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Objective. Evaluation of neuronal changes in an animal experimental model of normocapnic hypoxia- reoxygenation. Materials and Methods. Fifty male piglets were the study subjects; normocapnic hypoxia was induced in 40 piglets and ten were shamoperated (controls). When bradycardia and/or severe hypotension occurred, reoxygenation was initiated. Animals were allocated in 4 groups according to the oxygen concentration, they were resuscitated with 18%, 21%, 40%, and 100% O2. Persisting asystole despite 10 minutes of cardiopulmonary resuscitation and return of spontaneous circulation were the endpoints of the experiment. Surviving animals were euthanized and brain cortex samples were collected, hematoxylin and eosin-stained, and examined for apoptotic bodies observing 10 consecutive high power fields. Results.Histological examination of the control group did not showany pathological change. On the contrary, apoptosis of neurons was found in 87.5% of treated animals. When specimens were examined according to the oxygen concentration used for resuscitation, we found marked intergroup variability; a higher percentage of apoptotic neurons was observed in piglets of group 4 (100% oxygen) compared to the others (P = 0.001). Conclusions. This preliminary data shows that normocapnic hypoxia and reoxygenation in Landrace/Large White piglets resulted in significant histological changes in the brain cortex. The degree of pathological changes in cortical neurons was significantly associated with the oxygen concentration used for reoxygenation, with a higher percentage of apoptotic neurons being observed in piglets reoxygenated with 100% compared to 18% O2 and to 21% O2. [ABSTRACT FROM AUTHOR]

Aim Papillary thyroid carcinoma (PTC) is the most common malignant tumour of the thyroid gland. The immunohistochemical profile of PTC is characterized by immunoreactivity of tumour cells for cytokeratins, thyroglobulin, vimentin, EMA and S100 protein. Recently, the presence of a serum protease inhibitor, alpha-1-antitrypsin (A1AT), has been demonstrated in tumour cells of PTC. The aim of our study was to test immunoreactivity of PTC for another inhibitor of proteases, alpha-1-antichymotrypsin (A1ACT). Methods and results Serial paraffin sections of nine consecutive cases of PTC were tested with anti-A1AT and anti-A1ACT antibodies. No immunoreactivity for A1AT and A1ACT was found in the normal thyroid tissue surrounding each tumour. In seven out of nine cases, tumour cells of PTC showed cytoplasmic immunoreactivity for A1ACT. In two cases, A1ACT was detected even in the nuclei. Immunoreactivity for A1AT was found only in three cases. Two cases of PTC showed no staining for both A1ACT and A1AT. No significant correlation of A1ACT staining was found with various prognostic indices (age of patients, histological pattern, tumour size, presence of regional lymph node metastases). The two cases showing a lack of staining for both A1ACT and A1AT showed a more aggressive clinical behaviour. Conclusions Our preliminary study shows that A1ACT is expressed by tumour cells in a large proportion of papillary carcinomas of the thyroid gland. Its significance remains, to the best of our knowledge, still unknown. The observation of a more aggressive behaviour in the two cases characterized by the absence of immunoreactivity for both A1ACT and A1AT suggests that the presence or absence of protease inhibitors could play a role in controlling tumour progression in PTC. [ABSTRACT FROM AUTHOR]

Aims: The histochemical demonstration of hepatic copper is important in the diagnosis of Wilson's disease (WD). Conflicting results have been published with regard to the ability of different histochemical methods to demonstrate copper storage in the liver. Therefore, we evaluated the diagnostic value of three available histochemical methods in a large series of patients affected by WD. Methods and results Seventy-nine consecutive liver needle biopsies, from 74 patients, 39 males and 35 females, aged 4–60 years (mean age 28.5 years) were stained with orcein, rhodanine and using Timm's method. On the basis of the histological picture, liver biopsies were subdivided into three groups: group A, steatosis; group B, interface hepatitis; group C, chronic hepatitis with bridging fibrosis and/or cirrhosis. In group A, 30.4% of the cases were positive using Timm's method, vs 13.2% using the rhodanine and 17.5% using the orcein method. In group B, Timm's method was positive in 40.1% while rhodanine and orcein showed positivity in 26.7%. In group C, the Timm's method stained 58.6%, rhodanine 36.6% and orcein 29.3% positively. Conclusions Our data show that: (1) Timm's silver stain is the most sensitive method for the demonstration of copper in all cases of WD; (2) rhodanine and orcein have minor value in the diagnosis of WD, especially in the early stages of the disease; (3) to increase the diagnostic value of histochemistry for copper multiple histochemical stains in serial sections are required; and (4) although hepatic copper concentration is highest in the early stages of WD, the histochemical demonstration fails in a large number of cases. [ABSTRACT FROM AUTHOR]

