text:
Mad Men
by KMSpider
Chase sat quietly in the near-deserted cafeteria sipping coffee out of a Styrofoam cup, mulling over the events of the day. House taken Hostage, along with 13 and a group of clinic patients. Functions all over the hospital had been disrupted, which explained the empty cafeteria.
Chase looked up as Kutner plopped onto a chair next to him.
He watched as Kutner rested his elbows on the table and tiredly rubbed his face.
"Crisis over?" Chase ventured a guess.
Kutner spread his fingers and peeped out. "What a day," he moaned, clearly exhausted.
Silently, Chase used one finger to push his cup of coffee over to the younger man.
Kutner's hands fell away from his face and he claimed the cup with a sigh, taking a long pull of liquid.
"Thanks, man."
"House solve his case?"
"Yeah. Cameron got it, actually. Chronic melioidosis. Guy nearly killed 13, but Foreman's looking after her."
Chase raised an eyebrow at that. Foreman and 13? Interesting. He's have to tell Cameron.
Kutner fell silent and took another sip of coffee. It was probably getting cold by now.
Suddenly Kutner placed the cup on the table and began to talk in a low voice, looking down at his hands. "My parents owned a Mom & Pop store. When I was 6, a man robbed it and shot them both."
The cafeteria felt like a confessional, and Chase listened like a priest. When Kutner fell silent again, Chase said, "A couple of years ago, a man walked into Diagnostics in the middle of a differential and shot House."
Kutner's eyes widened.
"Shot him once in the stomach. Both Foreman and I stepped forward to help, but the gunman turned the gun on us, warning us off. House was already on the ground and the guy shot him again. This time in the neck."
"God," whispered Kutner.
"Then he just turned and walked away. Like it was nothing."
"Is that how he got the scar there?" Kutner asked, touching a spot on his own neck.
Before Chase could answer, a voice behind him said, "Is this gonna be like Jaws where Quint, Hooper, and Brody start comparing scars?"
Chase and Kutner looked up at the sound of House's voice. House's hand rested for a moment on each of their shoulders before releasing them. Then he moved to the other side of the table and sat down.
"Lethal Weapon," Kutner countered.
"Jaws did it first," House corrected.
"I see you survived," Chase commented.
"No thanks to you," House shot back, making Chase flinch.
"You had six other doctors working on it," Chase replied mildly.
"But not you," House pointed out, studying the Australian.
"There was a hospital full of people who needed help and decided not to use a gun to get it."
House gave him a probing look. "But that's not the reason you left, is it?"
Chase signed. It had been awhile since he'd been under House's lens of scrutiny.
Kutner's round eyes darted back and forth between his boss and the young surgeon, like a tennis match. "Maybe he just decided to not give in to a mad man," Kutner offered. "On principle."
"Wish I'd had that choice," House said, and Chase looked away guiltily. "Tell the truth, Chase. That's not the real reason either, is it?"
"Maybe I just don't like guns," Chase offered, and Kutner nodded agreeably.
"It's not like he shot YOU last time," House prodded.
"No. I just got to watch!" Chase snapped back, looking away, instantly regretting his outburst.
"Ah," House said, as if he had just solved something.
House's eyes flicked to Kutner than back to Chase.
"I can't promise that it will never happen again, but..." House's voice trailed off, then quietly finished. "I'll try."
Chase nodded, head bent, hair obscuring his face, but House noticed a slight easing of his shoulders.
Kutner grinned and pushed the coffee cup toward House.
House nodded in thanks and took a sip... and immediately spit it back into the cup.
"I survive a hostage crisis and you try to kill me with BAD COFFEE?" House gagged.
Kutner and Chase chuckled, and Kutner jumped up to fetch three new cups.
House and Chase watched him go.
"I'm glad you're okay," Chase said, eyes still on Kutner.
"Think I can claim Post Traumatic Stress whenever I have Clinic duty?"
Chase grinned. "Should work for about a month, at least. If you work Cuddy's guilt just right, maybe two."
Kutner set down the cups just as Wilson entered the room.
"House! The police want to take a statement. Cuddy's looking for you."
House grabbed his cup, and swung himself out of his chair. "This is worse than clinic duty. Have you seen that guy. He has less a sense of humor than Foreman," he declared.
"Is that even possible?" Kutner asked.
"Apparently. Come on, Jimmy, we've got to find a good place to hide!"
House and Wilson headed for the door. "Go home, boys," House tossed over his shoulder on his way out.
Chase and Kutner watched Wilson herd House out of the room, then silently clinked cups together, grinning.
The End.


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An Elephant Makes Love To A Pig
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An Elephant Makes Love To A PigAn Elephant Makes Love To A Pig (1997) Season 1 Episode 105- South Park Cartoon Episode Guide
This page has been viewed 46 times this month, and 517 times total.
>Unknown Tag: 'short_stud_crew'
- Comedy Partners
- Animated Characters: Principal Victoria, Liane Cartman, Sharon Marsh, Sheila Broflovski, Mrs. McCormick, Nurse Gollum, Wendy Testaberger, Mrs. Crabtree, Bebe Stevens, Stan Marsh, Eric Cartman, Randy Marsh, Mr. Herbert Garrison, Philip Niles Argyle, Timmy, Jimmy Swanson, God, Satan, Mr. Mackey, Tom the News Reporter, Clyde, Grandpa Marvin Marsh, Miss Diane Choksondik, Ned Gerblanski, Officer Barbrady, Big Gay Al, Mr. Hankey, Dr. Alphonse Mephesto, Dr. Doctor, Twong Lu Kim, Bill Clinton, George Bush, Kyle Broflovski, Kenny McCormick, Gerald Broflovski, Stuart McCormick, Jimbo Kearn, Terrance Henry Stoot, Leopold "Butters" Stotch, Tweek, Jesus, Saddam Hussein, Pip Pirrup, Priest Maxi, Shlomo, Chef.
- First Aired in 1997.
- Episode Number: 105
- Running Time: 30 minutes.
- Season: 1
- Color
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Working title: "An Elephant Fucks A Pig."
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subset: commoncrawl


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I have a hyper v setup, since It was done there have been odd occurrences on the network. People not being able to log in sporadically, or logging in to find that there drives haven't mapped.
This was happening all over the network (350 +), with nothing in common. It was never the same people, machines or locations and would only last a couple of minutes if that. Normally trying again would sort it out.
This has been going on for several months, but with little to go on, and the fact that it was merely annoying a couple of people a day I had to press on with other things.
Last week I was finally able to start digging. I believe it coming from DHCP, as this would explain the sporadic nature, and people not logging in due to not having an ip.
Ive been monitoring my dhcp service which is sitting on domain controller on Hyper V. I've found that it is dropping packets, returning nacks and queuing requests. It is doing these things more often when under higher loads, such as entire room starting up after lunch.
I would assume that the server is struggling with multiple processes. But im not an expert on such matters and would welcome advise. Is it good practice to have your dhcp on hyper V. What kind of resources should it have. Currently it has 1gig of RAM and is sharing 2 dual core xeons from about 3 years ago (I dont have the specifics to hand) with a file server, and small print server.
And if your still reading at this point thanks!
17 Replies
Jun 17, 2010 at 8:26 UTC
I've got a DHCP server running in a Hyper-V guest just fine. Have you checked the DHCP logs, normally in c:\windows\system32\dhcp ?
Jun 17, 2010 at 10:22 UTC
Yeah Ive checked the logs, theres nothing to pinpoint a cause. Its just a list of renews with the occational nack etc.
Jun 17, 2010 at 10:49 UTC
You say 350 devices, how is it subnetted? Is it running out if IP addresses? Are you sure there are no other DHCP servers running anywhere?
Jun 18, 2010 at 4:30 UTC
We get are address range from local council as were a college so we have a 255.255.252.0 mask on an internal a range. We have 4 ranges of 255, and about 100 - 200 left.
Is there an easy way to check for another dhcp server?
Jun 18, 2010 at 7:52 UTC
Probably the quickest way would be to check one of the computers the next time the issue happens - run ipconfig /all and it should tell you the DHCP server it received the address from.
You may also want to make sure Conflict Detection is set up with 1 or 2 tries before it hands out an address.
Jun 18, 2010 at 9:16 UTC
Ive done the ipconfig and theres no dhcp server entry and it will have 169. I think conflict detection is in place. But there was no mention of a conflict in the reports ive been running. Just drops.
Jun 21, 2010 at 10:53 UTC
I would check the vNic you have for the DHCP server, is it a legacy NIC?
Jun 22, 2010 at 5:33 UTC
Im not an expert in such matters, so if I say anything idiotic or miss the point do forgive.
In the vhds, network adapter settings, I have LAN set for the network, Dynamic for the MAC. Enable virtual LAN identification was not set.
I Dont think it is legacy as at the bottom the is a message saying Use a legacy network adapter instead of this network adapter.
Jun 22, 2010 at 6:32 UTC
You could try swapping the NIC for legacy NIC, I had a number of issues with Hyper-V and NIC when it 1st came out!
Jun 23, 2010 at 3:34 UTC
Could you give a step by step of what that would involve please? Unfortunatly it wasnt a natural upgrade for me to hyper V, they were dumped on my lap.
Jun 23, 2010 at 6:26 UTC
Hmmmm, dont have Hyper-V anymore, from memory, edit the VM settings, remove current NIC, add new legacy NIC...O/s shouldnt know any difference, you may need to bring the VM down while editing...
Jun 24, 2010 at 3:49 UTC
Cool, Ill have a look into it. Thanks for your help.
Jun 24, 2010 at 3:55 UTC
I have another hyper v issue thats worth asking. I expanded my fileservers vhd by 150 gb but the C:\ and D:\ drive on the fileserver dont reflect it, is there another process I need to do?
Jun 24, 2010 at 3:51 UTC
You'll have to use Disk Management (or commandline diskpart) to expand the volume inside the VM. This is the same as imaging the drive to another larger drive - you still have to expand the volume.
Jun 24, 2010 at 6:41 UTC
Probably easier to attach the partitions to another 2003 VM and expand from disk management, otherwise as c: is a system drive, you wont be able to do it on its own o/s
Jun 24, 2010 at 7:56 UTC
Server 2008+ it's possible :D
Jun 25, 2010 at 3:07 UTC
Whod a thought it would be that simple lol. Ill expand them today. I dont suppose anyone can reccomend any good reading for hyper V. The brass in my place brought them on the spur of the momnet after a smooth sales pitch. The company who got the sale, also said they would provide support and training. Then the only guy at the company who knew hyper v left. Which then resulted in me having to pick up as and when.
This discussion has been inactive for over a year.
You may get a better answer to your question by starting a new discussion.


