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Objective@#To investigate the clinical, radiological and pathological features of visceral parasitic migration of the liver.@*Methods@#Seven cases of visceral parasitic migration of liver were identified at the Affiliated Drum Tower Hospital of Medical School of Nanjing University from January 2008 to July 2017. Clinical data, enhanced CT image and pathological features were analyzed, combining with literature review.@*Results@#There were 5 male and 2 female patients. Five patients presented with abdominal pain or discomfort as the first symptom. Two patients were admitted to the hospital for physical examination with liver nodule. Blood eosinophils were mildly to moderately increased in 4 cases. Enhanced CT showed the liver irregular beaded nodules that showed no significant enhancement of arterial phase. Mild enhancement of round lesions (ring lesion) was seen in a few cases before surgery. By histopathology, the lesions showed central geographic necrosis, surrounded by epithelioid granuloma and inflammatory cell bands. A large number of eosinophils and scattered multinucleated giant cells were found, especially at the peripheral of the lesion. Charcot-Leyden crystals were present in all case and parasitic migrans was found in one case.@*Conclusions@#Visceral parasitic migration of liver is a rare liver disease and is easily misdiagnosed as other benign or malignant liver tumors. Combining clinical data, enhanced CT images and pathological examination can improve the preoperative and postoperative diagnosis of the disease.
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Objective To improve the recognition for infantile spinal muscular atrophy (SMA-Ⅰ) and the level of early diagnosis,intervention and treatment for SMA-Ⅰ.Methods The clinical data of 39 patients with SMA-Ⅰ were analyzed retrospectively, including the clinical manifestations, neural electrophysiological characteristics, geno-type, diagnosis,treatment and prognosis of SMA-Ⅰ.Results Of the 39 cases with SMA-Ⅰ , 37 cases (94.9％) had onset in 6 months after birth.The paralyses of the limbs were symmetrical and flaccid.The lower was more severe than the upper , and the proximal was more severe than the distal, hypotonia and tendinous reflex disappears.Thirty-two cases (82.1％) had normal serum creatine kinase, and 7 cases (17.9％) increased slightly.Nerve electrophysiological examination showed that 169 (96.0％) had spontaneous potentials in 176 muscles.Of 160 limb muscles,35 (21.8％) released few motor unit potential (MUP) ,117 (73.1％) extended the duration of MUP and 104 (65.0％) increased the amplitude of M UP.Of 167 peripheral motor nerves, 160 (95.8％)decreased the amplitude of the compound muscle action potential and 162 (97.0％) had normal motor conduction velocity.Of 93 peripheral sensory nerves, 93 (100.0％) had normal range of the conduction.The gene detection showed that 38 cases had homozygous deletion of exon 7,8, and 1 case had homozygous deletion of exon 7 and heterozygous deletion of exon 8.In the effective follow-up of 30 cases,6 cases died in the 2-3 months after birth,4 cases died in 10 months after birth, 12 cases died in 12-18 months after birth.Six cases survived to 2 years old,2 cases survived to 3 years old,and all of them died of pulmonary infection.Conclusions There are typical clinical and nerve electrophysiological characteristics for SMA-I.Nerve electrophysiological examination can be used as an important method for diagnosis and differential diagnosis for SMA-I.Genetic testing can be used to identify the disease and make prenatal diagnosis.Through comprehensive intervention the quality of life can be improved in SMA-Ⅰ children.
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Objective To investigate the role of SCF on neuronal apoptosis induced by diabetes and its possible mechanism.Methods Twenty-seven male C57 mice were randomly divided into control group,diabetes group,and diabe-tes plus stem cell factor(SCF)group.The diabetic mice were induced by streptozotocin.TUNEL staining was used to assess neuronal apoptosis and western blot were used to detect the protein level of BCL-2,BAX,CASPASE 3 and P-ERK/ERK.Results Compared with the controls,the number of apoptotic neuron death and the protein levels of active CASPASE 3 were significantly increased in the cortex of diabetic mice.Treatment with SCF significantly reduced apoptotic neuron death and attenuated the increased in protein levels of active CASPASE 3 in the cortex of diabetic mice.The levels of BCL-2 and BAX were significantly increased in the diabetic animals compared to the controls.Treatment with SCF could significantly attenuated the increase in the expression of BAX but could not affect the level of BCL-2 in the cortex of diabetic mice.P-ERK was significantly decreased in the diabete group but not in dibete plus SCF group.Conclusions SCF can protect a-gainst diabete-induced apoptotic neuron death through increasing the phosphorylation of ERK and influencing the expression of BCL-2/BAX.