective.
Even though the ketogenic diet is still continuing to be used efficiently, there is growing research interest in the development of a new diet which will further improve the quality of life in the patients.
We would like to thank Driton Vllasaliu (King's College, London) as a native English speaker for English language editing of our manuscript.
Armond Daci and Shaip Krasniqi conceived and designed the study; Armond Daci, Fisnik Jashari and Adnan Bozalija analyzed the additional analytical and clinical literature data; Armond Daci and Shaip Krasniqi wrote the paper.
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Becker, F.; Schubert, J.; Weckhuysen, S.; Suls, A.; Grüninger, S.; Korn-Merker, E.; Hofmann-Peters, A.; Sperner, J.; Cross, H.; Hallmann, K.; et al. Do Glut1 (glucose transporter type 1) defects exist in epilepsy patients responding to a ketogenic diet? Epilepsy Res. 2015, 114, 47–51. [Google Scholar] [CrossRef] [PubMed]
Ragona, F.; Matricardi, S.; Castellotti, B.; Patrini, M.; Freri, E.; Binelli, S.; Granata, T. Refractory absence epilepsy and Glut1 deficiency syndrome: A new case report and literature review. Neuropediatrics 2014, 45, 328–332. [Google Scholar] [CrossRef] [PubMed]
Srour, M.; Shimokawa, N.; Hamdan, F.F.; Nassif, C.; Poulin, C.; Al Gazali, L.; Rosenfeld, J.A.; Koibuchi, N.; Rouleau, G.A.; Al Shamsi, A.; et al. Dysfunction of the Cerebral Glucose Transporter SLC45A1 in Individuals with Intellectual Disability and Epilepsy. Am. J. Hum. Genet. 2017, 100, 824–830. [Google Scholar] [CrossRef] [PubMed]
Çolak, R.; Alkan, Ö.S.; Yangın, E.E.; Kağnıcı, M.; Çalkavur, Ş. A Different SLC2A1 Gene Mutation in Glut 1 Deficiency Syndrome: C.734A>C. Balkan Med. J. 2017, 34, 580–583. [Google Scholar] [CrossRef] [PubMed]
Figure 1. Disorder of glucose transport (GLUT1-DS) across the blood–brain barrier and its availability in the brain (astrocytes and neurons respectively) caused by the variety of mutations in the SLC2A1, genetic testing of pathogenic variants, and therapeutic approaches with alternative energy sources.
Table 1. Current treatment options and precautions for GLUT1 deficiency related to epilepsy.
Diet Treatment
Drug Combinations to Avoid with KD
Drugs to Avoid Due to GLUT1 Impairment
Ketogenic (gold standard) Acetazolamide Valproate Phenobarbital, Valproate
Modified Atkins Topiramate Zonisamide Tyrosine kinase inhibitors
Medium chain Triglycerides Zonisamide Acetazolamide Caffeine, Ethanol
Low glycemic index treatment Phenytoin Topiramate Diazepam, Narcotics
Triheptanoin (under investigation) Carbamazepine - Tricyclic antidepressants
(under investigation) - - General anaesthetics,
- - - Guanosine triphosphate analogues
Table 2. SLC2A1 pathogenic variants and phenotypes for GLUT1 deficiency syndrome 1.
DNA Nucleotide Change
Predicted Protein Change
dbSNP
c.49G>T p.Gly17Ter - NA
c.1089delG p.Trp363Terfs rs587784391 A
c.1296C>A p.Tyr432Ter rs75485205 A
c.1366A>T p.Lys456Ter rs80359829 A
c.19_28delAAGCTGACGG p.Lys7Valfs rs587784393 A
c.272G>A p.Gly91Asp rs80359814 A
c.376C>T p.Arg126Cys rs80359818 A,C
c.377G>A p.Arg126His rs80359816 A,C
c.574_57delAT p.lle192Hisfs rs878853161 A
c.724C>T p.Gln242Ter rs794729221 A
c.748C>T p.Gln250Ter rs587784396 NA
c.823G>A p.Ala275Thr rs121909740 A,B,C
c.907dupG p.val303Glyfs rs7960655334 A,B
c.940G>A p.Gly314Ser rs121909739 A,B
c.966_967delCG p.Ser324Alafs rs886044287 NA
c.980_981delTG p.Val327Glyfs rs80359838 A,B
c.997C>T p.Arg333Trp rs80359825 A,C
c.1198C>T p.Arg400Cys rs796053263 NA
c.1402C>T p.Arg468Trp rs267607059 A,B
c.377G>T p.Arg126Leu rs80359816 A,B
c.766_767delAAinsGT p.Lys256Val rs80359822 A
c.971C>T p.Ser324Leu rs796053253 B,C
c.988C>T p.Arg330Ter rs80359826 A,B,C
c.277C>T p.Arg93Trp rs267607061 C
c.458G>A p.Arg153His rs149585781 C
c.464C>T p.Ala155Val rs35313240 B
c.667C>T p.Arg223Trp rs757188030 B,C
c.844C>T p.Gln282 rs1057521066 A
c.884C>T p.Thr295Met rs80359823 A,C
c.998G>A p.Arg333Gln rs111033808 B
c.1372C>T p.Arg458Trp rs13306758 A,B
c.400G>A p.Gly134Ser rs1057518953 A,C
c.100A>G p.Asn34Asp rs587784390 A
Phenotypes: A = early-onset classical phenotype; B = late-onset classical; C = non-classical phenotype; NA = data not available.
Daci, A.; Bozalija, A.; Jashari, F.; Krasniqi, S. Individualizing Treatment Approaches for Epileptic Patients with Glucose Transporter Type1 (GLUT-1) Deficiency. Int. J. Mol. Sci. 2018, 19, 122. https://doi.org/10.3390/ijms19010122
Daci A, Bozalija A, Jashari F, Krasniqi S. Individualizing Treatment Approaches for Epileptic Patients with Glucose Transporter Type1 (GLUT-1) Deficiency. International Journal of Molecular Sciences. 2018; 19(1):122. https://doi.org/10.3390/ijms19010122
Daci, Armond, Adnan Bozalija, Fisnik Jashari, and Shaip Krasniqi. 2018. "Individualizing Treatment Approaches for Epileptic Patients with Glucose Transporter Type1 (GLUT-1) Deficiency" International Journal of Molecular Sciences 19, no. 1: 122. https://doi.org/10.3390/ijms19010122
Int. J. Mol. Sci., EISSN 1422-0067, Published by MDPI


