text:
Wudstay Hitech City Main Road
Call us 1800-300-2400-1 (Toll Free) and Get additional Discount upto 50% for this Hotel.
You are getting lowest possible rate for this hotel
- About Hotel
- Reviews
Room Description
Standard Room
Room Amenities
Room Inclusions
- Breakfast
- Air conditioning
- Cable/satellite television channels,
- Coffee/tea
- maker
- Daily housekeeping
- Direct-dial phone
- Hair dryer
- Iron/ironing board
- LCD television
- Minibar,Shower/tub combination
- Wireless Internet access
About Wudstay Hitech City Main Road
Offering free internet access and breakfast service to its guests, the Wudstay Hitech City Main Road is situated 0.5 km from the Chanda Naik Nagar Bus Stop and 8 km from the Borabanda MMTS Station. A total of 10 air-conditioned rooms are available for accommodation. In-room amenities offered are television, bottled drinking water, separate seating area and attached bathroom with hot/cold running water facility and toiletries.
Checkin Time: 1200 pm
Checkout Time: 1200 pm


text:
February 12, 2009
Parkland Memorial Hospital, the county hospital for Dallas, Texas, announced changes in emergency room procedures to improve care and reduce long waits. Included is a new process for evaluating patients entering the ER, allowing them to confer immediately with a nurse or paramedic.
Some of the changes were the result of an Oct. 21 evaluation of Parkland's emergency operations by the Joint Commission, a national health-care accreditation agency:
- The evaluation followed the death of Mike Herrera, a 58-year-old Dallas man who checked into the ER Sept. 19 and died of cardiac arrest after waiting 19 hours for treatment.
- The commission cited 11 deficiencies in Parkland's ER, including inadequate check-in procedures, failure to offer proper pain medication to waiting patients, and ineffective leadership in some areas.
Parkland's ER has become overwhelmed with nonemergency cases due to the rising number of uninsured Texans needing basic medical care:
- Last year, the ER handled more than 130,000 patient visits.
- With the new procedures in place, last month, only 14 percent of ER patients left without seeing a physician, compared with the 24 percent who walked away in July.
John Haupert, the hospital's executive vice president and chief operating officer, said public hospitals throughout the nation are struggling with the flood of nonemergency patients. "This is not just a Parkland issue," he said:
- Parkland determined that its sickest ER patients last year waited an average of 2.7 hours to see a doctor and spent an additional 10.7 hours being treated or waiting for a hospital bed.
- Patients who were not as sick waited an average of 5.6 hours for care and spent an additional 4.8 hours being treated and discharged.
Source: Sherry Jacobson, "Parkland hospital streamlines emergency room procedures," Dallas Morning News, February 11, 2009.
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subset: commoncrawl


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2016 Five Year History and Proposed 2016 Millage Rate Notice
The Pickens County Board of Commissioners has tentatively adopted a millage rate which will require an increase in property taxes by 13.84 percent over the rollback millage rate of 7.203 mills.
All concerned citizens are invited to the public hearings on this tax increase to be held at 1266 East Church Street, Suite 168, on Thursday, September 8, 2016 at 10 a.m. and at 6 p.m.
The time and place of an additional public hearing on this tax increase will be Thursday, September 15, 2016 at 5:00 p.m. prior to the regularly scheduled Board of Commissioners' meeting at 5:30 p.m.
The millage rate will be approved and adopted at the 5:30 BOC meeting on September 15, 2016.
This tentative increase will result in a millage rate of 8.2 mills, an increase of 1 mill. Without this tentative increase, the millage will be no more than 7.203 mills. The proposed tax increase for a home with a fair market value of $150,000 is approximately $55.00 and the proposed tax increase for non-homestead property with a fair market value of $100,000 is approximately $40.00.


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Below is a selection of search results matching: Animal Therapy StirlingshireView All Listings
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Based in St Andrews, Scotland, Alison offers a varied range of therapies to help us all back to being 'whole'.
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CONTACT NAME: Andy Eckley
Andy Eckley is a fully qualified sports massage therapist also qualified in Bowen and EMMETT therapy along with NAT (Trigger point Therapy) ...
Phone: 01253 726222 Mobile: 07902 449433
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Homeopath, Counsellor, Reiki Master and Flower Essences Practitioner, treating anxiety, depression, bereavement, relationships, illness and ...
Phone: 01254 246205 Mobile: 0790 7766 095
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Spiritual Healing has been practised for hundreds, even thousands of years in many communities and countries.
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Phone: 01283 535 458
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Discover the amazing and magical difference crystals can make to your life! Crystal Therapy, Crystal Courses and Spiritual Artwork
Phone: 07952516639
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Whether you have a physical or psychological condition or you are just feeling under the weather HOMOEOPATHY offers you a better way t...
Phone: 0121 733 7170 Mobile: 07907734101
Birmingham, Birmingham, Warwickshire B32 2HB
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About | Herbal Therapy | Animal Reiki | Reiki Healer/Reiki Master | Aromatherapy O.A.DIP | Seated Chair Massage | Personality Assessment Th...
Phone: 07984259979 Mobile: 07984259979
Northampton, Northamptonshire NN1 4DX
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The Old Convent, Stroud, Gloucestershire GL5 4AD
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Craniosacral Therapy , Reiki Usui Shiki Ryoho and Working with animals
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Bucknell, Shrewsbury, Shropshire SY7 0BN
Animal Therapy, Aromatherapy, Homeopathy, Reiki, Shiatsu
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Latton, Swindon, Wiltshire SN1 4NS
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Sports Massage, Indian Head Massage, Mum to Be Massage, Equine Sports Massage, Corporate Massage, Seated Massage
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Calne, Wiltshire
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Quality - What makes me different from the rest and what can I offer you? I am an experienced, qualified and fully insured Professiona...
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Weston Super Mare, Weston-Super-Mare, Somerset BS23 2PE
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Tracy is a Physiotherapist, Clinical Hypnotherapist, Psychotherapist, Acupuncturist, Reiki Master and Psychic Medium.
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I specialising in difficult to treat health conditions including Candida & Multiple Sclerosis. ' I use Bioresonance Technology' and Nutrit...
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Do you have aches or pains in joints or muscles? Feel like you've trapped a nerve? Do you want to get healthy and stay well?
Phone: 01932 857782 Mobile: 07787 514271
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Discover how you can calm your mind, allowing your body to heal itself naturally and effectively.
Phone: 01258 458340
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|08 Aug 2016
Not using the laptop or replacement of the hard drive is the only way to prevent increasement of the attributes.
It is a physical issue, the system had to 'reallocate' those sectors on the drive, eventually when there are no sectors in the reserved part left more problems will arise like system freezes, BSODs, performance decreases drastically, etc.
Please note, this is only when the hard drive has no reserved sectors left, a huge amount of bad sectors and is almost at the worst situation at which you are by far not
|My System Specs
|09 Aug 2016
I got another BSOD after running chkdsk...
Technical information
0x000000CE (0xFFFFF88001B0F577, 0x0000000000000008, 0xFFFFF88001B0F577, 0x0000000000000000)
I left my laptop on overnight to run chkdsk and it was like that when I woke up this morning.
|My System Specs
|09 Aug 2016
Upload the chkdsk log Check Disk (chkdsk) - Read Event Viewer Log
|My System Specs
|09 Aug 2016
I tried to get the log but apparently the chkdsk never finished/worked? Probably because of the BSOD I described in my last post.
I got yet another BSOD while using Chrome just now.
A process or thread crucial to system operation has unexpectedly exited or been terminated."
Technical information:
*** STOP: 0x000000F4 (0x00000000000003, 0xFFFFFA8008B09B10, 0xFFFFFA8008B09DF0, 0xFFFFF800037C5E40)
Physical memory dump FAILED with status 0xC0000010
|My System Specs
|10 Aug 2016
Chkdsk never finished, else a log would be present.
I see a replacement of the hard drive is necessary for this issue to be resolved.
I would recommend to backup all important data to an external hard drive as a priority.
|My System Specs
|Thread Tools
|Similar help and support threads
BSOD kernel_data_inpage_error 0x0000007a
Mostly happens when i browse the internet.I've attached the file hopefully it's enought for you to find what's causing it. :p
|BSOD Help and Support
Bsod kernel_data_inpage_error (0x0000007a)
Hi, I've been experiencing BSOD KERNEL_DATA_INPAGE_ERROR 0x0000007A in my laptop a few hours ago. After the BSOD occurred, the BSOD did not automatically restart my laptop. I had to unplug and restart the computer. After that, the computer run start up repair and restart the computer but the...
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KERNEL_DATA_INPAGE_ERROR - 0x0000007A and after 0x000000F4
Hi, i just got two BSOD's in a row this morning, the first one i checked and found this: KERNEL_DATA_INPAGE_ERROR - 0x0000007A - Microsoft Community which may well be the problem (and if it's hardware, i hope it is) but then right after i got another one with 0x00000f4 error, so before crashing...
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STOP 0x0000007A: KERNEL_DATA_INPAGE_ERROR
Hi everyone, I thought that I may have had a virus so I scanned malwarebytes etc. The system would take 20 minutes+ to load. This in now about 10 minutes to load. The virus removed a few bits and was dealt with in another thread. I have now been getting the following error/bsod: STOP...
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Hourly BSODs: Kernel_data_inpage_error 0x0000007A
Hi all, I've been having hourly BSODs since Saturday afternoon. They don't seem to happen for a particular reason that I can tell, they simply occur about an hour after my machine is booted. I have also managed to get a picture of the BSOD, if its of any help at all! Virus/malware...
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ES6 (ES2015) introduces a standardized module format to Javascript. We'll take a look at the various forms of defining and importing modules. Using Webpack to bundle up our modules and Babel to transpile our ES6 into ES5, we'll put this new module syntax to work within our project. Then we'll examine how to import 3rd party packages from npm, importing lodash with the
_ underscore alias using the ES6 module syntax.
es6 is the next generation of javascript. You can use it today with the traceur compiler library. Also be sure to check out es6fiddle to start playing with ECMAscript 6 right now.


