S and I had left the previous house with extra cans of paint, which we used in the Hobbit Hole, but haven't used up – so we're continuing these older colors through some of the smaller rooms. The big rooms need multiple gallons, and so we went paint shopping, brought home items called "knightly straw" and "mango bean" and got to work. Luckily, S had snagged speakers such that we could listen to the vast collection of 80s rock while we taped and slopped.
S: I think it's Thomas Dolbey.
R: That would explain much.
R: Radio KAOS, I believe.
R: This sounds like a carnival. It's from Grand Illusion, isn't it?
S: Well, it's Styx. Must be mine, I don't think you like Styx.
R: Sweetie, I had a complete Styx collection when I met you. Damn. I'm old.
R: "In touch with the ground/ I'm on the hunt I'm after you / Smell like I sound I'm lost in a crowd…" I'm having flashbacks the a recent Dr Who Episode.
S: The one on the sub, I know.
R: Forward to the next song, would you? This is music to be jittery to, and I don't want to spill.
R: I wonder if the neighbors now think that 10 hours of hair bands is going to be normal for the weekends.
Just what every new homeowner likes to see upon getting the keys: the neighbors tree blew down, taking out a small chunk of our fence and lightly brushing the garage roof. Sigh.
But we have the keys, and S spent a good day on the telephone making sure we had utilities and Internet, and even talked the power company into acknowledging us – apparently the property is on the border between 2 electric companies, and neither thought we belonged to them.
Hopefully we will get the interior paint done and other pre-live in stuff done shortly, and we'll be able to shift from the Hobbit Hole apartment to a place with tall ceilings soon.
Visit Wilsons Window Cleaning New Malden for house cleaning services!
Flying from Portland to Rome takes 14 hours, with a layover. Amanda is a seasoned world traveller, but Scott and I were new at this, and got some advice on medicating through the discomfort and jet lag. First, Billy our ear expert recommended a nasal spray called Afrin which, along with some ear plugs, prevented the post flight ear equalizing action. And we brought some sleeping meds for the long flight.
Scott, alas, took the Ambien shortly before discovering that dinner was being served. It takes about 10 minutes for this drug to take affect, and he stayed…conscious, I guess, for about a half hour, so that he could eat his dinner. Mobile might be a better term. He ate the main course, then started working on the dessert but couldn't open the wrapper. So he grabbed some plastic ware to assist. When we asked him why he was attempting to open his brownie with a fork, he drowsily told us it was armored. At this point, Amanda pulled out a camera and interviewed him. He, of course, remembers none of this.
I waited until after eating to take the temazepan I'd brought. It helped me fall asleep, but not stay asleep through the 8 hours of screaming babies on the plane. We negotiated our way through the short layover in the land of blonde people and then tried to doze on the short leg, but I have to say we were pretty wrecked when we arrived.
Finding our AirBnB apartment was fun in that condition. It's a nice little place with a double bed and a daybed, tiny kitchen and a tiled bathroom, with windows overlooking the light well. I recall describing to my companions the structure of a roman apartment building as I'd learned it in the Colleen McCollough books, but we all crashed for an hour nearly immediately.
At 4:30pm local time, we were showered and alive and exploring the city. We meandered through the cobbled streets, seeing old men hanging out of shuttered windows, streets cobbled with square rocks on a diamond pattern, street vendors with a carpet full of handbags, and weathered buildings. There are main thoroughfares are full of automobiles, busses, trams, and scooters. A lot of scooters. Most of the residential area roads are tiny twisty alleys between structures built off the walls of their neighbors. Pedestrians walk out in the streets, making way for slow moving cars and scooters on the tiny roads and waiting for a big enough break to cow the vehicles on the bigger streets. One mustn't flinch when crossing the street. Alas, I did, and got left at the median while Scott waved and Amanda took pictures of me, stranded amongst the autos and motorini.
We stopped in our neighborhood's church – Santa Maria in Travestere – but the services were going on, so we didn't stay to look for the plaque for Belisarius. The fountain out front was a common gathering place – people sat on the steps because basically there isn't much in the way of public seating anywhere in Italy.
We crossed a river in our wanderings, and realized its the Tiber. Shortly after, we happened upon a block fenced off, with signage in several languages, asking you not to feed the cats that inhabit the excavation below. This was the Torro del Argentina, rumored to be where Ceasar was stabbed. It's a tram destination (and there's a feline sanctuary run out of the ruins). History is literally laying out in the open here.
There's so much history, in fact, that it must be hard to run a city. I mean, they were laying some fiber optic or something and had a street torn up, and we could see brickwork from ancient times. Rome was built on Rome.
There was a nightly art market in booths beside the fountain of the four rivers in Piazza Navono, which was only a little way from the Pantheon. Which is free entry, so since we are here….
The backside of the building is pretty non descript, but the front has the standard rows of columns and the interior is full of warm, colorful inlaid stone and religious icons. The roof is coffered, and while the walls are 20 feet thick and basalt, the dome is made of lighter and lighter material unit its a concrete with pumice aggregate and then the opening at the top, which was the only light source. The interior of the portico roof had been decorated by bronze sheathing, but some Pope stole it to make some additional artwork in the Vatican – more on that later. Also more on the Pantheon later, when we returned in daylight.
But now we're starving and we pick a ristorante, nearly at random, and have a cheese plate and 3 pastas that we mix and match. Spectacular. On the way back to the apartment, we stopped for gelato in the square in front of Santa Maria, and sit and listen to street musicians and watch passersby while leaning against the fountain, while nearby other diners enjoy the ambiance (and the occasional large candle).
For the month of September, there is a hillside in NE Portland that fills with picnickers every evening at sunset. The blankets are laid out with little space in between, and people share treats with strangers. The reason for this gathering is up in the air, where the blue sky is full of Veux swifts.
I had gotten their first, and saved a space of til the pub crowd, the hashers, and the Aussies who had organized this outting had arrived from their separate busy days. My bike had held the chunk of grass in reserve, but got tossed into a car before the auto went blocks away to find a parking spot – both picnic land and parking becomes a premium as the evening wears on. We all nibbled on our respective meals – Scott had brought me a salad – and watched the sky, and the school below us.
The chimney of the school somehow became the rest stop for a large flock of migratory swifts years ago, maybe decades. It's such an institution that the Audebon association – with fundraising from the students and neighborhood – helped create and alternative heating system and shore up the now defunct chimney for the elementary school. The only purpose for this brick structure is a night time shelter tens of thousands of birds for a month in the fall.
It's not that they don't need the retreat. As the crowd watches, a peregrine swoops through the flock. It looks like he did not score a meal, and as he veers off, a couple thousand little swifts harass him. The picnickers applaud – and I'm not sure who they are rooting for, the falcon or the prey.
As sunset falls, the flock circles into tighter spirals and begin to descend Into the chimney. It's a bird tornado. We watch them disappear into their roost and packed up for our separate journeys home, to our own roosts. Tomorrow at dawn, the birds will emerge with less fanfare and hunt for insects all over town while children learn history & science next to the chimney, and at night the adults and families will gather again to watch the flock.
The fact that this is just a regular Portland outting warms the heart.
Sandy Ridge Trail is named after the town of Sandy, Oregon, that sits below and west of the trail…or maybe it's named after the Sandy River, which erodes the volcanic landscape from Mt Hood and flows past the aforementioned town. It is not a giant dune.
Well, Scott can say. He's the one who endo'd today.
The climb is 1600 feet and paved, and then we strike single track and continue climbing to the edge of the Bull Run watershed (which serves as Portland's municipal water supply) and then to an overlook to the Sandy River watershed – which by the way could be improved by topping a tree or two that are between the ledge and Mt Hood (hint hint, Jason/Shane/Chris). Then it's a lot of berm turns and terrain features all the way back down. An incredibly fun descent that actually takes twice as long as 'that damn road climb' (Scott really isn't fond of hills. Or roads). Even with the crash, we had a great 2.5 hour, 10 mile ride.
My honey and I tend to do a lot of activites apart, or in our own heads, but occasionally, we do go out on dates. The dates don't tend to be things other folks find …romantic.
Thursday after work, I got on my bike and pedaled, not to home (20 minute commute) but to where some of our toys are stored (40 minutes of bike time). I must have hit a pot hole because a mile or so from her place as I was getting some interesting shimmies and rubbing. I have wheel truing in my near future.
Anyway, I pulled into the drive a few minutes before my honey got there – his food gathering attempt was in vain, our favorite Chinese restaurant was closed. We did some major combobulating of gear (leaving my bike, changing racks, etc), then drove off to gas up the car and stop at subway for a couple of meal deals. Then we headed to the Riverside Boathouse and unshipped the kayaks. It's a short carry down to the floating docks where the dragonboaters and sculling crews were beginning to come in for the night, and we wiggled into neoprene and slipped our hulls into the water: his yellow, mine red.
We paddled across the Willamette and noted where the crowds were, and shortly headed upstream, passing several large boats at anchor, their crews relaxing on deck with a drink. Chatting a bit with the captain of the Luscious, a purple & red 54′ rig with a huge main mast, we found he was appreciative of finding kayakers with lights, and thought the headlamps we had on were curious. He takes the boat (ship?) up and down the coast, no further than Vancouver (BC, I assume). As we paddled away, we commented to ourselves that with that rig, we'd be sailing to Alaska or Hawaii.
Not far past the downtown area of Portland, we approached the construction of the new train/bike bridge. The west tower is up past the road deck, so (we speculated) the rest will be going up quickly, and then they'll get going on the east tower. Completing our inspection, we turned and had a short sprint downstream, back the the crowds in waterfront park.
Intermission was over, and the conductor of the Oregon Symphony Orchestra introduced some guest performers, and told stories we could not quite hear between performance pieces. The land bound audience was picnicking, sipping wine, chatting, and allowing their kids some time to skip stones in the river while the music played. The many boats moored up held small groups, complete independent of the size of the craft – a couple hung out in a large speedboat, and offered us snacks, a mob of 6 or more in a pair of canoes huddled around an anchor point, etc. we kept station, more or less, floating through the arts lovers, and trying to stay away from the kids on shore.
Alas, a trio of young boys got a hold of an aluminum canoe, and paddled out into the anchored boats and proceeded to scream at each other, threatening dunkings at the top of their voices. They'd been playing loudly close to shore, but after ten minutes of this out she we were, I powered over to them and asked them seriously and sharply if anyone was hurt, were they injured, is someone dying? They confusedly said no to all this, and so I pointed out that there was a concert going on and the people around them could not hear it. Then I paddled away. I assumed the applause about then was from something on stage, but my honey says it was the boaters around me. The kids stopped being annoying.
We got treated to some Swan Lake, complete with spotlighted ballet, though we were too far under the rise to see more than the impressive high jumps. And then they started in on the 1812 Overature, which was why I had made the arrangements.
I loved the story about the piece being a humdrum item that a Boston Pops conductor decided to dress up (and hopefully attract ticket sales) by firing off cannons on stage – pure genius. We never hear the piece without the firepower these days. Sure enough, after the orchestra did a fine job on the descants, the 218th Field Artillery, hanging out on the other side of the Hawthorn Bridge, started up their volleys. I'm not sure if it was the difference between hearing the music directly in front of us and the cannons downstream, but there was a bit of a lag – really didn't detract from the enjoyment of the combination.
Meanwhile, while this was going on, the Luscious began parading across the river with a house-sized US flag hanging from the main mast, lit by spots. They turned near the bridge, shifted the lines and came back the other way, just as the piece was wrapping up in the final echoing booms, and then the fireworks started.
I'm not sure how this worked for people on shore, or even in larger boats, but from the water level, the fireworks were exploding around the full blue moon like a halo. Our angle was perfect. For a while, the Artillery on shore competed with the showy stuff coming off the barge, and gun smoke wafted around us.
It was 10pm and we still had to pull ourselves across the river, load boats, drive them to their storage area, unload & hang, change racks back, load my bike, and drive home. But it was a spectacular evening. Dinner, a cruise, the symphony, and a light show. What else can you ask for in a weeknight date?
Woke to alarm (again? We're on vacation!) and drove back into the park – the kiosk was unmanned at this hour. We actually had to pay for the stream side site with composting toilet -$21- as we weren't up before the camp host. We went straight to Curry Village Camp Reservations and took turns packing or being in line waiting for them to open & get us on the waiting list for an inpark site. While this was going on, Scott chatted with a lady who was thinking of moving her rv & husband out of the park, as he was having issues with the altitude. They made a deal & we got on the list and headed up trail to Happy Isles for the day's hike – Vernal and Nevada falls.