Our 2018 Prospect National Conference was held from 3-6 June 2018 at the International Convention Centre (ICC), Birmingham.
The Education and Children's Services Group put forward two motions highlighting the challenges that our members face and the impact of education policy at this year's Prospect conference in Birmingham.
The European Commission's attempts to limit air traffic controllers' right to strike should be condemned in the strongest possible terms, delegates agreed.
There's no doubt that the energy sector is in the midst of a radical transition.
Later today, Prospect's biennial national conference will be debating a range of motions related to social and public policy.


BA Transmissions Ltd is a family run business with nearly three decades of experience in diagnosing, repairing and reconditioning automatic transmissions. Based in Keighley, West Yorkshire, we aim to provide our customers with a quick diagnosis of their transmission problems, as well as a plan of action to repair it.
As well as private customers, we also provide automatic transmission repair/rebuild services for a number of garages, with some transmissions being shipped overseas to be reconditioned by BA Transmissions Ltd.
If our reputation isn't enough, all of our work comes with a warranty, allowing our customers to drive away with the peace of mind that, in the unlikely event that f something does go wrong, we will take care of it. We will never begin work on a vehicle or transmission without first consulting our customer and providing as accurate an estimate as is possible, so you can be sure that there'll be no nasty surprises when you get your invoice.
Quality is key for BA Transmissions Ltd. We guarantee our work so it's in our best interests to make sure it's done well.


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We Host WebZ
DomainKeys Identified Mail
What lies behind the abbreviation DKIM? How can this feature help your e-mail marketing campaigns?
DomainKeys Identified Mail (DKIM) is an authentication system used to confirm that an e-mail message has been sent by an authorized server or person. A digital signature is added to the message's header by using a private key. When the email is received, a public key that's available in the global Domain Name System is used to validate who actually sent it and whether its content has been modified in any way. The primary task of DKIM is to obstruct the widely spread scam and spam email messages, as it makes it impossible to forge an email address. If an email message is sent from an address claiming to belong to your bank or financial institution, for instance, but the signature doesn't correspond, you will either not get the email message at all, or you will receive it with a warning alert that most probably it is not a genuine one. It depends on email providers what exactly will happen with an email message that fails the signature check. DomainKeys Identified Mail will also provide you with an added security layer when you communicate with your business allies, for example, since they can see for themselves that all the e-mail messages that you send are legitimate and have not been manipulated in the meantime.
DomainKeys Identified Mail in Website Hosting
When you buy any of the Linux website hosting packages that we're offering, the DomainKeys Identified Mail feature will be enabled by default for any domain name that you add to your hosting account, so you won't have to create any records or to activate anything manually. When a domain is added in the Hosted Domains section of our custom Hepsia Control Panel using our NS and MX resource records (so that the emails related to this domain name will be handled by our cloud hosting platform), a private encryption key will be created straight away on our mail servers and a TXT resource record with a public key will be sent to the DNS system. All addresses set up with this domain name will be protected by DomainKeys Identified Mail, so if you send out emails such as periodic newsletters, they will reach their target destination and the receivers will be sure that they are genuine, because the DomainKeys Identified Mail functionality makes it impossible for unauthorized persons to spoof your e-mail addresses.
DomainKeys Identified Mail in Semi-dedicated Hosting
The DomainKeys Identified Mail option comes by default with any domain that's registered through a semi-dedicated server account with our company. The domain must also use our name servers, so that its DNS resource records are managed by our system. The latter makes it possible for a special TXT record to be set up, which is in fact the public key that verifies if a certain email message is legitimate or not. Such a record is set up once a new domain is registered in a semi-dedicated server account through the Hepsia Control Panel and at the same time, a private key is created on our mail servers. If you make use of our web and email hosting services, your messages will always reach their target destination and you will not need to worry about unsolicited persons spoofing your addresses for scamming or spamming purposes, which is something rather important when you use emails to get in touch with your business collaborators.
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redpajama_set_name: RedPajamaCommonCrawl


