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Objective: To investigate the mechanism of MCP-1 and TGF-β regulation by TAK242 in COPD rats. Methods: Thirty-six SD rats were randomly divided into normal, COPD control, and TAK242 groups. The normal group was freely fed, and the other groups used the method of fumigation plus lipopolysaccharide tracheal drip to establish an experimental animal model of COPD. After successful modeling, each experimental group received 0.9% NaCl solution and corresponding drugs by intraperitoneal injection for 7 d. After drug administration, lung function was examined; pathological changes in lung tissue were observed by light microscopy with hematoxylin-eosin staining; mRNA expression of MCP-1 and TGF-β was detected by q-PCR; and protein expression of MCP-1 and TGF-β in lung tissue was detected by Western blot and IHC, TGF-β protein expression in rat lung tissue. Results: Compared with the normal group, rats in the COPD control group showed signs and symptoms of COPD, decreased lung function, and increased expression of MCP-1 and TGF-β. The TAK242 group showed decreased expression of MCP-1 and TGF-β compared to the COPD control group. Conclusion: MCP-1, and TGF-β played a crucial role in the early stage of COPD fibrosis. TAK242 could ameliorate airway inflammation and inhibit the progression of COPD lung fibrosis in pre-existing rats in COPD model rats.

Experience with allogeneic hematopoietic stem cell transplantation (HSCT) in mycosis fungoides/Sezary syndrome (MF/SS) is limited to a small number of case reports and case series [1,2]. The advantage of allogeneic HSCT has been indicated in progressive disease in the review of CIBMTR study groups [3]. A consensus is still not available about the intensity and the content of the conditioning regimen due to the rarity of the disease and heterogeneous patient groups.

Uterine torsion is a rare life-threatening event that happens at any age or any gestational age. By definition, it consists of a rotation of more than 45 degrees around the long axis of the uterus. The reported cases have variable presentations. The uterine torsion can happen without any sequelae either for the fetus or the mother. However, fetal and maternal mortalities were also reported in such a case. We hereby, report the case of a 29-year-old female patient, with previous four Normal Vaginal Deliveries, pregnant with twins, presenting at 36 weeks gestation with an irreducible uterine torsion at the third trimester of her pregnancy complicated by maternal and fetal deaths. We concluded that the prognosis is improved as long as the management is done rapidly. More data is needed to know about the genetic predilection and the characteristics of imaging workup for a rapid preoperative diagnosis of this condition. 

A case study on Jakob Erdheim-Chester disease. Jakob Erdheim, pathologist, collector, scientist and educator was born in 1874 in Galicia and received his medical degree from the University of Vienna in 1900. He became interested in pathology and joined the Pathology Institute of the Municipal Hospital (Lainz) of Vienna

Background: Subclavian venous access for pacemaker lead insertion is a common procedure and is normally considered safe in the hands of an expert. However, subclavian venepuncture is not without complications, starting from mild subcutaneous hematoma to pneumothorax. We here present a case of hemoptysis occurring after difficult subclavian vein puncture, which subsequently improved on conservative management only. Case Summary: A 65-year-old gentleman, post aortic valve replacement had persistent high-grade AV block and was taken up for a dual chamber pacemaker implantation. Immediately following venous access, he had a bout of hemoptysis, which recovered on its own. Post procedure chest x-ray was suggestive of alveolar hemorrhage which cleared gradually in next three-four days. Discussion: Post subclavian venepuncture hemoptysis is known; but it is a rare complication, arising either because of lung parenchyma injury or arterial injury. This is mostly benign and improves on conservative management only; however rarely it may be massive and life threatening where transcatheter arterial embolization may be required.

The Coronavirus disease-2019 (COVID-19), has become a worldwide pandemic and the scientific communities are struggling to find out the ultimate treatment strategies against this lethal virus, Severe Acute Respiratory Syndrome Coronavirus–2 (SARS-CoV-2). Presently, there is no potential chemically proven antiviral therapy available in the market which can effectively combat the infection caused by this deadly virus. Few vaccines are already developed but it is not clear to the scientific community how much efficient they are to combat SARS-CoV-2. Mode of transmission and symptoms of the disease are two important factors in this regard. Rapid diagnosis of the COVID-19 is very much important to stop its spreading. In this scenario, a complete study starting from symptoms of the disease to vaccine development including various SARS-CoV-2 detection techniques is very much required. In this review article, we have made a partial analysis on the origin, virology, global health, detection techniques, replication pathways, doses, mode of actions of probable drugs, and vaccine development for SARS-CoV-2.