We weren't the first people on the trail, but we were damn early and the hikers were sparce. We were expecting this to be an all day trail, calculating a turnaround time, but then fairly flew up the first 2 miles of it. It was steep, but paved and pretty and in the morning we had lots of energy. At the bridge, there was a restroom and water, and our hike turned a good deal more rustic as we headed up beside the stream. Very shortly, we hit stone stairs. Some 300 + stairs carved into the granite and being often misted in the spray of the waterfall are known to be slippery and dangerous, but someone must have turned down the valve, as it was simply cool. Vernal fall is 370 feet of gorgeousness, and Scott's progress suddenly slowed to a creep. He stopped a lot to photograph the falls, the mist, the rocks, the rainbows – even me on the steps going to the top. He'll have a lot of great pics of that fall! The last chunk of the trail to the precipice had a handrail that was required. The slick rock was about a foot or so wide, stuck on the edge of the cliff face, for twenty yards or so. There was no passing of slow hikers here. Then we were at the top, having a snack in the shade of a lone tree and watching people watching the water go over the edge.
We continued up beside Emerald Pool, which was a healthy green, though more dark than emerald in my opinion. The upper end was basically an angled granite slab, and the citified looked at it and proclaimed "waterside!" – I can only imagine what that sandpaper slope would do to someone's swimsuit, and then skin, if they tried to slide down it. We took photos as we poked along, crossed the bridge and continued up, spending more and more time adjusting poles and shoes and whatnot until we got to the bottom viewpoint for Nevada Fall, which is 320 feet. We lunched here, and the white-shouldered ground squirrel that claimed this plateau as his own was determined to see what was in our packs, and not shy about it. While Scott was taking pictures, I was defending the gear with my life. Then I lost sight of my Scott. A German couple had been interacting with him when last I saw him, and after a while I asked them if they'd seen him – jokingly asked if they'd tossed him in the river. They laughed and pointed downstream – "oh," I said, "you did toss him in the river!" More laughter, and Scott waved when he saw us looking at him. Eventually he came back, and we packed up & headed back down to the pool.
From here, we took the John Muir trail, which is supposed to be the milder way down. It started with a climb. Up we went, leapfrogging a pack of 11 girl scouts and 3 chaperones from San Diego (one of whom has in laws in McMinnville, so we talked sci pub, and another who was Not Active Enough for this Hike). At Clark Point, Scott took some infrareds, which took a bit longer than expected, and then we decided – since we had a 3:00 appointment – that we'd basically sprint down, and picked up the speed. Oddly enough, we had the best cell signal that we'd gotten in days, and we kept fielding texts from friends back home. However, we were basically off the trail before 3, but not back at camp reservations in time. Still, Scott's deal making earlier landed us a site, and we were able to meet our benefactor & pay for the site they were leaving.
The new camp was to be on Tioga Road, so we did the last of the valley stuff – making dinner in the crock pot, mailing postcards, eating ice cream, showers at housekeeping camp ($5!), and driving up to Tunnel View for evening light. Scott set up his camera, but wasn't impressed with the light that evening. I set up the table, and we dined with the best view, much to the amusement of the other photographers and tourists at the overlook.
A long drive down the valley, then up the other side, in order to find our new camp had us leaving long before the sun actually set. The new site, we discovered, was in Crane Flats, which is forested (ie, no cranes would land here) and at a 20% side slope (ie, not flat). Leveling the van was interesting.
There's no water hookup up here, so in the morning we loaded every water bottle from the tap near the restroom. Had a lazy-ish start and cooked breakfast on the bear box while a couple of neighbor teens stood nearby, fascinated by the four yearling doe wandering through our site. I warned the deer away from my pancakes by telling them they would be pretty when sizzling – this amused Scott for some reason. After packing up and shifting the van, we filled in the holes dug to level us & drove off to get high priced gas from the Crane Flats station, and give a couple a van tour since they say they only haul their big RV around for the fridge. Then across the high roads.
We stopped and puttered at the Yosemite Creek picnic area, playing on the logs & rocks, but otherwise spent a long time driving across the pretty woods. As we moved east, the occasional granite crag appeared, and at Olmstead point there is a lovely view down to the same features I'd been looking up at for the past several days. We're a long way from Half Dome, but the park volunteer had a spotting scope trained on its back slope, and we could see the line of hikers, like ants, using the cable to pull themselves up that last 1/4 mile. We identified all the peaks using an iPhone tool that works somewhat, and avoid the throngs of kidlets playing on the granite slab to take some infrared photos, commenting on how it would be nicer if there weren't a throng. A little further down the parking lot, or at least the next pull out, gave us a view of Tenaya Lake, and Scott clambered up onto the roof of the van to shoot it – just like the old Ansel Adams print he bought. I took pics of it from a near by slab.
We passed the lake, where people were swimming, and continued down to the Touelame meadows townsite, such as it is. All the capital expenditure for the park was really focused on the central valley, and this area has a tiny visitor center (we got stamped), a post office/grill (ate burgers), and a "lodge" which appeared to mostly be cabin tents – we were not impressed. There are more domes in this area, and plenty of high Sierra hikes…but it's now late afternoon, and we're on a rest day, so we headed back to the lake, set up an encampment of the hammock and sat & read, wrote postcards, and generally hung out. I stayed in the shade, and the wind was rather chill – I ended up attaching the legs to my zip offs, and putting on a long sleeved shirt. Our neighbors on the beach were actually in the sun, and wearing bikinis. We're wimps.
Navigating across northern California would have been easier if we'd remembered the gazetteer, but we were trusting google…and then we found there was a whole lot less Internet out here. We stopped in the town of Ukiah for dinner at their brewpub – their pilsner was a bit light- then continued across the central valley, finding a BLM land pull off that didn't actually have no camping signs, and settled in.
Wednesday morning we sprinted for Yosemite. It was a lumbering sprint, as we stopped at Amanda's favorite fruit stand for veggies and crack almonds just north of Modesto. We also swung through a grocery store in some nameless town and got supplies and gas.
We reached the park around noon, and plopped down below Bridal Veil Falls on the main drag to eat up our leftovers & decide what to do. All the campgrounds were full. We ended up spending some time orienting around The Village and the transit system, and then took the bus out to Camp 4. I've read about the climbers base camp in so many stories – Nevada Barr, John Muir, a couple movies, and it's always a lawless, drunken place, with dirty sloppy inhabitants. I didn't find it so – it was actually neat and peaceful, with a few children hanging out in the shade. It was much quieter than the 'family' campgrounds across the valley! Let's hear it for folks who do strenuous exercise, have a beer, then sleep silently in their tents.
We stopped at the trail sign, with one leg pointing to the famous El Capitan. We went the other way. We hiked towards Upper Yosemite Falls, which was a 3.8 mile stroll with an elevation gain of OMG. Scott has the actual numbers, but I recall we'd gained 1000 feet over the first 2 miles. We managed to do it almost entirely in the shade too, which definately helped my stability – my sun issues are something I hope to avoid this trip.
Scott took pictures of the falls, and we turned and headed back down, cursing the trail builders now and again. There were lots of rock stairs – an impressive number – and occassionally they were sloped, narrow, and offset – we ended up nicknaming it scale mail, and our feet slipped off it like arrows off a knight. Did I mention the elevation? We descended a long time, but it seems to be a ratio of 2 hours up:40 minutes down.
We took the bus to the van – one of our fellow bus stop waits walked up & said "hello hikers," in a boisterous voice and handed out snicker minis – must remember this as a way to meet people.
Since the campsites were all filled that we knew of, we headed out of the park to park the van in a dispersed camp beside a river.
You know there's been some stress around when I'm the one requesting a lazy morning in camp on the first day of vacation. Sunday we had packed up and drove out of Portland, saturday we had been completely booked with Tacit & Zaiah's commitment ceremony and visiting Floridian horde, and the entire week previous I was covering at work for various people. No wonder I slept in until Scott had finished creating coffee, then I made a leisurely omelet breakfast and eventually Scott pushed us to get going.
Our southern drive had a stop at Burlesque, which was about as fun as we remembered, and left us desiring a tree house. We bought nothing, but the woodworking roadside attraction left us smiling and still feel its a fine stop in the middle of a long driving day.
We're just north of Redwoods National Park, leaving a bandit campsite beside the Smith River. Yesterday we arrived in the area around dinner time and took a hike in Stout Grove. Only a half mile, but it was enough to banish the last of my all day headache while we enjoyed the big trees. Scott took a picture of me doing my squirrel imitation – I think he's got an identical shot from 2005 when we visited Redwoods while on walkabout.
We had just gotten across the continent and begun exploring new ecosystems when Scott came down with an itch – insect bites? No, by the time we hit Crescent City, not only was it obviously poison oak, it had gone systemic, and it was good drugs and weeks later before he'd slept through the night. We don't remember too much from that first trip through Redwoods because we're repressing those memories. Firmly.
This time, we were heading from north to south, knew what PO looked like, and wore long pants. It was summer, yes, but it was cool Northern California, and the day was successive rain showers. Stout grove was a short, 1/2 hour hike with a little scramble down to a river bank. The visitor center was a stop to chat with the rangers and stamp the passport – its getting particularly full in western states, I'm going to have to craft a new version of it soon. Continuing through the drive, we stopped at Moormon grove – not impressive – and Big Tree, which is. Big Tree is the widest and probably oldest tree in the park, and apparently the park has stopped trying to keep a large wooden sign with its vital stats near by – instead, they have a laminated photo of the old sign. Scott took a pic of it – very meta. And as we recall, is where we tried to have lunch with the van doors swung wide open and were harassed by a Stellars Jay until we retreated (back then, having the van doors wide was a treat, as we were still From the Land of Mosquitos). This time, we also hiked across the street in an unassuming grove near the creek, and Scott attempted to photograph big trees while perched on the trunk of their fallen brethren, in the middle of the creek.
Past the visitor center and looking for a turn off, we instead found a handful of cars pulled off and a herd of about 30 roosevelt elk munching in someone's front yard. We stopped and jumped out and were taking pictures when car 1 came around the corner and slowed down to see the spectacle, and then car 2 zoomed around the same corner and started an uncontrolled skid. It looked to me like we were out of the path of collision if they hit, but to be safe, I ran towards the elk. Into a bog. The cars pulled it out without incident – though the young driver of car 2 heaped verbal insult on to everyone legally off the road and watching wildlife, regardless of the speed he'd been recklessly driving at. I extracted myself, Scott checked that the phone I'd pulled from my pocket hadn't gotten more than a splash, and then I went back to the van to change – I was mud to my hips, and my shoes squished.
We headed up Bald Mtn Road to the Redwood River Overlook, which did not appear to show off the landscape as well as Scott had hoped. You could still see the clear cutting canopy differences from the logging that was still going on in 1978, though the trees are defiantly moving back in. On the way down, we hiked over an impressive bridge and through the Lady Bird Johnson grove – where Nixon, Johnson, & Reagan (then the gov) dedicated the national park opening. It was an interpretive trail, and while Scott took endless photos of rhododendrons blooming in front of misty redwoods, I read the interpretive flyer aloud – it sounded like marketing drivel, but most entries had a bite or two of actual education in it. At one point, Scott put his camera down in the center of a hollow tree, shooting upward on timer while we hid outside the bark. Another point he set up a times shot of the two of us. Mostly, though, he shot in the mist.
Back on the road, we found cell signal and answered emails and checked weather and our intended route, getting most of that data before we turned off the highway at Redway, and then became self contained again. From Redway to Shelter Cove, we'd been told, is 30miles and would take us 1.5 hours to drive, although the locals do it in about 40 minutes. (pull over if someone comes up behind you – really) It started in a small redwood grove, then twisted through a variety of ecosystems – forest, prairie, farmland – as it wound up the ridge line, with no flow, unexpected corners, and exposure. I expect anyone mildly suseptable will get carsick when following this route; it was extremely disconcerting. I don't want to drive it myself, and I was really glad we made it to our destination before sunset. Scott has declared this road the Californian equivalent of El Camino del Muerte.
We pulled into Tolkan Campsite, at a peak of a ridge line, in time to perform camp chores and fetch water, and then the sun went down. The two other occupied campsites soon quieted. Scott stood outside, shaving before bed, and called me to join him. After a day of rolling clouds and rain, the moon was up, half full and visible through the trees. "Most guys," I told him, "give their girls diamonds. You give me the moon. This works for me.". He chuckled when I kissed him, and finished using his electric razer by braille in the dark night.