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Offspring from families with alcohol dependence (AD) have been shown to exhibit brain morphological alterations that appear to be related to their familial/genetic risk for AD. Greater susceptibility for developing AD may be related to structural underpinnings of behavioral traits that predispose to AD. We examined white matter (WM) integrity in 81 individuals with either a high density of AD in their families (N=44) or without a family history for either alcohol or drug dependence (N=37). Magnetic resonance images were acquired on a Siemens 3 T scanner with fractional anistropy (FA) and the apparent diffusion coefficient (ADC), along with radial diffusivity (RD) and longitudinal (axial) diffusivity calculated for major white matter tracts in both hemispheres. Extensive personal histories of alcohol and drug use were available from longitudinal collection of data allowing for reliable estimates of alcohol and drug exposure. We found that the interaction of personal exposure to alcohol and familial risk for AD predicts reduction in WM integrity for the inferior longitudinal fasciculus (ILF) and the superior longitudinal fasciculus (SLF) in the left hemisphere and the forceps major tract. Only one tract showed a significant difference for exposure alone, the anterior thalamic radiation.
The neurotoxic effects of alcohol consumption have been evident since the time that Victor et al. (1971) published their classic work. Using autopsy data, it was shown that the debilitating behavioral and neurocognitive effects of long-term alcohol use seen in Wernicke–Korsakoff patients, who have among other deficits a profound short-term memory loss, were associated with significant neuropathological changes in a number of subcortical regions.
It is now clear from numerous reports focused on individuals with chronic alcohol dependence that long-term consumption of alcohol is associated with brain morphological changes (Chanraud et al., 2010), as well as neurocognitive changes (Sullivan and Pfefferbaum, 2005; Oscar-Berman and Marinkovic, 2007). Although alcohol diffuses throughout the brain, there is evidence that not all regions are equally affected by alcohol. Regional changes have been suggested by work showing impairment in frontal and parietal networks in long-term alcohol dependence (Pfefferbaum et al., 2010) and a tendency for lateralized effects to be seen, with the right hemisphere showing greater impairment (Oscar-Berman and Marinkovic, 2007; Pfefferbaum et al., 2009) in association with the neurotoxic effects of alcohol.
There is an intriguing possibility that some of the observed variation in structural and functional characteristics of individuals who are heavy consumers of alcohol may have existed prior to the initiation of drinking and that some of these characteristics may actually be markers of vulnerability. Structural differences have been observed family-history-positive youth selected for a high density of familial alcohol dependence. These include reduced volume of the right amygdala (Hill et al., 2001), reduced volume of the right orbitofrontal cortex (Hill et al., 2009a), and greater volume of cerebellum for age (Hill et al., 2007a; Hill et al., 2011a) suggesting a slower rate of neural pruning of grey matter in those with a family history of alcohol dependence. Also, youth with parental alcoholism have been reported to have smaller total brain volume (Gilman et al., 2007). Electrophysiological differences between family-history-positive and-negative youth were first identified using event-related potential (ERP) recordings in boys without any significant drinking history (Begleiter et al., 1984). Reduction in the P300 component of the ERP was seen in those with a family history. Several other studies have found similar effects (for reviews, see Polich et al., 1994; Hill, 2010). These deficits may reflect an inability to reach age-appropriate levels of P300 in high-risk youth (Hill et al., 1999) and, importantly, slower trajectories of P300 change are related to childhood psychopathology (Hill and Shen, 2002).
A variety of functional imaging paradigms have been used to address possible differences between high- and low-risk youth. Although the paradigms and functions have varied across studies (for review see Tessner and Hill, 2010), the general tendency has been to see reduced activation in frontal regions associated with attentional tasks (Spadoni et al., 2008) and with tasks requiring inhibition of a prepotent response (Schweinberg et al., 2004). Functional imaging studies that have focused on brain connectivity using functional magnetic resonance imaging (fMRI) in family-history-positive and -negative youth have reported weaker fronto-parietal connectivity (Wetherill et al., 2012) and weaker fronto-cerebellar connectivity (Herting et al., 2011) in family-history-positive youth.
Attempts to differentiate what is cause and what is consequence are complicated by the fact that youth from families with a history of alcohol dependence have a higher risk for developing an alcohol use disorder (AUD) or related substance use disorder (SUD) than do youth without such a history (Milberger et al., 1999; Merikangas et al., 2009). Follow-up of youth from multiplex, multigenerational families with multiple cases of alcohol dependence is associated with a four-fold increase in risk for substance use disorder (SUD) (Hill et al., 2008, 2011b). In addition, youth with a positive family history of alcohol dependence tend to start using alcohol at an earlier age than do those without a history (McGue et al., 2001; Hill and Yuan, 1999; Hill et al., 2000). Because of this earlier onset of substance use, those with a family history may be at greater risk for incurring alcohol- and drug-related exposures that could potentially affect brain morphology.
Magnetic resonance (MR) diffusion tensor imaging (DTI) provides an opportunity to investigate white matter microstructure often revealing disruption that is not apparent upon macrostructural inspection (Pfefferbaum and Sullivan, 2002). DTI studies are possible because of characteristics of water diffusion in the brain. Diffusion that is unconstrained is isotropic as is seen in the cerebrospinal fluid whereas anisotropy results from constraints imposed by fiber tracts. The metrics of DTI include fractional anistropy (FA) and the apparent diffusion coefficient (ADC), which can be decomposed into two components, the transverse (radial) diffusivity (λT), and the longitudinal (axial) diffusivity (λL). (Beaulieu, 2002). Specifically, FA reflects the tendency for water to diffuse along an axis parallel to the fiber tract such that higher values of FA are associated with more intact white matter microstructure. Radial diffusivity (RD), which measures water diffusion perpendicular to the tract, is associated with disruption of white matter integrity so that higher values are indicative of greater disruption. These DTI metrics provide a method for assessing the likelihood that white matter integrity has been affected. Radial diffusivity (RD) increases with loss of myelin integrity. Longitudinal diffusivity can be altered where disruption of axonal integrity or axonal deletion is present. Typically, disruption of white matter through breakdown of the myelin sheath is associated with decreased FA and increased radial diffusivity RD (Song et al., 2002).
Among the applications of DTI methodology are assessments of whether white matter integrity has been compromised by exposure to substances, whether neurodegenerative conditions may be taking place, or whether white matter variation might be the result of a familial/genetic characteristic of the individual. Evidence that FA may also vary due to inborn characteristics comes from recent studies showing a substantial heritability of FA in related healthy individuals (Jahanshad et al., 2010). FA values change during development, typically with changes in mean diffusivity. In their review of 30 studies that have addressed DTI in child, adolescent, young adult, and older adult samples, Schmithorst and Yuan (2010) conclude that there is an overall tendency for FA values to rise during childhood, adolescence and young adulthood, peaking at about 40 years of age and then declining. The rise in FA seen during this period is mirrored by a decrease in mean diffusivity, declining until age 40 and then rising again.
DTI studies have provided evidence that white matter micro-structural disruption occurs in alcohol-dependent men and women in the corpus callosum and spenium and in multiple white matter tracts (Pfefferbaum et al., 2006, 2009). DTI can reveal regional white matter disruption and assess white matter tracts (Lehericy et al., 2004). Applying quantified fiber tracking, Pfefferbaum et al. (2009) showed that alcoholism affected FA and diffusivity of several fiber bundles with frontal and superior regions most affected (frontal forceps, longitudinal fasciculi, internal and external capsules, fornix and superior cingulate). Curiously, more posterior and inferior structures were relatively spared.
Although there is substantial evidence that exposure to alcohol and drugs is associated with white matter microstructural changes (Sullivan and Pfefferbaum, 2005; Pfefferbaum et al., 2009), it is unclear if some of these microstructural changes may have been present in those with a family history of alcohol dependence before they started drinking. Only a few studies have examined white matter microstructure in youth with and without a family history of alcohol dependence (Medina et al., 2008; Bava et al. 2009, 2010; De Bellis et al., 2008; Herting et al., 2010; Wetherill et al., 2012). One study reported reduced FA for the inferior longitudinal fasciculus and right optic radiation in family-history-positive youth (Herting et al., 2010), while another (Wetherill et al., 2012) did not find altered white matter micro-structure in tracts connecting the frontal and parietal regions, though they did find evidence for reduced frontoparietal connectivity using fMRI. Bava et al. (2009) reported a family history effect for the right crus cerebri, though no other regions showed an association. Exposure to marihuana and alcohol predicted FA above and beyond parental history, though no interaction between family history and exposure was seen. However, in a later report, Bava et al. (2010) found FA in inferior longitudinal fasciculus (right) to be significantly correlated with parental SUD.
Alcohol or marihuana exposure during adolescence and young adulthood appears to have an adverse effect on white matter microstructure (Medina et al., 2008; De Bellis et al., 2008; McQueeny et al., 2009; Bava et al., 2009; Thatcher et al., 2010). Three of the studies that evaluated exposure effects also evaluated family history (Bava et al., 2009; Medina et al., 2008; De Bellis et al., 2008) with one reporting no effect of familial risk for alcohol dependence background (Medina et al., 2008), the other showing minimal effect (Bava et al., 2009), while the third found an unexpected increase in FA (De Bellis et al., 2008).
Because of the possibility that both familial loading for alcohol dependence and exposure to alcohol or drugs of abuse might affect white matter tracts, this study was designed to address these issues in a sample that varied in familial loading for alcohol dependence and for whom extensive data were available for personal exposure to alcohol, marihuana, and cigarettes. Based on results from previous studies that have assessed alcohol exposure, we predicted that subjects with heavier alcohol exposure would have reduced FA and increased ADC (either axial or transverse diffusivity) reflecting loss of white matter integrity. With previous reports of reduced FA in those with a family history of alcohol dependence, we predicted that individuals with multiplex family history would have reduced FA. It was also hypothesized that those with a multiplex family history who were among the heavier consumers of alcohol might have the greatest decline in FA and the largest increases in radial or longitudinal diffusivity. Our first goal was hypothesis-driven and was designed to assess whether or not previously identified changes in specific tracts (inferior longitudinal fasciculi and superior longitudinal fasciculi) would be seen in association with multiplex familial risk for alcohol dependence and determine if this would be modified by personal exposure to alcohol. Our second goal was to perform exploratory analyses with the remaining Johns Hopkins University Atlas tracts to determine if other tracts might reveal an association with these variables.
The sample included 44 subjects (24 male and 20 female) from multiplex for alcohol dependence families and 37 (20 male and 17 female) low-risk control subjects (Table 1). Overall the groups did not differ in mean age, though the high-risk males were on average somewhat older than the low-risk males. A similar proportion was left handed. There was a statistically significant difference in the socioeconomic status (SES) of the two groups. However, the mean Hollingshead Four-Factor Index scores (Hollingshead, 1975) for the high- and low-risk groups are in adjacent SES classes suggesting greater similarity in SES for the two groups than the mean differences indicate.
A three-generation study of multiplex alcohol dependence (AD) alcohol dependence families initiated in 1985 provided the participants for the present study. These multiplex AD families were originally identified through the presence of two adult brothers (proband pair) with AD. Extensive in person and family history information are available for these targeted families, including the probands' parents (first generation) and the second generation siblings of the identified probands. The multiplex sampling strategy used in this study resulted in a high density of AD in the targeted pedigrees (an average of 4.41 first and second degree relatives for the present sub-sample) as previously described (Hill et al., 2008). Third generation offspring of the brother pairs and offspring of their siblings in these multiplex families provided the high-risk offspring for the present report. These offspring have a greater familial loading for alcohol dependence than is commonly seen in studies designed to identify offspring of AD parents (Table 2).
Psychiatric status of the "marrying in" side of the offspring's family was also obtained. Among the high-risk offspring, 76% of the fathers and 33% of the mothers had AD by lifetime history. A total of eight offspring (18.2%) were from families where both parents were alcohol dependent. Although six high-risk offspring did not have a father or mother with a lifetime diagnosis of AD, the sampling design insured that each individual designated as high risk came from multiplex pedigrees. As a result, the average number of second degree relatives (aunts and uncles), even for the six high-risk offspring without AD parents, averaged 4.33 relatives who were alcohol dependent.
Low-risk control families were identified through two adult brothers without a lifetime history of alcohol or drug dependence. Parental AD among low-risk offspring was infrequent but did occur where "marrying in" spouses had AD. For fathers, 8.1% were alcohol dependent and 2.7% were dependent on drugs. For control mothers, 5.4% had a lifetime diagnosis of drug dependence. Two second degree relatives of the control offspring were alcohol or drug dependent.
All third generation offspring who were enrolled in a longitudinal follow-up initiated in 1989 were eligible to participate in the MRI portion of the study. Letters were sent to all offspring and appointments set up for MRI scans for those whose schedules would allow it.
In order to control for variables other than familial/genetic risk that might influence brain morphology, careful attention was paid to personal characteristics of the subjects including their personal history of prenatal use. Similarly, prenatal use of substances by mothers was obtained.
Mothers of both high- and low-risk offspring were administered a structured interview designed to assess quantity and frequency of use of alcohol, drugs and cigarettes during pregnancy. The assessment was retrospective, being obtained at the child's first longitudinal assessment (typically before the age of 12 years). Comparison of prospective and retrospective data for drinking during pregnancy has shown retrospective data to be valid (Griesler and Kandel, 1998). Moreover, follow-up of women for 4 and 5 years following their pregnancies has shown substantial reliability (r=0.53 and 0.67, respectively) between reports obtained during pregnancy and those obtained following the pregnancy (Ernhart et al., 1988; Jacobson et al., 1991).
All participants are currently enrolled in the ongoing longitudinal study that has followed youngsters from childhood through young adulthood. Extensive clinical information was available for determining if any psychiatric disorder including substance use disorder was present by the time the MRI assessment was performed. Children/adolescents were assessed yearly with the Kiddie Schedule for Affective Disorders and Schizophrenia for School-Aged Children (K-SADS) (Chambers et al., 1985) using separate interviews of parent and offspring to determine the presence or absence of Axis I DSM-III diagnoses. (DSM-III was the current methodology at the initiation of the study in 1989.) Young adults were assessed using the Composite International Diagnostic Interview (CIDI) diagnostic instrument (Janca et al., 1992) to obtain DSM-IV Axis I diagnoses. The CIDI-Substance Abuse Module (CIDI-SAM) was used to supplement the CIDI to obtain detailed substance use history.
Using quantity and frequency information available from the K-SADS, CIDI and CIDI-SAM, it was possible to determine the average yearly density of each substance and the number of years of use. This measure was used as an index of exposure to take into account the number of years the subject had been drinking and the number of visits that occurred between the age of onset to drink and the time the scan was performed. The total number of drinks reported collectively from all visits was divided by the number of years drinking. If the number of visits was less than the number of years, the estimate was adjusted accordingly.
All participants signed informed consent documents after having the study explained to them. All were screened to insure absence of ferromagnetic metal in or on their body. All female subjects were screened for absence of pregnancy using Icon® 25hCG pregnancy kits. A neuroradiologist reviewed any scan considered suspicious for abnormality.
All subjects were scanned on a Siemens 3T scanner located in the Department of Radiology MR Research Center. To verify subject position, cooperation, and image quality, a set of coronal and sagittal scout images (TE=2.5 ms, TR=250 ms, slice thickness=4 mm, FOV=256 × 256 4 mm, 24 slices) were obtained. The axial sections are obtained parallel to the anterior commissure/posterior commissure line (AC/PC) which provides a reproducible guide for image orientation.
The T1 weighted images were acquired using the MPRAGE sequence (TR=2300 ms, TI=1000 ms, TE=2.98, flip angle=9 degrees, NEX=1, FOV=256 × 256) with full coverage of the whole head for all subjects.
Using the Siemens technology, the proton density and T2 weighted images are acquired in a single scan, as a dual echo acquisition turbo spin echo. The parameters for this sequence are TR=3000 ms, flip angle=150 degrees, echo times TE1=11 ms and TE2=101 ms, NEX=1, FOV=256×256. The geometry of the acquisition is 48 slices (3 mm thickness) with zero gap.
A single shot echo planar imaging (EPI) dual spin echo sequence modified to include bipolar diffusion-sensitizing gradients in arbitrary directions was used to acquire the DTI raw data. The parameters for the sequence were TR=5300, TE=88, NEX=4, FOV=256×256. Twelve diffusion gradient orientations were used and a total of four signal averages were performed for each orientation with a b-value of 1000 s/mm2. A total of 40 slices with a thickness of 3 mm and an interslice gap of 0 mm were acquired for each subject.
The FMRIB Software Library (FSL; University of Oxford) linear image registration tool (FLIRT) was used for preprocessing, including eddy current correction for the diffusion-weighted images, correction for spatial distortions including head motion, and for transformation of each diffusion image. The Brain Extraction Tool (BET) was used to mask out all structures other than brain tissue. The eddy corrected images were used to calculate the diffusion tensor components. The program MedINRIA (Asclepios Research Project; INRIA Sophia Antipolis, Cedex France), which provides an initial estimate of DTI parameters using a method described by Basser and Pierpaoli (1996), was used to obtain three eigenvalues (λ1, λ2, and λ3,) and FA. An average of the l2 and l3 images provided a measure of radial diffusivity (RD). The method proposed by Basser and Pierapoli in which a family of tensor-derived scalar anistropy measures is used to characterize the diffusion in DTI remains a well recognized approach (Basser and Pierpaoli, 2011).
Using TBSS, images from all study scans were combined to provide a representative template for further analysis. Although a template from the low-risk control sample could have been used, use of all study scans provided a larger sample for constructing a representative template. We used an FA threshold of 0.2 for determining the FA skeleton for the first stage where registration is done. The 3-D FA images were nonlinearly registered and aligned to FMRIB58_FA_1mm MNI 152 standard-space image. Images were registered using a two-step process. First images were registered linearly using FLIRT. This normalized the brain volume, shape, and center of mass. Images were further registered locally using FNIRT to nonlinearly align local structures. Every image was reviewed for registration misalignment. If the registration resulted in a failure, we rejected the subject's scan. Using fslmerge, these images were then merged into a single 4-D image. Next, fslmaths was used to mask out voxels not belonging to all subjects. The remaining voxels were averaged over all 81 subjects to obtain the mean FA. The mean FA was then skeletonized and used as the basis for skeletonizing each individual subject.
Our goal was to map our findings to the Johns Hopkins University Atlas (JHUA), which describes nine bilateral major fiber tracts along with the forceps major and minor (Wakana et al., 2004). Included were four bilateral association tracts: the superior longitudinal fasciculus (SLF), inferior longitudinal fasciculus (ILF), inferior frontal-occipital fasciculus (IFOF) and uncinate fasciculus (UF). Additionally, bilateral tracts of the anterior thalamic radiation (ATR) and corti-cospinal tracts (CST), cingulum (CG) and cingulum-hippocampus (CH) were assessed. Also, the portion of the superior longitudinal fasciculus that courses through the temporal lobe was assessed bilaterally.
The JHUA atlas was used to mask the skeletonized voxels of interest with all voxels within the mask being included. The JHUA mask for each major tract was applied to all 81 subjects using fslmaths. Fslstats was then applied to all of the resulting images to calculate the mean, median, and center of gravity for that tract for each subject. Our method is most similar to voxel-based statistical techniques but uses a standardized region of interest (ROI), an atlas-defined tract. By registering all of the subjects' data into a common space and common skeleton, our method makes it possible to apply the same structural mask to the entire set of subjects which leads to less bias in the outcome.
The mean FA, and components of the apparent diffusion coefficient (ADC) components, the transverse (radial) diffusivity (λT) or RD values, and the longitudinal (axial) diffusivity (λ L) values were then analyzed using SPSS (Version 20) using mixed model analyses that included fixed effects (familial risk status, alcohol exposure, and their interaction) with mixed model covariates included for sex, age, SES and mother's lifetime drinking status. Although the self-reported drinking and drug use during pregnancy was minimal in all mothers, the most conservative method for correcting for any possible underreporting would be to presume that those with a lifetime history might have used more substances during pregnancy than was reported. A random effect was included in the model to account for the presence of multiple siblings in some of the families. Tracts showing significant effects of alcohol exposure and risk were further tested to determine if exposure to marihuana or cigarettes would change the results obtained.
The close correspondence between the JHUA SLF tract (illustrated in blue) and the clusters of voxels for our subjects (red) may be seen in Fig. 1.
The adjusted yearly drinking variable was used to group individuals into high- and low-consumption groups. Terciles were constructed based on the reported yearly quantity consumed, with individuals in the bottom two terciles contrasted with those falling in the top tercile. Also, a total lifetime exposure variable was calculated representing total drinks consumed which was then converted to kg. Results may be seen in Table 3.
Fractional anistropy varied with risk group membership and alcohol exposure for three tracts: inferior longitudinal fasciculus (ILF) (left), superior longitudinal fasciculus (SLF) (left), and the portion of the superior longitudinal fasciculus that courses through the left temporal lobe (Table 4A). To examine the effect of alcohol exposure, correlations were performed between FA and lifetime number of drinks first for the full sample and then confined to the high-risk sample. Correlations for the full sample were all nonsignificant. However, analysis confined to the high-risk sample showed significant results. For ILF left r=−0.313, p=0.038, for SLF left, r=0.297, p=0.05, and for the temporal portion of SLF left, r=0.301, p=0.047.
Gender was a significant covariate for ILF left, and for the SLF left (temporal lobe portion) for FA (Table 4A), but was not significant for any of the tracts showing significant changes in transverse (radial) diffusivity.
Age was entered into the analyses both as a linear and a quadratic term. The tracts that were found to differ in association with the main effects of risk and exposure (ILF left, SLF left, SLF left [temporal lobe]) did not appear to be influenced by age.
