Summary Mammalian pallial (cortical and hippocampal) and striatal interneurons are both generated in the embryonic subpallium, including the medial ganglionic eminence (MGE). Herein we demonstrate that the Zfhx1b (Sip1, Zeb2) zinc finger homeobox gene is required in the MGE, directly downstream of Dlx1&2, to generate cortical interneurons that express Cxcr7, MafB and cMaf. In its absence, Nkx2-1 expression is not repressed, and cells that ordinarily would become cortical interneurons appear to transform towards a subtype of GABAeric striatal interneurons. These results show that Zfhx1b is required to generate cortical interneurons, and suggest a mechanism for the epilepsy observed in humans with Zfhx1b mutations (Mowat-Wilson syndrome).

Non-O1, non-O139 Vibrio cholerae (NOVC) are genetically diverse strains that are generally non-pathogenic in healthy hosts. In immunocompromised patients or those with liver disease, NOVC have been shown to cause gastroenteritis, wound infections or sepsis and are often associated with high mortality rates. We report a case of a patient with liver cirrhosis and chronic venous insufficiency who was found to have NOVC bacteremia. The patient had recently visited Florida, USA but had no seafood consumption or exposure to aquatic environments. The patient was managed with antimicrobials, with a favorable outcome.

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den Tol MP, de Lange DC, Braaksma MM, IJzermans JN, et al. A comparison of suture repair with mesh repair for incisional hernia. N Engl J Med.

Objective: Over 200,000 incisional hernia repairs are performed each year in the United States at a cost of over $2.5 billion. Currently, hernias are repaired using either alloplastic meshes or soft tissue‐derived prostheses; however, recurrence rates remain 10‐20% after primary repair and as high as 60% after repair of recurrent hernias. We have developed cellular neotendinous constructs (CNTs), scaffoldless 3‐D tissue‐engineered prostheses for hernia repair. Our CNTs integrate into the native muscle of the abdominal wall and allow infiltration of host cells, which may prevent junction failure and chronic prosthesis attenuation, the primary causes of hernia recurrence. The purpose of this preliminary study was to assess the potential of our CNTs as improved tissue prostheses for chronic hernia repair in a rat model. Methods: Bone marrow stromal cells were isolated from Fischer 344 rats and used to produce the CNT constructs. Two‐centimeter incisional hernias were created along the abdominal midline in ten Fischer 344 rats and left unrepaired for one month. A single CNT was used to close each defect site and 56 days were allowed for recovery. Biomechanical analyses were performed using a novel burst pressure test. Results: After 56 days in vivo, our CNTs fully repaired seven of the ten hernias. When subjected to pressure testing, four of the repair sites resisted substantial pressures, bursting at a mean of 65 kPa, 57% of native abdominal wall burst pressure. Histological analysis of the repair sites indicated the formation of robust CNT‐host muscle junctions. Figure 1. A single CNT (A) was implanted into each chronic hernia site (B&C). After 56 days, seven of the ten hernias had been closed (D). Figure 2. Of the seven repaired abdominal walls, four were able to withstand significant hydraulic pressure, bursting at 56% of the mean control pressure. Error bars indicate standard error. Conclusions: These data indicate that our CNTs warrant further study as tissue prostheses for ventral hernia repair. In future work, we will develop more durable CNTs which we hypothesize will provide improved repairs with biomechanical properties approaching those of native abdominal wall.