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Cheree and Desaree Model
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About MeMy name is Mariah, I'm a junior at Nevada Virtual Academy. Doing my classes online gives me the flexibility to pursue my dream of becoming a model. I'm a hard worker quick learner and always put my all into everything. I take my future very seriously. I'm looking for new doors to open & seeking different modeling / fashion opportunities. I'm always smiling and laughing. I work well with other people. My passions are fashion, music & belly dancing. Under no circumstances will i shoot nude erotic or as implied. I look forward too meeting/working with people!
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The article you requested is
Low 24-Hour Adiponectin and High Nocturnal Leptin Concentrations in a Case-Control Study of Community-Dwelling Premenopausal Women With Major Depressive Disorder: The Premenopausal, Osteopenia/Osteoporosis, Women, Alendronate, Depression (POWER) Study
Giovanni Cizza, MD, PhD, MHSc; Vi T. Nguyen, MD; Farideh Eskandari, MD, MHSc; Zhigang Duan, MS; Elizabeth C. Wright, PhD; James C. Reynolds, MD; Rexford S. Ahima, MD, PhD; and Marc R. Blackman, MD, for the POWER Study Group
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Objective: Major depressive disorder (MDD) is associated with immune system dysfunction and disruption of multiple circadian systems. Adiponectin is an adipocytokine with anti-inflammatory and antiatherogenic effects. Circulating concentrations are inversely related to adiposity and risks of metabolic syndrome and diabetes mellitus. Our goals were (1) to establish whether premenopausal women with MDD exhibit decreased plasma adiponectin concentrations and/or disruption of circadian adiponectin rhythmicity; (2) to assess whether there is a relationship between adiponectin and MDD; and (3) to explore the temporal relationships among adiponectin, leptin, corticotropin, and cortisol secretion.
Method: We conducted a case-control study of community-dwelling premenopausal women with DSM-IV MDD (n = 23) and age- and body mass index (BMI)–matched control subjects (n = 23). Main outcome measures were circulating concentrations of adiponectin, leptin, corticotropin, and cortisol measured hourly for 24 hours. Subjects were recruited from July 1, 2001, to February 28, 2003.
Results: Women with MDD had approximately 30% lower mean 24-hour concentration of adiponectin than did control subjects. Adiponectin concentration was inversely related to depression severity and total duration of disease, suggesting a causal link. In contrast, mean nocturnal leptin concentration was higher in the MDD versus control groups. Mean leptin concentration was inversely related to cortisol and adiponectin concentrations, both in subjects with depression and in control subjects. In cross-correlation analyses, the relationship between corticotropin and cortisol concentrations was stronger in women with MDD than in control subjects, a finding consistent with hypothalamic-pituitary-adrenal (HPA) axis activation in MDD.
Conclusions: In premenopausal women with MDD, reduced daily adiponectin production may increase the risk of diabetes mellitus, and elevated leptin may contribute to osteoporosis.
J Clin Psychiatry 2010;71(8):1079–1087
Submitted: April 27, 2009; accepted November 17, 2009.
Online ahead of print: May 18, 2010 (doi:10.4088/JCP.09m05314blu).
Corresponding author: Giovanni Cizza, MD, PhD, MHSc, NIDDK/NIH, Bldg 10, CRC, Rm 6-3940, Bethesda, MD 20892-1613 (email@example.com).
© Copyright 2010 Physicians Postgraduate Press, Inc.
Major depressive disorder (MDD) is a mood disorder with important consequences for the endocrine and immune systems. It affects approximately 17% of the general population, with increased morbidity due to central obesity, type-2 diabetes mellitus (T2DM), and cardiovascular disease (CVD).1–4 Major depressive disorder is accompanied by disruption of the hypothalamic-pituitary-adrenal (HPA) axis5 and disordered corticotropin secretion.6 A disruption of circadian rhythms in MDD suggests that other endocrine systems are affected. The prevalences of T2DM and CVD are higher in subjects with MDD.7 White adipose tissue, an organ with endocrine functions, secretes the adipocytokines, leptin, and adiponectin. Leptin was described in 1994 by positional cloning of the ob gene.8 Leptin is produced in proportion to total body fat, and it signals to the central nervous system (CNS) the amount of energy stores to regulate food intake and energy expenditure.9 If adequate body fat is present, energy can be expended for costly processes like reproduction and growth.10 Leptin modulates several endocrine axes, including the HPA axis by negative feedback at the hypothalamus,11 and elevated leptin has been associated with osteopenia.12
Adiponectin was first reported as an adipocyte secretory protein in 1995,13 but only recently has its physiology been investigated. Plasma adiponectin concentrations are about 2 to 3 times greater than those of most other hormones, and its concentrations, unlike those of other adipocytokines, are inversely related to adiposity. Adiponectin receptors R1 (AdipoR1) and R2 (AdipoR2) have been identified in the periphery and CNS. Adiponectin receptor R1 is abundant in skeletal muscle, and AdipoR2 exists primarily in the liver. Adiponectin receptor R1 and AdipoR2 are also present in the paraventricular nucleus of the hypothalamus, amygdala, area postrema and, diffusely, in the periventricular areas and cortex.2 AdipoR1, and AdipoR2 have been observed in the human pituitary as well.14 Adiponectin inhibits gene expression and secretion of growth hormone (GH) and lutenizing hormone (LH) release in rat pituitary somatotropes and gonadotropes.15 In human anterior pituitary cells, adiponectin expression has been observed in cells that produce GH, follicle-stimulating hormone (FSH), LH, and thyrotropin but not in corticotropin-producing cells.14 Adiponectin has generated interest in relation to obesity-related diseases. Pima Indians and Asian Indians with higher adiponectin are less likely to develop T2DM16,17 because of enhanced glucose and fatty acid disposal by skeletal muscle.18 Adiponectin is lower in patients with CVD,19 and it prevents atherosclerotic progression by reducing smooth cell proliferation and improving angiogenesis and endothelial function.20
Leptin is a hormone produced by the white adipose tissue. Originally isolated by positional cloning, its discovery has prompted a new impetus in the field of the endocrinology of energy metabolism, and it has redefined the physiology of the adipose organ.21 Leptin modulates appetite, food intake, sexual maturation and reproductive functions, and immune functions, all of which are disrupted in depression. We originally studied the rhythmicity of leptin and discovered that this adipocytokine is secreted in an exquisitely pulsatile fashion and that its secretion is inversely related to the secretion of corticotropin and cortisol.23 Reports of serum leptin levels in depressed subjects are conflicting, with studies finding no differences, lower levels in depressed men, elevated levels in depressed men and women, or elevated levels only in depressed women.22
While leptin's rhythmicity is well described,23 the 24-hour secretory profile of adiponectin is not well known. Adiponectin exhibits diurnal and ultradian rhythms in normal weight men.24 Circulating concentrations of adiponectin have been reported in depressed patients, but only at single time points. In some studies, adiponectin was lower in newly diagnosed and drug-naive MDD subjects and was inversely related to depression severity.25 However, in others, there was no significant relationship between single adiponectin measurements and depressive symptoms.26 To date, 24-hour secretory profiles of adiponectin have not been described in MDD patients. Because MDD subjects have a higher CVD prevalence, and reduced adiponectin is associated with negative health consequences, adiponectin rhythmicity in patients with depression is of interest. The relationship of adiponectin to the HPA-axis and leptin also remains unknown in MDD subjects. Accordingly, the main goals of the current study were (1) to establish whether women with MDD have decreased circulating concentrations of adiponectin and/or disruption of adiponectin secretory rhythmicity; (2) to study the relationship of adiponectin and leptin secretion with depression; and (3) to explore the temporal correlations among circadian concentrations of adiponectin, leptin, corticotropin, and cortisol.
Study Design
This ancillary study was performed as part of the Premenopausal, Osteopenia/Osteoporosis, Women, Alendronate, Depression (POWER) study, a 36-month prospective study of bone turnover in 21- to 45-year-old premenopausal women with MDD conducted at the National Institutes of Health Clinical Center (NIH-CC).4 Recruitment was conducted from July 1, 2001, to February 28, 2003, in Washington, DC, and the metropolitan area by newspaper, radio, Internet, and flyer advertisements among community-dwelling women. We enrolled 89 women with MDD and 44 healthy control subjects. Controls were matched to subjects with MDD based on a standard deviation from the mean of ± 3.0 years for age and of ± 2.0 kg/m2 for body mass index (BMI). Subjects were seen at 0, 6, 12, 24, and 36 months.
Major depressive disorder was diagnosed by 2 psychiatric clinicians using the Structured Clinical Interview (SCID) for DSM-IV27 criteria. Women were enrolled if they met DSM-IV criteria for MDD and had experienced a depressive episode in the preceding 3 years, a limit chosen to minimize recall problems associated with remote depressive episodes. Exclusion criteria for women with MDD were suicidal risk, eating disorders, bipolar disorders, schizophrenia, and schizoaffective disorder. Patients with anxiety disorder or a history of alcohol or drug dependence in remission for 5 years were eligible. For controls, exclusion criteria were a history of any DSM-IV diagnosis other than past alcohol abuse.
From the whole POWER sample, we then individually matched 23 consecutively studied women with MDD with 23 control subjects, based on sample size analysis (see below). All participants were in good health, as assessed by medical history, physical examination, and screening evaluation (electrocardiogram, negative serum pregnancy test; tests of hematologic, thyroid, liver, and renal function). This study was approved by the Scientific Review Board and the Institutional Review Board of the NIMH. All participants provided written informed consent.
Psychiatric Assessment
Current severity of anxiety and depression was assessed using the Hamilton Anxiety Rating Scale (HARS, 14 questions) and the Hamilton Depression Rating Scale (HDRS, 24 questions). These 2 scales inquire about symptom severity over the past 2 weeks. As part of the SCID interview, we also inquired about age at onset, number and duration of the depressive episodes, current depressive state that met DSM-IV criteria, and antidepressant use.