To further explore the impact of age, all tracts were analyzed to determine if significant main effects of age would be apparent by regressing age on FA, testing for linear and quadratic components for the 81 subjects studied. Over the age range studied, significant age effects were not found with the exception of the corticospinal tract (CST) (left) (F=3.95, df=1,79, p=0.050). An analysis was then performed to address the age-related changes within each familial risk group. To control for gender, analyses were performed within a sub-sample of male low-risk controls (N=20) and a sub-sample of high-risk males (N=24). As may be seen in Fig. 2, a significant quadratic relationship (F=4.70, df=2,17, p=0.024) between age and FA was seen in the low-risk control males. In contrast, high-risk males did not show an age-related change in FA for any fit. For the quadratic fit that was significant in controls, high-risk males appeared to show minimal change with age (F=0.11, df=2,21, p > 0.05) (Fig. 3). Neither the high- nor the low-risk female groups displayed significant age-related changes.
Analysis to determine the extent of radial diffusivity across the nine bilateral tracts and the forceps major and minor (Table 4B) in association with familial risk, alcohol exposure and their interaction revealed marginally significant results for the inferior lon-gi-tu-dinal fasciculus … the forceps major (left) and significant results for the forceps major (p=0.046). Also, the anterior thalamic radiation showed increased radial diffusivity in association with alcohol exposure alone (p=0.025). Additionally, ADC for the anterior thalamic radiation (ATR) right tract differed significantly for those in the lower terciles of alcohol exposure versus those in the top tercile (p=0.014). Increased longitudinal (axial) diffusivity was also seen for this tract (p=0.023). To further examine factors associated with increased diffusivity, correlations were performed between lifetime drinking, ADC, RD, and λL for ATR right within the male only and female only sub-samples. Within the male sample (high and low risk) two significant correlations and one nonsignificant correlation were observed. For ADC r=0.355, p=0.018, for RD r=0.355, p=0.018, and for λL r=0.287, p<0.05. Results for the ATR right may be seen in Fig. 4.
Although the goal of the study was to evaluate the effects of alcohol exposure in offspring with and without a family history of alcohol dependence, the overlap with marihuana exposure and cigarette smoking suggested the need to analyze the results to account for possible effects of these substances. Models were run for the ILF left, SLF left and the SLF in the left temporal lobe to test for the effects of risk and alcohol exposure, covarying gender and age, and additionally evaluating first marihuana exposure and then cigarette smoking. As may be seen in Tables 4A and 4B, yearly adjusted use of marihuana and cigarettes when entered as covariates in the full model did not show an effect of these potentially contaminating variables.
Marihuana exposure was analyzed as a main effect without consideration of familial risk or alcohol exposure to assess the extent of its impact on white matter integrity. It should be noted that 42 subjects reported using marihuana with 39 reporting none. Of the 42 users 20 reported a 1–9 year history and 22 a history of 10–20 years. Lifetime number of marihuana smoking occasions was analyzed using a group analysis with (1) no previous use; (2) use between 2.5 and 263 occasions (lower exposure) and 365 or more occasions. The tracts showing significant exposure effects in association with alcohol use (Table 4A) were tested for main effects of marihuana. Although there was a trend for FA to be reduced in association with group membership, marihuana exposure did not prove to be statistically significant for these tracts. Correlation analysis for total lifetime marihuana use and FA for ILF left, SLF left and SLF left (temporal) were not significant with r values ranging between −0.01 and −0.07.
When cigarette smoking was analyzed as a main effect without consideration of alcohol consumption, no effect was seen using in a three group analysis in which lifetime number of cigarettes smoked was considered. Correlation analysis was performed for ILF left, SLF left and SLF left (temporal) and total lifetime exposure (number of cigarettes). All correlations ranged between r=−0.09 and −0.11 and were not significant. It should be noted that our results for the effects of smoking are based on a small sample of smokers (N=30) from the total group of 81 subjects. This may have limited the statistical power to uncover such effects.
Mothers of both high- and low-risk offspring were interviewed concerning their use of alcohol or drugs during pregnancy and found to be free of heavy use during pregnancy. Drinking among mothers in both groups was quite low. Of the 81 subjects studied, prenatal exposure data for drinking were available for 74, with data for drug use and cigarette smoking available for 70. A total of 81.1% of the mothers of the offspring studied reported no drinking with an additional 18.9% drinking less than one drink per day. A total of 1.4% reported using any drugs during pregnancy. Absence of cigarette use was reported by 77.1% of mothers. However, of those who smoked, a greater percentage were from high-risk families (30.7%) versus low-risk families (12.9%).
Although the reported level of drinking, drug use and cigarette smoking was low in this sample, poor recall or distortion of self-report can occur. Therefore, we performed two additional analyses to insure that our results were not influenced by prenatal exposure but rather reflected personal exposures and familial risk. First, a dummy variable was constructed in which any mother with a lifetime history of alcohol or drug dependence was coded as "1" and those without such a diagnosis coded as "0". These values were entered into the full analysis shown in Tables 4A and 4B as a covariate. This analysis showed that the mothers' potential use during pregnancy did not alter our results. Next, we removed the data for 14 offspring of these mothers. In spite of reduced sample size that could reduce power to detect differences for the major variables of interest (risk, exposure and risk × exposure), the results seen in Tables 4A and 4B were supported.
The results of the present study need to be interpreted in view of two separate goals: (1) to assess the effects of familial risk effects on the SLF and ILF association tracts and the forceps major and the effects of alcohol exposure, alone and in combination with familial risk effects, and (2) to explore these variables in other tracts. Accordingly, two different phases of our statistical analysis are reported. Our first goal was to determine if white matter integrity would differ in SLF, ILF and forceps major, tracts previously identified as being affected by either exposure to alcohol or other drugs or familial risk for alcohol dependence. Because this portion of the study was hypothesis-driven, the nominal p values can be taken largely at face value. Accordingly, the present results show significant familial risk group by alcohol exposure changes in FA for the ILF (left) and SLF (left) that are consistent with a previous report showing reduced FA in these tracts in 15–18 year olds with varying familial risk group membership (Herting et al., 2010). The present results are also consistent with findings in which binge-drinking youth differed from controls in FA in these tracts (McQueeny et al., 2009). Reduction of FA for ILF right and SLF left has been reported for youth with both heavy alcohol exposure and marihuana use in contrast to those without such history (Bava et al., 2009). Long-term alcohol exposure at a level that results in diagnosed alcohol dependence is clearly associated with reduced FA in the SLF in individuals studied at ages 28–59 (Pfefferbaum et al., 2009) and even in those with much shorter drinking histories who have significant exposure with early onset of alcohol dependence (mean=16.7 years) (Thatcher et al., 2010). Clearly, there are major age-related changes in WM microstructure (Lebel et al., 2008; Tamnes et al., 2010; Schmithorst and Yuan, 2010) as well as sex differences (Schmithorst and Yuan, 2010; Bava et al., 2011). Taking all of the studies reviewed in Table 5 together suggests a remarkable convergence in findings with respect to the effects of alcohol exposure, familial risk effects, and microstructural changes in the ILF and SLF tracts in view of variations in age, gender, and exposure histories across studies. Previous studies have typically not studied both variables and their interaction, however.
The ILF tract is a major pathway between the occipital lobe and the temporal lobe (Craig et al., 2009). It has been suggested that the ILF may be responsible for transmitting signals back to visual areas, signals that may pertain to the salience of observed stimuli so that visual processing of emotionally significant stimuli may be enhanced (Catani et al., 2003). Others have suggested that occipital-temporal connectivity may contribute to individual differences in social cognition, refinement of form, face and object representation (Barnea-Goraly et al., 2005). Previously we observed differences between high- and low-risk subjects in an fMRI paradigm designed to assess social cognition (Hill et al., 2007b). We have suggested that deficits in social cognition may be one mechanism whereby individuals may have greater susceptibility for developing alcohol use disorders.
The SLF tract contains bidirectional association fibers that link the frontal lobe to the occipital lobe and parts of the parietal and temporal lobes. The following three distinct components have been identified (1) a dorsal component originating in the parietal cortex and terminating in the frontal lobe and in the supplementary motor cortex; (2) a portion that originates in the caudal portion of the parietal cortex and ends in the dorsolateral prefrontal cortex; and (3) a ventral component that originates in the inferior parietal lobe and ends in the ventral premotor and prefrontal cortex. Although the SLF has extensive connections and shows a variety of branching patterns across its extent, nevertheless the primary connections appear to be between the parietal and frontal lobes. Functional relationships have been identified between FA in the SLF and neuropsychological performance (Karlsgodt et al., 2008; Hoeft et al., 2007). These appear to be lateralized with verbal performance being poorer in those with reduced FA in the left hemisphere (Karlsgodt et al., 2008) and visuospatial construction deficits in those showing abnormal white matter integrity in the right SLF. The present study identified less FA in the left SLF in association with familial risk and alcohol exposure.
Because neuropsychological data were not included in the present analysis, it is uncertain if impaired verbal performance was present in the subset of individuals with reduced SLF FA. Future analysis with a larger sample is planned for assessing this possibility.
Previous studies have reported impairment in frontal and parietal networks in long-term alcoholics (Pfefferbaum et al., 2010). Also, youth with a family history of alcohol dependence have been shown to have weaker frontal/parietal connectivity (Wetherill et al., 2012). The present results which find reduced FA in the left SLF in association with familial risk and greater exposure to alcohol appear to be consistent with these previous reports.
The significant RD effect found for the forceps major appears to be a new finding as previous reports addressing WM integrity by familial risk or exposure to alcohol and drugs have not noted this effect. The forceps major is a fiber bundle that connects the occipital lobes via the splenium of the corpus collosum. FA in the forceps major has been associated with the general factor of intelligence (Tang et al., 2010), although the relationship varies by gender, with males showing an inverse relationship and females a positive relationship.
The present study did not find main effects of exposure or familial risk alone for either the ILF or SLF but rather uncovered a significant interaction between risk and exposure. However, a significant main effect of alcohol exposure was seen for the anterior thalamic radiation (right). The average diffusion coefficient and both the radial and longitudinal diffusivity showed associations with the alcohol exposure variable. These results are of interest because further analysis by gender revealed that the effect was seen only in males and not females. This may not be surprising in view of the fact that males drank almost twice as much alcohol by the time of their scans as did females. Why this tract may be especially vulnerable to effects of alcohol is currently unknown. However, Pfefferbaum et al., (2009) have noted that fiber bundles showing the most consistent alcohol effects across DTI metrics in alcoholic men and women include the anterior association fibers with posterior fibers being relatively more spared.
A second phase of our statistical analyses was focused on determining if any other major tract would show differences by familial risk, exposure or their interaction. Here, a large number of exploratory tests were run so that nominal p values observed when correctly interpreted against an adjusted significance level could be interpreted as statistically nonsignificant. The additional would be viewed as tracts tested included the ATR, CST, CG, CH, IFOF, forceps minor, and uncinate. Only one of these tracts (ATR) was significant. The analysis did not show a familial risk by alcohol exposure interaction but showed a nominally significant effect due to alcohol exposure. Because this tract was part of the exploratory phase of our study, the result should be viewed with caution. However, detailed analysis of this tract did reveal changes in DTI metrics that would suggest that the association between alcohol exposure and white matter that was observed may be valid. Specifically, greater ADC and radial diffusivity were seen in association with level of alcohol exposure (highest tercile of consumption versus lower terciles).
In view of the many studies reporting main effects of either exposure or familial risk, it is of interest to examine why the present results only find interactive effects. First, most studies have not examined both familial risk and exposure within the same investigation (Table 5) so that some results reported as exposure effects may also reflect familial risk group differences as well. Second, although we attempted to characterize the exposure level by quantifying the estimated lifetime exposure for analysis of the main effect of this variable, there are collinear effects with familial risk that complicate analyses. Although our high- and low-risk subjects were studied at similar ages, the number of years drinking by the time they were scanned was significantly greater in the high-risk males studied than their low-risk counterparts (10 years versus 3.3 years). A greater number of high-risk individuals were also showing more extreme drinking and marihuana use with twice as many drinking in the top tercile of the sample distribution, and almost six times the number of high-risk subjects reporting marihuana use that would place them in the top tercile. A third possible explanation for the interactions found might be that those with a familial risk for alcohol dependence are somehow more sensitive to effects of alcohol exposure in these specific tracts (ILF and SLF). Recent attention to the important role that epigenetic factors can play across generations suggests that alcohol exposure in previous generations might confer changes in gene expression through methylation or his-tone modification of genes associated with white matter integrity (Feil and Fraga, 2012).
There are limitations to the present study that should be mentioned. First, the study sample consisted of individuals who were between the ages of 13 and 34 years at the time of scanning. This represents a period of both rapid and less accelerated development in major white matter tracts. In a sample of 168 individuals between the ages of 8–30, increases in WM volume were seen across many, though not all, brain regions (Tamnes et al., 2010). Similar findings have been noted by others (Lebel et al., 2008). Although significant age-related differences were not seen for most of the tracts examined, this may have been due to the wide variation in age across the subjects assessed. Additionally, the study did not include repeated scans of the same subjects so age-related effects were obtained from cross-sectional data.
With the use of standard TBSS procedures for developing a template, study scans from both high- and low-risk subjects were included. This may have made significant risk-group differences more difficult to detect because high-risk subjects with more substantial exposure were included. Because our goal was to perform an exploratory analysis aimed at identifying risk and exposure variation for 20 JHUA tracts with hypothesis-driven tests for specific tracts (ILF,SLF, and forceps major) FA, it appeared prudent to take a more conservative approach with respect to template formation. Our statistical approach to data analysis was not conservative (no corrections were applied). Therefore, it is possible that some of the differences seen might have been type I errors. We chose to report results without correction to best inform future studies, our own and those of others, by identifying regions most susceptible to alcohol effects and reporting all nominal p values.
Determination of lifetime exposure for alcohol presents challenges even in longitudinal studies where prospective data collection assures that subjects have minimal retrospective recall of quantity consumed. Our study design included a plan for yearly follow-up between the ages of 8 and 18 years and biennial follow-up during young adulthood (19 years and beyond). Nevertheless, subjects started drinking at varying ages, and some were unable to come in at exactly 1-year intervals. Therefore, we choose a drinking metric that was based on total reported quantity at all of the visits and adjusted to meet the number of years they had been regularly drinking. A limitation of this measure is that it assumes an equal quantity of drinking across the time period of interest, namely from drinking onset to time of scan. Clearly, quantity consumed may have shown an increase over time. However, yearly drinking density has the advantage of approximating the impact that alcohol use may have on white matter integrity by adjusting for the varying ages of onset seen in adolescent samples and the fact that timing of visits often does not conform to one's study design.
Another limitation of the study was that we were unable to conclusively determine if marihuana use is detrimental to WM integrity due to the collinearity between marihuana and alcohol use. More than half of the subjects who were the highest consumers of alcohol were also the highest consumers of marihuana making it difficult to conclude that alcohol or marihuana was causative in the observed lesser FA seen in association with such exposure. The absence of a main effect of marihuana use may reflect the fact that approximately half of the sample had never used marihuana. It is likely that years of marihuana smoking showed significance as a covariate in our analyses because those who regularly used alcohol were most likely to have used marihuana extensively.
Another possible limitation of our analysis was that some offspring were exposed to alcohol, cigarettes, or other drugs used by their mothers while they were in utero. The ideal situation would be to have offspring without in utero exposure when evaluating the effects of familial risk and personal exposure. The base rate of alcohol and cigarette use during pregnancy suggests this would probably not be possible even if a national sample were studied. Using data from a survey of eight obstetric clinics in Southeastern Michigan, Flynn et al. (2003) found that 81.9% of the mothers reported drinking less than one drink per week. In our sample, 81.1% reported no drinking during pregnancy. Thus, we find the rate of alcohol use reported by the mothers during their pregnancies is similar to that seen in the general population. Smoking during pregnancy was reported by 22.8% of the mothers in our sample. Survey data for the US and England reveal that 12–20% of mothers continue to smoke during pregnancy (Gilman et al., 2008; Office for National Statistics, 2006).
While it may be argued that mothers may not recall use during pregnancy accurately or simply choose to not disclose the full extent of their use, it appears that was not the case in our sample. Multiple points of inquiry were available for these mothers because they were most often the parent bringing in the child for follow-up evaluation. At each follow-up visit, a parent update interview covering major psychiatric disorders including alcohol and drug dependence was performed to determine the clinical status of the parent. With this information in hand, a time-line could be constructed that enabled us to determine if reported use during pregnancy was consistent with the overall picture emerging over several years of follow-up.
Moreover, performing the analysis using the mothers' lifetime history of alcohol or drug dependence as a covariate on the assumption that those with a lifetime history may have underestimated their pregnancy use did not alter our results. These considerations suggest that the risk-group differences seen in combination with the subject's own personal exposure was minimally influenced by the effects of prenatal use of substances by the mothers of these offspring.
The absence of a familial risk group effect might be considered a limitation of the present study in view of reported volumetric differences for specific brain regions (Hill et al., 2001; Hill et al., 2009a) and for total brain volume (Gilman et al., 2007). Also, family history effects on white matter integrity have been assessed previously (De Bellis et al., 2008; Medina et al., 2008; Bava et al., 2009) with one study (Herting et al., 2010) finding significant family history effects in youngsters between the ages of 11 and 15 years. However, one study that addressed family history did not find reduction in FA in the regions assessed (Medina et al., 2008) while another found only limited support for a family history effect with no significant familial risk by exposure effects (Bava et al., 2009), and one study found an increase in FA (De Bellis et al., 2008) in the corpus callosum. Another study (Bava et al., 2010) reported a correlation between ILF (right) FA and parental history of alcohol dependence in 16–19 year olds. Possibly white matter metrics associated with familial alcohol dependence risk are most apparent in younger children where exposure does not contaminate results. Alternatively, biological markers for alcohol dependence risk appear to show developmental effects so that they are most apparent in younger children as is the case for P300 amplitude, which has been shown to predict later SUD outcome best in 9-year-old children (Hill et al., 2009b).
Significant effects of age on FA were not seen for any of the tracts studied with the exception of the corticospinal tract. This may be viewed as a limitation of our study in view of previously reported increases in FA across adolescence and young adulthood (for review, see Schmithorst and Yuan, 2010). However, it should be noted that Lebel et al. (2008) reported substantial variability in age-related changes in tracts showing FA increases over the age range of 5 to 30 years. They note that the association fibers such as the SLF, and the superior and inferior fronto-occipto fasciculi reach 90% of maximum FA between ages 13 and 20 years. It should be noted that the median age for our sample was 22 years, making it more likely that across the age range studied (13–34 years) these tracts would not show age-related changes. In contrast, previous studies have consistently reported that continued brain maturation occurs during adolescence in the corti-cospinal tracts (Schmithorst and Yuan, 2010; Barnea-Goraly et al., 2005; Ben Bashat et al., 2005). Our findings indicate a significant nonlinear age-related change in FA for the CST in the full sample of 81 cases, a finding that is consistent with an exponential fit for CST age-related changes observed in 202 subjects, ages 5.6 to 29.2 years, by Lebel et al. (2008). In our study, a separate analysis within each risk group indicated that this pattern was only seen in the low-risk controls and not the high-risk sample. This finding merits further study in a larger sample to determine if familial risk confers a differing trajectory of FA development in the CST.
In spite of these limitations, there are a number of strengths that should be mentioned. Prospective collection of data on alcohol and drug exposure results in better recall of actual use than retrospective recall. Attempts to find familial risk factors that may influence FA are more likely to be revealed in studies of offspring from multiplex families selected for multiple cases of alcohol dependence within the family. Finally, it appears essential to address familial risk and lifetime exposure to drugs and alcohol to the degree it is possible within the same study. Herting et al. (2010) provided important data showing family history effects in adolescents but had minimal opportunity to find risk by exposure effects because of study design (heavier drinking youth [ > than 10 drinks by lifetime history] were excluded from the study). Three important DTI studies demonstrating exposure effects (Pfefferbaum et al., 2009; McQueeny et al., 2009; Thatcher et al., 2010) did not investigate family history and so could not have found an interaction.
Future studies need to address larger samples so that a sufficiently large number of subjects can be included by age and gender to identify critical periods when exposure is most likely to affect WM integrity and to provide an opportunity to determine the extent to which familial risk and alcohol exposure contribute to WM changes.
The authors thank the many research associates that have contributed to this research during the longitudinal study including Brian Holmes and Jeannette Wellman and research clinicians Bryan Kostelnik, M.S.W., and Carol Mazotta, M.S.W., Lisa Lowers, M.A., and Timothy Smith, Ph.D., and project statistician Bobby Jones, Ph.D. Also, the continued support of the families who have volunteered their time to this project is greatly appreciated. This research was supported by NIAAA grants AA018289, AA05909, AA08082, and AA015168 to SYH.
PubMed Central Canada is a service of the Canadian Institutes of Health Research (CIHR) working in partnership with the National Research Council's national science library in cooperation with the National Center for Biotechnology Information at the U.S. National Library of Medicine(NCBI/NLM). It includes content provided to the PubMed Central International archive by participating publishers.


