Penile rehabilitation following treatment for prostate cancer: an analysis of the current state of the art

Despite recent advances in surgical technique using laparoscopic and robotic approaches for the management of early organ-confined prostate cancer, most contemporary reports demonstrate significant rates of erectile dysfunction comparable to standard open approaches. Controversy remains related to many of the pre-and postoperative management strategies, including agents to enhance nerve recovery, erectogenic drugs, antioxidants, vasoactive injectables, vacuum erection devices and nerve grafting procedures. Additionally, the optimal timing of these interventions and their duration, dose, frequency and outcome thresholds remain ill-defined. In our paper, we provide a comprehensive literature review involving both the basic and clinical data surrounding rehabilitative approaches.     

Usefulness of erythrocyte protoporphyrin as a primary screening test for lead exposure in children

Erythrocyte protoporphyrin and blood lead concentrations were measured in samples from 583 Saudi children attending the outpatient clinics. Erythrocyte protoporphyrin concentrations showed poor correlation with blood lead concentrations of 25 ug dl^?1 and below. Measurement of erythrocyte protoporphyrin as a primary test for lead exposure is not recommended.     

Guillain-barré syndrome: A series observed at riyadh armed forces hospital january 1984–January 1994

A consecutive series of 47 hospitalized cases of Guillain-Barré syndrome seen over a 10-year period was analysed with respect to: (1) age and sex; (2) antecedent events and seasonal distribution; (3) patterns of clinical presentation; (4) CSF and neurophysiological findings; (5) results of treatment with plasma exchange; and (6) outcome. Twenty-two were children, 20 middle-aged and 5 aged; 37 were male and 10 were female. The most frequent antecedent event was upper respiratory tract infections; a seasonal peak incidence was found in winter. Clinical, CSF and neurophysiological findings concurred with those in the Western literature; 79% of the cases were severe. Plasma exchange performed within the first 2 weeks of onset benefitted in the short-term outcome, i.e. improvement by 1 grade at 4 weeks, but the long-term benefit, i.e. the ability to regain independent locomotion, was questionable. Plasma exchange helped in curtailing the time to walking unaided but had no benefit on the duration of artificial ventilation. Factors associated with an adverse outcome were: age over 15 years, severity of motor electrodiagnostic findings (especially a decreased distal CMAP amplitude and EMG signs of acute denervation), requirement for ventilation and slow progression (>3 weeks) to maximum deficit. After a mean follow-up of 11 months, 55% of the patients regained independent locomotion, which is a comparatively low proportion.     

Cross-linking of surface IgM or IgD causes differential biological effects in spite of overlap in tyrosine (de)phosphorylation profile.

Although displaying similar amounts of surface IgM and IgD, ECH 408-1 cells only succumb to apoptosis after cross-linking of IgM (not IgD), suggesting that different signaling pathways couple to both receptors. Immunoprecipitation studies revealed the presence of several proteins selectively associated with IgM and IgD, thus ruling out that the lack of inhibitory signaling mediated by IgD might be due to membrane expression in the absence of associated proteins belonging to the B cell receptor complex. 32P metabolic labeling and immunoprecipitation studies demonstrated that IgM and IgD are associated with phosphoproteins of 32-33 kDa in an isotype-specific fashion. Kinetic analyses of tyrosine kinase activity showed that cross-linking of surface IgM or IgD resulted in the rapid (1-3 min) phosphorylation of several protein substrates on tyrosine residues, followed by a dephosphorylation step. Isotype-specific changes of the phosphorylation status specifically affected molecules in the 32-33 kDa range, i.e. IgM (not IgD) cross-linking affected a approximately 32-kDa protein, whereas IgD (not IgM) cross-linking induced phosphorylation of a protein exhibiting a slightly lower mobility (33 kDa). These results suggest that isotype-specific immunoglobulin-associated molecules could be involved in the second messenger cascade leading to different biological effects upon IgM and IgD cross-linking.     

