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A healthy female, working in radiation field with a healthy,live issue reported to have tsh levels of 6.1
no other symptoms except occassional weight gain, hair fall and insomnia. No family history.
what researches indicate she should be put on thyroxin replacement therapy? The patient is also trying to conceive.
any researches to back up this?
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Healthy female with no other comorbidities should be started on thyroxine replacement when TSH levels are 10 or above.
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Are you a Parent in the UK?
Please take part in my survey about how parenting changes across the generations! Should take 10 mins and will help me complete my masters degree.
I only need 18 more respondents for a medium effect size power analysis and would appreciate any help. If you are also completing research, I would be happy to take part if I am eligible. Please email me or comment below.
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Self-Efficacy, Learned Helplessness and Parental Psychological Control: A Transgenerational Perspective
Dear all,
I am currently recruiting participants to take part in my thesis project. I am investigating the relationship between self-efficacy, learned helplessness and parental psychological control from a transgenerational perspective.
The study has received ethical approval from Northumbria University (45055).
We are looking for participants who meet the following criteria:
• A resident in the United Kingdom (UK)
• Grew up in a two-parent household
• Currently have school-aged children
• Parent those children with a stable long-term partner who lives in the same household
The study will involve answering a set of demographic questions, questions about the parenting style received from your own parents, the parenting style you use with your own children, and questions measuring your levels of both self-efficacy and learned helplessness.
If you have any further questions regarding the study, please contact me at beth.sheerin@northumbria.ac.uk.
To find out more information about the study and to take part, please go to: https://nupsych.qualtrics.com/jfe/form/SV_867ksXh3vg8Mnzg
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Sorry I don't have children. Will share it with those who do. Good luck with your research.
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Family history is an important risk factor for breast cancer incidence, but the parameters conventionally used to categorize it are based solely on numbers and/or ages of breast cancer cases in the family and take no account of the size and age-structure of the woman’s family. What are your views?
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العلم الحديث يقول الجينات الوراثية لها دور فعال
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I'm trying to study the relationship between a family history of depression and brain's intrinsic functional connectivity in individuals at high risk for depression (by virtue of having a first-degree relative with a lifetime history of depression). Unfortunately, owing to the inherent difficulty associated with using the gold standard way of examining families' diagnostic status (i.e., using SCID), I've been forced to obtain the required information by means of self-reports -using the participants as informants. I'm well aware that this imposes a serious limitation on my ability to interpret my findings. However, I need to know if there has ever been an effort to see how well the ideas of the general population regarding psychiatric diagnoses (particularly, a major depressive disorder diagnosis) are in line with diagnoses confirmed by a psychiatrist. In other words, have there been studies comparing the results of general population self-reports about mental disorders (either their own or that of their family members) with actual psychiatric diagnoses?
I would really appreciate your response.
Sincerely,
Hassan
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Hi,
Thank you Michael Uebel and Bhogaraju Anand for your answers. I found them really helpful.
All the best,
Hassan
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50 years old man who visited Internal medicine clinic doing well without any complain or any other disease. He said to the doctor that he is screening his blood sugar at home (finger prick device)He had family history of DM2 so he was anxious about his situation. All the readings during the day are normal except that at early morning which was around 107 mg/dl in average for the last 30 days. Knowing that he sleep at 11pm and glucocheck done at 9 am.
*Should I consider this reading Abnormal and treat him as a pre-diabetic person ?
*Note: This Q is only to improve my knowledge about DM
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Yes. He is a prediabetic individual. Why.....?
According to the Michigan Diabetes Center's recordings which were considerably accepted as references by the American Diabetes Association, it classified population using Fasting Plasma Glucose (FPG) into:
euglycemic 72-102 mg/dL
prediabetic 103-125 mg/dL
diabetic ≥ 126 mg/dL
therefore, the second group must be warry via periodic check, good glycemic food control, and body exercises
from my experience point of view, many prediabetic subjects consult my clinic, continuing to have their normal life on my instructions
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in addition, I'd like to study the interventions of several variable factors with the chromosomal aberrations in breast cancer such as age, breastfeeding, family history, and smoking effects.
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Try straight multiple regression of chromosome aberration score vs quantified or categoric independent variables and test significance of regression coefficients.
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Acquired aplastic anemia is of known itiology like drugs, toxins and radiation therapy but is there any relationship found like positive family history may also result in AAA ?
