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Newsletter: Apple: Amnesty International's Next Target & Google Map's New Feature
Srishti Sisodia, 2018-03-22
0 10 min read
"The medium is the message. This is merely to say that the personal and social consequences of any medium – that is, of any extension of ourselves – result from the new scale that is introduced into our affairs by each extension of ourselves, or by any new technology." ~ Marshall McLuhan
AMNESTY INTERNATIONAL ACCUSES APPLE OF DECEIVING CHINESE ICLOUD USERS
Amnesty International launches a social media campaign against Apple and accused it of deceiving iCloud users in China.
Amnesty International is an NGO marching a campaign to stop wrong happenings on social media. Their latest target is everyone's favorite tech brand, Apple. You might remember that last month Apple transferred the iCloud data of Chinese users to mainland China, when China insisted. Amnesty is taking charge and accusing Apple of deceiving Chinese iCloud users by letting Chinese government scrutinize their personal data. Apple transferred the operation of its iCloud service for Chinese users to Guizhou-Cloud Big Data. All the photos, contacts, documents, messages and other data of Chinese users were moved to Guizhou-Cloud Big Data.
The campaign is against the partial behavior done with Chinese users. Thanks to this decision, now their data could be under constant surveillance and the privacy is no longer a trait of saving the data online.
This decision itself mocks the famous super bowl ad 1984 when Apple first introduced Macintosh. The ad suggests that Apple is the company which beliefs in freedom of expression. This upheaval has just started when Tim Cook, is visiting Beijing to co-chair some reputable business forum. Impeccable Timing, isn't it?
IS APPLE REALLY GUILTY?
After all of this, there is a dilemma whether Apple is really guilty or not. According to the legislature laws ordained in China in 2017, all the cloud services should be handled by the Chinese companies. So, Apple was given with the choice to either establish joint ventures with Chinese partners or lease server space inside China.
So, Apple made its choice and transferred the data to Guizhou-Cloud Big Data. The step is posing risk for Chinese users. Now, merely expressing their emotions, communicating with people, basically doing things that are not approved by authorities can put them at risk and might result into imprisonment.
Nicholas Bequelin, East Asia Director at Amnesty International, stated, "Tim Cook is not being upfront with Apple's Chinese users when insisting that their private data will always be secure. Apple's pursuit of profits has left Chinese iCloud users facing huge new privacy risks. Tim Cook preaches the importance of privacy but for Apple's Chinese customers' these commitments are meaningless. It is pure doublethink. By handing over its China iCloud service to a local company without sufficient safeguards, the Chinese authorities now have potentially unfettered access to all Apple's Chinese customers' iCloud data. Apple knows it, yet has not warned its customers in China of the risks."
COULD THIS BE CONSIDERED AS A ROUGH PATCH FOR TECHNOLOGY?
With Twitter already in clutches of the NGO and Apple now added to the social media campaign due to its doublethink, it seems that no matter how technology has profited us but these shortcomings make us think that it would have been better if we were living in stone age.
Technology being the biggest help in many ways has been the need but it has also turned up as the risk of exposing your private life to the world and violating basic human rights. All of this needs to be toned down and we, the users and appreciators of technology need an assurance for security and privacy.
GOOGLE MAPS ON IPHONE CAN HELP YOU ESTIMATE WAIT TIME IN RESTAURANTS
Now with your iPhone, you can book a table and estimate wait time at your favorite restaurants using Google Maps.
WHAT IS THE FEATURE CAPABLE OF?
Ever thought of a day, on which all you want is a cup of coffee and muffin to get through the day. However, when you turn up to your favorite restaurant, you can't find a table for you, saddening, right?
One of the ways to avoid it would be booking a table in advance but what if you get a sudden urge to taste your favorite sushi at a Chinese restaurant around the corner, then what?
Well, if you have an iPhone, don't have to worry about it anymore, as Google Maps for iPhone now tells you the average wait time for restaurants around the world.
This feature already works for Google Search since November 2017 and now it is coming to Google Maps too.
So, now a restaurant's information card within the app will provide you detail info about the popular times hour by hour throughout the day, and how crowded the place is when you are looking. Moreover, it also informs you about the time of day when you might have to wait for the longest so that you could plan accordingly.
WHAT OTHER FEATURES WERE ADDED?
There are other features added to Google Maps with this update. The update brings improvements for transit directions which will let you know the most efficient route to your train.
The feature is available in New York, Los Angeles, Paris, Madrid, Barcelona, Budapest, Moscow, Kiev, Hong Kong, Taipei, Singapore, and Delhi. It is coming to more locations soon.
Google Maps has been working on the software to make it more efficient. The new design of the icons will make it easier to identify useful or interesting places nearby.
Also Read: How To Unlock Google Maps' Hidden Driving Mode?
According to Liz Hunt, product manager of Google Maps, the concurrent work follows a revamp in the interface design, with an aim to reflect "your world, right now,"
NEWSLETTER: FACEBOOK'S PETITION FEATURE & GOOGLE'S REVOLUTIONARY NEW TECH
Newsletter: Private Tweets Exposed & Fossil's Next Smartwatch Will Be Expensive
Newsletter: Amazon Web Services Announce AWS Backup & Google Hikes G Suite Prices
Newsletter: DuckDuckGo Inherits Apple Maps & New Official Battery Cases for iPhone


A week late, I know. I've been ridiculously busy and I have not even gone more than a few light years these past two weeks, its just been mine, eat, mine, sleep, repeat. First thing is first though, you know what I said 2 weeks ago about me thinking that I was close to Elite Status? Well I now have joined the Elite! A few days after I docked, Deep Space Surveys, who are running the station, bought the cartographic services online. I sold my huge batch of data for a nice wedge of credits, gaining numerous first discovered systems, earth like worlds and water worlds. Within a few minutes I had the notification come over my comms. "Right on, Commander, The Pilots Federation has bestowed its greatest honour on you and granted you the explorer rank of elite". I stared at the animated Elite emblem for a little while, feeling like I had just won the Federal Grand Lottery, a proud moment indeed.
The second Mining operation kicked off back on the 7th with just as much enthusiasm from the fleet as the first. There was a surprise announcement too, apparently as the fleet had mined so many extra tonnes of resources during the first operation it had been decided that a mega ship, The DSSV Distant World, would be built and situated in the same system as the new station, however, it's purpose still remains to be seen. We needed to mine tonnes of bauxite, water and liquid oxygen that the builders had specified was required to complete the projects. After the haulers had caught up to the fleet and delivered all my mining gear from the Omega Sector, I oversaw the refit and turned my ship back into a full-on Mining rig for the last time.
Once again, I felt instantly at home dropping into a gas giant's rings in a system next door, I could have been back in Delkar, apart from the intense backdrop being filled with hundreds of thousands of additional stars. If you'd told me a year ago that I would end up mining in the center of the galaxy, I would have laughed at you and told you to lay off the stims! This past month has been unlike any other, that's for sure. After chatting to the pros from the mining union (IMU) I settled into mining a bauxite hotspot for the week, less strenuous than shifts back home when we used to cram in multiple contracts at the same time, but still exhausting. All the while I could see the progress being made on the station, the habitat ring being built piece by piece, growing each day. My little Phantom did me proud once more, having allowed me to mine a not insubstantial amount of 1082 tonnes. The fleet smashed the requested quantities required again, although not reaching above 10.5 tiers this time. We will be leaving our mark on this extreme, remote spot in the galaxy, contributing to studying the super massive black hole and creating a haven for future expeditions for numerous decades to come. With the hard work done it was time to relax and unwind before the longest most dangerous part of the expedition started.
During the downtime, I'd got chatting to a few mechanics that were members of the Hull Seals, the dedicated lot that have been repairing explorers in need during the expedition. During a drinking session, they had joked about me letting them loose on my Phantom to give it an overhaul and face lift. As a treat to myself, I took them up on the offer and they eagerly went to work, once we were all sober obviously. The Voids Flame is now kitted out with two new tail fins, an engine exhaust heat shield and an overhaul of the exhaust systems, with new heat exchanger units and inlets build into the top of the ship that elegantly sweep down to the wing edges. I also had her completely repainted along with adding an Explorer Elite emblem above the cockpit. She now looks like a completely different ship, it's like Delacy have released the Phantom MK2 and it's just flown off the ship production line. Pretty sure she won't be looking quite so shiny by the time I next dock at a station though.
I managed to sleep through the mass jump at the weekend when the fleet moved on. I was ready to go, pre-flight done, nav points set and I somehow managed to fall asleep strapped in to my flight seat in the cockpit whilst in the hanger, the long "days" and my messed-up body clock having got the better of me. I managed to join a small group of commanders outside the station and we jumped once more onward, saying farewell to any form of civilisation.
Here I am then, some 2,000 ly from Sagittarius A* but not even half way to the next waypoint, numer 8, at 'Lower' Goliath's Rest in Hypiae Phyloi LR-C d22. It's going to be exciting and scary from here on out, with focus purely on science and exploration. There are over 50,000 ly still to go with only a third of our journey behind us. I must admit I have not even thought about the return trip from Beagle Point, neither do I want to, not yet anyway. So, no more stations, outposts or mega ships to land at, nothing but the black and new discoveries await us.


