Objective Recent studies have revealed that microRNAs (miRNAs) are involved in the regulation of cardiac development, physiologic, and pathologic processes via post-transcriptional control of gene expression. The stable circulating miRNAs offer unique opportunities for the early diagnosis of several diseases. In this study, we examined the circulating miR-133 and miR-328 levels from patients with acute myocardial infarction (AMI).
Patients and Methods Twenty-eight control subjects and fifty-one consecutive AMI patients were enrolled. The plasma and whole blood samples from AMI patients were obtained within 24 hours (n=51) and 7 days (n=6) after the onset of AMI symptoms. The circulating miR-133 and miR-328 levels were analyzed using quantitative real-time PCR.
Results The miR-133 levels in plasma from AMI patients exhibited a 4.4-fold increase compared with control subjects (p=0.006). Moreover, the increased miR-133 levels in whole blood were comparable with those in plasma samples. In contrast, the miR-328 levels in plasma and whole blood of AMI patients were markedly increased by 10.9-fold and 16.1-fold, respectively, compared to those in control subjects (p=0.033 and p<0.001). The elevated circulating miR-133 and miR-328 levels were recovered to the control levels at 7 days after AMI. In addition, there was a correlation between circulating miR-133 or miR-328 levels and cardiac troponin I. Furthermore, circulating miR-133 or miR-328 showed no significant changes in AMI patients with tachyarrhythmia (n=24) or bradyarrhythmia (n=26) compared to those in patients without arrhythmias. Receiver operating characteristic curve analysis revealed that the areas under the curve of miR-133 or miR-328 in plasma and whole blood were 0.890, 0.702 and 0.810, 0.872, respectively (all p<0.05).
Conclusion The miR-133 and miR-328 levels in plasma and whole blood in AMI patients were increased compared to those in control subjects. These miRNAs may represent novel biomarkers of AMI.

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Objective To investigate the prevalence of cardiovascular disease (CVD) in a Chinese patient population with different stages of chronic kidney disease (CKD).
Methods Six hundred and two CKD patients who were hospitalized in Ruijin Hospital between Jan. 2004 and Jan. 2006 were selected. Patients' medical histories and the results of laboratory tests were reviewed.
Results The prevalence of CVD in 602 patients with CKD stages 1 to 5 was 1.28%, 17.24%, 22.86%, 33.33%, 56.2% respectively. The prevalence of CVD in CKD stage 5 patients with dialysis was 78.51%. In all the patients, the prevalence of coronary artery disease (CAD), left ventricular hypertrophy (LVH), and congestive heart failure (CHF) was 8.64% (52/602), 26% (154/602), and 13% (78/602), respectively. Regarding co-morbidities of CVD, 34.52% of patients had 2 or more of the above abnormalities. The prevalence of CAD in patients with CKD stages 1 to 5 respectively was 1.28%, 5.75%, 7.86%, 10.26%, 12.33%;LVH was 0%, 11.49%, 16.43%, 29.49%, 44.75%; and CHF was 0%, 3.45%, 3.57%, 8.97%, 28.77%.
Conclusion The occurrence of CVD started from CKD stage 1 and increased with the progression of CKD. The screening and prevention of CVD should begin at CKD stage 1.

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Background Diffuse alveolar hemorrhage (DAH) of unknown cause has been characterized as idiopathic pulmonary hemosiderosis (IPH). IPH is a rare disease, which has a high prevalence in children and shows a poor prognosis. However, in adults, since there are few reports about collective cases, the details remain to be determined.
Methods Between January 2003 and June 2008, consecutive adult patients strictly defined as unknown cause DAH by chest images, fiberoptic bronchoscopy, autoantibody testing, and exclusion of systemic disease were enrolled. We investigated the clinical characterization and course of the enrolled patients.
Results Nine patients were included. All patients were middle-aged men (56.1 ± 4.2 year-old) with sudden onset. They did not present with anemia (the hemoglobin level was 13.9 ± 0.5 g/dL) despite the quantity of bleeding. In bronchoalveolar-lavage fluid analysis, the cell count was increased (7.6 ± 1.6×10⁵ cells/mL) with neutorophilia (33.3 ± 13.3%). The illness resolved within 2 weeks with or without corticosteroid therapy. All of the patients were alive without recurrence during the follow-up period (45.2 ± 6.2 months) after diagnosis.
Conclusion Adult IPH patients showed good prognosis. However, the present patients are clinically slightly different from the previously characterized IPH.

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Objective This study was aimed to identify the relationship between radiographic features of elderly pulmonary TB patients and nutritional deficiency.
Methods Ninety-two patients older than 70 years of age with pulmonary TB were retrospectively enrolled. The influence of nutritional parameters, such as serum albumin concentration and peripheral blood total lymphocyte count on CT findings was examined. CT findings of pulmonary TB patients were classified as those including atypical findings (segmental or lobar consolidation in an unusual location, miliary nodules, and hilar and mediastinal lymphadenopathy) or not. The number of segments involved by TB was also counted.
Results Age- and gender-adjusted analyses for the nutritional parameters and confounders revealed that hypoalbuminemia, lymphocytopenia, and steroid therapy were significantly related to the presence of atypical CT findings. Furthermore, hypoalbuminemia, lymphocytopenia, and the amount of acid-fast bacilli in sputum smears were significantly related to an increased number of involved segments. In multivariate analysis, only hypoalbuminemia was significantly related to the presence of atypical CT findings (OR: 0.335, 95% CI: 0.142-0.794, p = 0.013) and an increased number of involved segments (OR: 0.145, 95% CI: 0.047-0.453, p = 0.0009). Among the CT findings, the tree-in-bud pattern was the most common in all patients (79.3%). However, the presence of the tree-in-bud pattern was not significantly related to any nutritional parameter.
Conclusion Elderly TB patients of poor nutritional status, in particular those with hypoalbuminemia, tended to show atypical CT findings and widespread lesions. The tree-in-bud pulmonary pattern could be observed in TB patients in any nutritional state.