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Lego Star Wars Minifigure - Yoda Jedi Master 8018
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LEGOStar Wars Yoda Minifigure, mini-figure, minfig, minifig Lego made this figure. Small, but oh so powerful.. This figure is like the one that comes in the Armored Assault Tank 8018. Item Condition Figures are new, in excellent shape and have never been displayed or played with. Shipping I DO COMBINE SHIPPING (You must wait for me to send you a combined invoice) Shipping is 1.98 for this figure. SHIPPING FOR 4 ADDITIONAL FIGURES IS FREE!!! and then 10 cents for each figure after 4. Includes delivery confirmation. (for your peace of mind) You may bid on other auctions that end 7 days later before paying. So check out my many other minifigure auctions to save on shipping. I cannot ship internationally. Thanks for looking!!!! Email me through EBAY if you have any questions.
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A hammer is an essential addition in any toolbox. Whether you're working out on the jobsite or trying to hang a picture at home, you'll want to have the right model for the job. Here are some different types of hammers and features to consider before buying a new one.
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Hammer Features
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- I'm sad to say I resigned yesterday. 9 months ago
a little more around town
- RT @TylerGreenDC: Johm Singleton Copley was ~27 in ~1765 when he painted this portrait, @ColbyMuseum. It is creepy. https://t.co/pjaw7GWF8M 1 day ago
- RT @GalleryIMA: "Cloud Pear" by Sam Chung, Stoneware, Glaze, Copper Luster, 11.5 x 7 x 5 inches https://t.co/67dXlxrf2u 1 day ago
- RT @Whatcom_Museum: Take a docent tour this weekend to learn more about our exhibits. Check our web calendar for dates and times: https://t… 1 day ago
Tag Archives: First thursday Seattle
Shift en deux! An extended show and a new location!
This is a Blue Moon event: two Shift shows, two locations, both in the Tashiro Kaplan Bldg. First, the big news: Shift is moving to a new gallery, and it's gorgeous. More space, easier access, all kinds of good, so … Continue reading
Posted in New shows Tagged Art, Artists, First thursday Seattle, jen grabarczyk, Ken Barnes, painting, pioneer square, Ruthie V., sculpture, Seattle art 2 Comments
July @ Shift: Ken Barnes and Jen Grabarczyk, First Thursday July 11
Pretty much all of the Pioneer Square First Thursday scene is switching to July 11 this year, due to our national birthday celebration. Shift is very pleased to follow suit with its opening and artist reception for Ken Barnes and … Continue reading
Surprise! June @ Shift, works from Clamor, UW Literary & Arts
We're super excited to offer a bit of Clamor for you in June: Clamor is the UW-Bothell Literary & Arts journal, and Shift is honored to host intriguing selection of works from Clamor through the month of June. Think of … Continue reading
Posted in New shows Tagged clamor UW, collaborative, collaborative installation, First Thursday, first thursday art walk, First thursday Seattle, installation, Mixed Media, new works, Seattle art, Seattle Artwalk, Shift Collaborative, Shift Collaborative Studio, Tashiro Kaplan, UWB literary arts Leave a comment
Inside/Out @ Shift in May: Street Art Considered, by Daya B. Astor & Liz Patterson
PSquare streets will be buzzing with lots of new shows and free parking, so come on down. Shift Collaborative Studio is very pleased to present Inside/Out by Daya B. Astor and Liz Patterson–an exploration of urban street art. Mixed media artist … Continue reading
Posted in New shows Tagged Art, Art Walk, Artists, artwalk, Collaborative Studio, Daya B. Astor, First Thursday, first thursday art walk, First thursday Seattle, graffiti, graffiti artist, Liz Patterson, Mixed Media, new works, Seattle, Seattle art, Seattle Artwalk, Shift Collaborative, Shift Collaborative Studio, street art, Tashiro Kaplan Leave a comment
Adele Eustis @ Shift in April–lit from within
Adele Eustis has created an engaging installation of structures made of woven bent branches, wire, light, silk and jute–they are like nests, like a private world, illuminated and welcoming, strange and wonderful. Rosemary Ponnekanti of the Tacoma Tribune described them: … Continue reading
Posted in New shows, Uncategorized Tagged Adele Eustis, Art, Art Walk, Artists, artwalk, Cass Nevada, collaboration, Collaborative Studio, First Thursday, first thursday art walk, First thursday Seattle, illumination, installation, nature, sculpture, Seattle art, Seattle Artwalk, Shift Collaborative, Shift Collaborative Studio, Tashiro Kaplan Leave a comment
Adele Eustis and Cass Nevada @ Shift in April
Shift Collaborative Studio is pleased to present an engaging show of nature in April for your contemplation: Adele Eustis' new show Issue reveals a world illuminated from within. Around these cocoon-like structures are silk, wire, bent wood branches, jute and … Continue reading
Posted in New shows Tagged Adele Eustis, Art, art of nature, Art Walk, Artists, artwalk, Cass Nevada, cocoon sculpture, Collaborative Studio, drawing, First Thursday, first thursday art walk, First thursday Seattle, illuminated art, ink drawing, installation, Jen Graves at the Stranger, LED sculpture, murmuration, nature, nest sculpture, pioneer square, Seattle art, Shift Collaborative Studio, slog, swarm, Tashiro Kaplan Leave a comment
Shift in March: Ed McCarthy
Ed McCarthy likes to play with wood. And metal. And lots of other materials, so his work is usually pretty intriguing. His show in March is no exception; in his own words, he recalls a love of sculpture to which … Continue reading