A histological and ultrastructural study, coupled with transmission and scanning electron microscopy of the early changes in the liver following a single administration of cycloheximide (CHX), was carried out in male Wistar rats. At the histological level, apoptosis was already present in the liver 2 h after treatment. By scanning electron microscopy, the following sequential changes were observed: brightness and progressive detachment of hepatocytes from neighbouring cells, formation of surface infolds with multiple blebs and, finally, release of several membrane-bounded apoptotic bodies (ABs) in the extracellular space and into the sinusoidal lumen. Three hours after CHX administration, the apoptotic cycle was completed, as shown by the presence of phagocytosed ABs inside the cytoplasm of intact liver cells. Light microscopic examination of the liver 6 h after CHX administration showed ABs mainly located in the cytoplasm of intact hepatocytes and inside activated Kupffer cells. By transmission electron microscopy, it was possible to demonstrate that cells undergoing apoptosis were hepatocytes. At 24 h, the livers of treated animals appeared normal, with no evidence of apoptosis. [ABSTRACT FROM AUTHOR]

Recent observations on a correlation between fetal serum ferritin and gestational age, consistent with an increase in fetal iron stores during pregnancy, led us to study liver iron content in 22 human stillborns, newborns and infants of different gestational and postnatal age. At autopsy, a longitudinal liver slice was subdivided into ten blocks. Each sample was analyzed for iron content by atomic absorption spectroscopy. The mean iron concentration in the studied livers was 21.6 μM/g dry tissue (d.t.). A striking interindividual variability in iron content was observed: the hepatic concentration of the metal ranged from 3.3 to 64.4μM/g d.t. No correlation was found between the hepatic iron concentration and gestational age or other clinical parameters of the patients studied. Moreover, the total storage iron of the liver did not appear to be correlated with the gestational age. The analysis of iron concentration in ten blocks in each liver revealed an irregular distribution of the metal. Lobar differences were observed, with a tendency of the left lobe to accumulate more iron than the right one. Furthermore, striking differences in iron content were found between adjacent liver samples, ranging in one instance from 4.5 up to 109.0 μM/g of dry tissue. Perls' stain for iron was positive in 7 out of the 22 livers examined, showing an irregular acinar distribution, with preferential periportal localization. Our data show that the newborn liver can be considered an interesting model for the study of iron storage. The observed uneven distribution of the metal, even in the absence of fibrosis normally associated with iron storage in adults, casts doubt on the interpretation of iron concentration of a small liver sample as representative of the mean hepatic iron concentration. [ABSTRACT FROM AUTHOR]

Presents a clinical case of massive hepatic haemosiderosis in Wilson's disease. Presenting signs and symptoms; Results of diagnostic examinations; Disease characterization.

An abstract of the conference paper "Extrauterine undifferentiated endometrioid stromal sarcoma arising in endometriosis of the rectovaginal septum of a postmenopausal patient with recent onset of pelvic pain," by S. Guerriero and colleagues is presented.

Reports issued related to histopathology. Incidence of massive hemosiderosis in wilson's disease; Use of flatbed scanner to create digital images of pathology specimens; Assessment of multicentric breast carcinoma.

Background: The histological hallmark of alpha-1-antitrypsin deficiency (AATD) is the presence of periodic acid-Schiff diastase (PASD)-resistant positive globules in hepatocytes, with a heterogeneous distribution. It is noteworthy that hepatocellular carcinoma (HCC) arises specifically from the AAT-negative areas but the reason for this remains unclear., Aim: To determine whether the different distribution of AAT globules within neoplastic and non-neoplastic hepatocytes is the result of a self-induced correction of the genetic defect., Patients and Methods: Two HCV-positive patients with AATD-associated HCC were studied. One patient harboured a compound heterozygous PiSZ genotype whereas the other showed the rarer PiMMmalton in heterozygosity. In both cases, neoplastic hepatocytes appeared globule devoid, while non-neoplastic hepatocytes showed intracytoplasmic accumulation of PASD-positive globules. Laser-assisted microdissection was used to assess a genotype/phenotype correlation in single liver cells from HCC and from non-neoplastic hepatocytes., Results: Direct sequencing of DNA purified from globule-devoid and globule-filled hepatocytes demonstrated that all liver cells carried the same mutant genetic background., Conclusion: Our findings indicate that (i) both variants of HCC arising in AAT deficiency (Z and Mmalton) do not accumulate the mutant protein and (ii) the different phenotypic appearance of hepatocytes is not the result of a retromutation during neoplastic transformation, but other mechanisms should be investigated.