Identification of small subunit of serine palmitoyltransferase a as a lysophosphatidylinositol acyltransferase 1‐interacting protein

Lysophosphatidylinositol acyltransferase 1 (LPIAT1), also known as MBOAT7, is a phospholipid acyltransferase that selectively incorporates arachidonic acid (AA) into the sn‐2 position of phosphatidylinositol (PI). We previously demonstrated that LPIAT1 regulates AA content in PI and plays a crucial role in brain development in mice. However, how LPIAT1 is regulated and which proteins function cooperatively with LPIAT1 are unknown. In this study, using a split‐ubiquitin membrane yeast two‐hybrid system, we identified the small subunit of serine palmitoyltransferase a (ssSPTa) as an LPIAT1‐interacting protein. ssSPTa co‐immunoprecipitated and colocalized with LPIAT1 in cultured mammalian cells. Knockdown of ssSPTa decreased the LPIAT1‐dependent incorporation of exogenous AA into PI but did not affect the in vitro enzyme activity of LPIAT1 in the microsomal fraction. Interestingly, knockdown of ssSPTa decreased the protein level of LPIAT1 in the crude mitochondrial fraction but not in total homogenate or the microsomal fraction. LPIAT1 was localized to the mitochondria‐associated membrane (MAM), where AA‐selective acyl‐CoA synthetase is enriched. These results suggest that ssSPTa plays a role in fatty acid remodeling of PI, probably by facilitating the MAM localization of LPIAT1.     

Complete recovery of herpes zoster radiculopathy based on electrodiagnostic study: A case report

BACKGROUNDHerpes zoster is a painful infectious disease caused by the varicella zoster virus. Herpes zoster radiculopathy, which is a type of segmental zoster paresis, can complicate the disease and cause motor weakness. This complication should be considered when a patient with a rash complains of acute-onset motor weakness, and the diagnosis can be verified via electrodiagnostic study. CASE SUMMARYA 64-year-old female with a history of asthma presented to the emergency department with stabbing pain, an itching sensation, and a rash on the right anterior shoulder that had begun 5 d prior. Physical examination revealed multiple erythematous grouped vesicles in the right C4-5 and T1 dermatome regions. Because herpes zoster was suspected, the patient immediately received intravenous acyclovir. On the third hospital day, she complained of motor weakness in the right upper extremity. Magnetic resonance imaging of the cervical spine revealed mild intervertebral disc herniation at C4-C5 without evidence of nerve root compression. On the 12^th hospital day, electrodiagnostic study revealed right cervical radiculopathy, mainly in the C5/6 roots. Six months later, monoparesis resolved, and follow-up electrodiagnostic study was normal. CONCLUSIONThis case emphasizes that clinicians should consider the possibility of post-herpetic paresis, such as herpes zoster radiculopathy, and that electrodiagnostic study is useful for diagnosis and follow-up.     

Monocarboxylate transporter 4 plays a significant role in the neuroprotective mechanism of ischemic preconditioning in transient cerebral ischemia

Monocarboxylate transporters(MCTs), which carry monocarboxylates such as lactate across biological membranes, have been associated with cerebral ischemia/reperfusion process. In this study, we studied the effect of ischemic preconditioning(IPC) on MCT4 immunoreactivity after 5 minutes of transient cerebral ischemia in the gerbil. Animals were randomly designated to four groups(sham-operated group, ischemia only group, IPC + sham-operated group and IPC + ischemia group). A serious loss of neuron was found in the stratum pyramidale of the hippocampal CA1 region(CA1), not CA2/3, of the ischemia-only group at 5 days post-ischemia; however, in the IPC + ischemia groups, neurons in the stratum pyramidale of the CA1 were well protected. Weak MCT4 immunoreactivity was found in the stratum pyramidale of the CA1 in the sham-operated group. MCT4 immunoreactivity in the stratum pyramidale began to decrease at 2 days post-ischemia and was hardly detected at 5 days post-ischemia; at this time point, MCT4 immunoreactivity was newly expressed in astrocytes. In the IPC + sham-operated group, MCT4 immunoreactivity in the stratum pyramidale of the CA1 was increased compared with the sham-operated group, and, in the IPC + ischemia group, MCT4 immunoreactivity was also increased in the stratum pyramidale compared with the ischemia only group. Briefly, present findings show that IPC apparently protected CA1 pyramidal neurons and increased or maintained MCT4 expression in the stratum pyramidale of the CA1 after transient cerebral ischemia. Our findings suggest that MCT4 appears to play a significant role in the neuroprotective mechanism of IPC in the gerbil with transient cerebral ischemia.     

Delayed hippocampal neuronal death in young gerbil following transient global cerebral ischemia is related to higher and longer-term expression of p63 in the ischemic hippocampus

The tumor suppressor p63 is one of p53 family members and plays a vital role as a regulator of neuronal apoptosis in the development of the nervous system. However, the role of p63 in mature neuronal death has not been addressed yet. In this study, we first compared ischemia-induced effects on p63 expression in the hippocampal regions (CA1–3) between the young and adult gerbils subjected to 5 minutes of transient global cerebral ischemia. Neuronal death in the hippocampal CA1 region of young gerbils was significantly slow compared with that in the adult gerbils after transient global cerebral ischemia. p63 immunoreactivity in the hippocampal CA1 pyramidal neurons in the sham-operated young group was significantly low compared with that in the sham-operated adult group. p63 immunoreactivity was apparently changed in ischemic hippocampal CA1 pyramidal neurons in both ischemia-operated young and adult groups. In the ischemia-operated adult groups, p63 immunoreactivity in the hippocampal CA1 pyramidal neurons was significantly decreased at 4 days post-ischemia; however, p63 immunoreactivity in the ischemia-operated young group was significantly higher than that in the ischemia-operated adult group. At 7 days post-ischemia, p63 immunoreactivity was decreased in the hippocampal CA1 pyramidal neurons in both ischemia-operated young and adult groups. Change patterns of p63 level in the hippocampal CA1 region of adult and young gerbils after ischemic damage were similar to those observed in the immunohistochemical results. These findings indicate that higher and longer-term expression of p63 in the hippocampal CA1 region of the young gerbils after ischemia/reperfusion may be related to more delayed neuronal death compared to that in the adults.     

Prevalence of the Brugada-type ECG recorded from higher intercostal spaces in healthy Korean males.

BACKGROUND: Electrocardiograms (ECGs) recorded from the higher intercostal spaces (ICSs) are reported to be helpful for the diagnosis of Brugada syndrome (BS). However, the prevalence of Brugada-type ECG changes recorded from the higher ICSs is unknown in the healthy Korean population. METHODS AND RESULTS: A total of 225 healthy Korean male subjects with a mean age of 44+/-13 (20-69) years with no syncope or family history of sudden death were enrolled in the present study. ECGs were taken from 4th, 3rd, and 2nd ICSs and examined for Brugada-type ECG changes. There were none on the routine 12-lead ECGs, but 3 (1.3%) of the 225 subjects had a Brugada-type ECG recorded from the higher ICSs and 1 of them had a Brugada-type ECG recorded at both the 2nd and 3rd ICSs. The prevalence of the Brugada-type ECG was 1.3% at the 3rd ICS, 0.4% at the 2nd ICS. All were type 2. CONCLUSION: Some healthy Korean males with normal routine ECGs show Brugada-type 2 changes on ECGs recorded from higher ICSs.