Create that trusting bond between agents and callers that will set calls off on the right path from the get go and create good customer relationships, helping you improve service, increase sales and resolve issues.
Building rapport with customers means your agents have to be able to create a bond that demonstrates that each – the customer and the agent – trust and understand each other's feelings and where they're coming from.
In a call centre environment it's an essential way of building good relationships with customers, reflecting well on the image of your business and helping to increase sales and customer service performance.
This can involve the type and tone of language used during a call, right through to something as basic as getting the customer's name right and sets your agents up to handle calls successfully.
It sounds so obvious and is one of the first things an agent should tackle, but capturing the caller's name (if you don't know it already) is important and shows an agent is treating them as a real and unique individual, rather than a statistic on a screen.
Just as important is getting the pronunciation of a name right. Failing on this front can even cause offence, so it's crucial agents ask at first if they're not sure and then make sure they remember it. The same applies to names that can be said in different ways or shortened – for example saying "Katy" instead of "Kate" or "Steph" instead of "Stephanie".
Technology that provides screen-pop information boxes on the screen when an agent is connected to a customer can dramatically help agents in this regard. If a customer is dialled from a data set or has previously been in contact with an agent before, this information will readily be available for the agent to use at the beginning of the phone call.
If agents have notes or information at hand regarding a caller, in addition to any notes about them or their situation, agents can pick up where a previous colleague left off.
Not only does this cut back on wasted time by having to find out potentially a lot of the same information as before, it prevents the customer being irritated by having their own time wasted through having to repeat themselves. Your agents and organisation will come across as professional and help to complete an overall smoother process.
Simple box fields on a customer's account that allow agents to leave whichever notes on a customer they feel is necessary will help achieve this by presenting the information to a following agent on their screen, impressing your caller and improving customer service.
When agents are going to be dealing with calls that are more complex in nature or heavy on information, it significantly helps if they are pre-equipped with details prior to being connected to a customer.
In the case of an outbound campaign, utilising preview dialling will help your campaign's effectiveness in such scenarios. Agents will be able to preview important data attached to the customer before they click to initiate the call to be connected.
This strategy of outbound dialling is particularly popular for customer retention purposes or in B2B campaigns. When agents are ready for their next call they simply click to load the next record, allow time to preview the information that will instantly load to the screen, and then click again to initiate contact.
The language and tone used by an agent can set the mood for the rest of the call and have a real impact on how it pans out.
Just put yourself into the shoes of a customer on the other end of the phone and think how you feel if you hear a warm, welcoming and upbeat tone. It makes a big difference to your perception of the agent and how it seems they are treating you, making you far more likely to respond in a polite manner and have more patience.
Meanwhile, demonstrating a naturalness shows you are a real and normal personality. For example, making polite comments about any background noise or showing communality about a holiday the customer has just been on or going on, by talking about one you have just been on or going on, can make the customer feel comfortable and find a common ground with you.
Of course, there are a time and place when this will not be required, but it's down to your agents to use common sense and judge when appropriate.
An angry customer is usually the toughest type of caller an agent will have to handle, with rapport being very difficult to build compared to 'ordinary' calls – at least initially.
How an agent handles the caller in the early stages has a big impact on the outcome at the end of the call, typically resulting in either the customer being even more irate or (hopefully) being calmer. Allowing the customer to vent without interruption lets them get their issue off their chest, rather than risk exacerbating the situation.
What it also cleverly does is bide the agent time to figure out a solution to the caller's problem, whilst also thinking of the correct tone and language to use that will calm the caller down. Technology that provides call centre managers with silent monitoring and in-call coaching facilities can ensure on those even more difficult calls when reasoning and understanding is simply not working, an agent can be given a helping hand by their superior.


