Monday, August 29, 2016

ME/CFS has an objectively identifiable chemical signature in both men and women 

ME/CFS has an objectively identifiable chemical signature in both men and women 

  By: Robert K. Naviaux a ,b ,c ,d ,1 , * Jane C. Naviaux a ,e , * Kefeng Li a ,b , * A. Taylor Bright a ,b , * William A. Alaynick a ,b , * Lin Wang a ,b , * Asha Baxter f , * Neil Nathan f ,2 , * Wayne Anderson f , and * Eric Gordon

  "Patients with CFS showed abnormalities in 20 metabolic pathways. Eighty percent of the diagnostic metabolites were decreased, consistent with a hypometabolic syndrome."

"We studied a total of 84 subjects using these methods. Forty-five subjects (n = 22 men and 23 women) met diagnostic criteria for ME/CFS by Institute of Medicine, Canadian, and Fukuda criteria. Thirty-nine subjects (n = 18 men and 21 women) were age- and sex-matched normal controls. Males with CFS were 53 (±2.8) y old (mean ± SEM; range, 21–67 y). Females were 52 (±2.5) y old (range, 20–67 y). The Karnofsky performance scores were 62 (±3.2) for males and 54 (±3.3) for females."

Saturday, August 27, 2016

A doctor diagnosed with MUS (a diagnosis used by incompetent doctors) who was actually dying from cancer ...



A doctor diagnosed with MUS (Medically Unexplained Symptoms) who was actually dying from cancer ... Highlighting the fact that MUS is a diagnosis of incompetent doctors as evidence that something is MUS or psychosomatic does not exist ...

Dr Lisa Steen: the wilderness of the medically unexplained


This patient perspective essay was written by Lisa Steen. She has since died. We have permission to publish the piece from her husband, Raymond Brown.
I am a GP, formerly a trainee psychiatrist and now 43 years old. In July 2014, I was diagnosed as having kidney cancer with multiple bone metastases. The cancer was extremely rare, associated with a succinate dehydrogenase B (SDHB) mutation. This genetic condition was later also found to be the cause of my carotid body paraganglionoma which had appeared when I was 18 and was finally excised when I was 27.
I had felt unwell in terms of dizziness and visual symptoms since August 2012, and presented to my GP in September 2012, nearly two years before my diagnosis was made in July 2014. So I spent two years wandering in the wilderness of the medically unexplained.
In fact I had been feeling tired for several months even prior to this presentation in August 2012, and had felt like I was lacking concentration. I had been put on a series of antidepressants, each of which caused “side effects” which may have been symptoms of illness all along. Fluoxetine caused headaches, sertraline caused diarrhoea, and dosulepin caused visual disturbance—at least that’s what I thought at the time.
I had considerable difficulty describing my symptoms: primarily visual disturbance; a sense of being behind a wobbly TV camera; also of diplopia—another image slightly below causing blurring, and negative palinopsia, prompting the GP to refer me to the eye clinic urgently, where all examinations were shown to be normal.

There were many other minor symptoms too: fatigue, palpitations, cramps in my hands and feet, subtle cognitive impairments, difficulty finding words, memory problems, difficulty coping at work. I had time off sick even though I previously had an intact sick leave record. I had headaches which were worse on standing, also an altered sensation in a glove and stocking distribution, mild tremor, and gradual weight loss without dieting.
My GP insisted on sending me to a psychiatrist mainly because I had been on so many antidepressants, and we didn’t know which to choose next. But also because I had initially interpreted these symptoms as SSRI withdrawal or dosulepin side effects.
The psychiatrist’s immediate instinct was that the illness seemed “organic” not psychiatric, and neither was it SSRI withdrawal or dosulepin side effects.
A neurologist’s advice was sought and her first thoughts were of hypothyroidism or low calcium. The neurologist also requested an ultrasound of the neck as I had concerns that it was something to do with my previous carotid body tumour, and I wondered if it had returned.
The ultrasound and bloods proved normal. The neurologist did not find anything abnormal on examination apart from a Horner’s syndrome (longstanding and related to the previous carotid body surgery). An MRI of my head was subsequently normal.
The psychiatrist made a diagnosis of depression and health anxiety, but without much psychiatric evidence, I felt. This diagnosis not only perplexed me, and I wandered away from my own further diagnostic enquiry, but it impacted on consultations following this diagnosis.
I did not entirely believe my psychiatrist however, mainly because the visual symptoms were so florid. I considered myself very psychologically aware and was not convinced about the anxiety/depression diagnosis. Though, unfortunately I had proved a highly suggestible subject during the cognitive behavioural assessment, due to having been trained in CBT myself.