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Article Free access | 10.1172/JCI6572
Effects of a low-fat, high-carbohydrate diet on VLDL-triglyceride assembly, production, and clearance
Elizabeth J. Parks,1 Ronald M. Krauss,2 Mark P. Christiansen,3 Richard A. Neese,3 and Marc K. Hellerstein3,4
1Department of Food Science and Nutrition, University of Minnesota–Twin Cities, St. Paul, Minnesota 55108, USA2Department of Molecular and Nuclear Medicine, Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA3Department of Medicine, University of California–San Francisco, and the Medical Service, San Francisco General Hospital, San Francisco, California 94110, USA4Department of Nutritional Sciences, University of California–Berkeley, Berkeley, California 94720, USA
Address correspondence to: Elizabeth J. Parks, Department of Food Science and Nutrition, University of Minnesota–Twin Cities, St. Paul, Minnesota 55108, USA. E-mail: eparks@tc.umn.edu. Or to: Marc K. Hellerstein, Department of Nutritional Sciences, University of California–Berkeley, Berkeley, California 94720-3104, USA. Phone: (510) 642-0646; Fax: (510) 642-0535; E-mail: march@nature.berkeley.edu.
Find articles by Parks, E. in: JCI | PubMed | Google Scholar
Find articles by Krauss, R. in: JCI | PubMed | Google Scholar
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Published in Volume 104, Issue 8 on October 15, 1999
J Clin Invest. 1999;104(8):1087–1096. https://doi.org/10.1172/JCI6572.
Received: February 17, 1999; Accepted: August 30, 1999
Low-fat, high-carbohydrate (LF/HC) diets commonly elevate plasma triglyceride (TG) concentrations, but the kinetic mechanisms responsible for this effect remain uncertain. Subjects with low TG (normolipidemic [NL]) and those with moderately elevated TG (hypertriglyceridemic [HTG]) were studied on both a control and an LF/HC diet. We measured VLDL particle and TG transport rates, plasma nonesterified fatty acid (NEFA) flux, and sources of fatty acids used for the assembly of VLDL-TG. The LF/HC diet resulted in a 60% elevation in TG, a 37% reduction in VLDL-TG clearance, and an 18% reduction in whole-body fat oxidation, but no significant change in VLDL-apo B or VLDL-TG secretion rates. Significant elevations in fasting apo B-48 concentrations were observed on the LF/HC in HTG subjects. In both groups, fasting de novo lipogenesis was low regardless of diet. The NEFA pool contributed the great majority of fatty acids to VLDL-TG in NL subjects on both diets, whereas in HTG subjects, the contribution of NEFA was somewhat lower overall and was reduced further in individuals on the LF/HC diet. Between 13% and 29% of VLDL-TG fatty acids remained unaccounted for by the sum of de novo lipogenesis and plasma NEFA input in HTG subjects. We conclude that (a) whole-food LF/HC diets reduce VLDL-TG clearance and do not increase VLDL-TG secretion or de novo lipogenesis; (b) sources of fatty acids for assembly of VLDL-TG differ between HTG and NL subjects and are further affected by diet composition; (c) the presence of chylomicron remnants in the fasting state on LF/HC diets may contribute to elevated TG levels by competing for VLDL-TG lipolysis and by providing a source of fatty acids for hepatic VLDL-TG synthesis; and (d) the assembly, production, and clearance of elevated plasma VLDL-TG in response to LF/HC diets therefore differ from those for elevated TG on higher-fat diets.
Increases in fasting plasma triglyceride (TG) concentrations are commonly observed during the consumption of low-fat, high-carbohydrate (LF/HC) diets (1, 2). Other serum lipid changes include reductions in HDL, LDL, and total cholesterol concentrations. The potential atherogenicity of carbohydrate-induced elevations in TG has been the subject of current debate (1–5). Endogenous hypertriglyceridemia, which is observed in individuals on higher-fat diets, is associated with increased coronary heart disease risk (6), but it is not known whether carbohydrate-induced and endogenous TG elevations share underlying kinetic mechanisms and therefore similar atherogenic risk.
Differences in lipoprotein dynamics between the 2 forms of hypertriglyceridemia might contribute differently to the risk for cardiovascular disease. In the fasting state, most plasma TGs are carried in VLDLs. Overproduction of VLDL particles might generate a higher flux of atherogenic particles to LDLs in the plasma or into the artery wall. By contrast, reduced clearance of VLDL-TG does not increase the flux of cholesterol into the plasma. Moreover, nonpharmacologic regimens, such as weight loss and exercise training, may increase TG clearance.
Synthesis of VLDL-TG, and particle assembly and secretion, have been the subjects of much in vitro research (7–10). Much of this work, however, has been performed in HepG2 cells, which exhibit defective TG mobilization (9, 10). In humans, evidence has been presented for similar TG metabolism in the endogenous and carbohydrate-induced forms of hypertriglyceridemia. TG secretion rates are elevated in endogenous hypertriglyceridemia (11–15), and some (12, 16–19), but not all (20, 21), workers have reported high TG flux rates in subjects fed LF/HC diets. Nestel et al. (22) and Boberg et al. (23, 24) suggested, on the basis of indirect evidence, that the source of fatty acids supporting elevated TG synthesis on LF/HC diets may have been from de novo lipogenesis. If increases in dietary carbohydrate elevate de novo lipogenesis, this increase in fatty acid availability to the liver could drive hepatic TG overproduction.
Most previous studies examining the kinetic mechanisms of carbohydrate-induced hypertriglyceridemia have used either short-term (<10 days) feeding protocols (12, 13, 15), liquid diets nearly devoid of fat (19, 25, 26), or diets in which the carbohydrate was primarily in the form of simple sugars (12, 19, 27). Such high-sugar or liquid-formula diets may be metabolized differently than whole-food, high-fiber, low-fat diets consumed normally. Furthermore, the contribution from de novo lipogenesis to fatty acids in TG had not been quantified reliably, owing to the lack of accurate methods to measure this process in humans (28). Accordingly, the present study was designed to determine the metabolic and kinetic mechanisms underlying carbohydrate-induced elevations in TG in subjects consuming an isoenergetic diet that was composed of whole foods, rich in fiber and restricted in monosaccharides. Normolipidemic subjects and those with mildly elevated fasting TG levels were compared to determine whether these groups differed in their response to the LF/HC diet.
Human subjects. Volunteers were recruited by advertisement and gave written informed consent before enrolling in the study. The University of California–Berkeley and University of California–San Francisco Committees on Human Research approved the protocols. Subjects were eligible for inclusion in the study if their screening TG concentration was less than 100 mg/dL (normolipidemic [NL]; n = 6), or was 100–200 mg/dL (hypertriglyceridemic [HTG]; n = 5). We chose to study subjects with moderately elevated TG, on the basis of previous work (E.J. Parks, unpublished data; and ref. 29) showing that carbohydrate-induced elevations in TG tend to be more variable in individuals with higher TG concentrations (>250 mg/dL), whereas those with TG in this moderate range have a more reproducible response to LF/HC diets. TG values represented the average of at least 2 measurements, obtained approximately 2 weeks apart in subjects who had fasted 12 hours, were well hydrated, and had abstained from alcohol for at least 48 hours. All subjects were nonsmoking, healthy males who had normal liver enzyme concentrations and no history of medical disorders (liver disease, kidney disease, diabetes mellitus, etc.). One HTG subject had been on a hypolipidemic medication (niacin) previously; this subject's medication had been discontinued for 9 weeks before entry into the study. NL and HTG subjects did not differ in age (31 ± 7 and 37 ± 4 years, respectively; P = 0.25), but were significantly different in body weight (73.1 ± 6.9 and 87.3 ± 3.2 kg, respectively; P = 0.008), body mass index (BMI; 22.4 ± 1.3 and 27.6 ± 1.1 kg/m2, respectively; P = 0.008), and percentage of body fat (16.4 ± 3.3 and 26.5 ± 1.1%, respectively; P = 0.001).
Study design. Subjects consumed 2 isoenergetic diets: a control diet (35% fat) for 1 week, followed by an LF/HC (15% fat) diet for 5 weeks. The composition of the 2 diets is shown in Table 1. Foods making up the control diet were chosen to be similar to those routinely consumed by the subjects ad libitum during screening. Ad libitum consumption was determined over a period of 2–6 weeks, by 3 methods: 3-day food records, food-frequency questionnaires, and diet history interviews. Only those subjects whose ad libitum dietary fat intake was 30–35% were enrolled in the study. Both screening and subject participation in the study were scheduled to avoid public holidays and personal events (birthdays, anniversaries, etc.). The LF/HC diet was designed to replace dietary fat with carbohydrate, while limiting the consumption of monosaccharides and sucrose. As typically occurs when fat intake is reduced using whole foods, the content of other dietary components (e.g., cholesterol, fiber, and saturated fat) also changed (Table 1). Subjects were instructed to limit alcohol intake to 1 drink or less per week (equivalent to 12 oz of beer, 8 oz of wine, or 1 oz of hard liquor). For both diets, all meals, beverages, and snacks were prepared by the staff of the metabolic kitchen at the General Clinical Research Center (GCRC) of San Francisco General Hospital. Each subject reported to the GCRC 3–5 days per week to be interviewed by study staff, get weighed, and consume the main meal of the day. Food to be consumed until the next visit was packed and sent home with the subject for consumption as an outpatient. Subjects were instructed to consume all the study food and not to consume any other food during the 6-week study period. To ensure that metabolic changes on LF/HC diet were not confounded by weight loss, adjustments of dietary energy were made to maintain body weight within 1–2 kg of baseline. Frequent dietary interviews and inspection of returned food containers were used to assess subject compliance. Body composition was measured by bioelectric impedance analysis (model 1990B; Valhalla Scientific Inc., San Diego, California, USA), using calculations according to manufacturer's equations.
Composition of experimental dietsA