text:
Q: How do you check for duplicate data using Cypress.io? I have a table, using DIVs that contain customer data. I wan't to be able to test if there is duplicate customer data.  Below is an example of my table:

Holiday,John

8675309

Doe,Jen

123524

Holiday,John

8675309

I'm not how to approach this to say that, indeed, there is duplicate data (Holiday, John)
I'm hoping to say that, with Cypress, there "There are duplicates, therefore the step fails.
Thanks!

A: You should be able to do this to make sure there is only one
cy.get('a:contains("Holiday,John")').should('length',1);

If this fails you have more than one or none.. I tried it using your HTML and it seemed to work. It is basically counting how many A elements there are that contain Holiday,John. In this case you will get 2 which will fail the test

redpajama_set_name: RedPajamaStackExchange


text:
Screening for and Treatment of Polycystic Ovary Syndrome in Teenagers
Experimental Biology and Medicine 229:369-377 (2004)
© 2004 Society for Experimental Biology and Medicine
Darren J. Salmi, Howard C. Zisser1, and Lois Jovanovic
Sansum Diabetes Research Institute, Santa Barbara, California 93105
Requests for reprints should be addressed at Sansum Diabetes Research Institute, 2219 Bath St., Santa Barbara, CA 93105. E-mail: hzisser@sansum.org
Polycystic ovary syndrome (PCOS) usually arises during puberty and is marked by hyperinsulinemia and hyperandrogenism. Adolescents with PCOS are at an increased risk of developing health problems later on in life such as type 2 diabetes, cardiovascular disease, and infertility. Furthermore, the physical signs of PCOS can be detrimental to a teenage girl's self-image. Early diagnosis and treatment of PCOS in adolescents are essential in ensuring adulthood health and restoring self-esteem. Treatments for an adolescent with PCOS include diet and exercise, metformin, and oral contraceptive pills. Each of these options has been shown to be effective in improving certain aspects of PCOS, and probably the best treatment plan involves some combination of them.
Although the first description of polycystic ovary syndrome (PCOS) is generally credited to Stein and Leventhal in 1935, it may have been observed as early as 1721, when Italian scientist Antonio Vallisneri observed "young married peasant women, moderately obese and infertile, with two larger than normal ovaries, bumpy and shiny, whitish, just like pigeon eggs" (1). This depiction sounds similar to the subfertility and obesity commonly found in PCOS. It was not until 1921 that Achard and Thiers noticed a relationship between hyperandrogenism and insulin resistance in their study of the "bearded diabetic woman" (2). This relationship is present in PCOS in what might be called the "hirsute hyperinsulinemic woman." In 1935, Stein and Leventhal made the connection between amenorrhea and polycystic ovaries. In addition, they noticed the occurrence of "masculinizing changes" in many patients with polycystic ovaries, including hirsutism and acne (3). Several, though not all, of their original case studies involved women who were overweight. In all seven of their case reports, attempts to treat ovulatory dysfunction with estrogenic hormone failed, and wedge resection was employed. Surgery for PCOS is uncommon now, but all of Stein and Leventhal's patients gained normal menstruation, and two become pregnant. Still, much has changed in the way we understand and treat PCOS.
Although the exact etiology of PCOS is still debated, studies conducted with family members of women with PCOS have suggested that there is a genetic role in its pathogenesis. In a study group of 15 prepubertal daughters of women with PCOS, all but one were found to have polycystic ovaries by ultrasound (4). In a twin study of PCOS, there was a concordance rate of 60% among the sampled dizygotic twin pairs and 74% among monozygotic twin pairs (5). Hyperandrogenemia, either with or without menstrual irregularity, is present in about one-half of sisters of women with PCOS (6). Additionally, the parents of women with PCOS have a high prevalence of impaired glucose tolerance and type 2 diabetes (T2DM), 30%–31% and 16%–27%, respectively (7).
There is evidence that PCOS may be a lifelong disorder where certain precursors are present well before the full onset of disease. In fact, polycystic appearing ovaries have been found in girls as young as 6 years, and some girls are probably born with polycystic ovaries (8). Experimental studies of hyperandrogenism in animals prior to birth further suggest that the hormonal aspect of PCOS is genetically predetermined (9). It seems as though patients with PCOS have at least some form of it throughout life. However, diagnosing the disorder before puberty is difficult because patients with PCOS are generally diagnosed only after seeking help for irregular menses or skin changes that do not take place until puberty.
Although several specific genes have been suggested as markers for PCOS susceptibility, there has been no clear evidence of any of them being strongly associated with PCOS inheritance. The fact that insulin resistance is such a prominent feature of PCOS has led to the hypothesis that PCOS is the result of so-called thrifty genes being expressed in an environment of plentiful food and minimal exercise (10). Many suspected genes, including the Xbal polymorphism of the glycogen synthetase gene, the T228A polymorphism of the SORBS1 gene, and the D85 and Y85 variants of the UGT2B15 gene, have been found to be no more common in women with PCOS than in the general population (11–13). The v-LH gene variant has been shown to play a minor role in PCOS, but more research is still necessary (14). The C/T single nucleotide polymorphism at the tyrosine kinase domain of the insulin receptor (INSR) gene has been implicated in PCOS susceptibility, but only among the population of lean women (15). The INS VNTR and CYP11alpha genes also show some association with PCOS (16). Calpain 10, IRS-1, IRS-2, and sex hormone binding globulin (SHBG) genes have been suggested to contribute to PCOS (17). Also, the study of PCOS theca cells has suggested even more genes, including aldehyde dehydrogenase 6 and retinal dehydrogenase 2, that may factor into the inheritance of PCOS (18).
Despite the fact that there is a strong familial component to PCOS, it clearly has a multifactorial pathogenesis. It is widely agreed that among women genetically predisposed to developing PCOS, an additional event triggers the development of the full-blown syndrome. For example, the increase in insulin levels and IGF-I activity that naturally occurs during puberty can activate the expression of PCOS (19). Other such events could be prolonged stress or weight gain (20).
The underlying problem of PCOS is related to hyperinsulinemia (Fig. 1). Prolonged exposure to increased insulin concentrations may lead to acanthosis nigricans, increased body fat, and eventually the development of T2DM. Hyperinsulinemia also causes the pituitary to hypersecrete luteinizing hormone (LH), which in turn triggers anovulation. Additionally, high insulin concentrations contribute to the thickening of the ovarian theca, which in turn causes elevated production of androgens, specifically testosterone. Increased testosterone levels are responsible for the acne, hirsutism, and alopecia that often occur in PCOS.
Why It Is Important to Diagnose and Treat PCOS in Adolescence
PCOS is linked to a host of health problems, including T2DM, heart disease, hypertension, endometrial cancer, ovarian cancer, subfertility, and infertility. For example, women with PCOS have a higher incidence of gynecological cancer (21) and are about 2.5 times as likely as healthy women to develop ovarian cancer (22), and the persistent dysfunctional bleeding that affects some women with PCOS can lead to anemia. The early detection and treatment of PCOS during adolescence could delay the onset of, or even prevent, many of these maladies later on in adulthood. In addition, dermatological effects of PCOS, such as acne, hirsutism, acanthosis nigricans, and alopecia, have a deleterious effect on an adolescent's self-image.
When dealing with teenagers who have PCOS, one of the main concerns should be infertility as they mature. Although teenagers with PCOS do not complain about difficulty conceiving, they may later in life. Many adult patients are diagnosed with PCOS only after seeking treatment for infertility, but the emotional and financial strains that result could have been prevented if PCOS were diagnosed in the teenage years and closely followed by a physician. About one-third of pregnancies in women with PCOS end in spontaneous abortion (20). Obesity, which occurs frequently in about one-half of all women with PCOS, further complicates the situation as it increases the likelihood of gestational diabetes, preeclampsia, premature labor, neonatal macrosomia, and stillbirth (20). Therefore, effective treatment of an adolescent's PCOS and establishment of diet and exercise habits to prevent obesity will increase her likelihood of having a complication-free pregnancy and a healthy baby when the time comes.
Women with PCOS have a 5–10 times greater chance of being affected by T2DM than do women without PCOS (23). By the time they reach the age of 40, 40% of women with polycystic ovary syndrome have T2DM or impaired glucose tolerance (IGT; Ref. 24). It is not just obese women who are in danger. Nonobese women with PCOS have been shown to be at risk for IGT as well (25). The progression toward T2DM begins at an early age. Obese PCOS adolescents have one-half the peripheral tissue insulin sensitivity that obese non-PCOS adolescents have (26). Impaired ß-cell function and abnormal production of hepatic glucose have also been found in obese adolescents with PCOS (27). The defects in insulin activity and secretion, ß-cell dysfunction, and rise in hepatic glucose production are all precursors of T2DM. Since the average cost of health care for a person with diabetes is 2.4 times that of a nondiabetic person, this would not only improve the long-term health of PCOS patients but also reduce their health care expenses.
PCOS has been linked to unfavorable lipid profiles. As low high-density lipoprotein (HDL) levels are predictors of risk for coronary heart disease, it is significant to note that there is both a decline in the HDL levels of PCOS women when compared with healthy counterparts as well as a correlation between reductions in HDL and increases in obesity within the population of PCOS women (28). Rajkhowa et al. proposed that a modified activity of hepatic lipase or lipid transfer protein might be the culprit for the lipid abnormalities seen in PCOS (28). While obesity tends to play a large role in low-density lipoprotein (LDL), HDL, and cholesterol levels, it seems that hyperinsulinemia plays the greatest role in triglyceride levels (20). It is apparent that among PCOS adolescents who are obese, early efforts at weight loss would be very beneficial to their lipid profiles and therefore their risk of cardiovascular disease.
Hyperandrogenism, insulin resistance, hypertension, dyslipidemia, obesity, and ovulatory dysfunction regularly found in women with PCOS put them at much greater risk of developing heart disease, which is the most common cause of death among women (28).
Women with PCOS have an incidence of coronary artery calcification (a predictor of cardiac disease) that is greater than three times that of matched controls (29). Compared with healthy women, women with polycystic ovary syndrome are 7.4 times more likely to develop ischemic heart disease and myocardial infarction (28). Additionally, the disparity in risk between PCOS women and normal women is greatest in young adults, particularly between the ages of 18 and 24 (30). Obese PCOS adolescents with impaired glucose tolerance lack a dip in their nocturnal blood pressure, which may signal an increased risk of cardiovascular disease (27). It has been suggested that obese adolescents with PCOS are a population in considerable danger of developing cardiovascular disease when they become adults (27, 29, 31), and therefore intervention at an early age should be implemented in order to improve their chances of avoiding heart disease or at least postponing it for as long as possible (29).
Finally, one of the most important yet overlooked reasons for adequate screening and treatment of PCOS in adolescents is the quality-of-life issue that weighs so heavily on patients. Because of the phenotype of this disorder, girls with PCOS experience a great emotional and psychological burden. Many of the symptoms common to PCOS, such as excess hair growth, acne, alopecia, and obesity, cause the patients to experience social trauma during a period when social acceptance is especially greatly valued, leading to higher rates of depression. Some PCOS adolescents become unhappy with their appearance at a point in their life where personality growth occurs most dramatically, which can have a severe negative impact on their self-esteem, confidence, and self-respect during their teens and beyond. Coupling this with the usual emotional difficulties of adolescence creates a decreased sense of quality of life (32), and about half of all women with PCOS suffer from some degree of depression (33). The hirsutism that affects many PCOS adolescents leads to increased social fears and anxiety compared to nonhirsute adolescents (34, 35). Women with PCOS feel that hirsutism, irregular menstruation, and infertility make them "less feminine" (36), and one unfortunate result of this is that some teenagers with PCOS actively seek pregnancy as a way to prove their femininity to themselves. As mentioned earlier, fertility issues are of great concern among patients with PCOS. Not surprisingly, adolescents with PCOS are 3.4 more times as concerned with fertility as non-PCOS girls (37). Distressingly, about one-third of PCOS women have abnormal eating patterns, and 6% are bulimic, emphasizing a need to screen for such disturbances when dealing with PCOS patients (38).
How to Screen for PCOS in Adolescents