Anthropometric Measurements
Weight was measured to the nearest 0.1 kg using a digital scale. Height was measured 3 times to the nearest 0.1 cm using a stadiometer. Waist circumference was measured at the level of the natural waist. Hip circumference was measured at the level of maximum extension of the buttocks. The mean of 3 measurements at each site was used in all analyses.
Cooper Test (12-Minute Walk/Run Test)
The Cooper test, an indirect index of physical fitness, was performed on the morning of the third admission day after completion of the blood collection. Performance was measured in total meters traversed within 12 minutes on a standardized treadmill.
Dual Energy X-Ray Absorptiometry Dual energy x-ray absorptiometry (DXA) measurements for bone mineral density and body composition were performed by the Hologic DXA QDR 4500 (Hologic, Inc, Bedford, Massachusetts). Total body fat percent and abdominal area were reported from the T12/L1 interface to the L4/L5 interface, which includes visceral and subcutaneous fat.
Twenty-Four Hour Blood Sampling Protocol
Study participants were admitted to the NIH-CC in the late afternoon of the day before testing. All studies were performed after an overnight fast. Blood was collected via an intravenous catheter hourly from 0800 hours until 0800 hours the following morning, for a total of 25 samples. Plasma samples were saved at −80°C for subsequent measurements of adiponectin, leptin, corticotropin, and cortisol. The total amount of blood drawn from each subject was approximately 200 mL.
Hormone and Other Blood Measurements
Assays were performed blinded to group allocation. Intra-assay coefficients of variation (CVs) were < 15%. Hormones were measured as follows: plasma total adiponectin (Linco Research, St Charles, Missouri; radioimmunoassay [RIA]; sensitivity, 2 µg/mL; CV, 1.78%–6.21%); plasma leptin (Linco Research; RIA; sensitivity, 0.5 ng/mL; intra-assay CV, 8.3%). Plasma corticotropin was measured by chemiluminescent immunoassay using the Nichols Advantage apparatus (Nichols Institute Diagnostics, San Juan Capistrano, California). Serum insulin and cortisol were measured by chemiluminescent immunoassay using the DPC Immulite-2000 system (Diagnostics Product Corporation, Los Angeles, California). Insulin resistance was calculated using the homeostasis model assessment for insulin resistance (HOMA-IR).28 Measurements of high-density lipoprotein (HDL), low-density lipoprotein (LDL), total cholesterol, total triglycerides, glucose, and insulin levels were performed on morning samples after an overnight fast.
Statistical Analyses
Circulating adiponectin concentrations that are reduced by 15%–33% are known to be predictive of later T2DM.16,17 During the planning phase of this study, we conducted an analysis to determine the statistical power needed to detect a 15% difference in mean 24-hour adiponectin levels between groups and estimated that 23 subjects per group were needed (P < .05, 2-sided t test, power = 0.90; SD = 0.7).
Chronolab software (available from Universidade de Vigo, Vigo, Spain, Bioengineering & Chronobiology Laboratory, http://www.tsc.uvigo.es/BIO/) was used for cosinor analyses. By multiple regression analyses, we determined the relationship of adiponectin with measures of adiposity, clinical indices of depression, and with other hormones. Significance was accepted at a level of P < .05; all results are expressed as mean ± SD.
Cross-Correlation Analysis
To assess the temporal relationships of diurnal variations among hormones studied, we performed cross-correlation analyses on the following pairs of time series from each subject: corticotropin vs cortisol, leptin vs cortisol, and adiponectin vs leptin. The cross-correlation functions were then averaged for MDD subjects and controls, and the lag relationships of each pair were assessed. Mean correlation coefficients at any particular lag time were tested against the null hypothesis of no correlation by using Wilcoxon signed rank tests. The maximum correlation coefficients were compared between groups by using Wilcoxon 2-sample tests.
Click figure to enlarge
Demographic and Clinical Characteristics of Subjects
Demographic characteristics are reported in Table 1. The 2 groups did not differ in lifestyle characteristics examined. Table 2 illustrates the clinical characteristics of the MDD group. Women with MDD had a cumulative depression history of approximately 6 years. Mean age at onset was in the mid teens. Women with MDD on average exhibited mild symptoms of anxiety and depression, as indicated by HARS and HDRS scores. Six of 23 women with MDD were currently depressed, defined as an episode during the preceding 4 weeks. The majority of women with MDD were taking antidepressants. Two thirds had at least one other DSM-IV Axis I diagnosis.
Body Composition and Metabolic Features of Study Subjects
There were no significant differences in anthropometric measurements, body composition, lipid profiles, glucose, insulin, and insulin sensitivity (Table 3). However, women with MDD tended to have less lean mass than did controls. Total fat mass as measured by DXA, and waist-circumferences were similar. Women with MDD tended to have higher LDL, triglycerides, and total cholesterol levels. There were no differences in glucose or insulin levels or the HOMA-IR index between groups.
Twenty-Four Hour Hormonal Values
Figure 1, Table 4, and Table 5 illustrate mean adiponectin and leptin concentrations. In control subjects, diurnal fluctuation in adiponectin was about 30%. In both groups, mean adiponectin concentration was higher during the day, with a zenith occurring at approximately 1430 hours, an initial fall around 1600 hours, a further decline after 2300 hours, and then another increase at approximately 0300 hours. Women with MDD exhibited similar adiponectin rhythmicity. Mean adiponectin concentrations were about 25% lower at all 24-hour time points in women in the MDD versus control groups.
In both women with MDD and control subjects, leptin exhibited its typical diurnal variation, with higher concentrations during the night and a zenith at approximately 0200 hours. The lowest concentrations were observed during the day, with a nadir around 1100 hours. Mean leptin concentration was higher in women with MDD at all 24-hour time points. Leptin's rhythmicity was similar between groups.
Mean corticotropin and cortisol concentrations showed typical diurnal variations, with higher values in the morning (Figure 2A and 2B and Table 4). There were no differences in circadian corticotrophin secretion between groups; however, mean 0800-hour corticotropin concentration was somewhat higher in women with MDD than in control subjects (P = .0557).
Relationships of Adiponectin With Adiposity and Clinical Indices of Depression
The diagnosis of MDD accounted for approximately 25%–30% of the variability in adiponectin concentrations (0800-hour adiponectin, R2 0.285; P = .004; 24-hour mean adiponectin concentration, R2 = 0.267; P = .001). Adiponectin concentration was inversely related to the cumulative duration of depression (R = −0.51; P = .03) and tended to be inversely related to the duration and severity of depression (R = −0.41; P = .09). Adiponectin concentration accounted for approximately 20% of the waist-hip ratio variability (0800-hour adiponectin, R2 = 0.194; P = .002; 24-hour mean adiponectin concentration, R2 = 0.230; P = .007). Adiponectin concentration and waist-hip ratio were inversely related (R = −0.57; P = .04). No colinearity was observed between MDD and waist-hip ratio.
Temporal Relationship of Adiponectin, Leptin, Corticotropin, and Cortisol
Corticotropin and cortisol exhibited similar secretion with a zenith in the early morning and nadir in the afternoon. As expected, the cortisol peak followed the corticotropin peak with a time lag of < 1 hour. Leptin secretion was almost directly inverse to those of corticotropin and cortisol. Overall, temporal relationships were not different between the MDD and control groups.
Table 6 reports cross-correlations, including mean maximum coefficients of correlation, for various comparisons of 2 hormones as a paired time series. Corticotropin vs cortisol was related (mean maximum correlation: controls; r = .739, P < .001; MDD: r = .819, P < .001), and this relationship was stronger in women with MDD than in controls (P = .018).
Corticotropin versus cortisol secretion was synchronized with a lag of 0 hours (ie, an increase in corticotropin concentration was followed by an increase in cortisol concentration within 0 minutes to 1 hour). The maximum cross-correlation was observed at 0 minutes lag time in both groups.
Leptin versus cortisol concentration was inversely related in the MDD (r = −0.519, P < .001) and control groups (r = −0.531, P < .001). The maximum cross-correlation was observed at −2 hours' lag time. Leptin versus adiponectin concentration was weakly but significantly related (controls r = −0.273, P < .001; MDD: r = −0.254, P < .008). There were no significant differences in the leptin-cortisol, or leptin-adiponectin relationships between the MDD and control groups.
Premenopausal women with MDD exhibited lower circadian plasma adiponectin concentrations than did closely matched control subjects. As reduced adiponectin has been shown to predict T2DM and CVD, premenopausal women with MDD may be at increased risk for both conditions. Women with MDD also had increased nocturnal leptin, elevated morning corticotropin, and decreased nocturnal corticotropin and cortisol. Corticotropin and cortisol were more strongly related in women with MDD than in control subjects, suggesting HPA-axis activation in depression.
In the current study, women with MDD exhibited adiponectin concentrations that were reduced by an average of 25%, a magnitude of decrease that has been reported in prospective studies to increase the risk of T2DM and CVD.16,17,29 Our findings suggest that otherwise healthy premenopausal women with MDD may form a distinct subgroup at risk for these conditions. Lower adiponectin was related to increased severity of depression. Consistent with the current study, single adiponectin measurements were decreased in newly diagnosed MDD subjects and were inversely related to depression severity.25 Men with MDD also tended to have lower adiponectin than did controls.26 Our findings contrast, however, with data from 2 other reports.30,31 Both evaluated older populations, and one utilized broad inclusion criteria for depression and did not exclude subjects with comorbid illnesses. Different ethnicity may also have played a role, as one study was conducted in a Chinese population.30
