The influence of dietary nitrogen reduction and conjugated linoleic acid supply to dairy cows on fatty acids in milk and their transfer to ripened cheese.

The aim of this study was to investigate the consequences of reducing the dietary crude protein content, with or without a supply of protected conjugated linoleic acid (CLA), on the milk fatty acid (FA) yield and recovery in 90d ripened cheese. Twenty mid-lactation Friesian dairy cows were reared for 4 periods of 3wk each in groups of 5, following a 4×4 Latin square design. Cows were fed 4 different rations, consisting of a combination of the 2 dietary crude protein levels [150 (CP15) or 123 (CP12) g of crude protein/kg of dry matter], with or without a conjugated linoleic acid supply (80g/d, providing 5.57 and 5.40g/d of C18:2 cis-9,trans-11 and C18:2 trans-10,cis-12, respectively). Milk yield was recorded. Twice in each period, milk samples were analyzed for protein, fat, and lactose content, and 10 L milk samples (pooled by group) were processed to produce 96 cheeses, which were ripened for 90d. Milk and cheese fat were analyzed for their FA profiles. Milk and cheese FA were expressed as daily yields and relative proportions, and nutrient recoveries were computed. Dietary crude protein reduction had small or no effects on the yield and relative presence of FA in milk and cheese, except for a small increase in mid-chain branched saturated fatty acids. The CLA supply strongly reduced the yield of various categories of FA, and had major effects on short-chain FA of de novo synthesis, leading to changes in the relative proportions of the various FA in milk and cheese. The addition of CLA tended to reduce uniformly the recovery of all milk constituents and of short-, medium-, and long-chain FA groups, but we observed large differences among individual FA with apparent recoveries ranging between 640 and 1,710g/kg. The highest recoveries were found for polyunsaturated long-chain FA, the lowest for saturated or monounsaturated short- or medium-chain FA. A notable rearrangement of these FA components, particularly the minor ones, took place during ripening.

Clinical reactivation during lamivudine treatment correlates with mutations in the precore/core promoter and polymerase regions of hepatitis B virus in patients with anti-hepatitis B e-positive chronic hepatitis.

BACKGROUND: Drug-resistant mutants may emerge in patients with chronic hepatitis B receiving lamivudine therapy. AIM: To evaluate whether different viral mutational patterns may be associated with clinical reactivation during lamivudine treatment in patients with chronic B hepatitis. METHODS: Eight anti-hepatitis B e-positive patients with (group A) and 14 patients without clinical exacerbation (five anti-hepatitis B e-positive, group B1; nine hepatitis B e antigen-positive, group B2) during lamivudine treatment were investigated. RESULTS: 'Polymerase region': M204V/I variants were found in all group A patients, but in none of group B1 (P=0.0007) and in four of nine of group B2 (44%; P=0.02) patients. The L180M substitution was detected in four of eight (50%) of group A and in none of groups B1 and B2. 'Core promoter': the double basic core promoter (A1762T/G1764A) variant was detected in seven of eight (87%) of group A and in one of five (20%; P=0.03) of group B1 and one of nine (11%; P=0.002) of group B2 patients. 'Precore': the G1896A stop codon mutation was present in seven of eight (87%) of group A and in zero of five (P=0.004) of group B1 and one of nine (11%; P=0.002) of group B2. CONCLUSIONS: Different mutational patterns were observed in the lamivudine-treated patients with and without exacerbation. There was an association of the basic core promoter and stop codon mutations with lamivudine resistance in patients with disease exacerbation.

[Femoral and humeral head osteonecrosis in a patient with hypofibrinolysis and hyperhomocysteinemia. A case report and a review of the literature]. / Osteonecrosi delle teste femorali ed omerali in un paziente con ipofibrinolisi e iperomocisteinemia. Descrizione del caso e revisione della letteratura.

