Cystic precursors to invasive pancreatic cancer

Improvements in the sensitivity and quality of cross-sectional imaging have led to increasing numbers of patients being diagnosed with cystic lesions of the pancreas. In parallel, clinical, radiological, pathological and molecular studies have improved the systems for classifying these cysts. Patients with asymptomatic serous cystic neoplasms can be managed conservatively with regular monitoring; however, the clinical management of patients with intraductal papillary mucinous neoplasms and mucinous cystic neoplasms is far more challenging, as it is difficult to determine whether these lesions will progress to malignancy. Fortunately, prospective studies have helped to establish that proposed clinical and radiological criteria (the Sendai guidelines) can be used to guide the care of patients with cystic lesions of the pancreas. Despite this progress in imaging and clinical guidelines, sensitive and specific tests have not yet been developed that can reliably predict the histology and biological properties of a cystic lesion. Such biomarkers are urgently needed, as noninvasive precursors of pancreatic cancer are curable, while the vast majority of invasive pancreatic adenocarcinomas are not.     

Two subjects, each with a brain lesion and each prone to criminal behaviour: a plea for the involvement of a behavioural neurologist in the forensic psychiatric evaluation of such cases

Interest in the neurobiology of criminal behaviour is increasing. Recent research emphasises the important role played by the frontal lobe in the processing of emotional and social information and in the controlling of behaviour. Damage to specific frontal structures in the brain may therefore lead to antisocial and criminal behaviour. On the basis of the case histories of two suspects with brain lesions, the impact of such damage on the forensic psychiatric diagnosis is discussed. A plea is made for the more frequent involvement of a neurologist in the diagnostic evaluation usually undertaken by the forensic psychiatrist.     

A cellular model for the investigation of Fuchs' endothelial corneal dystrophy

Fuchs' Endothelial Corneal Dystrophy is the most common corneal endotheliopathy, and a leading indication for corneal transplantation in the US. Relatively little is known about its underlying pathology. We created a cellular model of the disease focusing on collagen VIII alpha 2 (COL8A2), a collagen which is normally present in the cornea, but which is found in abnormal amounts and distribution in both early and late-onset forms of the disease. We performed cellular transfections using COL8A2 cDNAs including both wild-type and mutant alleles which are known to result in early-onset FECD. We used this cell model to explore the cellular production of wild-type and mutant monomeric and trimeric collagen VIII and measured production levels and patterns using Western blotting and immunofluorescence. We studied the thermal stability of the mutated collagen VIII helices using computer modeling, and further investigated these differences using collagen mimetic peptides. The Western blots demonstrated that similar amounts of wild-type and mutant collagen VIII monomers were produced in the cells. However, the levels of trimeric collagen peptide in the mutant-transfected cells were elevated. Intracellular accumulation of trimeric collagen VIII was confirmed on immunofluorescence studies. Both the computer model and the collagen mimetic peptides demonstrated that the L450W mutant was less thermally stable than either the Q455K or wild-type collagen VIII. Thus, although both mutant collagen VIII peptides were retained intracellularly, the biochemical reasons for the retention varied between genotypes. Collagen VIII mutations, which clinically result in Fuchs' Dystrophy, are associated with abnormal cellular accumulation of collagen VIII. Different collagen VIII mutations may act via distinct biochemical mechanisms to produce the FECD phenotype.     

血小板血浆对人牙髓细胞增殖的影响

目的：观察血小板血浆及其细化成分对人牙髓细胞增殖的影响。方法：使用因正畸而拔除的人牙的牙髓细胞，用细胞定量测定试剂盒测定细胞增殖情况。结果：5％的多血小板血浆（platelet-rich plasma，PRP）、5％和10％的洗净血小板（washed platelet，WPLT）均明显地促进了人牙髓细胞的增殖，而且WPLT的作用较PRP更显著。乏血小板血浆（platelet-poor plasma，PPP）呈浓度依赖性地抑制了人牙髓细胞增殖，5％WPLT促进人牙髓细胞增殖的作用。结论：去除血浆成分的WPLT对培养的人牙髓细胞增殖有明显的促进作用；血浆中可能存在对抗血小板生长因子作用的因子。     

Regulation of primary Strongyloides ratti infections in mice: a role for interleukin-5.

C57BL/6 mice genetically deficient in interleukin-5 (IL-5-/-) and normal C57BL/6 (IL-5+/+) mice were infected with larvae of a homogonic strain of the nematode Strongyloides ratti. In primary infections both male and female IL-5-/- mice released two to four times more eggs and larvae than IL-5+/+ mice. IL-5-/- mice harboured about 60% more intestinal worms, which were more fecund, than IL-5+/+ mice. The duration of the infection was similar in normal and IL-5-deficient mice. Both IL-5-/- and IL-5+/+ mice resisted a secondary infection. IL5-/- mice lost more weight during the infection than normal mice and took longer to regain their initial weight after expelling the worms. The number of eosinophils increased in the bone marrow, peritoneal cavity and small intestine of IL-5+/+ mice, but not IL-5-/- mice, following infection. No significant differences between infected IL-5+/+ and IL-5-/- mice in mast cells or other leucocytes were observed in the peritoneal cavity. Thus, IL-5 functions to protect the host in a primary infection of S. ratti by limiting the number and fecundity of worms establishing in the small intestine. This protection is correlated with elevated blood and tissue eosinophilia which occurs in normal mice but not in IL-5-/- mice.     

Serum cholesterol and high density lipoprotein cholesterol distributions in patients with acute myocardial infarction and in the general population of Kuopio Province,Eastern Finland

Abstract. As part of the FINMONICA project, serum total cholesterol (TC) and high density lipoprotein cholesterol (HDLC) concentrations were determined in 1216 AMI patients (937 men. 279 women) aged 35–64 years in the province of Kuopio in eastern Finland during the 5-year period 1983–87. The distributions were compared with the corresponding distributions in a representative sample of the general population of the same area (1026 men, 1021 women). The mean serum TC levels did not differ between the AMI patients and the normal population. Only the prevalence of a very high serum TC level (> 8.0 mmol l^?1) among women was significantly higher in the AMI group than in the population sample. On the other hand, in both sexes the age-adjusted mean HDLC was significantly lower in the AMI group than in the population sample. Our findings emphasize the importance of HDLC measurement as a part of the assessment of the lipid risk factor profile in patients with AMI.