Cenani–Lenz syndrome and other related syndactyly disorders due to variants in LRP4, GREM1/FMN1, and APC: Insight into the pathogenesis and the relationship to polyposis through the WNT and BMP antagonistic pathways

Cenani–Lenz (C–L) syndrome is characterized by oligosyndactyly, metacarpal synostosis, phalangeal disorganization, and other variable facial and systemic features. Most cases are caused by homozygous and compound heterozygous missense and splice mutations of the LRP4 gene. Currently, the syndrome carries one OMIM number (212780). However, C–L syndrome‐like phenotypes as well as other syndactyly disorders with or without metacarpal synostosis/phalangeal disorganization are also known to be associated with specific LRP4 mutations, adenomatous polyposis coli (APC) truncating mutations, genomic rearrangements of the GREM1‐FMN1 locus, as well as FMN1 mutations. Surprisingly, patients with C–L syndrome‐like phenotype caused by APC truncating mutations have no polyposis despite the increased levels of β catenin. The LRP4 and APC proteins act on the WNT (wingless‐type integration site family) canonical pathway, whereas the GREM‐1 and FMN1 proteins act on the bone morphogenetic protein (BMP) pathway. In this review, we discuss the different mutations associated with C–L syndrome, classify its clinical features, review familial adenomatous polyposis caused by truncating APC mutations and compare these mutations to the splicing APC mutation associated with syndactyly, and finally, explore the pathophysiology through a review of the cross talks between the WNT canonical and the BMP antagonistic pathways.     

Kenny–Caffey syndrome: an Arab variant?

We describe 2 unrelated Bedouin girls who met the criteria for the diagnosis of Kenny-Caffey syndrome. The girls had some unusual features--microcephaly and psychomotor retardation--that distinguish the Kenny-Caffey syndrome profile in Arab children from the classical Kenny-Caffey syndrome phenotype characterized by macrocephaly and normal intelligence. The 2 girls did not harbor the 22q11 microdeletion (the hallmark of the DiGeorge cluster of diseases) that we previously reported in another Bedouin family with the Kenny-Caffey syndrome (Sabry et al. J Med Genet 1998: 35(1): 31-36). This indicates considerable genetic heterogeneity for this syndrome. We also review previously reported 44 Arab/Bedouin patients with the same profile of hypoparathyroidism, short stature, seizures, mental retardation and microcephaly. Our results suggest that these patients represent an Arab variant of Kenny-Caffey syndrome with characteristic microcephaly and psychomotor retardation. We suggest that all patients with Kenny-Caffey syndrome should be investigated for the 22q11 microdeletion. Other possible genetic causes for the Kenny-Caffey syndrome or its Arab variant include chromosome 10p abnormalities.     

Divergent genetic evolution of hemagglutinin in influenza A H1N1 and A H1N2 subtypes isolated in the south-France since the winter of 2001-2002.

BACKGROUND: Influenza A viruses are divided into subtypes based on their hemagglutinin (H1 to H15) and neuraminidase (N1 to N9) glycoproteins. Of these, three A subtypes H1N1, H3N2 and H1N2 circulate in the human population. Influenza A viruses display a high antigenic variability called "antigenic drift" which allows the virus to escape antibody neutralization. OBJECTIVES: Evaluate the mutations apparition that might predict a divergent antigenic evolution of hemagglutinin in influenza A H1N1 and A H1N2 viruses. STUDY DESIGN: During the three winters of 2001-2002 to 2003-2004, 58 A H1N1 and 23 A H1N2 subtypes have been isolated from patients with influenza-like illness in the south of France. The HA1 region was analyzed by RT-PCR and subsequently sequenced to compare the HA1 genetic evolution of influenza A H1N1 and A H1N2 subtypes. RESULTS: Our results showed that 28 amino acid substitutions have accumulated in the HA1 region since the circulation of A/New Caledonia/20/99-like viruses in France. Of these, fifteen were located in four antigenic sites (B, C, D and E). Six of them were observed only in the A H1N2 isolates, six only in the A H1N1 isolates and three in both subtypes. Furthermore, nine of twenty two A H1N2 isolates from the winter of 2002-2003 shared a T90A amino acid change which has not been observed in any A H1N1 isolate; resulting in the introduction of a new glycosylation site close to the antigenic site E. This might mask some antigenic E determinants and therefore, modify the A H1N2 antigenicity. CONCLUSIONS: The divergent genetic evolution of hemagglutinin may ultimately lead to a significant different antigenicity between A H1N1 and A H1N2 subtypes that would require the introduction of a new subtype in the vaccine batches.