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Hello Ashique,
As Geovanny and Raksha mentioned we should be very cautious in family history and aplastic anemia; However we should not forget that Idiopathic acquired aplastic anemia (AA) is typically a diagnosis of exclusion after inherited disorders, acquired MDS, infections, metabolic diseases, or nutritional deficiencies have been ruled out.
This paper might help:
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I'm in the process of deciding on my final topic for my dissertation for the MLitt in local and family history..... just wondered if you're doing the same!
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Sorry am not studying in that field
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Researching American composer's early career and life - looking for early family history. Know his grandparents settled in Saunders County, Nebraska, June, 1869. Looking for name of ship on which they sailed (immigrated) to America.
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There is no records of an emmigrant ship leaving Oslo (Christiania) on June 2, 1870. See for instance Link: http://norwayheritage.com/p_year.asp?ye=1870
I suggest to take direct contact with me on mail: morten.edvardsen@nmbu.no
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Is it possible a patient with profound family history, positive HLA B27, significant symptoms of pain in the sacroiliac region, hips, feet and hands to have Ankylosing Spondylitis? After 3 MRI scans there are small changes yet nothing significant enough to prescribe TNF treatment. Is an MRI the only firm way of diagnosis of AS, that in turn leads to TNF treatment in the uk? 
I would like like to add here... there is positive diagnosis of osteoarthritis in hands and feet. The 3 MRI scans span over 4 years. However each scan has been during a 'good period' of pain and movement restriction. Drug treatments made available thus far has been NSAIDs with no alleviation from traditional anti inflammatory drugs other than Arcoxia. This worked well to control pain and inflammation but the side effects meant that the course of treatment could not continue.
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According to me it is not the best way as per my opinion on basis of my research.
Diagnosis of Ankylosing Spondylitis
A rheumatologist is commonly the type of physician who will diagnose ankylosing spondylitis (AS), since they are doctors who are specially trained in diagnosing and treating disorders that affect the joints, muscles, tendons, ligaments, connective tissue, and bones. A thorough physical exam, including X-rays, individual medical history, and a family history of AS, as well as blood work (including a test for HLA-B27) are factors in making a diagnosis.
Note that AS can present differently at onset in some people. This tends to be the case in women more than men. Quoting Dr. Elaine Adams, "Women often present in a little more atypical fashion so it's even harder to make the diagnosis in women." For example, we have heard anecdotally from some women with AS that their symptoms started in the neck rather than in the lower back.
Varying levels of fatigue may also result from the inflammation caused by AS. The body must expend energy to deal with the inflammation, thus causing fatigue. Also, mild to moderate anemia, which may also result from the inflammation, can contribute to an overall feeling of tiredness.
The overall points taken into account when making an AS diagnosis are:
Onset is usually under 45 years of age.
Pain persists for more than three months (i.e., it is chronic).
Back pain and stiffness worsen with immobility, especially at night and early morning.
Back pain and stiffness tend to ease with physical activity and exercise.
A physical examination entails looking for sites of inflammation. Thus, your doctor will likely check for pain and tenderness along the back, pelvic bones, sacroiliac joints, chest, and heels. During the exam, your doctor may also check for limitations in spinal mobility in all directions and for any restriction of chest expansion.
Other symptoms and indicators are also taken into account, including a history of iritis or uveitis (inflammation of the eye), a history of gastrointestinal infections (for example, the presence of Crohn's Disease or ulcerative colitis), and a family history of AS, as well as fatigue due to the presence of inflammation.
 
 
Blood Work and the HLA-B27 Test
First, HLA-B27 is a perfectly normal gene found in 8 percent of the Caucasian population. Generally speaking, no more than 2 percent of people born with this gene will eventually develop spondylitis.
Second, it is important to note that the HLA-B27 test is not a diagnostic test for ankylosing spondylitis. Also, the association between AS and HLA-B27 varies among different ethnic and racial groups. It can be a very strong indicator in that more than 95 percent of people in the Caucasian population who have AS test positive for HLA-B27. However, close to 80 percent of AS patients from Mediterranean countries and only 50 percent of African American patients with AS are HLA-B27 positive.
Since there is no single blood test for AS, laboratory work may, or may not, be of help. Elevated erythrocyte sedimentation rate (ESR), also known as SED rate, and C-reactive protein (CRP) are common indicators of inflammation. Elevated levels of these markers, however, are not present in all AS patients and, when they are, it can be from other causes such as anemia, infection, or cancer. For example, it is estimated that less than 70 percent of people with AS have a raised ESR level.
