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Salt marshes are recognized as blue carbon ecosystems for their ability to rapidly sequester organic carbon (OC) via sedimentation. For this reason, there is growing interest in managing these systems to help mitigate climate change. However, in order for sediment accretion to offset ongoing CO2 emissions, organic matter undergoing burial must be derived from contemporary primary production. To investigate the provenance of OC sequestered by salt marshes, we analyzed the concentration and isotope composition (δ13C and Δ14C) of sedimentary OC in two minerogenic marshes in San Francisco Bay, California, USA. Data from the low marsh dominated by Spartinaspp. show that autochthonous OC is entering the sediment matrix and may in part be stabilized through incorporation into the mineral‐bound pool. However, the sedimentary OC stock as a whole is dominated by material with low values of δ13C (~ −20 to −25‰) and Δ14C (~ 100 to −300‰) indicating a preponderance of allochthonous OC that was retained in other OC reservoirs for 102 to 103 years prior to deposition in the marsh. Diagenetic modeling of OC and its δ13C values further shows that autochthonous OC is lost from the sediment profile at a much faster rate than allochthonous OC. The rapid turnover of contemporary autochthonous OC ("fast carbon") relative to the apparent stability of old allochthonous OC ("slow carbon") suggest that carbon burial at these sites is largely decoupled from ongoing CO2 emissions. [ABSTRACT FROM AUTHOR]

We have chosen to test the safety of human intracerebroventricular (ICV) brain injections of autologous non-genetically-modified adipose-derived stromal vascular fraction (ADSVF). In this IRB-approved trial, 24 patients received ICV ADSVF via an implanted reservoir between 5/22/14 and 5/22/17. Seven others were injected via their ventriculo-peritoneal shunts. Ten patients had Alzheimer's disease (AD), 6 had amyotrophic lateral sclerosis (ALS), 6 had progressive multiple sclerosis (MS-P), 6 had Parkinson's "Plus" (PD+), 1 had spinal cord injury, 1 had traumatic brain injury, and 1 had stroke. Median age was 74 (range 41–83). Injections were planned every 2–3 months. Thirty-one patients had 113 injections. Patients received SVF injection volumes of 3.5–20 cc (median:4 cc) containing 4.05 × 105 to 6.2 × 107 cells/cc, which contained an average of 8% hematopoietic and 7.5% adipose stem cells. Follow-up ranged from 0 to 36 months (median: 9.2 months). MRIs post injection(s) were unchanged, except for one AD patient whose hippocampal volume increased from < 5th percentile to 48th percentile (NeuroQuant® volumetric MRI). Of the 10 AD patients, 8 were stable or improved in tests of cognition. Two showed improvement in P-tau and ß-amyloid levels. Of the 6 MS-P patients all are stable or improved. Four of 6 ALS patients died of disease progression. Twelve of 111 injections (11%) led to 1-4 days of transient meningismus, and mild temperature elevation, which resolved with acetaminophen and/or dexamethasone. Two (1.8% of injections) required hospitalization for these symptoms. One patient (0.9% of injections) had his reservoir removed and later replaced for presumed infection. In this Phase 1 safety trial, ADSVF was safely injected into the human brain ventricular system in patients with no other treatment options. Secondary endpoints of clinical improvement or stability were particularly promising in the AD and MS-P groups. These results will be submitted for a Phase 2 FDA-approved trial. [ABSTRACT FROM AUTHOR]

This article focuses on the case of a generalized chondrodystrophy in newborns associated with dystrophic thoracic changes which caused respiratory distress and early death. Signs and symptoms of the disease displayed the following manifestations: (1) respiratory defects; (2) pinkish skin color and cyanosis; and (3) deformed and abnormal skeletal structure. Results of radiographic, anatomic, and pathologic studies indicates that the disorder is genotypic chondrodystrophy. The author claimed that asphyxiating thoracic dystrophy has resemblance to the Ellis van Creveld syndrome. Treatment procedures for the disease involves: (1) antibiotics; (2) facilities for adequate endotracheal suctioning; (3) postural drainage; (4) nasogastric-tube feeding; and (5) oxygen therapy.

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