While lower circadian adiponectin concentration was not associated in this study with altered insulin sensitivity or metabolic alterations, there was a trend toward increased LDL and triglyceride levels in women with MDD. These findings might not have reached statistical significance because of the relatively small sample size or insufficient time to develop metabolic alterations. As previously reported, this same cohort of women exhibited increased evening levels of factor VIII and plasminogen activator inhibitor-1, 2 markers of enhanced cardiovascular risk4; increased levels of C-reactive protein, a marker of inflammation32; an increase in 24-hour circulating proinflammatory cytokines and a decrease in anti-inflammatory cytokines.33 The POWER study and the current substudy, are notable in that several related variables were concurrently measured, adding validity to these results. However, given the cross-sectional nature of this report, we cannot establish whether decreased adiponectin concentrations were due to depression per se, to nonspecific lifestyle factors, or to antidepressant medications. Most of the women with MDD were taking selective serotonin reuptake inhibitors (SSRIs) or selective serotonin-norepinephrine reuptake inhibitors (SSNRIs). Selective serotonin reuptake inhibitors and SSNRIs may act to increase adiponectin secretion from adipocytes. Patients with remitted depression who received 6 months of SSRI therapy have been reported to have higher adiponectin levels than those in healthy controls.34 It is of note, therefore, that our sample of women with MDD had lower adiponectin concentrations than those in healthy controls, in spite of their being on SSRI therapy.
To our knowledge, this is the first report describing the circadian rhythm of adiponectin in women with MDD. Women with MDD had lower adiponectin around the clock, but no differences were observed between MDD and control groups in time of the peak or amplitude. More frequent sampling may have unraveled more subtle differences between the groups. A rhythm of adiponectin secretion characterized by higher values during the day with a peak in the late morning was originally reported in healthy men.22 Adiponectin's rhythmicity has also been studied in obese patients, in whom rhythmicity was preserved but there were higher daytime levels.35,36
It is possible that, in women with MDD, short sleep and/or sleep disruption decreased adiponectin secretion. Sleep disturbances are one of the components of the depressive syndrome, according to DSM-IV criteria, and approximately 60% of depressed patients have insomnia.37 In the Nurses Health Study Cohort,38 women with more frequent snoring, a proxy for sleep disruption, had proportionally lower adiponectin levels. Sleep-deprived men lose the typical day/night variations in adiponectin.39
Women with MDD had approximately 25% higher concentrations of leptin than those in healthy controls and exhibited the typical nocturnal rise in leptin concentrations.23 Because MDD is a state of increased sympathetic tone,40 higher leptin may have been secondary to activation of the sympathetic nervous system, which is known to stimulate leptin secretion. We have previously shown that this group of women with MDD has clinically relevant lower bone mass and that depression is a risk factor for osteoporosis comparable in magnitude to other well-established risk factors.3 Leptin has been shown in a mouse model to centrally inhibit bone formation via the sympathetic system. Apposition of new bone takes place mostly at night, as indicated by circadian measurements of markers of bone turnover41; therefore, higher nocturnal leptin levels may contribute to the development of osteoporosis in women with MDD.
HPA Axis
As expected, corticotropin and cortisol concentrations were strongly related, and this correlation was more pronounced in MDD subjects. These findings support MDD as a state of HPA axis activation and validate the notion that subtle alterations in the HPA axis are present in mild depression. Women with MDD exhibit diminished negative feedback of cortisol on corticotropin.42 The activation of the HPA axis in MDD subjects is caused in part by relative cortisol resistance at the glucocorticoid receptor.43 We previously reported that women with MDD were more likely to be homozygous for a glucocorticoid receptor polymorphism, resulting in higher sensitivity to dexamethasone.44
In the current study, lower nocturnal corticotropin and cortisol concentrations were associated with increased nocturnal leptin concentrations. Leptin and cortisol were strongly and inversely correlated in both MDD and control groups. Elevated leptin may have decreased nocturnal corticotropin and cortisol levels via inhibition of the hypothalamic–corticotrophin-releasing hormone neuron.23
Overall Clinical Relevance
We propose that this sample of women with MDD is representative of a distinct clinical phenotype that is emerging, characterized by an increased risk for insulin resistance, cardiovascular disease, and osteopenia. By use of sensitive analytic techniques and around-the-clock measurements, we have described a novel hormonal and immune profile that may enhance our understanding of the neuroendocrinology of major depression. In this study of adipocytokines, we found that women with MDD had decreased diurnal adiponectin concentrations, of sufficient magnitude to put them at elevated risk for T2DM. We have previously shown that this same cohort exhibits elevated circulating concentrations of Factor VIII and plasminogen activator inhibitor-1, and it may be at increased risk for thromboembolic events.4 Decreased adiponectin levels have also been implicated in CVD, and we have found changes in other markers related to CVD risk. Our study cohort also had alterations in the immune system, characterized by an increase in proinflammatory and a decrease in anti-inflammatory cytokines evident both in 24-hour plasma cytokines3 and in cytokine secreted in sweat,33 as well as increases in C-reactive protein, a well-accepted marker of inflammation.32 Although our MDD patients were not overtly hypercortisolemic, we identified subtle alterations in their HPA-axis function that may be partly related to genetic polymorphisms of the glucocorticoid receptor that we previously reported.44 Finally, this investigation on adipocytokines demonstrated that women with MDD exhibit elevated nocturnal leptin levels. Leptin has emerged as one regulator of bone formation through actions on osteoblasts, and it may account for bone deficits in women with MDD 3. These alterations in endocrine and immune systems, taken together, provide possible mechanisms for several of the medical consequences of depression, including insulin resistance, CVD, and osteopenia.
Strengths and Limitations
The current study had several strengths. The sample was well characterized from a metabolic and hormonal perspective; measurements of multiple hormones and immune outcomes were performed hourly over 24 hours; and the sample size was adequately powered. According to one large, recent survey,45 50.5% of men and 65.5% of women with MDD are pharmacologically treated. The adjusted odds ratio for a subject with MDD to have had generalized anxiety disorder in the previous 12 months increased severalfold to 8.6.45 Therefore, our sample may be representative of a large proportion of the general population. At the same time, because of these confounding factors we cannot absolutely attribute our findings to MDD per se versus concomitant medications and comorbidity.
Limitations included the cross-sectional nature of this analysis. The clinical sample was composed mainly of white women, and most subjects had mild depression. Hourly sampling did not allow for more detailed analysis of circadian secretion. Most of our subjects were pharmacologically treated and suffered from comorbid generalized anxiety disorder and other DSM-IV diagnoses.
Future Research Questions
Future studies appear warranted to establish whether a causal link exists between MDD and decreased daily production of adiponectin. These studies should be large enough and of sufficient duration to detect clinical events such as T2DM or CVD. The effects of antidepressants on adiponectin should be investigated, as should the mechanisms that lead to decreased adiponectin and increased leptin secretion, respectively.
We report herein decreased adiponectin and elevated leptin concentrations in premenopausal women with MDD. These changes in adipocytokines are of large magnitude, potentially clinically significant, and generalizable to the large population of young women who have mild depressive symptoms and who are on treatment. Given the high prevalence and chronic nature of depression, especially in women, and the increasing recognition of adiponectin as a risk factor for T2DM, these data are likely to have public health significance.
Drug name: bupropion (Aplenzin, Wellbutrin, and others).
Author affiliations: Clinical Endocrine Section, Clinical Endocrinology Branch, National Institute of Diabetes, Digestive and Kidney Diseases (NIDDK), National Institutes of Health (NIH), Bethesda, Maryland (Drs Cizza and Nguyen); Pediatric Endocrine Unit, Massachusetts General Hospital, Boston (Dr Nguyen); Section on Neuroendocrine, Immunology and Behavior, Integrative Neural Immune Program, Intramural Research Program, National Institute of Mental Health (NIMH), NIH, Bethesda, Maryland (Dr Eskandari); Office of the Director, NIDDK, Bethesda, Maryland (Mr Duan and Dr Wright); Radiology Department, Warren G. Magnuson Clinical Center, NIH, Bethesda, Maryland (Dr Reynolds); Department of Medicine, Division of Endocrinology, Diabetes and Metabolism, University of Pennsylvania School of Medicine, Philadelphia (Dr Ahima); and Endocrine Section, National Center for Complementary and Alternative Medicine (NCCAM), NIH, Bethesda, Maryland and Research Service, Veterans Affairs Medical Center, Washington, DC (Dr Blackman).
Potential conflicts of interest: None reported.
Funding/support: The study was fully supported by the Intramural Research Programs of the NIMH; NIDDK; and NCCAM, NIH, Bethesda, Maryland.
Previous presentation: This study was presented in poster format at the 64th Annual Scientific Convention & Meeting of the Society of Biological Psychiatry, May 14-16, 2009; Vancouver, British Columbia.
Acknowledgment: The following individuals were investigators of the POWER (Premenopausal, Osteopenia/Osteoporosis, Women, Alendronate, Depression) Protocol: Giovanni Cizza, MD, PhD (Principal Investigator); Ann Berger, MD; Marc R. Blackman, MD; Karim A. Calis, PharmD, MPH; Gyorgy Csako, MD; Bart Drinkard, BA; Farideh Eskandari, MD; Philip W. Gold, MD; McDonald Horne, MD; Christine Kotila, BSN; Pedro Martinez, MD; Kate Musallam, BSN; Terry M. Phillips, PhD; James C. Reynolds, MD; Nancy G. Sebring, RD; Esther Sternberg, MD; and Sara Torvik, BSN. All investigators are affiliated with the NIH, Bethesda, Maryland.
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Editor's Note: We encourage authors to submit papers for consideration as a part of our Focus on Women's Mental Health section. Please contact Marlene P. Freeman, MD, at firstname.lastname@example.com.


