Angiogenic activity of swine granulosa cells: effects of hypoxia and the role of VEGF.
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Biomedical subjects
Publications and source records attributed to F Bianco.
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We cryopreserved swine granulosa cells by a slow cooling rate system; FSH was added to the freezing medium to test its effectiveness in protecting the cells. After thawing, proliferative activity, viability, steroidogenesis and apoptosis were tested; moreover, we determined heat shock protein (HSP70) production, to investigate the recovery from stress and superoxide dismutase (SOD) and catalase activity to evaluate a possible impairment of the antioxidant pathway. E2 production was enhanced by cryopreservation in particular with FSH; on the contrary, P4 production was inhibited by the freezing process in particular without FSH. Only the higher FSH concentration (10 ng/ml) stimulated steroid secretion in freshly collected cells; P4 production by cells cryopreserved in the presence and in absence of FSH was increased by both 5 and 10 ng/ml while the lowest concentration was effective in stimulating E2 production only when FSH was added to freezing medium. Freezing did not modify proliferative activity, while apoptosis was higher in frozen than in fresh cells. HSP70 production was lower in cells cryopreserved in presence of FSH, whose antioxidant metabolism was also conserved: SOD and catalase activities were similar to control. In conclusion, cryopreservation does not seem to markedly affect granulosa cells, in particular if they are frozen in presence of FSH; the gonadotrophin somehow improves their performances after thawing, probably stimulating E2 production and the antioxidant metabolism.
Transient mutism was observed in a liver transplant patient under immunosuppressant therapy with cyclosporine A and antifungal prophylaxis with amphotericin B. Fluid-attenuated inversion recovery and diffusion-weighted images revealed reversible bilateral symmetric hyperintensity located in the frontal motor cortex and corticospinal tracts. These MRI abnormalities may be caused by acute edema, possibly a combination of cytotoxic and vasogenic edema, which resolved with a prompt change in therapy.
A rapidly progressing dementia, followed by focal neurological signs, and evidence of periodic sharp wave complexes (PSWC) in the EEG may lead to the clinical suspicion of Creutzfeldt-Jakob disease (CJD). Different clinical variants of CJD have been described in the past, with prominent extrapyramidal or occipital lobe involvement, all included in the sporadic form of CJD (sCJD). Familiar and iatrogenic forms of CJD are also known. More recently a new variant has been described, vCJD, casually linked to bovine spongiform encephalopathy (BSE) and it has attracted increasing attention toward each form of rapidly progressing dementia; likewise the differential diagnosis between sCJD vs. vCJD is not always easy. Magnetic resonance imaging (MRI) too seems to have a peculiar role in differentiating sCJD from vCJD, even if the role of MRI in the diagnosis of CJD is still debated. Diffusion MRI is expected to play an important role in the clinical setting of CJD, contributing to formulation of an early diagnosis, especially in cases with unusual clinical presentation. In fact, the sensitivity of diffusion MRI is superior to that of conventional MRI (T1, T2, FLAIR) in detecting specific basal ganglia and cortical abnormalities early in the course of CJD and these abnormalities correlate well with areas of the most severe and characteristic neuropathological changes. We describe a case of autopsy-proven sCJD, with an unusual clinical course without dementia as a presenting symptom and discuss the role of diffusion MRI and laboratory tests in making an early diagnosis.
The authors carried out genetic analyses and visual electrophysiologic evaluations in six asymptomatic sons and daughters of patients with symptomatic cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). Three subjects showed Notch3 Cys146Tyr missense mutation and a dysfunction of the outer, middle, and innermost retinal layers, with normal neural conduction in postretinal visual pathways, whereas in the remaining subjects without genetic mutations, no electrophysiologic abnormalities were found. An early vascular retinal impairment in CADASIL may precede the onset of clinical manifestations.
The treatment of faecal incontinence includes: the education of the patient, medical therapy, biofeedback and sphincteric exercises, surgical therapy. Conservative, non-surgical treatment is almost always the initial therapeutic approach, except in those cases in which an evident defect of the sphincter muscle is present. Surgical treatment has seen a noteworthy increase in the last fifteen years as a consequence of the development of new surgical techniques. These techniques include: external anal sphincter plasty, pelvic floor plasties, sacral neuromodulation, muscular transpositions with or without electrostimulation, artificial anal sphincter. These procedures may be employed as first or second level treatment depending on the type of pathology considered and its aetiology. The 1st results achieved by surgical treatment authorise us to believe that reconversion with artificial sphincter is a valid alternative to graciloplasty, notwithstanding the fact that its costs are higher. Attentive pre- operative assessment of patients is important. Patients must be strongly motivated and able to manage the new condition. Although further studies are necessary, the degree of satisfactory of the 1st patients operated is the best stimulus for pursuing the development of this technique.
Piriformis syndrome (PS) is an unusual cause of sciatica that, because of the lack of strict diagnostic criteria, remains a controversial clinical entity. The diagnosis of PS is still primarily clinical because no diagnostic tests have proven to be definitive. We report the case of a 30-year-old woman, affected by a severe scoliosis, who developed a persistent buttock pain resembling that of PS. The clinical suspicion was confirmed by magnetic resonance imaging (MRI) of the pelvis, which showed an enlargement of the left piriformis muscle with an anterior isplacement of the sciatic nerve. The role of MRI in the diagnosis, clinical definition, and therapeutic approach to PS is discussed.