Osteonecrosis is a disease characterized by the death of marrow and bone tissues. All bones may be affected, most commonly those of the hip, knee, shoulder, ankle as well as the small bones of the hands and feet. When the disease involves a weight-bearing joint there is a significant risk that subarticular fracture may develop leading to disabling arthrosis and requiring, therefore, arthroplasty surgery. Osteonecrosis typically affects patients in their third, fourth and fifth decades of life and is associated with many factors including other diseases and co-morbidities. Multifocal osteonecrosis is defined according to the involvement of at least three separated anatomic sites. We describe the case of a young man with osteonecrosis of the shoulder and hip joints which required total arthroplasty. Among biochemical investigations, an increase in the plasminogen activator inhibitor type 1 (PAI-1) levels associated with mild hyperhomocysteinemia was present. Another finding was the HLA B27, without signs of spondyloarthropathies. In patients with osteonecrosis, especially if multifocal, a careful medical history, a complete physical examination and some biochemical investigations, particularly those related to thrombophilia and hypofibrinolysis, should be performed.

A full scale application in the control of the filamentous bulking generated by Type 021 N F. thiothrix sp.

The presence of industrial effluent in the wastewater incoming to municipal activated sludge treatment plants sometimes causes bulking events. In order to control one of these events a strategy of bacterial selection was applied with an anoxic selector before the main oxidation basin utilising the screw pumps basin. The result of this work confirms what is reported in the literature about the possibility to utilize a metabolic control of some filamentous forms (particularly Type 021 N) with high organic load. The remedial action could be realized using already existing facilities, without any additional costs.

Hepatic fibrosis plays a central role in the pathogenesis of thrombocytopenia in patients with chronic viral hepatitis.

The pathogenesis of thrombocytopenia in chronic hepatitis is not well known. This study evaluated the relationship between liver injury, serum thrombopoietin, splenomegaly and thrombocytopenia in chronic viral hepatitis. Two hundred and nine patients were enrolled, 85 with splenomegaly and 124 without. Thrombocytopenia was present in 71% and 23% of patients with or without splenomegaly respectively. In subjects with low platelet count, those with splenomegaly showed significantly lower platelet numbers than those without splenomegaly. The spleen size correlated with portal hypertension. An inverse correlation between spleen size and platelet count was observed (r = -0.54; P < 0.0001). In patients without splenomegaly, thrombocytopenia was associated with the grade of fibrosis; platelet counts were the highest in patients with fibrosis 0-2, lower in those with grade 3 (P < 0.008) and lowest in those with grade 4 (P < 0.05). These findings were independent of demographic and biochemical characteristics, hepatic necroinflammatory activity, portal hypertension and splenomegaly. Patients with normal platelet counts showed higher thrombopoietin levels than those with low platelet counts (P < 0.0001). An inverse correlation between thrombopoietin levels and fibrosis grade was observed (r = - 0.50; P < 0.0001). Median thrombopoietin levels were 58 and 27 pg/ml for fibrosis grade 0-1 and grade 4 respectively (P < 0.001). These data indicate that advanced hepatic fibrosis, causing an altered production of thrombopoietin and portal hypertension, plays the central role in the pathogenesis of thrombocytopenia in chronic viral hepatitis.

Thrombosis of the subclavian vein in SAPHO syndrome. A case-report.

The hallmark of SAPHO Syndrome (Synovitis, Acne, Pustulosis, Hyperostosis, Osteitis) is osteitis of the anterior chest wall, which can be so pronounced as to cause thoracic outlet syndrome, thrombosis of the subclavian vein, and compression of the superior vena cava. Suggestive skin manifestations, namely palmoplantar pustulosis and severe acne, generally antedate the bone and joint lesions. We report a case of SAPHO syndrome that went unrecognized for many years and eventually caused compression and thrombosis of the right subclavian vein requiring cleidectomy. SAPHO syndrome should be considered in every patients with anterior chest wall inflammation, particularly when skin lesions are also present.

[Paget's disease of bone associated with autoimmune thyroiditis and joint chondrocalcinosis]. / Maladie osseuse de Paget associée à une thyroïdite auto-immune et à une chondrocalcinose articulaire.