Infusion protocol. Sodium [1-13C1]acetate, [5,5,5-2H3]leucine, [1,2,3,4-13C4]palmitate, [2-13C1]glycerol, and [U-13C6]glucose were purchased from Isotec (Miamisburg, Ohio, USA) or Cambridge Isotope Laboratory (Andover, Massachusetts, USA). Isotopic purity was greater than 98% for all tracers used. The subjects were admitted to the GCRC for 2 stable isotope infusion studies, one administered at the end of each diet phase. The infusion protocol is shown in Figure 1. The evening meal on day 1 (at 1700 hours) reflected the diet composition of the current feeding phase; that is, a 35% fat meal was fed the night before infusion study no. 1, and a 15% fat meal was fed the night before infusion study no. 2. After dinner, the subjects remained fasted until the end of the infusion study (1700 hours on day 2). At 2200 hours on day 1, an intravenous line was placed in the antecubital vein of each arm; one intravenous line was for administration of isotopes, and the other was for drawing blood. At 2400 hours, an infusion was started that contained [1-13C1]acetate and [5,5,5-2H3]leucine. At 0400 hours on day 2, a second infusion was started that contained [2-13C1]glycerol, [U-13C6]glucose, and [1,2,3,4-13C4]palmitate complexed with human albumin in a molar ratio of 2 fatty acids per albumin (30). Frequent blood samples were drawn between 0400 and 1700 hours on day 2. All blood was drawn into iced Vacutainers containing 1 mg/mL EDTA. Plasma was separated immediately by centrifugation (1,500 g for 20 minutes) at 4°C, kept on ice, and aliquoted for various analyses. Plasma samples for nonesterified fatty acid (NEFA) analysis were extracted with a 30:70 heptane/isopropanol mixture within 1 hour of the blood draw. An aliquot of plasma was also immediately deproteinized with perchloric acid (2:1, vol/vol) in preparation for isolation of glucose and glycerol by ion exchange chromatography as described previously (31). Subjects rested, watched television, or read during the infusion tests. Non–energy-containing, noncaffeinated drinks (e.g., herbal tea, diet soda) were available upon request. Indirect calorimetry was performed for 30 minutes between 0800 and 0900 hours on day 2. A Deltatrac metabolic cart (Sensor Medix, Yorba Linda, California, USA) in the hooded mode was used.
Stable isotope infusion protocol. Subjects were admitted to the GCRC for a 24-hour isotope infusion study; protocol and calculations are described in the text.
Analysis of metabolites. Analysis of plasma total, LDL and HDL cholesterol, TG, and apo A-I and B concentrations was performed by staff at the Lipoprotein Laboratory (Lawrence Berkeley National Laboratory, Berkeley, California, USA). Lipids were measured enzymatically on a Ciba-Corning Express Model 550 (Ciba Corning Diagnostics, Oberlin, Ohio, USA), and VLDL cholesterol was calculated by difference. Apolipoproteins were measured by maximal radial immunodiffusion (32). Fasting apo B-48 and B-100 concentrations within the d < 1.006 g/mL fraction were measured by SDS-PAGE in the laboratory of R. Havel (University of California–San Francisco, San Francisco, California, USA) (33). Concentrations of glucose in plasma samples and in the infusates were measured using a glucose analyzer (Yellow Springs Instrument Co., Yellow Springs, Ohio, USA); plasma insulin concentrations were determined by RIA (Diagnostic Products Corp., Los Angeles, California, USA).
VLDL isolation and subfractionation. Within 24 hours of each infusion study, plasma samples were subjected to ultracentrifugation at 35,000 rpm for 25 minutes in a 50.3 rotor at 15°C (1.6 × 106g) to separate chylomicrons (34); VLDL (d < 1.006 g/mL) was then isolated by ultracentrifugation for 20 hours in a 50.3 Beckman rotor (1.3 × 108g at 12°C). The total VLDL sample from each time point was divided into 2 aliquots. The first aliquot of VLDL was used for isolation of lipoprotein TG by thin-layer chromatography (TLC). After scraping the TG band from the TLC plate, VLDL-TG fatty acids were transesterified to fatty acid methyl esters, in preparation for gas chromatographic/mass spectrometric analysis (35). The second aliquot of VLDL was subjected to an additional ultracentrifugation step to separate large, buoyant VLDL particles for isolation of apo B. This strategy was used to isolate VLDL that most closely represented particles newly secreted by the liver. The longer VLDL circulates, the more it undergoes remodeling in the plasma compartment (36); the resulting smaller particles have an altered composition and are more prevalent in the plasma of HTG subjects (36). As described previously (37), total VLDL was dialyzed to d = 1.21 g/mL with 2 changes of dialysis buffer over a 2-day period, layered under a discontinuous gradient of salt solutions of 3 densities (1.02, 1.01, and 1.0 g/mL), and subjected to nonequilibrium density gradient ultracentrifugation in an SW41 swinging bucket rotor (Beckman Instruments, Palo Alto, California, USA) for 6 hours at 40,000 rpm and 17°C (1.8 × 106g). The top 1 cm3, denoted large VLDL, was aspirated. Because the sample quantity was limited, large VLDLs were analyzed only for apo B-100 [5,5,5-2H3]leucine enrichment.
Isolation of metabolites and gas chromatographic/mass spectrometric analysis. All gas chromatography/mass spectrometry columns were fused silica and were purchased from J&W Scientific (Folsom, California, USA). Gas chromatography/mass spectrometry was performed using an HP-5971 instrument (Hewlett-Packard, Palo Alto, California, USA) in the selected-ion monitoring mode. Plasma NEFA, containing 100 nmol pentadecanoic acid (Sigma Chemical Co., St. Louis, Missouri, USA) as an internal standard, were isolated by TLC and transesterified to fatty acid methyl esters. Methyl esters of plasma NEFA and VLDL-TG fatty acids were separated on a DB225 gas chromatography column, and fatty acid composition was measured by flame ionization detection, as described previously (35). The enrichment of [1,2,3,4-13C4]palmitate (monitoring m/z: 270, 271, 272, and 274) was assessed using electron impact ionization and a standard curve. Plasma glucose and free glycerol were isolated by ion exchange chromatography and derivatized with pyridine/acetic anhydride (38). Glucose-pentaacetate was analyzed using a 60-m DB17 column under methane chemical ionization for the molecular ions (monitoring m/z: 331, 332, 333, and 337). Glycerol triacetate was analyzed using a DB225 column under chemical ionization (monitoring m/z: 159/160). Standard curves were used to assess the enrichment of [U-13C6]glucose and [2-13C1]glycerol. Large VLDL-apo B was precipitated using the method of Egusa et al. (39). After protein hydrolysis in 6 N HCL, apo B amino acids were derivatized with MTBSTFA/acetonitrile and separated on a 30-m DB17 gas chromatography column. Positive fragments were measured under electron impact ionization (m/z: 200 and 203), and enrichments were calculated using a [5,5,5-2H3]leucine standard curve.
Calculations. Calculation of biosynthetic rates was done according to the precursor-product relationship (40). VLDL-TG synthetic rate was calculated in 2 ways from the incorporation of [1,2,3,4-13C4]palmitate (40). Fractional replacement (turnover) rates (Ks) were calculated by modeling the rise toward plateau enrichment of [1,2,3,4-13C4]palmitate into VLDL-TG. The data were fit to the equation y = A∞ × [1–e –Ks(t–c)], where y = VLDL-TG palmitate enrichment, A = the plateau or asymptote value of TG palmitate, t = time in hours, and c = lag period before isotope incorporation into secreted VLDL-TG. In the same manner, VLDL particle fractional replacement rate (Ks) was calculated from the enrichment of [5,5,5-2H3]leucine in large VLDL-apo B. Half-lives were calculated by dividing 0.693 by Ks (31). Plasma volume was estimated as described by Grundy et al. (41) to account for the differences in plasma volume between subjects of different body weight.
The transport rate of total VLDL-TG was determined as follows: VLDL-TG transport rate (μmol • kg fat-free mass [FFM]–1h–1) = VLDL-TG concentration (μmol/L) × plasma volume (L) × Ks (h–1) / FFM (kg).
The plasma apo B concentration in large VLDL was determined from the apo B concentration of VLDL after subfractionation. We corrected for dilution due to buffers added during the procedure, but recognize that subfractionation may result in inaccuracies of apo B pool size measurements. The transport rate of large VLDL-apo B was calculated as follows: Large VLDL-apo B transport rate (μmol • kg–1h–1) = plasma concentration (μmol/mL) × plasma volume (mL) × Ks (h–1) / total body weight (kg).
The clearance rate of a metabolite represents the amount of plasma completely cleared of the substance per minute and reflects its efficiency of removal (42). At steady state, clearance was calculated as the ratio of transport or turnover rate to plasma concentration. Thus, to calculate the clearance rates of large VLDL-apo B and VLDL-TG (mL/min), their transport rates (μmol/min) were divided by their respective plasma concentrations (μmol/mL).
The sources of fatty acids used for the assembly of VLDL-TG were determined as follows. The proportion of VLDL-TG palmitate derived from circulating NEFA was calculated by dividing the enrichment of [1,2,3,4-13C4]palmitate in VLDL-TG at plateau by the steady-state enrichment of the plasma NEFA pool. The infusion of [1,2,3,4-13C4]palmitate was between 0400–1600 hours, and enrichment within plasma NEFA reached steady state within 1 hour after the start of the infusion (data not shown). The NEFA enrichment used was the average of at least 6 time points. In all subjects, VLDL-TG [1,2,3,4-13C4]palmitate enrichment reached a plateau by the 9th hour of label infusion, and the plateau value was determined from an average of at least the final 2 time points taken. (An example of the calculation for the data of a NL subject follows: the plateau of TG palmitate enrichment was 1.51% and the steady-state enrichment of plasma nonesterified palmitate was 1.55%. Therefore, 97.4% (1.51/1.55) of TG palmitate was derived from the plasma NEFA pool; Figure 2). The proportion of VLDL-TG palmitate derived from hepatic de novo lipogenesis (i.e., made "new" from acetyl-CoA precursors) was calculated by mass isotopomer distribution analysis. VLDL isolated from plasma drawn at 0800–0900 hours was used for this analysis in 6 subjects; de novo lipogenesis was also measured at 8 additional time points (0200, 0400, 0600, 1000, 1200, 1400, 1600, and 1700 hours) and found not to vary during the course of the infusion. Mass isotopomer distribution analysis allows calculation of the isotopic enrichment of the true biosynthetic precursor from the labeling pattern in a polymer, as has been described in detail previously (43). The fractional contribution of gluconeogenesis to endogenous glucose production was determined from the incorporation of [2-13C1]glycerol into plasma glucose, using mass isotopomer distribution analysis to calculate the isotopic enrichment of the triose-phosphate precursor pool (43). The rate of endogenous glucose production was determined by the dilution of [U-13C6]glucose (31). The rate of adipose tissue lipolysis was calculated from the dilution of [1,2,3,4-13C4]palmitate and [2-13C1]glycerol in plasma (31). Indirect calorimetry was used to measure energy expenditure using standard equations to determine net substrate oxidation, nonprotein respiratory quotient, and energy expenditure (44). A fixed protein catabolism was assumed based on the daily protein intake of the prepared diets.