text: I have a major dilemma that I need some help with. Most of the time, when my band does not hire sound, I use only my amp w/ no mics, as we don't have a huge PA system. When we play larger clubs, house sound is provided, or we hire. I am trying to figure out what is best, going direct to the PA, or having my rig mic'd. The sound when I go direct sounds very thin and tinny to me, and the bad tone really screws with my mood/playing. I am used to the tone I play with, and most comfortable with it, so the most logical idea for me is to have my rig mic'd. I want to avoid the situation where my tone doesn't sound good to me (going direct), but don't want to sacrifice the sound of the entire band just for my sake. I do have a zoom b3, and was wondering if I just go direct from that, if it would be a good solution. Any help is appreciated. I have a gig on Thursday night that is a pretty big one for my band, and want to sound as good as possible. Thanks in advance!


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|04 Jul 2011
Issues with Mass Effect 1
About a year ago-ish, I recieved "Mass Effect 1" that my sister bought for me from eBay (much obliged, Sister-thing). However for the life of me I can't get the game to work and I was hoping if someone could help me with this problem.
Before someone asks, yes I have installed the recent patch for the game.
I started trying to get to game running again yesterday and one of the solutions I saw someone suggest was instead of choosing the default file locations (which was in Program Files (x86)), create a new folder in the C: section and put the game in there, so I tried that.
I have also tried setting it to the appropriate compatibility mode (I've tried several different compatibility modes), but that did work either.
I'll explain what's been happening:
So for my first try I right-clicked the desktop icon of the game and selected "Run as administrator". Then I selected the "Play" button when the box-thing showed up(I'm an idiot, forgive me). It began to load the game and then I was give a black screen where I waited for several minutes until I finally pressed the key at the bottom of my keyboard that has the white window on it (I forgot what that key is called), where I see I've recieved this message:
"General protection fault!
History: GMatrix2D::Swap() Address = 0x10bb5ed6 (filename not found) [in C:\Games\Mass Effect\Binaries\MassEffect.exe]
Address = 0x1c1f3ce4 (filename not found)"
The next thing I tried was going to the Binaries folder (C:/Games/Mass Effect/Binaries) and selected MassEffect.exe instead. So I right clicked it, selected "Run as administrator" and instead of taking me to the box where I click play before loading the game, it skipped it and went straight to loading the game. But then I recieved the same problem as I did with my 1st solution.
The next thing I noticed (it's not really important but I feel the need to mention it) is that when I go to My Documents, I find I have 2 Bioware folders for the game. The 1st one is the one that has "Mass Effect", "Dragon Age: Origins" and "Dragon Age 2", and the other one just has Mass Effect. I thought that was a little weird ....
I have a Windows 7 Home Premium x64 bit laptop developed by Toshiba.
|My System Specs
|04 Jul 2011
Windows 7 pro 64bit. (SP1)
it would be nice to know not only your pc brand and os but other specs.. like video card etc.
maybe you just need some drivers or software intall/upgrade
because games ofter require for example Visual C++ runtimes, .net framework etc.
|My System Specs
|04 Jul 2011
|My System Specs
|04 Jul 2011
Windows 10 Pro
First off system specs would be immensely helpful here.
Ok, first off we cant help if you dont supply the most basic of information systems specs. The importance of this cant be overstated since game performance is highly dependent on your hardware. Please see this tutorial on filling out system specs as well as my How To Ask For Help guide.
Also do you have SP1 installed for Windows 7? If so, see this post - https://www.sevenforums.com/gaming/15...installed.html
|My System Specs
|Thread Tools
|Similar help and support threads
Mass Effect
I bought Mass Effect (1) yesterday and was really looking forward to playing it today. The install went well. However when I start the game and press play it gives me an error message about the configuration utility not working. Details as follows: Problem signature: Problem Event Name: ...
mass effect 3
soooooo has anyone else seen the gameplay and new trailers from e3? thoughts/worries/rants? i think its looking great and the upgraded movement looks amazing. cannot wait for it to be released.
So I bought Mass Effect 2...
So I just picked up Mass Effect 2 Collectors Edition (PC) today. Beautiful looking package. According to Amazon.com, the package weighs about a pound which includeds a tin case containing 3 discs game install discs 1 & 2, bonus materials disc 3, manual. You also get another cardboard box...
Mass Effect 2 Help please.
Sorry to post this again cause someone already posted it I think but the situation was explained by faulty RAM but my issue is different. I got this awesome game Mass Effect 2 and got an FPS lag every 30 seconds or so. Here are my PC Specs: OS: Windows 7 Ultimate x64 Motherboard: MSI P6n...
Mass Effect 1
I'm sorry if this has been answered, if it has please point me in that direction since i've spent the last hour trying to find that answer. I've just installed mass effect 1, installed the new patch 1.02 and Bring down the sky, yet when i pull up ME and tell it to play, the mouse will turn to...
Mass Effect
Mass Effect (digital download) runs perfectly on build 7000. No problems. :)
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text: Shares in Finnish shipping company Finnlines plunged on Wednesday after it said 2000 profit would be worse than expected due to tough competition, higher oil prices and strikes hindering business. On Wednesday shares were trading down 12.5 percent at 23.99 euros, under-performing already soft Helsinki shares. In February Finnlines posted a 1999 profit before extraordinary items of 67.3 million euros ($64.46 million) and said the outlook for 2000 was uncertain due to factors such as tighter competition and a drop in import volumes. Finnline's released statement, reads in part as follows: A strong imbalance exists between exports and imports of unitized cargo in Finland. Since the company has wished to maintain its export service at the level requested by its customers, no measures have so far been taken to reduce cargo capacity. Competition for imported freight has led to unhealthy price levels. The volume of Russian transit traffic has remained low. The continuing high price of oil has raised operating costs significantly and it has been possible to transfer only a small proportion of these costs to freight prices owing to the intense competition. Ongoing industrial actions in Finland have caused substantial harm to the maritime industry and port operations. Sympathy strikes have been held at Finnish ports since March 14, 2000 to expedite negotiations in a dispute involving bus drivers in Tampere. This has severely curtailed material flow and hampered port and shipping operations. A strike by truck drivers on March 29, 2000, a consequent lock-out by employers, and a sympathy strike by seamen and stevedore workers called by the truck and transport workers union have effectively brought the entire sea transport business to a halt.


