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  • Jun. 11th, 2009 at 12:57 PM
Knowing the difference between an anxiety attack vs. heart attack is information that can be useful. This can be especially significant if you or someone close to you has experienced heart or anxiety attacks in the past. Every year thousands of people end up in emergency rooms in hospitals all over the country because they believe they have had a heart attack. There symptoms vary but usually include chest pains, shortness of breath and nausea. The remainder of this article will be to illustrate the differences between an anxiety attack vs. heart attack.

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  • Apr. 30th, 2009 at 1:54 PM
The Journal of Affective Disorders publishes papers concerned with affective disorders in the widest sense: depression, mania, anxiety and panic. It is interdisciplinary and aims to bring together different approaches for a diverse readership. High quality papers will be accepted dealing with any aspect of affective disorders, including biochemistry, pharmacology, endocrinology, genetics, statistics, epidemiology, psychodynamics, classification, clinical studies and studies of all types of treatment. The Journal of Affective Disorders is the official Journal of the International Society for Affective Disorders.

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  • Apr. 26th, 2009 at 1:57 PM
I am still a kid, fourteen turning fifteen, and after I recovered from my panic disorder I had another problem. While I was having my panic disorder, I also had GAD (Generalized Anxiety Disorder) and the GAD hasnt gone away.
For those who dont know, GAD is an anxiety disorder that makes you pretty much afraid of everything. Its not that bad though, because my parents trust me heaps, since I wont get myself into a remotely not-actually-but-possibly situation.
The problem is that the physical symptoms are killing me. The headaches, the muscle pains, small amounts of trembling, restless sleep (I go to bed 1AM. I cant sleep before then), nausea, a choking sensation that occasionally pops up for no apparent reason, and all these things are starting to get to me.
My mum doesnt even believe that theres a problem, because apparently this is normal. Which I dont really care about, except for the fact that she wont get me medication to help with the symptoms, or psychological treatment.
I cant wait for years to pass before I move out and earn my own money to get help. Ive had this thing for 1 and 1/4 years, and its really starting to get to me. Please help me find a solution that requires no money.
And my dad wants to help, but he simply wont go up against my mum. As for my mum, theres no possibility anyone can bring her to reason. I was shaking, barely breathing in my room, a 13 year old kid, her daughter, and she left me and told me to just relax.
So a year later and shes still making things worse, but I just want the symptoms to go away. The disorder itself isnt too bad, and its not worth the pain of fixing. Its just the pain, the headaches, and the occasional trembling that I need to control.

First off, Im sorry your mom wont help you get help. There are a couple of ways you can go by this.
First, talk with your counselor at school. By speaking with her she maybe able to help and even speak with your mom
Secondly, try to see if you have a local mental health department in your area. Im not sure theyll treat you since your a adolescent, but its worth trying.
Third and last, if you have a dad speak with him. He may be able to convince your mother.
Best of luck and keep going striving and never give up.

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Duloxetine surrounded by favour of pressure urinary incontinence be market by means of Lilly lower than the mass contempt against cross Yentreve.(R) References (1) Koponen, H., et al. Efficacy of Duloxetine for the Treatment of Generalized Anxiety Disorder: Implications for Primary Care Physicians. Prim Care Companion J Clin Psychiatry 2007: 9(2):100-107 (2) Rynn M., et al. Efficacy and Safety of Duloxetine in the Treatment of Generalized Anxiety Disorder: A Flexible-Dose, Progressive-Titration, Placebo-Controlled Trial. Depression and Anxiety 2007: 25(3): 182-189.

RE-VOLUTION (TM) isà anà extensiveà clinicalà trialà programmeà involvingà moreà than 38,000 patients complete.

(4) Nicolini H, et al. Improvement of telepathist and somatic symptom in seasoned patients beside generalized anxiety disarray: Examination from a duloxetine, venlafaxine extended-release, and placebo-controlled search. In Press at Psychological Medicine.

(5) Endicott, J., et al. Duloxetine Treatment for Role Functioning Improvement in Generalized Anxiety Disorder: Three Independent Studies. The Journal of Clinical Psychiatry 2007: 68(4):518-24 (6) Allgulander, C., et al. Pharmacotherapy of Generalized Anxiety Disorder: Results of Duloxetine Treatment from a Pooled Analysis of 3 Clinical Trials. Current Medical Research and Opinion 2007: 23(6): 1245-1252 (7) Davidson JRT, et al. Duloxetine remedy for lapse averting in adults with generalized anxiety disorder: A 26-week randomized placebo- controlled study. Poster presented at the American College of Neuropsychopharmacology annual convention 2007. Boca Raton, Florida (8) Lieb, R, et al. The epidemiology of generalised anxiety disorder in Europe. European Neuropsychopharmacology 2005 Aug;15(4):445-52.

(9) National Institute of Economic and Social Research. Summarized from the National Institute Economic Review,194, 28 October 2005.