Percentage of VLDL-TG palmitate derived from the plasma NEFA pool. Data are from 2 representative subjects on the control diet: an NL subject (top) and an HTG subject (bottom). The infusion of [1,2,3,4-13C4]palmitate (from 0400 to 1600 hours) reached steady state within the plasma NFA pool 1 hour after the start of the infusion.
Statistics. Data are mean ± SEM. Statistical analyses were performed using SPSS statistical software (SPSS Inc., Chicago, Illinois, USA), with P < 0.05 considered significant. Variables whose values were not normally distributed (e.g., plasma TG concentration) were log-transformed before statistical analysis. The subjects were stratified by baseline TG values into 2 groups (NL: subjects with TG < 100 mg/dL; and HTG: those with TG = 100–200 mg/dL). To compare the 2 groups for change in response, analysis of covariance was performed to control for differences in baseline values. Measures of glucose flux were collected in a subset of subjects (3 NL and 3 HTG subjects); analysis of covariance was not performed on these data because the sample size was deemed too small. A P value for the overall treatment effect was also calculated from a paired t test of the entire group (n = 11).
Analysis of diets and comparison of baseline values between NL and HTG subjects. The study diets differed in their percentage of energy from fat, as well as in other characteristics (Table 1). In particular, compared with the control diet, the LF/HC diet contained 50% more fiber and 89% less cholesterol. The percentage distribution of carbohydrate as simple sugars (sucrose, fructose, glucose, lactose, and maltose) remained constant, although the absolute intake of simple sugars increased by 38% on the LF/HC diet. There was no difference in baseline intake between the NL and HTG subjects with respect to total energy intake or macronutrient composition of the diet (in grams per day or percentage of energy of fat, protein, or carbohydrate). All subjects tolerated the LF/HC diet well, aside from a common complaint of feeling overly full. The groups had significantly different baseline values for TG, total cholesterol, LDL cholesterol, VLDL cholesterol, and apo B (P < 0.05), with the HTG subjects having higher values for all of these variables (Table 2). HTG subjects tended to have lower concentrations of HDL cholesterol (P = 0.09).
Fasting concentrations of plasma metabolites on the control and LF/HC dietsA
Plasma lipid and lipoprotein concentrations. The lipid responses to dietary fat reduction are shown in Table 2. All subjects experienced significant elevations in fasting TG concentration on the LF/HC diet. Significant reductions in LDL, HDL cholesterol, and elevations in VLDL cholesterol were observed, with no group effect observed for any of these variables. The relative increase in TG was similar for both groups, when the TG values were log-transformed (12% for NL and 9% for HTG). On the control diet, plasma insulin concentration was borderline/significantly higher in the HTG subjects (52 ± 10 pmol/L) compared with the NL subjects (31 ± 5; P = 0.06); no treatment effect was observed for this variable. The fasting concentrations of apo A-I, glucose, and NEFA remained unchanged with LF/HC feeding, with no difference in response between the groups. In the HTG group only, fasting concentrations of apo B-100 and B-48 from the TG-rich lipoprotein fraction were measured. LF/HC feeding was associated with significant, 2-fold increases in both the apo B-100 and apo B-48 content of the TG-rich lipoprotein fraction (Figure 3).
Apolipoprotein (apo) concentrations in the TG-rich lipoprotein (TRL) fraction in HTG subjects. Values are mean ± SEM. *P < 0.05, comparison between dietary treatments.
Fuel utilization. Measures of carbohydrate and fat metabolism are presented in Table 3. The energy expenditure of the subjects was not significantly different between the dietary phases (averaging 12,100 kJ/d for all subjects combined). In a subset of subjects (3 from each group), glucose flux data were obtained and showed no effect of diet on glucose production or the sources of endogenous glucose production. The 2 groups did not respond differently to the diets with respect to fatty acid flux or glucose oxidation. For the group as a whole, glucose oxidation was nonsignificantly higher on the LF/HC diet (P = 0.09, for treatment effect). Whole-body fat oxidation was significantly lower for the entire group after the LF/HC diet (18% reduced; P = 0.02 for the treatment effect).
Glucose and fatty acid kinetics and substrate oxidation ratesA
Lipoprotein kinetics. The dietary response of the subjects with respect to VLDL particle and TG transport is presented in Table 4. Analysis of covariance revealed that the 2 groups responded differently with respect to large VLDL-apo B transport rate (P = 0.03), although neither of the P values for changes in the individual groups was significant (P < 0.13 and 0.31 for the control and HTG subjects, respectively); this was most likely due to the small sample size and high variability. Use of a different statistical comparison (comparing the means for the groups at a given time point) showed that at baseline, the apo B transport rates were not different between the groups (0.11 vs. 0.24 μmol • kg total body weight [TBW]–1 h–1 for the control vs. HTG, respectively; P = 0.31), whereas this difference approached significance after the LF/HC diet (0.13 vs. 0.32 μmol • kg TBW–1h–1; P = 0.08). No group differences were observed for any of the other variables presented in Table 4. For all subjects combined, the mass of large VLDL-apo B was significantly increased on the LF/HC diet (94% and 51% for the controls and HTG, respectively); the fractional replacement rate was nonsignificantly slower (P = 0.09), but clearance rate did not change. The concentration of TG in the large VLDL fraction was significantly increased in both groups on the LF/HC diet: 62% in the control and 75% in the HTG subjects (treatment effect for the entire group: P = 0.04). VLDL-TG transport rate was not different between the dietary phases (P = 0.58). By contrast, VLDL-TG fractional replacement rate (Ks) was reduced significantly on the LF/HC diet (P = 0.03). This slower fractional replacement rate was accompanied by a 37% reduction in the clearance rate of VLDL-TG (overall P = 0.05), with no significant difference in response between the groups.
Kinetics of VLDL-apo B and VLDL-TGA
Assembly of VLDL-TG: sources of fatty acids. The percentage of VLDL-TG derived from the plasma NEFA pool was determined from the relative enrichments of this pool during infusion of [1,2,3,4-13C4]palmitic acid. Representative data from 2 subjects are shown in Figure 2. As demonstrated by the NL subject's data, more than 90% of palmitic acid found in VLDL-TG derived from the plasma NEFA pool at the end of the 12-hour infusion of label. By contrast, data from the HTG subject reveal that at steady state, about 72% of TG fatty acids were derived from NEFA. The contribution from de novo lipogenesis to palmitate in VLDL-TG was also measured. The summary data (Figure 4) show that de novo lipogenesis did not make a substantial contribution of fatty acids (<5%) to fasting TG on either diet, in either group. For NL subjects on both diets, plasma NEFA provided the primary source of palmitate in VLDL-TG (94% and 92% for the control and LF/HC, respectively). Compared with the NL subjects, the contribution of NEFA was significantly lower in the HTG subjects on both diets (84% and 67% from NEFA on the control and LF/HC diets, respectively). The total percentage of VLDL-TG accounted for by the sum from NEFA and de novo lipogenesis was similar in the NL subjects, regardless of diet (97%). In the HTG subjects, the total accounted for on the control diet was 87% (84% from NEFA, and 3% from de novo lipogenesis), which was significantly less than that of the NL group (P = 0.02). This difference became greater after the LF/HC diet, when the total accounted for by NEFA plus de novo lipogenesis dropped to 71% in the HTG (compared with 97% in NL subjects; P = 0.004 between groups). Within the HTG group alone, LF/HC feeding significantly reduced the percentage of VLDL-TG palmitate accounted for by fatty acid inputs (87% vs. 71% on the control and LF/HC diets, respectively; P = 0.04). A significant negative correlation was observed between the percentage of VLDL-TG palmitate derived from the plasma NEFA pool and the body fat percentage in subjects consuming a 35% fat diet (r = –0.70, P < 0.01; data not shown). This relationship was similar, although not statistically significant (r = –0.55, P = 0.07), after consumption of the LF/HC diet.
Sources of VLDL-TG palmitic acid. Values are mean ± SEM. The numbers on the bars represent the percentages of VLDL-TG palmitate derived from the NEFA pool alone (darker portion of the bar).
Fasting TG concentrations increased by 60% in subjects consuming the solid-food, high-fiber, LF/HC diet. These results underscore the ability of LF/HC diets to elevate fasting plasma TG even when the diet is composed of whole foods and is low in simple sugars. Increased secretion of TG was not the primary kinetic mechanism responsible for this carbohydrate-induced TG elevation, however; reduced TG clearance from the plasma was the major metabolic mechanism involved. This conclusion reveals a difference in the underlying mechanism from hypertriglyceridemia observed on higher-fat diets. Although lipoprotein kinetic studies are frequently limited in their ability to discern between primary effects on overproduction or reduced clearance of TG, the latter mechanism is supported by several independent measurements. First, the transport rate of VLDL-TG (as assessed by the kinetics of TG palmitate) was not increased on the LF/HC diet. Second, the half-life of VLDL-TG was prolonged, and the clearance of VLDL-TG was significantly reduced. Third, fasting apo B-48 concentrations were elevated. Finally, de novo lipogenesis was not increased.