The symptoms did indeed get worse with stressful situations, but this was partly because those situations occurred whilst standing—such as presenting patients on the morning ward round. This had been a factor in stopping work, because there were problems with my word finding and memory. On reaching the patient’s bedside I found myself almost hallucinating in terms of palinopsia, purple haze and blotches, all of which was very distracting whilst trying to contribute to the ward round. It was impossible really to continue working without working life becoming a total humiliation. This did indeed lead to low self worth and anxiety. The low level acute confusional state, as I now see it, meant that I was functioning at a suboptimal level at work, for no clear reason, this then led naturally to anxiety and concern. It was then difficult for me to untangle my own symptoms from psychiatric ones.
Since I was being paid to be off sick, I felt it my duty to follow orders. So therefore to pursue psychological cure—though at the same time I was reading about the physical causes of my symptoms.
I spent the next few months trying to address my apparent mental health problems with a psychologist, and I mainly considered myself to have a psychosomatic illness maybe some sort of conversion disorder. Unusually, I worked backwards, as it were, to exclude a psychiatric illness so as to realise I had a medical illness.
But I gradually became convinced that exertion and not anxiety caused the visual symptoms to worsen, I also thought that the nature of the symptoms “felt” organic because of the pronounced and ongoing visual symptoms.
I then started to look for threads, clues, and a way forward to get treatment. This was thwarted by my earlier diagnosis of health anxiety and having medically unexplained symptoms. One could not be dogmatic in further requests for investigations for fear of looking even more “anxious” or suffering from “health anxiety,” aka a hypochondriac. I wanted to ask the GP for a chest x-ray and abdominal ultrasound, and thought about paraneoplastic syndromes but I always tended to think it was not cancer, in view of the normal inflammatory markers and the length of time it had gone on. But I suspect also it was a pitfall of being forced into the “physician heal thyself” situation.
I saw a vascular surgeon, privately, wondering if the carotid was narrowed by scar tissue from the previous surgery, thinking maybe inadequate blood supply to the brain/retina could be occurring—which is the cause of physiological palinopsia. The carotid was not narrowed, but the vascular surgeon who performed the duplex ultrasound suggested that I might have a genetic disorder and have a phaeochromocytoma, which was something that impacted on his field. I persuaded my GP to order a 24 hour metanephrine test which frustratingly came back negative. At my behest the heart-sunk GP also did blood tests for SLE, and infectious serology screen.
In Spring 2013, I presented to Poole A&E in Dorset with palpitations, whilst on holiday (the palpitations unhelpfully disappeared on arrival in A&E). The heart rhythm was normal, but the A&E doctor was convinced she heard a third heart sound, and suggested a follow up.
So the next relevant thing seemed to be referral to a cardiologist, in June 2013. I suggested to the cardiologist the possibility of a genetic syndrome related to carotid body tumours. The cardiologist was a kindly man, but after exclusion of any cardiac conditions with an echo and 24 hour tape he began to consider the initial health anxiety diagnosis—or at least it looked like that to me. Once again a kind of consulting room glazing occurred and I was left once more looking like a goldfish. My mouth moving but no sound conveyed to the doctor’s ears. This was by now a familiar feeling to me.
The cardiologist did at least acquiesce to my suggestion that I may have POTS syndrome: postural orthostatic hypotension and suggested referral to a specialist. So I could have some excuse for being off sick.
By now I had gone back to work. There had been a rotation, and I was assigned to a consultant psychiatrist, who made it her mission to rehabilitate me back to work.
By August 2013, I hoped that I had found a thread, something tangible that the specialist could investigate secondary causes of. The POTS specialist did at least do a full examination, though he was not worried about my concerns of a possible pulsatile mass on the left flank, and thought my aorta was just rather left of centre. A tilt table test was organised which was “borderline positive.” In February 2014 further urinary and blood metanephrines were normal. All bloods were repeated and normal. The ESR and CRP remained very low.
At this point I gave up my quest: I was back at work, part time with a benevolent boss, and coping, though tired. I had adapted to my visual disturbance and could now function with it, though I was still embarrassed by my word finding difficulties. I tried to be more organised, and write everything down.
