Background: Glutamate is the main excitatory neurotransmitter. Excessive glutamate causes excitatory toxicity and increases intracellular calcium, leading to neuronal death. Parvalbumin is a calcium-binding protein that regulates calcium homeostasis. Quercetin is a polyphenol found in plant and has neuroprotective effects against neurodegenerative diseases. Objectives: We investigated whether quercetin regulates apoptosis by modulating parvalbumin expression in glutamate induced neuronal damage. Methods: Glutamate was treated in hippocampal-derived cell line, and quercetin or vehicle was treated 1 h before glutamate exposure. Cells were collected for experimental procedure 24 h after glutamate treatment and intracellular calcium concentration and parvalbumin expression were examined. Parvalbumin small interfering RNA (siRNA) transfection was performed to detect the relation between parvalbumin and apoptosis. Results: Glutamate reduced cell viability and increased intracellular calcium concentration, while quercetin preserved calcium concentration and neuronal damage. Moreover, glutamate reduced parvalbumin expression and quercetin alleviated this reduction. Glutamate increased caspase-3 expression, and quercetin attenuated this increase in both parvalbumin siRNA transfected and non-transfected cells. The alleviative effect of quercetin was statistically significant in non-transfected cells. Moreover, glutamate decreased bcl-2 and increased bax expressions, while quercetin alleviated these changes. The alleviative effect of quercetin in bcl-2 family protein expression was more remarkable in non-transfected cells. Conclusions These results demonstrate that parvalbumin contributes to the maintainace of intracellular calcium concentration and the prevention of apoptosis, and quercetin modulates parvalbumin expression in glutamate-exposed cells. Thus, these findings suggest that quercetin performs neuroprotective function against glutamate toxicity by regulating parvalbumin expression.

BACKGROUND: The neuropathy disability score (NDS) is a type of clinical grading method for diabetic polyneuropathy. In clinical practice, a nerve conduction study (NCS) is routinely employed as a non-invasive test for the evaluation of polyneuropathy. However, the consensus regarding the degree of abnormalities in NCS as a parameter for the severity of the disease is lacking. The objective of our study is to assess the relation between NDS and NCS parameters and thus verifying the reliability of our new NCS grading method in the representation of objective neurological defects. METHODS: Seventy three patients (man 31, women 42) with diabetes mellitus were included in the study. The NDS was scored in each patient by a single examiner and a NCS was performed on one side of extremities by an experiencedtechnician. Also, the gastrocnemius-soleus H-reflex was performed and analysed for the representation of a deep tendon reflex. The observed values of CMAP and CNAP were transformed into square root and log values. The transformed individual amplitudes and nerve conduction velocities were graded in relation to the mean normal values and standard deviations of our control group study. Then, the sum of the graded score was calculated in each individual and was correlated to the NDS using correlational analysis. RESULTS: There has been a significant linear relationship between NDS and our new NCS scoring system (Pearson's correlation coefficient r=0.703, p<0.01) CONCLUSIONS: The study showed significant correlations between NDS and our new grading system for NCS. Thus, NCS appears to reliably represent theobjective neurologic findings. In asddition, the quantititive grading of NCS would be useful in determining the grade of peripheral polyneuropathy in diabetic patients.
Consensus ; Diabetes Mellitus ; Diabetic Neuropathies* ; Extremities ; Female ; H-Reflex ; Humans ; Neural Conduction ; Neurologic Manifestations ; Polyneuropathies ; Reference Values ; Reflex, Stretch

A 42-year-old man presented with severe pancytopenia and uncontrolled epistaxis. The diagnosis of SLE was made and the pancytopenia was found to be due to myelofibrosis. The pulse therapy with methylprednisolone and maintenance therapy with prednisolone reversed both pancytopenia and myelofibrosis. Although myelofibrosis has been described in SLE, this coexistence must be very rare since there has been only 19 cases showing this combination. We report a case of SLE with myelofibrosis which was reversed by the treatment with glucocorticoid.
Adult ; Diagnosis ; Epistaxis ; Humans ; Lupus Erythematosus, Systemic* ; Methylprednisolone ; Pancytopenia ; Prednisolone ; Primary Myelofibrosis*