text:
Q: Why are all my Unreal Engine uasset files missing after using git lfs migrate import --include="*.uasset" I was trying to add large file support for my Unreal Engine project. After adding LFS support I then found the following command to make sure that all the large files where added throughout my version history.
git lfs migrate import --include="*.uasset"
After running this command I know notice that NON of my blueprints or assets inside the content browser are showing up. If I browse to the file system all the .uasset files are there.
I'm not sure how to get the .uassets to show up in Unreal Editor again.

A: I had the same problem.
It seems after the command:
    git lfs migrate import

You need to run:
    git lfs checkout

Original answer:
Broken git repo after git lfs migrate

redpajama_set_name: RedPajamaStackExchange


Today, the Lagos Islands Academy celebrates one of our awesome teachers, Michael Savage. We love you. Happy birthday!
Fun in the Lagos Islands Academy!
Meet the LION! Drama is fun! it's 'Dress up' and ACT-ion!
Children love drama. Enroll today!
It was great this last week as Mr. Duncan Rice visited the Lagos Islands Academy and Lagos principals and teachers. He attended classes at one of ours schools (Children International School- CIS).
It was beautiful to watch him teach. Our teachers were not left out on the fun and experience, as he took them on training sessions that was a journey of greatness. Indeed , Everyone is a STAR at the Helen O Grady drama Academy Lagos Islands, teachers and students.
Classes off to a GREAT start!
Classes are up and running at different centers. Children are excited and so are the teachers. This is one of our teachers, Emmanuel with our students at Children International school(CIS). Truly excellent at what he does.
The term starts in two weeks and indeed our teachers are very excited about this term. December production will be off the hook! We trust that our kids will have the time of their live this term.


Although he is a gifted psychic medium, Matt Fraser believes his job isn't just to reconnect friends and family with their loved ones who have passed. Each month Matt spends countless hours volunteering, hosting events and fundraisers to help give back to non-profit organizations. He strongly believes that it is his mission to help make the world a better place, in any way that he can.
In just the past year alone, Matt has helped numerous non-profit organizations and charities raise funds through his interactive and uplifting "Medium with a Message" events. It is his way of paying it forward and helping to support those organizations that have such a strong positive influence in helping the community. A few of the organizations that Matt has helped in the recent months through his live events include Westport Vietnam Veterans, Dana Farber via Pan America Mass Challenge, "Out of the Darkness" Suicide Prevention, Alzheimer's Finding a Cure, Pawtucket Fireworks Fundraiser, and Forever Paws Animal Shelter.
As well as extending a helping hand to charities in need, Matt holds a seat on the board of directors of Forever Paws Animal Shelter (above) and The National Cultural Diversity Council (NCDAC). Two non-profit organizations in New England that Matt holds close to heart.
For more information on hosting an event, or to have Matt as a guest speaker please fill out the form below.
mission is to increase awareness of the need for communication, understanding and respect among people of ethnically and racially diverse backgrounds. Through community events, workplace cultural diversity training, youth cultural diversity workshops, and alliances with corporations, educational institutions, government agencies and non-profit organizations, NCDAC addresses the important issues of multiculturalism facing our nation today.
Your organization is an important part of our community and Matt wants to lend a hand in helping! In a continuing effort to support worthy neighborhood causes, Matt Fraser would love to hear about how he can help you to raise funds for your organization. Matt's "Medium with a Message" LIVE Event is a inspirational, uplifting, and interactive way for you to raise money for schools, sports teams, non-profit organizations, and large clubs or specialty organizations. For more information on hosting an event, or to have Matt as a guest speaker please fill out the form below.


