Primary congenital glaucoma (PCG) is one of the primary causes of blindness in children and is characterized by congenital trabecular meshwork and anterior chamber angle dysplasia. While being a rare condition, PCG severely impairs the quality of life of affected patients. However, the pathogenesis of PCG remains to be fully elucidated. It has previously been indicated that genetic factors serve a critical role in the pathogenesis of PCG, although patients with PCG exhibit significant genetic heterogeneity. Mutations in the cytochrome P450 family 1 subfamily B member 1 gene have been implicated in PCG and further genes that have been reported to be involved in PCG are myocilin, forkhead box C1, collagen type I α1 chain and latent transforming growth factor β binding protein 2. The present review aims to provide an up to date understanding of the genes associated with PCG and the use of molecular technologies in the identification of such genes and mutations. This may pave the way for the development of preventative methods, early diagnosis and improved therapeutic strategies in PCG.Transthoracic echocardiography is a rapid, sensitive and non-invasive technique for diagnosing ventricular septal perforation. Furthermore, left ventricular angiography is generally used for left ventricular aneurysm but right heart catheterization is the gold standard for septal perforation following myocardial infarction. The objectives of the present study were to compare radiological and hemodynamic diagnostic parameters of non-invasive methods with those of right heart catheterization in patients with suspected ventricular aneurysm and interventricular septal perforation after acute myocardial infarction. Data regarding demographics and clinical characteristics, as well as right heart catheterization, echocardiography and angiographic parameters of 199 patients examined within 21 days after myocardial infarction due to suspected ventricular septal defect indicated by persistent colic pain in the pre-cardiac region were collected and analyzed. Coronary angiography identified 149 (75%) patients with single-vessel disease, 42 (21%) patients with two-vessel disease and 8 (4%) patients with triple-vessel disease. Transthoracic color Doppler echocardiography strengthened the diagnostic performance of right heart catheterization regarding segmental motor abnormalities but underestimated the right atrial pressure, systolic pulmonary artery pressure, mean pulmonary artery pressure and pulmonary capillary wedge pressure compared with right heart catheterization (P less then 0.0001 for all). Overall, there was no procedural complication requiring emergency intervention, no major complications and no conditions resulting in death due to diagnostic modalities. Transthoracic color Doppler echocardiography may strengthen the diagnostic performance of right heart catheterization regarding radiological measurements but underestimated hemodynamic measurements (level of evidence 3).The aim of the present study was to evaluate the role of ceftriaxone sodium combined with dexamethasone on the treatment of infant purulent meningitis (PM) and to measure brain-derived neurotrophic factor (BDNF) levels in children with PM. Of the 177 patients enrolled into the present study, 92 patients received ceftriaxone sodium+dexamethasone (combination group) and 85 patients received ceftriaxone sodium alone (monotherapy group). The time taken for the body temperature, peripheral blood (PB) and cerebrospinal fluid (CSF) white blood cell (WBC) counts to recover back to normal levels were compared between the two groups. In addition, changes in the CSF WBC counts, CSF protein and sugar concentrations, BDNF levels, effective treatment rates and incidence of adverse reactions three days before treatment (T1), after one week of treatment (T2) and after two weeks of treatment (T3) were compared between the two groups. In the combination group, the recovery time of body temperature, WBC counts in both PB and CSF were significantly lower compared with those in the monotherapy group. The combination group also exhibited lower CSF protein concentrations and higher CSF sugar concentrations at T2 and T3 compared with those in the monotherapy group (P less then 0.05). The effective treatment rate of the combination group was significantly higher compared with that of the monotherapy group (P=0.006). CSF protein at T1, T2 T3, and CSF sugar concentrations and BDNF levels at T1 were significantly lower in the combination group than in the monotherapy group (P less then 0.05) while the CSF sugar concentrations at T2, T3 were higher in the combination group than in the monotherapy group (P less then 0.05). Taken together, these observations suggest that ceftriaxone combined with dexamethasone was superior compared with that of ceftriaxone alone for the treatment of infantile PM, and that this combination therapy may improve the effective treatment rate and accelerate patient rehabilitation.Acute oxidative stress and mitochondrial dysfunction are crucial for acute myocardial ischemia-reperfusion (AMI/R) injury, which may induce cell or mitochondrial membrane rupture and myocardial infarction. Plasma homocysteine (Hcy) expression levels are positively associated with risk of cardiovascular disease, and ERK1/2 exert anti-apoptotic and cardioprotective effects on AMI/R injury. However, the precise molecular mechanism of action underlying the effects of Hcy and the ERK1/2 signaling pathway on mitochondrial dysfunction and oxidative stress in AMI/R injury remains unclear. In the present study, AMI/R injury models were established in an animal model treated with Hcy and in H9C2 cells that were treated with hypoxia-reoxygenation. Mitochondrial function and oxidative stress were evaluated. The results demonstrated that Hcy enhanced ERK1/2 protein expression levels and oxidative stress, induced cytochrome c translocation and mitochondria dysfunction, and caused cardiac dysfunction in rats with AMI/R injury. https://www.selleckchem.com/screening-libraries.html However, an ERK1/2 inhibitor effectively protected AMI/R injury rats from Hcy-induced cardiac dysfunction and oxidative stress. In conclusion, Hcy induced mitochondrial dysfunction and oxidative stress in AMI/R injury through stimulating ROS production and the ERK1/2 signaling pathway. An ERK1/2 inhibitor may be an effective new therapeutic method for treating Hcy-induced cardiac dysfunction in patients with AMI/R injury.