(10) Calculated extrapolations of have rates fractious the populations of a dyed-in-the-wool countryside or area, base upon prevalence of generalized anxiety disorder in the US, UK, Canada or Australia. Available at: Accessed on 2.4.08 (11) National Institute of Mental Cialis Professional (NIMH). Anxiety Disorders. Available at: Accessed on 2.5.08 (12) Bymaster, FP et al. The Dual Transporter Inhibitor Duloxetine: A Review of its Preclinical Pharmacology, Pharmacokinetic Profile, and Clinical Results in Depression. Current Pharmaceutical Design. 2005; 11: 1475-1493.

American Society of Nephrology (ASN) 1725 I St.

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Breast cancer is common. Breast cancer is one of the top two causes of cancer deaths together with lung cancer in most developed countries. 99% of breast cancers occur in women with 1% in men. Incidence increases with age. Breast cancer is rare in those under the age of 30, but presents in up to 1 in 14 women over the age of 70. 15-30% of breast cancers are of the in situ type whilst 70-85% are of the invasive type. Ductal carcinoma is the most common making up 80% of all breast cancers. DCIS has increased in incidence since the introduction of mammographic screening. It is now seen in 20-25% of women over 50 screened with mammography. Geographically, breast cancer is found worldwide.
Predisposing Factors
The main risk factors for breast cancer are:
* Increasing age
* A family history of breast cancer
* Proliferative breast disease
* Hormonal factors: women who begin menstruation early, women who have a late menopause, late or few pregnancies, or who are obese. Some evidence is emerging that long term oestrogen therapy (for example, long-term use of the oral contraceptive pill, or hormone replacement therapy (HRT)) may increase risk, as may a diet which is high in fat.
* Others: exposure to radiation; geographical factors.
Progression
Ductal carcinoma in situ (DCIS) is an form of breast cancer. In this case, cells lining the ducts of the breast have become abnormal and are growing more rapidly than usual, but are not able to spread beyond the ducts. Women with DCIS are at higher risk of developing invasive ductal carcinoma. Invasive ductal carcinoma has developed the ability to spread beyond the ducts of the breast. Ductal carcinoma of the breast spreads initially by direct invasion of overlying skin and adjacent fat. Spread into lymphatics and to lymph nodes in the axilla is the most important step, since from there it can spread to lymph nodes in the neck and supraclavicular region and into blood vessels. Once in the blood vessels, spread is possible to distant organs such as the bones, lung or liver.
Probable Outcomes
Early breast cancer has a good (greater than 80%) 5 year survival. Important prognostic factors which can help predict survival include involvement of lymph nodes, the size of the tumour, and how aggressive the tumour cells are. If the cancer has metastasised (spread) to lung, liver or bone at diagnosis, 5-year survival rates are significantly lower. As mentioned above, women with DCIS are at increased risk of developing invasive breast cancer in the future. However, as most cases of DCIS are now treated, it is not known exactly how high this risk is, or how quickly the progression from in situ to invasive cancer is likely to occur.
How is Breast Cancer Diagnosed?
Any breast symptom, such as a lump or nipple discharge, is assessed with the triple test. This includes examination of the breast, imaging of the breast through mammography or ultrasound, and sampling of the breast tissue with fine needle aspiration (FNA), core biopsy or open biopsy. Following a diagnosis of breast cancer, blood tests including Full Blood Count and Liver Function Tests may be used to assess the possibility that the cancer may have spread to the liver or bone marrow. Other imaging tests, including chest x-rays, bone scan, abdominal CT or liver ultrasound may also be used if symptoms suggest that the cancer has spread.
How is Breast Cancer treated?
Surgical treatment of breast cancer aims to achieve total disease control through removal of the primary breast tumour, along with any local extension.
Virtual Medical Centre Video
Surgical treatment can be divided into two major streams:
* Breast conserving surgery with complete local excision (CLE) and axillary dissection, or
* Total mastecomy with axillary dissection.
These two procedures are considered similar in terms of 5- and 10-year survival rates. The decision as to which procedure is more appropriate is therefore based on clinical features, such as the size and location of the tumour, and patient preference.
* Larger, widespread cancers or cancer near the nipple may usually require mastectomy (removal of the whole breast). This can be followed by reconstructive surgery.
* Smaller tumours, or tumours located in the outer quadrant in larger breasts may be removed by lumpectomy or partial mastectomy. Radiotherapy usually follows the procedure.
* Axillary dissection refers to the removal of lymph nodes in the axilla (armpit). These lymph nodes are commonly the first site of metastasis (spread) of a breast tumour, and axillary dissection is routinely done to ensure all cancer cells are removed. Rarely, with some very small and well-defined cancers, axillary dissection may not be necessary.
Adjuvant therapy refers to chemotherapy, radiotherapy or hormone therapy which is done with the aim of destroying any cancer cells not removed by surgery. Chemotherapy protocols include:
1. CMF:
* Cyclophosphamide 100mg/m2 PO days 1-14
* Methotrexate 40mg/m2 IV days 1+8
* 5-Fluorouracil 600mg/m2 IV days 1+8 (repeat every 4 weeks for 6 cycles)
ALL I.V. CMF:
* Cyclophosphamide 750mg/m2 IV day 1 (or 150mg/day)
* Methotrexate 60mg/m2 IV day 1
* 5-Fluorouracil 750mg/m2 IV day 1 (repeat every 3 weeks)
2. AC:
* Doxorubicin 60 mg/m2
* Cyclophosphamide 600 mg/m2
3. For High Risk Patients:
* TAC
* FEC 75
* FEC 100
* Docetaxel
* Paclitaxel
Modifications:
1. Post menopausal:
* Tamoxifen 20 mg PO daily
2. Locally Advanced FAC:
* 5-Fluorouracil 600 mg/m2 IV day 1 + 8
* Doxorubicin 60mg/m2 IV day 1 (vesicant)
