Sub- and super-shear ruptures during the 2023 Mw 7.8 and Mw 7.6 earthquake doublet in SE Türkiye

An earthquake doublet (Mw 7.8 and Mw 7.6) occurred on the East Anatolian Fault Zone (EAFZ) on February 6th, 2023. The events produced significant ground motions and caused major impacts to life and infrastructure throughout SE Türkiye and NW Syria. Here we show the results of earthquake relocations of the first 11 days of aftershocks and rupture models for both events inferred from the kinematic inversion of HR-GNSS and strong motion data considering a multi-fault, 3D geometry. We find that the first event nucleated on a previously unmapped fault before transitioning to the East Anatolian Fault (EAF) rupturing for ~350 km and that the second event ruptured the Sürgü fault for ~160 km. Maximum rupture speeds were estimated to be 3.2 km/s for the Mw 7.8 event. For the Mw 7.6 earthquake, we find super-shear rupture at 4.8 km/s westward but sub-shear eastward rupture at 2.8 km/s. Peak slip for both events were as large as ~8m and ~6m, respectively

Complex multi-fault rupture and triggering during the 2023 earthquake doublet in southeastern Türkiye.

Two major earthquakes (MW 7.8 and MW 7.7) ruptured left-lateral strike-slip faults of the East Anatolian Fault Zone (EAFZ) on February 6, 2023, causing >59,000 fatalities and ~$119B in damage in southeastern Türkiye and northwestern Syria. Here we derived kinematic rupture models for the two events by inverting extensive seismic and geodetic observations using complex 5-6 segment fault models constrained by satellite observations and relocated aftershocks. The larger event nucleated on a splay fault, and then propagated bilaterally ~350 km along the main EAFZ strand. The rupture speed varied from 2.5-4.5 km/s, and peak slip was ~8.1 m. 9-h later, the second event ruptured ~160 km along the curved northern EAFZ strand, with early bilateral supershear rupture velocity (>4 km/s) followed by a slower rupture speed (~3 km/s). Coulomb Failure stress increase imparted by the first event indicates plausible triggering of the doublet aftershock, along with loading of neighboring faults

Complex multi-fault rupture and triggering during the 2023 earthquake doublet in southeastern Türkiye

Abstract Two major earthquakes (MW 7.8 and MW 7.7) ruptured left-lateral strike-slip faults of the East Anatolian Fault Zone (EAFZ) on February 6, 2023, causing >59,000 fatalities and ~$119B in damage in southeastern Türkiye and northwestern Syria. Here we derived kinematic rupture models for the two events by inverting extensive seismic and geodetic observations using complex 5-6 segment fault models constrained by satellite observations and relocated aftershocks. The larger event nucleated on a splay fault, and then propagated bilaterally ~350 km along the main EAFZ strand. The rupture speed varied from 2.5-4.5 km/s, and peak slip was ~8.1 m. 9-h later, the second event ruptured ~160 km along the curved northern EAFZ strand, with early bilateral supershear rupture velocity (>4 km/s) followed by a slower rupture speed (~3 km/s). Coulomb Failure stress increase imparted by the first event indicates plausible triggering of the doublet aftershock, along with loading of neighboring faults

Invasive Saprochaete capitata Infection in a Patient with Autosomal Recessive CARD9 Deficiency and a Review of the Literature.

Purpose Autosomal recessive (AR) CARD9 deficiency is an inherited immune disorder which results in impaired innate immunity against various fungi. Superficial and invasive fungal infections, mainly caused by Candida or Trichophyton species, are the hallmark of CARD9 deficiency. Together with the increasing number of CARD9-deficient patients reported, different pathogenic fungal species have been described such as Phialophora, Exophiala, Corynespora, Aureobasidium, and Ochroconis. Saprochaete capitata is an opportunistic infectious agent in immunocompromised patients and is a common cause of invasive fungal disease in patients with hematological malignancies. In this study, we investigated the causative genetic defect in a patient with S. capitata fungal infection which disseminated to lymph nodes and common bile duct. Methods The identification of the isolated yeast strain was made by direct microscopic examination and confirmed by internal transcribed spacer (ITS) sequencing. We applied whole exome sequencing to search for the disease-causing mutation. Sanger sequencing was used to validate the mutation in the patient and his parents. Results S. capitata was isolated from the biopsy specimen as the causative microorganism responsible for the invasive fungal disease in the patient. Whole exome sequencing revealed a homozygous c.883C > T, (p.Q295*) mutation in CARD9, confirmed by Sanger sequencing. Conclusions This is the first report of invasive Saprochaete infection associated with autosomal recessive (AR) CARD9 deficiency in the literature and thereby further extends the spectrum of fungal diseases seen in these patients