[Objective]To investigate the reasons of misdiagnosis of colon cancer complicated with appendicitis and to sum up the experience of diagnosis. [Methods] Between May 1995 and September 2005, 1060 cases with appendicitis were undergone appendectomy. However, of them, 9 cases complicated with colon cancer had confirmative diagnosis during the operation or after, performed successfully suitable operations. [Results] All of 9 cases were misdiagnosed as appendicitis and undertook appendectomy for similar clinical traits. According to the signs of exploration in the appendectomy and the analysis of patient history, clinic characteristic and some radiologic features, we acquired confirmative signs of carcinoma and put up reasonable surgical intervention. [Conclusion] There are some imperative measures to decrease misdiagnosis by analyzing clinical manifestations comprehensively, observation dynamically, exploration in the appendectomy, and effective examination. Among them, the key to reduce misdiagnosis rate is exploration during the period of appendectomy.

Primary hyperparathyroidism (PHPT) is a disorder of calcium metabolism, which is characterized by elevated blood calcium and PTH urine calcium, which is easy to involve multiple systems. The disease is mainly caused by a benign adenoma of parathyroid tissue, a few of which are parathyroid hyperplasia or parathyroid adenocarcinoma. As awareness of physical examination increased, the proportion of asymptomatic PHPT patients gradually increased. The disease can be cured by surgical resection of the parathyroid gland, most of which is a real good prognosis, but a few of them are complex and difficult to diagnose and treat. At present, there continue to be many controversies about the diagnosis and treatment of PHPT.This article is a review of the progress in the diagnosis and treatment of PHPT.

Objective:This study aims to explore the potential effects of adipose-derived stem cell-extracellular vesicles(ASC-EVs) on TGFβ-Smad signaling pathway during myofibroblast trans-differentiation in vitro. Methods:ASCs were isolated from liposuction and flow cytometry was used to detect the surface protein markers. ASC-EVs were isolated from the supernatant of the third to fifth generation ASCs, and the microscopic morphology was observed by transmission electron microscope. The particle size distribution was detected by nano-particle tracking analyzer NanoSight and the membrane surface marker proteins CD63, Alix and TSG101 were detected by flow cytometry. The uptake of EVs by dermal fibroblasts co-cultured with PKH67 fluorescence labeled ASC-EVs was observed by confocal microscope. Dermal fibroblasts were continuously induced by TGFβ1 for five days, and ASC-EVs at the dose of 50 and 100 μg/ml were added. The expression of α-SMA and Smad-2/3/4 were detected by immunofluorescence staining, RT-PCR and Western Blot.Results:The results of flow cytometry showed that the surface markers CD73, CD49d, CD90 and CD105 of the third generation ASCs, were positive, and CD34 and CD45 were negative. Under transmission electron microscope, ASC-EVs was a round membranous vesicle with clear edge and surrounded by bilayer phospholipid membrane. The particle size of more than 95% of the ASC-EVs was distributed between 30 nm to 261 nm, with an average of (166.0±86.1)nm. The specific marker proteins of extracellular vesicle, CD63, Alix and TSG101 were highly expressed. Under confocal microscope, ASC-EVs with green fluorescence were uptake by dermal fibroblasts and distributed in the cytoplasm, and part of ASC-EVs was distributed around the nucleus.TGF-β1 induced a significant increase in the expression of α-SMA in dermal fibroblasts, and the addition of 50 or 100 μg/ml ASC-EVs reduced the expression of α-SMA genes and proteins, but did not show a dose-dependent manner. The gene and protein expression changes of Smad-2/3/4 were consistent with α-SMA. In addition, ASC-EVs could significantly reduced the content of type Ⅰ collagen in the supernatant, but had no significant effect on the secretion of type Ⅲ collagen.Conclusions:The mechanism of ASC-EVs inhibiting scar hyperplasia may be closely related to the suppression of TGF-β-Smad signaling pathway in dermal fibroblasts, inhibition of myofibroblast trans-differentiation and reduction of type Ⅰ collagen secretion.

Objective:This study aims to explore the potential effects of adipose-derived stem cell-extracellular vesicles(ASC-EVs) on TGFβ-Smad signaling pathway during myofibroblast trans-differentiation in vitro. Methods:ASCs were isolated from liposuction and flow cytometry was used to detect the surface protein markers. ASC-EVs were isolated from the supernatant of the third to fifth generation ASCs, and the microscopic morphology was observed by transmission electron microscope. The particle size distribution was detected by nano-particle tracking analyzer NanoSight and the membrane surface marker proteins CD63, Alix and TSG101 were detected by flow cytometry. The uptake of EVs by dermal fibroblasts co-cultured with PKH67 fluorescence labeled ASC-EVs was observed by confocal microscope. Dermal fibroblasts were continuously induced by TGFβ1 for five days, and ASC-EVs at the dose of 50 and 100 μg/ml were added. The expression of α-SMA and Smad-2/3/4 were detected by immunofluorescence staining, RT-PCR and Western Blot.Results:The results of flow cytometry showed that the surface markers CD73, CD49d, CD90 and CD105 of the third generation ASCs, were positive, and CD34 and CD45 were negative. Under transmission electron microscope, ASC-EVs was a round membranous vesicle with clear edge and surrounded by bilayer phospholipid membrane. The particle size of more than 95% of the ASC-EVs was distributed between 30 nm to 261 nm, with an average of (166.0±86.1)nm. The specific marker proteins of extracellular vesicle, CD63, Alix and TSG101 were highly expressed. Under confocal microscope, ASC-EVs with green fluorescence were uptake by dermal fibroblasts and distributed in the cytoplasm, and part of ASC-EVs was distributed around the nucleus.TGF-β1 induced a significant increase in the expression of α-SMA in dermal fibroblasts, and the addition of 50 or 100 μg/ml ASC-EVs reduced the expression of α-SMA genes and proteins, but did not show a dose-dependent manner. The gene and protein expression changes of Smad-2/3/4 were consistent with α-SMA. In addition, ASC-EVs could significantly reduced the content of type Ⅰ collagen in the supernatant, but had no significant effect on the secretion of type Ⅲ collagen.Conclusions:The mechanism of ASC-EVs inhibiting scar hyperplasia may be closely related to the suppression of TGF-β-Smad signaling pathway in dermal fibroblasts, inhibition of myofibroblast trans-differentiation and reduction of type Ⅰ collagen secretion.

OBJECTIVE To explore the clinical features of patients carrying deletions of the rod domain of the dystrophin gene. METHODS Clinical data of 12 Chinese patients with Becker muscular dystrophy (BMD) and such deletions was reviewed. RESULTS Most patients complained of muscle weakness of lower limbs. Two patients had muscle cramps, one had increased creatine kinase (CK) level, and one had dilated cardiomyopathy. CONCLUSION Compared with DMD, the clinical features of BMD are much more variable, particularly for those carrying deletions of the rod domain of the dystrophin gene. Muscular weakness may not be the sole complaint of BMD. The diagnosis of BMD cannot be excluded by moderately elevated CK. For male patients with dilated cardiomyopathy, the possibility of BMD should be considered.