Glutamate is a representative excitatory neurotransmitter. However, excessive glutamate exposure causes neuronal cell damage by generating neuronal excitotoxicity. Excitotoxicity in neonates caused by glutamate treatment induces neurological deficits in adults. The 14–3-3 family proteins are conserved proteins that are expressed ubiquitously in a variety of tissues. These proteins contribute to cellular processes, including signal transduction, protein synthesis, and cell cycle control. We proposed that glutamate induces neuronal cell damage by regulating 14–3-3 protein expression in newborn animals. In this study, we investigated the histopathological changes and 14–3-3 proteins expressions as a result of glutamate exposure in the neonatal cerebral cortex. Rat pups at post-natal day 7 were intraperitoneally administrated with vehicle or glutamate (10 mg/kg). Animals were sacrificed 4 h after treatment, and brain tissues were fixed for histological study. Cerebral cortices were isolated and frozen for proteomic study. We observed serious histopathological damages including shrunken dendrites and atypical neurons in glutamate-treated cerebral cortices. In addition, we identified that 14–3-3 family proteins decreased in glutamate-exposed cerebral cortices using a proteomic approach. Moreover, Western blot analysis provided results that glutamate treatment in neonates decreased 14–3-3 family proteins expressions, including the β/α, ζ/δ, γ, ε, τ, and η isoforms. 14–3-3 proteins are involved in signal transduction, metabolism, and anti-apoptotic functions. Thus, our findings suggest that glutamate induces neonatal neuronal cell damage by modulating 14–3-3 protein expression.

Background: Retinoic acid is a major metabolite of vitamin A and exerts beneficial effects including anti-oxidant and anti-inflammatory activities in neurons. The ubiquitin–proteasome system is an important biological system that regulates cell survival. Ubiquitination regulates protein degradation and plays an important role in oxidative stress. Deubiquitinating enzymes cleave ubiquitin from proteins and control ubiquitination-induced degradation. We detected decreases in ubiquitin carboxy-terminal hydrolase L1, ubiquitin thioesterase OTUB1, and proteasome subunit alpha types 1 and 3 in cerebral ischemic damage. In this study, we investigated whether retinoic acid regulates the expression of deubiquitinating enzymes ubiquitin carboxy-terminal hydrolase L1, ubiquitin thioesterase OTUB1, and proteasome subunit alpha types 1 and 3 in cerebral ischemic injury. Right middle cerebral artery occlusion (MCAO) was performed to induce cerebral ischemic damage in male rats. Retinoic acid (5 mg/kg) or vehicle was intraperitoneally injected every day from 4 days before surgery. Neurological behavioral tests were performed 24 h after MCAO, and right cerebral cortical tissues were collected. Results: MCAO damage caused neurological behavioral dysfunction, and retinoic acid alleviated these deficits. The identified proteins decreased in MCAO animals with vehicle, while retinoic acid treatment attenuated these decreases.The results of proteomic study were confirmed by a reverse transcription-PCR technique. Expressions of ubiquitin carboxy-terminal hydrolase L1, ubiquitin thioesterase OTUB1, and proteasome subunit alpha types 1 and 3 were decreased in MCAO animals treated with vehicle. Retinoic acid treatment alleviated these MCAO-induced reductions. The ubiquitin–proteasome system plays an essential role in maintaining cell function and preserving cell shape against ischemic damage. Conclusions These findings suggest that retinoic acid regulates ubiquitin- and proteasome-related proteins including ubiquitin carboxy-terminal hydrolase L1, ubiquitin thioesterase OTUB1, and proteasome subunit alpha types 1 and 3 in a brain ischemia model. Changes in these proteins are involved in the neuroprotective effects of retinoic acid.

