Banino et al.'s approach paves the way also to a potential approach towards a better comprehension of our "second brain", i.e., the myenteric plexus. We know that enthorinal grid cells are placed in exagons and fire when a moving animal crosses their firing fields. If we examine flat mounts of whole gut slices, we find the same nervous exagonal grid, which is located preferentially in the myenteric plexus. Therefore, a theoretical, testable hypotesis can be drawn: the same topological exagonal scheme found in the enthorinal regions might enable myenteric neurons to recognize the location of food volumes or chemical substances in the gastroenteric lumen, enabling our gut to "recognize" the location of its own content. We could, therefore, be in front of an "intestinal map", based on the same mechanisms of external environment's enthorinal recognition.
A SAFER APPROACH TO UMBILICAL GRANULOMA WITH SILVER NITRATE STICK
Tozzi A. 2017. Bacteria may produce resistance to antibiotics... although never exposed to them. BMJ, https://www.bmj.com/content/358/bmj.j3418/rr-9. Response to: Llewelyn MJ, Fitzpatrick JM, Darwin E, Tonkin-Crine S, Gorton C, et al. 2017. The antibiotic course has had its day. BMJ, 358:j3418.
Llewelyn et al. are concerned about antibiotic resistance caused by drug misuse. However, studies suggest that bacteria do not need exposure to antibiotics to gain resistance. Indeed, Bhullar et al. (2012) discovered bacteria at the bottom of a 1,000 feet deep cave (Lechuguilla Cave, New Mexico) that, although isolated from humans and antibiotic drugs for four million years, are resistant to 14 different commercially available antibiotics. This finding negates the theory that bacteria only develop resistance to antibiotics when directly exposed to them. Therefore, antibiotic resistance did not evolve in the clinic just through our use, rather is natural, ancient and hard wired in the microbial pangenome. Environmental organisms as reservoirs of resistance genes that can be vehicled to other bacteria through simple horizontal transmission.
A lesson for parents: why no-vax conspiracy theories are untenable. Electronic Response to: Pediatrics, January 2018, VOLUME 141 / ISSUE 1 MeetingAbstract. Time for Your Check Up: The Impact of Vaccine Refusal on the Frequency of Physician Office Visits
One of the main claims of no-vax movements is that Health Companies promote vaccination worldwide in order to earn more. Is such a tenet true? Imagine a world without vaccinations. In this case, we would face an huge increase of diseases characterized by long-lasting sequelae: in particular, the invalidating outcomes of Poliovirus and chronic hepatitis B would be foremost, therefore providing large money incomes to Health Companies. Concering Rotavirus, it is much more expensive to cure an acute diarrhea during an hospitalization, than to prevent it. Concerning Papillomavirus vaccination, if we remove it, we would achieve a large increase of venereal infections and cervix cancer, that would require a large amount of money to be managed. To make another example, without pertussis vaccination, one every two hundred infants would die, and a large amount of the survived ones would be affected by chronic pathologies that require expensive treatments. Furthermore, Diphteritis and tetanus are potentially mortal, but they also cause, in the few surviving individuals, tremendously expensive sequelae. Therefore, the claims that Health Companies have economic benefits from vaccination procedures does not hold true.
A weird urine sample.
A 5-year female, who had suffered from a very mild strangury in the last few days, brought to the primary care pediatrician a urine sample in a winter morning, in order to perform a urine test strip for the rapid determination of ten parameters. When the mother opened the disposable urine container in front of the pediatrician, they realized that three ivory-white, half-round objects, unnoticed during the sampling, floated on the urine surface. They displayed a diameter of approximately 1 centimeters. In order to appreciate their size, notice that, in the Figure, the total diameter of the 150 ml cylinder is 5,8 cm. The three cupola-shaped structures were hard to the touch. Despite their hard plastic consistency, they cracked in 4-5 smaller pieces after a strong pressure between two fingers. The test strip did not show urinary pathological findings. Physical examination did not reveal alterations in child’s perineal and genital areas. The young female did not suffer from systemic diseases, such as hyperoxaluria or metabolic alterations. She was taking levetiracetam (oral solution), because of a recent diagnosis of early onset occipital epilepsy The mother was fully reliable and trustworthy and did not suffer from any psychiatric or psycological diseases. Note that the well mixed, non-centrifuged, protected from light, not older than two hours urine was collected in a clean, well rinsed container, free of detergents and preservatives. No one manipulated the container after the sampling.