Previous studies comparing TG secretion in NL individuals with that in those with endogenous hypertriglyceridemia consuming high-fat diets have reported significantly higher rates (11–15). In the present study, the TG secretion rate of HTG subjects was 2.7-fold higher than that of the NL subjects on the higher-fat diet. In contrast, carbohydrate-induced elevations in TG were explained by reduced clearance of VLDL-TG rather than increased production. The reduction in TG clearance during LF/HC feeding observed here differs from some previous reports of elevated TG production in carbohydrate-induced hypertriglyceridemia (12, 19, 27). However, we fed a whole-food, high-fiber diet, whereas those previous LF/HC research diets were of liquid form and/or high in mono- and disaccharides (12, 19, 27). Hudgins et al. (45) have recently shown that the form of carbohydrate (simple sugar vs. starch) markedly influences fatty acid synthesis (de novo lipogenesis; see later here). The form of carbohydrate might also influence TG production. Reduced VLDL-TG clearance may be due to competition between VLDL and chylomicron remnants for TG hydrolysis in the plasma compartment, as fasting apo B-48 concentrations were elevated in the HTG subjects. Other possible causes of reduced VLDL-TG clearance can be proposed (46–48). The mechanisms responsible for reduced VLDL-TG clearance on LF/HC diets need further study.
A second goal of this work was to determine whether dietary fat reduction altered the assembly of VLDL-TG, in particular the sources of fatty acids used for TG synthesis. In the NL subjects, NEFA provided more than 93% of the fatty acids secreted in VLDL-TG by the liver, and the contribution of this source was unchanged by dietary fat reduction. The synthesis of fatty acids de novo contributed less than 5% of VLDL-TG palmitate, even on the LF/HC diet, excluding hepatic de novo lipogenesis as a basis for increased TG secretion (24). Compared with the NL group, HTG subjects consuming the control diet had significantly lower percentages of TG palmitate derived from plasma NEFA (84%), with newly synthesized fatty acids accounting for less than 3% of VLDL-TG palmitate. Thus, 13% of fatty acid precursors for TG synthesis were derived from neither NEFA nor de novo lipogenesis. The percentage of TG precursors not accounted for by either isotopic labeling route became even greater when HTG subjects consumed the LF/HC diet (29% of VLDL-TG palmitate remaining unaccounted for). Several years ago, Barter and Nestel reported that a substantial percentage of VLDL fatty acids were not derived from NEFA in obese individuals (49). Havel et al. (50) and Boberg et al. (24) also showed that for some HTG subjects, splanchnic NEFA uptake did not explain higher TG secretion rates and that other sources must have provided the precursors for TG synthesis. Furthermore, elevated BMI correlates with lower contributions of plasma NEFA to VLDL-lipid (49). A similar inverse relationship between body fat percentage and plasma NEFA contribution to TG synthesis was observed in the present study on the control diet.
One source of unlabeled TG fatty acids in HTG subjects could be splanchnic lipid, from hepatic or visceral sources (20), as peripheral blood NEFA enrichments are used in the calculation (Figure 2). Obese subjects have increased liver TG content (51, 52). Havel et al. (50) observed that about two thirds of the NEFA taken up by the HTG liver escaped oxidation and were apparently stored, with only one third of the NEFA being secreted as TG. This process could lead to the slow turnover of hepatic TG droplets in HTG subjects. In the present study, a contribution from unlabeled hepatic lipid stores to TG synthesis may be less likely, because the subjects had been fasted for 24 hours by the end of the infusion test, which should substantially reduce hepatic lipid stores. Visceral adipose stores are also a potential source of fatty acids for TG assembly. This adipose depot is metabolically active (53, 54) and is an important predictor of abnormal plasma lipoprotein concentrations (55). Furthermore, individuals with upper body obesity have elevated VLDL-TG production rates (41, 56, 57). Visceral fatty acid sources could have contributed to the unlabeled VLDL-TG observed in the HTG subjects on the control diet (Figure 4), but an increase in their contribution on the LF/HC diet is less likely, as we and others (e.g., 58) found no change in body composition on the LF/HC diet.
Finally, an interesting potential source of unlabeled lipid for TG assembly on the LF/HC diet is chylomicron remnants cleared to the liver. In rats, chylomicron remnants contain approximately 50% of their original TG when cleared to the liver (59, 60). Very little is known about this process in humans. The 2-fold elevation in fasting apo B-48 concentrations observed in the HTG subjects after the LF/HC diet suggests that chylomicron remnants might provide a significant source of VLDL-TG fatty acids in the fasting state. The increased presence of B-48–containing TG-rich lipoproteins was surprising, given that the blood draw for this measurement occurred after the subjects had fasted 15 hours and that the last meal they consumed contained very little fat (15% of energy). However, Karpe et al. (61) have shown that the chylomicron remnant pool contains lipoprotein populations that are heterogeneous. One population may have a very short half-life (<15 minutes), whereas others may circulate for much longer periods. The elevation in fasting apo B-48 associated with LF/HC feeding could have resulted from alterations in the intestinal secretion pattern of chylomicrons, such that more particles were secreted in the fasting state or that a subpopulation of the chylomicrons secreted postprandially circulated for a longer time. This result requires further investigation.
Another somewhat surprising result was the role of de novo lipogenesis in the response to the LF/HC diet. In the present study, the proportion of fatty acids synthesized de novo was extremely low, contrary to the results of our previous collaborative study with Hudgins et al. (27). Because the 2 investigations were similar with respect to duration of the high-carbohydrate diet, baseline TG concentrations of the subjects, the magnitude of TG responses to the diets, and the protocols used for infusion of labeled acetate, the most likely explanation for the difference between the 2 studies is the composition of the LF/HC diets administered. The liquid diet, high in simple sugars, that was used previously (27) might be more lipogenic than the present whole-food, LF/HC diet. In a subsequent study, Hudgins et al. (45) reported that consumption of longer-chain dietary carbohydrates, compared with short-chain glucose polymers and simple sugars, reduced the lipogenic response to low-fat feeding (45).
Subjects in this study received only 1 week of the prepared high-fat diet. A crossover design, with each diet fed for 5 weeks, would have been ideal but would have made subject compliance more difficult. Moreover, we took a number of precautions, including the use of 3 methods to assess baseline food intake, avoidance of screening over holidays or vacations, and the use of several screening visits for assessment of the subjects' background diets. With the baseline intake so well documented, we therefore consider it likely that the baseline research diet, containing 35% fat, was similar to the subjects' background diets.
In conclusion, carbohydrate-induced TG elevations occurred in both NL and HTG subjects switched from a higher-fat diet (35%) to a 15% fat, whole-food diet. The elevations in fasting TG concentration can be explained kinetically by reduced clearance of VLDL-TG concurrent with elevations in fasting chylomicron remnant concentrations in the HTG subjects. Production of plasma VLDL-TG was higher in HTG subjects compared with NL subjects on the higher-fat diet, but was not increased by the LF/HC diet, and fasting de novo lipogenesis remained low (<5% of VLDL-TG fatty acids, even on the LF/HC diet). The lack of stimulation of de novo lipogenesis with a whole-food, complex carbohydrate diet is in contrast to observations with simple sugars in the diet (45). This disparity has relevance to the current increase in consumption of commercially available low-fat foods, in that some LF/HC diets may be more lipogenic than others. In the present study, sources other than NEFA and de novo lipogenesis contributed significantly to VLDL-TG assembly in HTG subjects, and these sources contributed even more when HTG subjects consumed the LF/HC diet. The assembly, production, and clearance of elevated plasma VLDL-TG in response to the LF/HC diet differed from that associated with the elevated TG on the higher-fat diet. Caution should be used in extrapolating our findings to individuals with frank hypertriglyceridemia (TG > 300 mg/dL), because our subjects were recruited to have moderate elevations in baseline TG concentration (100–200 mg/dL). The results presented here, however, have potential public health significance, as this moderate degree of hypertriglyceridemia is highly prevalent in the population (62).
This work was done during tenure of a Postdoctoral Research Fellowship (to E.J. Parks) from the American Heart Association, California Affiliate. The project was supported, in part, by funds from the Nora Eccles Treadwell Foundation, the International Life Sciences Institute-North America, and Kellogg Inc., and by GCRC grant 5-M01-RR00083-37 from the Division of Research Resources, National Institutes of Health (NIH). Additional support was provided by a grant from the National Dairy Promotion and Research Board (to R.M. Krauss), administered in cooperation with the National Dairy Council, and by NIH Program Grant HL-18574 from the National Heart, Lung, and Blood Institute through the US Department of Energy under contract DE-AC03-76SF00098. The authors express their appreciation to Leila Kotite at University of California–San Francisco, Doris Dare, Kristie Frazier, and the nurses of the GCRC staff at San Francisco General Hospital for excellent subject care and data collection; to Mark Hudes for statistical advice; and to Katherine Haddock, Ken Abe, Eva Hughes, and the staff of Lipoprotein Analysis Laboratory of Lawrence Berkeley National Laboratory for their skilled technical assistance.
Portions of this work were presented in abstract form at the American Diabetes Association National Meeting, June 1998, in Chicago, Illinois, USA.
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Miller, M. Is hypertriglyceridaemia an independent risk factor for coronary heart disease? Eur Heart J 1998. 19(Suppl. H):H18-H22.