* Cyclophosphamide 600mg/m2 IV day 1 (repeat every 4 weeks)
4. Stage IV: First line chemotherapy:
* CMFP (oral or IV) (add prednisolone 40mg/m2 PO days 1-14 to CMF)
Reassess every 3 courses Treat until maximum response
* Trastuzumab (Herceptin) and Taxanes
* Herceptin 4 mg/kg IV over 90 minutes then 2mg/kg/week over 30 minutes until progression
o WITH Docetaxel 75 mg/m2 IV over 1 hour every 3 weeks for 6 cycles OR
o Paclitaxel 90 mg/m2 IV over 60 minutes weekly
5. Herceptin single agent:
* Herceptin 4 mg/kg IV over 90 minutes then 2mg/kg/week over 30 minutes until progression
6. Second line chemotherapy:
* Doxorubicin 60mg/m2 IV day 1 (vesicant) (repeat every 3 weeks)
7. Third line chemotherapy:
* Docetaxel 75 mg/m2/day over 1 hour as starting dose can escalate to 100mg.m2/day IV over 1 hour. In heavily pretreated patients or those with poor liver function can start at 60 mg/m2. (repeat every 3 weeks)
* Docetaxel (weekly) 36 mg/m2/week over 1 hour for 6 weeks then 2 weeks off
* Paclitaxel 175mg/m2/day over 3 hours IV (repeat every 3 weeks)
* Paclitaxel (weekly) 100 mg/m2 IV over 1 hour
8. Fourth line chemotherapy:
* Capecitabine 2500 mg/m2 divided into 2 doses daily po 2 weeks every 3 weeks
* Mitomycin C 10 mg/m2 IV Day 1 (vesicant)
* Vinblastine 5 mg/m2 IV Day 1 and 15 (vesicant) (repeat every 4 weeks)
9. Hormonal Therapy:
* Tamoxifen 20 mg. po daily or Anastrozole 1mg po daily
* Then Medroxyprogesterone acetate 500 mg po daily Or Exemestane 25 mg/day
10. Premenopausal Advanced Breast Cancer:
* Zoladex 3.6 mg SC every month
* Tamoxifen 20 mg/day
11. Bone metastases: When the tumour has spread to bone, zoledronic acid can be used to help prevent fractures.
* Zoledronic acid 4mg iv over 15mins every 28 days
12. Breast Cancer (Bone Predominant):
* Pamidronate 90mg IV over 2 hours.
If the tumour has spread to bone, treatment with zoledronic acid can help prevent tumour growth in bone and subsequent bone fractures. Symptoms that may require attention include bone pain from bone metastases, visceral (organ) pain from liver or lung metastases and neurogenic (nerve) pain if nerve tissue is compressed. Improvement in symptoms is an important measurement. Hormone therapies: Women with hormone receptor-positive tumours (eg. oestrogen-receptor positive tumours) should be offered adjuvant hormone therapies such as tamoxifen or ovarian ablation therapy. Click the links below to see for information on other breast cancers:
* Breast cancer - Adenocarcinoma of the breast
* Breast pain
* Male breast cancer
* Breast cancer - Lobular carcinoma of the breast
* Inflammatory breast cancer
Breast Cancer References
1. Australian Institute of Health and Welfare National Breast Cancer Centre 2006. Breast cancer in Australia: an overview, 2006. Cancer series no. 34. cat. no. CAN 29. Canberra: AIHW.
2. Braunwald, Fauci, Kasper, Hauser, Longo, Jameson. Harrisons Principles of Internal Medicine. 16th Edition. McGraw-Hill. 2001
3. Cotran RS, Kumar V, Collins T. Robbins Pathological Basis of Disease Sixth Ed. WB Saunders Company 1999.
4. Dr Guy Van Hazel, Oncologist, Mount Hospital, Perth
5. Kumar P, Clark M. Clinical Medicine. Fourth Edition. WB Saunders, 1998.
6. National Breast Cancer Centre. 2003. The clinical management of ductal carcinoma in situ, lobular carcinoma in situ and atypical hyperplasia of the breast, First Edition. National Breast Cancer Centre, Camperdown,NSW. [online] Available from: http://www.nbcc.org.au/bestpractice/resources/CMW_dcisbook.pdf
7. National Breast Cancer Centre. 2001. Clinical practice guidelines for the management of early breast cancer:Second edition. National Breast Cancer Centre, Camperdown,NSW. [online] Available from: http://www.nhmrc.gov.au/publications/synopses/cp74syn.htm
8. Schwartz, GF, Solin, LJ, Olivotto, IA, et al. Consensus Conference on the Treatment of In Situ Ductal Carcinoma of the Breast, April 22-25, 1999. Cancer 2000; 88:946.
9. Talley NJ, OConnor Simon. Clinical Examination. Fourth Edition. MacLennan Petty, 2001
Related Documents:
* For a PPT presentation titled NCCTG N9831: Whether Trastuzumab adds to the benefit of adjuvant paclitaxel in resected HER-2 positive breast cancer please click here.
* For a PPT presentation titled The Role of Bevacizumab in the Treatment of Metastatic Breast Cancer please click here.
* For a PPT presentation titled A Randomized Phase III Trial of Paclitaxel versus Paclitaxel plus Bevacizumab as First-Line Therapy for Locally Recurrent or Metastatic Breast Cancer please click here.
* For a PPT presentation titled Doxorubicin and Cyclophosphamide Followed by Paclitaxel with or without Trastuzumab as Adjuvant Therapy for Patients with Her-2 Positive Operable Breast Cancer please click here.
* For a PPT presentation titled Targeting HER-2 in the Adjuvant Setting please click here.
* To view these PPT slides with a free PowerPoint viewer 2003, please click here.
Regimens Used in the Treatment of This Disease:
* 5-Fluorouracil
* AC (Doxorubicin + Cyclophosphamide)
* ACE (Doxorubicin + Cyclophosphamide + Etoposide)
* Capecitabine + Docetaxel
* Capecitabine + Paclitaxel
* CMF (Cyclophosphamide + Methotrexate + 5-Fluorouracil)
* Docetaxel
* Doxorubicin
* Doxorubicin (Liposomal)
* EC (Epirubicin + Cyclophosphamide)
* Epirubicin
* FEC 100 (5-Fluorouracil + Epirubicin + Cyclophosphamide)
* FEC 75 (5-Fluorouracil + Epirubicin + Cyclophosphamide)
* Gemcitabine + Paclitaxel
* Mitomycin
* Mitozantrone
* Paclitaxel + Trastuzumab
* TAC (Docetaxel + doxorubicin + cyclophosphamide)
Treatments Used in This Disease:
* Breast Conserving Surgery
* Mastectomy
Drugs/Products Used in the Treatment of This Disease:
* Methotrexate Injection BP
(Methotrexate)
* Arimidex
(Anastrozole)
* Aromasin
(Exemestane)
* Avastin
(Bevacizumab)
* Femara
(Letrozole)
* Gemzar
(Gemcitabine hydrochloride)
* Haldol Decanoate
(Haloperidol decanoate)
* Herceptin
(Trastuzumab)
* Megace
(Megestrol acetate)
* Onkotrone
(Mitozantrone hydrochloride)
* Pamisol
(Disodium pamidronate)
* Provera
(Medroxyprogesterone acetate)
* Tamoxifen-BC
(Tamoxifen citrate)
* Taxotere
(Docetaxel)
* Tykerb
(Lapatinib Ditosylate)
* Xeloda
(Capecitabine)
* Zoladex 3.6mg and 10.