text:
19 October 2008,
Price realised GBP 157,250
Yue Minjun (b. 1962)
City No. 1
signed in Chinese, inscribed and dated 'LY.1993.11' (lower right)
oil on canvas
39¼ x 43 3/8in. (100.7 x 111.2cm.)
Painted in 1993
New York +1 212 636 2000
London +44 (0)20 7839 9060
Hong Kong +852 2760 1766
Shanghai +86 21 6355 1766
Yue Minjun's work questions assumptions about generally accepted reality -- personal, art historical or political -- by parodying and exaggerating everything he reproduces. His paintings operate on the postulation that the viewer recognises the subject -- we see the artists trade-mark self depiction with an over strung smile, or famous scenes from art historys most iconic paintings -- but any image is exaggerated to levels of the grotesque, irrevocably issuing a critique.
His paintings have been classified as Cynical Realist works and as answer to the history of the Tiananmen Square massacre and its aftermath. Characteristically, they feature images of the artist laughing uncontrollably and unaware. The humorous grimace, in its repetition and mindless characteristics, transforms Yue's works into something absurd. Yet, it is not absurdity born out of coincidence, but a choice by the author, where the absurd has dictated a large part of his life. Yue is known to have said that, after 1989, to laugh seemed the only possible reaction, the only available escape from the absurd reality, with which the Chinese people were confronted at the time. The absurdity of the hysterical laugh is also what continues to make his works contemporary in a sociopolitical context: the self-portrait has become standardised, making its repetition a direct comment on propaganda and advertisement in contemporary Chinese society.
All the above elements repeat themselves in City No. 1, where the viewer is confronted with Yue's familiar smile, which transforms the painting into something beyond a work of art: it becomes a trade-mark Yue Minjun branded object, like a luxury commodity. The latter attribute cynically comments on the state of contemporary reality. City No. 1 evokes an idea of a human collective, a city. And yet, two figures smile at us from what appears to be a sewer opening: from beneath the city, from a place outside of society, where they remain outsiders, humorous commentators and cynical bystanders all the same.
Special Notice
No VAT will be charged on the hammer price, but VAT at 15% will be added to the buyer's premium which is invoiced on a VAT inclusive basis.
Schoeni Art Gallery, Hong Kong.
Littmann Kulturprojekte, Basel.
Acquired from the above by the present owner.
Pre-Lot Text
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text: The NetCAN+ 120 WLAN is an easy to use gateway from Ethernet to CAN-Bus, based on state of the art RISC components. It provides CAN-BUS communication over Ethernet and WLAN, and allows completely secured communication for both data transfer and configuration to the attached CAN devices. CAN BUS is widely used in industrial applications as well as in automotive monitoring and control. The NetCAN+ can be used to monitor the data traffic as well as sending control information. Implemented in the NetCAN+ is an option to use the viaVPN system for Remote Access and Monitoring. viaVPN provides secure and strong encrypted access via Internet, without any re-configuration of firewalls. Once installed in the local network the NetCAN+ are used exactly as without the option viaVPN. But at the same time the operation can be monitored from remote locations. If the CAN port is not occupied by local access, also operation from remote is possible. NetCAN+ supports three operating modes: TCP Raw Server, CAN Bridge and Driver Mode. With TCP Raw Server the communication is handled directly via IP address and port number. The CAN Bridge connects two NetCAN+ devices to tunnel CAN data via Ethernet/WLAN. The Driver Mode requires the installation of a virtual com-port driver, which makes the network fully transparent for the application. NetCAN+ provides various software tools to interface the user application: • The ASCII conversion protocol is useful in developing and testing any CAN-BUS configuration. Users just connect directly via Telnet, and have a simple way to talk to the CAN controller. It can also be used to manually transmit and receive CAN frames. • Applications programmed by users should use the VScan API library (DLL), which transparently handles the ASCII conversion for the CAN frames. Programmers have to handle only the CAN frames and status information, they do not have to care more about the ASCII conversion in their applications. This API is supported in C/C++, C#, VB.NET, Delphi and LabVIEW.• In Linux SocketCAN can be used as alternative to vs_can_api library. VScom CAN devices support standard Serial Line CAN (slcan) driver (see this FAQ).• The NetCAN+ also supports CANFestival, an Open Source CANopen Framework. CANopen is a CAN-based higher layer protocol that is used in various application fields, such as medical equipment, offroad vehicles, maritime electronics, railway applications or building automation. CANopen unburdens the developer from dealing with CAN-specific details such as bit-timing and implementation-specific functions. It provides standardized communication objects for real-time data, configuration data as well as network management data. • CANHacker, a tool for analyzing and transmitting frames on the CAN BUS, is included in the product package. This requires the Driver Mode. • A set of Mapper DLLs simulates CAN hardware from other manufacturers. Users configure their system for those products or the NetCAN+ 110 adapter as a replacement. So existing software will use the NetCAN+ without replacing the application or modifying it.