Finally, there is no association between AS and rheumatoid factor (associated with rheumatoid arthritis) and antinuclear antibodies (associated with lupus.)
 
 
The Hallmark of Ankylosing Spondylitis
The hallmark of AS is involvement of the sacroiliac (SI) joints. Some physicians still rely on X-ray to show erosion typical of sacroiliitis, which is inflammation of the sacroiliac joints. Using conventional X-rays to detect this involvement can be problematic because it can take seven to 10 years of disease progression for the changes in the SI joints to be serious enough to show up on conventional X-rays.
Another option is to use MRI to check for SI involvement, but MRI can be cost prohibitive in some cases.  
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Asymtpmatic patient on cervical MRI and later added Head MRI due to transient left arm pain. No family history and no background diseases known. No weight loss. Any Idea?
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Hi Felix, interesting case. Can you give a follow-up? Do you have a diagnosis now? Kind regards, Michael
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Since FOP can usually be acquired through new mutations of the ACVR1 gene (meaning people with no family history of the disease can get it), what do you think are the factors that cause the gene mutation in cases like this? 
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If we are talking generally external factors such as radiation doses, chemical insults to dna, maternal age and increasing paternal age and triplet expansions have all been found to have an effect in various disorders
Some mechanisms for base mutations ( thank you Wiki) are
Spontaneous mutations on the molecular level can be caused by:[25]
Tautomerism — A base is changed by the repositioning of a hydrogen atom, altering the hydrogen bonding pattern of that base, resulting in incorrect base pairing during replication.
Depurination — Loss of a purine base (A or G) to form an apurinic site (AP site).
Deamination — Hydrolysis changes a normal base to an atypical base containing a keto group in place of the original amine group. Examples include C → U and A → HX (hypoxanthine), which can be corrected by DNA repair mechanisms; and 5MeC (5-methylcytosine) → T, which is less likely to be detected as a mutation because thymine is a normal DNA base.
Slipped strand mispairing — Denaturation of the new strand from the template during replication, followed by renaturation in a different spot ("slipping"). This can lead to insertions or deletions
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A 33 years primigravida with a family history of two first degree relatives with epithelial ovarian cancer, BRCA status not known, wants me to perform BSO during elective Caesarean section
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BRCA1/2 gene status should be known to the best of my knowledge. Around 10 - 15 %  chance of inheritence exists with ovarian cancers in this case.  Screening with annual mammography from age 30 and breast MRI from age 25 for BRCA1 and BRCA2 mutation carriers are suggested by some authors.
Also bilateral salpingo-oophorectomy can be offered to women with a BRCA1 or BRCA2 mutation once they have complete the desired number of children, around 35 - 40 years of age. Youngest age when the ovarian cancer appeared in the family should be questioned and considered.  However, at 33 year old, inducing menopause may adversely effect heart and bone status of the patient seriously and should be decided by a council of the doctors if the patient insists on having the bilateral salpingoophorectomy.  Early menopause may also affect the cognitive function, so if this women is a professional using cognitive functions/decision making processes, this should be taken into account. 
A single physician should not decide on bilateral salpingoophorectomy of a 33 year old patient just by the desire of the patient to the best of my understanding. 
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Two sisters 15 Yrs & 16 Yrs with medical and family history. They are exposed to  severe acute distress because  of gunshot near their home, after which they started to be Diabetic on insulin therapy. One of sisters died because she developed DKA with shortage of therapy.
What is the pathogenisis? 
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The mind-body connection is theoretically extended to suggest concrete impact of one on the other. (E.g., stress and heart disease). The specific diabetes-trauma relationship in children is less studied. The above article is a case study. I myself have noticed that children who are diabetic have had extreme trauma pre-diagnosis--but of course, one cannot say cause-effect. 
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Hans Jansz, the father of Adriaen Koerbagh, was born in Bergen op Zoom around 1594. Only the name of his mother, Anna van Coevorden, is known, but no more information about his family background can be found. It is possible that his ancestors originally lived at Korbach (Germany). All additional information is welcome.
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Thank you for the answer. I've already searched the baptismal records of Bergen op Zoom, which seem to be very incomplete in the relevant period. Furthermore, the name Hans Janz is so 'generic' (as both 'Hans' and 'Jan' are abbreviations of 'Johannes') that it is difficult to identify perosn with naems such as 'Hans Jansz', 'Jan Jansz', 'Johannes Hansz', etc.