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  • Feb. 25th, 2009 at 6:58 PM

Acute syndrome (positive symptoms)

Appearance and behaviour: preoccupied, withdrawn, inactive, restless, noisy, inconsistent
Mood: mood change, blunting, incongruity
Disorders of thought: vagueness, formal thought disorder, disorders of the stream of thought
Hallucinations: auditory, visual, tactile, gustatory, olfactory
Delusions: primary, secondary (esp. persecutory)
Orientation: normal
Attention: impaired
Memory: normal
Insight: impaired

Chronic syndrome (negative symptoms)

Lack of drive and activity
Social withdrawal
Abnormalities of behaviour
Abnormalities of movement: stupor and excitement, abnormal movement, abnormal tonus
Speech: reduced in amount, evidence of thought disorder
Mood disorder: blunting, incongruity, depression
Hallucinations: esp. auditory
Delusions: systematized, encapsulated
Orientation: age disorientation
Attention: normal
Memory: normal
Insight: variable

Schneider's 'first rank' symptoms of schizophrenia

Hearing thoughts spoken aloud
Third person hallucinations
Hallucinations in the form of commentary
Somatic hallucinations
Thought withdrawal or insertion
Thought broadcasting
Delusional perception
Feelings or actions experienced as made or influenced by external agents



Classification of psychotic disorders that do not meet the diagnostic criteria for schizophrenia:

1. Duration too short. Less than 1 month is called acute psychotic disorders. Between 1 month to 6 months is called schizophreniform.
2. Prominent affective symptoms. These cases are called schizoaffective.
3. Delusions without other symptoms of schizophrenia. These are called delusional disorders.