redpajama_set_name: RedPajamaCommonCrawl


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text:
Connor Cruise at Pacha Macau
Driven by passion and a deep-rooted connection to music, Connor Cruise's journey of becoming an international DJ started in his early childhood with his first musical encounter with the piano, leading him ultimately to discover the turntables.
Having grown up with famous acting parents, Connor has forged his own career moving away from the big screen to behind the decks. With his unique sound and natural abilities he has quickly amassed huge followings throughout the US and Europe, using his travels as inspiration for his musical expression while performing at major festivals, clubs and private events, earning the respect of his peers and fans alike.
With followers since his birth, Connor uses music as a forum to get in touch with people and to reach out to a new audience by bringing good music and good vibes to the world.
Join us on Saturday, August 6 at Pacha Macau
From 9PM till late
Advance Tickets: MOP150 (available until August 6)
At Door: MOP250 (including 1 drink)
For tickets and table enquiries: pacha@sc-macau.com | +853 8865 6699 | www.pachamacau.com


Nail fungus is a troubling chronic disorder that impacts self confidence and can lead to further health issues especially for those prone to diabetes or immune disorders. Treatment of nail fungus is difficult because the infection is within and below the nail plate, making it hard for other treatments to reach it.
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text:
Q: How do I do this in C#? The following Unit Test passes in VB.Net
<Test()> _
Public Sub VB_XMLLiteral_SyntaxRocks_Test()
    Dim XML = <Doc>
                  <Level1>
                      <Item id="1"/>
                      <Item id="2"/>
                  </Level1>
                  <Level1>
                      <Item id="3"/>
                      <Item id="4"/>
                  </Level1>
              </Doc>
    Assert.AreEqual(4, XML.<Level1>.<Item>.Count)
End Sub

How do I assert the same thing in C#?
To clarify, I 'd like to know how to express...
XML.<Level1>.<Item>

...in C#

A: Assert.AreEqual(4, XML.Elements("Level1").Elements("Item").Count());

And of course XML needs to be an XElement (that's what a VB literal produces too)

A: Using LINQ to XML:
var XML = new XElement("Doc",
    new XElement("Level1",
        new XElement("Item",
            new XAttribute("Id", 1)),
        new XElement("Item",
            new XAttribute("Id", 2))),
    new XElement("Level1",
        new XElement("Item",
            new XAttribute("Id", 3)),
        new XElement("Item",
            new XAttribute("Id", 4))));

Assert.AreEqual(4,
   (from element in XML.Elements("Level1").Elements("Item")
    select element).Count());

redpajama_set_name: RedPajamaStackExchange


Baba Ramdev backing for Sterlite and Anil Agarwal!
Protection: All original content on https://www.apherald.com/Politics/ViewArticle/311609/Baba-Ramdev-backing-for-Sterlite-and-Anil-Agarwal-/ is created by the website owner or published under permission including but not limited to text, design, code, images, photographs and videos are considered to be the Intellectual Property of the website owner, whether copyrighted or not, and are protected by DMCA.com Protection Pro Service using the Digital Millennium Copyright Act Title 17 Chapter 512 (c)(3). Reproduction or re-publication of this content is prohibited without permission.


text:
\section{Discussion}
\vspace{-.05in}
We find, using carefully designed datasets utilizing isomorphic symmetries in Sudoku, that transformer-based models can generalize well to out-of-distribution puzzles in the Rows and Columns conditions when component subtasks span the full space of the data distribution, and fail to do so without this training on the component subtasks.  These findings may be relevant to understanding the performance of large transformer-based models.  While they may receive restricted experience with complex multi-step problems, their ability to solve new ones may depend in part on more complete coverage of component sub-problems in their training data.   Future research should explore this hypothesis in larger and more naturalistic data sets.  We did find that the models struggled to generalize to held-out digits, and found evidence that this failure is due to a failure to attend to within-distribution digits during crucial steps within the Hidden Single task.  This is surprising in that the failure occurs during steps the model does succeed on in the component Naked Single task.  Future research that corrects this deficiency could have important implications for the success of larger models, perhaps helping them to achieve stronger performance in abstract reasoning than they have achieved thus far.
\section{Experiments}
\vspace{-.1in}

We use a 3-layer transformer encoder \citep{vaswani2017attention} to which
all grid and text embeddings are passed, and from which output vectors are then mapped to output text tokens.
We use teacher-forcing during training and greedy autoregressive generation during evaluation.

We first check if the network could solve the tasks by producing the final yes/no responses immediately after the prompt.
After training on 50,000 HS puzzles uniformly sampled from the full problem space, we find that these models only solve 87.8\% of held-out puzzles, compared to the 99.9\% of models trained to produce the full sequence of reasoning steps.
Taking complete success at within-distribution generalization as a pre-requisite, we use the full sequences as exemplified in Table \ref{table:problems} in all remaining experiments, which focus on out of distribution generalization in our models.

We define within-distribution (WD) puzzles as those that conform to the restrictions used to construct the training set and out-of-distribution (OOD) as puzzles that do not conform to these restrictions. All models included in our analyses solved held-out WD puzzles with near perfect accuracy, so we only report OODG performance in our results for conciseness.

\begin{figure}[t]
\vspace{-0.4in}
    \begin{center}
        \includegraphics[width=\linewidth]{figures/ood_accuracy.png}
    \end{center}
    \vspace{-0.1in}
    \caption{Out-of-distribution accuracy results. Small dots represent individual models (10 per condition). Large dots represent average accuracy in each condition. Left: accuracy based on final yes/no at the end of output sequence. Right: accuracy based on the entire output sequence.}
    \label{fig:ood-results}
    \vspace{-0.15in}
\end{figure}

\vspace{-0.1in}
\paragraph{Relevant related experiences.}
Based on the natural symmetries of Sudoku grids and the train/test split used in \cite{nam2021underlies}, we devised three distributional splitting schemes to probe for OODG.
Our first condition, \textit{Rows}, recognizes that the application of the HS, FH, or NS techniques is isometric relative to the row in question.
Thus, a successful model of abstract relational reasoning should solve HS puzzles applied to any of the 6 rows, even when trained on a strict subset of the 6 rows.
We train the models using HS puzzles applied to 4 of the 6 rows (i.e. the goal cell will only appear on these 4 rows), then test its OOD performance on the remaining 2 rows.
In our second condition, \textit{Columns}, we exclude all HS puzzles that are performed over columns from the training set, and test the models on these column puzzles.
The abstract principle of process of elimination remains the same, and the main challenge is knowing which cells to iterate over.
Our final condition, \textit{Digits}, uses the fact that swapping digits only superficially changes the puzzle without affecting the underlying structure (see Figure~\ref{fig:attention}.
We train the model on puzzles with 4 of the 6 digits as the candidate digits and test the model on puzzles with the remaining 2.