I still knew there was something wrong, but it seemed so fruitless going to see specialists. It was so humiliating, feeling like a goldfish with no voice. Watching doctors’ faces glaze over at the multitude of symptoms. Trying to fit it all in with work and looking after my family.
I decided it would have to wait for clinical events to become more diagnosable. I had tried as hard as I felt reasonably possible. It is also taboo to discuss one’s own health in any depth at work, and I was so exasperated by it all that I felt I would cry if anyone were too sympathetic—which doctors might then interpret as a psychiatric symptom.
In February 2014 I had a follow up with an occupational health doctor. This time the occupational health doctor became concerned, and noticed that I had lost weight and suggested seeing a bowel specialist in relation to a change in bowel habit and to see a neurologist about my numb hands and feet.
I went home and gave myself a full examination. This time I was sure. I found a large mass in my left flank.
I saw my GP, but they couldn’t feel it. I saw my POTS specialist a couple of weeks later and he thought it might be an enlarged spleen. He ordered a routine ultrasound.
One evening in June 2014 the junior radiology technician, working on a waiting list initiative, found a solid/cystic mass 10cm in diameter arising from the left kidney.
I was initially jubilant thinking this would turn out to be a phaeochromocytoma—maybe dopamine secreting. And now I could have an “anxietyectomy.” An urgent CT of the abdomen and pelvis was recommended.
The result was not cause for celebration. The CT showed that the mass was arising from the left kidney and was reported as looking like a renal cell carcinoma. There were also multiple sclerotic lesions in the spine, ribs, and pelvis reported as metastases.
By then I had abandoned my psychiatric training. I had felt unable to study because of “brain fog,” however I had managed to get over the many hurdles to get back my GP status, which involved three exams and six months of retraining.
I had just landed a job as GP Lead for Inclusion service, treating patients with drug and alcohol problems. But the news came just a few days after my interview and offer of the post. My progression through medical services was much more efficient after that and I saw an oncologist and the urologist urgently.
***
I do not know how long I’ll live. It probably won’t be for many weeks. But right now I am glad to be alive, I am grateful for the expensive drug which is holding back the cancer. I am angry at being left in the medically unexplained wilderness and I did not like the way my colleagues looked at me, when they believed me to have health anxiety.
If anyone of the doctors I saw had gone another mile they would’ve stumbled upon it. I almost told them the answer; I repeated over and over my belief of a genetic syndrome linked to the carotid body, something related to it, but they were unable to hear the answer from a patient. They were reluctant to lay their hands on and examine a fellow medic. I was disappointed in finding a very poor appetite for a diagnostic hunt, which may in part be the result of protocolisation and superspecialism. I disliked being unable to order my own tests, and I regret not pulling more strings. I was too embarrassed about my “psychiatric” condition, too confused by not having the whole answer ready.
My story is a cautionary tale to all of us health professionals when we get ill. Illness is somehow not the done thing. It upsets our “them/us” belief system, which helps us cope with the horror of what we see. “We do not get ill, they are ill.” We are a lot more military than we realise.
We are trained to keep going, as if there was a war on. Our workloads are superhuman, and we seriously do not appreciate it if those around us “slack off,” particularly those taking sick leave with depression or stress. “Heaven knows the rest of us are depressed and stressed, all right for some putting their feet up.”
I felt deeply ashamed of being too unwell to work.
The communication was different, it didn’t go the same way that it would have if I was a non-medic. Doctors do not like being told what to do, and if you try obliquely they don’t notice. They don’t worry much as they assume you’ll come back. But it is hard getting to appointments when one is working, and just how many times can you come back if it gets worse? I was beginning to think that our etiquette for being seriously ill is to drop dead on the job—it is fairly common practice, anecdotally anyway.
Mine is a cautionary tale to those treating health professionals, and those of us who are unwell—doctors do get ill, they don’t always know what is wrong with themselves: give them a class A service because it is actually harder getting treated as a doctor than a lay person.