Differential diagnosis

1.Organic syndromes: drug-induced, temporal lobe epilepsy, delirium, dementia 2.Psychotic mood disorders: distinction between mood disorder and schizophrenia need to made.
3.Personality disorder: need prolonged observations for first rank and other features of schizophrenia
4.Schizoaffective disorder



Factors predicting poor outcome in schizophrenia

1.Features of illness: insidious onset, long first episode, previous psychiatric history, negative symptoms, younger age of at onset
2.Features of the patient: Male, seingle, separated, widowed, or divorced, poor psychosexual adjustment, poor employment record, social isolation, poor compliance



Assessment and management of acutely disturbed patients

1.Make a provisional diagnosis: acute provisional diagnosis, alcohol/drug intoxication/withdrawal, personality disorder, schizophrenia, mania
2.Appropriate examination and blood and urine specimen (if patient permits)
3.Antipsychotic drug treatment if needed
4.Decide the need for admission to hospital



Hospital management of an acute episode of schizophrenia

-Antipsychotic medication
-Appropriate activites
-Counselling for patient and family
-Good response and good prognosis: continue medication for 6 months, gradual return to work and social activities; regular review and counselling
-Incomplete response and or poor prognosis: long-term medication (consider depot), counselling and support for family (reduce expressed emotion), assess needs for sheltered work or housing



Antipsychotic drugs with the normal daily dose range

-Conventional: Haloperidol (2-30 mg), Chlorpromazine (100-600mg), Trifiuoperazine (5-30mg), Sulpiride (400-800mg)
-Atypical: Risperidone (4-16mg), Olanzepine (5-20 mg), Sertindole (12-20mg), Clozapine (100-900mg).

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  • Jan. 3rd, 2009 at 4:31 PM

GTx, Inc. (Nasdaq: GTXI) today announced the submission of a New Drug Application with the U.S. Food and Drug Administration (FDA) for toremifene 80 mg, an oral selective estrogen receptor modulator (SERM), for the prevention of bone fractures in men with prostate cancer on androgen deprivation therapy (ADT).




ADT has helped improve survival for men with advanced prostate cancer. Unfortunately, ADT may cause unintended serious estrogen deficiency side effects, such as a high risk of fractures, which can shorten survival, said Dr. Mitchell Steiner, CEO of GTx. If approved, toremifene 80 mg could become the first cancer care agent for the prevention of fractures in men receiving ADT.




Ipsen Group has licensed European toremifene rights from GTx and is planning to submit a marketing application in 2009 in its licensed territories for the use of toremifene 80 mg for this indication.




The submission is supported by results from a two year, double blind, placebo controlled, randomized Phase III clinical trial of 1,382 men with advanced prostate cancer on ADT. The clinical trial, the first ever fracture prevention study in men on ADT, was conducted under a special protocol assessment with FDA. Toremifene 80 mg met the primary endpoint of the clinical trial, a reduction in new morphometric vertebral fractures compared to placebo, as well as other key secondary endpoints related to estrogen deficiency side effects of ADT. Because there are no FDA approved treatments for this indication, GTx has requested priority review for toremifene 80 mg.




Additionally, in the Phase III clinical trial, toremifene 80 mg was generally well tolerated. Among the most common adverse events that occurred in over 2 percent of study subjects in the toremifene and placebo groups were joint pain, dizziness, back pain, and extremity pain.




Toremifene has been marketed for the treatment of advanced breast cancer in more than 60 countries including the U.S. The Phase III ADT clinical trial safety data are consistent with the existing 17 year pharmacovigilance database which includes approximately 480,000 patient years use of toremifene citrate, said Ronald A. Morton Jr., MD, Chief Medical Officer of GTx.



About Prostate Cancer




Prostate cancer is the second most common type of cancer diagnosed in men in the U.S. An estimated 186,000 new cases of prostate cancer were diagnosed in the U.S. in 2008. Two out of every three prostate cancer diagnoses are in men over the age of 65.



About ADT




ADT is the primary treatment for advanced prostate cancer in the U.S. Approximately 700,000 men with prostate cancer are being treated with ADT and an estimated 100,000 are anticipated to initiate ADT each year.




Of patients on ADT, up to 77 percent develop significant bone loss, making them susceptible to fracture. Recent studies indicate that the annual risk of fracture in men on ADT is 5% to 8%, or three times higher than the risk of fracture for postmenopausal women. Fractures are serious and can reduce survival in men on ADT by more than three years.



About estrogen deficiency side effects of ADT




Although estrogen is commonly thought of as a female sex hormone, it plays a critical role in mens health. Estradiol is the primary hormone responsible for bone turnover and bone quality. It is also important for cognition and the regulation of certain central nervous system functions and metabolism. Testosterone, through the process of aromatization, is converted to estrogen, and healthy elderly men actually have higher levels of estrogen than do postmenopausal women. However, ADT reduces testosterone by up to 95% to castrate levels, thereby also depleting estrogen levels. Depletion of estrogen can result in serious side effects of ADT, including a high risk of bone fractures, adverse lipid changes and increased risk of cardiovascular disease, as well as common symptomatic side effects such as growth of breast tissue often accompanied by tenderness and pain, and hot flashes.



