Many Membrane Abnormalities in Hypertension Result from one Primary Defect

1991 ◽  
pp. 291-302 ◽  
Author(s):  
David F. Bohr ◽  
Philip B. Furspan ◽  
Anna F. Dominiczak
Keyword(s):  
Primary Defect

Live Confocal Analysis of Fertilization and Early Development

2001 ◽  
Vol 7 (S2) ◽  
pp. 1012-1013
Author(s):  
Uyen Tram ◽  
William Sullivan
Keyword(s):  
Drosophila Melanogaster ◽  
Embryonic Development ◽  
Real Time ◽  
Early Development ◽  
Fluorescent Probes ◽  
Primary Defect ◽  
Fluorescent Analysis ◽  
Dynamic Event ◽  
Enormous Amount ◽  
Fluorescent Studies

Embryonic development is a dynamic event and is best studied in live animals in real time. Much of our knowledge of the early events of embryogenesis, however, comes from immunofluourescent analysis of fixed embryos. While these studies provide an enormous amount of information about the organization of different structures during development, they can give only a static glimpse of a very dynamic event. More recently real-time fluorescent studies of living embryos have become much more routine and have given new insights to how different structures and organelles (chromosomes, centrosomes, cytoskeleton, etc.) are coordinately regulated. This is in large part due to the development of commercially available fluorescent probes, GFP technology, and newly developed sensitive fluorescent microscopes. For example, live confocal fluorescent analysis proved essential in determining the primary defect in mutations that disrupt early nuclear divisions in Drosophila melanogaster. For organisms in which GPF transgenics is not available, fluorescent probes that label DNA, microtubules, and actin are available for microinjection.

The Effects of Primary Defect Characteristics on Reconstruction Type and Adjunctive Intervention in Mohs Micrographic Surgery: A Retrospective Review

2020 ◽  
Vol 19 (3) ◽  
pp. 264-270
Author(s):  
Oscar Trujillo ◽  
Adetokunbo Obayemi ◽  
Gulce Askin ◽  
Kristina Navrazhina ◽  
Brienne Cressey ◽  
...  
Keyword(s):  
Retrospective Review ◽  
Mohs Micrographic Surgery ◽  
Micrographic Surgery ◽  
Primary Defect ◽  
Adjunctive Intervention

scholarly journals HMG-CoA reductase is not the site of the primary defect in phytosterolemia

1998 ◽  
Vol 39 (5) ◽  
pp. 1046-1054
Author(s):  
G.M.B. Berger ◽  
R.J. Pegoraro ◽  
S.B. Patel ◽  
P. Naidu ◽  
L. Rom ◽  
...  
Keyword(s):  
Primary Defect ◽  
Hmg Coa Reductase ◽  
Coa Reductase

scholarly journals Reconstruction of a secondary scalp defect using the crane principle and a split-thickness skin graft

BMC Surgery ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Yi Lu ◽  
Ke-Chung Chang ◽  
Che-Ning Chang ◽  
Dun-Hao Chang
Keyword(s):  
Skin Graft ◽  
Subcutaneous Tissue ◽  
Donor Site ◽  
Split Thickness Skin Graft ◽  
Salvage Procedure ◽  
Primary Defect ◽  
Scalp Defects ◽  
Thickness Skin ◽  
Scalp Defect ◽  
Secondary Defect

Abstract Background Scalp reconstruction is a common challenge for surgeons, and there are many different treatment choices. The “crane principle” is a technique that temporarily transfers a scalp flap to the defect to deposit subcutaneous tissue. The flap is then returned to its original location, leaving behind a layer of soft tissue that is used to nourish a skin graft. Decades ago, it was commonly used for forehead scalp defects, but this useful technique has been seldom reported on in recent years due to the improvement of microsurgical techniques. Previous reports mainly used the crane principle for the primary defects, and here we present a case with its coincidental application to deal with a complication of a secondary defect. Case report We present a case of a 75-year-old female patient with a temporoparietal scalp squamous cell carcinoma (SCC). After tumor excision, the primary defect was reconstructed using a transposition flap and the donor site was covered by a split-thickness skin graft (STSG). Postoperatively, the occipital skin graft was partially lost resulting in skull bone exposure. For this secondary defect, we applied the crane principle to the previously rotated flap as a salvage procedure and skin grafting to the original tumor location covered by a viable galea fascia in 1.5 months. Both the flap and skin graft healed uneventfully. Conclusions Currently, the crane principle is a little-used technique because of the familiarity of microsurgery. Nevertheless, the concept is still useful in selected cases, especially for the management of previous flap complications.

