The S-layer proteins of Tannerella forsythia are secreted via a type IX secretion system that is decoupled from protein O-glycosylation.

Conserved C-terminal domains (CTD) have been shown to act as a signal for the translocation of certain proteins across the outer membrane of Bacteroidetes via a type IX secretion system (T9SS). The genome sequence of the periodontal pathogen Tannerella forsythia predicts the presence of the components for a T9SS in conjunction with a suite of CTD proteins. T. forsythia is covered with a two-dimensional crystalline surface (S-) layer composed of the glycosylated CTD proteins TfsA and TfsB. To investigate, if T9SS is functional in T. forsythia, T9SS-deficient mutants were generated by targeting either TF0955 (putative C-terminal signal peptidase) or TF2327 (PorK ortholog), and the mutants were analyzed with respect to secretion, assembly and glycosylation of the S-layer proteins as well as proteolytic processing of the CTD and biofilm formation. In either mutant, TfsA and TfsB were incapable of translocation, as evidenced by the absence of the S-layer in transmission electron microscopy of ultrathin-sectioned bacterial cells. Despite being entrapped within the periplasm, mass spectrometry analysis revealed that the S-layer proteins were modified with the complete, mature glycan found on the secreted proteins, indicating that protein translocation and glycosylation are two independent processes. Further, the T9SS mutants showed a denser biofilm with fewer voids compared with the wild-type. This study demonstrates the functionality of T9SS and the requirement of CTD for the outer membrane passage of extracellular proteins in T. forsythia, exemplified by the two S-layer proteins. In addition, T9SS protein translocation is decoupled from O-glycan attachment in T. forsythia.

Esophageal motor function in laryngopharyngeal reflux is superior to that in classic gastroesophageal reflux disease.

Laryngopharyngeal reflux (LPR) in otolaryngology patients appears to be different from classic gastroesophageal reflux disease (GERD). In particular, esophagitis and its principal symptom, heartburn, considered the diagnostic sine qua non of GERD, are often absent in LPR. It has therefore been postulated that LPR patients have superior esophageal function. Esophageal acid clearance (EAC) is a measure of the ability of the esophagus to restore neutral pH after reflux events have occurred. It is considered an excellent overall measure of esophageal function. The mean EAC can be calculated from 24-hour pH monitoring data. A comparison of EAC in patients with GERD and LPR has not been previously reported. To compare the EAC of 1) patients with LPR alone, 2) patients with GERD alone, 3) patients with both LPR and GERD, and 4) patients without either LPR or GERD, we studied 200 otolaryngological patients who had undergone 24-hour double-probe (simultaneous pharyngeal and distal esophageal) pH monitoring, 50 in each group. The subgrouping of each patient was determined by previously established pH monitoring criteria. We defined GERD as abnormal esophageal reflux and LPR as abnormal pharyngeal reflux. The patients with GERD had a mean (+/-SD) EAC of 1.44 +/- 1.2 minutes, and those with LPR had a mean EAC of 1.00 +/- 1.00 minutes (p < .05). The patients with both GERD and LPR had a mean EAC of 1.53 +/- 1.01 minutes. The patients without reflux had a mean EAC of 0.53 +/- 0.38 minutes. We conclude that patients with LPR have significantly better EAC than those with GERD. These data suggest that patients with LPR have superior esophageal function. This finding may clarify our understanding of the differences in mechanisms, symptoms, and incidence of esophagitis in patients with LPR and GERD.

Localization of a gene for otosclerosis to chromosome 15q25-q26.

Among white adults otosclerosis is the single most common cause of hearing impairment. Although the genetics of this disease are controversial, the majority of studies indicate autosomal dominant inheritance with reduced penetrance. We studied a large multi-generational family in which otosclerosis has been inherited in an autosomal dominant pattern. Five of16 affected persons have surgically confirmed otosclerosis; the remaining nine have a conductive hearing loss but have not undergone corrective surgery. To locate the disease-causing gene we completed genetic linkage analysis using short tandem repeat polymorphisms (STRPs) distributed over the entire genome. Multipoint linkage analysis showed that only one genomic region, on chromosome 15q, generated a lod score >2.0. Additional STRPs were typed in this area, resulting in a lod score of 3.4. STRPs FES (centromeric) and D15S657 (telomeric) flank the 14. 5 cM region that contains an otosclerosis gene.

A novel locus for autosomal dominant nonsyndromic hearing loss, DFNA13, maps to chromosome 6p.

Nonsyndromic hearing loss (NSHL) is the most common type of hearing impairment in the elderly. Environmental and hereditary factors play an etiologic role, although the relative contribution of each is unknown. To date, 39 NSHL genes have been localized. Twelve produce autosomal dominant hearing loss, most frequently postlingual in onset and progressive in nature. We have ascertained a large, multigenerational family in which a gene for autosomal dominant NSHL is segregating. Affected individuals experience progressive hearing loss beginning in the 2d-4th decades, eventually making the use of amplification mandatory. A novel locus, DFNA13, was identified on chromosome 6p; the disease gene maps to a 4-cM interval flanked by D6S1663 and D6S1691, with a maximum two-point LOD score of 6.409 at D6S299.

[Hospital productivity and methods of evaluating utilization of beds]. / Produktivita nemocnice a metodika hodnocení vyuzití luzkového fondu.

The authors define the hospital (or departmental) productivity the criteria of which are the use of the hospital capacity: the average length of stay, the occupancy ratio, the turnover interval and the turnover. The authors describe the construction of a nomogram for the graphic evaluation of the position of all four indicators. They submit a formula for calculation of the global "index of hospital productivity". They consider the possibility to increase hospital productivity in particular by reducing the length of stay and turnover interval. They draw attention to the influence of external circumstances on hospitalization and the necessity to evaluate indicators of productivity in association with efficiency, effectivity and quality of hospital care.