Because PCOS is a collection of conditions, it lacks a definitive identifying test, and so a proper diagnosis depends on consideration of many factors. Furthermore, since an exact definition of PCOS is not universally agreed on, the criteria for its diagnosis are somewhat amorphous. The most widely accepted diagnostic criteria are oligomenorrhea/amenorrhea, hyperandrogenism (clinical or biochemical), and absence of other causes of hyperandrogenism (virilizing tumor, hyperprolactinemia, congenital adrenal hyperplasia, Cushing's syndrome, and so on), set forth by a 1990 NIH/ NICHHD conference (39). Insulin resistance, although not part of the NIH criteria, is a trademark feature of PCOS (40). Therefore, when a young female presents with irregular menses, hirsutism, acne, alopecia, central adiposity, acanthosis nigricans, and/or hyperinsulinemia, PCOS should be considered as a possible cause for her symptom(s), and an endocrine evaluation, including measurements of total and free testosterone and dehydroepiandrosterone sulfate (DHEAS), should be completed. Unfortunately, many adolescents with oligomenorrhea do not consult with a physician about their condition at all, and several who do seek help are prescribed oral contraceptives and not given endocrine evaluations. The basic screening formula provided in Figure 2 decreases the chance of such missed diagnoses. Table 1 shows our experience with a successful screening program in our teenagers in Santa Barbara County, California. Although hyperinsulinemia may be difficult to assess since a passing state naturally occurs during puberty, adolescents with hyperandrogenism have significantly higher insulin levels than otherwise normal pubertal adolescents (41). Oral glucose tolerance tests are useful in diagnosing PCOS, and they also determine IGT, which indicates an increased risk of T2DM. When diagnosing PCOS, it is important to rule out other possible causes of the patient's symptoms, such as runner's amenorrhea, hyperprolactinemia, hypothyroidism, ovarian or adrenal virilizing tumor, Cushing's syndrome, or idiopathic oligomenorrhea. Table 2 shows signs, symptoms, and laboratory values that are helpful with the differential diagnosis in our experience.
Furthermore, a proper medical history can help lead to a diagnosis of PCOS. Adolescents with a family history of PCOS or diabetes, male relatives with alopecia, or female relatives with infertility or menstrual problems should be assessed for PCOS because such familial associations put them at a much greater risk. Lifestyle parameters such as diet, exercise, and smoking should be evaluated, and appropriate recommendations should be given, as these factors have a significant effect on PCOS. Determining pubertal history is important since the first indication of PCOS is usually premature pubarche (42). Thus, hyperandrogenism should be checked for in such patients, as they are in danger of developing PCOS.
Despite the condition's name, not all women with polycystic ovaries have PCOS, and not all women with PCOS have polycystic ovaries. Polycystic ovaries are found in up to one-fourth of all women, so their presence alone is not enough for diagnosis. However, ovarian morphology can still be useful in diagnosis of PCOS. For instance, ovarian volumes of greater than 10 cm3 have a high sensitivity and specificity for PCOS (43, 44). Also, a ratio of ovarian stroma to total area of more than 0.34 is appreciably linked to PCOS (45).
Two other criteria that have been theorized to be indicators of PCOS are growth hormone and prolactin levels. However, prolactin secretion has not been found to be significantly greater in PCOS women, and amplified growth hormone secretion has been indicated only in nonobese adolescents with PCOS (46). Sometimes visual clues, like perceptible facial hair or skin changes, are good indications of PCOS. For example, acanthosis nigricans is an indicator of hyperinsulinemia (47), which has been suggested to lead to hyperandrogenism (48). Since both hyperinsulinemia and hyperandrogenism are identifying features of PCOS, women with acanthosis nigricans should be examined for PCOS.
A particular subgroup of women with an increased risk of PCOS is patients with epilepsy. PCOS is overrepresented in this group, occurring in about 26% of women with epilepsy (49). Although there is debate over the relationship between epilepsy and PCOS, it is thought either that the hypothalamic control of reproductive function is disturbed by the disorder itself or that valproic acid, a drug used in the treatment of epilepsy, is somehow responsible (50). Since the prevalence of PCOS among women with epilepsy is three to five times greater than normal, screening for reproductive endocrine disorders in this population is warranted.
Screening for PCOS in the general public may be a feasible endeavor. A study done in northern Finland demonstrated that a simple questionnaire asking questions about oligomenorrhea and hirsutism could help identify women with PCOS-like endocrine abnormalities and insulin insensitivity (51). Since adolescent and adult PCOS diagnostic features are fairly similar (52, 53), such self-completed surveys are an easy and apparently effective way of detecting possible PCOS patients of any age.
The course of treatment for women with PCOS largely depends on the severity of an individual's symptoms. For example, someone who is trying to become pregnant but cannot because of PCOS-related infertility will be most concerned with improving ovulation, whereas someone who is not trying to become pregnant but is hirsute will be most concerned with decreasing their androgen levels. Adolescents with PCOS tend to be troubled most by the cosmetic effects of PCOS, such as acne, hirsutism, and/or acanthosis nigricans. Therefore, treatment of the PCOS adolescent must address these issues as well as take into account the consequences of long-term hyperinsulinemia and ovulatory dysfunction. Surgical procedures, medications, and lifestyle changes all can improve symptoms of PCOS and prevent or delay the onset of complications associated with PCOS. Furthermore, since adolescents with PCOS suffer from lower quality of life, psychological factors must be taken into consideration as well.
A primary anxiety of adolescents with PCOS is the effect that hyperandrogenism has on their skin. Spironolactone has been shown to diminish hyperandrogenism and even improved fertility in one out of three women with infertility in one study (54). Another antihirsutism agent, flutamide, also lowers androgen levels and improves ovulation (55). In addition, many treatment measures used for acne and hirsutism in non-PCOS populations are used successfully among adolescents with PCOS.
It is imperative to discuss the possibility of the risk of unwanted pregnancies in sexually active patients treated for PCOS. Oral contraceptive pills (OCPs) should be used in conjunction with metformin. The use of OCPs is very helpful in alleviating acne and hirsutism. OCPs are also beneficial to the PCOS adolescent for many other reasons. They increase bone density, lessen follicular activity, reduce the risk of ovarian and endometrial cancers, return menstrual regularity, and ward off anemia (56). Although OCPs have been implicated in raising triglyceride levels and total cholesterol in adolescents with PCOS, LDL/HDL ratios remain constant (57–59). OCPs increase neither body weight nor body fat in teenage women with PCOS (58).
The most preferred and most effective method of treatment for PCOS is lifestyle modification. Exercise, such as regular walking, has been shown to reduce waist-to-hip ratio, an indicator of diabetes and other morbidities, and homocysteine levels, an indicator of cardiovascular risk, in overweight PCOS women (60). Weight loss improves practically every parameter of PCOS. In obese, anovulatory PCOS women, weight loss restores ovulation and pregnancy rates, decreases insulin levels, diminishes acanthosis nigricans, lowers testosterone levels while raising SHBG levels, and improves psychological considerations (61, 62). Modifying dietary intake by increasing the protein-to-carbohydrate ratio appears to be endocrinologically beneficial to overweight PCOS women (63). A large study in Finland demonstrated that an adolescent's weight at 14 years and how it changes over the next 17 years has the strongest predictive power on future hormonal and metabolic perturbations (51). Thus, weight control is possibly the best method to prevent PCOS complications.
Metformin is emerging as an important component of PCOS treatment. In addition to the expected improvements in insulin sensitivity and glucose metabolism, metformin therapy also ameliorates hyperandrogenism and menstrual irregularity (64–66). Although most studies of metformin have involved obese PCOS women, nonobese PCOS populations profit from treatment as well (67), and metformin is able to restore ovulation in about three-fourths of women who are resistant to clomiphene citrate (68). As beneficial as metformin can be for adults with PCOS, it appears even more effective in adolescents with PCOS. A summary of metformin treatments and outcomes in adolescents is given in Table 3. Hyperinsulinemia and hyperandrogenism improve just as much as in adults, but an even higher success rate at normalizing menses and decreasing hirsutism occurs in the younger group (69, 70, 71, 74). Also, metformin has reduced the total cholesterol, LDL cholesterol, and triglycerides of PCOS adolescents while increasing HDL cholesterol (71). In addition, metformin has been shown to decrease C-reactive protein levels, which are predictive of cardiovascular disease (75). Metformin's various beneficial effects, combined with its safety record in people with T2DM, make it an appealing choice of medication for PCOS. However, it should be noted that metformin use in the treatment of PCOS might be lifelong. Ibáñez et al. showed that in adolescents with PCOS, all the improvements in menstruation, hirsutism, hyperinsulinemia, dyslipidemia, and hyperandrogenism were lost 3 months after cessation of metformin treatment (71). Also, since metformin can improve ovulation, the risk of pregnancy can increase, and if pregnancy occurs, use must be discontinued immediately, as metformin crosses the placenta.
Another group of insulin-sensitizing agents, thiazolidinediones (TZDs), may be effective in treating PCOS. However, it should be noted that the use of TZDs is not indicated in teenagers, and the recent findings of hepatotoxicity of troglitazone will probably necessitate further study of the safety of other TZDs. Nevertheless, rosiglitazone has been shown to improve insulin sensitivity, decrease androgen levels, lessen hirsutism, and improve ovulation (76). Also, pioglitazone has been shown to improve androgen and lipid profiles in obese PCOS women as well as improve insulin secretion, sensitivity, and clearance (77). In a study of PCOS women who had difficulty responding to metformin, the addition of pioglitazone to their treatment regimen improved glucose/insulin parameters, lowered DHEAS levels, raised SHBG and HDL levels, and enhanced cycle regularity (78). D-chiro-inositol has also been implicated as an insulin sensitizer with possible benefits for PCOS patients (79), but very little research has been done in this area.
Drug therapy is not the only treatment option for PCOS. A study of the Chinese herb tiangui fang demonstrated its ability to ease hyperinsulinism, lower serum testosterone, and restore normal menses as well as metformin (80). The recent evidence for supplemental chromium as a potential aide in the treatment of T2DM has raised the possibility that it may be of benefit to PCOS patients. Chromium not only has been known to lower fasting blood glucose but also has been shown to improve glucose tolerance and potentiate insulin action (81, 82). Although it is believed that chromium supplementation may benefit only those with a deficiency, its excellent safety record and effect on glucose/insulin parameters commonly found in PCOS make further research worthwhile.
Although the use of insulin-sensitizing agents has diminished surgery's usefulness, it is sometimes added to the treatment regimen of the adult with PCOS who wishes to become pregnant. In Stein and Leventhal's time, surgery was the most effective treatment for PCOS-related infertility, while today it is usually the last resort after clomiphene citrate, insulin sensitizers, and gonadotropin therapy fail. Though ovarian drilling by diathermy or laser is probably the preferred method, improvements in wedge resection techniques have resulted in impressive pregnancy rates and fewer adhesions than ever before (83, 84). Still, surgery is not indicated in teenagers, as it does little to improve PCOS symptoms beyond infertility, and pregnancy induction is not desirable in this group.
Despite the prevalence of PCOS, its etiology has yet to be clearly elucidated. Evidence suggests there are familial and genetic roles in becoming predisposed to PCOS from birth, while an additional event such as puberty brings about the fully developed syndrome. Therefore, until more sophisticated methods of detecting PCOS before puberty are formulated, screening for PCOS in adolescents is the best chance at early diagnosis and treatment. PCOS should be considered in any adolescent female with irregular menses, acne, hirsutism, alopecia, insulin resistance, and/or acanthosis nigricans, and diagnosis should rule out other causes of hyperandrogenism. Adolescents with PCOS not only suffer from the psychological effects of acne and hirsutism but also have an increased risk of negative health consequences, such as subfertility, cardiovascular disease, T2DM, dyslipidemia, and gynecological cancers. Even though several treatment options exist, including the highly effective metformin, healthy diet and regular exercise are the most beneficial in treating PCOS symptoms and preventing further health dilemmas.
Kovacs G, Smith J. A Guide to the Polycystic Ovary: Its effects on health and fertility. Castle Hill Barns, UK: TFM Publishing, 2002.
Achard C, Thiers J. Le virilisme pilaire et son association à l'insuffisance glycolytique (diabète des femme á barbe). Bull Acad Natl Med 86:51–83, 1921.
Stein IF, Leventhal ML. Amenorrhea associated with bilateral polycystic ovaries. Am J Obstet Gynecol 29:181–191, 1935.
Battaglia C, Regnani G, Mancini F, Iughetti L, Flamigni C, Venturoli S. Polycystic ovaries in childhood: a common finding in daughters of PCOS patients. A pilot study. Hum Reprod 17:771–776, 2002.[Abstract/Free Full Text]
Jahanfar S, Eden JA, Warren P, Seppala M, Nguyen TV. A twin study of polycystic ovary syndrome. Fertil Steril 63:478–486, 1995.[Medline]
Legro RS, Driscoll D, Strauss JF III, Fox J, Dunaif A. Evidence for a genetic basis for hyperandrogenemia in polycystic ovary syndrome. Proc Natl Acad Sci U S A 95:14956–14960, 1998.[Abstract/Free Full Text]
Yildiz BO, Yarali H, Oguz H, Bayraktar M. Glucose intolerance, insulin resistance, and hyperandrogenism in first degree relatives of women with polycystic ovary syndrome. J Clin Endocrinol Metab 88:2031–2036, 2003.[Abstract/Free Full Text]
Bridges NA, Cooke A, Healy MJ, Hindmarsh PC, Brook CG. Standards for ovarian volume in childhood and puberty. Fertil Steril 60:456–460, 1993.[Medline]
Abbott DH, Dumesic DA, Franks S. Developmental origin of polycystic ovary syndrome—a hypothesis. J Endocrinol 174:1–5, 2002.[Abstract]
Holte J. Polycystic ovary syndrome and insulin resistance: thrifty genes struggling with over-feeding and sedentary life style? J Endocrinol Invest 21:589–601, 1998.[Medline]
Rajkhowa M, Talbot JA, Jones PW, Clayton RN. Polymorphism of glycogen synthetase gene in polycystic ovary syndrome. Clin Endocrinol 44:85–90, 1996.[Medline]
Witchel SF, Trivedi RN, Kammerer C. Frequency of the T228A polymorphism in the SORBS1 gene in children with premature pubarche and in adolescent girls with hyperandrogenism. Fertil Steril 80:128–132, 2003.[Medline]
Tomboc M, Witchel SF. Frequencies of the D85 and Y85 variants of UGT2B15 in children and adolescent girls with hyperandrogenism. J Pediatr Endocrinol Metab 16:719–726, 2003.[Medline]