We also had 3 conditions for how we trained the models.
In the first training condition, HS Only, we included 110,000 HS puzzles as part of the training set and not the FH or NS puzzles, and trained the model for 70,000 gradient updates (each based on 192 examples).
The second condition, \textit{Simultaneous}, included 50,000 HS puzzles and 30,000 FH and NS puzzles each, and the model was trained on all 3 tasks simultaneously for 70,000 updates.
The FH and NS puzzles were sampled completely at random without any systematic constraints.
The last condition, \textit{Curriculum}, uses the same materials as Simultaneous, but trains the model on the FH and NS puzzles for the first 20,000 updates, reaching ceiling performance, before training on all 3 tasks for 50,000 more updates.

Figure \ref{fig:ood-results} summarizes the out-of-distribution generalization results in each condition.
First, we compute the accuracy based on the final yes/no answer at the end of the output sequence, and we find that models trained only on HS puzzles struggle to exceed chance (50\%), suggesting that the model has no inherent inductive bias towards generalizing in these dimensions.
When trained with the FH and NS tasks, the model succeeds in generalizing to the held-out rows and columns to a high degree, especially when trained using the curriculum-based setup.
We consider the strong generalization in the Columns condition (though somewhat less complete than in the Rows condition) to be an important finding, since the Columns condition contained no training on column-wise puzzles, while the Rows condition included 4 of the 6 rows.
Our models generally failed to exceed chance on the held-out digit puzzles.
The relational neural network \citep{palm2018recurrent} also fails to transfer to held-out digits, but humans who learn to solve HS puzzles with a restricted set of targets show no decrement when tested on held-out digits \cite{nam2021underlies}.

We also measure the accuracy for entire sequences, in which a problem is considered solved if the entire model output sequence matches the target sequence, including the intermediate steps. This not only magnifies the differences, but also indicates that the models that generalize successfully do so in its entire reasoning process, not just at the correct final output.

\begin{wrapfigure}{r}{0.35\textwidth}
  \vspace{-0.25in}
  \begin{center}
    \includegraphics[width=0.33\textwidth]{figures/attention.png}
  \end{center}
  \caption{Attentional maps. Within- and out-of-distribution puzzle with candidate digits 3 and 4 on top and bottom, respectively}
  \label{fig:attention}
  \vspace{-0.25in}
\end{wrapfigure}

Although the Rows and Columns conditions successfully demonstrate out-of-distribution generalization, the Digits condition does not, as shown by the roughly 50\% accuracy in Figure~\ref{fig:ood-results}.
This is surprising, since human participants show no change in performance when the digits in the grid are swapped \citep{nam2021underlies}.
Its peculiarity is magnified by the fact unlike the Rows and Columns conditions, full sequence accuracy is well above the floor even when the models are trained with only HS puzzles.

Inspecting the model generated outputs, we find that the models correctly identify the relevant cells to iterate over, and the last line indicating the final answer is consistent with its intermediary outputs.
In other words, the errors are made when determining whether or not the cells can contain the candidate digit. Moreover, these errors only occur at empty cells, not at cells already containing a digit.

To gain further insight, we analyze the attention maps generated by the transformer that indicate which information the model considers.
We probe the model by taking held-out puzzles and rotating the digits in each grid such that 1 becomes 2, 2 becomes 3, 6 becomes 1, etc., thus producing 6 identical sets of puzzles that only differ by the digits involved, and each puzzle in the set has a unique candidate digit.
We inspect how the model queries the grid as it produces the yes/no responses at the end of each substep in the HS problem by taking the maximum attention weight given for each cell from the last transformer layer.
Figure~\ref{fig:attention} shows an example of one model's attentional map on the HS problem shown in Table~\ref{table:problems} when considering whether the candidate digit can be placed at the cell on (2, 2).
In the within-distribution problem, where 3 is the candidate digit, the model correctly identifies the 3 in the same row.
In contrast, the model does not attend to the same position in the out-of-distribution puzzle where 4 is the candidate digit.
This form of mis-attention is characteristic of the errors in the Digits condition.

\section{Supplementary Materials}

\subsection{Training Details}
\label{sec:sup:training}
The core of our model is a 3-layer transformer encoder \citep{vaswani2017attention} supported by embedding layers for grid digits, grid cell positions, and input text, and finally an output text decoder layer.
The digits of the encoded by a 256-dim embedding layer and the row and column coordinates are encoded by a 128-dim embedding, which are concatenated together and summed with the digit embedding.
All text tokens are encoded by a 256-dim embedding layer and position information is added to the vectors using the sinusoidal positional encoding scheme introduced in \cite{vaswani2017attention}.
The 36 grid cell vectors and all token vectors are passed to the transformer, which is composed of 3 encoder layers with 8 heads and 1024-dim feed-forward layers, and the output vectors are decoded using a linear layer to form the final logit values for the predicted output tokens.

During training, we use teacher-forcing to predict the next token at each sequence position and cross-entropy with the target sequence.
We mask the loss so that in the loss is only applied after the 'digit' token in the hidden single and full house tasks, and after the column number token in the naked single tasks.
The loss is computed using cross-entropy and the model is optimized using Adam \cite{kingma2014adam} with a learning rate of 0.0001.
When training with multiple tasks at once, we sum the losses in each batch from all the tasks before computing the gradient for backpropagation.
We keep the same batch size of 192 samples for each task, regardless of how many tasks are used to train at once.

Although we provide the model with seed sequences as exemplified in Table \ref{table:problems} including the candidate digit at evaluation time, we train the model to also predict the candidate digit to evaluate whether how accurately could identify the correct digit with the prompt alone.
During evaluation time, all output sequences are produced using greedy autoregressive generation.

\section{Task Description}
\label{sec:task}

We design base our tasks on the three simplest Sudoku techniques.
\textit{Full House (FH)} involves identifying a cell in which all other cells in one of its houses (row, column, or 2x3 box) are filled such that the empty cell's digit must be the only remaining digit.
\textit{Naked Single (NS)} involves identifying a cell in which 5 of the 6 possible digits already exist in its neighborhood (row, column, and 2x3 box) such that the empty cell's digit must be the remaining digit.
\textit{Hidden Single (HS)} involves identifying a cell $C$ in which all other cells $c_i$ in one of its houses cannot contain one of the digits, either due to $c_i$ already containing a different digit or the digit being present in $c_i$'s neighborhood, such that the only remaining cell that can contain the digit in the house is $C$.

For each technique, we create a task in which the model is presented with a 6x6 Sudoku grid and a string sequence prompt that provides the context for solving the problem, including the coordinates of the cell to solve for, the candidate digit, the name of the technique to use, and, for the Hidden Single (HS) and Full House (FH) tasks, the house type to inspect. By specifying all these details as part of the prompt, we simplify the task from conducting a search for a valid solution to verifying whether a goal cell should contain a candidate digit according to the rules of the specified technique.

The target sequence formats for each of the three tasks were designed to support composition of elements of the Full House and Naked Singles (NS) tasks (see Table \ref{table:problems}).
The HS task format steps through all of the cells other than the target cell in the specified target house, and checks to see if
the specified digit can go in any of these cells.  If it cannot, the answer is yes, it must go in the target cell
The FH task performs a similar iteration strategy, but identifies whether the cell contains a digit at all at each step.
The NS task matched the sub-tasks in the HS task, requiring the model to identify whether a given cell can contain a candidate digit based on any direct contradictions within its shared row, column, or box neighborhood.

redpajama_set_name: RedPajamaArXiv


text:
Q: Example of a measure which is not an $L^1$ function. If $f\in L^1(\Omega)$, then $f$ defines a measure on $\Omega$. I wonder, can a function $f\not\in L^1(\Omega)$ define a finite measure on $\Omega$?
I know that Dirac delta defines a measure which is not in $L^1$, but I am bit confused whether it is a function, because it is not defined on $\Omega$ but on $\mathcal{C}_c^\infty(\Omega)$ (the space of compactly supported smooth functions) . Thanks!!

A: To every measurable function $f:\Omega \to \mathbb{R}$ we can associate an expression $$v_f (A) =\int_A f(t) l_n (dt ) $$
where $l_n $ is $n$-dimensional lebesgue measure. If $v_f (A) $ is finite for every lebesgue measurable subset of $\Omega$ then it is easy to show that $f\in L_1 (\Omega ).$

A: The problem is that you are unsure on the identification between (some) functions and measures. Given a function $f\in L^1(\mathbb R^n)$, you can define a measure $\mu_f$ by
$$
\mu_f(A):=\int_{\mathbb R^n} f(x)\, dx, \quad \forall A\ \text{Lebesgue measurable},$$
or, more shortly, $d\mu_f := f\, dx$. The general theorem that governs this kind of constructions is the Radon-Nikodym theorem, but you do not need its full force, only the statement. If a measure $\mu_f$ is constructed like that, you say that it is absolutely continuous with respect to the Lebesgue measure $dx$, and you say that $f$ is the Radon-Nikodym derivative of $\mu_f$ with respect to $dx$, which alludes to the formal manipulation
$$
d\mu_f = f\, dx \quad \overset{\text{formal}}{\iff}\quad f=\frac{d\mu_f}{dx}.$$

Your question is now: can we do this construction with a function $f$ that does not belong to $L^1(\mathbb R^n)$? The answer is no: the writing
$$\tag{!!}
\int_A f\, dx $$
does not make sense for all measurable $A\subset \mathbb R^n$ unless $f\in L^1(\mathbb R^n)$.

A: In the whole space, $f = 1\not\in L^1$  as measure is the Lebesgue measure.