Yep, as any FOX host or talk radio jock will tell you, the real problem holding back America's economy is lazy welfare moochers.
Seriously though, as Ruth Marcus points out below, "Of 4.1 million in the ranks of the long-term unemployed, only 1.3 million are still receiving the unemployment checks that Paul asserts are holding them back."
The year's not over, but it's not too early to declare the hands-down winner of this year's Scrooge award: Sen. Rand Paul.
The Kentucky Republican wants to cut off people's unemployment benefits — not to save taxpayers' money from being frittered away by loafers unwilling to haul themselves out of their comfy hammocks to look for work. No, Sen. Scrooge wants to cut them out of solicitude for the long-term unemployed.
Because, as the kindly doctor explained (correctly) on "Fox News Sunday," it is clear that the longer people are unemployed the more difficulty they have finding work. Ergo, says Paul, the obvious solution: Limit the length of unemployment benefits — even if no jobs are available.
Paul is wrong, by the way, about the 99 weeks — the longest combined state and federal benefits can now last is 73 weeks, and then only in three states where unemployment has hovered above 9 percent. Elsewhere, depending on the severity of unemployment, the maximum duration is between 40 and 63 weeks.
Yes, I know about moral hazard. In a well-functioning economy, overly generous unemployment benefits may dissuade people from taking new jobs. But this is not a well-functioning economy. Even with unemployment at a five-year low, nearly four of 10 jobless workers count as long-term unemployed, out of work for 27 weeks or longer. In October, there were nearly three people unemployed for every available job.
One relevant data point: When President Bush signed an extension of unemployment benefits in June 2008, the unemployment rate was 5.6 percent, the long-term unemployment rate was 1 percent and the average duration of unemployment was 17.1 weeks. Today those numbers are 7 percent unemployment, 2.6 percent long-term unemployedand 37.2 weeks in duration.
Another point: This could easily be you. According to a new report by the White House Council of Economic Advisers, 40 percent of the long-term unemployed had a household income, prior to job loss, between $30,000 and $75,000. One in five has a bachelor's degree or higher. The more education you have, the less likely you are to fall into unemployment. But once you're unemployed, your education offers no shield against joining the ranks of the long-term unemployed.
And about those overly generous benefits. They average $300 a week. Would that be enough to keep you on the unemployment rolls? Ironically, long-term benefits help keep people in the job market — looking for work is a condition of receiving help — rather than simply giving up. Cutting them off would likely cause the unemployment rate to fall, but only because they would be out of the workforce.
Another indication that correlation is not causality: Most of those in the ranks of the long-term unemployed have exhausted their benefits. Of 4.1 million in the ranks of the long-term unemployed, only 1.3 million are still receiving the unemployment checks that Paul asserts are holding them back.
Republicans cite two recent studies as proof that, as the House Ways and Means Committee put it, emergency benefits are "the cause of the painfully slow labor market recovery." But the bulk of academic research suggests that extended benefits only slightly increase the length of time people are out of work, mostly because of flexibility to find a suitable job rather than grasping at the first offered.
If Paul and fellow Republicans had their way, 1.3 million jobless would be cut off by year's end, another 1.9 million in the first half of 2014. Two words suffice in response: Bah! Humbug!
Is it good the Saudis are mad at Obama?