Friday, August 26, 2016

Please Sign this PETITION: ME is not MUPS or SOLK (PACE trial proved ME/CFS is physical)



PACE trial proves ME/CFS is physical; it's not MUPS (Medically Unexplained Physical Symptoms) or SOLK  

A quick history:

56000 signatures were collected by very ill patients several years ago (Dutch Patient/Citizen Initiative Recognize ME) to get Parliament to listen. They asked Dutch Health council to write a new advisory report about state of the knowledge about ME. However serious conflicts of interest of the members of the Dutch Health Council (ie Dutch PACE colleagues) are ignored.

There are members on there who think along the lines of the Wessely school of vested interest psychiatry, ie the biopsychosocial model, a hypothesis disproven by 1000s of research articles and by Wessely's PACE trial itself !!

ME is a chronic complex multi-system disease, anyone who claims otherwise has no place in health care. Health care and treatment can no longer be based on people clinging to old paradigms, based on non-evidence based treatments. Lets Raise our voice together as this problem affects ME patients around the world.

Please SIGN this petition @  petities.nl

  Thank you for considering and / or signing !

Please remember the outcome of the INDEPENDENT review of the PACE trial, which amongst things showed that the real conclusions of this trial, based on the published results, contrary to the published conclusions, are that: 1. CBT and GET are ineffective to treat people with ME (also known as CFS or ME/CFS) also called a NULL effect; 2. A discovery by the trial which proves yet again that ME/CFS is a physical disease; 3. The disproval of the biopsychosocial model favored by the British (PACE trial) psychiatrists and their Dutch Nijmegen friends.

The full article "The PACE Trial Invalidates the Use of Cognitive Behavioral and Graded Exercise Therapy in Myalgic Encephalomyelitis/ Chronic Fatigue Syndrome: A Review" with it's other conclusions can be read here, free of charge.

 

Tuesday, August 23, 2016

In Argentina, Ampligen has just been commercially approved for severe ME/CFS



PHILADELPHIA, Aug. 23, 2016 (GLOBE NEWSWIRE)

  "“In Argentina, rintatolimod (Ampligen) has just been commercially approved for the severe disabling form of ME/CFS.  The number of patients with ME/CFS is estimated to be over three million worldwide, however, only a portion of these have the severe and disabling form of the disease which we are targeting with this drug,” stated Tom Equels."

  "Several post-approval activities are required to be completed before product launch, including manufacturing site inspections and reimbursement evaluation by the Health Services Authority (SSS), the central health authority in Argentina."

 

Thursday, August 18, 2016

OMG: Prof Chalder admits that they made up the death threats themself to ridicule patients



Prof Chalder admits that they made up the death threats to ridicule patients in trying to make sure that the PACEtrial data doesn't get released. Therefore it doesn't take a genius to conclude that the data is much worse than what they have presented and published because if it would have backed up their claims they would have long shared it ...

P 36 @ informationtribunal.gov.uk

Wednesday, August 17, 2016

Prof Chalder: Cochrane review not independent at all as all principal investigators of the PACE trial sat on it ...


P31:
"Professor Chalder states that disclosure to the Cochrane review does not count as disclosure to independent scientists as all three of the PACE principal investigators sat on the review panel."

 Which means that the principal investigators of the PACE trial were reviewing their own trial ...

So it is becoming clearer and clearer that the PACE trial is a bridge too far for the psychiatrists who have been lying about a debilitating neuro immune disease for decades.

More @ informationtribunal.gov.uk

Tuesday, August 9, 2016

That moment you realize there is an overlap in entry and recovery criteria in the 8 million dollars costing thing of beauty




The real thing of beauty is the review of the PACE trial, which amongst things showed that the real outcome of this trial, contrary to the published conclusions, is that:

1. CBT and GET are ineffective to treat people with ME (also known as CFS or ME/CFS) also called a NULL effect
2. A discovery by the trial which proves yet again that ME/CFS is a physical disease
3. The disproval of the biopsychosocial model favored by the British (PACE trial) psychiatrists

The full article "The PACE Trial Invalidates the Use of Cognitive Behavioral and Graded Exercise Therapy in Myalgic Encephalomyelitis/ Chronic Fatigue Syndrome: A Review" is available free of charge.

Sunday, July 31, 2016

Spinal fluid abnormalities in patients with ME/CFS

Spinal fluid abnormalities in patients with chronic fatigue syndrome

  @ PubMed:

  Natelson BH 1, Weaver SA , Tseng CL , Ottenweller JE . Spinal fluid abnormalities in patients with chronic fatigue syndrome. Clin Diagn Lab Immunol.  2005 Jan;12(1):52-5.