A key platform underpinning the traditional understanding of the cardiovascular system, with respect to the behavior of large arterial vessels, is Otto Frank’s Windkessel Hypothesis [1]. This hypothesis posits simply that the smooth muscle walls of large arteries do not undergo rhythmic contractions in synchrony with the heartbeat but, rather, behave as passive elastic tubes undergoing distension from pulsatile pressure waves. The Windkessel Hypothesis is elegant, well described for over a century, ingrained in the understanding of cardiovascular medicine and physiology, and simply wrong. Several groups have now shown that the arterial smooth muscle wall undergoes rhythmic activation in synchrony with the heartbeat in a variety of tissues, including human brachial artery; canine coronary, femoral, and carotid arteries; rabbit aorta; feline pulmonary artery and rodent aorta [2-8]. The phasing of these events is such that the upstroke of the contraction slightly precedes the upstroke of the pulse wave, suggesting nomenclature for the events as pulse synchronized contractions, or PSCs [3,6-8]. PSCs have been found to be of neurogenic origin, sensitive to the neural blocker tetrodotoxin [3,8]. Although the specific neural pathways regulating PSCs have not been elucidated, the alpha-adrenergic system is at least partially involved, as evidenced by reduction or blockade of PSCs by the alpha-adrenergic blocker phentolamine [8]. Further, PSCs have not been observed following vessel excision in in vitro studies, as an intact nervous system is not present. The pacemaker for the PSC resides in the right atrium, as suggested by two lines of evidence. First, pacing of the right atrial region to faster than spontaneous frequencies leads to a one-to-one correspondence of PSC frequency with the stimulation rate [3]. Additionally, excision of the right, but not the left, atrial appendage results in elimination of PSCs [3]. As the pacemaker region for PSCs and the heartbeat both lie in the right atrium, this may potentially allow for coordination between the heartbeat and pulse wave with PSCs [3,5,8]. Extensive evaluations also have been performed showing the PSC was not an artifact produced either by cardiac contractility or from the vessel distension from the pulse wave [3,5,6].

Symptomatic vasospasm represents an uncommon complication of perimesencephalic nonaneurysmal subarachnoid hemorrhage (SAH) which is a benign form of SAH without any recognizable source of bleeding accounting for about 15% of non-traumatic SAH [1,2]. 

Idiopathic Pulmonary Fibrosis (IPF) is a chronic and progressive disease without treatment that leads to death. Therefore, to control its progression to pulmonary hypertension is still a challenge. Moreover, there is no study that has investigated the Renin-Angiotensin System in patients with IPF. Objective: Verify the plasma concentrations of Angiotensin I, Angiotensin II (AngII), Angiotensin-(1-7) [Ang- (1-7)] and Alamandine in patients with IPF. Methods: Ten IPF patients, with or without PH, were included, and ten controls matched by sex and age. Quantitative plasma peptide concentrations (PPC) were expressed as mean and standard deviation or median and interquartile range. The Student Newman-Keuls t test was used for parametric data, Mann-Whitney for nonparametric data and, to compare proportions, the Fisher exact test was performed. The associations between clinical variables and the PPC were evaluated by Pearson or Spearman correlation coefficients. A p ≤ 0.05 was considered statistically significant. Results: The Alamandine plasma concentration was significantly (365%) lower in the IPF group and positively associated (r = 0.876) with pulmonary artery pressure (PAP). In addition, only in control group, the forced expiratory volume (FEV1%) was positively associated (p = 0.758) with Ang-(1-7). Conclusion: This study showed, for the first time, that there is a decrease in Alamandine participation in patients with IPF. The ACE-AngII-AT1 axis may be more active in this disease. In addition, our results suggest that Alamandine might be compensating the increase in PAP, as well as the Ang-(1-7) is improving the forced expiratory volume.

Introduction: Diffuse axonal injury (DAI) is a major cause of disability in the pediatric patient. Herein we describe the MRI/DWI findings in a case with DAI. We also discuss the current role of CT and MRI with DWI in the evaluation of DAI. Aim of the study: To stress the role of diffusion-weighted imaging in diffuse axonal injury. Methods: A pediatric patient, who was hospitalized in the ICU, was submitted to MRI with DWI for the evaluation of brain lesions. The patient was scanned with T1-weighted images, T2-weighted images, FLAIR, T2*-weighted images and diffusion weighted images. Result: Brain lesions caused by DAI were more conspicuous on diffusion-weighted images compared to FLAIR images. T2*-weighted images were a helpful adjunct in showing micro-hemorrhages. Conclusion: T2*-weighted images and FLAIR images alone underestimate the true extent brain lesions in DAI compared to DWI.