The Kennedy Center of Louisiana acts as host to volunteer community-based mentoring initiatives in Shreveport/Bossier.
Our goals are to educate and empower the children of the Caddo Parish by placing them with mentors that offer support.
Mentors build structured & trusting relationships by offering guidance, support, encouragement, and academic assistance.
Our mentors help young people develop into confident, competent, and contributing members of society.
All stayed in school, and their average attendance improved.
Grade point averages were almost half a unit higher.
Seniors were almost three times more likely to go to college.
More trusting of parents or guardians and less likely to lie to them.
The Kennedy Center of Louisiana is a community based non-profit organization founded in 2004 by Ms. Tonya Williams. Ms. Williams, a Licensed Professional Counselor, and Licensed Marriage and family Therapist has worked diligently to remove barriers and increase the quality of life for youth and adults with the most need for many years. It is her desire and the mission of The Kennedy Center of Louisiana to EMPOWER individuals to reach their full potential by supporting, teaching and linking them to resources in the community. It is our belief that all individuals are capable of SUCCESS and deserve the same quality of life regardless of their socioeconomic background and life circumstances.
In 2008, The Kennedy Center partnered with Queensborough Elementary School and Caddo Parish Schools to establish a school-based mentoring program entitled We All Winn Mentoring to combat the academic failure, poverty, delinquency, and illiteracy that is so prominent in the community. The Kennedy Center was awarded a grant by the Office of Safe and Drug Free Schools to implement this school based mentoring initiative that matches non-related adult mentors with children (grades 4th – 5th) with the greatest needs to promote positive development and social responsibility, as well as improved academic achievement.
As a result of the success of the elementary school mentoring program the Kennedy Center of Louisiana has taken steps to launch several programs with the mentoring component for juveniles and adults.
This organization is constantly seeking volunteers to serve as mentors, advisory committee members, assist with events, such as fundraisers or recreational outing with our program participants. Please continue to browse the website and contact us if any additional information is needed.
** The We all Winn Mentoring program is named in honor of Terrance Winn, a teenager tragically killed by gunfire at the age of 16.
The mission of the We All Winn Mentoring Program is to empower at-risk youth in our community to make positive life choices that enable them to maximize their personal potential. Through collaborative programming with schools and other community-based organizations, staff will provide educational, social and mentoring opportunities to enhance the academic performance, social, and community connections, and career options of the youth.
The year 2009 marked a time of expansion for the We All Winn (WAW) Mentoring Program to include extending their services to "second chance" youth in Shreveport, LA. The main objective of this program is to close the revolving penal door for juveniles and encourage them to reassess and the behaviors that made them active participants in the juvenile justice system and make better life sustaining choices when they are out by offering them a "second chance." We will offer them services that will; help combat the academic achievement gap that exist between minorities and their more affluent peers, bolster their job readiness and employability, that will result in them reducing their tendency to opt to choose to act on risky behaviors that may send them back to the juvenile justice system. Several of our program components include positive mentoring relationships with adult role models, academic assistance, career exploration, parental engagement, and psychological counseling.
The We All Winn (WAW) Mentoring Program will service approximately 50 youth per year that reside in the Shreveport/Bossier area. Our goals are to increase the academic achievement/GED completion/Graduation rates of the program participants, reduce/eliminate truancy incidents, disciplinary referrals resulting in suspensions, strengthen bonds to family and community, reducing gang involvement and potential for violence. Our progress will be measured through academic progress tracking, attendance and participation in program and school, along with pre and post surveys of youth, parents, mentors and other involved staff.
If you are interested in becoming involved in our mentoring program, contact us below.
Face Forward is a Caddo Parish juvenile diversion program using Cognitive Awareness Training published by the American Community Correction Institute. Participants (ages 16 – 24 and court involved prior to adjudication and/or juvenile) complete small same-gendered behavioral modification sessions for 2 hours a week over 12 weeks.
Functional Family Therapy targets youths 10-18 at risk for severe behavior problems and delinquency. It is a cornerstone service of the Face Forward program. Intensive family therapy changes interaction patterns and develops skills such as communication, problem solving, conflict resolution and effective parenting. Five phases of treatment are tailored to the unique characteristics of each family.
The We All Winn second chance mentoring program is a re-entry program designed to provide assistance and support to motivated individuals being released from prison. By providing intensive case management and matching these individuals with a life coach that will be a friend and inspiration, we anticipate that these individuals with have an opportunity to turn their lives around and become productive individuals. This program is funded by the bureau of justice assistance.
Safehavens of Shreveport is a Transitional Living Program designed to give runaway, homeless, and throw away young men between the ages of 16-21 safe and stable shelter for up to 18 months with adult supervision. The ultimate goal is to help build independence and self-sufficiency by improving life skills, educational completion, job training/placement, and other necessary referrals to supportive community services and positive long term connections. Service provision includes individual goal setting, aftercare services, and mentoring to strengthen participant's relationships with positive role models to assist in them developing into responsible adults. Referrals will come through community partners, individual referrals, and Safehaven's Street Outreach workers.
Street Outreach is a program that has focused on touching an often overlooked and neglected aspect of homelessness, the throwaway, homeless, and runaway youth. It is designed to help these individuals get back on the right track and leave the streets. We may be able to offer the participants options that they have not considered or know about. Our main goal is reducing the number of youth living on the streets often becoming victims of sexual/ drug abuse, violence and exploitation.
We provide crisis intervention, temporary youth shelter referrals, safe alternate living arrangements or transitioning back to the home if that is the best option for the youth. We also work to address their immediate needs such as food, clean clothing, survival aid items, hygiene kits, showers and a listening ear. We also offer skill building workshops that will equip them with necessary ,pertinent information for life on or off the streets.
To refer to Safehavens of Shreveport contact the Transitional Living Program Director or print off and fax an application to 318-675-1124. If you would like to be involved with our Street Outreach of Shreveport Program, contact us below.
The target client base for the Chance 4 Success program is the under educated, disadvantaged and individuals with special needs. While society has seemingly cast these individuals aside we are here to offer them education, job training opportunities coupled with rehabilitation efforts that align with the current and projected labor market needs and employer defined skill sets. Concurrently we will work to form partnerships with local business and industry so the result will be that participants will have an opportunity to garner sustained meaningful work that will promote self sufficiency.
If you would like to participate in our Chance 4 Success program, contact us below.


text:
Ardeadoris egretta es una especie de babosa de mar, del orden nudibranchia, un molusco gasterópodo sin concha de la familia Chromodorididae. Se trata de la especie tipo de su género.

Distribución
Fue descrita en el arrecife Escape Reef y otras localizaciones de la Gran Barrera de Coral australiana. Se encuentra en el Océano Índico y el Pacífico occidental en Malasia, Indonesia y las Islas Solomon.

Descripción
Los bordes del manto son amarillos, y puede llegar a medir 12 cm.