A case of scapular Paget's disease of bone with concurrent autoimmune thyroiditis and articular chondrocalcinosis is reported. Although infrequent, this combination suggests the involvement of common pathogenic mechanisms: thyroiditis and Paget's disease may stem from the same viral infection and/or autoimmune disorder, whereas chondrocalcinosis may be the consequence of thyroiditis-related hypothyroidism. In contrast, the association of Paget's disease and chondrocalcinosis may be fortuitous, since both disorders are common.

Interrelationships between interleukin (IL)-1, IL-6 and IL-8 in synovial fluid of various arthropathies.

High levels of many cytokines, including interleukin (IL)-1, IL-6 and IL-8, were found in various arthropathies suggesting that they play a role in the pathogenesis of disease, although their relationship with the type and activity of disease is still not clear. The synovial fluid (SF) of 24 patients with rheumatoid arthritis (RA), 19 with psoriatic arthritis (PA) and 33 with osteoarthritis (OA) was analyzed for IL-1 beta, IL-6 and IL-8. The highest concentration of the three cytokines was found in the SF of RA. IL-beta detectable levels (> or = 20 pg/ml) were observed in 8/24 (33.3%) patients with RA, in one patient with PA but in no patient with OA. IL-6 (mean +/- SD) (1610.37 +/- 1781.65 pg/ml) was higher in RA than in PA (672.47 +/- 867.40 pg/ml, p = 0.043) and OA (89.45 +/- 120.52 pg/ml, p = 0.0001). IL-8 (1042.72 +/- 698.64 pg/ml) was higher in RA than in PA (660.36 +/- 625.11 pg/ml, p = 0.03) and OA (89.9 +/- 45.88 pg/ml, p = 0.0001). A correlation between IL-1 beta, IL-6 and IL-8 was found in RA. In all patients a correlation between IL-6 and IL-8 levels was found; moreover, these two cytokines were associated with SF indices of inflammation, such as white blood cells (WBC) count and total protein (TP) concentration. Our findings suggest that these interrelationships play a role in the evolution of more severe erosive arthropathy such as RA.

Effect of prednisone priming followed by alfa-interferon in treatment of children with chronic hepatitis B: an interim analysis of a controlled trial.

A six-month analysis of a controlled trial on the treatment of chronic hepatitis B in children shows that prednisone priming followed by alpha-interferon 2A was effective in 6 of 9 treated patients in reducing HBV replication and disease activity.

Prolonged treatment of children with chronic hepatitis B with recombinant alpha 2a-interferon: a controlled, randomized study.

A prospective study was conducted to evaluate the efficacy and tolerance of alpha-interferon in 20 children with biopsy-proven HBsAg/HBeAg/HBV-DNA-positive, anti-delta-negative chronic hepatitis. Patients were randomized to receive alpha 2a-interferon (INF), 3 MU im three times weekly for 12 months, or no treatment (10 patients per group). Five patients receiving IFN showed a marked decrease or negativization of HBV-DNA during treatment. At the end of the study (after 18 month), three patients lost HBV-DNA permanently, and two of them seroconverted to HBeAb 10 and 11 months after disappearance of HBV-DNA with normalization of aminotransferase values. In the control group, one patient had spontaneous clearance of HBV-DNA with conversion to HBeAb and normalization of aminotransferase levels. All treated patients had a febrile reaction in the first month of treatment. The dose of IFN had to be decreased in two patients and was discontinued for persistent intolerance in one of them. Patients who showed a decreased viral replication had higher initial biochemical and histological activity than nonresponders. The data suggest that IFN treatment may favorably influence the progression of chronic B hepatitis in children with a history of acute hepatitis and active chronic disease.

Progressive myoclonic encephalopathy in X-linked hypogamma-globulinemia. Case report, review of the literature and its relationship with progressive encephalopathy in children with A.I.D.S.