The connection with Bergen op Zoom is found in the registration of the banns for the intended marriage of Hans Jansz and Trijntje Adriaens, dated 2 june 1617 (Stadsarchief Amsterdam, DTB source 421, p. 224). The original text is in full:
"Compareerden als vooren Hans Jansz van Bergen op Zoom plateelbacker oud 23 Jaren, geass[isteer]t met Anne van Couuerden, syn moeder wonen [added above the previous word: ‘apuero’] opde Lindegraft, ende Trijntjen Adriaens oud 17 Jaren, wiens vaders consent de coster belast is te halen wonen opde Lindegraft’, and in the margin was added: ‘de vad[e]r heeft sijn consent v[er]claert"
The 'apuero' or 'a puero' indicates that Hans Jansz has lived in Amsterdam from childhood, implying that he moved there, probably from Bergen op Zoom, as an infant or child.
Although more documents about Hans Jansz can be found in the Amsterdam archives, this is the only source that tells us something about his ancestors. 
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I am looking for a questionnaire to measure family psychiatric history among young adult informants. I have come across a number of procedures for acquiring this information via structured interviews, but nothing questionnaire-based. Any recommendations? I am primarily interested in family history of psychosis and mood disorders.
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What do you mean by 'measuring" family  psychiatric history? Do you mean having it on record? Would something simple like:
Family Psychiatric History:
Any thought or mood disturbances, mood altering substance abuse, neurological  deficits, learning problems noted or  diagnosed?  Include grandparents, parents, siblings, cousins.
Please list relationship, followed by diagnosis/problem.
....   ....    ....
(You could create a check-off list of problems but this may be less likely to be answered)
You may also wish to inquire about exposure to mental illness + substance abuse in the environment of care, since a patient may have been raised outside of their family, or in multiple environments.
Good luck finding what you require.
PS You may alsowish to consier possible drug/medication exposure dure pregnancy.
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What are the defining characteristics or factors which make up a family's well-being?
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Great question Nicolette. One of the messy issues in studying families is what is family process and what is family outcome.  The use of systems perspectives suggests both are interrelated. I think both prior posts suggest good ideas. My view (following up on earlier work from Joan Patterson on family resilience) is that families are functioning competently when they show evidence of individual competence, family competence in fulfilling basic family functions, and good family-ecosystem fit.
Take a look at these publications for more insights:
Henry, C. S., Morris, A. S., & Harrist, A. W. (2015). Family resilience: Moving into the third wave. Family Relations, 64(1):22-43. doi: 10.1111/fare.12106
Patterson, J. M. (2002). Integrating family resilience and family stress theory. Journal of Marriage and the Family, 64, 349-360. doi:10.1111/j.1741-3737.2002.00349.x
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I am conducting archival research on the issues that parents have communicated about with their children in letters they mailed to their children. I am interested in things that gratified parents and things that upset them. I want to examine how these issues changed or remained the same over time. I am particularly interested in locating good archives for such letters in the NY, NJ, PA area. I have found good material at the New York Historical Society and at historical societies in Princeton and Morristown NJ. I would appreciate any information about letter archives that have already been digitized and are available online (if there are such resources). Thanks.
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There are lots of letters from Alfred Russel Wallace (co-discoverer of natural selection) to his children William and Violet in Wallace Letters Online - see http://www.nhm.ac.uk/research-curation/scientific-resources/collections/library-collections/wallace-letters-online/database.html?from=h
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Part of the Ricardo family was expelled from Spain in 1492. It is not a Jewish name, but they were Jews. I need suggestions about the origin of the surname.
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Yes, ii has a Gothic origin, or I would say a Germanic origin.
But I understand the issue which has been propossed here is related with a much later problem. It's related with the fact of a jewish Ricardo family (Ricardo as family name) who were expelled form Castilla in 1492. The original question was if somebody could give any idea about the origin of that name... as a Jewish name (because it is clearly not a Jewish family name). The problem is, then, how a Jewish family got that family name. it is not jewish, and it is not even a family name, but a personal name.
I think it is realted with a situation of "crypto-judaism": maybe they were forced to bapthize as Christians and they took the name of their godfather (there are other testimonies of that practice), or of their lord (or maybe both). There are also examples of some other personal names working in this same way, some times woth an article in fornt: (de) María, (de) Pedro.
Thanks, once more.