Examiners’ Ratings of Color Transparencies of Clinical Signs Associated with Vitamin Deficiencies

1957 ◽  
Vol 5 (1) ◽  
pp. 56-61 ◽  
Author(s):  
SUSAN B. MERROW ◽  
MARY M. CLAYTON ◽  
CHESTER A. NEWHALL ◽  
WALTER D. FOSTER
Keyword(s):  
Clinical Signs ◽  
Vitamin Deficiencies

A rapid method for the direct identification of paramyxovirus in canine CSF by ultracentrifugation and negative staining as a rule out for distemper

1990 ◽  
Vol 48 (3) ◽  
pp. 594-595
Author(s):  
W.L. Steffens ◽  
M.B. Ard ◽  
C.E. Greene ◽  
A. Jaggy
Keyword(s):  
Subacute Sclerosing Panencephalitis ◽  
Clinical Signs ◽  
Viral Disease ◽  
Etiologic Agent ◽  
Mucosal Inflammation ◽  
Worldwide Distribution ◽  
Negative Stain ◽  
Viral Particles ◽  
Systemic Manifestations ◽  
Rule Out

Canine distemper is a multisystemic contagious viral disease having a worldwide distribution, a high mortality rate, and significant central neurologic system (CNS) complications. In its systemic manifestations, it is often presumptively diagnosed on the basis of clinical signs and history. Few definitive antemortem diagnostic tests exist, and most are limited to the detection of viral antigen by immunofluorescence techniques on tissues or cytologic specimens or high immunoglobulin levels in CSF (cerebrospinal fluid). Diagnosis of CNS distemper is often unreliable due to the relatively low cell count in CSF (<50 cells/μl) and the binding of blocking immunoglobulins in CSF to cell surfaces. A more reliable and definitive test might be possible utilizing direct morphologic detection of the etiologic agent. Distemper is the canine equivalent of human measles, in that both involve a closely related member of the Paramyxoviridae, both produce mucosal inflammation, and may produce CNS complications. In humans, diagnosis of measles-induced subacute sclerosing panencephalitis is through negative stain identification of whole or incomplete viral particles in patient CSF.

Hormone Replacement Therapy and Voice

2019 ◽  
Vol 4 (4) ◽  
pp. 607-614
Author(s):  
Jean Abitbol
Keyword(s):  
Replacement Therapy ◽  
Symptom Severity ◽  
Low Dose ◽  
Hormone Replacement ◽  
Clinical Signs ◽  
Female Voice ◽  
Fat Cells ◽  
High Pitch ◽  
Endocrine Effects ◽  
The Voice

The purpose of this article is to update the management of the treatment of the female voice at perimenopause and menopause. Voice and hormones—these are 2 words that clash, meet, and harmonize. If we are to solve this inquiry, we shall inevitably have to understand the hormones, their impact, and the scars of time. The endocrine effects on laryngeal structures are numerous: The actions of estrogens and progesterone produce modification of glandular secretions. Low dose of androgens are secreted principally by the adrenal cortex, but they are also secreted by the ovaries. Their effect may increase the low pitch and decease the high pitch of the voice at menopause due to important diminution of estrogens and the privation of progesterone. The menopausal voice syndrome presents clinical signs, which we will describe. I consider menopausal patients to fit into 2 broad types: the “Modigliani” types, rather thin and slender with little adipose tissue, and the “Rubens” types, with a rounded figure with more fat cells. Androgen derivatives are transformed to estrogens in fat cells. Hormonal replacement therapy should be carefully considered in the context of premenopausal symptom severity as alternative medicine. Hippocrates: “Your diet is your first medicine.”

Die Aplasie der Vena cava inferior als Ursache rezidivierender Bein- und Beckenvenenthrombosen

VASA ◽  
1999 ◽  
Vol 28 (4) ◽  
pp. 289-292 ◽  
Author(s):  
Tiesenhausen ◽  
Amann ◽  
Thalhammer ◽  
Aschauer
Keyword(s):  
Inferior Vena Cava ◽  
Inferior Vena ◽  
Heart Defects ◽  
Vena Cava ◽  
Clinical Signs ◽  
Vena Cava Inferior ◽  
Caval Vein ◽  
Rare Finding ◽  
Thrombotic Complications ◽  
Asplenia Syndrome

Congenital anomalies of the caval vein are often associated with other abnormities such as heart defects, situs inversus or a polysplenia-asplenia-syndrome. An isolated, congenital malformation like aplasia of the inferior vena cava is a rare finding. A review of the embryology and abnormities, diagnostics, clinical signs and treatment is given together with the histories of two patients having thrombosis of the lower extremities and pelvic veins, caused by aplasia of the inferior vena cava. After thrombotic complications caused by vena cava aplasia there is high risk of recurrence. Those patients should be anticoagulated for lifetime.