Tapanainen JS, Koivunen R, Fauser BC, Taylor AE, Clayton RN, Rajkowa M, White D, Franks S, Antilla L, Pettersson KS, Huhtaniemi IT. A new contributing factor to polycystic ovary syndrome: the genetic variant of luteinizing hormone. J Clin Endocrinol Metab 84:1711–1715, 1999.[Abstract/Free Full Text]
Siegel S, Futterweit W, Davies TF, Concepcion ES, Greenberg DA, Villanueva R, Tomer Y. A C/T single nucleotide polymorphism at the tyrosine kinase domain of the insulin receptor gene is associated with polycystic ovary syndrome. Fertil Steril 78:1240–1243, 2002.[Medline]
Xita N, Georgiou I, Tsatsoulis A. The genetic basis of polycystic ovary syndrome. Eur J Endocrinol 147:717–725, 2002.[Abstract]
Legro RS, Strauss JF. Molecular progress in infertility: polycystic ovary syndrome. Fertil Steril 78:569–576, 2002.[Medline]
Wood JR, Nelson VL, Ho C, Jansen E, Wang CY, Urbanek M, McAllister JM, Mosselman S, Strauss JF III. The molecular phenotype of polycystic ovary syndrome (PCOS) theca cells and new candidate PCOS genes defined by microarray analysis. J Biol Chem 278:26380–26390, 2003.[Abstract/Free Full Text]
Nobels F, Dewailly D. Puberty and polycystic ovarian syndrome: the insulin/insulin-like growth factor I hypothesis. Fertil Steril 58:655–666, 1992.[Medline]
Carmina E, Lobo RA. Polycystic ovary syndrome (PCOS): arguably the most common endocrinopathy is associated with significant morbidity in women. J Clin Endocrinol Metab 84:1897–1899, 1999.[Free Full Text]
Meirow D, Schenker JG. The link between female infertility and cancer: epidemiology and possible aetiologies. Hum Reprod Update 2:63–75, 1996.[Abstract/Free Full Text]
Schildkraut JM, Schwingl PJ, Bastos E, Evanoff A, Hughes C. Epithelial ovarian cancer risk among women with polycystic ovary syndrome. Obstet Gynecol 88(4, Pt 1):554–559, 1996.[Abstract]
Ovalle F, Azziz R. Insulin resistance, polycystic ovary syndrome, and type 2 diabetes mellitus. Fertil Steril 77:1095–1105, 2002.[Medline]
Kidson W. Polycystic ovary syndrome: a new direction in treatment. Med J Aust 169:537–540, 1998.[Medline]
Legro RS, Kunselman AR, Dodson WC, Dunaif A. Prevalence and predictors of risk for type 2 diabetes mellitus and impaired glucose tolerance in polycystic ovary syndrome: a prospective, controlled study in 254 affected women. J Clin Endocrinol Metab 84:165–169, 1999.[Abstract/Free Full Text]
Lewy VD, Danadian K, Witchel SF, Arslanian S. Early metabolic abnormalities in adolescent girls with polycystic ovarian syndrome. J Pediatr 138:38–44, 2001.[Medline]
Arslanian SA, Lewy SD, Danadian K. Glucose intolerance in obese adolescents with polycystic ovary syndrome: roles of insulin resistance and beta-cell dysfunction and risk of cardiovascular disease. J Clin Endocrinol Metab 86:66–71, 2001.[Abstract/Free Full Text]
Rajkhowa M, Neary RH, Kumpatla P, Game FL, Jones PW, Obhrai MS, Clayton RN. Altered composition of high density lipoproteins in women with the polycystic ovary syndrome. J Clin Endocrinol Metab 82:3389–3394, 1997.[Abstract/Free Full Text]
Christian RC, Dumesic DA, Behrenbeck T, Oberg AL, Sheedy PF, Fitzpatrick LA. Prevalence and predictors of coronary artery calcification in women with polycystic ovary syndrome. J Clin Endocrinol Metab 88:2562–2568, 2003.[Abstract/Free Full Text]
Talbott E, Guzick D, Clerici A, Berga S, Detre K, Weimer K, Kuller L. Coronary heart disease risk factors in women with polycystic ovary syndrome. Arterioscler Thromb Vasc Biol 15:821–826, 1995.[Abstract/Free Full Text]
Macut D, Micic D, Cvijovic G, Sumarac M, Kendereski A, Zoric S, Pejkovic D. Cardiovascular risk in adolescent and young adult obese females with polycystic ovary syndrome (PCOS). J Pediatr Endocrinol Metab 14(Suppl 5):1353–1359 (discussion, 1365), 2001.[Medline]
Trent ME, Rich M, Austin SB, Gordon CM. Quality of life in adolescent girls with polycystic ovary syndrome. Arch Pediatr Adolesc Med 156:556–560, 2002.[Abstract/Free Full Text]
Rasgon NL, Rao RC, Hwang S, Altshuler LL, Elman S, Zuckerbrow-Miller J, Korenman SG. Depression in women with polycystic ovary syndrome: clinical and biochemical correlates. J Affect Disord 74:299–304, 2003.[Medline]
Barth JH, Catalan J, Cherry CA, Day A. Psychological morbidity in women referred for treatment of hirsutism. J Psychosom Res 37:615–619, 1993.[Medline]
Sonino N, Fava GA, Mani E, Belluardo P, Boscaro M. Quality of life of hirsute women. Postgrad Med J 69(809):186–189, 1993.[Abstract]
Kitzinger C, Willmott J. "The thief of womanhood": women's experience of polycystic ovarian syndrome. Soc Sci Med 54:349–361, 2002.[Medline]
Trent ME, Rich M, Austin SB, Gordon CM. Fertility concerns and sexual behavior in adolescent girls with polycystic ovary syndrome: implications for quality of life. J Pediatr Adolesc Gynecol 16:33–37, 2003.[Medline]
McCluskey S, Evans C, Lacey JH, Pearce JM, Jacobs H. Polycystic ovary syndrome and bulimia. Fertil Steril 55:287–291, 1991.[Medline]
Zawadzki JK, Dunaif A. Diagnostic criteria for polycystic ovary syndrome: towards a rational approach. In: Dunaif A, Givens JR, Haseltine F, Merriam GR, Eds. Polycystic Ovary Syndrome. Boston: Blackwell, pp377–384, 1992.
Lewis V. Polycystic ovary syndrome: a diagnostic challenge. Obstet Gynecol Clin North Am 28:1–20, 2001.[Medline]
Apter D, Bützow T, Laughlin GA, Yen SSC. Metabolic features of polycystic ovary syndrome are found in adolescent girls with hyperandrogenism. J Clin Endocrinol Metab 80:2966–2973, 1995.[Abstract]
Kent SC, Legro RS. Polycystic ovary syndrome in adolescents. Adolesc Med 13:73–88, 2002.[Medline]
Herter LD, Magalhaes JA, Spritzer PM. Relevance of the determination of ovarian volume in adolescent girls with menstrual disorders. L Clin Ultrasound 24:243–248, 1996.
Dramusic V, Goh VH, Rajan U, Wong YC, Ratnam SS. Clinical, endocrinologic, and ultrasonographic features of polycystic ovary syndrome in Singaporean adolescents. J Pediatr Adolesc Gynecol 10:124–132, 1997.
Fulghesu AM, Ciampelli M, Belosi C, Apa R, Pavone V, Lanzone A. A new ultrasound criterion for the diagnosis of polycystic ovary syndrome: the ovarian stroma/total area ratio. Fertil Steril 76:326–331, 2001.[Medline]
Garcia-Rudaz MC, Ropelato MG, Escobar ME, Veldhuis JD, Barontini M. Amplified and orderly growth hormone secretion characterizes lean adolescents with polycystic ovary syndrome. Eur J Endocrinol 147:207–216, 2002.[Abstract]
Richards GE, Cavallo A, Meyer WJ III, Prince MJ, Peters EJ, Stuart CA, Smith ER. Obesity, acanthosis nigricans, insulin resistance, and hyperandrogenemia: pediatric perspective and natural history. J Pediatr 107:893–897, 1985.[Medline]
DeClue TJ, Shah SC, Marchese M, Malone JI. Insulin resistance and hyperinsulinemia induce hyperandrogenism in a young type B insulin-resistant female. J Clin Endocrinol Metab 72:1308–1311, 1991.[Abstract]
Bilo L, Meo R, Valentino R, Di Carlo C, Striano S, Nappi C. Characterization of reproductive endocrine disorders in women with epilepsy. J Clin Endocrinol Metab 86:2950–2956, 2001.[Abstract/Free Full Text]
Meo R, Bilo L. Polycystic ovary syndrome and epilepsy: a review of the evidence. Drugs 63:1185–1227, 2003.[Medline]
Taponen S, Martikainen H, Jarvelin MR, Laitinen J, Pouta A, Hartikainen AL, Sovio U, McCarthy MI, Franks S, Ruokonen A. Hormonal profile of women with self-reported symptoms of oligomenorrhea and/or hirsutism: Northern Finland birth cohort 1966 study. J Clin Endocrinol Metab 88:141–147, 2003.[Abstract/Free Full Text]
Bili H, Laven J, Imani B, Eijkemans MJ, Fauser BC. Age-related differences in features associated with polycystic ovary syndrome in normogonadotrophic oligoamenorrhoeic infertile women of reproductive years. Eur J Endocrinol 145:749–755, 2001.[Abstract]
Gulekli B, Turhan NO, Senoz S, Kukner S, Oral H, Gokmen O. Endocrinological, ultrasonographic and clinical findings in adolescent and adult polycystic ovary patients: a comparative study. Gynecol Endocrinol 7:273–277, 1993.[Medline]
Vetr M, Sobek A. Low dose spironolactone in the treatment of female hyperandrogenism and hirsutism. Acta Univ Palacki Olomuc Fac Med 135:55–57, 1993.[Medline]
De Leo V, Lanzetta D, D'Antona D, la Marca A, Morgante G. Hormonal effects of flutamide in young women with polycystic ovary syndrome. J Clin Endocrinol Metab 83:99–102, 1998.[Abstract/Free Full Text]
Jensen JT, Speroff L. Health benefits of oral contraceptives. Obstet Gynecol Clin North Am 27:705–721, 2000.[Medline]
Creatsas G, Koliopoulos C, Mastorakos G. Combined oral contraceptive treatment of adolescent girls with polycystic ovary syndrome. Lipid profile. Ann N Y Acad Sci 900:245–252, 2000.[Abstract/Free Full Text]
Lloyd T, Lin HM, Matthews AE, Bentley CM, Legro RS. Oral contraceptive use by teenage women does not affect body composition. Obstet Gynecol 100:235–239, 2002.[Abstract/Free Full Text]
Mastorakos G, Koliopoulos C, Creatsas G. Androgen and lipid profiles in adolescents with polycystic ovary syndrome who were treated with two forms of combined oral contraceptives. Fertil Steril 77:919–927, 2002.[Medline]
Randeva HS, Lewandowski KC, Drzewoski J, Brooke-Wavell K, O'Callaghan C, Czupryniak L, Hillhouse EW, Prelevic GM. Exercise decreases plasma total homocysteinc in overweight young women with polycystic ovary syndrome. J Clin Endocrinol Metab 87:4496–4501, 2002.[Abstract/Free Full Text]
Clark AM, Ledger W, Galletly C, Tomlinson L, Blaney F, Wang X, Norman RJ. Weight loss results in significant improvement in pregnancy and ovulation rates in anovulatory obese women. Hum Reprod 10:2705–2712, 1995.[Abstract/Free Full Text]
Apter D. How possible is the prevention of polycystic ovary syndrome development in adolescent patients with early onset of hyperandrogenism. J Endocrinol Invest 21:613–617, 1998.[Medline]
Moran LJ, Noakes M, Clifton PM, Tomlinson L, Norman RJ. Dietary composition in restoring reproductive and metabolic physiology in overweight women with polycystic ovary syndrome. J Clin Endocrinol Metab 88:812–819, 2003.[Abstract/Free Full Text]
Chou KH, von Eye Corleta H, Capp E, Spritzer PM. Clinical, metabolic and endocrine parameters in response to metformin in obese women with polycystic ovary syndrome: a randomized, double-blind and placebo-controlled trial. Horm Metab Res 35:86–91, 2003.[Medline]
Kazerooni T, Dehghan-Kooshkghazi M. Effects of metformin therapy on hyperandrogenism in women with polycystic ovary syndrome. Gynecol Endocrinol 17:51–56, 2003.[Medline]
Moghetti P, Castello R, Negri C, Tosi F, Perrone F, Caputo M, Zanolin E, Muggeo M. Metformin effects on clinical features, endocrine and metabolic profiles, and insulin sensitivity in polycystic ovary syndrome: a randomized double-blind, placebo-controlled 6-month trial, followed by open, long-term clinical evaluation. J Clin Endocrinol Metab 85:139–146, 2000.[Abstract/Free Full Text]
Morin-Papunen L, Vauhkonen I, Koivunen R, Ruokonen A, Martikainen H, Tapanainen JS. Merformin versus ethinyl estradiol-cyproterone acetate in the treatment of nonobese women with polycystic ovary syndrome: a randomized study. J Clin Endocrinol Metab 88:148–156, 2003.[Abstract/Free Full Text]
Vandermolen DT, Ratts VS, Evans WS, Stovall DW, Kauma SW, Nestler JE. Metformin increases the ovulatory rate and pregnancy rate from clomiphene citrate in patients with polycystic ovary syndrome who are resistant to clomiphene citrate alone. Fertil Steril 75:310–315, 2001.[Medline]
Arslanian SA, Lewy V, Danadian K, Saad R. Metformin therapy in obese adolescents with polycystic ovary syndrome and impaired glucose tolerance: amelioration of exaggerated adrenal response to adrenocorticotropin with reduction of insulinemia/insulin resistance. J Clin Endocrinol Metab 87:1555–1559, 2002.[Abstract/Free Full Text]
Glueck CJ, Wang P, Fontaine R, Tracy T, Sieve-Smith L. Merformin to restore normal menses in oligoamenorrheic teenage girls with polycystic ovary syndrome (PCOS). J Adolesc Health 29:160–169, 2001.[Medline]
Ibáñez L, Valls C, Potau N, Marcos MV, de Zegher F. Sensitization to insulin in adolescent girls to normalize hirsutism, hyperandrogenism, oligomenorrhea, dyslipidemia, and hyperinsulinism after precocious pubarche. J Clin Endocrinol Metab 85:3526–3530, 2000.[Abstract/Free Full Text]
Ibáñez L, de Zegher F. Flutamide-metformin therapy to reduce fat mass in hyperinsulinemic ovarian hyperandrogenism: effects in adolescents and in women on third-generation oral contraception. J Clin Endocrinol Metab 88:4720–4724, 2003.[Abstract/Free Full Text]
Freemark M, Bursey D. The effects of metformin on body mass index and glucose tolerance in obese adolescents with fasting hyperinsulinemia and a family history of type 2 diabetes. Pediatrics 107(4):E55, 2001.[Medline]
Loverro G, Lorusso F, De Pergola G, Nicolardi V, Mei L, Selvaggi L. Clinical and endocrinological effects of 6 months of metformin treatment in young hyperinsulinemic patients affected by polycystic ovary syndrome. Gynecol Endocrinol 16:217–224, 2002.[Medline]
Morin-Papunen L, Rautio K, Ruokonen A, Hedberg P, Puukka M, Tapanainen JS. Metformin reduces serum C-reactive protein levels in women with polycystic ovary syndrome. J Clin Endocrinol Metab 88:4649–4654, 2003.[Abstract/Free Full Text]
Ghazeeri G, Kutteh WH, Bryer-Ash M, Haas D, Ke RW. Effect of rosiglitazone on spontaneous and clomiphene citrate-induced ovulation in women with polycystic ovary syndrome. Fertil Steril 79:562–566, 2003.[Medline]
Romualdi D, Guido M, Ciampelli M, Giuliani M, Leoni F, Perri C, Lanzone A. Selective effects of pioglitazone on insulin and androgen abnormalities in normo- and hyperinsulinaemic obese patients with polycystic ovary syndrome. Hum Reprod 18:1210–1218, 2003.[Abstract/Free Full Text]
Glueck CJ, Moreira A, Goldenberg N, Sieve L, Wang P. Pioglitazone and metformin in obese women with polycystic ovary syndrome not optimally responsive to metformin. Hum Reprod 18:1618–1625, 2003.[Abstract/Free Full Text]
Nestler JE, Jakubowicz DJ, Iuorno MJ. Role of inositolphosphoglycan mediators of insulin action in the polycystic ovary syndrome. J Pediatr Endocrinol Metab 13(Suppl 5):1295–1298, 2000.[Medline]
Hou J, Yu J, Wei M. Study on treatment of hyperandrogenism and hyperinsulinism in polycystic ovary syndrome with Chinese herbal formula "tiangui fang." Zhongguo Zhong Xi Yi Jie He Za Zhi 20:589–592, 2000.[Medline]
Anderson RA. Chromium, glucose tolerance, and diabetes. Biol Trace Elem Res 32:19–24, 1992.[Medline]
Anderson RA, Cheng N, Bryden NA, Polansky MM, Cheng N, Chi J, Feng J. Elevated intakes of supplemental chromium improve glucose and insulin variables in individuals with type 2 diabetes. Diabetes 46:1786–1791, 1997.[Abstract]
Duleba AJ, Banaszewska B, Spaczynski RZ, Pawelczyk L. Success of laparoscopic ovarian wedge resection is related to obesity, lipid profile, and insulin levels. Fertil Steril 79:1008–1014, 2003.[Medline]
Yildirim M, Noyan V, Bulent Tiras M, Yildiz A, Guner H. Ovarian wedge resection by minilaparatomy in infertile patients with polycystic ovarian syndrome: a new technique. Eur J Obstet Gynecol Reprod Biol 107:85–87, 2003.[Medline]
PCOS: uncovering polycystic ovary syndrome (in an 11-year old girl!)
Filed Under: Diagnosis, PCOS Research, Teens and PCOS Tagged With: diagnosis, PCOS Research, teenagers, Teens, treatment
« [VIDEO] Can I Get Pregnant With PCOS? An Experts Weighs In…
Mothers Of Women With PCOS Have Increased Risk Of Cardiovascular Disease »