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Articles tagged with 'Hacking Chinese'
Back-to-school Hacking Chinese course discount
The start of a new semester is the right time to accelerate your learning with Hacking Chinese – A Practical Guide to Learning Mandarin. Get $10 off the course and bonus extra content until Saturday, August 19th!Read →
Chinese New Year and New Semester Course Discount
To mark the Chinese New Year and the start of a new semester, I offer a time-limited discount for my video/audio/text course, valid until the end of Thursday next week (February 2nd).Read →
Extra course content and new-semester discount
I have added content to my course in the form of a study checklist highlighting things you can do to upgrade the way you're learning Chinese. I also offer a new-semester discount for the course, valid until the end of Thursday next week (September 8th).Read →
I have published a book!
I have published a book! It's called Hacking Chinese: A Practical Guide to Learning Mandarin. Get the paperback now and get the audio version for free!Read →
Launching Hacking Chinese: A Practical Guide to Learning Mandarin
I'm proud to announce the launch of a new course: Hacking Chinese: A Practical Guide to Learning Mandarin. It's the result of thousands of hours of work and just like the Hacking Chinese website, it is about how to learn Chinese in a better way. The course consists of video episodes, an in-depth e-book and an audio version. Get it before Christmas for a handsome discount!Read →
Launching Hacking Chinese Resources
"Resources" is a new section of Hacking Chinese that strives to provide you with resources for learning Chinese suitable to you. Everything is neatly tagged by difficulty level, topic/skill and type of resource, enabling you to find whatever you need, whenever you need it.Read →


