Bispectral Index Changes during Acute Brainstem TIA/Ischemia

We describe a 76-year-old patient who suffered a brainstem TIA just before being anesthetised for cardiac surgery. The TIA was registered on BIS and resulted in a drop in BIS to a value of 60. When consciousness returned spontaneously, the BIS increased to 85. The relative use of the BIS during an operation is discussed. We believe that the lack of input from the brainstem to the frontal cortex resulted in the reduced cortical electrical activity as registered with the BIS

HPV infections and flat penile lesions of the penis in men who have sex with men.

Background: Flat penile lesions (FPL) in heterosexual men are thought to play a role in the transmission of HPV. We investigated the association between FPL and penile HPV, and explored determinants of FPL in men who have sex with men (MSM). Methods: In 2015–2016, MSM were recruited based on HIV and penile HPV status in a previous cohort. MSM self-completed a questionnaire. Peniscopy was performed after application of acetic acid to visualize FPL. Penile physician-collected samples were tested for HPV-DNA using the highly sensitive SPF10-PCR DEIA/LiPA25 system. HPV viral load (VL) was determined using a quantitative type-specific (q)PCR targeting the L1-region. Presence of HPV and HIV, HPV VL and circumcision status were compared between MSM with and without FPL. Results: We included 116 MSM, of whom 59/116 (51%) MSM were HIV-positive and 54/116 (47%) had FPL. A penile HPV infection was present in 31/54 (57%) MSM with FPL and 34/62 (55%) MSM without FPL (p = 0.8). There was no difference between MSM with and without FPL regarding presence of penile HPV infection, HPV VL, HIV status or circumcision status (p > 0.05 for all). Conclusion: Among MSM in Amsterdam, we found no association between FPL and penile HPV, HPV VL, HIV status or circumcision status

Molecular heterogeneity in human papillomavirus-dependent and -independent vulvar carcinogenesis

Vulvar squamous cell carcinoma (VSCC) and precancerous vulvar intraepithelial neoplasia (VIN) can develop through human papillomavirus (HPV)-dependent and -independent pathways, indicating a heterogeneous disease. Only a minority of VIN progress, but current clinicopathological classifications are insufficient to predict the cancer risk. Here we analyzed copy number alterations (CNA) to assess the molecular heterogeneity of vulvar lesions in relation to HPV and cancer risk. HPV-status and CNA by means of whole-genome next-generation shallow-sequencing were assessed in VSCC and VIN. The latter included VIN of women with associated VSCC (VINVSCC) and women who did not develop VSCC during follow-up (VINno VSCC). HPV-testing resulted in 41 HPV-positive (16 VINVSCC, 14 VINno VSCC, and 11 VSCC) and 24 HPV-negative (11 VINVSCC and 13 VSCC) lesions. HPV-positive and -negative VSCC showed a partially overlapping pattern of recurrent CNA, including frequent gains of 3q and 8q. In contrast, amplification of 11q13/cyclinD1 was exclusively found in HPV-negative lesions. HPV-negative VINVSCC had less CNA than HPV-negative VSCC (P =.009), but shared chromosome 8 alterations. HPV-positive VINno VSCC had less CNA than VINVSCC (P =.022). Interestingly, 1pq gain was detected in 81% of HPV-positive VINVSCC and only in 21% of VINno VSCC (P =.001). In conclusion, HPV-dependent and -independent vulvar carcinogenesis is characterized by distinct CNA patterns at the VIN stage, while more comparable patterns are present at the cancer stage. Cancer risk in VIN seems to be reflected by the extent of CNA, in particular chromosome 1 gain in HPV-positive cases