redpajama_set_name: RedPajamaCommonCrawl


text:
Teddy Sheringham Back Signed Manchester United Shirt
ICTSMUS1
This shirt was personally signed by former Manchester United striker Teddy Sheringham. Don't miss out on this special piece of memorabilia.
Categories: Premier League, Manchester United, Players, Teddy Sheringham, All, Under £200, Under £400, Under £1000
Known as one of the most intelligent footballers of his generation Teddy Sheringham, enjoyed one of the longest and most successful careers in Premier League history. Born in Highams Park in 1966, he began his career with Millwall helping the Lions to reach the top flight of English football for the first time in 1988. Brian Clough soon spotted Sheringham's talents taking him to Nottingham Forest in 1991 but despite scoring the first ever Premier League goal - the Londoner was soon sold to Tottenham Hotspur the following year. During five successful years at White Hart Lane Sheringham scored 76 goals, and earning himself international recognition with England in the process. Always excelling himself in an England shirt, he struck up a successful partnership with Alan Shearer and was a key man during Euro 96. With 51 caps to his name, Sheringham also scored 11 goals. As he entered the twilight of his career Sheringham was given a new lease of life when Sir Alex Ferguson signed him for Manchester United in 1997. Two years later he helped United win the Treble, scoring United's famous equaliser against Bayern Munich at the Nou Camp. In 2001, after enjoying his best ever season at the age of 35, Sheringham was named PFA Player of the Year and FWA Footballer of the Year. After quitting Old Trafford in the summer of 2001, Sheringham returned to Spurs before enjoying spells with West Ham United, Portsmouth and finally Colchester United - before announcing retirement from the game in 2008. Own a piece of sporting history Teddy Sheringham's famous equaliser against Bayern Munich in the 1999 Champions League final will go down as one of the most legendary moments in the history of the competition - helping his side claim an unprecedented Treble.