text:
18th Century Louis XV Armoire
An extraordinarily tall mid-18th century Louis XV provincial fruitwood narrow armoire/bonnetiere with a rectangular cornice.The frieze is centered by a basket of flowers, the mire mesh inset door is carved with laurel leaves, straw hat and gardening tools. The entire piece is ready to be finished out however it suit the new interior space.
Originally purchased from Sotheby's New York Auction House)
DIM: 7'9"H x 29"W x 22.5"D


text:
Alif Setiawan
Web Developer, Designer, and Filmmaker in Central Java, Indonesia
I am a web developer, designer, and filmmaker currently living in Central Java, Indonesia. My interests range from photography to design. I am also interested in entrepreneurship, travel, and movies.
You can click the button above to visit my website. If you'd like to get in touch, feel free to say hello through any of the social links below.


text:
As Week 8 games approach, we take a spin around the NFL and offer quick-hits on the status of big names nursing injuries:
- 49ers TE Vernon Davis (ankle) was limited in practice Friday and is listed as questionable for Sunday's game against the Broncos in London. He is expected to play.
- Broncos RB Knowshon Moreno (hamstring) is not listed on the Broncos' injury report for Sunday's game against the 49ers in London and is expected to start. WR Eddie Royal (groin) is listed as probable after practicing fully on Friday.
- Chargers TE Antonio Gates (toe) practiced fully Friday, but is listed as questionable for Sunday's game against the Titans. Gates missed practice last week but still started against the Patriots, catching his eighth touchdown of the year. Gates will face added pressure to shore up the Chargers passing game with the likelihood that WRs Malcom Floyd (hamstring, doubtful) and Legedu Naanee (hamstring, doubtful) will not play.
- Colts RB Joseph Addai (neck) did not practice Friday and will likely miss Monday night's key rematch with the Texans. The onus falls on Mike Hart and Donald Brown to carry the Indy backfield. Brown has missed time with a nagging hamstring injury, but said Friday, "if the game was today, I'd play."
- Panthers RB DeAngelo Williams (foot) did not practice Friday and is listed as doubtful, clearing the way for Jonathan Stewart to take the bulk of the carries against the Rams.
- Rams RB Steven Jackson (finger) was limited in practice Friday and is listed as questionable for Sunday's game against Carolina after having surgery on a broken ring finger on his left hand. He insists he will play, but coaches have not announced a decision.
- Saints RBs Reggie Bush (fibula) and Pierre Thomas (ankle) will not play against the Steelers, leaving Chris Ivory to carry the load Sunday.
- Titans QB Vince Young (knee/ankle) practiced all week and is listed as probable for Sunday's game against the Chargers. He has not officially been named the starter in place of backup Kerry Collins but coach Jeff Fisher said, "I think there is a good chance Vince will start."
Nate Davis is a reporter, blogger and editor who's been at USA TODAY since 2000. He has covered the NFL since 2005. No, he did not play quarterback for Ball State. Davis' succession of our esteemed colleague Sean Leahy at The Huddle is considered a Brady-for-Bledsoe swap by most "insiders."More about Nate


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Let us know when your receive great advice so we can thank our lawyers and point others with similar questions in the right direction.Got it!
I received the original amount of child support at the beginning of the month, but on the 11th it was changed so that he owed more, he was told to pay the rest of the amount this month and hasn't done so yet. compared to what it was changed to, he has only paid a small amount.
Although child support may be "due" at the beginning of the month or on some other date, it is not considered delinquent until the end of the month. If the full (increased) amount is not paid by the last date of the month, you can make a demand for the shortfall and determine whether enforcement action is necessary.
** This response is provided as general information only and does not constitute legal advice or otherwise establish an attorney-client relationship. **Ask a similar question
You should review the Order that modified child support. Generally, the Order sets forth a date that the new amount of child support begins. If your statement "he was told to pay the rest of the amount this month" then the month is not over so he may not be late. Usually the Order would set forth more definite terms.
Kindly be advised that the answer above is only general in nature cannot be construed as legal advice, given that not enough facts are known. It is your responsibility to retain a lawyer to analyze the facts specific to your particular situation in order to give you specific advice. Specific answers will require cognizance of all pertinent facts about your case. Any answers offered on Avvo are of a general nature only, and are not meant to create an attorney-client relationship.Ask a similar question
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Regulators Prepare To Question QuattroneDec 11, 2002 | FT.com
Massachusetts securities regulators' efforts to question Frank Quattrone and other leading Credit Suisse First Boston executives as part of their probe into Wall Street's conflicts of interest are heating up.
Massachusetts has informed Mr Quattrone through CSFB that he must appear on January 13 to answer questions about alleged misconduct in the CSFB technology investment banking group he heads.
The formal deposition is part of the endgame in broader settlement talks with Wall Street's leading investment banks, which could result in huge fines and an overhaul of the way banks do business, and it may be a tactic to increase pressure on CSFB before a deal is reached.
Still, it has raised questions about the banker's fate just months after CSFB had appeared free of regulatory problems.
William Galvin, the Massachusetts secretary of state, has filed a civil suit against CSFB, accusing Mr Quattrone's tech group of overly optimistic stock research and handing initial public offerings to executives to win investment banking business.
Mr Galvin has also referred evidence against the group to New York attorney general Eliot Spitzer and the US Attorneys Office to consider possible criminal charges. More ominously, regulators have hinted they will pursue cases against individual executives after they conclude the broader settlement.
There are questions as to whether Mr Quattrone, arguably the most prominent banker of the tech bubble, will survive the crusade inspired by its collapse.
He would be one of the largest names to fall, alongside Jack Grubman, the former telecoms analyst, who resigned from Salomon Smith Barney under pressure in August.
CSFB has declined to comment, but for the moment, Mr Quattrone is going about business as usual and in spite of trimming staff by half, CSFB's tech group is still the leader in Silicon Valley. "There isn't anyone with a better understanding of this business," a prominent venture capitalist said.
CSFB snatched Mr Quattrone and his team from Deutsche Bank five years ago, luring them with an unusual deal that gave the tech share of its own revenues.
But other elements of the deal are now drawing scrutiny. Most notably, Mr Quattrone was given oversight of the tech group's analysts, controlling coverage and determining compensation.
Massachusetts regulators argue that this led to a culture in which analysts did bankers' bidding. In one email uncovered by investigators, Mr Quattrone asked a research analyst about to initiate coverage of a company what investment banking business had been "extracted" in return.
"The system worked as they wanted it to work, so that analysts served investment banking," one investigator said. "Quattrone knew, or should have known."
CSFB notes that it never received any banking business from the company in question, Agile Software.
Mr Quattrone's regulatory problems seemed safely behind him this time last year. In November, he was pronounced clean by John Mack, then newly installed chief executive, after an internal probe into IPO abuses in the division.
Not only did Mr Mack publicly attest to the banker's good ethics, but also promoted him to the management committee.
A month later, the tech group's problems appeared to be resolved when prosecutors declined to pursue criminal charges, letting the bank off with a $100m civil settlement in which it admitted no wrong-doing.
CSFB has dismissed the Massachusetts complaint as "flawed" and "riddled with factual mistakes".
That may be so and it is far from certain that state or federal regulators will pursue Mr Quattrone. But even if they do not, the current scandal is taking a toll on banker and firm.
CSFB may have to pay as much as $250m as its portion of the global settlement, according to people familiar with the negotiations, and possibly several times that amount to deal with resulting class-action lawsuits filed by investors. It is likely Mr Quattrone will be tied up with legal matters for years.