  Abstract

  Arguments exist as to the cause of chronic fatigue syndrome (CFS). Some think that it is an example of symptom amplification indicative of functional or psychogenic illness, while our group thinks that some CFS patients may have brain dysfunction. To further pursue our encephalopathy hypothesis, we did spinal taps on 31 women and 13 men fulfilling the 1994 case definition for CFS and on 8 women and 5 men serving as healthy controls.

  Our outcome measures were white blood cell count, protein concentration in spinal fluid, and cytokines detectable in spinal fluid. We found that significantly more CFS patients had elevations in either protein levels or number of cells than healthy controls (30 versus 0%), and 13 CFS patients had protein levels and cell numbers that were higher than laboratory norms; patients with abnormal fluid had a lower rate of having comorbid depression than those with normal fluid.

  In addition, of the 11 cytokines detectable in spinal fluid, (i) levels of granulocyte-macrophage colony-stimulating factor were lower in patients than controls, (ii) levels of interleukin-8 (IL-8) were higher in patients with sudden, influenza-like onset than in patients with gradual onset or in controls, and (iii) IL-10 levels were higher in the patients with abnormal spinal fluids than in those with normal fluid or controls.

  The results support two hypotheses: that some CFS patients have a neurological abnormality that may contribute to the clinical picture of the illness and that immune dysregulation within the central nervous system may be involved in this process.

Tuesday, July 19, 2016

Neuromuscular Strain causes symptom flare-ups in ME/CFS

RESEARCH ARTICLE

Neuromuscular Strain Increases Symptom Intensity in Chronic Fatigue Syndrome

Peter C. Rowe , Kevin R. Fontaine , Megan Lauver , Samantha E. Jasion , Colleen L. Marden , Malini Moni , Carol B. Thompson ,Richard L. Violand

 * Abstract* Chronic fatigue syndrome (CFS) is a complex, multisystem disorder that can be disabling. CFS symptoms can be provoked by increased physical or cognitive activity, and by orthostatic stress. In preliminary work, we noted that CFS symptoms also could be provoked by application of longitudinal neural and soft tissue strain to the limbs and spine of affected individuals. In this study we measured the responses to a straight leg raise neuromuscular strain maneuver in individuals with CFS and healthy controls. We randomly assigned 60 individuals with CFS and 20 healthy controls to either a 15 minute period of passive supine straight leg raise (true neuromuscular strain) or a sham straight leg raise. The primary outcome measure was the symptom intensity difference between the scores during and 24 hours after the study maneuver compared to baseline. Fatigue, body pain, lightheadedness, concentration difficulties, and headache scores were measured individually on a 0–10 scale, and summed to create a composite symptom score. Compared to individuals with CFS in the sham strain group, those with CFS in the true strain group reported significantly increased body pain (P = 0.04) and concentration difficulties (P = 0.02) as well as increased composite symptom scores (all P = 0.03) during the maneuver. After 24 hours, the symptom intensity differences were significantly greater for the CFS true strain group for the individual symptom of lightheadedness (P = 0.001) and for the composite symptom score (P = 0.005). During and 24 hours after the exposure to the true strain maneuver, those with CFS had significantly higher individual and composite symptom intensity changes compared to the healthy controls.

We conclude that a longitudinal strain applied to the nerves and soft tissues of the lower limb is capable of increasing symptom intensity in individuals with CFS for up to 24 hours.

These findings support our preliminary observations that increased mechanical sensitivity may be a contributor to the provocation of symptoms in this disorder.

Citation: Rowe PC, Fontaine KR, Lauver M, Jasion SE, Marden CL, Moni M, et al. (2016) Neuromuscular Strain Increases Symptom Intensity in Chronic Fatigue Syndrome. PLoS ONE 11(7): e0159386. doi:10.1371/journal.pone.0159386

Editor: Ute Vollmer-Conna, University of New South Wales, AUSTRALIA

Received: March 17, 2016; Accepted: July 3, 2016; Published: July 18, 2016

More @ Plosone

 

Saturday, June 25, 2016

Professor Hanson: further evidence against the ridiculous concept that ME/CFS is psychological


Professor Maureen Hanson: "our detection of a biological abnormality provides further evidence against the ridiculous concept that the disease is psychological in origin"

By Krishna Ramanujan, June 24, 2016, Cornell University:

  ksr32@cornell.edu

  Indicator of chronic fatigue syndrome found in gut bacteria

  In a study published June 23 in the journal Microbiome, the team describes how they correctly diagnosed myalgic encephalomyeletis/chronic fatigue syndrome (ME/CFS) in 83 percent of patients through stool samples and blood work, offering a noninvasive diagnosis and a step toward understanding the cause of the disease.