A 7-year-old boy suffering from X-linked hypogammaglobulinemia and progressive myoclonic encephalopathy is reported. The onset of neurological disturbances is at four years of age with ataxic gait and myoclonic jerks. The EEG shows a progressive slowing of background activity, bilateral diffuse and repetitive, pseudoperiodic, high amplitude slow waves, myoclonic jerks polygraphically documented. The CT-scan shows generalized cerebral atrophy, white matter hypodensity--principally in the frontal regions -, multiple nodular calcifications, also in the basal ganglia. Two years after the onset of neurological signs, the boy is completely bedridden, spastic, dement and blind; the myoclonic jerks persist. Finally the relationship is discussed with both the previously reported patients with the same affection, and with similar progressive encephalopathy in children suffering from A.I.D.S.

Thoracic complications of pancreatitis.

Pancreatitis may be associated with thoracic complications, notably chronic massive pleural effusion (CMPE) and, rarely, pseudocysts with mediastinal extension (PME) and enzymatic mediastinitis (EM). Our personal experience with 14 cases of thoracic complications (nine CMPE, two PME associated with pleural effusion, and three EM of 670 patients who underwent surgery; of these, 191 had acute and 479 had chronic pancreatitis) during 16 years (1970-1986) is reported. In the patients with CMPE, the initial symptoms were progressive dyspnea eventually associated with cough and chest pain. In the PME cases, there was dysphagia associated with left subscapular pain and left chest pain. The initial signs in the patients with EM were sudden dyspnea, cyanosis, retrosternal pain, tachycardia, and acute heart failure. A fistula between the pancreatic ductal system and the pleural cavity in seven of the nine patients with CMPE was demonstrated by intraoperative pancreatography and/or cystography. On the contrary, preoperative endoscopic pancreatography demonstrated the sinus tract in only three of the seven. In both cases of PME, computed tomography (CT) provided a correct diagnosis that was confirmed at surgery. In the patients with EM, the diagnosis was suggested by the clinical appearance and was confirmed by the chest roentgenogram and by CT. All patients had operations after varying periods of unsuccessful 2-4-week-long conservative treatment. One patient with infected ascites died postoperatively. There were no thoracic recurrences of pancreatic disease among the other patients at a 10-month-10-year follow-up observation after surgery.

Kojewnikow's Epilepsia Partialis Continua: two cases associated with striatal necrosis.

The authors report two cases of children suffering from Epilepsia Partialis Continua (EPC). The first case concerned a boy primarily affected by abdominal neuroblastoma and secondarily by bilateral EPC; "pallidal posture" was the prominent clinical feature. An acute measles encephalitis was diagnosed and the CT scan showed necrosis of the putamina. The second case concerned a girl suffering from increased intracranial pressure due to suprasellar craniopharyngioma. Seven days after intervention, Diabetes Insipidus and EPC appeared. Enlargement of rolandic and sylvian spaces and lacunar necrosis of the putamen on the left side were also evident on the CT scan. The authors emphasize the significance of occasional metabolic disturbances, especially natremia, in the development of EPC.

Liver disease in hemophiliacs: etiological and biochemical data on 159 cases from our geographical area.

A total of 159 hemophiliacs (149 treated) from our geographical area were screened in 1983 for serological evidence of HBV infection and biochemical evidence of liver disease. All were asymptomatic. HBsAg was detected in 16 cases (10%); anti-HBs and anti-HBc in 106 (67%); 19 (12%) subjects were susceptible to HBV. The HBV infection rate evaluated in 70 patients followed-up from 1980 to 1983 was 28% per year. The cumulative risk of HBV infection as well as the rate of seroconversion to HBV increased with increasing age and with increasing frequency of treatment given during the last 12 months. Anti-delta was detected in the serum of 5 (28%) out of 13 HBsAg-positive cases. Follow-up data showed that in 61% of subjects with liver dysfunction, hepatic damage could not be accounted for by HBV infection. AST and/or gamma-globulin increase was detected in 80% of patients. Abnormalities were more pronounced in HBsAg-positive cases and among them in subjects carrying anti-delta. Further follow-up studies are needed to clarify the long-term prognosis of liver disease in hemophiliacs.