275 research outputs found
Sweet's syndrome associated with cellulitis - a challenging diagnosis
Sweet's syndrome is a neutrophilic dermatosis with worldwide distribution that has been associated with inflammatory autoimmune diseases, infections, malignancies, drugs, and pregnancy. The disease is idiopathic in up to 50% of patients. A 64-year-old woman, diagnosed with right limb cellulitis (4 days of evolution), was seen at our department, due to persistent cellulitis and progressive appearance of painful nodules and plaques in both shins and the right forearm (2 days of evolution). Taken together, clinical, laboratory and pathological data suggested the diagnosis of Sweet's syndrome, probably secondary to cellulitis of the right inferior limb. We suggest that cellulitis may be associated with Sweet's syndrome, a rare association in the literature
Immunohistochemistry of the uterine cervix of rats bearing the Walker 256 tumor treated with copaiba balsam
Bacteria arise at the border of mycoplasma-infected HeLa cells, containing cytoplasm with either malformed cytosol, mitochondria and endoplasmic reticulum or tightly adjoined smooth vacuoles
A study with transmission electron microscopy of mycoplasma-contaminated HeLa cells using five cell donors referred to as donors A, B, C, D and E, observations are herein presented. Experiments performed with cells from donors B, C and D, revealed the presence of Mycoplasma hyorhinis after PCR and sequencing experiments. Bacteria probably originated from a cytoplasm with compacted tiny granular particles replacing the normal cytosol territories, or from the contact with the cytoplasm through a clear semi-solid material. The compact granularity (CG) of the cytoplasm was crossed by stripes of smooth and rough endoplasmic reticulum cisternae. Among apparently normal mitochondria, it was noted, in variable proportions, mitochondria with crista-delimited lucent central regions that expand to and occupied the interior of a crista-less organelle, which can undergo fission. Other components of the scenarios of mycoplasma-induced cell demolition are villus-like structures with associated 80-200 nm vesicles and a clear, flexible semi-solid, process-sensitive substance that we named jam-like material. This material coated the cytoplasmic surface, its recesses, irregular protrusions and detached cytoplasmic fragments. It also cushioned forming bacteria. Cyst-like structures were often present in the cytoplasm. Cells, mainly apoptotic, exhibiting ample cytoplasmic sectors with characteristic net-like profile due to adjoined vacuoles, as well as ovoid or elongated profiles, consistently appeared in all cells from the last four cell donors. These cells were named “modified host cells” because bacteria arose in the vacuoles. The possibility that, in some samples, there was infection and/or coinfection of the host cell by another organism(s) cannot be ruled out
Inhalation anesthesia equipment for rats with provision of simultaneous anesthetic and oxygen
Molecular and cellular mechanisms underlying the evolution of form and function in the amniote jaw.
The amniote jaw complex is a remarkable amalgamation of derivatives from distinct embryonic cell lineages. During development, the cells in these lineages experience concerted movements, migrations, and signaling interactions that take them from their initial origins to their final destinations and imbue their derivatives with aspects of form including their axial orientation, anatomical identity, size, and shape. Perturbations along the way can produce defects and disease, but also generate the variation necessary for jaw evolution and adaptation. We focus on molecular and cellular mechanisms that regulate form in the amniote jaw complex, and that enable structural and functional integration. Special emphasis is placed on the role of cranial neural crest mesenchyme (NCM) during the species-specific patterning of bone, cartilage, tendon, muscle, and other jaw tissues. We also address the effects of biomechanical forces during jaw development and discuss ways in which certain molecular and cellular responses add adaptive and evolutionary plasticity to jaw morphology. Overall, we highlight how variation in molecular and cellular programs can promote the phenomenal diversity and functional morphology achieved during amniote jaw evolution or lead to the range of jaw defects and disease that affect the human condition
Dyadic adjustment, family coping, body image, quality of life and psychological morbidity in patients with psoriasis and their partners
Background Psoriasis is an incurable and chronic disease
that includes unpredictable periods of remission and relapse
requiring long-term therapy.
Purpose This paper focuses on the relationship among
family coping, psychological morbidity, body image,
dyadic adjustment and quality of life in psoriatic patients
and their partners.
Method One hundred and one patients with psoriasis and
78 partners comprised the sample. They were regular users
of the Dermatology Service of a Central Northern hospital
in Portugal and a private dermatology clinic. Patients with
psoriasis were assessed on anxiety, depression, body image,
quality of life, dyadic adjustment and family coping.
Partners were assessed on the same measures except body
image and quality of life.
Results A positive relationship among dyadic adjustment,
psychological morbidity and family coping in patients and
their partners was found. Also, patients with lower levels of
quality of life had partners with higher levels of depressive
and anxious symptoms. Better dyadic adjustment predicted
family coping in the psoriatic patient. High levels of dyadic
adjustment in patients and low partners’ trait anxiety
predicted better dyadic adjustment in partners.
Conclusion The results highlight the importance of incorporating
family variables in psychological interventions in
psoriasis’ care, particularly family coping and dyadic
adjustment as well as the need for psychological intervention
to focus both on patients and partners
The Targeting of Plasmalemmal Ceramide to Mitochondria during Apoptosis
Ceramide is a key lipid mediator of cellular processes such as differentiation, proliferation, growth arrest and apoptosis. During apoptosis, ceramide is produced within the plasma membrane. Although recent data suggest that the generation of intracellular ceramide increases mitochondrial permeability, the source of mitochondrial ceramide remains unknown. Here, we determine whether a stress-mediated plasmalemmal pool of ceramide might become available to the mitochondria of apoptotic cells. We have previously established annexin A1—a member of a family of Ca2+ and membrane-binding proteins—to be a marker of ceramide platforms. Using fluorescently tagged annexin A1, we show that, upon its generation within the plasma membrane, ceramide self-associates into platforms that subsequently invaginate and fuse with mitochondria. An accumulation of ceramide within the mitochondria of apoptotic cells was also confirmed using a ceramide-specific antibody. Electron microscopic tomography confirmed that upon the formation of ceramide platforms, the invaginated regions of the plasma membrane extend deep into the cytoplasm forming direct physical contacts with mitochondrial outer membranes. Ceramide might thus be directly transferred from the plasma membrane to the mitochondrial outer membrane. It is conceivable that this “kiss-of-death” increases the permeability of the mitochondrial outer membrane thereby triggering apoptosis
Suboccipital craniectomy with or without duraplasty: what is the best choice in patients with Chiari type 1 malformation?
- …