Fanconi-Bickel syndrome - the original patient and his natural history, historical steps leading to the primary defect, and a review of the literature

1998 ◽  
Vol 157 (10) ◽  
pp. 783-797 ◽  
Author(s):  
R. Santer ◽  
R. Schneppenheim ◽  
D. Suter ◽  
J. Schaub ◽  
B. Steinmann
Keyword(s):  
Natural History ◽  
Review Of The Literature ◽  
Primary Defect

Limb deformity proteins: role in mesodermal induction of the apical ectodermal ridge

Development ◽  
1997 ◽  
Vol 124 (1) ◽  
pp. 133-139 ◽  
Author(s):  
J. Kuhlman ◽  
L. Niswander
Keyword(s):  
Sonic Hedgehog ◽  
Limb Development ◽  
Apical Ectodermal Ridge ◽  
Primary Defect ◽  
Limb Deformity ◽  
Normal Morphology ◽  
Fibroblast Growth Factor 8 ◽  
Skeletal Pattern ◽  
Two Phases ◽  
And Function

During early limb development, distal tip ectoderm is induced by the underlying mesenchyme to form the apical ectodermal ridge. Subsequent limb growth and patterning depend on reciprocal signaling between the mesenchyme and ridge. Mice that are homozygous for mutations at the limb deformity (ld) locus do not form a proper ridge and the anteroposterior axis of the limb is shortened. Skeletal analyses reveal shortened limbs that involve loss and fusion of distal bones and digits, defects in both anteroposterior and proximodistal patterning. Using molecular markers and mouse-chick chimeras we examined the ridge-mesenchymal interactions to determine the origin of the ld patterning defects. In the ld ridge, fibroblast growth factor 8 (Fgf8) RNA is decreased and Fgf4 RNA is not detected. In the ld mesenchyme, Sonic hedgehog (Shh), Evx1 and Wnt5a expression is decreased. In chimeras between ld ectoderm and wild-type mesenchyme, a ridge of normal morphology and function is restored, Fgf8 and Shh are expressed normally, Fgf4 is induced and a normal skeletal pattern arises. These results suggest that the ld mesenchyme is unable to induce the formation of a completely functional ridge. This primary defect causes a disruption of ridge function and subsequently leads to the patterning defects observed in ld limbs. We propose a model in which ridge induction requires at least two phases: an early competence phase, which includes induction of Fgf8 expression, and a later differentiation phase in which Fgf4 is induced and a morphological ridge is formed. Ld proteins appear to act during the differentiation phase.

Allergic Rhinitis

1992 ◽  
Vol 13 (9) ◽  
pp. 323-328
Author(s):  
Frank S. Virant
Keyword(s):  
Allergic Rhinitis ◽  
Clinical Signs ◽  
Upper Airway ◽  
Allergic Patient ◽  
The United States ◽  
Specific Ige ◽  
Interferon Γ ◽  
Interleukin 4 ◽  
Primary Defect ◽  
Primary Focus

Epidemiology Allergic rhinitis affects as many as 8% to 10% of children in the United States. Many of these children suffer significant morbidity, leading to millions of lost school days annually. Morbidity is amplified when these children concurrently suffer from complications of allergic rhinitis, such as recurrent otitis media or chronic sinus disease. Typically, children who have allergic rhinitis have a family history of atopic disorders. Upper airway allergy may become manifest at any age, but the appearance of symptoms is most common during childhood or young adulthood. Clinical signs of rhinitis may be perennial, seasonal, or episodic, and the primary focus of complaints may relate to secondary problems, including ear, sinus, or lung disease. Pathophysiology In the allergic patient, disease is mediated by the production of antigenspecific IgE by the patient's B lymphocytes. Current research suggests that the primary defect may be the excessive production of interleukin 4 (IL-4) or a deficient level of gamma interferon (γ-INF) when a T-cell is presented with an antigen. This constellation of immunomodulators directs the B-cell to produce IgE rather than the IgG response of the non-allergic patient. Clinical disease occurs when an allergen reacts with antigen-specific IgE on the patient's nasal mast cells. When these factors combine, the mast cell is activated to release a variety of preformed and newly produced mediators, including histamine, leukotrienes, and prostaglandins (Fig 1).

