32^nd World Pediatrics Conference December 04-05, 2019 Barcelona, Spain

Biography:

K. M. Yacob is a practicing physician in the field of healthcare in the state of Kerala in India for the last 31 years and very much interested in basic research. His interest is spread across the fever, inflammation and back pain. He is a writer. He has already printed and published nine books on these subjects. He wrote hundreds of articles in various magazines. After scientific studies, we have developed 8000 affirmative cross checking questions. It can explain all queries related to fever.

Abstract:

As you aware, if temperature increases (Absence of  fever)after 31 degree Celsius , Warm sensitive neurons increase their firing rate and inhibit Cold sensitive neurons as core temperature increases. As temperature drops, the firing rate of Warm sensitive neurons decreases, reducing their inhibition, and Cold sensitive neurons which respond by increasing their firing rates. On the contrary to increase of temperature, in fever the firing rate of Warm sensitive neurons decreases, the firing rate of Cold sensitive neurons increases as core temperature increases. inhibit warm sensitive neurons. The temperature increasing and decreasing controlled by the brain. The firing rate of Warm sensitive neurons and Cold sensitive neurons also controlled by the brain.When the disease becomes threat to life or organs, blood circulation decreases. Temperature of fever will emerges to increase prevailing essential blood circulation. WBC and their products stimulate the brain to increase temperature by increasing the firing rate of Cold sensitive neurons and decreasing the firing rate of Warm sensitive neurons. And it acts as a protective covering of the body to sustain life. There is no  way other than this for a sensible and discreet  brain to increase temperature. If the aim of   Cold sensitive neurons increasing their firing rates in hypothermia is to increase temperature, then the aim of Cold sensitive neurons  increasing their firing rates during fever is also to increase temperature.

How can we prove that W neurons decreases and C neurons increases in fever to protect the  life or organ?

If we ask any type of question related to fever by assuming that the Warm sensitive neurons decreases and Cold  neurons increases in fever to protect the  life or organ we will get a clear answer. If avoid or evade from this definition we will never get proper answer to even a single question If we do any type of treatment  by assuming  that the Warm sensitive neurons decreases and Cold  neurons increases in fever to protect the  life or organ , the body will accept, at the same time body will resist whatever treatment to decrease temperature and blood circulation. No further evidence is required to prove The Warm sensitive neurons decreases and Cold  neurons increases in fever to protect the  life or organ.

Biography:

K. M. Yacob is a practicing physician in the field of healthcare in the state of Kerala in India for the last 31 years and very much interested in basic research. His interest is spread across the fever, inflammation and back pain. He is a writer. He has already printed and published nine books on these subjects. He wrote hundreds of articles in various magazines. After scientific studies, we have developed 8000 affirmative cross checking questions. It can explain all queries related to fever.

Abstract:

All treatments for fever are based on the belief  that  fits is the result of  41 degree Celsius temperature and  it  damages cells of  brain and body. At the same time there is no evidence based   tests or concrete  diagnosing  methods  to the  belief  that  fits and brain damage  is the result of  pyrexia. Necessary ingredients to destroy brain cells  and fits cannot be seen  in fever.In pyrexia or absence of fever  a fainted  patient fell on the floor with unconscious state and destroy cells of brain, and necessary ingredients to  become conscious are same.

When disease increases essential blood circulation and energy level also decreases. The vertical height between heart and brain is more than one feet. When the disease becomes severe, ability to pump the  blood to the brain decreases. As a result of this   brain cells are damaged. so the patient might be paralyzed or may even die.

In pyrexia or absence of fever,  when blood flow to the brain decreases and fits are formed. There is no other  way than  this  to increase  blood circulation  to the brain.It is  a sensible and discreet  action of brain to protect the  life or organ.

 Recovery from  Fits.

The patient become conscious before the time to get decreasing the temperature of fever. When the fainted patient lie on the floor, the vertical height between heart and brain is decreased, blood circulation increased to brain.

Self checking  methods.

When the fainted patient lie on the floor,The patient can stand straight and lie on bed alternatively.Then the patient can experience  himself the intensity of blood circulation.T he patient can experience when he stand  his blood circulation decreases and when lie on the bed the blood circulation decreases.Besides that he can also experience increased blood circulation when lie on the bed raise the foot higher than head.

Biography:

Natalia Antonova completed her PhD in the year 2013 from North-Western State Medical University named after I.I. Mechnikov, St-Petersburg, Russia. She works as a paediatrician and children at the Tallinn Children's Hospital. Dr. Antonova is an author of 15 articles and 10 oral presentations and lectures for family doctors in Estonia. In 2011 she completed Clinical attatchment in paediatrics at Al Wasl Maternity & Paediatric Hospital in Dubai, UAE. She is a member of Open American/Austrian University and participated in 2 in Saltzburg CHOP seminar in Pediatric Pulmonology (2010) and Pediatric Infectious Diseases (2017) with the clinical cases presentations. X.2016-VI.2017 she completed a EULAR on-line course in Paediatric Rheumatology.

