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Gut Fermentation Syndrome also known
as Auto-Brewery Syndrome is a relatively unknown phenomenon in modern medicine.
Very few articles have been written on the syndrome and most of them are
anecdotal. This article presents a case study of a 61 years old male with a well documented case
of Gut Fermentation Syndrome verified with glucose and carbohydrate challenges.
Stool cultures demonstrated the causative organism as Saccharomyces cerevisiae. The patient was treated with antifungals
and a low carbohydrate diet and the syndrome resolved. Helicobacter pylori was also found and could have been a possible confounding variable
although the symptoms resolved post-treatment of the S. cerevisiae.
Several modes of eukaryotic of DNA double strand break
repair (DSBR) depend on synapsis of complementary DNA. The Rad51 ATPase, the S.
cerevisiae homolog of E. coli RecA, plays a key role in this process
by catalyzing homology searching and strand exchange between an invading DNA
strand and a repair template (e.g. sister chromatid or homologous chromosome).
Synthesis dependent strand annealing (SDSA), a mode of DSBR, requires Rad51.
Another repair enzyme, the Rad1-Rad10 endonuclease, acts in the final stages of
SDSA, hydrolyzing 3￠ overhanging
single-stranded DNA. Here we show in vivo by fluo-rescence microscopy that the ATP binding function of yeast Rad51 is required to recruit
Rad10 SDSA sites indicating that Rad51 pre-synaptic filament formation must
occur prior to the recruitment of Rad1-Rad10. Our data also show that Rad51 ATPase
activity, an important step in Rad51 filament disassembly, is not absolutely
required in order to recruit Rad1- Rad10 to DSB sites.
Hereditary diffuse gastric cancer is a rare, autosomal dominant hereditary cancer syndrome associated with germline mutations in CDH1 in which 60% - 80% of affected individuals develop advanced diffuse gastric cancer, many as young adults. At clinical presentation, ~90% of these malignancies represent advanced, surgically incurable disease. As such, presymptomatic identification of germline CDH1 mutation carriers followed by early prophylactic total gastrictomy is the sole effective management strategy available. DNA sequence analysis of the CDH1 gene to identify the affected germline allele is the diagnostic standard of care; however, CDH1’s relatively high frequency of polymorphisms and the limited amount of experience available regarding them dictate that many identified variants are, as yet, of unknown clinical significance. Given the dramatic consequences of inappropriately offered or withheld treatment, careful clinical selection of at-risk individuals is critical. To facilitate this, multiple groups have published screening criteria recommendations, and while there is disagreement regarding the optimal diagnostic approach, the most widely-used overlap to a considerable degree.