Physiology of erection

In these article we review the main mechanisms involved in human erection. We review and update in detail the biochemical (nitric oxide and Rho-kinase pathways), cellular (smooth muscle relaxation mechanisms), neural (autonomic and somatic pathways) and microscopic penile principles.     

Hiperhidrosis primaria. Situación actual de la cirugía del simpático

Primary hyperhidrosis-PH is an excessive sweating without known etiology. The PH is more frequent in women and in palms, soles and axillae. Medical treatment is not effective. The objective of the surgery is to remove or to disconnect sympathetic ganglia T2 (craniofacial PH or facial blushing), T3 (palmar PH) and T3–T4 (axillary PH). The surgical techniques are mainly resection/transection, ablation with electrocoagulation, sympathetic block by clipping and radiofrequency. Anhidrosis is achieved in 95% of the patients. The overall rate of complications is less than 5% and these are minor complications. The most important unwanted effect is reflex sweating, presented in 48% of the patients. Reflex sweating is more frequent in back, thorax and abdomen and it appears independently of the surgical technique. Ninety percent of the patients are very satisfied after surgery. Nowadays, thoracic sympathetic surgery is the gold standard for primary hyperhidrosis.     

Deletions in 16p13 including GRIN2A in patients with intellectual disability,various dysmorphic features,and seizure disorders of the rolandic region

Seizure disorders of the rolandic region comprise a spectrum of different epilepsy syndromes ranging from benign rolandic epilepsy to more severe seizure disorders including atypical benign partial epilepsy/pseudo‐Lennox syndrome, electrical status epilepticus during sleep, and Landau‐Kleffner syndrome. Centrotemporal spikes are the unifying electroencephalographic hallmark of these benign focal epilepsies, indicating a pathophysiologic relationship between the various epilepsies arising from the rolandic region. The etiology of these epilepsies is elusive, but a genetic component is assumed given the heritability of the characteristic electrographic trait. Herein we report on three patients with intellectual disability, various dysmorphic features, and epilepsies involving the rolandic region, carrying previously undescribed deletions in 16p13. The only gene located in the critical region shared by all three patients is GRIN2A coding for the alpha‐2 subunit of the neuronal N‐methyl‐d ‐aspartate (NMDA) receptor.     

The earliest evidence of true lambdoid craniosynostosis: the case of “Benjamina”, a Homo heidelbergensis child

Background  

The authors report the morphological and neuroimaging findings of an immature human fossil (Cranium 14) diagnosed with left lambdoid synostosis.     

Pancreatic pseudocyst drainage guided by endoscopic ultrasound

Pancreatic pseudocysts can be managed conservatively in the majority of patients but some of them will require surgical, endoscopic or percutaneous drainage. Endoscopic drainage represents an efficient modality of drainage with a high resolution rate and lower morbidity and mortality than the surgical or percutaneous approach. In this article we review the endoscopic pseudocyst drainage procedure with special emphasis on technical details.     

A Study of the Bibliometry and Areas of the Research Groups of Archivos de Bronconeumología (2003–2007)

IntroductionScientific cooperation is essential for the advance of biomedical research. Scientists set up informal groups to work together on common issues, who are the main units in the research funding system. Bibliometric and Social Network Analysis methods allow informal groups in scientific papers to be identified and characterised. The objective of the study is to identify research groups in Archivos de Bronconeumología between 2003 and 2007 period with the aim of characterizing their scientific collaboration patterns and research areas.MethodsCo-authorships, institutional collaboration relationships and the main research areas of papers published in Archivos de Bronconeumología have been identified. Co-authorship networks and institutional collaboration networks have been constructed by using Pajek software tool.ResultsA total of 41 research groups involving 171 investigators have been identified. The Collaboration Index for articles was 5.59 and the Transcience Index was 73.11%. There was institutional collaboration in 60.33% of papers. The collaboration between institutions of the same region prevails (41.03%), followed by collaborations between departments, services or units of the same institution (39.74%), inter-regional collaboration (14,97%) and international collaboration (6.83%). A total of 83.03% of articles were cited. The main research areas covered by groups were chronic obstructive pulmonary disease, asthma, lung neoplasm, bronchogenic carcinoma, smoking and pulmonary embolism.ConclusionsThe scientific production of a large number of Respiratory System Spanish research groups is published in Archivos de Bronconeumología. A notable collaboration and citation rate has been observed. Nevertheless, it is still essential to encourage inter-regional and international collaboration.     

