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Reaction of lithium tris(trimethylsilyl)silanide · 3 THF with R2GaCl (R = 2,2,6,6‐tetramethylpiperidino, Me, Cl) yields tmp2GaSi(SiMe3)3 (3) and R2Ga(THF)Si(SiMe3)3 (R = Me, Cl) (7, 9). Both gallium nitrogen bonds in 3 are cleaved by protic reagents. Depending on the acidity of these agents, either oligomeric gallanes [(RO)2GaSi(SiMe3)3]n (R = Et, H, n = 2, 3) (11, 12) or tetramethylpiperidinium gallates [X3GaSi‐(SiMe3)3]– (X = OPh, Cl) (13, 14) are formed. Hydroxide 11 adds lithium hydroxide to afford the mixed lithium gallium hydroxide 15. Single‐crystal X‐ray diffraction studies confirm the suggested constitutions. The gallium‐silicon bond can adopt values between 236 and 247 pm. Here electronic influences of the substituents on the gallium center are of great importance as well as their steric demand. This is underlined by quantum chemical calculations on the ab initio (SCF) level.

Cervical cancer is responsible for around 5% of all human cancers worldwide. It develops almost exclusively from an unsolved, persistent infection of the squamocolumnar transformation zone between the endo- and ecto-cervix with various high-risk (HR) human papillomaviruses (HPVs). The decisive turning point on the way to persistent HPV infection and malignant transformation is an immune system weakened by pathobionts and oxidative stress and an injury to the cervical mucosa, often caused by sexual activities. Through these injury and healing processes, HPV viruses, hijacking activated keratinocytes, move into the basal layers of the cervical epithelium and then continue their development towards the distal prickle cell layer (Stratum spinosum). The microbial microenvironment of the cervical tissue determines the tissue homeostasis and the integrity of the protective mucous layer through the maintenance of a healthy immune and metabolic signalling. Pathological microorganisms and the resulting dysbiosis disturb this signalling. Thus, pathological inflammatory reactions occur, which manifest the HPV infection. About 90% of all women contract an HPV infection in the course of their lives. In about 10% of cases, the virus persists and cervical intra-epithelial neoplasia (CIN) develops. Approximately 1% of women with a high-risk HPV infection incur a cervical carcinoma after 10 to 20 years. In this non-systematic review article, we summarise how the sexually and microbial mediated pathogenesis of the cervix proceeds through aberrant immune and metabolism signalling via CIN to cervical carcinoma. We show how both the virus and the cancer benefit from the same changes in the immune and metabolic environment.

Die Umsetzung von Bis(2,2,6,6‐tetramethylpiperidino)chlorgallan mit Kaliumthiocyanat führt nicht zu einfacher Substitution des Halogenids, sondern es bildet sich unter Abspaltung des Cyanamids tmp‐CN das Heterokuban (tmpGaS)4. Das auf diese neuartige Weise dargestellte amino‐substituierte GaS‐Kuban wurde NMR‐spektroskopisch und mittels Röntgen‐Einkristallstrukturanalyse charakterisiert.

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