Referencias

Enlaces externos

Chromodorididae

redpajama_set_name: RedPajamaWikipedia


text:
Music Video New Music Singles Bar TAPSheet
EXCLUSIVE PREMIERE – NEW HOLIDAY SINGLE/VIDEO: SOFIA TALVIK, "This Mess We're In"
ByRob Ross
Dec 14, 2020 Gothenburg SWE, MusicTAP.net, neo-folk, non-traditional holiday music, Rob Ross, singer-songwriter, Sofia Talvik
As many of you probably know, if you've followed the career of singer/songwriter Sofia Talvik, by now she releases a new original Christmas single (as a free download) every year. Her Christmas songs are generally on the darker side, so 2020 did not pose any obstacles for achieving that this year. Her new Christmas single is called "This Mess We're In"; please listen to and watch the video below.
Ms. Talvik's explanation and motivation is clear: "I think many artists, including myself in the beginning of this pandemic, thought that we'd finally have lots of time to create, something that can easily be pushed aside by a busy tour schedule a regular year. I also think that more artists than just me, then sat down with a deep sigh and no inspiration and no creative urge to do anything. Because touring, playing live and meeting people is what feeds inspiration, and we haven't been able to do any of those things this year.
So that is the grounds to this Christmas single, as well as reflection of the craziness of this whole year with people calling the pandemic a hoax, and the general fail of most of the world to handle it in a good way. All the while, we have lots of other problems on this planet as well. So I guess you could call it a "doomsday Christmas" song, because why not – it's 2020.
What I did have time to do this year was to put extra work into the production. When I initially started my tradition of Christmas songs, it was also a way for me to experiment and just have fun with the sound, and it didn't have to follow the sound of my albums. But as years passed, my Christmas songs became just another part of my repertoire and lost their experimental flare. So this year I am bringing it back with a big "dream-folk" production. I use 5 different guitars and a banjo on this track. I brought in bass from Sweden (by Janne Manninen) and drums all the way from New Orleans (by Marc Pagani).
Poignant and fitting for the moment, indeed.
"This Mess We're In" is available now on all streaming platforms, etc.
https://sofiatalvik.com/
DOCUMENTARY REVIEW: "Long Hot Summers: The Story Of The Style Council"
New Ken Hensley (Uriah Heep) Solo Album Expected
By Rob Ross
Rob Ross has been involved in the music industry for over 30 years - as guitarist/singer/songwriter with The Punch Line, freelance journalist, producer, manager and working for independent and major record labels. He resides in Staten Island, New York with his wife and cats; he works out a lot, reads voraciously, loves Big Star, traveling down South and his orange Gretsch. He's pretty groovy!
Lisa Gerrard (Dead Can Dance), and Jules Maxwell To Release Album, Burn


The actual Kansas Town Chiefs sit down on top of the actual AFC Western having a 5-1 report. Dealing with a few difficult groups to begin the growing season can make this particular report even more amazing.
Nobody understood precisely what the actual Kansas Town Chiefs' report might seem like following the very first 6 video games from the period. Once the Chiefs chosen at hand the actual reigns in order to second-year quarterback, Meat Mahomes II, it might possess ended up being the growth or even bust line kind of period. Fortunately, https://www.nflchiefsonlinestore.com/spencer-ware-jersey-c-43/ this appears to become much more of the growth kind of the period.
Lots of enthusiasts understood which Mahomes experienced an extremely higher roof arriving since the beginner, however most likely wouldn't possess speculated which he'd end up being top the actual MVP competition following the very first 6 video games.
Viewing this particular gauntlet associated with groups to begin the growing season had been most likely the key reason which a few thought which Kansas Town would want annually to determine the way the second-year quarterback might change. Because as it happens, Mahomes didn't require that point. Tossing with regard to 13 touchdowns within the very first 3 video games shattered the actual NATIONAL FOOTBALL LEAGUE report along with the majority of touchdowns tossed on the three-game extend to begin the period.
Within the very first 7 days from the period, the actual Chargers had been selected in your own home to place the beating about the Chiefs. Kansas Town rapidly created the declaration through displaying everybody the reason why they're the actual protecting AFC Western champs. Eric Berry Jersey Mahomes as well as organization exited M. THE. having a 38-28 conquer the actual Chargers.
Proceeding in to 7 days 3 as well as their own very first online game in your own home, the actual Chiefs appeared assured to visit 3-0. Actually sickness 37 factors about the Jimmy Garoppolo-lead Bay area 49ers had been required since the protection permitted the overall game to become a lot nearer compared to this must be. Following successful this particular online game 38-27, the actual Chiefs had been seated nicely from 3-0.