About GTx




GTx, Inc., headquartered in Memphis, Tenn., is a biopharmaceutical company dedicated to the discovery, development, and commercialization of small molecules that selectively target hormone pathways to treat cancer, osteoporosis and bone loss, muscle wasting and other serious medical conditions. GTx is developing toremifene citrate, a selective estrogen receptor modulator, or SERM, in two separate clinical programs in men: first, a completed pivotal Phase III clinical trial evaluating toremifene 80 mg for the treatment of serious side effects of androgen deprivation therapy for advanced prostate cancer, and second, an ongoing pivotal Phase III clinical trial evaluating toremifene 20 mg for the prevention of prostate cancer in high risk men with high grade prostatic intraepithelial neoplasia, or PIN. In 2006, GTx and Ipsen Group entered into a development and collaboration agreement for toremifene in all indications except breast cancer for Europe and the Commonwealth of Independent States (CIS). GTx has made application for marketing approval and, if approved, plans to commercialize toremifene 80 mg in the United States. In December 2007, GTx and Merck Co., Inc. formed a collaboration to discover and develop selective androgen receptor modulators (SARMs), a new class of drugs with the potential to treat sarcopenia, which is the loss of skeletal muscle mass resulting in reduced physical strength and ability to perform activities of daily living, cancer cachexia (muscle wasting), as well as other musculoskeletal conditions. Merck and GTx are conducting several Phase I and Phase II clinical trials evaluating multiple SARM product candidates, including Ostarine™ (also designated as MK-2866) for sarcopenia. Merck and GTx are evaluating additional muscle loss indications for potential SARM clinical development. GTx also is developing its preclinical compound GTx-758, an oral luteinizing hormone inhibitor, for advanced prostate cancer. www.gtxinc.com



Forward-Looking Information is Subject to Risk and Uncertainty




This press release contains forward-looking statements based upon GTxs current expectations. Forward-looking statements involve risks and uncertainties. GTxs actual results and the timing of events could differ materially from those anticipated in such forward-looking statements as a result of these risks and uncertainties, which include, without limitation, the risks that (i) GTx and its collaboration partners will not be able to commercialize their product candidates if clinical trials do not demonstrate safety and efficacy in humans; (ii) GTx may not able to obtain required regulatory approvals to commercialize product candidates; (iii) clinical trials being conducted by GTx and its collaboration partners may not be completed on schedule, or at all, or may otherwise be suspended or terminated; and (iv) GTx could utilize its available cash resources sooner than it currently expects and may be unable to raise capital when needed, which would force GTx to delay, reduce or eliminate its product development programs or commercialization efforts. You should not place undue reliance on these forward-looking statements, which apply only as of the date of this press release. GTxs quarterly report on Form 10-Q filed November 6, 2008 contain under the heading, Risk Factors, a more comprehensive description of these and other risks to which GTx is subject. GTx expressly disclaims any obligation or undertaking to release publicly any updates or revisions to any forward-looking statements contained herein to reflect any change in its expectations with regard thereto or any change in events, conditions or circumstances on which any such statements are based.
[Via http://www.medicalnewstoday.

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This is a piece of prose written by an anonymous author about her struggle with Anorexia. I said I would come back to the psychological suffering of ED's because it can't be described in a short paragraph. I think first-hand accounts are the only way one can really begin to appreciate the living hell that is an Eating Disorder. Some people might find it upsetting.

Our Anorexic was a sweet girl. Always did as she was told, always got good grades, always did the best in her class. At 15 depression hit. The vitality of youth replaced by the slow, sluggish misery of depression. There's a weight on her shoulders, holding her below real life, it's hidden from her by a black veil, and she can only watch and pass through passively, helpless and unable to feel anything but sadness. She no longer laughs when she should, or smiles when she should. All the things she used to like have no meaning any more. Friends don't understand it, they leave her to herself. Increasingly isolated, she turns her pain inwards to self-anger and self-hatred. "It's all your fault. You've made them hate you." On the worst days she can't even get up. Parents shout at her, teachers roll their eyes when she hands work in late. Her whole body is a lead weight, and she tries her best but it takes her forever to do work now.

What's to be done? She's ugly. Nobody likes her, as she sees it. She hates every part of herself and she cannot change it. Well, she could stand to lose a few pounds, maybe that will help a bit. The couple of pounds drop off, and suddenly something clicks. She feels accomplishment and positivity for the first time in a year, at the lower number on the scales. And it becomes her drug. Soon diet pills and diet coke replace actual food, except for the dinner she eats with her family. "I'd rather eat in my room" she says. Mum doesn't mind. She throws away half the pasta and smiles as she does her stomach crunches. Today has been a good day.


No. Stop it. Don't think about it. Stop. Get over it. Your friends don't want you any more. Probably because you are so pathetic. Listen to the happy laughs, the playful chatter, look at the photos of other people, smiling, having fun. Don't flatter yourself, there's no point longing for it. You were not meant to have friends and fun, you were meant to be alone. Still, you want people to like you, better go out.

