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Biomedical subjects

A Stella

Publications and source records attributed to A Stella.

At least 109 records · Page 6Linked to original sources

An immunohistochemical study of inflammatory abdominal aortic aneurysms.

Seven cases of inflammatory abdominal aortic aneurysms (IAs) were studied by light microscopy, transmission electron microscopy (TEM) and immunohistochemistry. Microscopically, atherosclerosis coexisted with adventitial fibrosis and inflammation. The inflammatory component showed a follicular and a diffuse pattern. Fibrous entrapment of fatty tissue, adventitial vasculitis, neuritis were also common findings. By TEM, sparse smooth muscle cells having dilated cisternae of rough endoplasmic reticulum, large bundles of collagen fibres and oedematous, amorphous fibrillary elastin were observed. By immunohistochemistry, the follicles mostly contained CD22+ B-cells. T4- (CD2+/CD4+/CD8-), T8-(CD2+/CD4-/CD8+) cells as well as macrophages (CD4+/CD11c+) and follicular dendritic reticulum cells (DRC1+) were also detected. The monoclonal antibody Ki-67 reacted with 2-48% of germinal center cells. In the fibrous extrafollicular adventitia, actively synthesizing plasma cells prevailed over T4-cells, and macrophages. Some of the macrophages were also activated (CD4+/CD11c+/CD25+/CD30-). IgM, IgG and C3c deposits were detected in the fibrous zone, in the germinal centers, within adventitial vessels and nerves. HLA-DR antigen was diffusely expressed in cells populating both the fibrous and the follicular zones as well as in endothelial and Schwann cells. These findings suggest that IAs could develop in some individuals affected by advanced atherosclerosis of the abdominal aorta through a pathogenic B-cell response to locally presented antigens.

Antigens, CD↗

Exclusion of the APC gene as the cause of a variant form of familial adenomatous polyposis (FAP)

Familial adenomatous polyposis (FAP) is a premalignant disease inherited as an autosomal dominant trait, characterized by hundreds to thousands of polyps in the colorectal tract. Recently, the syndrome has been shown to be caused by mutations in the APC (adenomatous polyposis coli) gene located on chromosome 5q21. We studied two families that both presented a phenotype different than that of the classical form of FAP. The most important findings observed in these two kindreds are (a) low and variable number of colonic polyps (from 5 to 100) and (b) a slower evolution of the disease, with colon cancer occurring at a more advanced age than in FAP in spite of the early onset of intestinal manifestations. To determine whether mutations of the APC gene are also responsible for this variant syndrome, linkage studies were performed by using a series of markers both intragenic and tightly linked to the APC gene. The results provide evidence for exclusion of the APC gene as the cause of the variant form of polyposis present in the two families described.

Adenomatous Polyposis Coli↗

Familial adenomatous polyposis: identification of a new frameshift mutation of the APC gene in an Italian family.

Familial Adenomatous Polyposis (FAP) is a premalignant disease of the gastrointestinal tract inherited as an autosomal dominant trait assigned to chromosome 5q21. The 15 exons of the APC gene responsible for the defect were amplified from the DNA of one FAP patient. SSCP analysis of the amplified DNA revealed a variant conformer of exon 10. The sequencing of the cloned PCR product showed a 1 base insertion at position 1370, creating a stop codon four nucleotides downstream. SSCP analysis of 20 family members and nucleotide sequencing of exon 10 in three affected members confirmed the Mendelian inheritance of the mutant allele.

Adenomatous Polyposis Coli↗

Hypertension due to an aneurysm of the left renal artery in a patient with neurofibromatosis.

Arterial lesions in patients with neurofibromatosis are rarely described and in most cases are stenotic. The aneurysmal changes reported in the literature are usually characterized by multiple microaneurysms due to the dysplastic lesions of the artery. We report a case of a single aneurysm of the inferior hilar branch of the left renal artery of a young female with neurofibromatosis. The patient showed hypoperfusion of the renal pole fed by this branch and was hypertensive. The aneurysm had a diameter of 4 cm and showed the histological findings typical of dysplastic lesions of neurofibromatosis. The hypertension and the renal pole hypoperfusion recovered after surgical excision of the aneurysm and end-to-end anastomosis of the hilar branch stumps.

Adult↗

The kidney as a sensor: functional evidence.

PURPOSE: To evaluate the effects of afferent renal nerve activity on reflex control of the cardiovascular system and volume balance. ANATOMICAL AND ELECTROPHYSIOLOGICAL EVIDENCE: In the kidney, receptors sensitive to mechanical and chemical stimuli have been identified. Afferent fibres from the kidney have been shown to travel along renal nerves and dorsal roots, mainly from T9 to L4, and to project to the central nervous system at spinal and supraspinal levels. Most of the brainstem regions involved in cardiovascular control and several regions of the anterior hypothalamus (including vasopressin-secreting neurons) receive inputs from renal afferents. REFLEX EFFECTS ON THE CARDIOVASCULAR SYSTEM: The electrical stimulation of afferent renal nerve fibres can either increase or decrease systemic arterial pressure. The hypertensive response to electrical stimulation of renal afferents is the result of widespread activation of the sympathetic nervous system, leading to an increase in peripheral vascular resistance. Activation of afferent renal nerve fibres by an intrarenal artery infusion of adenosine elicits sustained increases in arterial pressure, heart rate and cardiac output without changing total peripheral resistance, indicating reflex activation of the sympathetic nervous system, predominantly restricted to the heart. An increase in the plasma vasopressin concentration, observed during the electrical stimulation of renal afferents, might help to mediate the hypertensive response to afferent renal nerve stimulation. RENORENAL REFLEXES: The existence of neural renorenal reflexes, by which one kidney can influence the functioning of the opposite kidney, is well established. Contralateral renorenal reflexes, which are inhibitory in nature, are tonically active and mainly control the secretion of renin from juxtaglomerular cells and the tubular reabsorption of sodium and water. CONCLUSIONS: The evidence suggests that sensory information from the kidney contributes to the overall regulation of cardiovascular homeostasis and volume balance.