SelenoproteinN1-related myopathy: From clinical signs to diagnosis

2011 ◽  
Vol 42 (S 01) ◽  
Author(s):  
E Alberg ◽  
S Lutz ◽  
W Kress ◽  
U Schara
Keyword(s):  
Clinical Signs

Sonographically guided, transcatheter foam sclerotherapy of the great saphenous vein

Phlebologie ◽  
2007 ◽  
Vol 36 (06) ◽  
pp. 309-312 ◽  
Author(s):  
T. Schulz ◽  
M. Jünger ◽  
M. Hahn
Keyword(s):  
Saphenous Vein ◽  
Great Saphenous Vein ◽  
Clinical Stage ◽  
Clinical Signs ◽  
Cost Effective ◽  
Duplex Sonography ◽  
Foam Sclerotherapy ◽  
Average Loss ◽  
One Year ◽  
The Cost

Summary Objective: The goal of the study was to assess the effectiveness and patient tolerability of single-session, sonographically guided, transcatheter foam sclerotherapy and to evaluate its economic impact. Patients, methods: We treated 20 patients with a total of 22 varicoses of the great saphenous vein (GSV) in Hach stage III-IV, clinical stage C2-C5 and a mean GSV diameter of 9 mm (range: 7 to 13 mm). We used 10 ml 3% Aethoxysklerol®. Additional varicoses of the auxiliary veins of the GSV were sclerosed immediately afterwards. Results: The occlusion rate in the treated GSVs was 100% one week after therapy as demonstrated with duplex sonography. The cost of the procedure was 207.91 E including follow-up visit, with an average loss of working time of 0.6 days. After one year one patient showed clinical signs of recurrent varicosis in the GSV; duplex sonography showed reflux in the region of the saphenofemoral junction in a total of seven patients (32% of the treated GSVs). Conclusion: Transcatheter foam sclerotherapy of the GSV is a cost-effective, safe method of treating varicoses of GSV and broadens the spectrum of therapeutic options. Relapses can be re-treated inexpensively with sclerotherapy.

Cystic Bone Lesions in Horses and Humans: A Comparative Review

1998 ◽  
Vol 11 (01) ◽  
pp. 08-18 ◽  
Author(s):  
C. W. McIlwraith ◽  
J. A. Auer ◽  
Brigitte von Rechenberg
Keyword(s):  
Recurrence Rate ◽  
Subchondral Bone ◽  
Fibrous Tissue ◽  
Clinical Signs ◽  
Bone Lesions ◽  
Anatomical Location ◽  
Cystic Lesions ◽  
Bone Cysts ◽  
Biological Behaviour ◽  
Comparative Review

SummaryCases of cystic bone lesions in horses and humans were reviewed in the literature. These lesions are radiolucent areas of bone, recognized as subchondral cystic lesions in the horse (SCL), intra-osseous ganglia (IOG), subchondral bone cysts secondary to osteoarthrosis (OAC), and unicameral bone cysts (UCB) in humans. Their morphology is quite similar, consisting of lesions with a distinct cyst wall, and a cavity filled with fibrous tissue and yellowish mucoid fluid. The lesions are surrounded by sclerotic bone and can be easily diagnosed radiographically. SCL, IOG and OAC occur in the subchondral bone close to the adjacent joint, whereas UCB occur in the metaphysis of long bones. Their aetiology and pathogenesis is still unknown, although primary damage to the subchondral bone, cartilage or local blood supply and growth disturbances are discussed. In this review 703 lesions of SCL in horses, 289 lesions of IOG and 1460 lesions of UCB in humans were compared in their anatomical location and clinical signs. SCL and OAC resembled each other with respect to anatomical location. A correlation of affected bones could not be found for all four groups. Clinical presentation concerning age was most similar for SCL and UCB with both lesions mainly occurring in young individuals. Gender predominance of males was present in SCL, IOG and UCB. Clinical diagnosis was either incidental, or connected with intermittent pain in all lesions except for OAC. Additionally, the lesions were also found in conjunction with degenerative joint disease (SCL, OAC) or pathological fractures (UCB). Cystic bone lesions were either treated conservatively, surgically with curettage alone, curettage in combination with grafting procedures, or intra-lesional application of corticosteroids. SCL and UCB were similar in their biological behaviour concerning their slow response to the therapy and relatively high recurrence rate. None of the cystic bone lesions were comparable, and a common aetiology and pathogenesis could not be found.In a literature review cases of cystic bone lesions in horses and humans were compared with the goal to find a common aetiology and pathogenesis. Cystic bone lesions occur in horses as subchondral cystic lesions (SCL), and in humans as either intra-osseous ganglia (IOG), subchondral cystic lesions secondary to osteoarthrosis (OAC) or unicameral bone cysts (UCB). IOG and OAC compare with SCL mainly in the anatomical location. IOG and SCL resemble each other in size, clinical signs and histology, whereas UCB and SCL show a similar biological behaviour regarding their therapeutic response and recurrence rate. None of the cystic bone lesions in humans were comparable to the SCL in horses in all aspects. A common aetiology and pathogenesis could not be established.

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