It has been reported that sodium intake can be estimated in dialysis patients by the increment in the body sodium pool from the end of a dialysis session to the beginning of the following one. To verify the reliability of this method we compared the sodium intake, estimated by the interdialytic changes in plasma sodium concentration (C) and body water volume (V), to sodium removal during three consecutive sessions. For this purpose we investigated 9 nondiabetic patients, 5 females and 4 males, under chronic hemofiltration treatment. Sodium intake was estimated by the formula (C(pre) V(pre)) - (C(post) V(post)) using a flame photometer and electrical bioimpedance to determine the plasma sodium concentration and total body water, respectively. Sodium removal was calculated by the difference between sodium loss into the ultrafiltrate and sodium gain with the reinfusion fluid. The mean values of sodium intake calculated during the three intervals corresponded with the sodium losses measured during the three hemofiltration sessions in each patient (338+/-55 vs. 329+/-67 mEq; r = 0.92, p<0.0001). A direct relationship was also observed between sodium intake and both interdialytic body weight increase (r = 0.89, p< 0.0001) and fluid loss during the sessions (r = 0.88, p<0.0001). This data demonstrates that sodium intake can be properly estimated by the interdialytic changes in body water and plasma sodium concentrations. They also suggest that fluid intake may be influenced by sodium consumption and that sodium intake monitoring could be useful for the control of excessive interdialytic fluid gain.
The authors notice that, though the duodenal involvement in patients with acute pancreatitis is very common, the duodenal obstruction is quite exceptional and the reported cases are very few. The Authors describe; then, the case of a patient with duodenal obstruction caused by a peri-duodenal phlegmon due to an acute pancreatitis treated with a gastro-jejunostomy and a drainage of the abscess.
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BACKGROUND & AIMS: Hepatic involvement in hereditary hemorrhagic telangiectasia is common but often asymptomatic. However, in some cases, the vascular lesions that involve the liver may lead to high-output cardiac failure and pulmonary hypertension that is predominant over hepatobiliary manifestations. Liver transplantation and treatment of these complications are described and discussed in this article. METHODS: Three patients with hereditary hemorrhagic telangiectasia and hepatic involvement received transplants. They had pulmonary hypertension and chronic right-sided heart failure caused by disseminated intrahepatic telangiectasias with shunts between the hepatic artery and hepatic veins or portal vein. Left-to-right intrahepatic shunt output was estimated to range between 51% and 57.5% of cardiac output. RESULTS: Hyperdynamic circulation disappeared after liver transplantation in all patients. Results of computed tomography and right-sided heart catheterization performed 6 months later were normal. Follow-up periods currently are 65, 53, and 29 months, and each patient continues to be asymptomatic. CONCLUSIONS: This report suggests that liver transplantation can be considered as an alternative and successful curative treatment that may prevent the irreversible evolution of cardiopulmonary disease.
The DEFECT11 syndrome is a contiguous gene syndrome associated with deletions in the proximal part of chromosome 11p. In this study, we describe in an Italian family the co-existence of multiple exostoses (EXT) and enlarged parietal foramina (FPP), the two major symptoms of this syndrome, with abnormalities of the central nervous system. The latter may be a yet undescribed feature of DEFECT11 syndrome. FISH and molecular analysis allowed us to identify a small deletion on 11p11-p12, further refining the localisation of the FPP gene involved in the DEFECT11 syndrome.
We describe the clinical case and MRI findings of a patient with acquired immune deficiency syndrome and pathologically confirmed cytomegalovirus encephalitis. Prevalent brainstem and cerebellar signs together with almost exclusive involvement as seen on MRI of posterior fossa structures at the onset of the symptoms were the main features of our case.
We report the case of a 41 year-old woman with a slight mental retardation and epilepsy. MRI showed a diffuse subependymal heterotopia. The cognitive level supports the view that the ectopic cells are probably not important for the normal cortical functions but that they are likely able to maintain some of the electric properties of normal neurons, even if with altered discharge modalities. The genetic etiology of subependymal neuronal migration disorders is discussed. This is the second reported case of diffuse subependymal heterotopia in a female patient.
High signal in the globus pallidus on T1-weighted images was observed in two patients who underwent early MRI, after exposure to carbon monoxide (CO). We compare these MRI abnormalities with those previously reported, and with CT findings which suggested that the damage to the globi pallidi is of vascular origin. We discuss also the hypothesis that haemorrhagic infarction is an early manifestation of CO poisoning.
Cardiovascular disease is the major cause of death in patients with end-stage renal disease, and the incidence of atherosclerosis-related complications is significantly higher in dialysis patients than in nonuremic controls. This study aimed at evaluating atherosclerotic involvement of carotid vessels in hemodialysis patients and in a group of subjects with a similar cardiovascular risk factor pattern using echo color Doppler ultrasonography. Carotid lesions have been evaluated, taking into account plaque characters (surface, echogenicity), the most severe luminal narrowing, and the number of vessels involved. A large number of vascular plaques has been observed in uremic patients: 73.8% versus 44% in the control group (chi square test = 10.98; P < 0.01). A high prevalence of carotid lesions has been found in both patients and controls with clinical evidence of cardiovascular complications. Finally, we have considered the presence of carotid lesions with a topographic evaluation. The presence of atheromatous lesions in hemodialysis patients compared with control subjects was statistically significant different in all the vessels except common carotid (internal carotid: chi-square test = 8.59, P < 0.01; external carotid; chi-square test = 13.46, P < 0.01; bulb chi-square test = 7.90; P < 0.01). Our data clearly show that the hemodialysis population suffers from a higher degree of atherosclerosis than age- and sex-matched controls with similar cardiovascular risk patterns, suggesting that the uremic state in conservative and substitutive treatment per se may contribute to "advanced" atherosclerosis. However, this does not enable us to state that hemodialysis accelerates atherosclerosis. In fact, the progression of atherosclerosis might be related to atherogenic factors operative before regular dialysis.
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