These images are available for media use. Check back often as we continue to update the gallery.
Browse the Executive's official Flickr gallery for images you can use in publications, websites, blogs, and more.
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Gathering of the Vibes starts this Thursday and is set to be a mid summer spectacular. GOTV is on the waterfront in beautiful Seaside Park in Bridgeport, Connecticut with beaches to swim at in the festival! There are still some tickets available online although with 4 day passes and individual day passes available but VIP tickets are sold out.
Get your tickets to Gathering of the Vibes: here.
Headlining this year's GOTV will be Furthur featuring Phil Lesh & Bob Weir of the Grateful Dead, Jane's Addiction and Elvis Costello. Elvis Costello made a surprise appearance with Furthur at Radio City Music Hall on Furthur's spring tour.


text:
Showing results for tags 'movement'.
Test environment for player movement
peter_spy posted a topic in TDM Editors Guild
One of basic rules of level design is that a map has to be fun to navigate. And yet even the most seasoned authors seem to struggle with that, to the point that some players are led to believe that player movement in TDM is clunky, which couldn't be further from the truth. So I thought it would be good to have a reference test map to check player abilities and blockout your geometry accordingly. This is by no means final, but hopefully it will give you some idea about when the player movement shines, and what should be avoided. For the sake of simplicity I tested the most common measurements and indicated when things start to be trial and error. Feel free to extend the map with your own ideas, more granular measurements, etc. mantle_ref.pk4
player character
Idea for movement in narrow passages
Plutonia posted a topic in The Dark Mod
Although the Dark Mod has already expanded the movement possibilities of the Thief games significantly, why couldn't there be more still? I actually got this idea from the atrocious poorly disguised loading screens that constantly hinder your progress in NuThief. I'm absolutely certain that a bunch of modders could program a better system than those so-called professionals in Canada, who were eager to sacrifice any amount of gameplay or control freedom, if it allowed them to implement body animations with even less effort. Usually in games, the player character has a cylindrical collider. Meaning that if he can't fit through something facing straight, he can't fit through at all. But what it we could simulate the character turning his body but facing forward with his head, seamlessly without any interference in the player's input or the character's movement? The idea is basically that if you come to a narrow passage, the game checks which side of the passage your view is pointed at. Either left or right. It's almost impossible to face 0° away from the surface normal, so your facing will fall under the category for left, or the one for right. When the player moves into the passage, the game orients the character's virtual body accordingly, and restricts the player's ability to turn the head based on which way the character is oriented in the passage. The player is also unable to crouch because that would take more horizontal space for the body. Now, when in this narrow passage, facing up and pressing forward would allow the player to slowly climb up the passage by leaning against the walls. The controls would be identical to climbing vines on a wall. If there is a window or ledge up there, the player could use the standard mantling key to climb up the wall that he's facing. The problem I could see with a system like this would be that players would have a hard time recognizing the possibility to do this kind of navigation in the levels. There isn't a ladder, or a piece of wood for a rope arrow. Just two walls close to one another.


What happens on Find adult friendz, stays on Find adult friendz. Chances are you will come across someone you know, so please exercise the utmost discretion when using the site.
Respect your fellow members. Remember, Find adult friendz users are people just like you, who are looking to have fun and explore their sexuality in a safe environment.


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text:
This Site Comes With Music!
Do you want to hear the music?
Sankofa Speakers
Send Email To: Please enter up to 3 valid emails. From: Please put in a valid email address. Message:
Please include a comment.
In April of 2012, the Sankofa Lecture Series entered into public discourse as the only conference in the Colorado region that focused on the use of art and culture to enhance educational praxis. We accomplished this, in part, through unwavering community support and partnerships between the Denver community and local colleges and universities. The curator of the Sankofa Lecture Series in tandem with dedicated volunteers produced activities and programs that situate the pedagogy and influence of Hip Hop as a site of cultural literacy, identity formation, and tool for innovative teaching.
In 2015, the lecture series culminated on the campus of Metropolitan State University of Denver (MSU Denver), however, the movement to contextualize traditional fields of study through the conceptual framework of Hip Hop scholarship continues.
Now in its fourth year, the Sankofa Lecture Series has transitioned to a consultant group. We pledge to offer institutions guidance on how to use the canon of Hip Hop as a means to compliment subject-specific instruction, and foster meaningful dialogue among high school and college/university stakeholders (i.e., students, staff, administrators, faculty, alumni, community and so on).
Overall objectives of the Sankofa Lecture Series are:
To increase curriculum connections and innovative approaches to teaching through the use of didactic concepts of Hip Hop culture.
To increase knowledge of how elements of Hip Hop culture have been used to communicate the perspective of marginalized communities on issues of race, identity, and (regional) space.
To critically examine the artistic conflict between affirming and harmful representations of Hip Hop culture, and how such issues impact identity formation and literacy.
The Sankofa Lecture Series has been awarded the Inclusive Excellence Shield for our steadfast commitment to advancing cultural competence through reflection, professional development and education. This recognition was bestowed by the Equity in Excellence (EiE) Steering Committee in collaboration with the MSU Denver Office of Institutional Diversity.
Twitter @ Sankofalecture
or E-mail: sankofalecture@gmail.com
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text:
Q: Mysql function DATE() on sql server? I need to convert this MYSQL query to sql server:
DATE(datetime_field);
How can i translate this query on sql server language?
Thanks.

A: You can use either of the following ..
SELECT CONVERT(DATE,datetime_field)

OR
 SELECT CAST (datetime_field as date)

A: Simply use the following:
 SELECT CONVERT(date, getdate())

A: If you are using SQL server 2008 or above, try this:
SELECT CONVERT(date, GETDATE())

A: You can use
select try_convert(date, datetimefield)

or
select try_cast(datetimefield as date)

If you get invalid date it will not error out instead it will return null

A: CONVERT also has an handy 3rd argument which allows to format the date using some predefined styles (returns varchar)
so for example:
SELECT CONVERT(varchar, GETDATE(), 112)

will output today's daye in ISO format like 20160831
SELECT CONVERT(varchar, GETDATE(), 103)

would output 31/08/2016
...and so on...
see: https://msdn.microsoft.com/en-us/library/ms187928.aspx

A: Try this
Select Convert(varchar(10),GETDATE(),103) AS CurrentDate


ALBUQUERQUE, N.M. (KRQE) – A New Mexico doctor and firefighter are about to embark on a very dangerous lifesaving mission.
Doctor Chris Hammond, who works at Los Alamos Medical Center, and Tylerr Jones, who is a firefighter, EMT and registered ER-nurse in Los Alamos, are going to Mosul, Iraq.
They will be treating casualties in the war zone.
Both volunteered as part of the group Global Outreach Doctors.
They've been told to prepare to treat blast and gunshot injuries in the field.
Chris Hammond and Tylerr Jones wanted help others and when they were asked if they were willing to do this they agreed.
Both said they are nervous, especially since news of the strikes in Syria, but also excited.
Jones said he's going for his young daughter and said he's extremely thankful to have a happy and healthy daughter.
He will have a constant reminder of her on his arm, which is a tattoo of her signature.
Hammond and Jones head out Friday night and will be gone through April 25.


When pretty college student Maggie Shanner receives and invitation to her great grand-father "Big Daddy" Wingfield's 104th birthday celebration, it's a chance for her to get out from under her mother's thumb for an entire week. Her over-protective mother, Catherine, wants her to dump her boyfriend and live at home until she meets Mr. Right and gets married... and stay away from her crazy great-grandfather. Big Daddy Wingfield is a patent medicine millionaire who lives alone on private island off the coast of Florida. No one has seen him for decades. Catherine hints that he's a recluse because of some strange dark incident in his past. A sinister family secret.
Maggie and her abrasive opportunist boyfriend Stanley join the other great grandchildren for a week on the private island paradise: failed ex-quarterback Brick and his trailer-trash wife Charlotte, plus aggressive lesbian poet Blanche. Why would Big Daddy invite only the great grand kids... unless he's thinking of revising his will to include some of them? All five begin plotting against each other to gain "first position" in Big Daddy's will, with Stanley pulling every dirty trick in the book to come out on top.
A frightening genetic mutation: half-man, half-alligator. A ferocious freak that hides in the tall grass, lurks in the shadows, and attacks when you least expect it. Tearing off limbs with its razor-sharp teeth. Chomping a human torso in half with its powerful jaws. The result of one of Big Daddy's experiments gone wrong?
With no way off the island, Maggie and the others must stay alive long enough to discover the family secret behind the half-man, half alligator freak. The secret to why Big Daddy may be 104 years old, but only looks 50. The secret to why Catherine waited until she was in her late 30s before giving birth to Maggie.
Because these five aren't in competition for a place in the will, Big Daddy is really trying to find the best experiment subject (with his DNA) so that he can create a new half-man, half-gator to regenerate internal organs so that he can stay forever young. He's found the fountain of youth in Florida... and it's gators! That creature who stalks the swamps at night, feeding on human flesh... is Maggie's half-brother!
GATORBABY is a tale that blends the terror of JAWS with the Southern Gothic sensibilities of CAT ON A HOT TIN ROOF. One horror-filled week trapped on an island with a monster... and no way to escape it's powerful jaws.
Every family has its secrets, but this one has teeth!
To read the script online... GATORBABY.