  “Our work demonstrates that the gut bacterial microbiome in ME/CFS patients isn’t normal, perhaps leading to gastrointestinal and inflammatory symptoms in victims of the disease,” said Maureen Hanson, the Liberty Hyde Bailey Professor in the Department of Molecular Biology and Genetics and the paper’s senior author.

  “Furthermore, our detection of a biological abnormality provides further evidence against the ridiculous concept that the disease is psychological in origin,”

  More @ cornell.edu

Friday, June 3, 2016

Ester Crawley given a million pounds to replicate FITNET's NULL effect


Ester Crawley given a million pounds to replicate FITNET's NULL effect

http://www.nets.nihr.ac.uk/projects/hta/14192109

Ester Crawley's Study will be based on the following Dutch study also called FITNET which ignored their own NULL effect just like the PACE trial did.




Because it's obviously more important to make sure that people who are severely ill do not get proper treatment and to make sure that their kingdom which is based on fake tan doesn't come tumbling down. The Sad State of Affair of greed and denial medicine ...

  Nijhof SL, Priesterbach LP, Uiterwaal CS, Bleijenberg G, Kimpen JL, van de Putte EM, Internet-based therapy for adolescents with chronic fatigue syndrome: long-term follow-up. Pediatrics. 2013 Jun;131(6):e1788-95. doi: 10.1542/peds.2012-2007. Epub 2013 May 13.

  ( Bleijenberg G aka the Dutch Peter D White or Simon Wessely and van de Putte EM aka the Dutch Ester Crawley)

  "Cognitive behavioral therapy (CBT) is known to be an effective treatment of adolescents with chronic fatigue syndrome (CFS), but its availability is limited." No it's not known to be effective but they want us to believe it is effective which is a totally different thing ... The reality is, as a recent review of the PACE trial showed, that CBT and GET are totally useless !!! But the BIG LIE must obviously continue ...

  "Fatigue in Teenagers on the Internet (FITNET), an Internet-based CBT program for adolescents with CFS, has been developed as an alternative to face-to-face CBT. Recently, its short-term effectiveness has been proven in a randomized clinical trial. Here we aimed to assess the long-term outcome of CFS in adolescents after FITNET treatment and after usual care."

  "Conclusion: The short-term effectiveness of Internet-based CBT on adolescent CFS is maintained at LTFU. At LTFU, usual care led to similar recovery rates, although these rates were achieved at a slower pace."

  "At LTFU, usual care led to similar recovery rates" aka as a NULL effect ...

  http://www.ncbi.nlm.nih.gov/pubmed/23669515

 

Tuesday, May 17, 2016

Unexpressed feelings towards lying psychiatrists? Then here is the reason why ...

Unexpressed feelings towards lying psychiatrists? Then here is the reason why ... If you have some unexpressed feelings towards lying psychiatrists like Simon Peasley, Pizza White, Michael Blushing and Trudies Itchyshoulder then here you can read why you have them ... Please make sure you have got a bucket ready otherwise you will need some urgent CeeBeeTea If you are really desperate then here is the link to the study http://psycnet.apa.org/psycinfo/2016-23898-001/

Wednesday, April 20, 2016

Great letter by Professor Hooper asking for retraction of the PACE trial 

Great letter by Professor Hooper asking for retraction of the PACE trial via meactionuk.org.uk, April 15, 2016:

  Dear Dr Horton,

  I write to call again for the retraction of the PACE study paper by White PD et al. (Comparison of adaptive pacing therapy, cognitive behaviour therapy, graded exercise therapy, and specialist medical care for chronic fatigue syndrome (PACE): a randomised trial. "Lancet "2011;377:823-836).

  MORE @ meactionuk.org.uk

 

LinkWithin

Related Posts with Thumbnails