Increased hemangioblast commitment, not vascular disorganization, is the primary defect in flt-1 knock-out mice

Development ◽  
1999 ◽  
Vol 126 (13) ◽  
pp. 3015-3025 ◽  
Author(s):  
G.H. Fong ◽  
L. Zhang ◽  
D.M. Bryce ◽  
J. Peng
Keyword(s):  
Endothelial Cells ◽  
Population Density ◽  
Cell Fate ◽  
Vascular System ◽  
Primitive Streak ◽  
Cellular Level ◽  
Wild Type ◽  
Primary Defect ◽  
Knock Out ◽  
Vascular Channels

We previously demonstrated the essential role of the flt-1 gene in regulating the development of the cardiovascular system. While the inactivation of the flt-1 gene leads to a very severe disorganization of the vascular system, the primary defect at the cellular level was unknown. Here we report a surprising finding that it is an increase in the number of endothelial progenitors that leads to the vascular disorganization in flt-1(−/−) mice. At the early primitive streak stage (prior to the formation of blood islands), hemangioblasts are formed much more abundantly in flt-1(−/−) embryos. This increase is primarily due to an alteration in cell fate determination among mesenchymal cells, rather than to increased proliferation, migration or reduced apoptosis of flt-1(−/−) hemangioblasts. We further show that the increased population density of hemangioblasts is responsible for the observed vascular disorganization, based on the following observations: (1) both flt-1(−/−) and flt-1(+/+) endothelial cells formed normal vascular channels in chimaeric embryos; (2) wild-type endothelial cells formed abnormal vascular channels when their population density was significantly increased; and (3) in the absence of wild-type endothelial cells, flt-1(−/−) endothelial cells alone could form normal vascular channels when sufficiently diluted in a developing embryo. These results define the primary defect in flt-1(−/−) embryos at the cellular level and demonstrate the importance of population density of progenitor cells in pattern formation.

The Central Slip Tenodesis Test for Early Diagnosis of Potential Boutonnière Deformities

1994 ◽  
Vol 19 (1) ◽  
pp. 88-90 ◽  
Author(s):  
P. J. SMITH ◽  
D. A. ROSS
Keyword(s):  
Early Diagnosis ◽  
Conservative Management ◽  
Primary Defect ◽  
Non Invasive ◽  
Boutonniere Deformity ◽  
Invasive Method ◽  
Central Slip ◽  
Boutonnière Deformity

Disruption of the central slip is the primary defect leading to boutonnière deformity. In the closed injury early diagnosis of this lesion is rarely achieved due to the limitations of current methods and difficulties encountered in assessing a painful finger. We describe a simple, non-invasive method of diagnosis which can be carried out on all patients and with minimal discomfort. This test is also beneficial in monitoring the progress of conservative management of central slip disruption.

scholarly journals An electrophysiological investigation of skeletal muscle in human chronic Chagas' disease

1978 ◽  
Vol 36 (4) ◽  
pp. 319-326 ◽  
Author(s):  
Olga P. Sanz ◽  
A. F. Ratusnu ◽  
G. G. Aristimuño ◽  
E. M. O'Neill ◽  
R. E. P. Sica
Keyword(s):  
Chagas Disease ◽  
Electrophysiological Study ◽  
Motor Units ◽  
Normal Range ◽  
Primary Defect ◽  
Repetitive Nerve Stimulation ◽  
Conduction Velocities ◽  
Muscle Changes ◽  
Chronic Chagas Disease ◽  
Extensor Digitorum Brevis

An electrophysiological study has been made of the thenar, hypothenar, soleus and extensor digitorum brevis muscles and their inervation in 90 patients with chronic Chagas' disease. Some of them showed a reduced number of functional motor units with increased size of many of the surviving units. No decremental muscle response was found to repetitive nerve stimulation. Motor and sensory conduction velocities as well as motor terminal latencies were on the normal range. These findings suggested that the muscle changes resulted from a primary defect of the alpha spinal motoneurone soma.

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