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A 40-year-old man was admitted with a continuous high grade fever accompanying a relatively large solitary liver abscess with septations. A puncture of the abscess revealed gram-negative rods that could be identified histologically as Fusobacterium necrophorum, which was later confirmed by tissue culture. The patient was switched to meropenem and penicillin, and cured of the infection. Fusobacterium necrophorum is a rare bacterium causing potentially fatal liver abscesses in humans. Clinicians should bear Fusobacterium necrophorum in mind when treating patients with an enlarged solitary liver abscess.

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Parasitic infections lead to significant morbidity and mortality, especially in tropical regions. The renal damage caused by these infections occurs via various mechanisms. Two forms of parasitic echinococcus infection widely responsible for infection in humans are Echinococcus granulosus and Echinococcus multilocularis. E. multilocularis causes Alveolar echinococcus infection in humans. Alveolar echinococcus has high mortality, and the possible limits of surgery are generally exceeded by the time of diagnosis. The literature contains no case reports of comorbidity of alveolar echinococcus and glomerulonephritis. Here we discuss the treatment of a patient with comorbid mesangioproliferative glomerulonephritis and alveolar echinococcus, behaving like a tumor, using albendazole since there was no possibility of surgery. This is the first ever such case report.

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A 32-year-old man was diagnosed as having thrombotic microangiopathy (TMA) and treated by plasma exchange (PE). During the course of admission, he was also newly diagnosed with pulmonary tuberculosis, tuberculous peritonitis and pleuritis, which was thought to be the cause of the TMA. There are only a few previous reports on TMA associated with tuberculous infection. Although its pathogenetic mechanism is not well understood, it would be valuable to recognize that this worldwide infectious disease could cause TMA.

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Swyer-James syndrome (SJS) is a rare disease probably resulting from bronchiolitis obliterans. The radiological findings of this entity are characterized by hyperlucent appearance of one or more lobes of a unilateral lung, decreased lung volume, diminished ipsilateral hilar shadow and hardly visible arterial structure on chest radiography. We report a 50-year-old patient, who had unilateral right lower lung hyperlucency on chest radiography. However, the patient reported a history of pulmonary atelectasis of lobus centralis dexter in the course and the corresponding affliction of ipsilateral pulmonary vein, that rendered the diagnosis more complicated. The radiological and pathological features of this syndrome, as well as differential diagnosis were also discussed.

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A 78-year-old woman with rheumatoid arthritis treated with methotrexate and corticosteroid was admitted to our hospital for dry cough and dyspnea. She was diagnosed as having Pneumocystis pneumonia based on elevated beta-D-glucan and positive PCR analysis of bronchoalveolar lavage fluid for Pneumocystis jirovecii. We started trimethoprim-sulfamethoxazole and high-dose corticosteroid therapy. Her pulmonary lesions gradually improved; however, she developed perforation of the ileum and subsequently died from sepsis. Histology of the perforated site was compatible with cytomegalovirus enterocolitis.

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Spinal segmental myoclonus is defined as a rare involuntary movement characterized by myoclonic jerks of spinal origin. We describe the case of a 62-year-old woman who developed spinal segmental myoclonus 4 months after undergoing cervical laminoplasty for ossification of the posterior longitudinal ligament. Myoclonic jerks were observed in the upper trapezius innervated by C3-4, which corresponded to the level of myelomalacia. These jerks were elicited and aggravated in the sitting and standing positions but were completely suppressed in the supine position. The myoclonus was refractory to medication but improved with the use of a soft neck brace.

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Hemophagocytic syndrome (HPS) is a severe, potentially life-threatening disorder characterized by an excessive activation of macrophages, such as may occur in the setting of lupus. A 62-year-old Japanese woman treated with etanercept for rheumatoid arthritis developed persistent fever, cytopenia, coagulopathy, and hyperferritinemia. Simultaneously, lupus-like features including pleuritis, hypocomplementemia, and positive autoantibodies were observed. She was diagnosed with HPS related to etanercept-induced lupus, and underwent immunosuppressive therapy with successful recovery. To our knowledge, this is the first case of etanercept-induced lupus accompanied by HPS. This case suggests that HPS should be considered as a complication during TNF-α inhibitor therapy.

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A 56-year-old HTLV-I-positive woman, initially diagnosed as having Sjögren's syndrome, presented with muscle weakness, myalgia, face erythema and leg edema. Based on the presence of various autoantibodies, the diagnosis of overlap syndrome (dermatomyositis/Sjögren's syndrome) was made. Treatment with high-dose corticosteroid plus cyclosporine improved her symptoms. However, three months after the start of these treatments, exacerbation of myositis occurred. A muscle biopsy revealed prominent perivascular accumulation of mononuclear cells with perifascicular atrophy, which were consistent with dermatomyositis. Tacrolimus, which was substituted for cyclosporine led to marked improvement of the myositis symptoms.

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