Where did the objects come from? After a careful anamnestic investigation, it sorted out that the child suffered from a recent onset otalgia, and that the mother treated the painful symptoms with paracetamol by rectal suppository in the past two days. In order to confirm the “diagnosis”, a rectal examination was performed: traces of a white, semisolid material, compatible with the remnants of a paracetamol suppository, were found 2-3 centimeters above the dentate line.
Prevalenza di faringotonsillite da streptococco β-emolitico di gruppo A in una popolazione della Campania.
Aim of the study: to evaluate the prevalence of group A streptococcal pharyngitis in a pediatric population in a rural area of south Italy. Patients and methods: we have performed a transversal, observational study on 108 patients (median age: 5,5±3,1 years, 53 males and 55 females) with acute pharyngitis diagnosed by mean of streptococcal rapid test. Results: we outlined the presence of group A streptococcus in 39,8% of the patients examined.
Tozzi, A. A "nonlinear approach to pediatric diseases (electronic response to Hymel KP et al. Validation of a clinical prediction rule for pediatric abusive head trauma. Pediatrics. 2014 Dec;134(6):e1537-44. doi: 10.1542/peds.2014-1329). DOI: 10.13140/2.1.3360.8007
Buccigrossi V, Armellino C, Tozzi A, Nicastro E, Esposito C, Alicchio F, Cozzolino S, Guarino A. Time- and segment-related changes of postresected intestine: a 4-dimensional model of intestinal adaptation. J Pediatr Gastroenterol Nutr. 2013 Jan;56(1):40-5. doi: 10.1097/MPG.0b013e318268a9a4.
The aim of the present study was to investigate the segment- and time-related changes in rat short bowel syndrome and construct a 4-dimensional (4D) geometrical model of intestinal adaptation. Sprague-Dawley rats were divided into 3 groups: 2-day, 7-day, and 15-day postresection groups in which 75% of the jejunoileum was removed. Histological and morphometrical parameters in the remaining proximal to distal intestinal segments, from the jejunum to the distal colon, were comparatively evaluated in the groups. The data were used to construct a 4D geometric model in which villi were considered as cylinders, and their surface area was expressed as cylinder lateral area. Major adaptive changes were observed in the ileum consisting of an increase in both the diameter of base and the height of villi. A parallel reduction in their number/mm was observed. The resulting ileal architecture was characterized by a limited number of large villi. An opposite pattern was observed in the jejunum whose postresection structure consisted of an increased number of villi. No changes were observed in the colon. Postresection restructuring was early and faster in the ileum than in the jejunum resulting in an increase in absorptive area of 81.5% and 22.5% in the ileum and jejunum, respectively. Postresection adaptation is intestinal segment-specific because all of the major changes occur in the ileum rather than in the jejunum. Sparing ileal segments during resection may improve the outcome of patients undergoing extensive intestinal resection. Our 4D model can be used to test interventions aimed at optimizing postresection intestinal adaptation.
IL PEDIATRA TRA 5-10 ANNI
- Staiano A, Basile P, Simeone D, Stanco A, Tozzi A, Caria MC. 1996. Proximal esophageal pH metry in children with respiratory symptoms. The Italian journal of gastroenterology 05/1996; 28(3):136-9
- Staiano A, Santoro L, De Marco R, Stanco A, Fiorillo F, Tozzi A. 1996. Autonomic dysfunction in children with Hirschsprung’s disease. Journal of Pediatric Gastroenterology and Nutrition 05/1996; 22(4)., DOI:10.1097/00005176-199605000-00065.
- Tozzi A, Mossetti G, Miele E, D’Armiento FP, Toraldo C, Staiano A. 1997. Development of submucosal and myenteric plexuses in relation to gestational age. Journal of Pediatric Gastroenterology and Nutrition 04/1997; 24(4)., DOI:10.1097/00005176-199704000-00122.
