Perfluorooctanoic
acid (PFOA) is a persistent organic pollutant
that has received concerns worldwide due to its extreme resistance
to conventional degradation. A mechanochemical (MC) method was developed
for complete degradation of PFOA by using alumina (Al2O3) and potassium persulfate (PS) as comilling agents. After
ball milling for 2 h, the MC treatment using Al2O3 or PS caused conversion of PFOA to either 1-H-1-perfluoroheptene
or dimers with a defluorination efficiency lower than 20%, but that
using both Al2O3 and PS caused degradation of
PFOA with a defluorination of 100% and a mineralization of 98%. This
method also caused complete defluorination of other C3∼C6 homologues
of PFOA. The complete defluorination of PFOA attributes to Al2O3 and PS led to the weakening of the C–F
bond in PFOA and the generation of hydroxyl radical (•OH),
respectively. During the MC degradation, Al2O3 strongly anchors PFOA through COO––Al coordination
and in situ formed from Lewis-base interaction and PS through hydrogen
bond. Meanwhile, mechanical effects induce the homolytic cleavage
of PS to produce SO4
•–, which
reacts with OH group of Al2O3 to generate •OH.
The degradation of PFOA is initiated by decarboxylation as a result
of weakened C–COO– due to Al3+ coordination. The subsequent addition of •OH, elimination
of HF, and reaction with water induce the stepwise removal of all
carboxyl groups and F atoms as CO2 and F–
, respectively. Thus, complete defluorination and mineralization
are achieved.
Mood disturbances have been documented in cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). The highly varied morbidity indicates that the affective symptoms in CADASIL have not been cataloged systematically, leading to ineffective treatment, affecting the patients’ quality of life, and possibly resulting in suicide. We present a case of CADASIL with bipolar II disorder as the first manifestation. A middle-aged female reported recurrent depressive episodes and appeared treatment resistant to adequate dosages and durations of antidepressants. Following a structured psychiatric interview and neuropsychological assessment, a past episode of hypomania was identified. Added treatment with sodium valproate alleviated most symptoms. Considering late-onset bipolar disorder with unexplained decline in cognition, a medical history of migraine, and a suspected family history of stroke, further cranial magnetic resonance imaging scan was performed and revealed severe leukoencephalopathy, prompting further investigation. The diagnosis was revised to CADASIL after Arg587Cys NOTCH3 mutation was confirmed. This case highlights the evolving process of affective disorder diagnosis and underlying organic etiologies. Based on the overlap of white matter hyperintensities, NOTCH3 mutation, and valproate therapy in bipolar disorder and CADASIL, bipolar II depression may be a poorly recognized manifestation of CADASIL. Well-designed clinical trials are warranted to verify the current findings.
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