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$200.00 7 months ago
Scooter - $200 (Joplin)
mgp mfx deckurban art barsPhoenix wheels odi grips ao pegs
7 months ago
Joplin, MO
$120.00 11 months ago
Pro scooter - $120 (Fresno)
Ethic grips Black ethic bars 21W 24TCrome sacrifice scsBlack 5 star headset Black Urbanartt ompressor forks Random front wheel proto gripper back wheel Purple MGP MFX 4.5W 21.5LNeed 120 but taking best offer
11 months ago
Fresno, CA
$140.00 1 year ago
District and Mgp scooter - $140
I would like to sell my district and my MGP stunt scooters. They are just to small and wanting a upgrade. The district brand new is almost $200 and the Mgp is almost $100 new.Dristact: I am asking $100 obo. I just put an new head set on it and new odi grips and rides smooth.It has a lot of scratches but runs great. No cracks tho. It has all district parts except the headset, grips, wheels, and bea
1 year ago
Medford, OR
$200.00 1 year ago
mgp nitro custom scooter - $200 (Elizabeth wv)
I have a mgp nitro custom scooter with eagle sport metal spoke wheels district triple clamp district headset all new part just put on not to long ago the scooter is very dialed and very trustworthy the only thing it would need is new grips it has about $400 in it and runs an hic compression system am willing to negotiate on price let me know what you think
1 year ago
Parkersburg, WV
$50.00 1 year ago
Misc. bike parts - $50
I have a box of bike parts for sale.... Here's the listScooter stemRaw metal handlebars6 Allen bolts2 new brake padsPedal bearing assembly2 15mm lug nutsNever been used MGP gripsSalt brake lever and brake assemblySalt rear hub ( needs new bearings )I'm asking 50 bucks OBO trying to get rid of all of it instead of just having it lay around...Send me a text at
1 year ago
Yakima, WA


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Root Beer Barbecue Sauce
Recipe by Kittencalrecipezazz
I doubled the recipe and baked my chicken pieces in it browning the chicken pieces first, I added in 1 tablespoon chili powder and some cayenne pepper, for a sweeter sauce add in more brown sugar to taste, if you like a thick sauce then mix in a little water mixed with cornstarch towards then end of cooking then simmer for a couple minutes to thicken.
Top Review by wicked cook 46
I added a bit more rootbeer and more brown sugar it was a bit to ketchupy for us. But then I used my homemade ketchup LOL so that changes it a bit. I browned my chicken and then pour the sauce all over and baked YUM. Made for Newest Zaar Tag
See Discussion:1 Review
Ingredients Nutrition
- 1 cup root beer (don't use sugar-free!)
- 1 cup ketchup
- 1⁄4 cup fresh lemon juice
- 1⁄4 cup orange juice
- 3 tablespoons Worcestershire sauce
- 2 tablespoons dark brown sugar
- 1 tablespoon light molasses
- 1 teaspoon liquid smoke (optional, but good to add in)
- 1 teaspoon grated lemon zest
- 1⁄2 teaspoon ginger powder
- 1⁄2 teaspoon onion powder
- 1⁄2-1 teaspoon garlic powder (I used fresh garlic)
- salt and pepper
Directions See How It's Made
- If you are adding in onion and garlic, then saute first in a couple tablespoons oil in a heavy saucepan for about 5 minutes until soft.
- Add in the remaining ingredients, except salt and pepper; bring to a boil, stirring occasionally.
- Reduce heat to medium-low and simmer for about 25-30 minutes.
- Season with salt and pepper to taste.
- Cool to room temperature, cover then chill overnight or tightly covered for up to 2 weeks.


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1124 Griggs Street, Grand Rapids 49507
See more homes for sale in Grand Rapids, MI
This property has been Sold!
07/08/2016 at $65,000
Charming home located on the SE side of Grand Rapids. MOVE IN READY with 2 bedrooms and 1 full bath. Open living room, dining and kitchen areas. All appliances shown remain with the home. New paint and carpet is present in this well cared for home. Fenced in rear patio and nice front and rear porches with new landscape so it is all ready for the new buyer. Home is SOLD AS IS. Hurry before this one is gone.
Property Information
- Status
- Sold
- Address
- 1124 Griggs Street
- City
- Grand Rapids
- Zip
- 49507
- County
- Kent
- Township
- City of Grand Rapids
- Possession
- At Close
- Zoning
- residential
- Total Finished SqFt
- 748
- Above Grade SqFt
- 748
- Garage Desc.
- 1, Detached
- Water
- Public
- Sewer
- Public
- Year Built
- 1925
- Taxes
- $1,210
Rooms and Land
- MasterBedroom
- 1st Floor
- Bedroom2
- 1st Floor
- Dining
- 1st Floor
- Kitchen
- 1st Floor
- Laundry
- Lower Floor
- Living
- 1st Floor
- Basement
- Michigan Basement
- Heating
- Forced Air, Natural Gas
- Acreage
- 0.08
- Lot Dimensions
- 42 x 80
- Appliances
- Oven, Range, Refrigerator
- Features
- All Window Treatments
- Exterior Materials
- Vinyl
- Exterior Features
- Fenced Back, Patio, Porch(es)
Listing Video for 1124 Griggs Street, Grand Rapids MI 49507
Mortgage Calculator
Listing Broker
Listing Courtesy of City2shore Real Estate Inc.
Office Address 6501 Balsam Drive
Listing Agent Laura A Carr
Listings last updated: . Some properties that appear for sale on this web site may subsequently have been sold and may no longer be available.
Our Michigan real estate agents can answer all of your questions about 1124 Griggs Street, Grand Rapids MI 49507. Real Estate One, Max Broock Realtors, and J&J Realtors are part of the Real Estate One Family of Companies and dominate the Grand Rapids, Michigan real estate market. To sell or buy a home in Grand Rapids, Michigan, contact our real estate agents as we know the Grand Rapids, Michigan real estate market better than anyone with over 100 years of experience in Grand Rapids, Michigan real estate for sale.
The data relating to real estate for sale on this web site appears in part from the IDX programs of our Multiple Listing Services. Real Estate listings held by brokerage firms other than Real Estate One includes the name and address of the listing broker where available.
IDX information is provided exclusively for consumers personal, non-commercial use and may not be used for any purpose other than to identify prospective properties consumers may be interested in purchasing.
All information deemed materially reliable but not guaranteed. Interested parties are encouraged to verify all information. Copyright© 2017 MichRIC LLC, All rights reserved.


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Home > What Is Siddha Yoga > Philosophy & Culture
Siddha Yoga Philosophy & Culture
Imagine looking at the world you live in and recognizing divinity in everything you see and everyone you meet. Imagine facing every situation in your life with the unwavering strength and delight that come from the certainty of the divine presence within you. The Siddha Yoga tradition embraces the universal principle of love and respect for one another, as expressed in one of the core teachings of this path -- See God in each other.
The Siddha Yoga philosophy asserts that this attainment is not only possible, it is our birthright. The goal of the Siddha Yoga path is Self-realization — the unceasing experience of yoga, or unity with God. Within each of us, behind the mind, the body, the ego, is a divine power. We practice yoga to recognize this divine power, the Self, and harmonize all our actions, thoughts, and words with it. The key to this divine vision of ourselves and the world is shaktipat, or spiritual awakening. When we receive shaktipat, we gain entry to our inner spiritual realms. Then, through our self effort in the form of spiritual practices, together with the grace of the Guru, our own spiritual awareness unfolds.
Gurumayi Chidvilasananda, as head of the Siddha Yoga lineage, continues a sacred tradition of making shaktipat available to spiritual seekers. Under the guidance of her teachings, Siddha Yoga students embrace the spiritual practices of yoga including meditation, chanting, contemplation and study, and selfless service (seva), as the means to the goal of Self-realization.
The Siddha Yoga philosophy springs from the timeless scriptural traditions of Kashmir Shaivism and Vedanta, as well as from the experience of the enlightened Siddha masters. Study of the texts of yoga deepens our understanding and appreciation of our inner experiences and helps us apply what we learn in our daily lives.
Siddha Yoga philosophy is made easily available to seekers around the world through the work of the SYDA Foundation. If you are new to Siddha Yoga meditation, you may find books by the Siddha Yoga Gurus helpful. These books and other items are available from the Ashram Bookstore and the Siddha Yoga Online Bookstore.
Please review our Terms of Useand Privacy Policy before using this site
© 2012 SYDA Foundation®. All rights reserved.