Afferent Pathways↗

Prognostic value of captopril renal scintigraphy in renovascular hypertension.

This study evaluates the prognostic value of captopril renal scintigraphy in hypertensive patients undergoing renal artery revascularization. Preoperative studies of 51 patients were correlated with blood pressure results at 6- and 12-mo follow-up. Captopril-renal scintigraphy was carried out 1 hr after oral administration of 50 mg of captopril, using either 220 MBq of 99mTc-DTPA or 74 MBq of 99mTc-MAG3, followed by a baseline study in case of abnormal results. Evidence of amelioration or normalization in relation to captopril study was considered predictive of blood pressure control following treatment. Blood pressure response was favorable in 37 patients, but failed to show any improvement in 14. The scintigraphic test was positive in 33 patients (15 cured, 17 improved, 1 failed) and negative in 18 (3 cured, 2 improved, 13 failed). Sensitivity and specificity for renovascular hypertension was 86.5% and 93%, respectively. For blood pressure cure and improvement, the test had positive and negative predictive values of 97% and 72%, respectively. A positive preoperative captopril renal scintigraphic result is a strong predictor of hypertension curability by renal artery revascularization.

Adult↗

Aneurysmal change at or above the proximal anastomosis after infrarenal aortic grafting.

We conducted a retrospective review of all patients undergoing repair of abdominal aortic aneurysm at or above the proximal anastomosis of a previous infrarenal aortic graft between 1986 and 1991. Infected grafts and patients with suprarenal aneurysms present at the time of the original graft were excluded. Twenty-one patients, 19 men and two women, were included. The original indication for surgery was aneurysm in 14 patients and occlusive disease in seven; the mean interval from initial surgery to presentation was 10 years (range, 3 to 23 years). Twelve lesions were anastomotic false aneurysms, and nine were true aneurysms beginning in the proximal juxta-anastomotic aorta. Fourteen patients had an asymptomatic abdominal mass. Seven patients had symptoms of acute expansion (three), rupture (three), or thrombosis (one). True aneurysm and symptomatic presentation were correlated with aneurysm as the original indication for surgery. Repair was accomplished by an interpositional graft in 13 and graft replacement in eight. Seven patients required suprarenal anastomosis or renal and visceral reconstruction. Five operative deaths (24%) occurred, including two of three patients with rupture (67%) and two of seven patients (28%) in the suprarenal group. The mortality rate for elective repair with an infrarenal anastomosis was 11%. Two additional late deaths occurred during the follow-up period.

Aged↗

Total excision and extra-anatomic bypass for aortic graft infection.

Reports of high mortality and amputation rates following total excision and extra-anatomic bypass for aortic graft infection have prompted the use of alternate approaches including local antibiotics, partial resection, in situ revascularization, and graft excision without revascularization. Experience with aortic graft infection was reviewed to establish current morbidity and mortality rates and evaluate our bias in favor of total excision and extra-anatomic bypass. Aortic graft infection was identified in 32 patients, 8 with aortoenteric fistulas. The mean interval between graft placement and infection was 34 months. History of groin exposure (75%) or multiple prior vascular surgery (50%) was common. Clinical signs included fever and/or leukocytosis (23 patients), false aneurysm (9 patients), graft thrombosis (6 patients), groin infection (11 patients), and gastrointestinal hemorrhage (6 patients). Microbiologic data, available in 26 patients, demonstrated gram-positive organisms in 15 patients and gram-negative in 9. Multiple organisms were seen in 11 patients. Patients were treated by partial removal with (8 patients) or without (4 patients) revascularization or total removal with (18 patients) or without (2 patients) revascularization. Revascularization was by an extra-anatomic route, either simultaneous or staged. Overall morbidity/mortality was less in the revascularized groups (p = 0.01), while late complications were seen only after partial removal (p less than 0.01). The best results were found after total excision with revascularization. No patient in this group experienced late infection or amputation during a mean follow-up of 34 months (range: 1 to 168 months). Complications after total excision and extra-anatomic bypass for aortic graft infection are lower than generally appreciated. This approach should remain the standard to which other approaches are compared.

Aged↗

The cellular component in the parietal infiltrate of inflammatory abdominal aortic aneurysms (IAAA).

Eight cases of inflammatory abdominal aortic aneurysm (IAAA) (group I) and a control group of ten cases of atherosclerotic abdominal aortic aneurysm (AAA) with little or no parietal inflammatory infiltrate (group II) were studied; using light microscopy, transmission electron microscopy (TEM), and immunohistochemistry. These were used to define cell composition in the inflammatory process, the degree of cell activation and alteration of connective tissue. Large numbers of B lymphocytes were present in IAAA with preservation of the T4/T8 ratio. In addition, HLA-DR and the IL2-R antigen (specific for activated cells) were widely expressed in the cell population. The interstitial matrix contained deposits of IgG, IgM and C3c together with an increase in type III collagen and a reduction in elastin which appeared fragmented and swollen. This study, therefore, characterised the cellular component of the parietal inflammatory infiltrate in IAAA. The degree of activation shown by these cell elements and the activation of complement suggest that the relevant antigen may have been localised in the aneurysm wall at the time of observation.

Aged↗