Do something useful. You have loads of work to do and you're just sitting here. You're an awful student. You should be studying. Throw yourself into your work. Go to your lectures, then go to the library, and stay there until after dinner so you can skip it. Do you know how many calories there could be in that food? It could be over a thousand and you wouldn't even know. Imagine how quickly you will get even fatter if you eat dinner! No, it's out of the question. Everything feels fuzzy.

You're just eating too much, that's all. Cut things out of your diet. You don't need them. Sweets are banned and carbs should be as little as possible. Those are in the "no" pile. Cut out breakfast. Just have an apple. Or just some coffee. Salad for lunch. And sugar free red bull for energy. You have to get through all that work after all. Prove you can resist. Restrict, restrain, get smaller. Shrink. Feel your stomach growl, your mouth water. Now refuse. No big deal, it's just a couple of pounds. You can stop any time. You're racing ahead. The hunger has disappeared and you feel light as air. Don't stop now.

No. Don't think about it. Don't think about being sad. That's pathetic, remember? Push it aside. You have to be the best. Top marks, top of the class, push yourself. Time to go out. Look at all those thin, pretty girls. Your competition. Raise your game. Don't go out. Think of all the calories in the alcohol, about the girls who are prettier than you. Stay in and do sit-ups. It's never fun any more anyway, you stand there and you watch them dance and you can't even smile. You can't think of anything, too hungry, too tired, nothing to say. You can stand and pretend to listen to people talk but you know you never hear what they say. Why bother? They will only tell you, like everyone else, that you are thin and that you need to eat. All lies. Pinch your belly. Look at the rolls of fat, god, it's disgusting. Look at your tree-trunk thighs and your barely-visible hipbones. Do those ribs stick out a little more than yesterday? No. Still fat. Keep going, you can do it, you can lose another pound.


She doesn't seem to have a shape any more. The mirror only shows fat blobs and imperfections, the whole doesn't seem to exist. Soon there is a psychiatrist and there are antidepressants. Soon she finds herself saying "I hate myself. I hate the way I look. I hate how fat I am". Alarm bells go off. The psychiatrist asks all about food and she tries to put it into words but she can't. Before she knows it she leaves him a note. "Food is all I think about. I think I need help. Please don't tell my mum." Measurements are taken, height 168cm, weight 94lbs, BMI 15.2. Blood tests are prescribed. An eating disorders specialist at a hospital that looks more like a hotel. "Maybe you should come in to the unit, just for 10 days, to kick-start your treatment." She flatly refuses. No, nobody is going to make me. I won't. So she goes in every day.

The nurse weighs her on the electric scales and she can't help but cry. "I'm not thin enough yet". The nurse sighs. "If I ever heard the voice of Anorexia talking, that was it." A kind-faced dietician, lots more nurses, and the other girls. Shouting over dinner tables, tears over ice cream or chips and other scary things. She tries to hide the food but it's impossible so she pretends to go to therapy and throws up in the bathroom instead. "I can't gain weight. I have to be thin, they just don't understand." But they don't give up, so she has a new plan. Make them think you're better until they let you go. So she eats a bit more, puts on a bit of weight, starts vomiting more as a result but at least her weight is going up. She fabricates diet diaries for the nice dietician. Yes I'm doing much better, thanks. Yes I really did have breakfast this morning. Porridge. It was delicious. She and another girl exercise in secret, it feels so exciting to break the rules.

But her hunger gets worse and she eats more and more and she throws up more and more, but at least there is a boyfriend now. Got to pretend to be OK for the boyfriend. Got to pretend to want to get well. Got to smile and meet his friends. Got to go drinking. Got to take in calories. Dancing is exercise though. "Look how ugly you are, look how little you deserve him. See how you make him cry? How he smiles and laughs with his friends and you make him upset because you're hurting yourself? You're so pathetic. Starve, starve, you must starve away your sins and your guilt. Throw up, you deserve the punishment. You're not good enough for him."

"I'm fine honestly. Look how many biscuits I'm eating. Look, I'll even eat a doughnut. I'm much better." It all comes back up behind closed doors and she sighs with exhaustion. Soon binging and purging is all she knows. Wake up, go to the shop, buy food, binge, purge, sleep, wake up, binge, purge, each day is an endless cycle of binges, purges and naps in between because it's all so tiring.

Soon there's no hiding it any more. Stuck in a hospital bed now, medication being increased again. Carted upstairs every morning in her pale pink satin nightdress and fluffy dressing gown and weighed. "If you lose any more weight we're going to make you stay on the eating disorders unit." She heads for lunch, she knows she has to eat. She stops. She sees the faces of the people eating staring back at her. "No. They're all watching. They'll all think I'm fat." She runs outside and sits on a bench. She tries time and time again to get up and go into the dining room but she can't. Paralysed by fear.

If Anorexia is a place in the mind, a mental space, in the doorway to it are the gates of hell, and the inscription from Dante would be written on them - "All hope abandon, ye who enter in.