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Prada Saffiano Men's Wallet
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Prada Saffiano Men's Wallet. But at the end of a long (eight-hour) and very hot flying programme, how better to end than with the birthday boys themselves, the Frecce? It was named Caledonia, and served on long-distance routes such as those across the Atlantic, its passengers able to enjoy the comfort (if not, by today's A380 standards, the space) of the lower deck lounge and bar areas. Prada Saffiano Men's Wallet. It must be stressed at this point that little or nothing can be seen from landside at the terminal and, whilst the rarity and exclusivity of this visit cannot be called into question, the activity levels are noticeably a little slow. As the airfield fell quiet, everyone realised that Marineflieger jets had finally become history. Prada Saffiano Men's Wallet. Prada Antic Nappa Gauffre Tote. The crowds are, amazingly, pretty modest ' and it is a low-key affair, for sure ' but when the short spells of action kick in it's like nothing else you can imagine (and your ears will ring for days). There is no definitive colour match because the paint was mixed and watered down to ensure there was enough to go around. Prada Saffiano Men's Wallet.
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Prada Saffiano Men's Wallet. Calvert The Harrier has in many ways found its way into the British psyche over the past 40 years. He could look at the target, and, with a single stick-top button press, enter the co-ordinates into the navigation system ' all without needing to overfly the target or punch in numbers. Prada Saffiano Men's Wallet. Daino Prada Belts. So, the 747 does not actually operate to meet the rest of our European Air Network at Liege, because of the time zone differences. Thus, the engines were changed to the 260hp Lycoming 0-540-E with Hartzell two-bladed, constant speed propellers. Prada Saffiano Men's Wallet. The new aircraft will swell the Pakistani Orion fleet to 10 aircraft, with the existing pair already engaged being overhauled in Pakistan. As well as being a detailed account of the aircraft's history and painstaking rebuild to flying condition, it is also an interesting and readable story. Prada Saffiano Men's Wallet.
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Prada Saffiano Men's Wallet. A proportion of the proceeds from the sale of all these products is donated to the Vulcan to the Sky campaign. But Ukraine is a large country and events in Kiev are not necessarily echoed across the rest of the land. Prada Saffiano Men's Wallet. Prada Bag Women. It was a common thing for John Britten's mother Zoe, a wonderful lady, to arrive at the factory with refreshments for those working into the night ' and sometimes all through it. Running the data link involved establishing the link, which allowed verbal communication with the ground station operator using secure 'voice over data' technology. Prada Saffiano Men's Wallet. In those early days, a large aircraft scrapyard was located nearby, but today nothing is left there. Formerly of Harmony Airlines, which recently ceased flying operations, the aircraft transferred to Zoom on 2 May and was photographed two days later at Pearson International Airport, Toronto. Prada Saffiano Men's Wallet.


text:
- truckful
- noun see truck III
New Collegiate Dictionary. 2001.
New Collegiate Dictionary. 2001.
truck — I. verb Etymology: Middle English trukken, from Anglo French *truker, *troker, from Vulgar Latin *troccare, probably of imitative origin Date: 13th century transitive verb 1. to give in exchange ; swap 2. to barter or dispose of by barter… … New Collegiate Dictionary
John Berryman — John Allyn Berryman (originally John Allyn Smith) (October 25, 1914 – January 7, 1972) was an American poet, born in McAlester, Oklahoma. He was a major figure in American poetry in the second half of the 20th century and often considered one of… … Wikipedia
Buck Barrow — Main article: Bonnie and Clyde Buck Barrow Blanche and Buck Barrow, 1931 Born March 14, 1903(1903 03 14) Marion County, Texas … Wikipedia
truckload — noun a) A full truck or lorry We were expecting just a handful of people to come to the festival, but then a truckload of revellers started arriving at the festival gates b) A large number Syn: truckful, busload … Wiktionary
lorryful — noun As much as a lorry can hold. Syn: lorryload, truckful, truckload … Wiktionary
explosive — ex|plo|sive1 [ ık splousıv ] adjective * ▸ 1 able to explode (something) ▸ 2 likely to cause problems ▸ 3 suddenly increasing ▸ 4 showing sudden emotion ▸ 5 very powerful ▸ 6 loud and unexpected 1. ) used for causing an explosion: an explosive… … Usage of the words and phrases in modern English
explosive — I UK [ɪkˈspləʊsɪv] / US [ɪkˈsploʊsɪv] adjective * 1) a) used for causing an explosion an explosive device (= a bomb) b) able to explode This gas is highly explosive. 2) likely to create difficulties or to have a dangerous or violent effect The… … English dictionary


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iZotope RX3 (Download)
Audio Restoration Software
- Description
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iZotope RX3 (Download) Product Description
iZotope's amazing RX 3 is a complete audio restoration standalone suite designed fix common audio problems such as hums, hisses, buzzes, clicks, clipping, and unwanted noises. RX 3 is a must-have for broadcasters, podcasters, archivers, and every studio that needs pristine audio quality. You'll love how easy it is to remove noise and crackles, take out hum, and even remove specific sounds like coughs or passing traffic. Plus, you can use these tools both as plug-ins in your DAW or in the standalone editor. iZotope RX 3 sets an incredible new standard in restoration technology!
- Standalone or plug-in application for restoring and repairing "damaged" audio
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text:
All public logs
From ArchWiki
Combined display of all available logs of ArchWiki. You can narrow down the view by selecting a log type, the username (case-sensitive), or the affected page (also case-sensitive).
- 04:36, 19 May 2013 Kynikos (talk | contribs) automatically marked revision 257694 of page Category:Norsk Bokmål patrolled


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Barkman Furniture Collection
This lovingly handcrafted Amish Chaili Sofa Table is the perfect accent table for your living room. This handmade sofa table is built to order with your choice of hardwood and stain, paint or finish. This sofa table is handcrafted by genuine Amish woodworkers in the United States, using only the finest North American lumber.
© Copyrights 2003 - 2017 DutchCrafters All rights reserved.


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A clinical trial can offer you the chance to try new treatments and possibly benefit from them. Learning a new therapy is better than the standard treatment can also help others.
Whether a new therapy or test becomes part of standard treatment for breast cancer depends largely on the results of clinical trials.
Some clinical trials compare a new treatment to the standard of care. So, not everyone in the trial gets the new treatment. However, even those who don't get the new treatment will still get the standard treatment, just as they would if they didn't join the trial.
Talk with your oncologist about clinical trials. But remember, like all aspects of cancer care, the decision to join a clinical trial is a very personal one.
Learn more about clinical trials, including how to enroll and the informed consent process.
Find a list of questions to ask your doctor about clinical trials.
Some people worry they will get a placebo instead of an effective treatment in a clinical trial. However, placebos aren't used in metastatic breast cancer clinical trials. You will get either the new treatment or the standard treatment.
If your medical center does not offer clinical trials, you may want to get a referral to a cancer center that does.
BreastCancerTrials.org in collaboration with Susan G. Komen® offers a custom matching service to help you find a clinical trial for people with metastatic breast cancer.
2016 Research Fast Facts
Metastatic Breast Cancer
Fact Sheet
Facts for Life: Metastatic Breast Cancer
Related Video


text:
Forums: Index → Adoption requests → Plant Tycoon Wiki
What is your username? Mark Polner
Please link to the wiki here: planttycoon.wikia.com
How many edits have you made on that wiki? 5
How many days/months have you been editing there? 2 days
On the Special Pages -> Special:ListUsers when was the last time an admin edited, and who was it? Beny175 Pretty long ago
Any other information: There was cursing and other things and the wiki seemed neglected
- Hi. In order to adopt a wiki you need to have edited there for at least a week and have created at least one new article. Please start working on the wiki and we will check back in a week or so. -- Wendy (talk) 01:51, December 6, 2012 (UTC)


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Capcom has revealed several exciting details about Resident Evil Revelations 2. The game was formally announced at Sony's pre-TGS 2014 conference on Sept. 1, 2014, and due for release in Japan sometime in early 2015. The game will be available for the PS3, PS4, Xbox 360, Xbox One and Steam. Capcom has confirmed that the development team responsible for Revelations will be working on the game.There was a playable demo at Capcom's booth at TGS this year.
Despite its nominal status as a sequel to Revelations, the game will not feature Chris Redfield or Jill Valentine as main characters, and will instead feature a new set of characters in a new setting. Instead, Revelations 2 will mark the return of protagonist Claire Redfield and a new character named Moira Burton (who is the daughter of S.T.A.R.S. member Barry Burton).
A new enemy type will make its debut, known as the "Afflicted". While looking like zombies, it's said they are "...something quite different." Players need to choose how react to them when in combat.
Capcom released several screens of the game along with a teaser trailer, check them out below!