Abstract:

The pathogenesis of the pediatric disorder periodic fever, aphthous stomatitis, pharyngitis, cervical adenitis (PFAPA) syndrome is unknown. It is regarded as an autoinflammatory process. Disease onset is usually before the age of five and generally resolves before puberty with no consequences for the patient. Children are asymptomatic between episodes and show normal growth. No specific diagnostic test for PFAPA is currently available. Syndrome has overlapping symptoms with other periodic fever syndromes with a known genetic cause. Genomic analysis of familial cases by genome-wide linkage analysis and whole-exome sequencing did not reveal rare variants in a single, common gene. In addition, genetic variants that are known to cause other autoinflammatory syndromes have been found in PFAPA patients, but the impact of these genetic variants in PFAPA syndrome is still unknown.

A 2-year Caucasian/Azerbaijan girl demonstrated repeated fever episodes with high levels (90-200 mg/l) of C-reactive protein (CRP) since 6 mo. She was observed regularly because of microcephalus, slight developmental delay and growth retardation, muscle hypotonus and dysmorphic phenotype (broad forehead, hypertelorism, micrognathia, and retrognathia, fluffy eyebrows, long and tight eyelashes, long filtrum, narrow lips). On genetic consultation, she was diagnosed with 7p22 microdeletions. During a period of January-October 2018, she was hospitalized 6 times with high fever, cervical l/adenitis and sore throat (3 times with aphthous pharyngitis). Different laboratory tests and instrumental investigations were performed and were normal: abdomen ultrasound, chest X-ray, EKG and EHHOKG, ANA, HIV, Borreliosis serology and Quantiferron test, urine test, and urine culture. Cervical ultrasound revealed increased lymphoid nodules with normal structure. In a period of January-July of 2018, she received 4 antibiotic courses because of high CRP levels and pharyngitis. A blood test revealed no neutropenia, Sedimentation rate was always increased up to 20-40 mm/t, procalcitonin level and blood culture repeatedly negatives. Brain MRI with spectroscopy was performed to exclude intracranial pathology because of congenital problems. ENT repeated consultations excluded otitis media, but adenoid hypertrophy was considered.

PFAPA was suspected because of typical clinical symptoms (repeated episodes of fever with aphthous pharyngitis, cervical l/adenitis and high CRP levels, absence of neutropenia).  Prednisolone treatment 1 mg/kg per os was used twice with excellent effect. Adenotomy with tonsillectomy was performed in October 2018. After this treatment in a period of November 2018- May 2019 the patient was ill 4 times with no high fever (gastroenteritis, conjunctivitis, rhinopharyngitis and Varicella with otitis media ) and just once needed antibiotic treatment.

Sequencing of genes was performed to exclude MEFV, MVK, TNFRSF1A, IL1RN, and other gene abnormalities, using Illumina TruSightOne expanded panel (6700 genes). No monogenic fever syndrome was revealed.

Biography:

Dr. Harvinder Kaur obtained her Doctoral (PhD) degree on the Growth of Symmetric and Asymmetric SGA infants from PGIMER, Chandigarh, India. Currently, she is working as Assistant Professor in Child Growth & Anthropology Unit of the Department of Pediatrics. She has over 15 years of experience in conducting longitudinal, auxological, nutritional and maturational studies on normal and sick children. She has published 22 research papers in Journals of National and International repute.

Abstract:

Age and sex specific percentile growth charts for body weight and crown-heel length (CHL) of full-term 100 symmetric small for gestational age (SGA) (boys: 50, girls: 50), 100 asymmetric SGA (boys: 50, girls: 50) and 100 appropriate for gestational age (AGA) (boys: 50, girls: 50) infants representing upper socioeconomic strata have been presented. Ponderal Index (PI) was used to categorize SGA babies into symmetric SGA (PI ≥ 2.2 g/cm³) and asymmetric SGA (PI < 2.2 g/cm³). Body weight and CHL of the babies were measured at birth, 1, 3, 6, 9 & 12 months of age in the Growth Laboratory/Clinic of Advanced Pediatrics Centre, PGIMER, Chandigarh, India using standardized techniques and instruments following a mixed-longitudinal growth research design. The 3rd, 5th, 10th, 25th, 50th, 75th, 90th, 95^th and 97th percentiles were computed using formulae given by Tanner et al (1966) after applying Healy’s (1962) correction. The 50^th percentile plotted for body weight & CHL of SGA and AGA infants demonstrated a continuous increase throughout infancy. As compared to their normal Indian, Western, MGRS and AGA counterparts, the curves plotted for SGA infants of the two types and sexes ran below throughout infancy. However, the magnitude of this deficit was recorded to be more in symmetric than asymmetric SGA infants. Growth charts provided may be used for comparative purpose and to detect nutritional deficits and growth aberrations of full-term SGA and AGA infants inhabiting north-western parts of India.