Mechanistic contribution of ubiquitous 15-lipoxygenase-1 expression loss in cancer cells to terminal cell differentiation evasion

Loss of terminal cell differentiation promotes tumorigenesis. 15-Lipoxygenase-1 (15-LOX-1) contributes to terminal cell differentiation in normal cells. The mechanistic significance of 15-LOX-1 expression loss in human cancers to terminal cell differentiation suppression is unknown. In a screen of 128 cancer cell lines representing more than 20 types of human cancer, we found that 15-LOX-1 mRNA expression levels were markedly lower than levels in terminally differentiated cells. Relative expression levels of 15-LOX-1 (relative to the level in terminally differentiated primary normal human-derived bronchial epithelial cells) were lower in 79% of the screened cancer cell lines than relative expression levels of p16 (INK4A), which promotes terminal cell differentiation and is considered one of the most commonly lost tumor suppressor genes in cancer cells. 15-LOX-1 was expressed during terminal differentiation in three-dimensional air-liquid interface cultures, and 15-LOX-1 expression and terminal differentiation occurred in immortalized nontransformed bronchial epithelial but not in lung cancer cell lines. 15-LOX-1 expression levels were lower in human tumors than in paired normal lung epithelia. Short hairpin RNA-mediated downregulation of 15-LOX-1 in Caco-2 cells blocked enterocyte-like differentiation, disrupted tight junction formation, and blocked E-cadherin and ZO-1 localization to the cell wall membrane. 15-LOX-1 episomal expression in Caco-2 and HT-29 colon cancer cells induced differentiation. Our findings indicate that 15-LOX-1 downregulation in cancer cells is an important mechanism for terminal cell differentiation dysregulation and support the potential therapeutic utility of 15-LOX-1 reexpression to inhibit tumorigenesis.     

Osteocalcin as a negative regulator of serum leptin concentration in humans: insight from triathlon competitions

Osteocalcin is a hormone produced by osteoblasts which acts as a negative regulator of fat mass, protecting against diet induced obesity and insulin resistance in rodents. To determine if an acute increase in osteocalcin concentration is associated with opposed changes in circulating leptin levels and insulin resistance we studied 15 middle and long distance male triathletes, (age 32.1 ± 6.9 years), before and 48 h after an Olympic (OT) or an Ironman (IT) triathlon competition. Muscle power, anaerobic capacity, body composition (dual-energy X-ray absorptiometry), and serum concentrations of testosterone, dihydrotestosterone, osteocalcin, leptin, glucose, insulin and insulin resistance (HOMA) were determined pre- and post-race. Pre- and 48 h post-race total and regional lean body mass was not altered, but fat mass was similarly increased (~250 g) 48 h after the competitions. This elicited an increase in plasma leptin of 33% after the IT while it remained unchanged after the OT, likely due to a 25% increase in plasma osteocalcin which occurred only after the OT (all p < 0.05). Post-race HOMA remained unchanged in OT and IT. Performance was normalized 48 h after the competitions, with the exception of a slightly lower jumping capacity after the IT. Serum testosterone concentration tended to decrease by 10% after the IT whilst dihydrotestosterone was reduced by 24% after the IT. In conclusion, an acute increase in serum osteocalcin concentration blunts the expected increase of serum leptin concentration that should occur with fat mass gain. This study provides evidence for osteocalcin as a negative regulator of serum leptin in humans.     

Epidermal growth factor receptor and K-Ras mutations and resistance of lung cancer to insulin-like growth factor 1 receptor tyrosine kinase inhibitors

BACKGROUND:

Most patients with nonsmall cell lung cancer (NSCLC) have responded poorly to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs). The authors investigated the involvement of insulinlike growth factor 1 receptor (IGF‐1R) signaling in primary resistance to EGFR TKIs and the molecular determinants of resistance to IGF‐1R TKIs.

METHODS:

Phosphorylated IGF‐1R/insulin receptor (pIGF‐1R/IR) was immunohistochemically evaluated in an NSCLC tissue microarray. The authors analyzed the antitumor effects of an IGF‐1R TKI (PQIP or OSI‐906), either alone or in combination with a small‐molecular inhibitor (PD98059 or U0126) or with siRNA targeting K‐Ras or mitogen‐activated protein kinase/extracellular signal‐regulated kinase kinase (MEK), in vitro and in vivo in NSCLC cells with variable histologic features and EGFR or K‐Ras mutations.

RESULTS:

pIGF‐1R/IR expression in NSCLC specimens was associated with a history of tobacco smoking, squamous cell carcinoma histology, mutant K‐Ras, and wild‐type (WT) EGFR, all of which have been strongly associated with poor response to EGFR TKIs. IGF‐1R TKIs exhibited significant antitumor activity in NSCLC cells with WT EGFR and WT K‐Ras but not in those with mutations in these genes. Introduction of mutant K‐Ras attenuated the effects of IGF‐1R TKIs on NSCLC cells expressing WT K‐Ras. Conversely, inactivation of MEK restored sensitivity to IGF‐TKIs in cells carrying mutant K‐Ras.

CONCLUSIONS:

The mutation status of both EGFR and K‐Ras could be a predictive marker of response to IGF‐1R TKIs. Also, MEK antagonism can abrogate primary resistance of NSCLC cells to IGF‐1R TKIs. Cancer 2012. © 2012 American Cancer Society.