text:
HOME CENSORSHIP NEWS RESOURCES DO SOMETHING
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"New" Torture Tactics at Pelican Bay
Postage is one of our biggest expenses. Why not send a book of stamps or two to POB 40799 SF, CA 94140 next time you're at the post office? help out
WARNING: FBI tracks our visitors
May 17: Tor Hidden Service Mirror
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MIM(Prisons) is a cell of revolutionaries serving the oppressed masses inside U.$. prisons, guided by the communist ideology of Marxism-Leninism-Maoism.
Shut Down the Control Units (1/30/2020)
We Demand Our Grievances are Addressed in Texas (1/09/2020)
We Demand Our Grievances are Addressed! (9/25/2019)
Build a United Front for Peace in Prisons (9/05/2019)
We Demand Our Grievances are Addressed in North Carolina (8/29/2019)
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My Peers
Staff Ignoring Assaults
Under Ground Revolutionary
Ambivalence in Texas Prisoner Organizing
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Under Lock & Key is a news service written by and for prisoners with a focus on what is going on behind bars throughout the United States. Under Lock & Key is available to U.S. prisoners for free through MIM(Prisons)'s Free Political Literature to Prisoners Program, by writing:
MIM(Prisons)
[Abuse] [Campaigns] [Pelican Bay State Prison] [California] [ULK Issue 47]
by a California prisoner August 2015 permalink
I want to inform you about a new torture tactic being used here in the Security Housing Units (SHU). Since August 3 [2 weeks ago] the staff have been doing what has been termed "security/welfare checks" which entails staff walking by every prisoner's cell every 30 minutes 24/7 and pressing a button that has been installed next to our cells. Due to the design of the SHU the sound everyone and everything makes is louder than it should be and at night we are woken up every thirty minutes due to staff opening/closing the pod door, which is extremely loud, stomping up the stairs to the top tier and back down, and making a loud bang sound when hitting the button next to our cells as they are hitting metal on metal.
During the day it's the same thing except the wand makes a high-pitch beeping sound when hitting the button. So 24/7 it's non-stop excessive noise that doesn't allow us to sleep longer than 30 minutes without being woken up. I feel like I'm living in a dream 24/7 as I'm always stirred and feeling the effects of being denied sleep and not being able to go through my normal sleep cycles. Anyone with common sense can see this is cruel and unusual punishment. The ironic thing is staff say it's to prevent suicides. Yeah let's make a bunch of excessive noise all day and night and not let anyone sleep longer than 30 minutes at any given time, that should prevent suicides. If it's driving relatively stable prisoners crazy I'm sure it's pushing those with mental health issues over the edge.
Also by doing this, even though it's misguided and unnecessary, the CDCR is admitting that the SHU makes people more likely to commit suicide if they need to check on everyone every 30 minutes. I have filed an administrative appeal on this to have it stopped or modified and plan to file a lawsuit if we are not allowed to sleep normally again. In the mean time I'm writing friends/family to call the prison/CDCR head quarters and complain about this, and I'm writing all prison organizations and public servants to make them aware of this new form of torture being conducted.
MIM(Prisons) adds: This sleep deprivation torture tactic has been reported on from San Quentin for some time, and we recently received word from a comrade on pending litigation on this issue:
"I am challenging a blatantly obvious psychological torture program put in play by Jeffrey Beard, Secretary of the gulag system in California, as a payback to the SHU guys for the hunger strikes. The CDCR had to throw us, death row, under the bus too, to make it less obvious who the target really is.
"There is a program whereby they come and shine lights in eyes, bang and yell, using a 'beeper' stick to hit the cell tray slots, every 20 to 30 minutes, all day and night.
"In my moving papers I proved it is utterly pointless as stated, as a suicide prevention program. Anyone knows you can commit suicide during the half hour between walks, and also in our unit it takes them over 20 added minutes to get the keys, get shields, and race in and pounce on a guy hanging by the neck. It is specious.
"So I filed saying this is far too onerous to be a mere act of stupidity, it is a malicious torture of the SHU units only (including PSU, psych wards, all lock-up units). If this does not cause suicide, what would? Ha!"
This latest tactic of inhumane sleep deprivation reinforces our point that the settlement of the Ashker v. Brown lawsuit will do nothing to end torture in California prisons. As the comrade above points out, this is not rogue COs, this is facility policy. We received reports over a year prior about the new Guard One torture program. As one comrade pointed out at the time, most deaths in cells are due to medical neglect.
Calling this a "new tactic" is a bit of a misnomer. This same exact system of "security checks" every 30 minutes has been used in recent history in Texas and North Carolina. Though in these cases they seemed more targeted, and the comrade in North Carolina grieved the abuse and won. In fact, this type of sleep deprivation dates back more than 50 years when prisoners suffered similar conditions in Walpole, Massachusetts. All these examples go to show that the system is inherently oppressive, and only by overthrowing imperialism will we ever begin to see humane treatment of prisoners.
We view the latest behavior by guards at Pelican Bay as a form of retaliation against the prisoners held in SHU, to show them who is in charge and that torture is alive and well in spite of the "successful" settlement. Exposing this consistent mistreatment of prisoners in California is a must to counter the narrative that the modern prison movement has succeeded in transforming the CDCR, or the conditions they submit their prisoners to, in any way.
The acute threat of this form of torture requires an immediate response.
A concerted effort has been taken up by a number of groups supporting the California prison movement to contact the warden to demand an end to this torture.
Warden Clark E. Ducart
Pelican Bay State Prison
Crescent City, CA 95531-7000
call: (707) 465–1000 ext. 9040
Campaign info:
Stop Sleep Deprivation Torture in California Lockdowns
The New Court-Approved Device of Torture in California SHUs: Guard One
Fighting Back Works
Isolation and Torture in Texas
Sleep deprivation to control oppressed
Torture Continues: CDCR Settlement Screws Prisoners
← Return to ULK News Page
All content produced by the Maoist Internationalist Ministry of Prisons is under the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported License.