You are here: Home / eCommerce / Amazon India / What are the Alternatives to Amazon India Easy Ship Program?
The main pain-point of any online e-commerce business is to deliver the product to customers. The cost-effective, reliable and robust logistics solution can be a bottleneck.
Amazon has done all the heavy lifting to provide better logistics services to its sellers. Hence, sellers have peace of mind when selling on Amazon India. Furthermore, Amazon is able to deliver sellers' products hassle-free pan India.
Amazon's "easy ship" is one of the solutions towards making the life of the seller easy. They pick and deliver the product. You can read about Amazon India "easy ship" service here.
The "easy ship" service doesn't make sense if you are selling a low-price product. The cost of using "easy ship" service for a single product may go beyond the actual selling price of the product.
If you still haven't registered as a seller at Amazon India in the first place then here is a step by step guide.
Amazon India FBA is a different program by Amazon India itself. It is an alternative to Amazon easy ship program.
Under the Amazon India FBA program sellers stock, their products at Amazon's fulfillment centers (warehouse) and upon receiving an order amazon does the picking, packing, shipping, delivery, and product return on behalf of them.
Amazon charges a nominal amount to deliver products across India. If FBA charges are a concern, optimize the product listing to make more sales and cover up the cost.
Read about Amazon India FBA program, its benefits, how it works, how to enroll for FBA, and more importantly who should use the Amazon FBA service.
Amazon's FBA program offers many other benefits. Here I will reiterate the critical logistic benefits a seller can avail.
The second alternative to Amazon India "easy ship" service is MFN. Merchant fulfilled network (MFN) means the seller has to deliver products on his own. He/she can use a private logistics or courier company like Blue Dart, FedEx or DHL.
There is no obligation on sellers to use Amazon's logistics solution. When a seller opts out of Amazon Easy Ship and FBA, then they can use with any third party logistics company which is cost-effective.
Below is the list of top courier companies in India to be considered.
Usually, shipping charges of these company start with minimum Rs. 30/500 grams to maximum Rs. 80/500 grams with applicable taxes. You can check each site for their rates.
The points mentioned above are generic and differ from one courier company to other. Consider every aspect before choosing the right logistics solution.
The postal service in India is one of the most reliable and accurate logistics solutions. The Indian Post covers PAN India delivery. No private courier services can match "India post" regarding serviceable pin codes across India. It is a preferred choice of logistics solution if you plan to consider launching your e-commerce website.
It is one of the better alternatives to Amazon India Easy Ship program. Amazon India has a tie-up with Indian postal services.
Indian post allows you to calculate the shipping cost of your product using a variety of postal services including both domestic and international locations. It takes a minimum of three and a maximum of seven days to deliver a product using postal services.
Before selecting an alternative to Amazon "easy ship" service, a seller should consider the following factors.
My advice will be to try Amazon FBA first. If things don't work out, try Indian postal service then.


What are the best times and days to visit popular UK attractions?
4 Blenheim Palace - www.blenheimpalace.com – is the historic home of the Dukes of Marlborough and birthplace of Sir Winston Churchill. As a major draw for visitors from all over the world, it can become crowded, especially during holiday periods. As with many of the attractions mentioned here, the general rule is that early arrival is the best way of avoiding the rush and enjoying the treasures in relative calm. Wednesdays at 9am are best of all.
5 Anybody hoping for a secluded visit to Windsor Castle - www.rct.uk/visit/windsorcastle - at any time during official opening hours is almost certain to be disappointed, but for some reason the crowds are at a minimum on Wednesdays at 2pm. In addition to architectural delights, the castle offers a fascinating exhibition of historic treasures. Visitors should note that airport-style security screening is in operation.
6 Like all London attractions, Kew Gardens - www.kew.org - are well within day trip range of the Swindon area. Established in 1840, it is the most famous location of its kind on the planet, and generally thought of as the greatest, with more than 30,000 individual types of plant and fungal life represented. The collection is distributed among a variety of large greenhouses, and other features include a popular treetop walkway. The best time to visit is on Wednesdays at 2.30pm.
8 Free and frequently packed to the rafters with fascinated visitors, the Natural History Museum in London - www.nhm.ac.uk - is a must-see for anybody with an interest in the world around us as it was, as it is and as it shall be. Exhibitions span everything from earthquakes to evolution, and from the most enormous dinosaurs to the tiniest microscopic life forms. Many of the exhibits are geared toward telling visitors what everybody can do to conserve the world's living things and natural resources. Wednesdays at 10am are the best time to visit.
9 The best time to visit Tower Bridge - www.towerbridge.org.uk – is at 9am on a Thursday. Sometimes described as the capital's most iconic landmark, although Big Ben is surely also a contender, the bridge offers visitors the chance to discover the stories behind the architecture an the feats of engineering which made its existence possible.
10 The Tower of London - www.hrp.org.uk/tower-of-london - is almost always lacked with visitors, but 9am on Wednesdays seems to be the best bet for those who want to keep queueing to a minimum before exploring this national architectural and historic treasure whose most famous exhibits are the Crown Jewels, and whose keepers are living symbols of the city.


text:
A step closer to the mine: Commerce Resources releases economic assessment
Published on : November 17, 2011 Published by : The Goat
Chris Grove, corporate communications with Commerce Resources, says they are increasingly fielding calls from Chinese business people asking them in broken English if they can supply them with mineral. Above are drill samples used to test the quality and quantity of mineral. Courtesy Commerce Resources.
Commerce Resources manager Jenna Hardy talks to the Goat about the potential for a Tantalum-Niobium mine 90km south of Valemount:
Do the positive results in the preliminary economic assessment mean a mine will happen in Blue River in the next few years?
No. It's a step in the process that gives you more certainty about that answer. When we do these sorts of reports, we're handicapped by a certain framework of engineering requirements. The biggest one is the prices we're required to use for the metals. These maybe don't reflect what's happening in the world where Tantalum and Niobium prices have risen substantially in the last year. Right now, the prices are 40 per cent plus (what was used in the preliminary economic assessment) … which would give us a much better business case.
What does the report say?
The report says let's move forward. As prices stand right now it's worth spending more time and money doing the next steps of engineering and valuation.
What has to happen before it's developed?
There are several steps. We did a lot of drilling in 2010 and 2011. That information isn't integrated into this study. Our next milestone will be to update the base on which we did the analysis. We'll update the body of mineralized material with the improved price. The results from the latest drilling assays won't be available until spring 2012. We can't really pull together a picture of what we've found until we get those assays back. The pre-feasibility and then feasibility study could take one year each if all the information is available – but it's going to be more than that. We've tried to tell people the mine is a few years out.
Will Commerce Resources develop the mine itself or find another company to do that work?
We are looking for a strategic partner. We need to raise more money to take it to pre-feasibility and feasibility. We could do that in the markets if times were good, but right now times aren't so great in the markets. There's other options open to us. We could try to make an alliance with someone already in production or you could sell forward some of your product if there was a company interested in getting a secure supply of both. With the situation in the Congo, with less than ideal labour practices, the money from some of the mining in Africa is being used to funding militia activities. We're Canadians and our mine would be in Blue River and we'd be required to operate to a very high standard. Somebody like a Sanyo or Samsung is quite interested in getting a safe and secure supply. That has an extra value to them. We have been approached by some of the electronic manufacturers to have a talk with them. We're spending a lot of time and effort on building a number of relationships to find the right prospective partner.
How strong is the market for tantalum and niobium?
The markets are quite strong because there aren't a lot of supplies that are safe and clean and ethical. In Canada right now there aren't any other tantalum mines. The existing mine that's the biggest in the world is in Australia. They're just ramping up after having been out of production for a few years. It's not like there's a lot of excess supply that isn't already coming from the Congo or other places.
What about bans on conflict minerals like tantalum coming from the Congo?
The US government did put a program into place (Dodd-Frank Act) to make companies declare where they were sourcing minerals from. There's been a bit of a delay in implementing the requirements. In that time, a couple of companies have gone into the Congo and tried to implement a safe supply chain with third party auditors. But it hasn't quite happened yet. So it's happening but it isn't there yet. There's a fair bit of skepticism about how sure you can be in a country where there's a fair bit of corruption. We think maybe there is some clean material coming out of Africa but it has to be third-party provable.
How long will the potential mine be operational based on the numbers right now?
It's got about a 10-year mine life (once it becomes operational). But at a higher tantalum and niobium price, more of the material becomes worth mining. If our third party engineer does accept the higher price for the next study, what will that really do? We know it will increase (the mine's) life but if it's by ex) 10 or 15 per cent, we don't know.
What would be the spinoffs for the area?
We would try to source labour from the local area. It would mean anyone who isn't an engineer, who had transferable skills from logging or something else. We'd probably do a bus system to collect people. There are enough people in the Valley with the right set of skills. Sourcing local is the right way to go.
Do you know how many jobs this could create?
The Preliminary Economic Assessment gives numbers for various areas (between 260-400 operators and administrators, depending on the year). I have to caution about the exact number at this point, but it's a significant number of jobs. (Author's Note: According to the PEA, the mine is scheduled for three 8-hour shifts/day, 360 days/year, which would require an equivalent of 4.5 mine crews working a rotating schedule for activities scheduled seven days a week and three crews for activities scheduled five days a week.)
Is this mine dangerous? What would the mining operation look like?
The host rock the mineral is in is really quite stable. We'd go in with a flat tunnel at a couple locations in the hillside. You go in on the upper tunnel and mine and drop stuff down to the lower tunnel which brings stuff out of the earth. These kinds of mines are very safe. Employees would go into the mine with heavy equipment and trucks. I visited a similar Niobium mine in Quebec. The rooms in there are the size of football fields. They don't have rockfalls – they're very stable. That's sort of our model. It's in the Sagueney area of Quebec – dairy country. You come out of the mine and there's farmers' fields and cows all around.
Mining enthusiasts check out Blue River deposit
Letter: Electrical dead-ends
Editorial: Problem solving isn't the way
Assessed property values go skyward in Valemount
Greenland's Gamble
TRC signs $6M in new contracts
Remembrance Day 2011 Photo Gallery


See below for information regarding: History, Children's Miracle Network Hospitals, DQ® Cares Product Grant Program, & Local Community Partnerships.
Although much has changed in the world and in the DQ® system through the years, one constant has remained: DQ® restaurants are still, and always have been, the place to find kids' sports teams celebrating a victory, business people on their lunch break and families taking time out to enjoy great food and soft serve treats. And success for the DQ® system is as simple today as it was in 1940. Satisfied customers lead to successful restaurants. Each owner of our independently owned and operated establishments worldwide is committed to nothing less than the "So Good It's RiDQulous®" slogan.