Surgical treatment of small hepatocellular carcinomas in cirrhosis

Over the last five years a policy of systematic screening for small hepatocellular carcinomas (HCC) in patients at risk has led to an increasing number of resections in patients with cirrhosis. Remarkable progress in the surgery of HCC in cirrhosis has been accomplished through: (a) a better understanding of the surgical anatomy of the liver, (b) the definition of new types of liver resection aimed at reducing the amount of parenchyma removed while still being oncologically satisfactory, (c) the reduction of intraoperative blood loss by various techniques of clamping afferent and efferent vessels, (d) the systematic use of intraoperative ultrasonography, and (e) the prevention of postoperative variceal bleeding and the formation of ascites. Results of resection of small HCC in cirrhosis have been quite impressive in Japanese series, with a low operative mortality and above 50% three-year survivals. Results in the West have been somewhat less good. Differences in the pathology of these tumours and particularly in the rate of encapsulation could account for these differences. Clearly, surgical resection has become an established treatment for small HCC in cirrhosis. More information is needed on the results of surgery in operated patients and this should be compared with the natural history of small HCC in cirrhosis in order to better define the patients who will most benefit from these operations and which tests performed at which intervals, are most reliable in screening patients at risk.     

A "crackleware" oesophagus

This case report describes a 70 year old woman with excessive diffuse keratinisation of the oral cavity and oesophagus harbouring a squamous cell carcinoma. This excessive diffuse keratinisation of normally non-keratinised squamous epithelium could not be identified in normally non-keratinised epithelia in other parts of the body (the vagina), arguing against a genetic basis for this disorder. The term "crackleware" oesophagus was used to describe this entity, which has not been described previously in the English literature.     

Comparative genotyping of Campylobacter jejuni by amplified fragment length polymorphism,multilocus sequence typing,and short repeat sequencing: strain diversity,host range,and recombination

Three molecular typing methods were used to study the relationships among 184 Campylobacter strains isolated from humans, cattle, and chickens. All strains were genotyped by amplified fragment length polymorphism (AFLP) analysis, multilocus sequence typing (MLST), and sequence analysis of a genomic region with short tandem repeats designated clustered regularly interspaced short palindromic repeats (CRISPRs). MLST and AFLP analysis yielded more than 100 different profiles and patterns, respectively. These multiple-locus typing methods resulted in similar genetic clustering, indicating that both are useful in disclosing genetic relationships between Campylobacter jejuni isolates. Group separation analysis of the AFLP analysis and MLST data revealed an unexpected association between cattle and human strains, suggesting a common source of infection. Analysis of the polymorphic CRISPR region carrying short repeats allowed about two-thirds of the typeable strains to be distinguished, similar to AFLP analysis and MLST. The three methods proved to be equally powerful in identifying strains from outbreaks of human campylobacteriosis. Analysis of the MLST data showed that intra- and interspecies recombination occurs frequently and that the role of recombination in sequence variation is 50 times greater than that of mutation. Examination of strains cultured from cecum swabs revealed that individual chickens harbored multiple Campylobacter strain types and that some genotypes were found in more than one chicken. We conclude that typing of Campylobacter strains is useful for identification of outbreaks but is probably not useful for source tracing and global epidemiology because of carriage of strains of multiple types and an extremely high diversity of strains in animals.     

A gene for autosomal recessive limb-girdle muscular dystrophy maps to chromosome 2p

The limb-girdle muscular dystrophies are a clinically and geneticallyheterogeneous group of disorders. We have ostudied two largeinbred families of different ethnic origin and excluded linkageto LGMD2 on chromosome 15q and SCARMD on chromosome 13. Proceedingto a genomic linkage search, we have now identified linkageto markers D2S134 and D2S136 on chromosome 2p (maximum lod score3.57 at zero recombination). The phenotype in the two familieswas similar, with onset in the pelvic girdle musculature inthe late teens and usually relatively slow progression. Thiswork Identifies a second locus for autosomal recessive limb-girdlemuscular dystrophy.