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A major pest control company claimed that Chicago has the biggest rat problem in the country in 2013. However, an animal shelter in the city of Chicago has come up with an environmentally friendly way to both solve some of this problem, and give several hard-to-adopt cats a permanent home. The Tree House Humane Society not only has sweet adoptable cats, but also manages hundreds of feral cat colonies containing thousands of feral cats which they trap, neuter and release. Taking care of these cats cost the shelter a lot of money and time, and since Chicago has a severe rat problem, they thought they should put the animals to work as natural pest controllers.
Residents and business owners who want to take part in the problem must be willing to pay about $500 to $600 dollars to set up three cats. The cats aren't just rounded up from the streets and released into a new area as they would quickly leave. Instead, they are slowly trained to get used to their new surroundings. Most people in the program notice an immediate improvement to the rat problem as soon as the cats arrive. Business owners say that the program costs are worth it because the cats save them money on rat-damaged merchandise which must be disposed. Currently, there is a 30-day waiting period for those who want to get into the program.


text:
Den Haag Ypenburg railway station
Den Haag Ypenburg
52°03′33″N 4°23′23″E / 52.05917°N 4.38972°E / 52.05917; 4.38972Coordinates: 52°03′33″N 4°23′23″E / 52.05917°N 4.38972°E / 52.05917; 4.38972
Line(s)
Gouda–Den Haag railway
Ypb
Preceding station
Following station
toward Den Haag Centraal
NS Sprinter 9800
2x/hour
toward Utrecht Centraal
NS Sprinter 19800
2x/hour; Not on evenings and weekends
toward Gouda Goverwelle
Den Haag Ypenburg is a railway station in the Leidschenveen-Ypenburg district of The Hague, Netherlands. It was opened on 11 December 2005. It is situated on the Gouda–Den Haag railway.
The following train services currently call at Den Haag Ypenburg:
2x per hour local service (sprinter) The Hague - Gouda - Utrecht
2x per hour local service (stoptrein) The Hague - Gouda Goverwelle
The railway station under construction (November 2005)
The railway station (January 2007)
NS website (Dutch)
Dutch Public Transport journey planner (Dutch)
Railway stations in South Holland
Boven Hardinxveld
Capelle Schollevaar
De Vink
Laan van NOI
Mariahoeve
Stadspolders
Goverwelle
Hardinxveld Blauwe Zoom
Hoek van Holland Haven
Leiden Centraal
Lammenschans
Rotterdam Alexander
Lombardijen
Vlaardingen Centrum
Future stations:
BleiZo
Leerdam Broekgraaf
Gorinchem Noord


Mac Design Nerd humor commentary on the new iTunes interface.
This entry was posted on Friday, September 9th, 2005 at 10:41 am	and is filed under Funny, Mac OS X. You can follow any responses to this entry through the RSS 2.0 feed. You can leave a response, or trackback from your own site.


Esquire is looking for a senior editor to oversee our digital coverage of movies, TV, music, books, and internet culture. This is a big role. Culture is one of the main pillars for Esquire, and the ideal candidate will manage not only the ongoing drumbeat of stories we publish every day, but also editorial franchises, celebrity profiles, and feature stories.
The ideal candidate should possess a wide-range of knowledge about culture, an instinct for what audiences desire, and the ability to parse data to find trends among readers.
This position is based in New York City and reports to the digital director of Esquire.


The Fire Department and the Cemetery Board are both looking for volunteers. Please contact the Township Office for more information.
If anyone wishes to address the council at the scheduled meetings, you must provide the Township Clerk with a written request by the Thursday prior to the meeting.
Tags are available at the Township Office. $5.00 for spayed or neutered dogs and $15.00 for non-spayed or non-neutered dogs.
In order to be better prepared, the Township is providing an opportunity for its residents to voluntarily self identify needs they may have in times of emergency to ensure their personal health and safety.
You are invited to identify those needs in the following brief survey. Residents who identify needs will be listed in an appendix of the plan. The appendix will be kept confidential and available only to those who will require the information in the event the Township's emergency response plan must be activated. Please print the form below and follow the instructions.
Notices relevant to residents and visitors will appear here from time to time.