Volume 7, Issue 2

Influenza pandemics with different extent occur every year in the world. It can cause high morbidity and mortality, arouse fear panic in public, and attract extensive attention worldwide. This paper reviews the research progress in epidemiological characteristics, detection methods, pathogenesis, treatment and prophylactic measures of influenza in China. It will be helpful for us to understand the current situation of influenza.

Background and Objectives Calcium-sensing receptor (CaSR) is known to regulate hypoxia-induced pulmonary hypertension (HPH) and vascular remodeling via the phenotypic modulation of pulmonary arterial smooth muscle cells (PASMCs) in small pulmonary arteries. Moreover, autophagy is an essential modulator of VSMC phenotype. But it is not clear whether CaSR can regulate autophagy involving the phenotypic modulation under hypoxia. Methods The viability of human PASMCs was detected by cell cycle and BrdU. The expressions of proliferation protein, phenotypic marker protein, and autophagy protein in human PASMCs were determined by western blot. Results Our results showed that hypoxia-induced autophagy was considerable at 24 h. The addition of NPS2390 decreased the expression of autophagy protein and synthetic phenotype marker protein osteopontin and increased the expression of contractile phenotype marker protein SMA-ɑ and calponin via suppressing downstream PI3K/Akt/mTOR signal pathways. Conclusions Our study demonstrates that treatment of NPS2390 was conducive to inhibit the proliferation and reverse phenotypic modulation of PASMCs by regulating autophagy levels.

Background and Objectives Significant rather than moderate coronary artery stenosis has been postulated to be the main substrate of plaque rupture in acute myocardial infarction (AMI). We evaluate if cavitation could influence the coronary artery plaque rupture contributing to the progression of thrombotic process. Methods We reconstructed a 3D model of the left anterior descending coronary artery (LAD) after reviewing the intravascular ultrasound (IVUS) data of 30 consecutive patients with mild to severe coronary artery disease. Results Turbulent flow or cavitation occurs in both concentric and eccentric coronary artery stenosis (≥ 75% for the former and ≥ 50% for the latter). The analysis of vapor phase demonstrated that cavitation propagated downstream, creating microbubbles, which exploded when the fluid pressure was lower than the vapor pressure at a local thermodynamic state. The relative higher vorticity magnitude (as turbulent flow in vivo angiogram) observed on the distal cap of the atherosclerotic plaque created a higher turbulence, probably able to destabilize the plaque through a micro-erosion process. Conclusions Cavitation seems to be able to promote the thrombotic occlusion within the coronary vessels due the ‘constant injuries’ created by the micro-explosion of bubbles.

The authors describe two cases of metabolic acidosis, caused by diabetic ketoacidosis in the first case and by dehydration following gastroenteritis in the second one. Both patients were followed with noninvasive end-tidal CO 2 (ETCO 2 ) monitoring. A correlation between EtCO 2 and PCO 2 and HCO 3− has been established in the literature. Noninvasive ETCO 2 is used in only 5–6% of metabolic emergencies. In contrast, users described its use as easy and convenient.

Our aim was to explore the relationship between liver cirrhosis (LC), portal hypertension (PH), and diabetes mellitus (DM). LC displayed hemodynamic alterations reflected by signs and symptoms of hypertension and hyperdynamic circulation. Portal hypertension also caused splenomegaly because of the blood flow into the spleen from the portal vessels and portal flow. The alcoholic cirrhosis displayed abnormal values (AST, ALT, AST/ALT, albumin, ammonia, bilirubin, blood platelet, erythrocytes, glucose, Hb, international normalized ratio (INR), PT, prothrombin index (PI), thymol test, white blood cell (WBC) count), which demonstrated the presence of portal hypertension, ascites, DM, infection, and coagulopathy. The evaluation of liver enzymes and other laboratories data helped to determine the severity of the condition and prognosis. Diabetes appeared to be less affecting the prognosis of patients with cirrhosis than LC itself, showing that hepatocellular failure was largely responsible for patients’ mortality rather than diabetes and its complications. Patients displayed a BMI correlating obesity, although affected by concomitant diseases that commonly cause a severe weight loss. The elevated BMI in this case was accentuated by the presence of ascitic fluid, which is responsible for the increase in weight and the inaccurate BMI evaluation. Ascites affect patients’ recovery from liver diseases. Obese patients with cirrhosis can be related to have a large amount of ascites and that physicians should be expecting to notice changes in their BMI pre- and postoperatively, subsequently making a prior classification as obese inappropriate. Disease severity could be assessed through the evaluation of PH stage, which was characterized by a significant depletion of WBC and as well as platelet counts.