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Part of the work we do at PI is to promote national legislation and public policies for the protection of HRDs. We believe that taking the necessary measures to guarantee appropriate protection of HRDs is the responsibility of the executive and the judiciary. We understand national protection mechanisms as public policies designed to improve the protection of HRDs in countries where they are attacked as a consequence of their work. These mechanisms are created by governmental policies and pieces of legislation and run by official bodies (i.e. recently created or ad-hoc bodies, or newly created functions attached to pre-existing bodies, like the Office of the Ombudsman).
Why is it necessary for the state to create specific mechanisms (laws, offices, policies) dedicated to the protection of defenders? Would it not be enough to make sure the existing institutions (the legal system and the security forces) fulfill their obligations and guarantee protection? Because mechanisms made available to HRDs generally have very limited power for implementation, in a legal sense as well as in a practical one, since these bodies lack the necessary resources and are unable to either launch an investigation or to wield any political power to guarantee appropriate protection for defenders. Although we admit the potential weaknesses of such legislation and mechanisms, we also feel that they can open a door to an improvement in protection, be it by making it easier to access otherwise inaccessible places, or by providing immediate support that can solve serious protection issues, at least in the short-term.
As part of our commitment to promoting national legislation and mechanisms for the protection of HRDs, we have undertaken research work and systematization of best practices and lessons learn. On this basis we have published a handbook titled "Protection of human rights defenders: best practices and lessons learnt". It is a symbol of our work in many aspects, a compilation of the effective work carried out by defenders in many countries, with whom we collaborate directly in many cases through our Protection Desks.
In addition to this we have been working in a training and advisory capacity for different defenders´ organizations, United Nations and Government officials on this topic.
To the same end, we have created another tool: Focus, a Global Observatory for Public Policies on the Protection of Human Rights Defenders.