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  • Nov. 19th, 2008 at 11:27 AM
Under Health and Fitness
Depression must first be understood before its treated.Depression is no joke; it is a very serious disease that affects millions and millions of Americans each and every year. The alarming dilemma is that over a third of those Americans will not seek any type of treatment. The old stereotypes of mental illness still bother too many people.
Their character is so important that they dont want a label like to tarnish it. To be diagnosed, those that suffer have to seek assistance. Thats the terrible merry go round of depression.
Many factors lead to depression. Depression stems from chemical, emotional, environmental and even physical causes . The genetic link cannot be ignored as well. Many diseases are passed on through a family. It is not just family history but family life in general. Daily life includes tremendous stress.
Some undergo a daily fight just to make ends meet. Even success and fitting into society can be the problem for others. Abuse such as sexual, physical or even emotional can overload people with anxiety. Its a long list.
Depression Treatment
Depression is often hard to find in its early form. Even while a loved one suffers from this disease the signs may be hard to notice. Everyone gets down in the dumps once in a while. This is natural.
Depression is more than just temporary sadness. Early detection is no longer an option when your whole life begins changing. Those suffering from depression tend to feel all alone and disgusted with life. Signs of hope in their lives are gone. Sleep habits and enjoyment from life no longer exist. At this point treatment has become literally a matter of life and death.
The afflicted needs a renewed sense of hope and meaning for an effective depression treatment. This stage of treatment comes through talking. This treatment can take months or years to bring about positive results but it is effective.
The medical professional also has the option of prescribing anti-depressants like Prozac, Paxil, Zoloft, Lexapro, Celex, or Luvox . Although they have some serious side effects, these medicines work. Studies also show that some herbs can be effective as depression treatment. There are also many depression support groups geared towards working with depressed individuals. If you or someone you love are feeling the affects of depression please consult a medical professional immediately.

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  • Nov. 3rd, 2008 at 9:36 PM
gamma-aminobutyric acid (GABA), the most common inhibitory transmitter in the brain, is reduced by nearly 30 percent in individuals who have been suffering from primary insomnia for more than six months. These findings suggest that primary insomnia is a manifestation of a neurobiological state of hyperarousal, which is present during both waking and sleep at physiological and cognitive levels.
"GABA is reduced in the brain of individuals with insomnia, suggesting overactivity is present not only at the level of excessive thoughts and emotions, but can also be detected at the level of the nervous system," said principal investigator Dr John Winkelman of Brigham and Women's Hospital, which is a teaching affiliate of Harvard Medical School in Boston, Mass.
GABA decreases overall activity in many brain areas, helping the brain to "shut down." Having a "racing mind" and an inability to shut down at night is a common complaint of people with primary insomnia.
Chronic insomnia, or symptoms that last for at least a month, affects about 10 percent of all adults in industrialized countries and is the most common sleep disorder. Most often insomnia is a "comorbid" disorder, present with another medical illness, mental disorder or sleep disorder, or associated with certain medications or substances. Approximately 25 percent of people suffering from insomnia are considered to have primary insomnia, which is defined as a difficulty falling asleep or maintaining sleep in the absence of coexisting conditions.
According to Winkelman, the recognition that primary insomnia is associated with a specific neurochemical deficiency helps validate the often misunderstood complaint of insomnia.
"Recognition that insomnia has manifestations in the brain may increase the legitimacy of those who have insomnia and report substantial daytime consequences," he said. "Insomnia is not just a phenomenon observed at night, but has daytime consequences for energy, concentration and mood."
This preliminary study included 16 participants (eight men and eight women) who were screened to be free of medical and sleep disorders, as well as anxiety and mood disorders, and who were not taking prescription medication. Ages ranged from 25 to 55 years. Researchers recruited people who had difficulty initiating or maintaining sleep with resulting daytime distress or dysfunction for a period of at least six months. The average duration of participants' symptoms was 10 years. Objective data were collected by actigraphy and overnight polysomnography. Proton magnetic resonance spectroscopy (1H-MRS) was used to non-invasively determine GABA levels. For statistical comparison the study included a well-matched control group consisting of seven women and nine men.
Significant correlations were found between GABA levels and both subjective and objective sleep measures after adjusting for age, body mass index (BMI) and gender. In subjects with primary insomnia, sleep continuity, as measured by minutes of wake after sleep onset (WASO) on sleep study, was strongly associated with GABA levels.
According to the study, reductions in brain GABA levels also have been observed with 1H-MRS in major depressive disorder (MDD) and anxiety disorders. Primary insomnia shares many features with anxiety and depressive disorders, including sleep disturbance, elevation in anxiety, and impairments in concentration and energy. In addition, primary insomnia is an important risk factor for incident mood and anxiety disorders. The study raises the possibility that GABA deficiencies seen in people with mood and anxiety disorders may be based on disturbances in sleep.
The study also reports that many of the hypnotic medications that are most effective in treating insomnia are benzodiazepine receptor antagonists (BzRAs), which increase activity at the GABA neurons. According to a new clinical guideline for the evaluation and management of chronic insomnia in adults, which was published by the American Academy of Sleep Medicine in the Journal of Clinical Sleep Medicine, hypnotic treatment should be supplemented with behavioral and cognitive therapies whenever possible.

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