Endovascular Treatment of Acquired Atheromatous Postsubclavian Aortic Coarctation

Coral reef aorta is a rare calcifying obstructive disease that involves the thoracoabdominal aorta. Similar presentations in the postsubclavian aorta may result in acquired atheromatous aortic coarctation leading to systemic hypertension and heart failure. The associated calcification makes surgical anatomic or extraanatomic bypass and thromboendarterectomy challenging. Extensive circumferential calcification often precludes endovascular intervention. We present the case of a 25-year-old man with an acquired atheromatous coarctation of the postsubclavian aorta who underwent successful endovascular treatment with use of a balloon-expandable covered stent.     

Exploring the Gut Microbiome in Myasthenia Gravis

The human gut microbiota is vital for maintaining human health in terms of immune system homeostasis. Perturbations in the composition and function of microbiota have been associated with several autoimmune disorders, including myasthenia gravis (MG), a neuromuscular condition associated with varying weakness and rapid fatigue of the skeletal muscles triggered by the host’s antibodies against the acetylcholine receptor (AChR) in the postsynaptic muscle membrane at the neuromuscular junction (NMJ). It is hypothesized that perturbation of the gut microbiota is associated with the pathogenesis of MG. The gut microbiota community profiles are usually generated using 16S rRNA gene sequencing. Compared to healthy individuals, MG participants had an altered gut microbiota’s relative abundance of bacterial taxa, particularly with a drop in Clostridium. The microbial diversity related to MG severity and the overall fecal short-chain fatty acids (SCFAs) were lower in MG subjects. Changes were also found in terms of serum biomarkers and fecal metabolites. A link was found between the bacterial Operational Taxonomic Unit (OTU), some metabolite biomarkers, and MG’s clinical symptoms. There were also variations in microbial and metabolic markers, which, in combination, could be used as an MG diagnostic tool, and interventions via fecal microbiota transplant (FMT) could affect MG development. Probiotics may influence MG by restoring the gut microbiome imbalance, aiding the prevention of MG, and lowering the risk of gut inflammation by normalizing serum biomarkers. Hence, this review will discuss how alterations of gut microbiome composition and function relate to MG and the benefits of gut modulation.     

The Occurrence of Nymphal Stage of Linguatula serrata in Water Buffaloes (Bubalus bubalis): Nymphal Morphometry and Lymph Node Pathology

The mesenteric lymph nodes (MLN) of buffaloes (n = 100) were examined for the presence of parasitic infection. The nymphal stage of Linguatula serrata was observed in two buffaloes. A single white‐coloured nymph with transversely striated spines on a segmented body, two pairs of oral suckers and hooks was observed in the MLN. The morphometrics of the nymphs were studied. The affected lymph nodes were grossly enlarged with cyst and showed pathological lesions of fibroblastic reaction with a mild underlying inflammatory zone.     

Deafness and CMT disease associated with a novel four amino acid deletion in the PMP22 gene

The molecular basis for the clinically distinct entity of deafness with Charcot-Marie-Tooth disease has not been established with certainty. The authors report deafness associated with a demyelinating neuropathy in three individuals of a family in whom a novel four-amino acid deletion in the PMP22 gene was identified. The data and review of literature suggest that in the PMP22 gene, some point mutations and small deletions in the transmembrane domain that are in close proximity to the extracellular component of the protein result in this clinically distinct entity.     

Coil occlusion of the small patent arterial duct without arterial access

BACKGROUND: Arterial access is traditionally considered mandatory during coil occlusion of the patent arterial duct. Arterial access necessitates heparinization and carries the risk of femoral artery occlusion in small children. METHODS AND RESULTS: Between July 1999 and May 2001, we attempted coil occlusion of patent arterial ducts in 104 patients without arterial access. The patients were aged from 3 months to 14 years. The median age was 2 years. They weighed 3-35 kg. The median weight was 9.8 kg. The duct diameter at pulmonary artery insertion was 1.8-3.5 mm. The patients were selected on basis of echocardiographic evaluation of duct diameter at pulmonary artery insertion and morphology of the ampulla. Doppler color flow imaging was used in the catheterization laboratory to confirm duct closure. Arterial access was required in 21 patients. The reasons included accidental puncture in 5 patients, failure to obtain venous access in 1 patient, aortic embolization in 3 patients, poor echo images in 2 patients, requirement for additional coils in 8 patients and, failure to cross the duct from pulmonary artery in 2 patients. The fluoroscopic time ranged from 2.2 to 20 min with a mean of 5.3+/-3.8 min. Immediate closure was achieved in 98 patients and this included 79 of the 83 patients in whom arterial access was avoided. Color Doppler 3-24 h later showed residual flow in 2 patients. Four patients had new-onset left pulmonary artery turbulence with peak gradients below 5 mm of mercury. Coil embolization occurred in 6 patients and all coils were retrieved. Three-month follow up information was available for 78 patients. Small residual ductal leaks were seen in 4 patients, 2 of whom had leaks at 24 h. Two patients had recanalized their ducts. CONCLUSION: It is feasible to occlude small patent arterial ducts with coils using venous access alone in carefully selected patients with excellent immediate and short-term results.     

Radiation exposure impairs luteinizing hormone signal transduction and steroidogenesis in cultured human leydig cells.

Therapeutic, accidental, and experimental radiation exposures decreased serum testosterone in males, leading to various sexual problems. Since testicular Leydig cells are the predominant source of circulating testosterone, findings on the direct effects of radiation on Leydig cell steroidogenesis and the mechanism behind such effects would be of greater importance to the use of safer radiation doses in cancer therapy and to adopt preventive or therapeutic measures to alleviate postirradiation lesions, respectively. Therefore, this study was undertaken to explore the same using cultured human Leydig cells. Testicles removed from advanced prostatic carcinoma patients were used for isolation and purification of Leydig cells. Purified Leydig cells were cultured and then exposed to different doses (2, 4, 6, 8, and 10 Gy) of fractioned gamma radiation. Normal and irradiated cells were used for luteinizing hormone (LH) receptor quantification or total RNA isolation to study LH receptor mRNA expression or LH/cyclic AMP (cAMP) stimulation test. While LH-stimulated cells were used for cAMP assay, LH- and cAMP-stimulated cells were used for the estimation of steroidogenic enzymes, testosterone and estradiol production. Radiation exposure caused adverse effects on Leydig cell steroidogenesis in a dose-dependent manner. While lower doses (2 and 4 Gy) were ineffective, higher doses (6 Gy and above) drastically decreased LH receptor, basal and LH-stimulated cAMP generation, and basal, LH-, and cAMP-stimulated steroidogenesis. While 2 Gy of radiation exposure increased the LH receptor mRNA level, other doses did not induce any significant change. Therefore, it is concluded that higher doses of radiation impair Leydig cell steroidogenesis by affecting LH signal transduction at the level of both pre- and post-cAMP generation. Decreased level of LH receptors following higher doses of radiation exposure is not coupled with impaired expression of its mRNA.     

Immunotherapy of rheumatoid arthritis: past, present and future

Rheumatoid arthritis (RA) is a chronic autoimmune disease, characterized by inflammation of the synovial lining of joints, and the destruction of cartilage and bone. Seminal studies demonstrating that pro-inflammatory cytokines, such as tumor necrosis factor-alpha (TNFalpha), are expressed in RA, has resulted in the approval of anti-TNFalpha biological therapies for its treatment. Although groundbreaking in themselves, these studies have also paved the way for further research to determine whether the targeting of other cytokines and immune pathways might aid in development of the next generation of drugs for the treatment of RA.