- Tozzi A, Ascione G, Carpentieri ML, Staiano A. 1997. Intestinal neuronal dysplasia associated with cystic fibrosis. Archives of Disease in Childhood 10/1997; 77(3):277. DOI:10.1136/adc.77.3.276a.
- Oderda G, Palli D, Saieva C, Chiorboli E, Bona G, Tozzi A. 1998. Short stature and Helicobacter pylori infection in italian children: prospective multicenter hospital based case-control study. The Italian Study Group on Short Stature and H pylori. BMJ Clinical Research 09/1998; 317(7157):514-5.
- Staiano A, Tozzi A. 1998. Diagnosis and treatment of constipation in children. Current Opinion in Pediatrics 11/1998; 10(5):512-5., DOI:10.1097/00008480-199810000-00011.
- Fitzgerald JF, Troncone R, Tozzi A, Tramontano A, Toraldo C. 1998. Clinical Quiz. Journal of Pediatric Gastroenterology and Nutrition 11/1998; 27(5):546-+., DOI:10.1097/00005176-199811000-00005.
- Tozzi A, Tramontano A, Toraldo C. 1998. Clinical quiz. Long-segment Hirschsprung's disease (total colonic aganglionosis). Journal of Pediatric Gastroenterology and Nutrition 12/1998; 27(5):546,559.
- Auricchio A, Griseri P, Carpentieri ML, Betsos N, Staiano A, Tozzi A, Priolo M, Thompson H, Bocciardi R, Romeo G, Ballabio A, Ceccherini I. 1999. Double Heterozygosity for a RET Substitution Interfering with Splicing and an EDNRB Missense Mutation in Hirschsprung Disease. The American Journal of Human Genetics 05/1999; 64(4):1216-21., DOI:10.1086/302329.
- Miele M, Staiano A, Troncone R, Tozzi A, Ciarla C, Paparo F. 1999. Clinical Response to Amino Acid-Based Enteral Formula in Neurologically Impaired Children With Refractory Esophagitis. Journal of Pediatric Gastroenterology and Nutrition 05/1999; 28(5):561., DOI:10.1097/00005176-199905000-00090.
- Tozzi A, Staiano A, Tramontano A, Miele E, Toraldo C. 1999. Hyperganglionosis and Hirschsprung's disease. Journal of Pediatric Gastroenterology and Nutrition 05/1999; 28(5)., DOI:10.1097/00005176-199905000-00132.
- Staiano A, Tozzi A. 2000. Approccio alla stipsi cronica.
- Staiano A, Simeone D, Del Giudice E, Miele E, Tozzi A, Toraldo C. 2000. Effect of the dietary fiber glucomannan on chronic constipation in neurologically impaired children. Journal of Pediatrics 02/2000; 136(1):41-5., DOI:10.1016/S0022-3476(00)90047-7.
- Miele E, Tozzi A, Staiano A, Toraldo C, Esposito C, Clouse RE. 2000. Persistence of abnormal gastrointestinal motility after operation for Hirschsprung's disease. The American Journal of Gastroenterology 06/2000; 95(5):1226-30., DOI:10.1111/j.1572-0241.2000.02014.x.
- Tozzi A, De Angelis A, Tramontano A, Scoppa A, Pinto L, Staiano A. 2001. Colonic transit times in children with anorectal malformations. Journal of Pediatric Gastroenterology and Nutrition 04/2001; 32:S55., DOI:10.1097/00005176-200104001-00048.
- Tozzi A, Staiano A, Paparo F, Miele E, Maglio M, Di Meo M, Simeone D, Troncone R. 2001. Characterization of the inflammatory infiltrate in peptic oesophagitis. Digestive and Liver Disease 08/2001; 33(6):452-8., DOI:10.1016/S1590-8658(01)80021-9.
- Miele E, Staiano A, Tozzi A, Auricchio R, Paparo F, Troncone R. 2002. Clinical Response to Amino Acid-Based Formula in Neurologically Impaired Children With Refractory Esophagitis. Journal of Pediatric Gastroenterology and Nutrition 10/2002; 35(3):314-9., DOI:10.1097/00005176-200209000-00014.