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MOVIE SYNOPSIS [ General Audiences ] When a crown Crystal Empire stolen, Twilight Sparkle chases the thief into an alternate world where she will become a teenager who must survive his biggest challenge ... high school. With the help of her new friends that remind Applejack, Rarity, Rainbow Dash, Pinkie Pie and Fluttershy of Ponyville, she embarks on a quest to find the crown and change the fate of these two parallel worlds. You can watch My Little Pony: Equestria Girls online on TV cable or theaters with original audio in English at different dates. This film premiered in theaters in 2013.
Rating: 5 by 2892 users./
Runtime: 72 minutes
Tara Strong, Ashleigh Ball, Andrea Libman, Tabitha St. Germain, Cathy Weseluck, Rebecca Shoichet, Lee Tockar, Richard Ian Cox, Nicole Oliver, Vincent Tong, Britt McKillip, Shannon Chan-Kent, Kazumi Evans, Kathleen Barr, Claire Corlett and Michelle Creber.
Animation, Family, Comedy.
72-minute film (full movie) directed by Jayson Thiessen.
The original audio of My Little Pony: Equestria Girls has dialogues in Dolby Digital, it was produced in Canada, USA.
It premiered in cinemas or television in 2013.
Screenplay written by Meghan McCarthy and Lauren Faust.
Chris Bartleman, Sarah Wall, Devon Cody, Kirsten Newlands and Stephen Davis.
This film was produced and / or financed by DHX Media and Hasbro Studios.
Composed by William Anderson.
Strategic Entertainment Solutions, Screenvision, Clear Vision, Tiny Pop, The Hub, Shout! Factory, Edel Media & Entertainment, Pop TV, Cineplex and Madman Entertainment.
Without commercial breaks, the full movie My Little Pony: Equestria Girls has a duration of 72 minutes; the official trailer can be watched in streaming on the Internet. You can watch this full movie free in EnglishDolby Digital in movie TV channels, renting the DVD or with VoD services (Video On Demand player, Hulu) and PPV (Pay Per View, Netflix).
See the page of this full movie, My Little Pony: Equestria Girls in FULLTV Movies.


text:
Websites Made With Pride !
New Jersey School Buildings & Grounds Assoc.
Content managed responsive website with
Membership Portal, News and Events Manager
& SEO Friendly URLS.
Expand Placement Group
Responsive and Retina Ready Website Design
for New Jersey based financial placement firm,
Expand Placement Group.
Sparta Dragon Boat Festival
Northern Pride donated Strategic Consulting,
Web Design and Development services to
create the Sparta Dragon Boat responsive web site.
This annual event benefits the school children
of Sparta, New Jersey public schools.
I.D. Systems, Inc.
Database driven content managed
responsive web design.
A diverse client base, from a wide variety of industries,
organizations and backgrounds.
organizations and backgrounds.


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Well, it looks like it might be another one of 'those' winters and I can tell you that I am NOT happy about it!
I decided I should just make the best of it and thought I would share some snowy ideas straight from Canada! My friend Jane Feener has some ideas you will want to check out.
And if you want to make today even better, be sure to check out this dollar sale I'm having with a few of my Indiana buddies. Did I say that everything here is just a dollar? Can't beat that! Happy Shopping!


text:
The following Official Record for Rigoberto Cornejo is being redistributed by LCN and is protected by constitutional, publishing, and other legal rights. This Official Record was reported on 2014-01-21 08:58:30. The person named in this listings has only been arrested on suspicion of the crime indicated and are presumed innocent.
Arrest Information for Rigoberto Cornejo
|Arrest Name
|Rigoberto Cornejo
|XXXXXXek Ct (VERIFIED)
|City, State
|Newman, CA
|Arrest Date
|Arrested For
|Possession of Controlled Substance
Possess Control Substance Para
Possess With Intent To Use Vehicle Master Key
Stop Requirement
Wish to be removed?
If you wish to remove your arrest information from our website, please use our removal form found by clicking "unpublish record" below.Unpublish Record


text:
The Download link for Backtrack 5 has changed to, http://www.wirelesshack.org/backtrack-5-download
Reaver now comes installed with Backtrack 5 R2 and higher, so installing it is no longer necessary. Use the command reaver –help to see if it is installed.
Here is step by step tutorial for Reaver and Backtrack 5 WPA WPA 2 crack. Once running it should take no more then 2 to 10 hours to crack a WPA WPA2 encrypted router and spelen roulette online voor geld.
For more information check out the Kindle eBook "Step by Step Kali Linux and Wireless Hacking Basics" http://amzn.to/1HAaUS0


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Orlando Pirates Under-19 winger Siboniso Liedson Baraka Junior has stated his desire to play for Ghana rather than South Africa.
The 18-year-old wing wizard, who has been likened to Portugal international Cristiano Ronaldo because of his skills, pace and eye for goal, is one of the highly rated young footballers in South Africa.
"My mother is a Ghanaian and my dream is to play for Ghana. I am currently in Ghana for holidays and I like the country so much," Baraka told Goal Ghana.
"I am looking forward to play in the next Under-20 for Ghana and I am working hard towards that."
The teenager has featured for the Malaga Academy in Spain, Black Leopards, Italian Serie C side FC Catanzaro and also the U17 side of Danish club FC Fyn. He also played for the Dutch national U16 during his stay in the Netherlands.


text:
HB Racing Hard Steel Driveshaft 76mm (Cyclone D4)
HB Racing
This item is discontinued and no longer available for purchase. You may want to search our site for a similar item.
|Low Price:
Discontinued Online
This is a replacement 76mm hard steel front drive shaft from Hot Bodies. This drive shaft connects to the front axle to provide drive to the wheels.
This product was added to our catalog on September 12, 2007.


text:
September 4, 2016
Man City captain Vincent Kompany nearing fitness: Belgian has had series of blood tests
The Manchester City captain, 30, suffered a thigh injury nine minutes into the Champions League semi-final clash away to Real Madrid in May.
It was the latest in a long list of cruel muscle injuries which wrecked large chunks of last season and forced Kompany out of Euro 16.
But City specialists now report that the damaged muscle is "clean" – although blood tests last week were still not perfect.
Kompany, though, is well on the road to full recovery and came through a midweek practice match behind closed doors without a problem.


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The new 80kmh speed limit; the Me-First-Drivers and those rude cyclists
Tell Eddie
After reading: "Now it's up to you to set your own, lower speed limit" (Motors, 25th March) I'm beginning to wonder if our Road Safety Authority has finally lost it.
With much fanfare, including full-page ads in the national press, they have informed us that the old 80kmh speed limit signs are to be replaced by new ones which mean, and I quote, "drive at the right speed for the road, and always under 80 kmh". Isn't that exactly what the old ones meant?
As you say yourself regarding posted speed limits: "...a speed limit is not a target; it is the maximum permitted on a given stretch of road".
So, very often, prevailing conditions and common sense will dictate that a speed far lower than that posted should be chosen. This has always been the case.
So, how much has been squandered on this useless exercise? The article includes a photograph of the Road Safety Authority CEO and the Minister for Transport demonstrating the new signs.
The minister is holding one which seems to depict an adult and a child playing football on a road, with a vehicle approaching.
When I was a lad, we were always told by our parents that roads were for cars, not for playing football on.
Am I now to assume that the official line from both our Government and the Road Safety Authority is that this principle has gone out the window?
Denis, Dublin
I live in a quiet country area but drive a fair bit to and from nearby large towns.
I cannot believe how rude some drivers are in towns.
The last thing they think of is a bit of courtesy towards other drivers or letting someone out of a side road.
I was always taught to give others a chance. The mantra now seems to be to give them no chance.
How have we become such a nation of Me-First-Drivers?
Marianne, Galway
I know many motorists don't like to be seen to criticise cyclists because they can be accused of bias.
But I feel compelled as someone who does a fair bit of driving in the general Dublin area to say that some of those on two wheels are a disgrace.
I could take up all your letters space with examples of what I can only describe as boorish behaviour.
All I can say is that if motorists carried on like that - going up one-way streets, cutting across in front of others - they would be banned.
I have nothing against cyclists in general but there are some, I agree a small number, who are giving the rest a bad name.
Ian, Malahide
Indo Motoring


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Burden is the degree to which you are distracted from your own patterns, your own rhythms. Anything that doesn't resonate with your internal sense of self will be perceived as a burden. The reason burden, and bearing it arises, is because we have come to ignore our true natures, often to the detriment of our physical and mental health.
There is a way that we can be in the world, but it begins by putting our personal presence first. Only then can we be present for others and others be fully present for us. The only good you have to offer is your own good. The only good you can really receive is your own good.
All burden is paradox. In every vision of burden, you have the secret of freedom as well. If life is burden then Atlas will inevitably weep, but if life is the place where you live, then even the biggest challenges will leave no lasting scars.
"Every burden is a blessing." Walt Kelly
"No burden is so heavy for a man to bear as a succession of happy days." Max Planck


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Facilities Maintenance Regional Service Process
Over the past decade, the department has been faced with continued reductions in General Fund resources, tremendous growth in University facilities and more technologically complex facilities systems. FM has set out to improve its operating model by shifting to a highly planned and scheduled service process.
By moving to a regional approach for providing maintenance services to the campus community, we are creating cost and performance efficiencies through
- reducing travel time between the Central shops and campus
- having all job classifications present on-site
- implementing planning/scheduling for all staff
- pre-planned procurement or kitting for job materials
- increased use of electric vehicles
Each region has been fully staffed with our skilled tradespersons in HVAC, plumbing, pumps, steam distribution, electrical, fire systems, elevators, roofing, central monitoring and specialty preventive maintenance work. We continue to provide quick response to service calls and focus on preventive and predictive maintenance.
Through it all, Facilities Maintenance remains committed to meeting our customers needs and we continue to tailor our customer service through service level agreements.
We welcome your questions, concerns, and compliments via email, at FM COMMENTS (get address), or telephone, at (734) 763-5075.
To request services see "Obtaining Work Orders".
Content modified: 11:25 am September 09, 2016


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welcome to join this travel party!
Reply from Kevin Chen is flagged as not relevant.
cOOL...I LOVE travel....
Reply from Jenny&King is flagged as not relevant.
sorry 。。 No english
u can read some chinese right my darling!
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