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Articles by A Singh
Total Records ( 2 ) for A Singh
  A Singh , M. J Harnett , J. M Connors and W. R. Camann

Factor XI (FXI) deficiency is a rare inherited coagulation disorder associated with prolonged activated partial thromboplastin time. The severity of bleeding often does not correlate with plasma factor levels. We reviewed the medical and anesthetic records of 13 parturients with FXI deficiency that presented for delivery. Nine cases were managed with neuraxial anesthesia. (epidural, seven; spinal, one; combined spinal-epidural, one). Three received general anesthesia for cesarean delivery, and one had an unmedicated vaginal delivery. Baseline factor levels ranged from severe (<15%) to mild (near 50%) deficiency. Fresh frozen plasma was administered to correct activated partial thromboplastin time in most, but not all, cases. Hematology consultation was obtained for all. No hematological or anesthetic complications were noted. FXI deficiency is not an absolute contraindication to neuraxial anesthesia, provided appropriate hematology consultation has been obtained, and factor replacement is provided as guided by clinical and laboratory hemostatic evaluation.

  X Ma , K Takeda , A Singh , Z. X Yu , P Zerfas , A Blount , C Liu , J. A Towbin , M. D Schneider , R. S Adelstein and Q. Wei

Rationale: Germline ablation of the cytoskeletal protein nonmuscle myosin II (NMII)-B results in embryonic lethality, with defects in both the brain and heart. Tissue-specific ablation of NMII-B by a Cre recombinase strategy should prevent embryonic lethality and permit study of the function of NMII-B in adult hearts.

Objective: We sought to understand the function of NMII-B in adult mouse hearts and to see whether the brain defects found in germline-ablated mice influence cardiac development.

Methods and Results: We used a loxP/Cre recombinase strategy to specifically ablate NMII-B in the brains or hearts of mice. Mice ablated for NMII-B in neural tissues die between postnatal day 12 and 22 without showing cardiac defects. Mice deficient in NMII-B only in cardiac myocytes (BMHC/BMHC mice) do not show brain defects. However, BMHC/BMHC mice display novel cardiac defects not seen in NMII-B germline-ablated mice. Most of the BMHC/BMHC mice are born with enlarged cardiac myocytes, some of which are multinucleated, reflecting a defect in cytokinesis. Between 6 to 10 months, they develop a cardiomyopathy that includes interstitial fibrosis and infiltration of the myocardium and pericardium with inflammatory cells. Four of 5 BMHC/BMHC hearts develop marked widening of intercalated discs.

Conclusions: By avoiding the embryonic lethality found in germline-ablated mice, we were able to study the function of NMII-B in adult mice and show that absence of NMII-B in cardiac myocytes results in cardiomyopathy in the adult heart. We also define a role for NMII-B in maintaining the integrity of intercalated discs.

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