Background: and Purpose Fatigue is common in demyelinating disorders of the central nervous system (CNS), including multiple sclerosis (MS), neuromyelitis optica spectrum disorder (NMOSD), and myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD).We aimed to validate the usefulness of the Functional Assessment of Chronic Illness Therapy– Fatigue (FACIT-F) and the Fatigue Severity Scale (FSS) relative to the Korean version of the Modified Fatigue Impact Scale (MFIS-K) in Korean patients with MS, NMOSD, and MOGAD. Methods: There were 294 patients with MS (n=120), NMOSD (n=103), or MOGAD (n=71) enrolled in a prospective demyelinating CNS registry. Fatigue was measured using the FACIT-F, MFIS-K, and FSS. Sleep quality, quality of life, depression, and pain were evaluated using the Pittsburgh Sleep Quality Index (PSQI), 36-item Short-Form Survey (SF-36), and Beck Depression Inventory-II (BDI-II). Results: The MFIS-K, FACIT-F, and FSS scores showed high internal consistencies and strong correlations with each other in the MS, NMOSD, and MOGAD groups. The scores on all three fatigue scales were correlated with PSQI, SF-36, and BDI-II results in the three groups. The areas under the receiver operating characteristic curves for the FSS and FACIT-F were 0.834 and 0.835, respectively, for MS, 0.877 and 0.833 for NMOSD, and 0.925 and 0.883 for MOGAD. Conclusions These results suggest that the MFIS-K, FSS, and FACIT-F are useful and valuable assessment instruments for evaluating fatigue in Korean patients with MS, NMOSD, and MOGAD.

Broncholithiasis is uncommon in patients with silicosis. Bronchoesophageal fistula complicated by broncholithiasis is especially rare and only one case has been reported in Korea. Surgical treatment of broncholithiasis should be as conservative as possible to preserve the adequate pulmonary function. Meticulous dissection and division of the fistula with the interposition of viable tissues will prevent recurrence. We report a rare case of bronchoesophageal fistula complicated by broncholithiasis in a patient with silicosis.

Ectopic pregnancy (EP) is diagnosed based on laboratory values and ultrasonography (US) findings. Evaluation for suspected EP should begin with a quantitative measurement of the serum β-human chorionic gonadotropin levels and transvaginal US. MR imaging is not preferentially performed in the evaluation of EP; however, if the findings of transvaginal US are uncertain, MR imaging can be used, as it has the advantages of superior soft-tissue contrast resolution and a wide scanning range. Identifying the exact location of implantation transfer using MR imaging can help in the diagnosis and establishment of treatment strategies for ectopic pregnancies, including laparoscopy. In particular, as the incidence of heterotopic pregnancy has increased with the recent increase in use of assisted reproductive technology, the scope of application of MR imaging is expected to expand further. This pictorial essay describes the various manifestations of EP and related conditions on MR imaging and US. Familiarity with the clinical setting and the US and MR imaging features of EP and associated conditions can lead to a more accurate diagnosis and treatment.

Ectopic pregnancy (EP) is diagnosed based on laboratory values and ultrasonography (US) findings. Evaluation for suspected EP should begin with a quantitative measurement of the serum β-human chorionic gonadotropin levels and transvaginal US. MR imaging is not preferentially performed in the evaluation of EP; however, if the findings of transvaginal US are uncertain, MR imaging can be used, as it has the advantages of superior soft-tissue contrast resolution and a wide scanning range. Identifying the exact location of implantation transfer using MR imaging can help in the diagnosis and establishment of treatment strategies for ectopic pregnancies, including laparoscopy. In particular, as the incidence of heterotopic pregnancy has increased with the recent increase in use of assisted reproductive technology, the scope of application of MR imaging is expected to expand further. This pictorial essay describes the various manifestations of EP and related conditions on MR imaging and US. Familiarity with the clinical setting and the US and MR imaging features of EP and associated conditions can lead to a more accurate diagnosis and treatment.

Ectopic pregnancy (EP) is diagnosed based on laboratory values and ultrasonography (US) findings. Evaluation for suspected EP should begin with a quantitative measurement of the serum β-human chorionic gonadotropin levels and transvaginal US. MR imaging is not preferentially performed in the evaluation of EP; however, if the findings of transvaginal US are uncertain, MR imaging can be used, as it has the advantages of superior soft-tissue contrast resolution and a wide scanning range. Identifying the exact location of implantation transfer using MR imaging can help in the diagnosis and establishment of treatment strategies for ectopic pregnancies, including laparoscopy. In particular, as the incidence of heterotopic pregnancy has increased with the recent increase in use of assisted reproductive technology, the scope of application of MR imaging is expected to expand further. This pictorial essay describes the various manifestations of EP and related conditions on MR imaging and US. Familiarity with the clinical setting and the US and MR imaging features of EP and associated conditions can lead to a more accurate diagnosis and treatment.